Disclaimer 

The contents of this document do not necessarily reflect the views and policies of the 

National Oceanic and Atmospheric Administration (NOAA) or the United States Coral 

Reef Task Force (USCRTF), nor is it intended to be an opinion beyond the scientific or 

other results of its authors. The mention of trade names or commercial products does not 

constitute endorsement or recommendation for their use by NOAA or USCRTF.

About This Document 

Editor’s Acknowledgements – This document was prepared and printed with support 

from NOAA through the Coral Reef Conservation Program. Layout and design were 

provided by Sylvia B. Galloway, Cheryl M. Woodley, NOAA NOS NCCOS CCEHBR, 

and Andy Bruckner, NOAA NMFS HC. Andy Bruckner, Sylvia Galloway, Jennifer 

Kozlowski, Jo-Ann Leong, Stephanie Venn-Watson, Cheryl Woodley and Thierry Work 

provided technical edits. 

Cover Photographs - The front cover photograph was contributed by Thierry Work and 

the back cover composite photographs were contributed by Thierry Work with artwork 

by Jim Nicholson. 

Citation – Please cite this report as follows: 

 

Galloway, S.B., Bruckner, A.W. and Woodley, C.M. (eds.), 2009. Coral Health and 

Disease in the Pacific: Vision for Action. NOAA Technical Memorandum NOS NCCOS 

97 and CRCP 7. National Oceanic and Atmospheric Administration, Silver Spring, MD 

314pp. 

Citation for an individual ‘white paper’ (e.g., Issues Unique to the Pacific paper) 

Gawal M, 2009. Overview of Issues Unique to the Pacific: Biological & Social 

Perspectives. pp. 162-167. In: Galloway, S.B., Bruckner, A.W. and Woodley, C.M. 

(eds.), 2009. Coral Health and Disease in the Pacific: Vision for Action. NOAA 

Technical Memorandum NOS NCCOS 97 and CRCP 7 National Oceanic and 

Atmospheric Administration, Silver Spring, MD 314pp. 
 

Coral Health and Disease in the Pacific: 

Vision for Action

Report Editors: 

SB Galloway, CM Woodley 

NOAA/NOS/NCCOS 

Center for Coastal Environmental Health and Biomolecular Research 

AW Bruckner 

NOAA/NMFS 

Habitat Conservation 

NOAA Technical Memorandum NOS NCCOS 97 

NOAA Technical Memorandum Coral Reef Conservation Program 7 

June 2009 

United States Department 

 of Commerce 

National Oceanic and 

Atmospheric Administration 

National Ocean Service 

Gary Locke Jane Lubchenco John (Jack) H. Dunnigan

Secretary Administrator Assistant Administrator 

 
 
i 

TABLE OF CONTENTS

TABLE OF FIGURES............................................................................................ iii

TABLE OF TABLES............................................................................................. iii

EXECUTIVE SUMMARY....................................................................................... 1

Recommendations............................................................................................. 4

OPENING REMARKS............................................................................................ 8

PREFACE............................................................................................................ 11

INTRODUCTION................................................................................................. 14

Physiology & Pathology Working Group (PPWG)..................................................... 16

Toxicology & Ecological Epidemiology Working Group (TEEWG)................................ 16

Pathology of Infectious Disease Working Group (PDWG)........................................... 16

Preventing & Responding to Coral Disease in the Pacific Region: 

Management Perspectives Working Group (MWG)............................................... 16

A. PHYSIOLOGY & PATHOLOGY........................................................................ 18

Background.................................................................................................... 18

Challenges and Recommendations........................................................................ 19

Physiology & Pathology Working Group Members................................................... 37

B. TOXICOLOGY & ECOLOGICAL ASSESSMENT.................................................. 38

Background.................................................................................................... 38

Challenges and Recommendations........................................................................ 39

Toxicology & Ecological Assessment Working Group Members................................... 55

C. PATHOLOGY OF DISEASE.............................................................................. 56

Background.................................................................................................... 56

Challenges and Recommendations........................................................................ 57

General Recommendation.............................................................................. 58

Pathology of Disease Working Group Members....................................................... 63

D. MANAGEMENT PERSPECTIVES....................................................................... 64

Background.................................................................................................... 64

State of coral Disease Understanding and Management in the 

Pacific........................... 

65

Challenges and Recommendations........................................................................ 67

General Recommendation.............................................................................. 69

Management Perspectives Working Group Members................................................ 81

E. WHITE PAPERS............................................................................................. 82

I. INTRODUCTION - SETTING THE STAGE..................................................... 83

Coral Disease And Health Consortium By Cheryl Woodley...................................... 83

Studying Coral Diseases: Understanding the Norm By E. Kramarsky-Winter................. 89

II. GLOBAL PERSPECTIVE OF CORAL DISEASE.............................................. 90

The GlobalPerspective of Incidence and Prevalence of Coral Diseases 

By Andrew Bruckner.................................................................................... 90

World Bank Project: Coral Disease Working Group By Bette Willis............................ 122

III. HISTORICAL PERSPECTIVE – LESSONS LEARNED...................................... 126
 

ii 

Progress in Understanding Coral Diseases in the Caribbean by Andrew Bruckner........... 126

IV. STATE OF KNOWLEDGE IN THE PACIFIC.................................................... 162

Overview of Issues Unique to the Pacific: Biological & Social Perspectivies 

By Michael J. Gawel................................................................................ 162

Baseline Levels of Coral Disease in the NorthwesternHawaiian Islands 

By Greta Aeby....................................................................................... 168

Report 1: Baseline Levels of Coral Disease in the Northwestern Hawaiian Islands 

by Greta Aeby........................................................................................ 168

Report 2: French Frigate Shoals Reef Health Surveys by Thierry Work et al........ 169

Current Knowledge of Diseases in US Territories/Freely Assoc. States 

By Thierry Work..................................................................................... 189

Report 1: Coral and Crustose Coralline Algae Disease on the Reefs of American 

Samoa by Greta Aeby et al....................................................................... 190

Report 2: Johnston Atoll Reef Health Survey by Thierry Work et al.................. 214

Coral Disease on the Great Barrier Reef and in the Western Pacific 

By Bette Willis et al................................................................................. 234

V. PATHOLOGY AND EPIDEMIOLOGY........................................................... 242

Disease and the Diagnostic Process By Gary Wobeser............................................. 242

Evolutionary Ecology and Disease Emergence: The Big Picture By Bruce Wilcox......... 244

Emerging Infectious Diseases By Stephanie Venn-Watson...................................... 245

Wildlife Disease Investigations 101 By David A. Jessup.......................................... 248

VI. COMMUNICATION TO MAKE A DIFFERENCE............................................ 256

Scientists, the Public and the Politicians: How Do We Connect for Reef’s Sake? 

 By Jeffery Allen..................................................................................... 256

VII.TECHNOLOGIES FOR THE FUTURE OF CORAL HEALTH............................. 261

Potential Technological Developments for Coral Disease Monitoring 

By Melissa Bos..................................................................................... 261

Leveraging Post Genomic Tools and Systems Biology Approaches to Accelerate the 

Understanding of Coral Disease and Effectively Monitor the Health of Tropical Reef 

Ecosystems By Eric J. Mathur......................................................................... 264

ACKNOWLEDGEMENTS...................................................................................... 266

REFERENCES...................................................................................................... 269

APPENDIX I. MEETING AGENDA.......................................................................... 284

APPENDIX II. PREVIOUSLY RECOMMENDED CNIDARIAN ‘MODEL SPECIES’ AND 

THEIR JUSTIFICATION FROM PEER-REVIEWED LITERATURE............................... 287

APPENDIX III. CORAL MODEL SPECIES SUPPLEMENTARY INFORMATION.............. 290

APPENDIX IV. BIOGRAPHICAL SKETCHES............................................................. 291

APPENDIX V. LIST OF PARTICIPANTS................................................................... 309

APPENDIX VI. OPINION PAPER – TRANSMISSION EXPERIMENTS............................ 312

 
iii 

TABLE OF FIGURES 

Figure I.1a Global Distribution of Coral Diseases Reported in 1984 .........................15 

Figure I.1b Global Distribution of Coral Diseases Reported in 2004 ........................16 

Figure A.1 Pocillopora damicornis .................................................................................24 

Figure A.2 Stylophora pistillata ......................................................................................25 

Figure A.3 Porites rus .....................................................................................................25 

Figure A.4 Galaxea fascicularis .....................................................................................26 

Figure A.5 Fungia scutaria .............................................................................................27

Figure A.6 Acropora formosa .........................................................................................28 

Figure A.7 Acropora millepora .......................................................................................29 

Figure B.1 Methodology for Ecosystem Epidemiology ...............................................41 

Figure B.2 Integrated Framework for Environmental Assessment ...........................55 

Figure C.1 Disease Outbreak Response ........................................................................59 

Figure C.2 Scheme for Determining the Nature of a Communicable Disease ..........61 

TABLE OF TABLES 

Table B.1 Coral Health/Disease Indicators ..................................................................43

Table B.2 Indicators of Coral Health & Disease: Field Observations .......................46

Table B.3 Indicators of Coral Health & Disease: Laboratory Data...........................47

Table B.4 Identification of Risk Factors .......................................................................49
 
 

1 

EXECUTIVE SUMMARY 

“We are studying arguably the most complicated ecosystem on the face of the Earth, and 

it is under serious threat.....We have an incredibly important message, if this ecosystem 

dies, if this ecosystem is otherwise perturbed to an extent that it cannot recover, not only 

does it spell potential disaster for this spaceship we call Earth, but there is no less than 

80 emerging economies, nations that are entirely or nearly entirely dependent on coral 

reef ecosystems whether it be for the economy or for the subsistence.” (Gary Ostrander, 

Vice Chancellor for Research at the University of Hawaii, opening remarks) 

Shallow coral reefs in the IndoPacific contain the highest diversity of marine organisms 

in the world, with approximately 1500 described species of fish, over 500 species of 

scleractinian corals, and an estimated 1-10 million organisms yet to be characterized 

(Reaka-Kudla et al. 1994). These centers of marine biodiversity are facing significant, 

multiple threats to reef community and habitat structure and function, resulting in local to 

wide-scale regional damage. Wilkinson (2004) characterized the major pressures as 

including (1) global climate change, (2) diseases, plagues and invasive species, (3) direct 

human pressures, (4) poor governance and lack of political will, and (5) international 

action or inaction. 

Signs that the natural plasticity of reef ecosystems has been exceeded in many areas from 

the effects of environmental (e.g., global climate change) and anthropogenic (e.g., land 

use, pollution) stressors is evidenced by the loss of 20% of the world’s coral reefs 

(Wilkinson 2004). Predictions are that another 24% (Wilkinson 2006) are under 

imminent risk of collapse and an additional 26% are under a longer term threat from 

reduced fitness, disease outbreaks, and increased mortality. These predictions indicate 

that the current list of approximately 30-40 fatal diseases impacting corals will expand as 

will the frequency and extent of “coral bleaching” (Waddell 2005; Wilkinson 2004). 

Disease and corallivore outbreaks, in combination with multiple, concomitant human 

disturbances are compromising corals and coral reef communities to the point where their 

ability to rebound from natural disturbances is being lost. 

Pacific reefs, in general, have been considered in good condition and most resource 

managers have no real concern about coral disease (regardless of whether the cause is an 

infectious agent or anthropogenic pollution); this ‘good’ condition status may only be a 

reflection of inadequate information for many areas. In fact, the U.S. state of coral reef 

ecosystems 2005 report (Waddell 2005) refutes this by showing an increase in disease 

reports throughout U.S. states, territories and freely associated states and documents a 

growing perception that coral disease may be a threat to Pacific reefs. Increased findings 

of coral disease from the World Bank Coral Disease Working Group (WBCDWG) and 

NOAA/USGS disease monitoring programs provide ample evidence that disease is 

present in Pacific reefs and may, in fact, be increasing. For example, in 2004, the 

WBCDWG recorded 12 syndromes at six survey sites; including four syndromes that had 

not been previously recorded (Waddell 2005). Some experts warn that Pacific coral reefs 

are on a trajectory of degradation similar to that experienced in the Caribbean Basin 

where coral reefs are decimated. 
2 

Though the proliferation of coral reef diseases is a sign of a sick ocean environment, this 

realization can also be used as an instrument of change. There is growing evidence that 

the increased severity and prevalence of these diseases is directly linked to human 

activities, such as pollution washing off the land, heat stress to corals, and through 

overfishing of organisms that can control macroalgae and pest species like corallivores. 

By developing an understanding of disease dynamics, causal links can be determined and 

factors driving these system failures can be identified. Developing such an understanding 

can move us toward the goal of health management and preventative care for coral reefs. 

Recognizing the need for a strategic plan of action to combat and avert a possible health 

crisis for Pacific Reefs, the Coral Disease and Health Consortium (CDHC) convened a 

workshop to help organize and coordinate a U.S. scientific effort focused specifically on 

coral health issues in the Pacific. The goal was to develop an action plan that would 

enable regional scientific efforts to detect, identify, characterize, and manage coral 

diseases in the Pacific. This report documents the proceedings of this workshop: Coral 

Health and Disease in the Pacific: Vision for Action. The goals of the workshop were 

to: 

Synthesize the state of knowledge of Pacific coral diseases; 

Discuss the concepts and principles of disease, their use in investigating causation 

and how this can be applied to corals; 

Characterize the difficulties in identifying, defining and managing disease in coral; 

and 

Develop a Strategic Research Plan that 

identifies knowledge gaps that impede understanding coral disease mechanisms 

(i.e., pathology), and limit elucidation of causes, significance or control of coral 

disease (i.e., epidemiology); 

recommends directed research and education to fill these knowledge gaps; 

standardizes methods for investigating coral disease outbreaks considering both 

biotic and abiotic etiologies; 

addresses issues relative to the management of coral reef resources; and 

fosters collaboration among CDHC partners, stakeholders, key marine resource 

management agencies, and regional networks in the Pacific. 

The workshop incorporated diverse viewpoints from experts representing biomedicine, 

coral disease, toxicology, and resource management. The opening day focused on 

presentations from 14 position papers (Appendix VI), to provide context and concepts for 

the break-out group discussions. These presentations covered key topics that included: 

What do we currently know about coral diseases in the Pacific? 

What lessons have we learned from Caribbean disease outbreaks? 

Diagnostic methods, systems biology and leveraging post-genomic technologies 

Emerging diseases, disease outbreak investigations and ecological epidemiology 

How to integrate science with social, economic and political values? 

The participants were then assigned to one of four groups: (1) Coral Cellular Physiology 

& Pathology; (2) Coral Toxicology & Ecological Epidemiology; (3) Pathology of 
 

3 

Infectious Disease; and (4) Preventing and Responding to Coral Disease in the Pacific 

Region: Management Perspectives. Each team was charged with identifying key 

impediments and making recommendations for strategic research priorities that comprise 

this Strategic Plan of Action. 

The opening presentation provided a context for the workshop, identifying and discussing 

the features that set U. S. Pacific reefs apart from those in the Caribbean and other parts 

of the world. The U. S. Pacific and Atlantic reef areas have similar political histories and 

both were exploited through plantation agriculture. Recently, the economies of both 

regions are shifting from agriculture to tourism, and to a lesser extent fisheries, mining 

and logging. All of these activities have an impact on the region’s coral reefs. The 

Pacific coral reefs have the highest biodiversity with at least 200 genera and 580 

recognized species of coral. The hub of this diversity is located in Southeast Asia around 

Indonesia and the Philippines in portions of the Indian and Pacific Oceans referred to as 

the ‘coral triangle’. This diversity then diminishes from one island to the next across the 

Pacific to the east. The eastern Pacific (e.g., Pacific coast off central and South America) 

has the lowest coral diversity in the Pacific, followed by Hawaii. However, Hawaii has 

the highest regional endemicity, with an estimated 25% endemic organisms that inhabit 

these coral reefs. The region is also distinguished by resource management practices that 

are shaped by traditional cultural knowledge and practices that remain active in many of 

the Pacific islands today. These customs and tribal governance are unique in that U. S. 

Pacific Islanders perceive their natural resources as valuable and an integral part of their 

lives. In areas where these practices occur, their influences have successfully guided 

community-based management practices that contrast “western” ideas and National and 

regional management practices. The most obvious difference between the Caribbean and 

Pacific is the sheer area of coral reef habitat, the number of islands and atolls that exist in 

the Pacific, and the amount of open ocean between these islands, all of which greatly 

exceed those found in the Atlantic. This in itself creates a degree of isolation for many of 

the Islanders. However, this vastness and high biological diversity creates logistical, 

biological and cultural challenges to research as the Pacific Islander population is spread 

over numerous islands often at great distances, resulting in diluted scientific resources 

and insufficient personnel to monitor and combat any potential disease crisis in their 

reefs. 

Our most comprehensive records (1972-2005) of coral disease are compiled in the Global 

Coral Disease Database (WCMC Wcmc 2006) developed through a partnership between 

NOAA and UNEPs World Conservation Monitoring Centre (WCMC). Dr. Andy 

Bruckner presented a report on the global diversity and distribution of coral diseases 

(Appendix VI). To date, this effort has documented reports of over 40 coral diseases 

from the western Atlantic, 28 from the Indo-Pacific and 5 from the Red Sea, and covers 

63 countries. Over 150 species representing 39 genera have been observed with disease. 

In the Caribbean, this translates to 80% of all taxa (41 species of scleractinian, 8 

gorgonians, 2 hydrozoans) being afflicted with disease. In the Indo-Pacific 97 species 

(approximately 17%) from 34 genera have been identified with disease and this is on the 

rise. These numbers reflect a 25% increase in genera and 45% increase in species number 

since 1999, with 7 new genera in the Indo-Pacific observed with disease over the last 5 
4 

years. Recent surveys conducted in strategic locations across the Indo-Pacific (Australia, 

the Philippines, American Samoa, Northwest Hawaiian Islands (NWHI) and elsewhere) 

illustrate the widespread, global distribution of coral diseases with prevalence varying 

from a low of 0.14% in American Samoa to 0.5% in the NWHI and highs of 10% along 

the Great Barrier Reef (GBR) to 14% in the Philippines (see white papers in Appendix VI 

of this report by Willis, Aeby and Work). In these areas, over the last five years, regions 

previously unaffected are reporting disease, while in other locations (i.e., GBR) the 

percentage of reefs affected by disease has increased, and several new disease 

manifestations have been reported since 2002 (Willis et al. 2004). Based on this and 

other information, it is reasonable to conclude that diseases in the Indo-Pacific are 

undergoing a rapid expansion in range and types of disease and now is the time to 

recognize the signs of a pending problem and take action. 

Our understanding of coral diseases and thus ability to combat the declining health of our 

reefs is limited by our lack of understanding of the basic biology and physiology of coral 

hosts, and their responses and tolerances to changes in their environment. We are at the 

cross-roads---we can remain in the dark ages of medicine, as our understanding of coral 

disease has been described, or we can take advantage of the established principles of 

wildlife veterinary medicine and the technologies of a post-genomics era, apply them to 

coral health, and accelerate the evolution of this field....not only to determine the cause, 

but how to manage disease in the reef environment. The approach undertaken by the 

CDHC and strategies recommended by the workshop participants can help move the 

coral disease field into the 21st century, through implementation of wildlife and human 

medical approaches and tools. This requires enhanced funding, improved training and 

capacity building efforts, education initiatives, and development of new tools and 

information resources. 

Recommendations: 

Provide Competitive-based Grant Opportunities to Fill Knowledge Gaps. 

Our ability to understand coral disease pathology is hampered by a limited 

knowledge of molecular and cellular physiological functions of corals. An 

understanding of these critical features of coral biology could be rapidly advanced 

by tapping into a knowledge-base and skills that exist in the wider research 

community, is just beginning to be applied to corals. Funding is a key impediment 

to filling these gaps. Partnerships with funding agencies (NSF, EPA NIEHS) to 

offer directed grant opportunities can provide the impetus needed to engage a 

broader research community in developing a knowledge-base of coral cellular 

physiology.

Adopt Model Coral Species for Research. Identify representative reef building 

coral species from the Atlantic and Pacific that could be used in research studies 

to better characterize normal coral physiology and biological stress responses, 

then support culture facilities to propagate these corals (i.e., living stock 

collection), and make specimens readily available to researchers. 
 

5 

Adopt an Ecological Epidemiology Approach to Identify Risk Factors and 

Assess their Contribution to Coral Reef Degradation. The principles and 

methodologies of epidemiology can be used to identify and quantify risk factors 

that impact coral health (e.g., toxins and pollutants that make corals more 

susceptible to disease) and quantify the contribution of the various factors leading 

to adverse health effects. Implementation requires developing standardized 

methods and tools to detect and track biological responses of corals which can 

focus diagnostic efforts, and help direct and prioritize management and research 

actions toward risk reduction. 

Develop a Systematic Approach to Investigate and Study Diseases in Corals. 

Identify and recommend standardized approaches to systematically investigate 

coral diseases, including a system of nomenclature and terminology to 

describe diseases, survey approaches and laboratory techniques to provide 

compatibility among data. 

Develop a protocol for responding to coral disease outbreaks, train regional 

and local teams in disease investigative methodologies, including 

documenting case histories, assessing the area and extent of an outbreak using 

appropriate survey techniques, sampling techniques for specific laboratory 

analysis, and implementing systematic investigations in response to unusual 

coral disease outbreaks and mortality events. 

Develop a bioinformatics system to track outbreaks, synthesize case data to 

identify drivers in outbreaks and provide data in a format easily accessible to 

researchers and resource managers. 

Manage Coral Reefs to Reduce Stressors that may make Corals more 

Vulnerable to Disease. Managers often discount the study of coral disease 

because conceptually they believe disease is part of nature or even if causes of 

disease are identified, nothing can be done so why bother. However, management 

of disease in animal populations cannot occur in absence of information. Indeed, 

several tools are available to manage disease in human and animal populations 

(including wildlife), and these tools were developed precisely because targeted 

research identified the key interactions between agent(s), host, and their 

interactions with their environment that drive the occurrence of disease. Similar 

concepts also apply to corals. The key to managing coral health and mitigating 

disease impacts is not through stereotypic routes of medication, vaccination, and 

treatments, but rather by identifying causes of coral diseases, pathogenesis and 

factors that may modulate the resulting pathologies, including interactions with 

manageable anthropogenic and environmental stressors. The most controllable 

environmental factors are those associated with land-based sources of stressors; 

understanding disease dynamics can identify control points in a disease cycle that 

can also be used in management strategies. This will require researchers working 

collaboratively with key marine resource management agencies and regional 

networks in the Pacific such as the U.S. All Islands Coral Reef Initiative 

Coordinating Committee. 
6 

Create and Support Advanced Educational Opportunities. There is a critical 

need to build scientific capacity in the field of coral pathology and disease 

management skills in reef resource management. These programs should include 

development of advanced degree programs in coral pathology, cellular 

physiology, toxicology or epidemiology as well as continuing education in 

specialty topics (e.g., disease identification for resource managers; disease 

investigation methods; environmental forensics) for professionals (i.e., resource 

managers).

Develop Guidance for the Proper Handling and Containment of Corals in 

Infectious Disease Experiments. Most experimental studies involving corals 

have occurred under conditions that, in a medical setting, would be unacceptable. 

Typically, corals are placed in water tables, exposed to a suspect agent, and 

monitored for development of gross lesions whereupon the conclusion is made 

that agent ‘A’ caused disease ‘B’. Critical oversights in such experiments include 

lack of environmental controls (e.g. use of water tables with little monitoring of 

what microorganisms go in and out of the system), lack of morphologic follow-up 

to confirm that a gross lesion is indeed due to the putative infectious agent being 

investigated, and lack of knowledge regarding the normal physiology and biota of 

the host being investigated. Other studies have been conducted in the field with 

no containment or control over the dispersal of the inoculum into the surrounding 

environment. These types of experimental studies are analogous to attempting to 

elucidate the cause of a farm animal disease by conducting studies in the 

barnyard. An important outcome of this workshop was the recommendation by 

the participants to the CDHC to accept the following guidelines for the care 

and handling of corals in experimental settings:

Field Challenges using agents grown in a laboratory setting should not be 

done. Just as we would not grow bacteria or viruses in the lab and infect 

livestock, wild animal populations or humans (vaccines being the one 

controlled exception), in open systems with no containment, nor should we do 

it in corals. 

The export of laboratory reared coral back into the field is not currently 

recommended, until suitable tests are available for assuring these coral do not 

pose a threat to the wild populations. 

The need for biosecurity and bio-containment guidelines for conducting 

laboratory challenge experiments with candidate infectious agents and 

toxicants is recognized and it is recommended that CDHC establish a steering 

committee to develop these guidelines that are consistent with existing 

guidelines for handling and containment of infectious agents in wildlife as well 

as protocols for hazardous materials handling. 

 
 

7 

Foster the Development of a Cohesive Coral Disease Research Community. 

The goals outlined in this document can only be achieved through a cohesive 

group of people focused on common goals and a passion for healthy coral reefs. 

The participants of this workshop recommend that the CDHC provide a focus for 

cross-cutting priority research needs and a framework for interaction and 

collaboration among the coral disease research community. 
8 

OPENING REMARKS 

(Transcribed from this Workshop's Opening Address presented by Gary K. Ostrander) 

When I was thinking about my comments last night, since I do publish in the field of coral reef 

biology, I realized that I had a unique opportunity today to talk to the leadership in my scientific 

community. This is in addition to my responsibility as the Vice Chancellor to welcome you to 

Hawaii. This is significant to me in that you are a special group of scholars. You were all invited 

to this meeting because you are outstanding researchers and many of you represent and/or 

collaborate with top research groups and laboratories in the world. 

I realized that if I actually had something significant to say, that it might impact you and in doing 

so it might extend to others in the field. So, my initial comment is as follows: 

When are we going to get our act together as a research community? 

At best, we’re pathetic. If that puts you on the defensive or makes you uncomfortable, that’s my 

intent. We are studying, arguably, the most complicated ecosystem on the face of the Earth and it 

is under serious threat. Yet, we are disproportionately under-funded, in terms of funding whether 

it’s in the United States, at NSF or EPA, in Europe, Australia, etc. We are disproportionably 

under-represented in the top research journals: Science, Nature, PNAS, Cell and even in the 

second and third-tier research journals. 

What’s the problem, what are we doing wrong? 

I tell my graduate students and staff that I don’t have a problem if you come to me with your 

problems, but I do have a problem if you don’t come to me with a solution or a starting point for a 

solution. So, I am going to hold myself to the same standard this morning and I’m going to offer 

the following for your consideration. 

What are the causes of the problem that we currently face and what is a possible solution? 

Are we stupid? I don’t think so. I’ve met a lot of very smart people in this field. I didn’t start out 

in this field--I’m a guest. I started my career in cancer biology. When I think of the solution and I 

think of the causes, I turn my attention to the zebrafish community. Does anybody in this room 

not know what a zebrafish is? Of course you do! 

Twenty years ago, when I started working in fish cancer, nobody was working on zebrafish. In 

fact, I would argue that there was probably an order of magnitude, if not two orders of magnitude, 

more people working on coral reefs than on zebrafish. Yet in 20 short years, zebrafish have 

become recognized as a predominant model for developmental biology. They were on the cover 

of Science a few weeks ago. They continue to be in the top journals. If you sit on the panels at 

NIH, NSF and EPA, etc. in the United States, it’s zebrafish work that’s getting funded. They (i.e. 

the zebrafish community) did two things well. One is they asked important questions. I don’t 

think that’s a problem for us. But, secondarily and most important, they came together as a 

community very early on. They supported each other. Before there was an Internet, they put 

together the zebrafish handbook, the bible for zebrafish researchers. They went out of their way 

to make it easy for people to join the community, to work in the community. If someone had a 

line of zebrafish, if someone had a cell line, you could ask them for it, they would FedEx it to you 

and they would pay the shipping, and then they’d call you to find out if you had questions or 

needed help. When you sat on a NIH Study Section or an NSF panel and a zebrafish grant would 

come through, it would get the “regular” reviews from everybody. However, from the fish 

people, whether they supported the grant or not, they supported the particular application of fish, 

they supported the individual, and they were an advocate for the type of work. Zebrafish 

scientists joined the boards in the major societies in North America and throughout the rest of the 
 

9 

world as well as journal editorial boards. And though they could be just as critical and just as 

scathing, and just as nasty as we are to our colleagues, they didn’t do that. When they were 

critical, they were critical in a positive and a productive way. Look at where it’s gotten them. 

Sadly, this is not the case for the coral reef community. I am on the Editorial Board for Aquatic 

Toxicology. When’s the last time you saw a coral reef paper in Aquatic Toxicology? It’s a top 

journal, there’s lots of coral work in aquatic toxicology. It’s amazing, when you send a coral 

paper out to someone who is not a coral biologist, you get a reasonable review, when you send it 

out to a coral biologist, you usually get a pretty scathing review, because everybody’s defending 

their own territories. I see this when I sit on study sections at EPA or NSF. When I was in the fish 

community, you wanted a fish person to review your stuff, not because they would automatically 

approve it. No, you wanted them because you would get a constructive review if they didn’t. 

In my brief time in the coral reef community, I have learned that I don’t want coral biologists 

reviewing my work. I am willing to take my chances with competent reviewers who don’t know 

anything about coral biology. 

Five years ago, approximately, Cheryl convened the first of these workshops. They have 

tremendous potential to help the coral community. Out of that workshop came the idea: could we 

sequence the coral genome? So, Craig Downs, Craig Venter, Claire Fraser, Steven Salzsberg and 

I got together to write a ‘white paper’. The middle three individuals are some fairly significant 

names in the human genome community. Let me tell you a little bit about that effort and where it 

got us. The first question we had to address was which species do we sequence? That created 

quite a bit of controversy in the coral reef community. In the end, Porites lobata was suggested. 

And, parenthetically, I will tell you that was not my first choice even though I was leading the 

effort to write the white paper. Once the species was selected it was necessary to get letters of 

support. NHGRI had mandated that we be able to demonstrate that the community was going to 

rally around the organism selected and would actually use it because of the high costs of 

sequencing a genome. I’m not going to name names, but I have to tell you that I was really 

disappointed that when I went to colleagues who had “lost” as they viewed it, in their efforts to 

get “their species” sequenced, that they didn’t provide letters of support, even when I emailed 

them a couple times. 

We ended up submitting an application with 45 letters, and it was a good application. However, I 

was further disappointed that after it was submitted to NHGRI, some of our colleagues, hopefully 

nobody in this room, took it upon themselves to go to members of the panel to lobby for their 

own species and to disparage the rest of us and the species that had been selected. This did not 

send a good message to the NIH. They eventually came back to us with their decision: they said 

they would support pilot sequencing on three species, which they did. Ironically, one of the 

species they came back to us with was not even among the final three we had selected ourselves. 

Obviously, more politics was involved. At one point, somebody from the coral community went 

to the officials overseeing the website that runs the listserv we were using to solicit letters of 

support for the effort and wanted everything taken down because they presupposed members of 

our team were using this effort to patent sequences to make drugs. That is, we were doing this as 

a money making venture. Nobody came to ask me if that was the intent. No one came to me and 

said, ‘Hey, we heard this rumor, is this true.’ No one ever talked to us about it, they just went 

around us. Clearly, it was not true and it was not even possible if you understood the NHGRI 

program. 

In the end, NHGRI provided funds and we did pilot sequencing on three coral species. I am told 

they are still planning to select one of them for full sequencing. However, I am also told it is not a 
10 

priority right now. What’s I have heard through back-channels is that there’s concern on the part 

of NHGRI as to whether our community is going to embrace whatever species that was selected 

and whether it would be used. Some people mistakenly assumed that if it was not their species 

that was sequenced, that it would have no value to their research. Now whether they are just 

ignorant of RT-PCR or some of the other technologies, or whether they are just being selfish, I 

don’t know, but it’s a real problem for our community. 

So let me conclude. I challenge you, all of you, to take the first steps to create a more cohesive 

community, a community that works together. People will follow by example, it’s been done 

before. We have an incredibly important message, if this ecosystem dies, if this ecosystem is 

otherwise perturbed to an extent that it cannot recover it spells disaster not only for this spaceship 

we call Earth, but for more than 80 emerging economies, nations that are entirely or nearly 

entirely dependent on coral reef ecosystems for their existence. This is an incredible opportunity, 

an incredible moment. One of our colleagues posted something on the coral list-serve that said in 

part ‘....the problem with the coral reef community is that they eat their young.’ It’s a nice 

analogy, I think its time we do something to reverse it. So with that I will conclude my welcome 

from the University of Hawaii. 

Thank you for your time.” 

Gary K. Ostrander, Ph.D. 

Professor of Biochemical Oncology and Marine Biology 

Vice Chancellor for Research & Graduate Education 

University of Hawai‘i at Mnoa 

June 19, 2006
 

11 

PREFACE 

Over the past three decades, coral reefs worldwide have experienced major changes in 

structure and function due to numerous anthropogenic stresses and natural factors. In 

particular, the prevalence and severity of coral diseases and the diminishing health 

condition among corals have contributed to unprecedented declines in live coral cover 

and altered the productivity of coral reef ecosystems. The Caribbean is referred to as a 

“hot spot” for diseases due to a rapid emergence and high virulence of new diseases, an 

increasing geographic distribution and wider host ranges of known diseases, and an 

increased frequency of epizootic events. The number of diseases and their distribution 

across the Indo-Pacific also appears to be on the rise. Increased anthropogenic stress, 

overfishing, changing environmental conditions associated with global climate change, 

and the synergistic effect of multiple stressors have been implicated as significant factors 

contributing to escalating disease levels. However, our ability to address the recent 

increases in coral disease is hampered by a paucity of relevant epizootiological data, an 

incomplete understanding of the mechanisms responsible for the diseases and their 

consequences, and few diagnostic tools to help managers evaluate and mange diseases. 

Responding to this growing threat requires improved scientific understanding and tools 

to: (1) detect and assess trends in coral diseases at scales relevant to scientific 

investigation and policy development; (2) determine the causes and consequences of 

increasing disease frequency and distribution; and (3) evaluate possible management 

options to mitigate the effects of disease on coral reef ecosystems and their users. 

In 1998 the United States government issued Executive Order 13089 on coral reef 

protection. This Order called for the creation of the U.S. Coral Reef Task Force (US 

CRTF 2008) to develop, in partnership with federal agencies whose actions affect U.S. 

coral reef ecosystems, measures needed to understand, manage and restore coral reef 

ecosystem, with emphasis on reduction of impacts from pollution, sedimentation and 

fishing. The CRTF developed the National Action Plan to Conserve Coral Reefs (March 

2000), which outlines 13 major themes focused on improving our understanding of reefs 

and quickly addressing human impacts to these ecosystems. This Plan, together with the 

National Strategy and the Coral Reef Conservation Act of 2000 has outlined a realistic 

strategy to improve the condition and health of coral reefs, and has helped focus our 

conservation efforts, especially in waters of the United States, our territories and 

commonwealths and the Freely Associated States. One of the key initiatives of the CRTF 

was the creation of the Coral Disease and Health Consortium (CDHC), focused 

specifically on coral health issues, with emphasis on the diagnosis and etiology of coral 

diseases and bleaching. The CDHC is a network of field and laboratory scientists, coral 

reef managers, and agency representatives devoted to understanding coral health and 

disease. Currently over 150 partners, including three federal agencies (EPA, DOI, 

NOAA), academia, non-profit groups and industry are working to understand and 

address the effects of natural and anthropogenic stressors on corals in order to 

contribute to the preservation and protection of coral reef ecosystems. 
12 

In January 2002 the CDHC convened its first official meeting where recommendations to 

address the major gaps in coral disease and health research were identified and are 

detailed in Coral Disease and Health: a National Research Plan (Woodley et al. 2003).

The major needs include: 

Establishing standard terminology, methodology and protocols; 

Expanding knowledge in basic coral physiology, biology and disease etiology; 

Developing model coral species; and 

Developing a centralized data/knowledge system, website, repository and core 

diagnostic facilities. 

The CDHC working closely with partners have focused on five main activities. These 

include: 

Developing standardized procedures based on medical principles that clearly 

define the terminology, pathology and diagnostic criteria; 

Developing diagnostic tools to assist researchers in identifying coral stressors; 

Applying advanced technologies in functional genomics, proteomics and systems 

biology to expand our knowledge in coral health and disease dynamics; 

Providing local response capabilities to carry out formal disease investigations; 

Establishing culture facilities to maintain reef organisms for research. 

The CDHC in cooperation with the research and management community has worked to 

1) strengthen multidisciplinary collaborations and provide training for scientists and 

managers, 2) develop diagnostic capabilities (e.g., IRCP), 3) establish culture facilities to 

propagate model coral species for use in research and 4) develop educational materials, 

databases and web-based tools for scientists, managers and the public. 

The CDHC recognized the need to improve collaboration among our U.S. Pacific and 

international colleagues. In June, 2006 experts from multiple disciplines were brought 

together in Honolulu, Hawaii to help chart a course for coral health and disease activities 

in the Pacific and Indo-Pacific. The intent of this meeting was to generate a strategic plan 

that addresses 1) research needs to help understand etiologies, epidemiology and ecology 

of Pacific coral diseases; 2) management needs in the context of identifying innovative 

strategies for disease management on coral reefs and 3) outreach and education needs to 

combat the spread of coral disease through novel strategies that engage the public and 

political sectors and enhance partnership with the CDHC. During the working group 

deliberations, participants identified five key areas for the CDHC to assist in organizing 

and coordinating scientific resources in: 

establishing diagnostic criteria and diagnostic tool development 

conducting mechanism-based research on coral health and disease 

leading outbreak investigations, training efforts, and epizootiological studies 

providing training and advanced continuing-education opportunities 

developing web-based communication and database tools
 

13 

 
14 

INTRODUCTION 

Over the last 25 years there has been a worldwide increase in reports of disease affecting 

coral reef organisms, with the Caribbean basin emerging as a hot spot for diseases. The 

first documented Caribbean-wide epizootic was the mass mortality of the keystone 

herbivore, the long-spined black urchin (Diadema antillarum) (Lessios et al. 1984); this 

was followed by fungal infections that devastated seagrass (Thalassia testudinum) 

(Roblee 1991) populations in Florida Bay. Outbreaks of white band disease (WBD) were 

first reported from the US Virgin Islands in the late 1970s (Gladfelter et al. 1977). The 

disease spread throughout the region during the 1980s and over the next decade WBD 

contributed to the near elimination of Acropora palmata and A. cervicornis (Aronson 

and Precht 2001). The regional pattern of decline from these stressors is alarming, with 

coral cover decreasing from an average of 50% in 1977 to 5-10% in 2006 (Harvell et al. 

2007; Miller et al. 2006; Waddell 2005). 

In the Pacific Ocean, the threat of coral diseases has been thought to be relatively minor 

due to the spatial vastness of the region. Recent studies, however, indicate an escalating 

abundance and prevalence of disease throughout the Pacific (Harvell et al. 2007; Waddell 

2005; Willis et al. 2004). While diseases affecting corals were first reported in the IndoPacific and Red Sea in the late 1970s (black band disease (BBD) and WBD), it is only in 

the last five years that coral disease survey efforts have increased throughout the region. 

These data are providing key findings that the number and distribution of diseases across 

the Indo-Pacific is on the rise. Scientists working in Australia, Philippines, Palau, Africa, 

American Samoa, the Red Sea and other locations have detected some of the more 

common and infectious diseases seen in the Caribbean, and have also discovered several 

diseases unique to each region. Recent data also suggest diseases may play a more 

important role in structuring Indo-Pacific reef communities than previously thought. 

These alarming trends emphasize the need for a comprehensive and collaborative 

research program to better understand biotic and abiotic diseases affecting Pacific coral 

reefs, and relationships between anthropogenic and environmental factors and their 

effects on coral health. 

As evidenced by the loss of Caribbean acroporids and concurrent impacts on associated 

coral reef species, coral diseases have the potential to alter reef community structure and 

function. Several diseases are playing an increasingly important role in controlling coral 

population size, diversity and demographic characteristics. This decline in the health and 

living cover of reef building corals has created an urgent need for trans-disciplinary 

studies to understand mechanisms governing coral health and disease processes. 

However, much of the work on coral diseases to date has focused on the morphological 

characteristics of diseases and the search for specific pathogens that can be implicated in 

disease causation, without detailed investigation of the underlying cellular and structural 

characteristics. Furthermore, environmental and anthropogenic stressors (e.g., degraded 

water quality and climate change) have been cited as potential factors causing coral 

disease and mortality, yet few studies have adequately characterized causal links between 

disease and specific environmental stressors (Turgeon et al. 2002; Wilkinson 2002; 

Wilkinson 2004). 
 

15 

As an initial step to identify and address coral health and disease needs in the Pacific, the 

CDHC Pacific Workshop: Vision for Action was convened in Honolulu, Hawaii in June 

2006. The goals of this meeting were to synthesize the state of knowledge of Pacific coral 

diseases and develop a strategic research plan that: 

identifies standardized methodologies for diagnosing coral disease in the Pacific 

identifies information gaps 

recommends strategic research for understanding coral disease etiologies 

addresses issues relevant to the management of coral reef resources and diseases 

fosters collaboration among CDHC partners and key stakeholders. 

Workshop participants included recognized experts in biology, ecology, pathology, coral 

disease, molecular biology, cellular physiology, environmental microbiology, toxicology, 

veterinary medicine as well as the coral reef management community. These individuals 

were selected from academia, state and public health services, the biotechnology 

industry, U.S. government agencies and non-profit institutions, with representatives from 

Israel, the Indo-Pacific, western Pacific and Atlantic regions. 

Several workshop participants were asked to develop position papers (Appendix VI). 

These included a variety of topics such as: 1) issues unique to Pacific coral reefs and 

coral health; 2) the current knowledge of coral disease in the Pacific; 3) lessons learned in 

the Caribbean that could be applied to Pacific efforts; and 4) key areas for the CDHC to 

assist in organizing and helping coordinate efforts in the Pacific. These papers were 

distributed to all participants prior to the workshop. 

The authors of the position papers presented summaries of their reports during the 

plenary session on the first day. A number of complex biological and social issues 

unique to the Pacific were discussed including geographic expanse (i.e., a large number 

of islands and reefs), higher biodiversity, historical and cultural importance of reefs, the 

value of traditional knowledge, and considerations regarding traditional and local 

community ownership of reef resources. A brief background on the CDHC helped clarify 

the vision of the consortium, provided highlights of ongoing efforts in the Caribbean, and 

outlined possible opportunities for cross-disciplinary collaborations and training for 

scientists and managers in the 

Pacific. This was followed by a 

historical perspective of coral 

disease research in the wider 

Caribbean, including the 

current state of knowledge of 

Caribbean diseases, and what 

was missed during the 

emergence of diseases. Future 

considerations for Pacific 

efforts were also discussed, to 

help avoid some of the 

confusion that has arisen in the 

Figure I.1a Global distribution of 

Coral Diseases Reported in 1984. 
16 

Caribbean, and to better understand emerging infections and the drivers in disease 

outbreaks. This was followed by a series of presentations on the current knowledge of 

coral diseases in the Pacific, including the 

global distribution of diseases (Figs. I.1a 

and I.1b) and recent observations from 

Hawaii and NWHI, U.S. Territories and 

Freely Associated States, and the Western 

Pacific. The remainder of the session 

included discussions on diagnostic 

methods, disease outbreak investigations, 

and application of new tools and 

technologies for disease research, drawing 

heavily on approaches that have worked 

well in other wildlife veterinary and 

animal health programs. 

Four working groups were convened on the second day to 1) compile and synthesize 

available knowledge of coral disease for the Pacific and Indo-Pacific regions; 2) identify 

gaps in knowledge and technology; and 3) recommend strategic actions to improve our 

ability to respond to emerging infections in the Pacific: 

Physiology & Pathology Working Group (PPWG) was tasked with identifying 

what knowledge is needed regarding coral physiology to advance understanding 

and capabilities in coral pathology. 

Toxicology & Ecological Epidemiology Working Group (TEEWG) was tasked 

with identifying knowledge and needs related to toxicological impacts on coral, 

interactions with infectious agents and how to discriminate among them and the 

ecology of diseases. 

Pathology of Infectious Disease Working Group (PDWG) was tasked with 

identifying diagnostic approaches needed to move the coral disease field forward, 

including toxicology, microbiology, parasitology, pathology and diagnostic 

criteria to characterize the pathology associated with various infectious diseases. 

Preventing and Responding to Coral Disease in the Pacific Region: 

Management Perspectives Working Group (MWG) was tasked with evaluating 

management options that currently exist for diseases in corals and identifying 

existing tools and new approaches that can assist managers in the Pacific region in 

preventing and/or responding to coral disease. 

Each of the working groups developed a series of goals, objectives and recommendations 

to address the identified tasks. These were presented to all participants in a plenary 

session at the end of the workshop, and are compiled in the following sections of these 

workshop proceedings. The participants also identified a number deliverables that will 

be produced as additional outputs of the workshop, including a series of resource manuals 

on 1) systematic approaches to disease investigations, 2) standardized laboratory 

methodologies, 3) diagnostic criteria and identification tools for Pacific diseases, and 4) 

culture facilities and husbandry approaches for a model species for coral research. 

Figure I.1b Global Distribution of 

Coral Diseases Reported in 2004. 
 

17 

The four working groups identified numerous recommendations for CDHC activities 

related to coral disease research, monitoring, assessment, management, and 

communication to address coral disease and health in the Pacific. Specific objectives 

presented by each working group include: 

Identify tools and technologies, including available biomarkers, baseline assays, 

and targeted cellular research on coral physiology, to determine the health status 

of a coral and as a basis to understand coral pathology. 

Incorporate ecological epidemiology concepts into coral disease studies to 

identify predictors (ecological risk assessment model) for changes in coral health 

and ecosystem condition, quantify the strength of those associations, and focus 

diagnostic efforts toward identifying etiology. 

Develop diagnostic criteria and identification tools for Pacific diseases, including 

approaches to determine the suspected etiology of infectious disease in corals. 

Support the development of a Coral Disease Manager’s Guide that includes 

standard nomenclature, survey protocols, outbreak response protocols, guidelines 

for research involving live organisms including biosecurity protocols, options for 

management responses, and resource materials available for managers. 

Compile a training manual on existing laboratory methods to investigate coral 

diseases. 

Develop a Manual for Selection and Husbandry of Model Species for Laboratory 

Investigations. 

Develop and implement coral disease monitoring programs for the Pacific, 

incorporating epizootiological surveys with assessment of relevant environmental 

parameters. 
18 

A. PHYSIOLOGY AND PATHOLOGY

Advancing Knowledge and Capabilities to Understand Coral Physiology and 

Pathology 

Background 

Signs abound in many areas that the natural plasticity of reef ecosystems to successfully 

respond to environmental (e.g., global climate change) and anthropogenic (e.g., land use, 

pollution) stressors has been exceeded. Vulnerable habitat conditions overlaid with 

multiple, concomitant stressors have compromised many coral communities to the point 

where their ability to rebound from natural disturbances is being lost. This is evidenced 

by the 27% loss of the world’s coral reefs (Wilkinson 2002) and by predictions that 

estimate another 30% will be lost or impaired in less than 25 years. These predictions 

indicate that the current list of approximately 30-40 fatal diseases impacting corals will 

expand as will the frequency and extent of “coral bleaching” (Wilkinson 2002) resulting 

in effects ranging from reduced fitness, to community shifts, and ultimately to destruction 

of reef physical and biological functioning as we know it today. 

Faced with many degrading environments over the planet, coral reefs are one of the key 

sentinels of ocean health and can serve as an indicator that links ocean and human health. 

Elevated disease levels among coral reefs serve as a sign of a sick ocean environment. 

With escalating disease reports throughout Pacific coral reefs, and predictions that point 

to a fate similar to that of Caribbean reefs, coral research and management are at a 

crossroads. This realization can instigate despair reflecting a hopeless inevitable fate that 

nothing can be done for reefs, or conversely be used as an instrument of change. It is our 

position that by developing an understanding of disease etiologies, causal links can be 

determined and factors driving these system failures can be identified. Developing such 

an understanding can move us from a triage mentality toward the ideal goal of health 

management and preventative care for coral reefs. 

We are handicapped, however, in achieving preventative health care for coral reefs, in 

large part, because of a weak foundation in the basic sciences (e.g., biochemistry, cell 

biology, genetics, organismal and cellular physiology) of coral biology and the tools to 

enable rapid advancements. This has resulted in a fragmented research community, a 

menagerie of observations describing various coral afflictions with little coherence in 

how to make precise, defined observations in ways that promote comparative analysis, 

and almost no ability to discern mechanisms of disease. 

The ability to successfully manage for healthy coral reefs depends on the inroads that are 

made into understanding the causes and effects of disease on coral vitality, i.e., coral 

pathology. Pathology however is rooted in the basic sciences of anatomy, physiology, 

microbiology, immunology, biochemistry and cell-molecular biology while integrating 

basic science with clinical applications. The very nature of pathology is predicated on the 

ability to discriminate between biological structures and functions occurring within a 

normal range and alterations resulting from disease processes. The depth at which we are 
 

19 

able to understand the normal structure and functions that govern corals at the colony 

level, individual, cellular and biochemical levels (i.e., their physiology) will dictate the 

speed and degree to which advancement is made in combating the spread of disease and 

ultimately proactively managing with the goal of healthy reefs. 

Challenges and Recommendations 

The Physiology & Pathology Working Group (PPWG) was tasked with identifying the 

information needed to advance knowledge and capabilities in coral physiology to better 

understand coral pathology. Thus providing a means to identify strategies to stop further 

reef degradation and create suitable conditions for natural restorative processes to take 

hold and flourish. 

Coral biologists are challenged today with overcoming a void in information related to 

the functional processes of coral at cellular and organismal levels and the normal ranges 

in the functional parameters that define a healthy status, i.e., physiology. An adequate 

understanding of normal coral physiology and biochemistry is a prerequisite for building 

a sufficient foundation to competently study pathological conditions of corals. 

Understanding coral physiology and pathology requires defining the role of functional 

components at the cellular, systems, and organismal levels however the relationship 

between specific physiological sub-system (e.g., digestive, energy metabolism, nervous, 

reproductive, etc) processes, their regulation and the function of the whole animal has yet 

to be demonstrated for most coral species. This complicates discerning when or how 

normal biochemical/physiological processes have been disrupted to the extent that normal 

tolerance ranges of disease agents have been exceeded resulting in a pathogenic condition 

with lasting detrimental effects. Only when a full understanding of normal coral 

functions, as influenced by specific stressors, is achieved will the clinical manifestations 

of a specific disease be understood. 

The pathogenesis and the etiology of a specific 

coral disease is partially known for only a few of 

the diseases described in the literature. Clinical 

manifestations have been described using a broad 

spectrum of biological/medical/veterinary terms 

that have been haphazardously applied to coral 

disease. The resulting nomenclature has painted a 

confusing picture that has led to misidentifying one 

syndrome for another. Another challenge for the 

coral disease community is to recognize the state of 

confusion within the field that can only be rectified 

by adopting standardized nomenclature and 

methodologies that will support exchange of 

information and ideas among coral disease 

investigators as well as with cross-disciplinary colleagues in fields not traditionally 

involved in coral disease research. 

Pathogenesis: the pathologic, 

physiologic, or biochemical 

mechanism resulting in the 

development of a disease or 

morbid process 

Etiology: the science and study 

of the causes of disease and their 

mode of operation 

Clinical manifestations:

gross morphological observations 

of corals
20 

Compared to other wildlife diseases, coral disease research is in its infancy. Only recently 

have coral disease researchers begun applying technologies and methodologies routinely 

used in human and wildlife clinical and diagnostic medicine and pathology. 

Epidemiology is virtually nonexistent in the field. A growing number of scientists have 

begun applying biomedical approaches and adapting molecular biology tools in an effort 

to understand and characterize healthy corals and their responses when exposed to 

different stresses. These efforts show us the potential for understanding coral pathology 

and mechanisms for disease, and how a firmer grasp on this type of information can 

contribute to developing predictive indicators of adverse change in community health. 

However, there is a vast need to engage other researchers in the various aspects of coral 

health and disease. Persuading established researchers, in fields not traditionally part of 

marine science, to incorporate coral in their investigations or attracting new researchers 

to this field is difficult. The main challenges limiting progress in this arena include: 1) the 

availability of funding to conduct research on coral functional biology; 2) lack of a 

readily available source of research models; 3) few trained experts able to conduct the 

necessary research; and 4) lack of standardized field and laboratory approaches, including 

diagnostic criteria. 

There is a critical need to equip scientists involved in coral research with the knowledge 

and skills to meet the challenges of health assessment and management. First and 

foremost, addressing information gaps on the functional biology of corals and their 

disease processes will require a broad integration of relevant disciplines that include 

health specialties (i.e., veterinary and medical science, pathology, medical microbiology, 

toxicology, epidemiology), marine scientists (i.e., wildlife and marine ecologists, marine 

biologists, oceanographers), basic scientists (i.e., biochemistry, cell physiology, 

microbiology, toxicology) and those who help interface with the public and politicians 

(i.e., resource managers, sociologists, economists). It is imperative to develop and 

provide advanced cross-disciplinary educational opportunities to encourage and equip the 

next generation of scientists to meet the challenges of coral reef health issues.

In addition to the strong support for strategic research in cellular physiology and funding 

routes pursued through directed funding by NOAA (i.e., grants program) and partnerships 

with NSF, EPA and other funding agencies, the PPWG recognized that a significant 

challenge to achieving success and a key underpinning is access to a valid research model 

(i.e., defined species, cell lines and zooxanthellae cultures). Agreement on selection of 

the model presents a significant challenge as many criteria need to be considered such as 

species range, growth forms, taxa with varying susceptibility to disease and bleaching, 

and known, reproducible genotypes. The PPWG also recognized the need to identify risk 

factors and preventative steps to reduce risks associated research activities (e.g., transport 

and introduction of pathogens via dive gear and tools, containment mechanisms to 

prevent the spread of coral disease under investigation in field and laboratory settings). 

Therefore, the PPWG devoted most of their time and effort in setting criteria for defining 

and selecting a model species for cellular physiological research which included 

identifying key information needs to support successful husbandry of the research animal 

model and identifying an initial set of candidate parameters to consider in delineating a 

normal physiological condition. 
 

21 

In the following section the PPWG identified six Strategic Objectives and associated 

Recommendations on practical approaches that can help address major gaps in the 

understanding of coral physiology and pathology. Achieving this goal will require 

instituting standard nomenclature to facilitate clear exchange of research and field 

observations, coral research models (species & cell lines) to elucidate physiological 

functions and morphological changes, and establishing standard culture conditions for 

consistency in use of model systems. 

Strategic Objective A.1 - Obtain strategic information needs in coral functional 

biology (e.g., cellular physiology, immunology, genetics, biochemistry). 

Recommendation A.1.1: Provide targeted merit-based competitive grant 

opportunities to address knowledge gaps in the basic functional biology of corals 

through various Grants Programs offered by NOAA, NSF, EPA, NIEHS as well 

as private foundations. 

There are limited sources of funding to conduct the research necessary to define 

physiological parameters and their natural variations in healthy coral. Most coral disease 

and health related funding has been targeted towards field monitoring that incorporates 

identification of gross lesions on coral to determine prevalence and incidence rates; 

microbiology to identify causative agents; histopathology to describe microscopic 

lesions; and a few biochemical and toxicological studies to measure responses of corals 

to various stressors, while few funding sources are specifically directed towards coral 

functional biology. The PPWG recommends establishing partnerships among granting 

agencies to develop a targeted RFP to support long term research and multi-investigator 

teams to determine baseline measures of coral health at the genetic, molecular, cellular, 

tissue and whole organismal level. This should include efforts to actively seek 

partnerships among the broader research community as a means of infusing new ideas 

and technologies from areas not traditionally considered as relevant to marine biology 

issues. 

The PPWG identified five key information gaps that need to be addressed if the research 

and management community hopes to improve our understanding of coral pathology: 

Determine relationships between normal physiology and alterations caused by 

disease processes; 

Determine relationships between function at sub-system levels and functions at 

the whole organism and system levels; 

Elucidate how disruptions of normal physiological processes lead to pathologic 

processes; 

Determine the etiology, pathogenesis, and clinical manifestations of specific 

disease processes; and 

Predict clinical manifestations and appropriate treatment options for defined 

medical diagnoses. 
22 

By expanding research activities in areas of cellular physiology, genomics and 

proteomics, the research community will be better able to define nominal ranges of 

diagnostic parameters in healthy coral under normal spatial, temporal conditions and 

identify normal species-specific differences as a differential to recognize compromised 

health states. Through implementation of the recommendations put forward by this 

group, we can better characterize the complex mechanisms and factors underlying 

increases in bleaching events and coral disease outbreaks, as well as how human 

activities influence these processes. Understanding the mechanisms that confer resistance 

and susceptibility to disease, and deciphering the interactions between disease and 

environmental parameters will also provide the necessary information to support 

innovative development of diagnostic tools for rapid assessment of health and predictive 

capabilities of changes in health before disease signs manifest. 

Strategic Objective A.2 – Identify laboratory model(s) for coral research to enable 

rapid advances in our knowledge by focusing on fundamental biological 

concepts that are broadly applicable. 

Model species have been the key to rapid advances in disciplines such as developmental 

biology, genetics, toxicology, immunology, biochemistry and medicine. Model species 

have been developed in a number of taxa. Examples include E. coli, lambda phage, 

Drosophila, and C. elegans that have been instrumental in stimulating progress in our 

understanding of genetics and molecular biology. Selective breeding of species such as 

the brown rat and the common house mouse have produced white lab rats and mice that 

have been the workhorse of modern medicine. Arabidopsis thaliana (or Thale cress), 

Medicago truncatula (legume) and rice are three plant model species that have been 

essential for developing our understanding of the genetic and physiological bases 

responsible for fundamental biological functions that affect crop performance. 

Developmental genetics and cell biology have benefited enormously from studies of a 

non-mammalian vertebrate model, the zebrafish. Since its first recognition in the early 

1970s, the zebrafish research community undertook several activities to promote uniform 

research conditions and open-exchange of information. Early on this included developing 

a manual for raising zebrafish for experiments and making it freely available and widely 

distributed among the research community. More recently, this free exchange of 

information has expanded to website resources and an enlarged zebrafish manual (see the 

following website for more information: http://zfin.org/zf_info/zfbook/zfbk.html), 

followed by the adoption of standard criterion for laboratory use of zebrafish. The 

website provides a large variety of resources in support of the zebrafish model, including 

products and supplies, gene collection, sequencing project, microarrays, funding 

opportunities, meeting information, and all types of document resources. The model is 

now listed on the NIH webpage for model organisms (Nih 2007) as one of eight nonmammalian models for biomedical research. 

Our search for knowledge to date for hexacorals and octocorals has not been focused on a 

‘model species’, but rather often represents the species readily available to a particular 

researcher. This has resulted in disparate studies involving hundreds of species or 
 

23 

subspecies, thus limiting the ability to compare data between studies and species. The 

PPWG recognized that all corals and their diseases are not the same, but an 

understanding of coral physiology requires focused development of one or two laboratory 

models that are most representative across scleractinian corals. There will always be a 

need to develop alternate models for specific diseases, but understanding basic coral 

physiology and the changes in these functions that result in disease will benefit from 

focused work on a few models. 

Recommendation A.2.1 Establish criteria and select model species to focus basic 

coral physiological research. 

Several suggestions for a cnidarian ‘model species’ have been published in the peerreviewed literature, but only a few have recommended a scleractinian species. A brief 

summary of several recommended species and the disciplines for which they are most 

applicable are described in Appendix II and III. This literature review served to establish 

the currently available cnidarian models as well as to provide suggestions as to which 

criteria would be important in selecting a scleractinian model species for health and 

disease research. 

Based on a review of the literature 

and the available expertise among 

working group members a list of 

criteria was developed for selecting 

a laboratory model for scleractinian 

coral physiology (see inset). The six 

possible candidates for the IndoPacific coral models identified by 

the PPWG are Pocillopora 

damicornis, Stylophora pistillata, 

Porites rus, Galaxea fascicularis, 

Fungia scutaria, and Acropora 

formosa. Each of these species has 

a different set of characteristics that 

make it a suitable candidate for a 

laboratory model for coral 

physiology studies. A brief 

rationale from published 

information is provided for each of 

these six species below. 

Pocillopora damicornis (aka, lace coral, cauliflower coral, bird’s nest coral) is often 

referred to as the laboratory “white mouse” by coral biologists (Fig A.1). It is a major 

reef building coral widely distributed throughout the Indo-Pacific and Red Sea, and 

occurs in all shallow water habitats. It is affected by bleaching and disease worldwide, 

and has often served as an experimental subject for studies on coral physiology and 

reproduction. Its reproductive cycle is well described (Miller and Ayre 2004; Permata et 

Criteria for Selecting a Laboratory 

Model 

1. Easy adaptation to long term captive 

rearing in closed, recirculation systems 

2. Possible to provide many replicates through 

fragmentation

3. Widespread, geographical distribution in 

the Indo-Pacific 

4. Reasonably common

5. Exhibits differences in susceptibility and 

resistance to disease 

6. Representative of different habitat types 

(e.g., shallow water back reef and deeper 

water species) 

7. Potential for sexual reproduction in 

captivity 

8. Relatively rapid rates of growth

9. Branching and boulder growth forms
24 

al. 2000; Richmond 1987; Sherman et al. 2006; Stoddart 1983; Ward 1992; Ward 1995; 

Whitaker 2006) and includes sexually produced planulae that are brooded to a fully 

developed Halcampoides-stage (Harrigan 1972). It is easily grown in a laboratory setting 

from fragments as well as larvae, and can be induced to produce planula year round by 

altering the night irradiance (Jokiel et al. 1985). The cryopreservation of P. damicornis 

larvae was reported by Hagedorn and colleagues (2006b). Its skeletal morphology, 

biochemical character and biomineralization process have been described (Brown et al. 

1983; Domart-Coulon et al. 2004; Holden and Davis 2006; Letissier 1988; Tissier 1988; 

Vandermeulen 1975; Vandermeulen and Watabe 1973; Wainwright 1963). Conditions of 

stress and disease have been studied, 

including temperature extremes, 

bleaching, physical damage, 

sediment loading, ammonium 

enrichment, and infection by Vibrio 

coralliilyticus (Ben-Haim and 

Rosenberg 2002; Ben-Haim et al. 

2003a; Ben-Haim et al. 2003b; 

D'croz and Mate 2004; MullerParker et al. 1994; Te 1992; Ward 

1995). P. damicornis is susceptible 

to black-band disease (Dinsdale 

2002; Willis et al. 2004), brown band 

disease (Willis et al. 2004), bacterial 

bleaching (Ben-Haim and Rosenberg 

2002; Ben-Haim et al. 2003a; BenHaim et al. 2003b; Rosenberg and Ben-Haim 2002), mycelial fungal infections 

(Raghukumar and Raghukumar 1991) rapid tissue necrosis (RTN) (Luna et al. 2007), 

white syndrome (Willis et al. 2004) and skeletal eroding band disease (SEB) (Page and 

Willis 2008; Page et al. 2006; Willis et al. 2004). Primary cell cultures have been 

generated from P. damicornis and were demonstrated to produce aragonite crystals in 

adherent multicellular isolates (Domart-Coulon et al. 2001). Information is also available 

on growth characteristics following fragmentation, phylogenetic and symbiotic 

relationships, as well as histology and morphology. Recently the entire mitochondrial 

genome of P. damicornis was sequenced in a study designed to elucidate 

phylogenetically unique features of the family Pocilloporidae (Chen et al. 2008). 

Stylophora pistillata (aka, false finger coral, cauliflower coral) is another well 

characterized scleractinian coral (Fig. A.2), whose widespread geographic distribution in 

the Indo-Pacific and commonality in shallow-water reef fringes make it an ideal 

candidate for a model species. It is a brooding species whose reproductive seasonality 

and lunar periodicity have been well described (Guest et al. 2005a; Guest et al. 2005b; 

Hall and Hughes 1996; Zakai et al. 2006). The larvae are easily induced to metamorphose 

in the laboratory (Baird and Morse 2004). S. pistillata has been used for many years as a 

key species for coral research in many fields, including coral biology, ecology, 

physiology, biochemistry, geochemistry, immunology, evolution, paleoecology, and 

biogeography (Loya, unpublished). Various features of the S. pistillata morphology 

Figure A.1 Pocillopora damicornis, 

photo by Greta Aeby. 
 

25 

(Baird and Babcock 2000; Muscatine et al. 1997), physiology (Rinkevich and Loya 1986) 

and biochemistry (Dove et al. 2001; Dove et 

al. 1995; Richier et al. 2003; Rinkevich and 

Loya 1983; Tom et al. 1999; Zoccola et al. 

2004; Zoccola et al. 1999) have been 

described, including characterization of the 

calcification process (Furla et al. 2000; 

Gattuso et al. 2000; Mass et al. 2007; Moya 

et al. 2006; Puverel et al. 2007; Puverel et al. 

2005; Raz-Bahat et al. 2006) and dietary 

requirements (Houlbreque and Ferrier-Pages 

2009; Houlbreque et al. 2003; Houlbrèque et 

al. 2004). The species has also been used in 

population level studies such as regional 

variations in population structure and 

dynamics, life history strategy, growth and 

regulation of populations, regeneration, 

competitive networks and reproductive 

strategy. Major contributions have been 

made on coral physiology, including insight into the symbiotic relationship between the 

coral host and its zooxanthellae, such as environmental effects on photosynthesis 

(Bhagooli and Hidaka 2003; Bhagooli and Hidaka 2004a; Ferrier-Pages et al. 2000), 

respiration (Hill and Ralph 2008; Leletkin 2005; Reynaud-Vaganay et al. 2001) and 

calcification mechanisms (Tambutte et al. 1996; Tambutte et al. 2007), energy budgets, 

carbon partitioning and utilization (Houlbrèque et al. 2004; Muscatine 1984; Reynaud et 

al. 2004), adaptive mechanisms of algal regulation and causes and effects of coral 

bleaching (Hoegh-Guldberg et al. 1987; Hueerkamp et al. 2001; Jones et al. 1999). The 

species has also been used to better understand obligatory, mutualistic or parasitic 

relationships and effects of marine pollution (crude oil, sewage and phosphates) at the 

population, individual and cellular levels (Loya et al. 2004; Rinkevich and Loya 1979; 

Walker and Ormond 1982). Recently the entire mitochondrial genome of S. pistillata

was sequenced in a study designed to elucidate phylogenetically unique features of the 

family Pocilloporidae (Chen et al. 2008). S. 

pistillata is susceptible to Black-Band 

Disease (Dinsdale 2002; Willis et al. 2004), 

skeletal eroding band disease (SEB) (Page 

and Willis 2008; Willis et al. 2004) and 

Acroporid white syndrome (Roff et al. 2008; 

Willis et al. 2004). 

Porites rus (aka, plate and pillar coral) can 

form submassive, laminar branching, 

columnar structures, commonly over 5 

meters across (Fig. A.3). It occurs 

throughout shallow reef environments in a 

wide variety of habitat types, where it may 

Figure A.2 Stylophora pistillata, 

photo by Andy Bruckner. 

Figure A.3 Porites rus, 

photo by Greta Aeby 
26 

be the dominant coral. Kolinski and Cox (2003) reviewed the modes and timing of 

gamete and planula release for Hawaiian scleractinian corals; they listed, but failed to 

provide information on P. rus. This coral exhibits high survivorship when exposed to 

anthropogenic stressors such as pollution and elevated temperatures and is fairly resistant 

to bleaching (Yap 2004; Yap and Molina 2003). It can rapidly colonize areas after 

disturbance, exhibits relatively rapid growth rates and can be readily propagated from 

fragments (Dizon and Yap 2006a). The Tahitian P. rus was shown to produce four 

MAAs (mycosporine-like amino acids) (Teai et al. 1997). The sea-floor spectral 

reflectance (R) is a characteristic utilized in remote sensing; P. rus exhibits a spectral 

reflectance pattern consistent with “blue” corals (Hochberg et al. 2004). Porites rus from 

Guam was shown to harbor the “C” phylo-type of Symbiodinium-like (Rodriguez-Lanetty 

2003). Although the response was not real strong, P. rus did show antimicrobial activity 

against cyanobacteria in a study conducted by Koh (1997). P. rus was reported in 2003 

as one of the six branching species of coral in the Indo-Pacific that exhibited signs of 

PUWS (Porites ulcerative white spot disease) (Raymundo et al. 2005; Raymundo et al. 

2003). In addition, Work and co-workers (white paper, this report page 189) reported 

discoloration as a result of a sponge infestation in P. rus in American Samoa.

Galaxea fascicularis (aka, tooth coral, moon coral, galaxy coral) is a hermatypic coral 

with a gonochoric (distinct sexes) breeding system (Fig. A.4). G. fascicularis has been 

grown successfully in culture with a >200% weight increase over a 37 month period 

(Carlson 1999); although coral 

extension rates and calcification rates 

in some aquarium systems are close to 

those reported for natural reefs, 

anomalies have been observed such as 

decreased skeletal density and unusual 

changes in colony morphology (Clode 

and Marshall 2003b). This species can 

be difficult to maintain in an aquaria 

due to high light requirements and a 

high susceptibility to infections (brown 

jelly). Various features of the G. 

fascicularis morphology, physiology 

and biochemistry have been described 

in the literature: characterization of the 

mucus (Fung and Ding 1998; Fung et al. 1997); characterization of a GFP-like protein 

(Karasawa et al. 2003); calcification processes (Al-Horani et al. 2007; Al-Horani 2005; 

Al-Horani et al. 2005a; Al-Horani et al. 2005b; Clode and Marshall 2002; Marshall and 

Clode 2004a; Marshall and Clode 2004b; Marshall et al. 2007); corallite morphology 

(Crabbe and Smith 2006); stress studies (Bhagooli and Hidaka 2003; Bhagooli and 

Hidaka 2004b; Philipp and Fabricius 2003); egg proteins (Hayakawa et al. 2006; 

Hayakawa et al. 2005); skeletal matrix (Clode and Marshall 2003a; Fukuda et al. 2003); 

various genomic studies (Fukuda et al. 2002; Watanabe et al. 2005); characterization of 

their algal symbionts (Huang et al. 2006; Watanabe et al. 2006); dietary requirements 

(Houlbrèque et al. 2004); and micosporine-like amino acid (MAA) abundance 

Figure A.4 Galaxea fascicularis, 

photo by Andy Bruckner.
 

27 

(Yakovleva and Hidaka 2004). In an electrophoretic analysis, four soluble egg proteins 

were present in high abundance in the female egg, but were not found in the pseudo-eggs 

of functional males (Hayakawa et al. 2005). Gene expression, studied at the 

transcriptional level, was compared between female and functional male colonies. One 

of the vitellogenin-like proteins, GfEIP-4 protein, was cloned, sequenced and found to be 

expressed in both female functional eggs as well as male pseudo-eggs (Hayakawa et al. 

2007). Although specific reports of disease in G. fascicularis have not been made, 

Winkler and colleagues (Winkler et al. 2004) reported SEB disease in coral reefs of 

Aqaba in the Red Sea including Galaxea sp. In addition, Work and co-workers (White 

paper, this report page 189) reported discoloration in Galaxea sp. in American Samoa. 

Fungia scutaria (aka, mushroom coral) is the most common mushroom coral of the 

Indo-Pacific (Fig. A.5). It is free living and easy to collect. The species has separate 

sexes and releases eggs and sperm in the late afternoon, one or two days after a full 

moon. The larvae are azooxanthellate for 24 hours after fertilization and the process for 

establishing symbiosis can be 

observed without confounding 

background (Wood-Charlson et 

al. 2006). Krupp (1983) 

reported spawning to occur 

between 1700 and 1900 hours, 

1-4 days following the full 

moon with only one short 

spawning event per lunar cycle. 

Krupp also reported that the 

oral pit formed by 24h and that 

the mouth became clearly 

visible by 39h; ingestion of 

zooxanthellae was not 

observed, but in a few days the 

planulae possessed 

zooxanthellae. F. scutaria also 

reproduce asexually (Krupp et 

al. 1993) and can regenerate 

from polyp stalks or from septal fragments (Krupp et al. 1996a). Their host-algal 

interactions have been studied, including means of infection and localization in tissues 

(Rodriguez-Lanetty et al. 2004; Rodriguez-Lanetty et al. 2006; Schwarz et al. 1999; Weis 

et al. 2001). Their sperm and planulae have been cryopreserved (Hagedorn et al. 2006a; 

Hagedorn et al. 2006b). The toxicity of the pesticide chlorpyrifos was tested against F. 

scutaria’s gametes and planulae (Krupp et al. 1996b). From the examination of mucus 

samples for C,N,P composition (Krupp 1982) and their immunochemical nature (Krupp 

1985), it was deduced that one of the components is sulfated acid polysaccharide and that 

the mucus was predominantly carbohydrate composition with some protein and of low 

nutritional quality. Although specific reports of disease in F. scutaria have not been 

made, Winkler and colleagues (Winkler et al. 2004) reported SEB disease in coral reefs 

of Aqaba in the Red Sea including Fungia sp. 

Figure A.5 Fungia scutaria, 

photo by Thierry Work. 
28 

Acropora formosa (Dana 1846) (aka, staghorn coral) is a common branching coral that 

forms large thickets in shallow water on reef slopes, fringes, and lagoons (Fig. A.6); the 

species often coexists with other acroporids such as A. nobilis and A. grandis and is 

widely distributed throughout the Red Sea, the Pacific and Indian Oceans. This species 

reproduces sexually and can also be easily propagated from fragments (Okubo et al. 

2005) but successful sexual reproduction following fragmentation is dependent upon the 

fragment size and the stage of oocyte development during fragmentation (Okubo et al. 

2007). Staghorn-type Acropora sp. grows rapidly making it an ideal candidate for 

captive breeding/propagation. A. formosa calcification involves active Ca++ transport 

(Chalker 1976) and is 

impacted by ambient 

seawater temperature 

(Crossland 1984) with 

temperature exceeding light 

in determining growth and 

survival on a high-latitude 

reef. The development of 

scleractinian larvae from 

gamete-spawning coral, 

including A. formosa, was 

described in detail by 

Babcock and Heyward 

(1986) and in great detail for 

5 related acroporid species 

(Okubo and Motokawa 

2007). There are numerous 

papers describing the zooxanthellae associated with A. formosa: characterizing their 

DNA (Huang et al. 2006); describing their phosphate uptake (Jackson and Yellowlees 

1990) and metabolism (Jackson et al. 1989); examining their potential for ammonia 

metabolism (Dudler and Miller 1988); and describing their turnover during bleaching 

(Jones and Yellowlees 1997). Toxic reactions to external chemicals both natural and 

anthropogenic have been reported: defensive chemicals exuded by soft corals can cause 

expulsion of A. formosa’s algae, followed by release of nematocysts and eventual tissue 

necrosis and death (Aceret et al. 1995) while herbicides have been shown to decrease the 

effectiveness of dinoflagellate photosynthesis by inhibiting the Photosystem II system 

(Jones and Kerswell 2003; Jones et al. 2003). A. formosa is susceptible to disease 

including Skeletal Eroding Band Disease (Page and Willis 2008; Riegl and Antonius 

2003; Willis et al. 2004), brown band disease (Willis et al. 2004; Yarden et al. 2007), 

white syndrome (Willis et al. 2004), black-band disease (Willis et al. 2004) and skeletal 

anomalies (Peters et al. 1986; Sutherland et al. 2004; Work et al. 2008a). Photoprotection 

of A. formosa may be provided by both mycosporine-like amino acids, UV-absorbing 

compounds (Dunlap and Chalker 1986; Dunlap and Shick 1998) and by photopigments, 

one being a unique blue pigment in A. formosa, produced by the coral host (Dove et al. 

2001; Dove et al. 1995). Another protective barrier, mucus, has been described in detail 

for A. formosa; the composition was reported to be polymers of proteoglycan crosslinked 

Figure A.6 Acropora formosa, photo by Greta Aeby. 
 

29 

by disulfides (Richards et al. 1983). Further characterization of the mucus side-chains 

indicated that they were sulfated oligosaccharides terminating with a mannitol (Meikle et 

al. 1987). In a comparative study, Meikle and colleagues found that there is not a 

common mucus structure for 6 different species of coral, rather the mucus was either 

dominated by unique protein or carbohydrate polymers (Meikle et al. 1988). Although 

complete genome information is not available for A. formosa, numerous studies have 

reported both genomic and mitochondrial DNA sequences. 

Acropora millepora (a staghorn-type coral, no common name) is a hermatypic 

scleractinian coral with a digitate to branching growth form (Fig. A.7). It has a broad 

geographic distribution in the Indo-Pacific, found mainly in shallow water on reef slopes, 

fringes, and lagoons. A. millepora is a broadcast spawner that release eggs and sperm 

bundles once a year. Their embryology has been described in detail and the molecular 

cues have been investigated in parallel (Ball et al. 2002). They acquire their 

zooxanthellae during the planula larval stage (Van Oppen 2001). Ralph and co-workers 

demonstrated strong down-regulation of photosynthesis under conditions of high 

irradiance and observed little photoinhibitory damage to photosystem II (Ralph et al. 

2002). High sea-surface temperatures lead to thermal stress in A. millepora with rapid 

bleaching, followed by recovery (with 

high retention of reproductive 

capacity) or death within 14 weeks; 

this in contrast to Platygyra sp. that 

resisted bleaching longer and took 

longer to recover (with loss of 

reproductive capacity) or die (Baird 

and Marshall 2002). Recently it was 

shown that there are shifts in the 

composition of the ‘coral-associated 

bacterial assemblages’ sampled from 

colonies of A. millepora during a 

natural bleaching event (Bourne et al. 

2008a). The herbicide diuron did not 

inhibit fertilization in A. millepora but 

it did significantly impact 

metamorphosis in symbiont free larvae 

of this species (Negri et al. 2005). 

Other toxics, tributyltin, copper (Negri and Heyward 2001) and petroleum products 

(Negri and Heyward 2000), all inhibit A. millepora fertilization and metamorphosis to 

some extent. A. millepora is susceptible to black band disease (BBD) (Dinsdale 2002; 

Willis et al. 2004), skeletal eroding band disease SEB (Page and Willis 2008; Willis et al. 

2004) and potentially skeletal growth anomalies (Work et al. 2008a). The innate immune 

capacity of A. millepora was characterized by scanning available EST and genomic 

resources; neither the Toll/TLR or the complement pathways were identified, but the 

presence of complement C3 and several MAC/PF are encouraging (Miller et al. 2007). 

Recently, the isolation and characterization of a mannose-binding lectin was reported; 

this pattern recognition protein binds bacterial pathogens as well as the coral symbiont 

Figure A.7 Acropora millepora, 

photo by Andy Bruckner. 
30 

Symbiodinium (Kvennefors et al. 2008). There are over 10,000 EST sequences listed in 

Genbank for A. millepora (Ball et al. 2002; Miller et al. 2007; Technau et al. 2005). 

The working group submitted two candidate models for the Indo-Pacific region during 

the plenary discussion, P. damicornis and S. pistillata. After additional discussion in the 

plenary session, the following two species were adopted as the recommendation of the 

Workshop, P. damicornis and A. millepora 

Strategic Objective A.3: Establish culture facilities to propagate corals, coral tissue and 

zooxanthellae cell cultures from the model species to augment laboratory studies. 

Recommendation A.3.1: Determine the requirements and methodologies for 

establishing in vitro tissue culture and cell lines. 

Coral tissue culture or zooxanthellae cell lines are not commercially available to 

researchers currently. The special requirements needed to establish and maintain coral 

cell cultures have not been fully elucidated and published such that this procedure is 

widely available and those reported successes of coral cell culture report only short term 

viability as primary cultures. There are however, private collections of zooxanthellae cell 

cultures, but only a handful of researchers are able to grow and maintain these cultures. 

The PPWG recommended the CDHC contact these investigators to assist in the 

development of a manual detailing the special requirements for establishing these 

cultures, and identify possible facilities that could maintain living cultures and provide 

them to researchers for a nominal cost, such as has been done in the harmful algal bloom 

(HAB’s) community. 

Several studies have undertaken the challenge to develop tissue/cell cultures of coral 

species. The importance of the presence of the extracellular matrix (ECM) was 

demonstrated by Schmid and colleagues (Schmid et al. 1999) as well as others (Dizon 

and Yap 2006a; Dizon and Yap 2006b; Lewis et al. 2006; Okubo et al. 2005; Permata and 

Hidaka 2005; Raymundo and Maypa 2004; Yap 2004). They noted that “when cultured, 

most cnidarian cells survive only when attached to ECM substrates; they rarely divide 

and die within short times.” A review of the obstacles, approaches and improvements in 

culturing was published in 1999 (Schmid et al. ) and updated in 2005 (Rinkevich). 

Moderate success was achieved in developing short-term primary cultures by several 

groups. Kopecky and Ostrander (1999) successfully cultured multicellular endothelial 

isolates from branching scleractinian coral (Acropora micropthalma and P. damicornis) 

that survived in primary culture for 300h. In addition, five other species were 

successfully cultured: Montipora digitata, S. pistillata, and Seriatopora hystrix with 

Porites sp. less successfully. In a study conducted by Domart-Coulon et al. (2001) cells 

of apical coral colony fragments (P. damicornis) were isolated by spontaneous in vitro

dissociation. Single dissociated cell types were separated by density in a discontinuous 

Percoll gradient. Primary cell cultures displayed a transient increase in alkaline 

phosphatase (ALP) activity, to the level observed in intact corals. Unique to this study 

was the demonstration of aragonite ‘precipitation’. Continuous cell cultures of four 
 

31 

species of Octocorallia were reported by Frank et al. (2001) as well as a method to 

produce primary cell cultures for 10 cnidarian species including three Hexacorallia (S. 

pistillata, Porites lutea, F. favus). The primary cell cultures underwent cell proliferation 

within 2-3 weeks, and produced a collagenase soluble gelatinous matrix on the bottom of 

the wells. In another study focused on whole tissue isolation, soft tissue detachment from 

the skeleton of two branching coral species (S. pistillata and P. damicornis) yielded 

viable tissue capable of 70% survival for 3 days (Frank et al. 1994); these tissue pieces 

(containing whole polyps) quickly lost their morphology in dilute cell culture media, i.e., 

radial symmetry and oral-aboral polarity both were lost. After two days, in high glucose 

media, the tissue isolates dissociated layer by layer into individual cells, spreading in a 

circular outgrowth. 

Recommendation A.3.2: Create the infrastructure and community-base to make 

experimental animals accessible and explore mechanisms to provide coral 

fragments from model species and in vitro tissue culture or cell lines to research 

community. 

There are several groups interested in providing coral fragments or nubbins for coral 

research. The University of Miami’s hatchery facility has been conducting feasibility 

studies with the goal of expanding their current culture capabilities (i.e., providing 

aplysia for neurological research) to coral production. However the major impediments, 

to establishing living stock collections of coral specimens of well defined genetic lines, 

are lack of funding and permit issues. 

The PPWG identified one possible funding source to develop a coral culture facility. 

‘Living Stock Collections’ is a potential source of short-term (36 months) support with 

the goal of developing innovative handling of stocks or well designed improvements in 

handling stocks. This is funded by the U.S. National Science Foundation 

(http://www.nsf.gov/pubs/2006/nsf06574/nsf06574.htm). There are only about 2-4 

awards per year and the anticipated funding is limited with $1,000,000 available for all 

awards (new and renewed). Limitations of this program are: limited support for storage 

and distribution; no funds to conduct research beyond normal and appropriate curatorial 

efforts; and, no direct support for development of new reagents. Due to the short-term 

nature and limited support of this source of funding it is apparent that other resources 

must be explored. 

To implement this recommendation, it will be necessary to obtain sustained government 

funding and/or assemble a team to actively identify benefactors from the private sector 

and secure long term funding until such a facility(ies) can be self-sustaining. 
32 

Recommendation A.3.3: Identify culture parameters that support normal 

physiologic condition and normal growth of the coral host model species. 

The PPWG recommended the development of informational resources on coral 

husbandry, with emphasis on selected model species. These resources would describe 

optimal environmental parameters for culture facilities (e.g., light levels, water quality, 

food sources); identify potential stressors that may affect the system; develop protocols 

and methodologies for propagating corals through asexual and sexual reproduction with 

enhanced growth rates; and develop protocols for treating known diseases that affect 

aquarium invertebrates: 

Define tolerance ranges and optimum culture conditions (temperature, salinity, 

light intensity-wavelength, saltwater composition, density). Some information is 

presented in (Delbeek and Sprung 1994; Sprung and Delbeek 1997). 

Describe culture induced conditions, such as excess worms, macroalgae, 

parasites, and diseases, and provide protocols for treatment. See Borneman (2001) 

for more information. 

Define conditions required for sexual reproduction; provide protocols. See 

(Delbeek and Sprung 1994; Hagedorn et al. 2006a; Hagedorn et al. 2006b; Sprung 

and Delbeek 1997). 

Describe methods to promote optimum growth following fragmentation of coral. 

See (Ayre et al. 1997; Dizon and Yap 2006a; Okubo et al. 2005; Tarrant et al. 

2004; Tsounis et al. 2006). 

To implement this recommendation for developing these information products, the 

CDHC will need to identify experts in this field and assemble a team to draft the 

informational resources described above. 

Recommendation A.3.4: Provide support to researchers in the optimal care and 

handling of the organisms by providing standard protocols for culturing the 

experimental animals through development of a manual for coral model 

laboratory organism. 

The PPWG suggested that this manual could be patterned after the Zebrafish Manual. 

Once developed it should be published in hard copy and made available on the NOAA 

CDHC and CoRIS webpages. The group suggested the manual should include the 

following sections: 

a. Introduction 

b. Background [information on basic biology and biochemistry, nutritional 

requirements, physiological systems, reproductive characteristics, symbiotic 

relationships (algal and bacterial), susceptibility to stressors and genetics] 

c. Distribution 

d. Morphology 

e. Developmental Biology 

f. Molecular Biology (EST libraries, known gene sequences, phylogenetic 

relationships) 

g. Husbandry 
 

33 

h. Availability and Processes for obtaining organism 

i. Shipping instructions 

j. Biosecurity 

k. Permits, etc. 

l. Histology: protocols and photographs 

m. Standardized procedures for research studies 

n. Research tools available (primers, specific antibodies, histological stains, etc.) 

Creation of this manual is a team effort and will require experts to be identified who are 

willing to collaborate on the development of this manual. The CDHC could facilitate the 

team interactions by providing meeting logistics and publishing the manual after final 

peer-review. 

Strategic Objective A.4: Determine key physiological parameters that typify a normal 

or healthy condition for the model coral species. 

Recommendation A.4.1: Define a suite of physiological parameters that represents 

gross, cellular and subcellular levels of biological function and establish normal 

ranges for each parameter as criteria for determining health status of the model 

species. 

The PPWG considered a number of possible assays that could be used to assess health 

status that include assays to assess photosynthetic potential, biochemical and cellular 

responses of coral to various stressors, regeneration of tissue, growth and reproduction. 

The group recognized that many of the specialized needs (e.g., immune function, cellular 

diagnostics, cell type and functional probes), would require a focused effort to develop 

the necessary assays. One approach to begin defining the physiological parameters 

suggested was to summarize methodologies and assays currently available as a resource 

manual for the model species. The initial list of factors to consider is as follows: 

1. PAM fluorometer measurements, range and conditions, and standardized 

parameters for making the measurement; 

2. Calcification rates under standard growing conditions; 

3. Histology and morphology descriptions, and protocols for preparation of samples 

for light microscopy, SEM, TEM; 

4. Microbial communities (culture-independent vs culture-dependent methods) 

under standard growing conditions. 

5. Zooxanthellae symbionts characterized with respect to number, mitotic index, 

chlorophyll levels, and genotype; 

6. Lesion development and regeneration; 

7. Response to nutrient levels; 

8. Developmental biology; and 

9. Identification of cellular parameters useful in diagnosing environmental stressors 

and disease 
34 

The group recognized that much of the information proposed for inclusion in the resource 

described above may not be available, depending on the model species of interest. They 

identified seven key parameters that should be further explored in detail: 

Determine the specific ratio of protein-carbohydrate-fat in diet to support 

maximal growth. 

Determine nutritional requirements of the host, specifically any essential 

compounds, elements, vitamins, or trace elements required for successful 

metabolic homeostasis (i.e., nutrients provided by symbionts, mutualistic bacteria, 

etc that cannot be synthesized by the coral host) (Grover et al. 2002; Houlbreque 

and Ferrier-Pages 2008; Mills and Sebens 2004; Muscatine 1973; Muscatine and 

Hand 1958). 

Define the basics of the calcification process and required conditions for maximal 

growth. (Abramovitch-Gottlib et al. 2002; Al-Horani et al. 2005a; Elahi and 

Edmunds 2007; Fine and Tchernov 2007; Gattuso et al. 2000). 

Define the requirements to support normal reproduction and describe the 

developmental biology (Abramovitch-Gottlib et al. 2002; Lewis et al. 2006). 

Define specific metabolite levels or enzymatic activities describing critical 

cellular and tissue function and characteristics of microbial communities (TRFLP 

versus culture) under standard growing conditions. (Achermann 1980; Ball et al. 

2002; De Jong et al. 2006; Gajewski et al. 1996; Holland 2004; Kopecky and 

Ostrander 1999; Miller and Harrison 1990; Seipel and Schmid 2006; Torras and 

Gonzalez-Crespo 2005; Watson and Mire 1999). 

Recommendation A.4.2: Define markers of disease, both from a structural (e.g., 

histology) and functional (e.g., clinical diagnostic assays) perspective, that 

establish criteria for determining abnormal health condition in the coral host 

model species. 

The PPWG identified four key research needs that could fill gaps in our understanding of 

changes in coral health, including morphological characterization using histology and 

electron microscopy; identification of cellular diagnostic parameters; characterization of 

patterns of lesion regeneration; and responses of the coral and associated symbionts to 

human and natural stressors: 

Reference materials (e.g., an atlas of coral tissue samples) with histological and 

morphological descriptions and photographs of healthy, stressed and diseased 

conditions in representative Pacific coral species. The Atlas should include 

protocols for preparation of samples for light microscopy, SEM, and TEM. 

(Ainsworth et al. 2006; Bourne et al. 2008a; Bourne et al. 2008b; Breitbart et al. 

2005; Bythell et al. 2002; Gil-Agudelo et al. 2006; Klaus et al. 2007; Rosenberg 

et al. 2007; Work and Aeby 2006; Work et al. 2008a; Yokouchi et al. 2006). 

Characterize and describe cellular biomarkers for disease and develop a manual 

on assay and/or test protocols. (Downs and Downs 2007; Downs et al. 2005a; 

Downs et al. 2005b; Mc Clanahan et al. 2004; Peters 1984a; Peters 1984b; Peters 

2001; Work and Aeby 2006; Work and Rameyer 2005). 
 

35 

Understanding of conditions that support regeneration following lesion 

development (Hall 1997; Hall 2001; Henry and Hart 2005; Kramarsky-Winter 

2004; Kramarsky-Winter and Loya 2000; Titlyanov et al. 2007). 

Characteristics of the response of the holobiont (coral host, zooxanthellae 

symbionts, and microbial community) to stressors (Branton et al. 1999; 

Hashimoto 2005; Lejeusne et al. 2006; Mc Dougall et al. 2006; Mitchelmore et al. 

2007; Readman et al. 1996; Rougee et al. 2006). 

Strategic Objective A.5: Create and support advanced educational opportunities. 

Recommendation A.5.1: Develop an advanced degree program in coral pathology, 

offer continuing education in specialty topics for professionals and support 

fellowships for career development or cross-specialty training. 

There is a critical need to build scientific capacity in the field of coral pathology and offer 

a health management perspective in resource management (Mullen et al. 2004; 

Sutherland et al. 2004; Woodley et al. 2008; Woodley et al. 2007; Work and Rameyer 

2005). This will require a broad integration of relevant disciplines that assimilate 

expertise, tools and information from the coral research community as well as human, 

veterinary and wildlife scientists (e.g., pathologists, microbiologists, ecologists, cell 

physiologists). It is imperative to develop and provide advanced cross-disciplinary 

educational opportunities to encourage and equip the next generation of scientists to meet 

the challenges of coral reef health issues. This could include continuing education 

courses for professional development in histology/histopathology, environmental 

forensics, ecotoxicology, risk assessment and other disciplines. It should also include 

opportunities for advanced education such as a Master’s program in coral pathology and 

graduate courses in cnidarian cell biology, histology and physiology. 

Strategic Objective A.6: Organize a system of methodologies to investigate coral 

disease. 

Recommendation A.6.1: Provide conceptual approaches to support sound science as 

coral biology merges with the field of medicine to understand disease causes and 

mechanisms that include guidance for the proper handling and containment 

regimes for laboratory and field experiments. 

The PPWG discussed the concerns associated with the potential transfer of pathogenic 

organisms between locations and the lack of national or international guidelines for 

cleaning and disinfecting methods for vessels, equipment and divers that can prevent the 

transmission and/or introduction of pathogens to new hosts or locations. The potential for 

transmission may be elevated by researchers in direct contact with diseased corals or on 

reefs with disease outbreaks especially through 1) transfection experiments involving the 

removal of diseased tissue and transplantation to other presumably healthy hosts; 2) 

transfer of dive gear and tools that have not been decontaminated from a reef with a 
36 

disease outbreak to a neighboring reefs, or even to other locations within the same or 

different oceans; and 3) research to identify a causative agent via infection experiments 

conducted in situ. Other concerns include potential human health issues arising from the 

handling of infectious agents either in the field or laboratory. 

A variety of groups have begun to develop protocols to protect against the introduction of 

pathogens or spread of disease including health certification for corals raised in 

laboratory settings and subsequently transplanted onto coral reefs, as well as protocols for 

cleaning and disinfecting vessels, dive gear and equipment prior to the transport between 

locations. Medical and veterinary containment measures may also be easily applied to 

potentially infectious disease outbreaks in the aquatic environment. It is recommended 

that a working group consider the available information and propose SOPs; an external 

review by a recognized authority of the SOPs is suggested to validate the process. 
 

37 

Physiology & Pathology Working Group Members: 

Jo-Ann Leong (Chair) – Hawaii Inst. of Marine Biology, University of Hawaii, Kane‘ohe, HI 

Sylvia Galloway (Recorder) – NOAA NOS, Charleston, SC 

Fenny Cox - NOAA NMFS, Pacific Islands Regional Office, Honolulu, HI 

Marion Henry - Resource Management & Development, The Federated States of Micronesia 

Margaret Miller - NOAA NMFS, Miami, FL 

Mac Terzich – Pacific East Aquaculture, DelMarva Springs, MD 

Stephen Victor - MS Research Department, Palau Int. Coral Reef Center, Koror, Palau

Esti Winter – Tel Aviv University, Tel Aviv, Israel 

Gary Wobeser – University of Saskatchewan, Saskatoon, Saskatchewan, Canada 
38 

B. TOXICOLOGY & ECOLOGICAL EPIDEMIOLOGY

Identifying the Current State of Knowledge and Knowledge-gaps for Toxicological and 

Infectious Impacts on Coral using Ecological Epidemiology 

Background 

The deterioration of many coral reef ecosystems worldwide is a clear example of not only 

the effects global environmental damage can have on our oceans’ health, but also damage 

from local sources of pollution. This damage is multi-factorial as are its consequences. 

Since the 1970’s, mounting evidence has built a convincing argument that human 

activities are a prominent cause (e.g., coastal urban and industrial development, 

agricultural runoff, sedimentation, over-harvesting, marine pollution, disease and climate 

change) (Bellwood et al. 2004; Bryant et al. 1998; Risk 1999; Turgeon et al. 2002; 

Walker and Ormond 1982). Anthropogenic factors (i.e., physical, chemical and 

biological) can be exacerbated by natural factors (e.g., climate: water temperature, UV, 

weather pattern changes, volcanic/tectonic activity; biological: nutrient cycling, 

bioerosion, infectious disease) resulting in adverse health effects collectively recognized 

as disease (Wobeser 1981). 

Reef species experiencing persistent environmental disturbances (e.g., coastal 

development and land-based pollution) may respond with acute mortality, resulting in 

rapid loss of diversity and abundance; but may also display non-acute, sub-lethal effects. 

These effects often present as increased incidence of disease (i.e., gross lesions), reduced 

growth, diminished reproductive effort and recruitment, and ultimately reef systems can 

cascade into irreversible deterioration (CRMP 2001; Downs et al. 2005c; HoeghGuldberg 1999; Knowlton 2001; Nystrom et al. 2000; Patterson et al. 2002; Porter and 

Tougas 2001; Richmond 1993). On a global basis, attempts to arrest overall coral reef 

decline have failed with reef degradation continuing (Bellwood et al. 2004; Jameson et al. 

2002; Wilkinson 2002). 

Why are we failing to stop the declines? How can we change this? 

An examination of coral reef health assessments conducted over the last 30 years show 

detailed descriptions at the population and community levels in terms of coral cover, 

diversity and population dynamics of other reef species (usually fish abundance and 

diversity) but with little change in methodology (Downs et al. 2005c). Though necessary, 

these well-defined descriptions are not sufficient to answer why or what to do about the 

continuing decline of reef condition. Similarly, contaminant chemistry programs that 

detail the array of chemicals found at a site cannot answer whether these contaminants 

are benign or causal in disrupting coral health. A better understanding of the root cause of 

reef decline is necessary if mitigation decisions are to be successful. This requires 

integrating descriptive data with efforts to elucidate mechanisms of action and causal 

analyses to determine if there is an association between a biological response and a 

putative stressor, the nature of that association (e.g., impairment) (Boehm et al. 1995a; 
 

39 

Boehm et al. 1995b; Downs et al. 2005c; EPA 2000; Suter 2006) and in turn determine 

the associated ecological risk for better informed management options. 

By its very nature, toxicology is an integrative science that is designed to uncover 

fundamental mechanisms of action governing chemical effects on biological systems. 

Drawing from the basic disciplines of molecular biology, biochemistry and physiology, 

toxicological principles and methods can be applied to subcellular systems and extended 

to ecosystems by evaluating ecological effects of chemicals or ecotoxicology (Hahn and 

Stegeman 1999; Suter 1993). With only a few studies recently published, toxicology and 

its relationship to infectious disease is only beginning to be applied to coral. It is 

however a critical underpinning for developing sound evidence that provides causal links 

between stressors and their biological effect(s) on corals and reef systems. 

By merging toxicology, causal analysis and risk assessment information with measures of 

health condition (e.g., pathology, and health assessment), epidemiological methods can 

be used to understand disease incidence, distribution and causes while identifying and 

characterizing risk factors (predictors) that drive its occurrence, regardless of the root 

causation (biotic or abiotic). While classical epidemiology explores the statistical 

relationships between disease agents (both infectious and non-infectious), a related field, 

ecological epidemiology views disease as a result of the ecological interactions among 

populations of hosts and parasites (pathogens) and is concerned with the identification of 

critical parameters (e.g. the incubation period or latency) as well as the chemical and 

physical nature of the environment and how each contributes to the health of the 

organisms within the particular ecosystem (Cormier 2006; Suter 2006). Since most 

disease is multi-factorial, identification of risk factors for coral health can direct and 

prioritize management strategies toward risk reduction without requiring knowledge of 

specific etiologies. 

Challenges and Recommendations:

The ultimate challenge is to move from a triage approach to coral reef decline to a state 

of knowledge where causal links can be determined and factors driving these system 

failures can be identified. This can then support ecological risk assessments that lead to 

the formulation of risk reduction strategies and mitigation actions. Developing this 

understanding can move us toward the ideal goal of health management and 

preventative care for coral reefs. To achieve a position of coral health management, 

however, will require recognizing that we currently lack the understanding and the ability 

to mitigate the problem and current approaches to environmental assessments for corals 

are not effective. The necessity for a change in the paradigm and approaches that 

currently dictate how the welfare of coral reefs is assessed must also be recognized. This 

requires a new approach to the science, new assessments and methodologies and a 

different focus of effort. 

To effectively protect coral reef resources, resource managers need sound information 

that can clearly 1) characterize baseline health of coral reef communities, 2) demonstrate 

resource injury and determine its extent, 3) forensically link causal factors to the injured 

resource, and 4) routinely and consistently evaluate effectiveness of the management 
40 

response and thus, enhance resource protection (Boehm et al. 1995a; Boehm et al. 

1995b). A mechanistic understanding of modes of action, susceptibility differences 

among species, interaction between chemicals and environmental variables (e.g., 

temperature, salinity, light, pressure), and tools that allow monitoring for exposures and 

effects will enable causal and risk analyses to be used for coral reef assessments (Hahn 

and Stegeman 1999). Obviously not all human activities that cause environmental 

damage can be eliminated, however by adopting an environmental risk assessment 

strategy, decision-making can be improved to better protect coral reef resources by 

characterizing risks and quantifying them. Thus risk assessments enable prioritizing 

actions and provide quantitative measures for evaluating management actions and their 

consequences. While risk assessment is a process that assigns probabilities to adverse 

effects of human activities or natural damaging events, it does not address health 

assessment which is concerned with determining the occurrence and causes of 

impairments of non-human populations and communities, a field known as ecological 

epidemiology (Cormier 2006; Suter 2006). Thus integrating ecological epidemiology 

(biological assessment and causal analyses) with risk assessment (risk models that link 

alternative decisions to future conditions) provides a systematic means to improve 

understanding of the causal chain of events and the factors involved for informed 

management decisions (Suter 2006). 

The Toxicology and Ecological Epidemiology working group (TEEWG) recognized the 

need to be able to detect change in coral health at the ecosystem, community and 

individual level before the system is damaged. Detecting change however requires 

establishing a baseline of health and disease indicators using standardized and accepted 

methodologies. The Group also emphasized that in order to determine the significance of 

the impacts that toxicants or pathogens have on coral ecosystems there is a greater need 

to track biological responses (i.e., health changes) than to measure the presence/absence 

of toxicants. The ability to discern biological consequences (direct and isolated effects) 

of toxicants will rely on the availability of laboratory studies. The integration of this 

process would call for adopting an epidemiological approach and then integrating it with 

ecological risk assessments for improving coral health and disease management options. 

As a result of their deliberations, TEEWG recommended a systematic approach to begin 

the process (Fig. B.1). The first step is to adopt specific health indicators in field research 

and monitoring efforts to be able to detect change (i.e., condition assessment)(Cormier 

and Suter 2008) in coral health at the ecosystem, community, and individual organism 

levels; 2) conduct surveillance to determine baselines for health indicators and detect 

change resulting in impairment; 3) identify probable causes for impairment and (i.e., 

causal pathway analysis); 4) identify and assess risk factors as predictors of health effects 

(i.e., ecological risk assessment); 5) implement risk management decisions (i.e., 

management assessment); and 6) conduct outcome assessments to evaluate the success of 

the management decisions. The output of the Group provides a framework to move 

forward and a start at populating this framework with a) a list of predictors and outcomes; 

b) identification of data gaps and resources; c) a list of recommendations to enhance field 

monitoring efforts; d) a draft list of data variables and a standardized formaat for 

recording information; and e) specific recommendations to move forward. 
 

41 

B. Overall Strategic Objective: Improve understanding of the causal links involved 

in coral reef decline to better inform decision makers for health management of 

reefs. 

B. Overall Recommendation: Adopt a formal environmental assessment framework 

that integrates ecological epidemiology with ecological risk assessment to 

provide decision makers with a coherent and consistent description of risks 

associated with management options that is transparent, reproducible and 

defensible. 

In the following sections, the TEEWG identifies a series of key steps in the application of 

an integrated environmental assessment framework based on ecological epidemiology, 

that can help improve the detection, identification, and remediation (cure/management) of 

coral reef diseases and increase our understanding of the incidence, distribution and 

causes of harmful effects of chemical, physical, or biological agents (i.e., ecological 

epidemiology)(Suter 1993) on coral reef communities. The methodology involves: 

1. Development and implementation of an ecological monitoring program to 

characterize coral community structure and function (Objective 1) 

2. Establishment of baseline risk factors present at the site (Objective 2) 
42 

3. Use of epidemiology to identify potential risk factors associated with change (e.g., 

toxin, emerging disease) if a health change is detected, (Objective 3) 

4. Use of these data to choose the most appropriate diagnostic tools to assess 

etiology, recognizing that the cause is likely multi-factorial (Objective 4) 

5. Implementation of practical management strategies with the objective of reducing 

or eliminating risk factors associated with coral disease (Objective 5) 

6. Conduct outcome assessments to evaluate the success of the management 

decisions (Objective 6) 

Strategic Objective B.1 Identify and measure indicators of coral health and disease 

(morbidity) at the following levels: ecosystem, community, and individual for 

assessing condition and detecting impairments. 

Recommendation B.1.1: Adopt a unified list of indicators of coral health and 

disease. 

Indicators of health and disease are often referred 

to as bioindicators or biomarkers. There are 

three general classes defined as biomarkers of 

exposure, effect or susceptibility. Changes in 

these biomarkers are used to identify delayed or 

sublethal effects in individuals that survive an 

initial exposure to an adverse event. They can 

reveal exposures that result in compromised 

health as well as help define causal linkages and 

risk of adverse health effects. The most crucial 

characteristic of a health indicator is that it not only can detect biological changes but has 

diagnostic value in determining the nature of the change in association with a given 

stressor(s). Health indicators can range from remote satellite imagery to subcellular 

biochemical or cellular physiological endpoints. Integrating across levels of biological 

organization from cellular parameters to higher levels can help develop mechanistic 

profiles for certain cellular functions and disease states, and contribute to a suite of 

indicators for overall performance. The behavior of these indicators and the identification 

and quantification of pattern changes provides a basis for defining health status (i.e., 

diagnosis) and providing a prognosis. 

An initial list of biological indicators at the ecosystem, community and individual level is 

presented in Table B.1, and examples of the type of information they may produce.

Morbidity – the relative incidence 

of disease 

Bioindicator / Biomarker – a 

distinctive biological or biologically 

derived indicator (as a metabolite) of 

a process, event, or condition (as 

aging, disease, or oil formation) 
43 

Table B.1 CORAL HEALTH/DISEASE INDICATORS 

Indicator Comments 

ECOSYSTEM  Ecosystem structure and function  Calcification balance  Trophic level interactions  Ecosystem metabolism  Bioturbation  Changes in algal community composition and cover 

(abundance/biomass) 

Increases in certain types of algae are indicative of impacts associated with increased nutrients and/or removal of herbivores. 

 Bioindicators, e.g., foraminifora COMMUNITY  Species diversity and abundance Identify organisms of special interest and their abundance: species of high commercial 

value, species of ecological importance, or pest species such as corallivores 

 Bioerosion  Bleaching event Extent of bleaching, species or genera affected,  Rugosity/topographic analysis Change on reef structure (topography or structural complexity) over time. Especially 

relevant for communities dominated by branching corals that may be detached and flattened during storms 

 Bioindicators/symbionts: e.g. Butterfly fish (prevalence, 

feeding rates); stomatopods; sea cucumbers; 

 Catch per unit effort for reef fish. 
Table B.1 CORAL HEALTH/DISEASE INDICATORS (Cont’) 

Indicator Comments

POPULATION  Age (size) Representation of different size classes  Recruitment Diversity and abundance of coral recruits, an indication of the potential for 

recovery and whether a reef is a source or sink. 

 Intraspecific genetic diversity INDIVIDUAL  Bleaching Amount of colony surface bleached, duration of bleaching, patterns of recovery 

and/or partial or total mortality 

 Respiration/individual metabolism  Change in immune response Susceptibility to disease  Coral morphology Growth form may be an alternate measure of species diversity  Zooxanthellae content  Skeletal density/skeletal strength  Density banding.  Depth of tissue penetration  Abnormal growth/hyperplasia.  Growth/division rate of zooxanthellae vs coral growth rate. 

Growth rate; ratio; photosynthesis/respiration; proteins in PCP complex; photosynthetic efficiency 

 Autotrophic/heterotropic status of coral: C13 analysis, 

retrospective 

 Fecundity, gamete production. Changes in life history 

stages. 
 

 45 

Strategic Objective B.2: Establish a baseline of health and disease indicators 

Recommendation B.2.1: Implement targeted surveillance programs for monitoring 

coral health and detecting biological change to develop a condition assessment. 

The TEEWG identified examples (Table B.2 and Table B.3) of parameters, tools, and data that 

could provide detailed information on the structure, composition, functioning and health of the 

community. All of the variables identified may not be 

relevant to every region/location. For each location a 

detailed review of existing monitoring efforts, 

available baseline information and known threats 

should be undertaken to establish core baseline data 

variables. The TEEWG pointed out that the most 

prominent indicators in use today are associated with 

mortality and therefore identified a substantial need 

for more indicators of coral morbidity (rather than 

mortality). Examples include lesion regeneration 

rates, molecular indicators of stress, measures of 

genetic integrity, cellular physiological parameters 

indicative of immune status, detoxification, 

metabolism and various cellular and tissue-level 

processes. As new indicators for detecting biological 

change are identified, adopting a variable should be 

based on the criteria highlighted in the inset.

Criteria for Selecting 

a Biomarker 

Relevant 

Measurable 

Easy to collect 

Cost-worthy 

Reliable & valid 

(trustworthy) 

Amenable to standardized 

collection protocols 

Comparable 
Table B.2 INDICATORS OF CORAL HEALTH & DISEASE: FIELD OBSERVATIONS: Variables are ranked in terms 

of difficulty in acquiring information and reliability of measurements with the minimum recommended frequency of monitoring. Difficulty of collecting: 1 = no training, no extra cost, less than 10 minutes during a survey; 5 = augmented 

funding, years of training, high cost, long time to collect). Reliability: is there an accepted protocol in place or standardized 

protocol that would be accepted? 1 = low trust in data; 5 = high trust, given that consortium has come up with an accepted protocol and data are collected using this protocol. 

Variable Difficulty Reliability Minimum Required Frequency of Monitoring 

Species diversity 3 5 Annually Trophic level interactions 2 3 Annually Benthic community analysis 2 5 Annually Remote sensing data 4.5 4 Annually Population demographics 

Age/size Recruitment 

2 2 

2 5 

Every 2 years 

Bioerosion 1 5 Annually Bioturbation (high, med, low: categorical designation) 1 5 Annually Fish indicators: catch/unit effort; transects “fish counts” 

2 5 1-4 times/year. 

Bioindicators: sea cucumbers, butterfly fish. 1 3 At least annually Algal blooms 1 5 Event driven/choice. Rugosity 1 5 Every 2 years Algal cover 2 5 Quarterly Benthic algal community 2 5 Seasonal; 4 times a year. Bleaching 1 4 Choice/ annual Abnormal tissue growth 1 2.5 Annual Fecundity assessment: Gamete presence/pigmentation 

1 3.5 Seasonal 

Human activity--use observations to guide further analysis. Natural: provide a list of potential risk factors. 
47 

Table B.3 INDICATORS OF CORAL HEALTH & DISEASE: Laboratory Data (Definitions same as Table 2.2) 

Variable Difficulty Reliability Required frequency of monitoring

Calcification balance 3 5 Once Life history stages; bioassays on different stages; controlled laboratory exposures 

4 4 Most spawning events are annual. 

Bioerosion--15N isotope analysis. 1 5 (data) 

3.5 

(interpretation) 

Once 

Bioindicators: foraminifora 2 5 Annually; event driven Algal blooms: algae characterization 2 5 Event driven/choice Skeletal density. 1 5 once; opportunistic/event driven Density banding 2 5 Once Fecundity, gamete analysis (quantify, viability, fertilization study) Gamete histopathology 

4 Annually or 

seasonally 

Sediment analysis: size, petrographic 1 4 Once Water quality: pH, turbidity, salinity, temperature, wave action, e.g., routine YSI measurements. 

1 4 Routinely 

Tissue depth ND ND RESEARCH NEED Zooxanthellae: growth rates, ratio, photosynthesis/respiration; PCP complex. Normals yet to be established. 

ND ND RESEARCH NEED 

Autotrophic/heterotrophic balance. 13C Requires large 

sample size 

 RESEARCH NEED 

Intraspecific genetic diversity ND ND RESEARCH NEED Contaminant chemical analyses: persistent organic pollutants (POPs). Water, tissue, skeletal. 

1-5 

metals: 1 

persistent 

organics: 5 

Variation--

established 

methodology for 

some, not 

others. 

RESEARCH NEED 

Testing based on probability; not shotgun 

contaminant analysis. Tends to be patchy in 

time and space. 
48 

Strategic Objective 3: Identify risk factors associated with a change in coral health 

status. 

Recommendation 3.1 3.1: Establish site specific risk factors that may affect the 

location of interest and incorporate these into research and monitoring 

programs. 

The TEEWG identified an initial list of possible risk factors (Table B.4) that may be 

associated with coral disease outbreaks. All categories of risk factors are not applicable 

to all situations. Potential risk factors must be measurable and quantifiable to allow 

detection of associations. 

Many of the risk factors (i.e., causal factors) are anthropogenic in nature and affect water 

quality either from land-based sources of pollution or groundwater discharges. As these 

predictors of coral disease are more specifically characterized, the TEEWG identified 

types of anthropogenic and natural risk factors to consider in developing research and 

monitoring programs. These risk factors include: 

Anthropogenic (human activity) 

Agricultural 

Manufacturers / Industrial 

Aquaculture 

Fishing 

Residential Activities 

Recreational Activities 

Natural (general environmental) 

Pathogens 

Climate 

Water Quality (temperature, salinity, turbidity, etc) 

Strategic Objective B.4: Use risk factor assessments to choose the most appropriate 

diagnostic tools. 

Recommendation B.4.1: Standardize methodologies for all variables. 

The cause of most coral diseases are likely multi-factorial and investigations of these 

factors require a trans-disciplinary approach, drawing on many types of information to 

develop quantitative comparisons among groups and various factors. Adopting an 

Integrated Environmental Assessment (IEA) provides a logical, defensible and systematic 

approach to understand the complexities of disease. It blends concepts and 

methodologies of ecological epidemiology (i.e., biological assessment and causal 

analyses) with risk assessment (i.e., risk models that link alternative decisions to future 

conditions) to provide a systematic means to better identify causal factors and their path 

from source to impairment. A deliberate environmental assessment will provide a 
Table B.4 IDENTIFICATION OF RISK FACTORS ASSOCIATED WITH A CHANGE IN CORAL HEALTH STATUS

PREDICTORS OF CORAL DISEASE (Risk Factors) Measurement 

Agriculture 

Sediment runoff Measure: turbidity, sediment traps, YSI [sediment--can be held by fleshy algae, re-release of 

metals/toxicants. Both measure of stress on reef and recorder of historical stress. Lead to causation.]

Pesticides, herbicides Measuare: quantify products. Separate water soluble and lipophilic--divide out risk, which associated

with which disease processes. Also consider effects on different life history stages. 

Fertilizer Measure: Nitrogen, Phosphorus, Sulfur, heavy metals. Can fingerprint nitrogen (isotope suite); can tell 

fecal waste from industrial waste. Chlorophyll a: best measure of nutrient availability in the water 

Salinity changes due to freshwater runoff Measure: salinity Animal waste Measure: coliforms (total enterococci), antibiotics or other pharmaceuticals 

Industrial/manufacturing: 

Oil/hard mineral extraction. 

Measure: industrial solvents, processing waste, petroleum products, Inorganic waste: easy to monitor and use as diagnostic fingerprint (e.g. vanadium) Evolution of chemicals used in manufacturing. Testing done does not look at effect on coral reef organisms. 

Mining coral, beach sand (destructive, but not toxic). Ore transport: potent source of nasty things. Measure: easy to monitor/identify--e.g. mussel shells. Perchlorates--present everywhere, in high levels in corals. Landfill runoff Mining tailings (sediment waste produced by mining). 

Marine transport/maritime activities 

Anti-fouling paints, copper used (processing waste). Diagnostic indicator of a certain type of activity Ballast water Oil spills/grounding Military activities Historical artifacts: bombs, sunken ships, 

Fishing activities 

Measure: recreational, commercial, cultural, economic: fleshy algae dominate if consumers removed Destructive fishing practices--dynamite fishing, may predispose to ciguatera, etc 

Overharvesting of large predators; effects on the food chain. 
Table B.4 IDENTIFICATION OF RISK FACTORS (Con’t) 

50 

PREDICTORS OF CORAL DISEASE (Risk Factors) Measurement

Mariculture/aquaculture 

Shrimp ponds: a major source of toxic materials, shoreline modification process. loss of mangrove ecosystem, biological filters. (Demonstrated human health impacts in Indonesia with shrimp ponds.) Measure: presence or absence of aquaculture, distance, species cultured, type of aquaculture, 

pathogens Escape of invasive species, predation 

Pond vs. cage: different downstream epidemiological implications Introduced pathogens 

Pharmaceutical/personal care products 

Endocrine disrupters 

Residential activity 

Household pesticide use: contributes to non-point source pollution. Chemical; pharmaceutical/personal care products Sewage Organic: Measure coliforms (E.coli not a good measure in seawater) total enterococci; estrogen. 

Inorganic: Measure stable isotopes of nitrogen, caffeine--measures of human plumes 

Polybromated diphenylethers: plasticizers, persistent. Industrial chemical, but also residential. 

Measure: prevalence in water; if associated, look for primary source. 

Recreational activity: water quality vs. direct impacts Water quality 

Hotel industry / golf courses / residential--sewage management. Measure: Concentration of visitors/area as a risk factor for coral health. Jet skis/waterskiing; pollution. Only burn about 80% of fuel. Divers as vectors of disease 

Direct impacts 

Water sports: anchoring dive boats, stepping on corals Measure: number of snorkelers/divers in the area. Jet skis: compression waves, effect of vibrations on fish. Measure: compare management practices e.g. Palau vs. elsewhere. Presence of mooring buoys, 

controlled access. Jet ski rentals. 

Anchor damage Invasive species--any maritime transport could vector. People or equipment. Algae, diseases, invasive species 
Table B.4 IDENTIFICATION OF RISK FACTORS (Con’t) 

PREDICTORS OF CORAL DISEASE (Risk Factors) Measurement

Long range transport: 

Maritime: Ballast water Commercial: Transport of materials: e.g. sand Humans as fomites: wetsuit transport of disease 

Socioeconomical; ethics/values NATURAL 

Consider with all risk factors that there are synergistic effects/multiple factors involved 

Measure: look at geological record for baseline. Case control: what could be the control time or 

location (place or time in which risk factor did not exist.) 

Baseline processes 

Bioerosion Disease 

Climate: 

Water temperature UV Change in weather patterns Ocean level related to die-offs. Sea level fluctuations in geological time: big killers of reefs. Volcanoes/tectonic activity/volcanic ash Long range transport: 

Atmospheric transport--African dust 

Substratum/water quality Affected by runoff and sedimentation; heavy rainstorms, events occur naturally. 

Community 

Natural pathogens part of coral reef system Crown of thorn starfish, corallivorous gastropods and fishes HABs: cause of anoxia, coral damage. Natural vs. anthropogenic? 

Population 

Intraspecific variation/protection against population demise. 
52 

quantitative basis for informed management decisions (Suter 2006). While relatively few 

diagnostic tools are available for corals, tools and approaches routinely applied to the 

study of other wildlife and human diseases are available to adapt for the study of coral 

diseases. These tools should be evaluated and tested on corals, with the goal of their 

application in a routine, standardized manner to Pacific coral disease and health studies. 

The TEEWG identified key actions that can help achieve standardized methodologies and 

integrate them into standard practices in the field of coral reef health assessments:

Solicit standardized protocols from subject matter experts 

Publish selected protocols in peer-reviewed literature and central handbook (hard 

copies and web-based) 

Provide training for standardized protocols 

Educate users in the importance of standardized data to participants 

Recommendation B.4.2: Develop and pilot a plug-and-play database 

Standardized methods and protocols will help provide uniformity in data reporting and 

facilitate analyses and interpretation. However, the available data currently resides in a 

variety of databases and there is no integrated or centralized portal available to support 

the organization, analysis or interpretation of data that may be obtained through the IEAs 

outlined in Recommendation 4.1. The TEEWG recognizes that it is imperative to 

synchronize data from institutions to central location that is accessible, and is also 

equipped with computational tools to interrogate the data, conduct analyses and 

synthesize data into usable information for management decisions. To address this 

recommendation will require the creation of a sub-committee to develop such a database 

and agency support to house and maintain the database and develop analytical tools for 

end users. The TEEWG also pointed out that communication with participants and key 

stakeholders is critical and could be facilitated by providing an annual summary report, a 

valuable communication tool. 

Recommendation B.4.3: Capacity building 

The approach outlined by the TEEWG is not commonly used in the coral reef research 

and assessment community, yet it provides a valuable new thinking process for problem 

solving that logically organizes information, develops causal pathway models and builds 

weight of evidence arguments. This provides a transparent course of action to develop 

compelling information for causation and causal links that is vital for management 

decisions and selection of appropriate management actions. To successfully implement 

this integrated approach to environmental assessment will require education for the users. 

To this end, the TEEWG identified 7 key actions: 

Identify and acquire personnel (empower local resources & use traditional 

knowledge) 

Conduct training courses with subject matter experts 

Establish local infrastructure 

Ensure open communication / training among data collectors 

Address data sharing concerns regarding publication 
 

53 

Assess potential reporting requirements with federal funds 

Consider using data routinely to: 

Communicate with politicians, managers & legislators 

Conduct long distance diagnostics with remote subject matter experts 

Enable evidence-driven decisions 

Identify risk factors (anthropogenic & natural) 

Assess response to policy changes and other mitigation strategies 

Strategic Objective B.5: Implement management strategies with the objective of 

reducing or eliminating risk factors associated with coral disease. 

Recommendation B.5.1: Adopt an adaptive management approach whereby specific 

risk factors of concern are reduced or eliminated in certain areas. 

To achieve a position of proactive coral health management requires being equipped to 

recognize new and reemerging infectious as well as non-infectious disease conditions, 

and understand the factors involved in disease emergence, prevention, and elimination. 

This requires: 

Adopting a methodology appropriate for assimilating and synthesizing numerous 

and diverse data points that encompasses the ability to detect chemical, physical 

and biological impairments; identify sources and pathways leading to the 

impairment; predictive capabilities to estimate risks (e.g., societal, economic, 

environmental) for different management options; and a means to evaluate the 

success of the management decisions. 

Providing training courses for equipping individuals to conduct risk analysis and 

ecological epidemiology and translate these analyses for decision making. 

As Pacific Coral Reef Management evolves, it is critical to acknowledge, embrace and 

incorporate the traditional system of resource management into each of the steps in the 

process. A wealth of knowledge and success is espoused in these traditional methods that 

need to be incorporated into any contemporary coral reef management regime. Pacific 

Islanders are in tune with their local environment and are keenly aware of indicators of a 

healthy ecosystem as well as those that strike an alarm of impairment. Because of this 

knowledge and inherent value and respect this culture brings to coral reef management, it 

is important that it play a prominent role in developing a surveillance system to work 

with contemporary scholastic knowledge to understand and identify causes of ecosystem 

impairment and solutions. The Pacific Islander culture also provides a vital quality: once 

a problem is recognized they take local ownership and action to attain the solution, 

quickly before further harm is done to their resource. Given the vast area of Pacific coral 

reefs, and the limited capacity per area, training and capacity building efforts should 

empower local resources and take advantage of traditional knowledge. 
54 

Recommendation B.5.2: Identify a central facility to compile and share information 

in a timely manner with researchers, managers and other stakeholders, and to 

train local responders in risk factor assessments. 

When conducting condition assessments, causal analyses, risk assessment or 

epidemiological investigations it is important to summarize the investigation in a report 

that includes the reason for the investigation; general summary characterizing the 

investigation, the clinical descriptions, results and possible source and conclusions on the 

nature of the disease, source of outbreak and method of transmission and any possible 

recommendations for control or management. These reports should be provided to 

relevant resource managers, researchers participating in the assessment, key stakeholders, 

and other decision makers in a timely manner to allow implementation of management 

responses, as necessary, as soon as possible after identification of the event. This will be 

best achieved through: 

Centralized facilities and web-accessible databases to compile, analyze and share 

data and information in a timely manner; 

Involving experts capable of conducting detailed analysis of these data, including 

local participants, with the goal of developing a hypothesis to explain the most 

likely cause, source and risk of distribution of the cases and suggest tools and 

strategies to mitigate the disease and or its impacts. 

Because many Pacific communities still utilize traditional management systems it is 

important to ensure local ownership of the problem/solution and encourage local 

participation at every stage of the process while reaching resolution of the problem. 

Strategic Objective B.6: Conduct outcome assessments to evaluate the success of the 

management decisions. 

Recommendation B.6.1: Institute performance measures appropriate for evaluating 

the success or weakness of each component of the environmental assessment 

process, decisions and actions. 

Once a problem has been detected, Resource Managers attempt to determine causes and 

evaluate solution options. Although their decisions are based on the ‘best available 

science’, it is essential to have a means to evaluate the performance of their actions, 

detect inadequacy in the evidence (i.e., science) used as a basis for their decisions or 

determine whether the action was effective. This may be accomplished by comparisons 

to similar areas without management intervention or through monitoring and surveillance 

to determine whether changes have occurred compared to baselines. This evaluation is 

key to identifying knowledge gaps and directing research and monitoring activities 

strategically in support of a successful adaptive management process. 

 
 

55 

Toxicology & Ecological Epidemiology Working Group Members: 

Stephanie Venn-Watson (Chair) – U.S. Navy Marine Mammal Prog., San Diego CA 

Katie Tucker - Mohl (Recorder) - University of PA, School of Veterinary Medicine 

Craig Downs – Haereticus Environmental Laboratory, Clifton VA 

Mike Gawel - Guam Environmental Protection Agency, Guam 

Eugene Joseph - Conservation Society of Pohnpei, Federated States of Micronesia 

Qing Xiao Li – University of Hawaii, Manoa 

Robert Richmond – University of Hawaii, Kewalo Laboratory 

Mike Risk – McMaster University, Ontario Canada 

Figure B.2 Integrated Framework for Environmental 

Assessment. Adapted from Cormier & Suter 2008. 
56 

C. PATHOLOGY OF DISEASE

Identifying Diagnostic Tools Necessary to Adequately Characterize the Pathology 

Associated with Coral Disease 

Background 

Over the past three decades, coral reefs worldwide have experienced significant losses in 

living coral cover and changes in the structure and function of these communities. 

Infectious diseases have been recognized as a prominent cause of mortality in 

scleractinian corals in the western Atlantic since the 1980’s, but until recently there were 

few reports of coral disease from the Indo-Pacific region. Current efforts to 

systematically assess the types and prevalence of coral disease in the Indo-Pacific suggest 

that coral disease also occurs commonly on Indo-Pacific reefs, and these diseases may 

have a greater role in structuring coral communities in the region than previously thought. 

Unfortunately, few diseases affecting Indo-Pacific corals have been adequately 

characterized, quantitative data on the spatial and temporal variability of diseases and 

their impacts are lacking for most locations, and linkages between environmental 

parameters and diseases affecting Indo-Pacific corals are unknown. 

‘Disease’ is a word with many different connotations, depending on one’s particular 

perspective or experiences. Coral biologists use disease almost exclusively to describe 

gross changes in a coral’s appearance and usually assume that a disease is due to an 

infectious agent. Disease however, includes “any impairment that interferes with or 

modifies the performance of normal functions, including responses to environmental 

factors such as nutrition, toxicants, and climate; infectious agents; inherent or congenital 

defects; or combinations of these factors” (Wobeser 1981). Therefore, as in other animal 

diseases, it is imperative that an unbiased approach is used when investigating coral 

disease. 

Literally speaking pathology is the study 

(logos) of suffering (pathos); practically, it 

involves studying the structural and 

functional changes in cells, tissues and 

organs that define disease processes. There 

are four aspects that are investigated to 

understand disease processes: etiology, 

pathogenesis, morphologic changes, and 

clinical significance (Kumar et al. 2005). It 

is in this context that adopting concepts and 

principles of pathology will help to organize 

our observations and direct conclusions 

about coral disease in a rigorous and 

organized manner. Two recent publications address these issues for coral pathology 

(Work and Aeby 2006; Work et al. 2008b). 

Etiology: its cause 

Pathogenesis: mechanisms of 

disease development; sequence of 

events in response to etiologic agent 

Morphologic changes: structural 

alterations in cells and organs 

Clinical significance: functional 

consequences of the changes
 

57 

Challenges and Recommendations: 

The Pathology of Diseases Working Group (PDWG) was charged with identifying gaps 

in knowledge, research needs, and potential approaches that could be used to address 

pathology, pathogenesis and etiology of diseases in animals applicable to corals with 

appropriate modifications. Given the limited knowledge of the cause of many diseases in 

corals and the lack of uniformly applied methods to investigate disease, this topic was 

considered critical and timely. 

The challenge for coral pathology is to develop approaches, procedural guidelines, and 

analytical methodologies that take advantage of the advances made in the study of the 

pathology and pathogenesis of disease in humans and other animals. There was general 

agreement within the group that the study of diseases in corals suffers from a lack of 

systematic investigation, particularly in regards to establishing case definitions and 

arriving at causality of disease. A case definition encompasses all the factors that define a 

particular disease, and can serve as a standardized point of reference for tracing the 

disease across different populations or geographic areas. Case definitions can change as 

new data on the particular disease appear. As a starting point, case definitions for newly 

described coral diseases should include good morphologic descriptions encompassing 

gross and microscopic pathology. More complete case definitions will include 

information about the causative agent and the pathogenesis of the disease. Many of the 

methods currently used to characterize diseases in terrestrial and other marine animals are 

applicable to corals. 

For diseases that are novel or previously undescribed, carefully controlled laboratory 

studies can help elucidate the pathogenesis and cause of the disease. This includes studies 

evaluating host-agent interactions such as exposure of corals to suspected infectious or 

non-infectious agents in attempt to replicate clinical signs observed in the field. In cases 

where an etiologic agent is suspected to be necessary and sufficient to cause disease, this 

can be demonstrated through the use of Koch’s postulates, where the animal is exposed to 

the isolated infectious agent, clinical signs reproduced, and the agent re-isolated from the 

animal (Work et al. 2008b). Unfortunately, Koch’s postulates have often been applied to 

coral diseases based on identification of external characteristics (e.g., disease signs) 

without more detailed investigation of underlying cellular and structural characteristics of 

the experimentally reproduced lesion. These efforts have failed to distinguish between 

primary and opportunistic pathogens and have served only to enhance confusion in the 

literature. In addition, many diseases are complex making them difficult to study using 

Koch’s postulates alone. Furthermore, many marine microorganisms are not culturable 

in laboratory settings thereby complicating their experimental manipulation. Through 

application of culture-independent methods, the presence of multiple disease-associated 

pathogens may be identified. In addition to traditional methods of morphological 

pathology (e.g. histopathology) and culture methods, the application of genomic, 

proteomic, and metabolomic-based approaches may be necessary to understand the 

pathology, pathogenesis and etiology of coral diseases. 
58 

General Recommendation: Develop key questions that might be asked in regards to 

a disease outbreak in corals. 

At the outset, there was a consensus that great confusion existed on nomenclature of 

gross lesions in corals and 

that a good morphologic 

description provided a 

foundation for describing 

any disease. This led to 

considerable digression 

and discussion, however, 

in the end, the group 

decided on a decision tree 

that would give a broad 

outline on the process of 

disease investigations. In 

addition, three products were identified that were judged critical to sorting out existing 

knowledge gaps regarding disease in corals. These products included: 

Field identification cards for major lesions in corals from the Pacific. 

A summary of existing approaches to coral disease diagnostics. 

An approach to arrive at the suspected etiology of infectious disease in corals. 

Strategic Objective C.1: Develop a decision tree for standardized investigation of coral 

diseases. 

Recommendation C.1.1: The disease investigation process should follow a standard 

course of events. 

An unusual mortality or morbidity event is signaled via presence of dead or dying corals 

(field signs) (Fig. C.1). Recognition of the event is followed by a systematic description 

of lesions (morphology) in affected corals leading to a decision point. Either a 

management decision is made (Management) based on field signs and gross morphology 

(e.g. continue observing, implement intervention, do nothing) or samples are taken for 

further laboratory diagnostics (Sample). The focus of laboratory diagnostics is to arrive 

at the cause of a lesion or to begin building a database of information that will add to the 

foundation of the case definition (morphology). If a causal agent is identified (or as 

information is accrued from the laboratory), this information is fed back to management. 

This communication has several purposes. First, it promotes “buy in” to the disease 

investigation on the part of management. Second, sharing of laboratory information with 

managers provides a forum for generation of further hypotheses and further sampling to 

arrive at cause of disease. Finally, if an etiology is identified, input from managers is 

critical in helping elucidate the ecology of the agent so that the disease can be effectively 

mitigated or potentially stamped out. 

Key questions related to a disease outbreak 

1. How do you describe the disease? 

2. Does it have a significant demographic 

effect? 

3. Does it move rapidly? 

4. Do corals recover? 

5. Do you know what causes it? 

6. Does it correlate with environmental factors?
 

59 

Strategic Objective C.2: Develop a field guide of common lesions observed in corals 

from the Indo-Pacific.

Recommendation C.2.1: A simple field guide to common lesions of corals in the 

Indo-Pacific should be developed, based on the approach identified for western 

Atlantic corals. This guide would include: accepted common name of lesion, 

morphologic description and representative photos (distance and macro). 

Over the last 35 years coral reef researchers have identified and named over 50 diseases 

in scleractinian corals through field monitoring programs and targeted coral disease 

Fig. C.1 Disease Outbreak Response

FIELD SIGNS

MORPHOLOGY

MANAGEMENT SAMPLE

ETIOLOGY

research projects (Bruckner 2007; Green and Bruckner 2000; Weil 2004). While these 

observations have increased the visibility of coral diseases and have led to the recognition 

of the importance of coral diseases as a community structuring agent, the lack of a 

standardized approach to describe diseases has caused much confusion thereby limiting 

our ability to apply management tools in order to prevent disease occurrence and spread. 

Currently, coral disease is typically diagnosed in the field by identifying lesions, with 

comparative observations by different researchers and in different regions relying 

primarily on available photographs of gross signs and general descriptions based on the 

locations of lesions, the color of affected tissue or exposed skeleton, species affected, and 

rates of mortality. Unfortunately, this has led to a profusion of new names, including the 

use of different terminology to describe presumably similar gross field signs and similar 

terminology for syndromes observed in different ocean basins that have vastly different 

signs. Part of the problem has been that those describing coral diseases often infer 

causation based on gross appearance alone, however, the determination of causation is 
60 

something done more appropriately in a laboratory setting. Some progress has been 

made towards standardizing nomenclature of coral lesions (Work and Aeby 2006). More 

recently, the CDHC convened a workshop to establish diagnostic criteria (including 

nomenclature and case definitions) for coral syndromes affecting western Atlantic corals. 

Through this workshop, the CDHC developed a three-tiered approach to identify and 

differentiate coral diseases (Raymundo et al. 2008; Work and Aeby 2006) 

Strategic Objective C.3: Review of existing laboratory methods to investigate coral 

diseases. 

Recommendation C.3.1: Develop a white paper on investigative processes applied to 

coral diseases. 

This review should include detailed information on pathology, microbiology (including 

bacteriology, virology, mycology and protozoology), toxicology, genomics/proteonomics 

and parasitology. 

 A variety of methods exist to investigate various aspects of coral disease, however, 

whether these methods are sufficiently standardized or adequate as currently applied 

remains questionable. The group recommended that a comprehensive literature search be 

implemented to review what methods have been used to investigate diseases of corals 

(from sampling to analysis), their limitations, and their potential. 

Strategic Objective C.4: Identify a standardized approach to elucidate etiology of 

disease in corals. 

Recommendation C.4.1: Assemble a model approach that could be used to 

determine whether a particular etiologic agent would have high probability of 

being associated with (or causal of) a lesion. 

The model approach is based on answering certain critical questions: 

Can a potential etiology be consistently visually associated with the lesion? For 

example, in some cases, an etiologic agent (bacterium, fungus, parasite or virus) is visibly 

associated with cellular damage either at the light or electron microscope level. Strong 

presumptions of causality can be inferred in cases where such findings are consistently 

associated with lesions. 

Is the lesion transmissible? The group judged that transmission experiments 

could be done in the field (and also the lab) under the following conditions: 

These are limited to a restricted geographic area (currently unspecified but 

probably carried out in the immediate area such as a 0.5 km radius). 

That healthy fragments be attached to diseased colonies (and not vice versa). 

That appropriate controls be run for all transmission experiments. 

[Editor’s note: In the final plenary session of the Workshop, the participants of all the 

working groups discussed field transmission experiments and decided they should be put 
 

61 

on hold until specific guidelines could be developed. See the OPINION paper by Cheryl 

Woodley in Appendix VI.] 

The illustration below (Fig. C.2) shows the general concept in determining the nature of a 

communicable agent. If field or laboratory trials indicate the lesion to be communicable, 

subsequent experiments are moved into the laboratory. There, tissues from the diseased 

corals are extracted (methods vary), filtered or unfiltered extracts are inoculated onto 

susceptible colonies, and those observed for development of lesions. If lesions are 

reproduced using 0.1μm filterable extracts, it is assumed that causative agent is 

subcellular element (virus, protein, nucleic acid or chemical). If lesions are reproduced 

using non-filtered extracts, it is assumed that causative agent is cellular (e.g. bacteria, 

parasite). A more comprehensive schema and approach is available elsewhere (Work et 

al. 2008b) 

For non-filterable agents, clues can sometimes be gained by visual association (e.g., light 

or electron microscopy) as to its identity. In many cases, however, there are too few 

organisms to visualize effectively, and attempts must be made to culture. Although many 

bacteria in the marine environment are not culturable, attempts should be made to rule 

out culturable bacteria by using a variety of selective and non-selective media (including 

anaerobic conditions) to compare flora between sick and healthy individuals in efforts to 

target potential organisms in trials to fulfill Koch’s postulates. Genomic approaches can 

also be used to compare sick and healthy corals; however, because of the large number 

and variety of organisms detected using these methods, large samples sizes may be 

necessary and this approach, though helpful in generating hypothesis, rarely gives a 

definitive cause of the lesion. Methods to detect culture-independent flora associated 

with corals are still under development and will continue to develop. In addition, there is 

a need to develop primers to detect bacteria associated with corals. 

Fig. C.2 Scheme for Determining the Nature of a Communicable Disease

DISEASED COMMUNICABLE

HEALTHY

EXTRACT

FILTERABLE, 0.1u NOT-FILTERABLE

Virus/Protein/Chemical/DNA Bacteria/Rickettsia/etc.

FIELD/

LAB

LAB
62 

Standard methods exist to identify filterable agents such as viruses. These include 

electron microscopy, sucrose density gradients (physical separation based on density), 

degenerate primers and PCR, and susceptibility to chloroform or ether (to assess whether 

enveloped or unenveloped particles are present). A major limitation to the study of 

virology in corals is the current lack of laboratory cell culture systems (see 

Recommendation 3.2 in the PDWG section indicating the need for coral cell lines). 

Standard methods also exist to identify filterable agents that are not viruses. Extracts can 

be treated with chloroform and the aqueous and lipid soluble phase assayed for effect 

(lesion) in corals. Such methods coupled with gas chromatography-mass spectrometry 

can help identify compounds (chemicals) that may be associated with presence of lesions. 

Strategic Objective C.5: Build critical scientific capacity in the field of coral pathology 

and offer a health management perspective in resource management. 

Recommendation C.5.1: Create and Support Advanced Educational Opportunities. 

Strategic Objective C.6: Improve capacity to Manage Coral Disease Outbreaks. 

Recommendation C.6.1: Establish a Coral Disease Outbreak and Unusual Mortality 

Response Program. 

A response program should be developed that involves a National Center that provides 

guidance in responding to disease outbreaks and serves as a repository for information, 

regional coordinators and local responders. The National Center should organize training 

programs for Response Teams in strategic Pacific and Caribbean locations and whenever 

possible should assist in the investigation of coral disease outbreaks, facilitate processing 

of samples, and ensure relevant results and recommendations are provided to resource 

managers, participants and stakeholders in a timely manner. The National Center should 

also develop, with input from experts, a manual with a set of tools and procedures for 

investigating coral disease.
 

63 

Pathology of Disease Working Group Members: 

Thierry Work (Chair) – USGS, Honolulu, HI 

Julie Higgins (Recorder) – NOAA NOS, Charleston, SC 

Andrew Bruckner – NOAA NMFS, Silver Spring, MD 

Dave Jessup - California Dept. Fish and Game, Santa Cruz, CA 

Robert Jonas – George Mason University, Fairfax, VA 

Ariel Kushmaro- Ben-Gurion University, Be'er-Sheva, Israel 

Emmett Shotts – USGS (retired), Cleveland, GA 

Pamela Parnell - Professional Veterinary Pathology Services, Columbia, SC 

Meir Sussman - James Cook University, Townsville, Australia 

Bette Willis - James Cook University, Townsville, Australia 
64 

D. PREVENTING AND RESPONDING TO CORAL DISEASE 

IN THE PACIFIC REGION: MANAGEMENT PERSPECTIVES

Background 

Coral reefs are biologically diverse ecosystems that provide numerous economic and 

social benefits including sources of revenue and jobs as well as a variety of ecosystem 

services such as shoreline protection, recreation and ecotourism. In addition, they 

provide biomedicals, minerals, chemicals, food, curios and ornamentals, and building 

materials to over 100 developing and developed countries. Impacts associated with 

landscape changes that introduce sediments and pollutants (e.g., agriculture, industry, 

coastal development and physical alteration of habitats) and over-exploitation of coral 

reef resources are among the most pervasive localized stressors. Furthermore, localized 

impacts are being compounded by threats from global climate change such as increased 

sea water temperatures, elevated UV radiation and changes in ocean acidity. While we 

already know these ecosystems are easily damaged, we are only beginning to understand 

what can be done to prevent continued degradation. The complexity of these ecosystems, 

along with a growing list of human activities and demands placed on them by multiple 

user groups, is an enormous challenge for managers, who must find a balance between 

protection and continued use. 

One of the most widely recognized management systems for long term sustainable use of 

coastal resources involves integrated coastal zone management (ICZM). To achieve 

ICZM, concurrent steps are undertaken that address anthropogenic threats to coastal 

watersheds, including implementation of coastal development policies, measures to 

reduce industrial discharges, environmentally friendly agricultural practices, and sewage 

treatment measures. To be successful, these measures must be applied in concert with 

other actions to ensure sustainable commercial and recreational fishing and tourism. For 

example, typical efforts to mitigate land-based sources of pollution have focused on 

tertiary treatment of wastes, regulated use of fertilizers and pesticides, controlling 

nutrient loss and sediment run-off by replanting native coastal vegetation, and 

environmentally friendly development, dredging and beach renourishment practices. An 

excellent example of successful coral reef ecosystem management is provided by the 

Great Barrier Reef Marine Park, where multi-use zoning limits or prohibits specific 

activities. Fishing, curio collecting and tourism are permitted in certain areas by 

designating different intensities of use through the establishment of habitat protection 

zones (e.g., MPAs), National Parks, preservation areas, and general use zones. Together, 

these steps can help address localized human impacts to reefs; however, successful 

implementation requires strong government, industry and community support and 

participation, a strong lead agency, and sufficient capacity in planning, monitoring, 

education and enforcement. 
 

65 

General efforts to mitigate anthropogenic stressors are likely to reduce pressures enabling 

coral reef ecosystems to better tolerate natural stresses and more resilient to climate 

change and bleaching. However, biodiversity at genetic, species and ecosystem levels 

differs among locations and localized impacts to coral reefs are often site specific and 

may influence a coral reef’s ability to resist disease and/or recover from impacts. These 

factors require consideration when implementing management strategies. Furthermore, 

the state of knowledge regarding 

diseases and disease impacts is 

highly variable between Pacific 

and Atlantic regions, and between 

local jurisdictions. It is likely that 

additional targeted management 

measures need to be derived 

specifically for each jurisdiction, 

territory, state or country to 

identify, understand, and respond 

appropriately to disease events on 

their reefs. These measures could 

be identified through an 

assessment of multiple factors 

such as the types of reefs and their 

distribution, biodiversity, social 

and economic uses of reef resources, existing human and environmental stressors and 

current state of knowledge of these ecosystems. Management needs for coral diseases 

should initially focus on 1) building infrastructure and capacity to proactively respond to 

disease outbreaks; 2) increasing public awareness about diseases and their potential 

impacts; and 3) collaboration between managers and scientists to fill critical gaps in our 

understanding of disease in the Pacific. In addition to key proactive management 

responsibilities, reactive measures geared towards addressing impacts and restoring 

degraded coral reef ecosystems are also a critical responsibility of the management 

community. 

State of coral disease understanding and management in the Pacific 

Coral diseases have been reported on 39 genera and 148 species from 63 countries. The 

vast majority of all observations to date (86%) are from the wider Caribbean, with only 

14% of the records from the Red Sea and Indo-Pacific. Coral diseases (BBD and WBD) 

were first reported from the Indo-Pacific and Red Sea during the late 1970’s and 1980’s 

by a single researcher (Antonius 1977; Antonius 1982; Antonius 1985) working in three 

countries (Philippines, Egypt and Saudi Arabia). By 1994, diseases had only been 

reported from six countries, including several new conditions first observed on reefs in 

Australia. Indo-Pacific diseases appear to be exhibiting a rapid expansion in range and in 

the types of disease since 2000. For instance, recent surveys conducted in Australia 

(Willis et al. 2004), western Indian Ocean (Mc Clanahan et al. 2004), Philippines 

(Raymundo et al. 2005; Raymundo et al. 2003), Red Sea (Loya et al. 2004), Palau 

(Sussman et al. 2006), Hawaii (Aeby 2005; Aeby 2007) and American Samoa (Work and 

What do we need from the managers? 

1. Better defined response process 

2. Monitor the response 

3. Quarantine the reef or eliminate certain 

activities 

4. Restrict or modify activities that may be 

problematic 

5. Policy and regulation changes 

6. Possible depopulation of the reef 

7. Treatment 

8. Prevention 

9. Community outreach 
66 

Rameyer 2005) illustrate the widespread, global distribution of coral diseases. Through 

annual and semi-annual monitoring programs, researchers are also identifying coral 

diseases on a greater number of reefs and species, and at higher levels since the late 

1990’s, suggesting that diseases have become more prevalent in the Indo-Pacific over the 

last five years (Kaczmarsky 2006; Raymundo et al. 2003; Willis et al. 2004). This 

includes reports from new regions that were previously presumed to be unaffected (South 

Africa and Solitary Islands, Australia), a higher percentage of reefs with disease and 

recent increases in disease incidence in certain locations (e.g., Great Barrier Reef in 

Australia), and an emergence of several new conditions. 

Based on lessons learned from dealing with disease and the devastating effect disease has 

had in the Caribbean, coordinated and strategic preventative measures, with a focus on 

maintaining overall ecosystem health, need to be taken now in the Pacific Region. 

Managers need to be engaged with the scientific community 1) to better direct and assist 

with research efforts, 2) to identify possible options for responses to disease outbreaks, 

and 3) to identify realistic management strategies for Pacific coral reefs. While efforts to 

document diseases has certainly increased in the Indo-Pacific, the numbers of trained 

experts and the numbers of jurisdictions with routine coral disease monitoring programs 

remains very low. Furthermore, few research activities are directed towards an 

understanding of causative agents, sources of pathogens, linkages with environmental 

stressors, monitoring of the impacts of diseases on the physiology/biology of affected 

corals, or the role of disease in structuring coral reef communities. Some of these 

limitations may be overcome through educational programs targeted towards graduate 

students and researchers, and development of centers of excellence in Pacific 

jurisdictions with the necessary staff, infrastructure and training to process samples and 

identify and develop specific tools and informational materials directed at coral diseases. 

Approaches undertaken to manage or mitigate coral diseases have been limited in scope 

and the effectiveness of these measures is not fully understood. For instance, massive 

corals affected by black-band disease have been “treated” by aspirating the microbial 

band and covering the affected area with clay or underwater epoxy, while antiobiotics 

have been successfully applied to diseased corals in aquarium environments. Pilot 

experiments involving the removal of corallivores (e.g. crown of thorns starfish and 

corallivorous gastropods) have been undertaken to reduce predation pressure on corals, 

secondarily eliminating potential vectors of disease. Reintroduction of the herbivore, 

Diadema antillarum, is being undertaken in parts of the Caribbean to stem increases in 

macroalgae, which may also improve the health of corals, thereby indirectly reducing the 

likelihood of disease. Researchers are also attempting to identify disease resistant clones 

of certain species of corals, with the goal of propagating and transplanting these into 

degraded areas. In 2003, the Florida Keys National Marine Sanctuary (FKNMS) closed a 

portion of the reef to recreational divers in attempt to prevent transmission and spread of 

a disease affecting A. cervicornis (Federal Register 2003). Other efforts have focused on 

improving resilience of reefs, such as the implementation of no-take MPAs and reduction 

in the discharge of certain land-based stressors to specific locations; these measures have 

not been implemented as a strategy to mitigate disease, but they may indirectly reduce 

morbidity and enhance the health and resistance of corals. 
 

67 

Challenges and Recommendations 

There are numerous factors that have hindered recognition by the management 

community of the importance of diseases and the need for management actions directed 

towards an improved understanding of diseases, surveillance of the occurrence, 

distribution and impact, and responsive (proactive and reactive) actions to address 

diseases. This includes the existence of very limited basic knowledge on locations and 

species affected by diseases, numbers of different diseases and their abundance, causes, 

and links to other anthropogenic and natural stressors. Moreover, few studies from the 

Pacific have quantified the extent to which disease has or could contribute to overall reef 

decline. 

The general lack of knowledge on Pacific coral diseases severely limits our ability to 

gauge the severity of the problem. In light of current and future funding limitations and a 

paucity of information on diseases, managers may be reluctant to direct their limited 

available resources towards implementing proactive measures to address disease and in 

so doing, fail to protect unimpacted coral reefs from possible disease outbreaks. We need 

to develop a dialogue with managers that will communicate the urgency to prevent 

Pacific coral reefs from being thrust on the same trajectory as their Caribbean 

counterparts; improving our understanding of diseases through strategic research and 

surveillance as well as developing and implementing proactive conservation measures 

can help avert this impending threat to Pacific reefs. Engaging stakeholders, and raising 

their awareness to the benefits of prevention rather than treatment is not only costeffective but more likely to be successful than efforts to treat diseases and/or restore reefs 

after diseases have degraded coral reef habitats. 

The goal for the managing coral disease should focus on the maintenance or 

improvement of coral ecosystem 

health, using a comprehensive 

ecosystem-based approach through 

implementation of adaptive 

management practices. In general, 

coordination and communication 

among research scientists and 

managers can be facilitated with an 

inter-disciplinary approach that 

brings scientists and managers 

together to work closely to address 

disease, using a single ecosystem 

approach to science and 

management that exemplifies the 

land-sea connection since many 

potential stressors are believed to be land-based. This includes support for: 

What do managers need to know with 

regards to disease outbreaks? 

1. What is it? 

2. What is affected? 

3. Location of infection within the reef, and 

where is the reef? 

4. Time frame, seasonality? 

5. What are the population impacts? 

6. Is it transmissible? 

7. What causes the disease? 

8. What should be done? 

9. How widespread is the disease in 

neighboring areas? 
68 

a. Monitoring and assessment of the current state of coral reefs and condition of 

important reef building corals. Current efforts to monitor disease are minimal, 

and typically include attempts to gather baseline data or opportunistic reporting of 

disease signs noticed during field research or other routine monitoring. There is a 

need for adopting standardized disease protocols to ensure signs and stages of 

disease are reported consistently as well as uniform reporting guidelines to ensure 

the information is being communicated to the correct management agencies. 

Institution of these standardized procedures would enhance the opportunity to 

obtain the funding required to support long-term monitoring efforts. 

b. Research geared towards an improved understanding of potential stressors, 

causes and sources of disease such as identification of specific vectors, sources 

of pathogens, and measurable indicators of change in the health status of corals 

(e.g., specific biomarker expression). Existing efforts have been primarily 

directed towards counts of corals with and without specific disease signs, with 

few studies focused on understanding physiological changes in coral health before 

the coral manifests visible signs of mortality. Data pinpointing disease sources 

are also lacking, making it difficult to convince managers, politicians and the 

public to care about and seek management alternatives to address coral disease. 

In other disciplines, such as in most veterinary practices and management of wild animal 

(terrestrial) populations, cost-benefits of proactive and precautionary management 

measures have been fruitful. Some of the major actions that have improved animal health 

without actually treating a disease have included addressing contaminated sources of 

water, good cleanliness practices. Management of human activities is likely to be the key 

to improve the health of coral reefs, taking into account social systems and considerations 

of the regulatory/legislative framework, and whether managers are able to be proactive. 

Our ability to characterize and address coral disease in the Pacific is hampered by a 

paucity of spatially and temporally relevant epizootiological data, an incomplete 

understanding of underlying mechanisms responsible for the occurrence, spread and 

impact of diseases, and limited technical information and few diagnostic tools to help 

managers evaluate, track, predict or mitigate diseases. In an attempt to identify specific 

management needs that can help address coral disease on Pacific coral reefs, the 

Management Working Group (MWG) identified a series of broad strategic objectives and 

accompanying recommendations for actions to achieve these objectives. 

Vision: To understand and manage impacts to reef ecosystems from climate change, 

bleaching and disease for increased resistance and resilience by: 

a. Understanding the types of diseases present and their distribution; 

b. Monitoring the prevalence, incidence and impacts of disease with emphasis on 

stakeholder participation in monitoring and reporting of bleaching and disease; 

c. Determining existing legal mandates and identifying new authorities as necessary 

to address priority gaps and research needs for diseases and human impacts 

known to affect the health of corals and other reef organisms; 
 

69 

d. Identifying and mitigating manageable factors that exacerbate the occurrence of 

diseases and testing the effectiveness of these measures by employing an adaptive 

management approach; 

e. Increasing public awareness regarding diseases; 

f. Improving policy support to address diseases and enhance communication among 

managers, scientists, and policy makers; 

g. Implementing training and capacity building programs for managers, graduate 

students, scientists and other stakeholders with the goal of improving research and 

management capacity directed towards disease; and 

h. Developing tools and technologies to respond to and mitigate diseases and their 

impacts. 

General Recommendations 

Address management needs for coral disease outbreaks in the U.S. Pacific 

through the U.S. Coral Reef Task Force Local Action Strategy Process 

The U.S. Coral Reef Task Force (US CRTF 2008) developed a National Action Plan in 

20001

 to improve our understanding of coral reefs and implement actions to mitigate 

human impacts to these ecosystems. As part of this plan, Local Action Strategies (LAS) 

were developed in partnership with the U.S. All Islands Coral Reef Committee during the 

fall of 2002 to help increase and link the goals and objectives of the National Action Plan 

to Conserve Coral Reefs (U.S. Coral Reef Task Force 2000) with priorities and actions 

that are relevant for particular areas. The LAS are locally driven, short-range roadmaps 

for collaborative and cooperative efforts among federal, state, territory, and nongovernmental partners to identify and implement priority projects that reduce key threats 

to valuable coral reef ecosystems in each region. Together, the LAS from the seven U.S. 

coral jurisdictions (American Samoa, the Commonwealth of the Northern Mariana 

Islands (CNMI), Florida, Guam, Hawaii, Puerto Rico, and the U.S. Virgin Islands) have 

identified projects to address five priority threats to coral reef ecosystems: land-based 

sources of pollution; overfishing; recreational overuse and misuse; lack of public 

awareness; and climate change, coral bleaching, and disease. Hawaii and Guam are the 

first jurisdictions to complete a LAS for coral disease and bleaching. There is a key need 

for other U.S. Pacific jurisdictions to create LAS that identify key activities, partners and 

funding needed to tackle coral disease-related issues throughout the region. 

 

 

1

 The US Coral Reef Task Force National Action Plan was the first national blueprint for US action to address the loss and degradation 

of US and international coral reef ecosystems. Based on input from government and non-government organizations, scientists, 

resource managers and other. http://coralreef.gov/ 
70 

Unify the coral disease research community with emphasis on efforts to bring 

together the World Bank Coral Disease Working Group (DWG) and the CDHC. 

The World Bank Coral Disease Working Group (DWG) has identified a number of needs 

and activities to address coral diseases globally, many of which overlap with priorities 

outlined in the CDHC National Research Plan (Woodley et al. 2003). For example, both 

groups recognize the need for standardized methodologies, nomenclature and diagnostics 

to improve the comparability of coral disease reports across jurisdictions and among 

different researchers. One of the most cost-effective ways to address gaps in knowledge 

and to facilitate the development of tools, technologies and informational products that 

can help resource managers respond to disease is through an enhanced collaborative 

partnership between the CDHC and DWG. This is a key step to help advance the field of 

coral disease research and ensure accurate and comparable results of coral disease 

research efforts. 

Develop web-accessible database and informational resources for Pacific coral 

diseases 

In the coral reef arena there is often a period of several years between conducting a 

research project and publication of its findings, with limited communication of pertinent 

results to the management community by researchers. Furthermore, these findings are 

most often published in peer-reviewed journals that may be highly technical in nature, 

with inclusion of few management options in response to the findings. Managers need to 

have information presented in a manner that will enhance: 

a. Recognition of the need for management actions in response to coral diseases; 

b. Understanding the risks posed by diseases and risks associated with lack of 

management actions; 

c. The ability to determine the state of their coral reefs, including baseline levels of 

diseases, changes in disease prevalence or linkages between disease occurrence 

and manageable human impacts; and 

d. A comparison of what is happening in waters under their jurisdiction to 

surrounding areas, including status, trends, types and benefits of proposed and 

implemented management actions. 

Develop a manager’s guide for coral disease

The MWG requested that the CDHC develop a guide that brings together the latest 

scientific knowledge and management experience to assist managers in responding 

effectively to coral disease outbreaks. This guide might be modeled after the Reef 

Manager’s Guide to Coral Bleaching (Marshall and Schuttenberg 2006) and should 

include: a) survey/assessment protocols; b) outbreak response protocol; c) protocols for 

post-disease response actions; d) guidelines for research involving live organisms 

including safety and biohazard containment strategies; e) disease identification guides 

and standardized nomenclature and diagnostics; f) possible management responses to 

reduce the occurrence of disease and control spread; and g) resource materials for 

managers. 
 

71 

Strategic Objective D.1: Enhance the state of knowledge of coral diseases. 

Recommendation D.1.1: Conduct baseline surveys on coral diseases throughout the 

region. 

The accurate and thorough documentation of the type, prevalence and geographic 

distribution of diseases currently present in each jurisdiction is fundamental to attempting 

to effectively manage these diseases. As a first step, baseline surveys are needed at 

relevant spatial scales (e.g., different depths, habitats, reef types, and at varying distances 

from land within each jurisdiction) to identify what diseases are present now, how 

common they are and what coral species and/or other marine organisms are being 

affected. These surveys could be easily incorporated into existing survey efforts that 

examine the community structure and cover of corals, other benthic invertebrates, 

commercially and ecologically important mobile invertebrates (e.g., lobsters and crabs), 

and coral reef dependent fishes. 

At minimum, efforts to characterize the baseline prevalence of diseases should include 

parameters that address: 

Coral species diversity at lowest possible taxonomic resolution (e.g., genus or 

preferably species level data) 

Coral community structure including size class and other population parameters 

Coral cover and colony condition 

Abundance of diseases and presence of possible disease vectors (e.g., gastropods, 

crown of thorns, fireworms) 

In order to collect comparable data, the group recommended that coral disease surveys be 

conducted using standardized methodologies, disease nomenclature and forms. 

Strategic Objective D.2: Develop and implement proactive management strategies. 

Recommendation D.2.1: Develop a disease monitoring program for Pacific reef 

areas or integrate disease into an existing monitoring program. 

Long-term monitoring of coral disease using standardized techniques is essential to detect 

and assess changes in disease prevalence, types, and organisms affected and to provide 

regular, up-to-date information to managers. Most areas in the Pacific with established 

monitoring programs do not include disease monitoring in their protocols. Furthermore, 

in areas where disease monitoring is occurring, survey approaches are highly variable, 

allowing only limited comparisons between programs and jurisdictions. The development 

of a disease monitoring program capable of assessing changes and trends in reef 

ecosystem health is recommended. This program should be appropriate for the specific 

reef areas of each jurisdiction and record comprehensive data exceeding current efforts at 

presence/absence of disease. It is further recommended that the effort be integrated into 
72 

existing monitoring programs whenever possible. Regular long-term monitoring, that 

includes disease surveys along with surveillance of high priority environmental stressors, 

can potentially be used strategically to identify and address emerging threats to specific 

areas (anthropogenic and natural threats). 

 

The MWG identified some of the basic information that should be included in the 

disease monitoring program and recommended four documents that could serve as 

a starting point for the development of an integrated, Pacific-wide disease 

assessment and surveillance effort:

IOC/UNESCO Coral Reef Targeted Research & Capacity Building for 

Management (CRTR) Program; Coral Disease Working Group assessment 

protocol 

A Reef Manager’s Guide to Coral Bleaching (Marshall and Schuttenberg 2006) 

CDHC’s Field Manual for Investigating Coral Disease Outbreaks (Woodley et al. 

2008) 

Priorities for Effective Management of Coral Diseases (Bruckner 2002) 

Recommendation D.2.2: Identify potential stressors that may influence susceptibility 

or resistance to disease and the potential to recover following disease outbreaks 

Ecosystem condition, including biological attributes such as coral cover, condition and 

biodiversity, other ecosystem parameters (e.g., abundance diversity and structure of 

associated fish and invertebrate communities), and environmental attributes such as water 

quality, influence the resistance of corals and resilience of coral reef ecosystems. 

Variations in the local environments, including unusual exposure to heat stress, excessive 

sedimentation and nutrient loading, can play an important role in triggering coral disease 

outbreaks by increasing the susceptibility of corals to disease and potentially increasing 

the virulence of coral pathogens. Environmental stressors, along with other factors such 

as connectivity can also influence the ability of corals to recover from disease as well as 

the ability of degraded reef ecosystems to recover through recruitment. While managers 

can do little to address increasing sea water temperatures and other stressors associated 

with global climate change, it is possible to manage and mitigate local or regional 

human impacts such as unsustainable removal of keystone species (through fishing and 

other activities), excessive input of pollutants and sediments, boat anchoring and other 

physical impacts to reef ecosystems, and marine pollution associated with recreational 

and commercial vessels. 

There is a growing body of evidence linking environmental stressors to coral disease 

outbreaks. However, few programs are conducting detailed monitoring of water quality 

in concert with disease studies, and few attempts have been made to tease out 

relationships between specific stressors and occurrence of disease, or the threshold of 

these stressors that will trigger a change in the health of corals and/or manifestation of 

disease signs. Through concurrent water quality monitoring, it may be possible to 

statistically compare disease abundance at single time points with the concentrations of 

specific stressors, as well as relationships between changes in input of stressors (e.g., 

during periods of high rainfall vs low rainfall) and the incidence of disease. For sites 
 

73 

known to be affected by specific contaminants or environmental stressors, it may also be 

possible to identify specific physiological/biochemical responses of the coral host that 

can be used as an indicator for that parameter. The MWG proposed a number of actions 

that could help to elucidate the responses of corals to various stressors and ultimately 

identify those stressors that can be managed to reduce disease occurrence: 

Identify stressors in specific area(s) of concern (i.e., water quality: content of 

nutrients, suspended sediments, agricultural or industrial chemicals, 

pharmaceuticals, secondary petroleum products, temperature, recreational uses) 

and characterize their effect and impact on corals and coral reef ecosystems. As a 

first step to identify possible stressors that may exacerbate diseases, monitoring 

programs could be established along a gradient including reefs adjacent to a 

known impact (e.g., adjacent to a sewage outfall) and sites varying distances 

upstream and downstream. If adverse effects were detected, this could be 

supplemented with more detailed studies on responses of individual corals to 

those stressors (i.e., bioaccumulations targeted biomarkers analyses and 

ecotoxicological assays). 

Identify site-specific stressors of major concern and determine “threshold for 

action” based on clearly defined acceptable/unacceptable percent change. 

Metrics or parameters should be selected that are appropriate for the local area 

and acceptable/unacceptable percent change should be defined. 

Natural fluctuations should be considered when selecting metrics. 

Scientists and managers should be encouraged to work together in developing 

general guidelines to reduce specific stressors of concern. A guidebook for “best 

management practices” (BMP) for addressing key environmental stressors should 

be created and encompass alternative management practices such as limiting 

development to specific low-impact places, reducing recreation in sensitive areas, 

and offering other protocols for addressing specific problems in a given area. In 

areas where these BMP guidelines or manuals already exist, scientists and 

managers should work to reference, communicate and apply this information in 

management activities. 

Recommendation D.2.3: Develop disease education and outreach materials and 

incorporate these as components of existing educational programs (knowledge, 

attitude, behavior). 

Most communities know that their coral reef resources are steadily being depleted but 

often they do not understand why. Local citizens in the Pacific Region are generally 

unaware of the presence of coral disease and therefore the potential impacts that disease 

could have on the coral ecosystem. This lack of understanding poses a challenge to the 

coral disease research community in that they may have difficulty in convincing the 

public, politicians and managers that they should care about coral diseases and consider 

preventative actions to address coral diseases and their impacts. 

Educational efforts should include some very basic messages about coral disease and why 

they should care about disease, with a strong emphasis on encouraging stakeholders to 

take actions designed to improve overall coral ecosystem health. Because governments 
74 

usually do not have sufficient resources to enforce regulations effectively, education and 

awareness programs should target all stakeholders, emphasizing the need for local 

citizens to take ownership of the resources, including steps to address harmful activities 

they are responsible for, and to promote community based management. An essential 

component of education is actual participation, including involvement in assessing and 

monitoring status and trends of coral reefs and diseases. 

Additionally, specific educational materials should be developed for targeted agency 

administrators, policy-makers, managers and legislators that: 

Improve their general understanding of coral biology and factors as well as 

consequences associated with declining health of corals 

Provide detailed information on: 

Interconnected relationships between corals and manageable environmental 

stressors, 

Effects of these stressors on coral organisms and reef ecosystems, 

Importance of understanding when and why changes to reefs and ecosystems 

are occurring, and 

Rationale for taking action before visible signs of disease appear (e.g., tissue 

loss). 

Identify consequences of non-action in addressing disease situations, including 

economic ramifications of coral mortality and reef degradation. 

Communicate lessons learned from other reef areas – including regulations, 

legislation issues, and management responses that helped mitigate disease and/or 

improve the resistance and resilience of corals and associated organisms. 

Encourage local stakeholder advocacy to decision-makers. 

Recommendation D.2.4: Identify management actions needed to reduce other 

stressors that may make corals more vulnerable to disease 

Four very basic messages for local citizens and tourists were identified 

by the working group: 

Diseases can and do kill coral reefs. Death of these keystone species has 

caused major shifts in community structure in some locations which results 

in losses of valuable ecosystem function and services. 

Corals are living animals that often have algal symbionts. They are 

susceptible to disease, as all animals are, and therefore can get sick and die. 

Exposure to stressors can make corals more vulnerable to disease; the 

stressors include physical damage, land-based pollution and overfishing. 

Many of these stressors can be reduced or eliminated through adoption of 

best management practices.

Disease can kill reef organisms, including corals, and in some locations has 

caused major shifts in community structure and concurrent losses of 

ecosystem function.
 

75 

A variety of natural and anthropogenic factors place substantial stress on reef building 

corals long before any visible signs of disease appear. These can include: 

a. Contaminants and pollutants associated with degraded water quality that directly 

affect the growth, reproduction and ability of the coral to resist pathogens, such as 

certain chemical contaminants; 

b. Excessive growth of macroalgae and cyanobacteria that affect the long term 

survival of the coral and future recruitment potential (due to top-down factors 

such as loss of key herbivores or bottom up factors such as increased nutrients); 

c. Injuries to corals caused by physical impacts associated with ship groundings, 

anchoring and diver contact that provide an entry point for a pathogen; 

d. Population explosions of coral predators such as crown of thorns sea stars and 

corallivorous snails which may serve as vectors for disease; 

e. Increases in temperature and UV radiation as a result of climate change that affect 

the resistance of corals; and 

f. Direct introduction of pathogens through run-off, discharge of human sewage, 

atmospheric deposition, subsequent transport to reef ecosystems via water 

circulation as well as ship traffic (hull microbial communities and bilge water). 

Reefs are likely to be affected by several of these factors simultaneously, making it 

extremely difficult to tease out the importance of any specific factor(s) or a critical 

threshold for individual factors in terms of the relationship with coral disease. 

Furthermore some of these factors (e.g., temperature change) may be out of direct control 

by managers. However, management efforts geared towards reducing specific human 

impacts negatively affecting a given reef system (i.e., nutrient loading, sedimentation, 

overfishing, recreational and other human activities) may increase the local survivorship 

of corals and the resilience of reef ecosystems, thereby improve their resistance to 

infections and recovery following disease outbreaks. Therefore, it is crucial that initial 

management actions target efforts to reduce known land-based stressors by implementing 

best-management practices. 

Recommendation D.2.5: Develop and implement training modules for coral disease 

and health surveillance methodologies, field and laboratory research, and 

potential management actions in the Pacific Islands 

There is a critical need to develop and deliver training programs for multiple audiences 

covering a variety of topics related to coral health and disease in the Pacific Region. 

Effective training programs are needed to identify various coral disease research methods 

and to promote adoption of standardized methodologies across the region to allow 

comparative analysis of data to reveal regional patterns and trends, and allow 

comparisons among locations affected by different stressors. The WG suggested that the 

CDHC lead these efforts with assistance from the U.S. All-Islands Coral Reef 

Coordinating Committee2

. 

 

2 The US All Islands Coordinating Committee is a collaboration of marine resource managers working together with federal agencies

to strengthen the conservation and protection of coral reef ecosystems in the United States. http://allislandscorals.org/
76 

Key training areas identified by the WG include: 

a. Basic survey methodologies for coral disease; 

b. Disease outbreak incidence response protocols; 

c. Disease identification and standardized nomenclature (The workgroup suggests 

creating “disease-cards” that depict and describe distinctive disease signs, and 

diagnostic criteria to distinguish these signs, along with general information on 

coral species that are typically affected, reef areas where the disease may be 

observed, and how/where to report disease sightings); 

d. Advanced curriculum on coral disease-related topics with emphasis on field and 

laboratory investigation, including surveillance and sampling procedures, coral 

histology and physiology studies, disease epidemiology, and molecular methods 

including biomarker and toxicology studies; 

e. Management practices and options for coral disease prevention and outbreak 

response. Coral and natural resource managers in the Pacific would tremendously 

benefit from training on recommended management alternatives and lessons 

learned from Caribbean experiences, including the “A Reef Manager’s Guide to 

Coral Bleaching”, and management efforts in Australia. Instruction and guidance 

is also needed to assist agency personnel with determining whether the existing 

infrastructure in each jurisdiction is appropriate for managing disease events. 

This would include an assessment and evaluation of existing agency mandates 

and legislation, current regulatory processes and enforcement capabilities. 

Strategic Objective D.3: Develop a management program to respond to disease 

outbreaks. 

Recommendation D.3.1: Evaluate local agency mandates and existing legislation, 

regulations and legal framework for addressing disease 

Many aspects of coral reef research and monitoring, responses to unusual events or 

emerging issues, and proactive management actions can be delayed or obstructed due to 

lack of existing authorities to conduct an activity, complications with a permit process or 

policy documents with unclear provisions for disease-related activities. Existing 

mechanisms for permitting and implementing various coral reef activities, especially 

those directed at coral disease research and management should be evaluated to 

determine whether they are adequate and allow timely implementation of actions. 

Managers can participate by assisting responders with specific permitting processes and 

permissions and regulatory responsibilities that are required to allow rapid responses in 

the event of disease outbreaks. If existing permits or policies are insufficient, action can 

be taken to work with administrators, legislators, and local authorities to establish 

authority for timely and thorough responses to a disease outbreak to allow experts to 

conduct surveillance efforts, collect and transport appropriate specimens quickly, and 

take appropriate emergency response measures. This may include the establishment of a 

Memorandum of Agreement between responsible agencies. 
 

77 

Recommendation D.3.2: Develop local and regional infrastructure to respond to 

disease outbreaks and unusual mortality events. 

While the MWG recognized the need for and benefits of proactive management 

responses for diseases, they also acknowledged the likelihood of future disease outbreaks 

and the need to obtain timely information on the occurrence, extent, cause and impact of 

these events. The MWG also recognized the advantages of an organized, systematic 

approach to create diagnostic case definitions of the disease (e.g., What is it?), identify 

risk factors (Where did it come from? How is it spreading?), formulate possible measures 

to control and manage the outbreak, and predict the consequences under various 

scenarios. Currently, one of the largest limitations in our ability to respond is a lack of 

appropriate infrastructure, including: 

People capable of identifying and reporting unusual outbreaks when they first 

occur; 

Standardized surveillance and sampling protocols; 

Trained response teams; 

Capacity (e.g., boats, supplies, diagnostic laboratories) to respond in an effective 

and timely manner; and 

Existing system for reporting observations. 

The MWG was supportive of the CDHC’s proposed Incident Command System for 

responding to disease outbreaks. For this effort to be successful the MWG acknowledged 

the importance of outlining the desired response process, assigning roles and 

responsibilities, creating necessary response protocols, databases and communication 

mechanisms, and identifying gaps in permitting procedures and funding sources. The 

MWG recommended the following infrastructure elements: 

a. Develop a local response protocol following the CDHC basic response 

framework; 

b. Create local “Eyes of the Reef” initiatives including public education on various 

aspects of response such as disease identification, reporting, and volunteer 

monitoring (divers, reef check, NGO’s, academics); 

c. Create a response team with defined roles and responsibilities and identify 

training, equipment and permissions needed to be a responder; 

d. Define the communication structure between the response team and coral reef 

managers; 

e. Set up a central system and/or database for reporting observations and data; 

f. Explore mechanisms for setting up permits for emergency response and 

mitigation to include standard permits for defined coral disease responses; and 

g. Identify additional funding sources needed for a fully functional response system 

(i.e., response activities, communications, data analysis). 

Additionally, based on a cursory evaluation of agency mandates, legislation and 

regulatory processes there may be a need to revise or create clear policy guidelines that 

will allow for immediate decision making and response activities in the event of a disease 

incident. We recommend that proactive steps be taken, if needed, to develop appropriate 

policy statements and Memorandums of Agreement between local agencies that would 
78 

allow immediate resource-based decision making to implement timely response activities 

and protective measures, such as temporary closures or activity restrictions in critical 

areas. 

The CDHC model response protocol (Woodley et al. 2008) follows a tiered approach for 

responding which allows the level of response to be determined based on an assessment 

interview of the original observer of the disease outbreak (Level I response). 

If a Level II or Level III response is deemed appropriate, the MWG identified the need 

for timely reporting of findings to managers to allow implementation of possible 

management actions in a timely manner. This includes a recognized need for follow-up 

surveys to determine impacts on affected corals, fisheries resources and the ecosystem in 

general. The MWG identified the importance of adopting standardized monitoring 

protocols and ensuring sufficient human and financial capacity to support post-incident 

monitoring before the disease event occurs. Moreover, a communication plan should be 

outlined to ensure that critical post-incident monitoring information reaches coral 

managers in a timely manner so suitable management decisions can be made and 

corrective or protective actions can be implemented. 

Recommendation D.3.3: Identify ecological and economic cost and benefits of 

various management actions in response to disease outbreaks. 

In response to a disease 

outbreak or incident specific 

management actions may be 

called for to control the 

potential exchange of disease 

vectors to other reef areas 

during outbreaks, to 

minimize long-term damage 

to the ecosystem and to 

allow for enhanced recovery 

of the affected reef. 

Recommended actions to be considered by 

managers to enhance reef recovery: 

Modify MPA boundaries or zoning 

Temporary closures, activity restrictions 

Containment of affected area and adjacent 

reef area 

Decrease or limit adjacent land use and 

development for specified times

Use the permit process to control field 

activities related to coral disease
 

79 

Strategic Objective D.4: Identify priority coral disease and health research needs to aid 

in management. 

The MWG also recognized the need for enhanced collaboration with and support for 

local scientists conducting coral reef research with emphasis on encouraging activities 

that will lead to increased understanding of coral disease and disease processes. 

Recommendation D.4.1: Create a CDHC Pacific Research Plan that emphasizes 

regional disease priorities. 

The MWG identified the need for additional meetings involving both scientists and 

managers to: 

More thoroughly review existing knowledge of coral diseases in the Pacific; 

Identify specific critical gaps hindering effective responses to disease outbreaks 

and management actions to mitigate diseases; and 

Identify a strategy to address these information gaps. 

As a starting point, the Strategic Objectives originally laid out in the 2003 CDHC 

National Research Plan (Woodley et al. 2003) should be revisited and reviewed to 

identify outstanding research priorities that apply nation-wide and identify an approach to 

fill these gaps. Eight regional research needs were identified by the MWG which will 

ultimately provide essential information to make better management decisions for 

preventing, responding to and managing disease outbreaks in the Pacific include:

Conduct economic valuations of coral reef ecosystems and associated resources 

where valuations have not been completed yet. 

Explore the potential to incorporate disease factors into modeling. 

Investigate how Pacific island cultural and social practices enhance or detract 

from management efforts and how are they can be better incorporated into 

management strategies. 

Conduct targeted disease transmission experiments under controlled conditions. 

Develop research projects to explore potential treatments and possible cascading 

effects of disease. 

Conduct research aimed at developing feasible and effective recommendations for 

action and mitigation strategies and establishing thresholds for action. 

Establish links between ecosystem health and organism health in coral reef 

ecosystems. 

Encourage interdisciplinary research following a watershed approach to link landbased stressors to coral disease. 

Strategic Objective D.5: Environmental and Human Health Safety Issues. 

Inherent in disease studies is some measure of risk to human and environmental health. 

Those working with diseased organisms and putative infectious agents must recognize 

that a potential exists for humans to become infected (though most likely a small risk) or 

they and/or their equipment may serve as inadvertent vectors to other corals and to other 
80 

locations. Just because coral disease occurs in an aquatic environment, does not make it 

completely safe to study and without risk. There are common practices that medical 

science adheres to when dealing with potentially infectious disease outbreaks (of known 

or unknown origin) or toxic events and are applicable, regardless of whether the focus is 

human disease or coral disease. Preventative containment measures are a logical option 

to mediate risk. Containment measures are relatively easy to apply in the aquatic 

environment and therefore should be included as part of each response activity 

particularly to limit the possible spread of infectious agents. The three recommendations 

listed below target important areas where managers can assist in coral disease 

management. 

Recommendation D.5.1: Create an awareness of the dangers of outplanting aquaria 

raised corals. 

There are significant issues related to placing captive animals into the wild. If not closely 

scrutinized catastrophic consequences can occur, even with the best of intentions. 

Though restoration efforts are important considerations for reef management in certain 

locations, it is also important to conduct a hazards analysis to avoid bringing modified 

organisms (through captive conditions) into the wild that may present an unacceptable 

risk to other wild species within the ecosystem. To fully explore the benefits and dangers 

will require a focus group to evaluate this issue and provide recommendations. 

Recommendation D.5.2: Develop requirements for containment measures needed 

for conducting disease transmission studies 

Bio-safety and bio-containment are critical issues when conducting disease research. 

Veterinary research facilities for aquatic and terrestrial animals have rigorous guidelines 

for handling sick and diseased organisms, as do domestic (e.g., U.S. Department of 

Agriculture) and international groups (OIE, World Organization for Animal Health). 

The guidelines and practices of these groups should function as a role model for adopting 

similar guidelines tailored for coral disease research. Development of these guidelines 

will require a team of coral disease researchers to interface with experts and practitioners 

of animal health, bio-security and bio-containment to develop methods appropriate for 

tropical marine systems. 

Recommendation D.5.3: Develop recommended methods for decontamination of 

dive gear. 

This is a specific project that can have wide spread management applications and is an 

obvious follow on to Recommendation 5.1. Determining the risk associated with dive 

gear in transmitting disease to either humans or marine organisms is vital to provide a 

basis for risk management options. Once the risk level is determined it is important to 

provide a means of decontamination that is safe and effective for both the user and the 

environment. Results of such a focused study can provide an unambiguous tool to help 

manage coral disease on a local level. 
 

81 

Management Perspectives Working Group Members: 

Jennifer Kozlowski (Chair) –NOAA CRTF efforts, Silver Springs, MD 

Amanda McLenon (Recorder) - NOAA, Charleston, SC 

Greta Aeby - HIMB, UH, Honolulu, HI 

Jeff Allen - Clemson University, Clemson SC 

Melissa Bos - DAR and Alliance, Honolulu, HI 

Kay Briggs - U. S. Geological Survey, George Mason Univ., Reston, VA 

Takiora Ingram - All Islands Committee Secretariat, Honolulu, HI 

Katie Siegler - NOAA Fellow- Honolulu, HI 

Bernardo Vargas - NOAA, Honolulu, HI 

Dana Williams - NOAA NMFS, Miami, FL 
82 

E. ‘WHITE PAPERS’ 

The opening day of the workshop focused on presentations derived from 14 position 

papers, to provide context and concepts for the break-out group discussions. The 

presentations, included in this section, covered key topics: 

What do we currently know about coral diseases in the Pacific?

What lessons have we learned from Caribbean disease outbreaks? 

Diagnostic methods, systems biology and leveraging post-genomic technologies 

Emerging diseases, disease outbreak investigations and ecological epidemiology 

How to integrate science with social, economic and political values? 
 

83 

I. INTRODUCTION—SETTING THE STAGE

CORAL DISEASE AND HEALTH CONSORTIUM (CDHC) 

Cheryl M. Woodley 

NOAA NOS CCEHBR 

Hollings Marine Laboratory 

331 Ft Johnson Rd. 

Charleston, SC 29412 

cheryl.woodley@noaa.gov 

CDHC - VISION 

“To understand and address the effects of natural and anthropogenic stressors on 

corals in order to contribute to the preservation and protection of coral reef 

ecosystems.” 

CDHC - WHO ARE WE? 

The Coral Disease and Health Consortium (CDHC) was created in 2002, in response to 

the U.S. Coral Reef Task Force’s (USCRTF) National Action Plan to Conserve Coral 

Reefs (United States Coral Reef Task Force 2000). Our goal is to provide coastal and 

ocean managers with scientific understanding and tools to help protect healthy coral reef 

ecosystems and restore degraded ones. The CDHC is a network of field and laboratory 

scientists, coral reef managers, and agency representatives devoted to understanding coral 

health and disease. It is extensive, highly collaborative, and completely voluntary. 

Currently over 150 partners, from federal agencies, EPA, DOI, NOAA along with 

academia, non-profit and industry, contribute their time and expertise to the CDHC, 

while the organizational 

infrastructure is supported by the 

congressionally funded NOAA’s 

Coral Reef Conservation Program. 

The commitment to share 

information, ideas, and common 

goals led to the development of a 

national research plan, Coral 

Disease and Health: A National 

Research Plan (Woodley et al. 

2003), that has inspired many to 

seek funding and devote new 

resources to the study and 

amelioration of coral disease. 

Members of the CDHC come from a variety of backgrounds, but all have a common 

commitment to share information, ideas, and common goals to further the study of coral 
84 

disease and in so doing identify ways to better manage coral disease. We encourage 

participation of anyone sharing our vision and goals. 

CDHC - WHY? 

Recent reviews have documented an explosion in the incidence of disease, particularly in 

the Caribbean. The first disease report occurred in 1965 related to skeletal anomalies 

(Squires 1965), with the next report coming 8 years later by Antonius (1973), from these 

reports through the early 1990s, only four diseases had been recognized: skeletal 

anomalies, Black band, White plague Type I, and Shutdown reaction (Sutherland et al. 

2004). Since the early 1990s, monitoring programs in the Florida Keys have documented 

a sharp increase in the number and prevalence (the ratio, for a given time period of the 

number of occurrences of a disease or event to the number of units at risk in the 

population) of coral diseases. Reports from the Indo-Pacific suggest an emerging crisis 

in coral disease as monitoring efforts are able to explore new areas. 

The picture of coral disease has expanded from the simple perception of an infectious 

disease agent to a plethora of possible interactions with a variety of possible agents 

attacking not just the coral animal, but an intricate group of organisms consisting of plant, 

animal and microbial associates. The complexity of this growing disease problem made it 
 

85 

more difficult to design management regimes and increased significantly the need for 

cross-disciplinary tools to combat the problem (see diagram below). 

Realizing these were complex and complicated issues, we recognized that our lack of 

understanding of the underlying mechanisms of coral pathologies was inhibiting our 

ability to manage the growing number of coral health problems. Also, to improve our 

ability to identify the factors responsible for coral health decline and increased disease 

incidence would require embracing a new paradigm of scientific investigation that 

incorporates new methods and new technologies able to help elucidate mechanisms that 

link cause and effect relationships so the field could move from just descriptive science 

into mechanistic science. 

There was an obvious need to unify the coral disease community, build scientific skills 

and capacity, and provide standardization in investigative nomenclature, methodologies 

and technologies in order to competently communicate and interact with other main 

stream disease fields (e.g., pathology, cell biology, physiology, infectious disease, 

toxicology, medicine). In response, the CDHC was organized in 2002 when 50 experts 

from various disciplines and perspectives from science to management, met and 

developed what we now refer to as the Coral Disease and Health: A National Research 

Plan (Woodley et al. 2003). This document provided an integrated roadmap that began 

tying these ideas together. This document outlined gaps in our knowledge and 

recommended research directions needed to support this new paradigm. Four major 

themes with accompanying strategic objectives were identified: Biology (6), Disease 

Identification and Disease Investigation (4), Disease Diagnostics (5) and 

Environmental Factors Affecting Susceptibility and Infectivity (11). The 26 

recommendations encompassed 9 topic areas: Nomenclature, Model System(s), Field 

Assessment of Coral Reef Condition, Microbiology, Toxicology, Histopathology, 

Molecular, Bioinformatics, and Advanced Education and Outreach. 

CDHC: WHAT ARE WE DOING? 

Research 

Information is limited on the physiological parameters that define healthy coral and even 

less on coral pathology. Our challenge is to apply advanced technologies in functional 

genomics, proteomics, toxicology, and systems biology to expand our knowledge to 

understand and recognize coral health and elucidate disease dynamics. The knowledge 

gained from this research approach is positioning us to move aggressively toward 

characterizing the processes that control ecological connectivity among reefs and 

discover critical control points for management strategies. The first step is to establish 

and make available tools that can support discovery and applied research. For example, 

CDHC efforts have helped establish transcriptomic resources from expressed sequence 

tag (EST) cDNA projects with over 30,000 coral EST sequences publically available 

from five species: Montastraea annularis, Oculina varicosa, Porites astreoides, 

Acropora palmata and A. millipora. There are also over 28,000 ribosomal gene 

sequences cloned from coral-associated bacteria available to assist in microbial diversity 
86 

and pathogen research efforts. This type of information is vital and basic to developing 

an understanding for how an organism responds to its environment, is key to developing 

diagnostic tools to assess coral health and lays the foundation for identifying critical 

control points and viable management options. 

Diagnostic Resources 

There is limited application of medical/veterinary knowledge or protocols to the study of 

coral health and disease, resulting in ambiguous and often misleading communication of 

findings. Compounded by inadequate diagnostic tools and insufficient application of 

diagnostic procedures, the challenge is to develop standardized procedures based on 

medical principles that clearly define terminology, pathology and diagnostic criteria. 

Education 

Experts in coral biology, pathology and veterinary science are developing resources and 

web-enabled tools for use in recognizing gross signs of disease and in clinical diagnostic 

pathology as well as developing case definitions for selected coral syndromes. The webtool will be used to guide investigators in the diagnostic process. Additional modules are 

planned that will include virtual slide technologies for distance learning coral histology 

and histopathology, consultation with experts on disease cases, and continuing education 

through regular ‘grand round’ web meetings. 

Diagnostic Tools 

Consortium members have achieved significant advances in diagnostic assay 

development that assist researchers in identifying coral stressors. Examples of new 

techniques include: 

DNA probe for the White Plague agent – Dr. Laurie Richardson, Florida Atlantic 

Univ. 

DNA sequence analysis for the White Pox agent Serratia marcescens (newly 

designated 'White Pox Serratiosis' when the presence of S. marcescens is 

confirmed) - Dr. Kathryn Sutherland, Rollins College, Winter Park FL 

Coral immuno-competence (IMCOMP) assay to assess the presence of 

antimicrobial agents within coral tissue by using a modified bacterial viability 

assay – Dr. Craig Downs, Haereticus Environmental Laboratory 

PCR-screening test for recognized pathogens – Dr. Shawn Polson, Univ. Delaware 

& NOAA NOS Charleston, SC

DNA Abasic site lesions – NOAA NOS Charleston, SC

Various toxicity tests are being adapted or modified to address development, 

mutagenesis, and cellular pathologies associated with toxicant exposures. 
 

87 

Specialized Resources 

Several specialized resources that help build capacity and provide outreach and 

educational opportunities are being made available by members of the CDHC. These 

include: 

International Registry of Coral Pathology (IRCP) supported by NOAA, Oxford, 

MD, is a research tool and resource of voucher materials for the coral research 

community. Submission, holdings and acquisitions are located at 

http://www.chbr.noaa.gov/InternationalRegistry.html. For more information 

contact Dr. Shawn McLaughlin, shawn.mclaughlin@noaa.gov 

Annotated cnidarian bibliography containing >5000 references and abstracts 

available as an ENDNOTETM library or on CD, is supported by a complete set of 

reprints and is accessible on an individual basis on site in Charleston, SC. Contact 

Dr. Sylvia Galloway, sylvia.galloway@noaa.gov for more information. 

CDHC Website and Listserve – Supported by NOAA's Coral Health and 

Monitoring Program at the Atlantic Oceanographic and Meteorological 

Laboratory in Miami, FL. http://coral.aoml.noaa.gov/mailman/listinfo/ 

http://www.coral.noaa.gov/coral_disease/ 

CDHC – VISION FOR ACTION - WHY ARE WE HERE AT THIS MEETING? 

The overarching goal for us is to “Promote the effective detection, identification and 

management of coral reef diseases”. To do this a plan of action is needed that will 

‘Chart a course for coral health and disease in the Pacific and Indo-Pacific’. We have 

convened this meeting to: 

Synthesize the state of knowledge of Pacific coral diseases 

Develop a strategic plan to: 

Identify research needs to help understand etiologies, epidemiology and ecology 

of coral diseases 

Identify innovative strategies for disease management on coral reefs 

Identify novel strategies to engage public and political sectors in partnering with 

us to combat the spread of coral disease 

Disease 

“any impairment that interferes with or modifies the performance of normal 

functions, including responses to environmental factors such as nutrition, 

toxicants, and climate; infectious agents; inherent or congenital defects, or 

combinations of these factors” Wobeser 1981.
88 

References: 

Antonius, A. 1973. New observations on coral destruction in reefs, Abstract, p. 3-3. 

Tenth Meeting of the Association of Island Marine Laboratories of the Caribbean. 

University of Puerto Rico. 

Squires, D. F. 1965. Neoplasia in a coral? Science (Wash.) 148: 503-505. 

Sutherland, K. P., Porter, J. W. and Torres, C. 2004. Disease and immunity in Caribbean 

and Indo-Pacific zooxanthellate corals. Mar. Ecol. Prog. Ser. 266: 273-302. 

United States Coral Reef Task Force. 2000. The National Action Plan to Conserve Coral 

Reefs. Washington, DC. 34pp. 

Woodley, C. M., Bruckner, A. W., Galloway, S. B., Mc Laughlin, S. M., Downs, C. A., 

Fauth, J. E., Shotts, E. B. and Lidie, K. L. 2003. Coral Disease and Health: A 

National Research Plan. National Oceanic and Atmospheric Administration, 

Silver Spring, MD. 72p. 
 

89 

STUDYING CORAL DISEASES; UNDERSTANDING THE NORM

E. Kramarsky-Winter 

Dept. of Zoology 

Tel Aviv University 

Tel Aviv, Israel 69978 

wintere@post.tau.ac.il 

Coral disease incidence has been on the rise for the past thirty years. Within that 

time frame approximately 30 new syndromes and diseases have been identified. To date, 

only few diseases or syndromes have been characterized in terms of causality and even 

fewer have been characterized in terms of the physiological effect on the coral. 

The coral holobiont may be considered a "super-organism" composed of the coral 

host, its algal symbionts, and accompanying microorganisms. Since disease is defined as 

"any deviance from normal physiological function of an organism" it then becomes no 

trivial task to ascertain the physiological norm of this complex "super-organism". 

In corals, disease signs and symptoms are usually classified by superficial signs, 

such as color change, tissue loss pattern, or changes in gross colony architecture. This 

simplistic classification is due to the inadequacy of information available describing basic 

biological and physiological processes that could provide the baseline for comparison. 

For example, information pertaining to cellular processes responsible for coral 

calcification and growth is still rudimentary. This is also true for information pertaining 

to biochemical regulation of coral reproduction. Similarly though mechanisms of tissue 

repair and regeneration have been studied at the organismal level, only recently have they 

begun to be assessed at cellular and molecular levels. Since these are all vital biological 

processes without which corals could not survive, understanding them is crucial to our 

perception of normal coral physiology. In turn understanding the norm will allow for a 

proper diagnosis of deviation from it. 

The use of "the diagnostic method" borrowed from the world of medicine may 

prove useful in elucidating disease processes. This method incorporates performing a 

"clinical" examination that includes historical and current information about the coral in 

order to determine its state and provide a diagnostic interpretation. The purpose of this 

examination is to detect overt changes in carefully chosen assessment end-points with 

known reference values. This will only really be possible though, once basic reference 

values have been established. The elucidation of physiological regulatory pathways will 

improve our understanding of how the coral holobiont responds to stress and will assist in 

formulating standards for proof of cause-and-effect relations and provide information on 

how environmental change could affect host-pathogen relations and immune defenses. 

 It is clear that assessment of coral health should be not be carried out only on a 

single level of biological organization, but should be evaluated across a hierarchy of 

organization including molecular, biochemical, cellular and tissue-level and whole 

organism phenomena, and include population metrics as well. Once these parameters are 

evaluated as a whole, we will be much better equipped to properly diagnose and mitigate 

coral disease. 
90 

II. GLOBAL PERSPECTIVE OF CORAL DISEASE

THE GLOBAL PERSPECTIVE OF INCIDENCE AND PREVALENCE OF 

CORAL DISEASES

Andrew Bruckner 

NOAA Fisheries 

Coral Reef Conservation Program 

Office of Habitat Conservation 

1315 East West Highway 

Silver Spring, MD 20910 

andy.bruckner@noaa.gov

ABSTRACT 

Diseases occur globally in most coral reef habitats whether near human 

population centers or remotely offshore. They generally affect a low proportion of the 

susceptible species, although localized outbreaks have produced significant mortalities to 

scleractinian corals, gorgonians, sea urchins, reef fish, sponges, algae and other coral reef 

organisms (Peters, 1993; Harvell et al., 1999; Williams and Bunkley-Williams, 2000). 

There are now over 30 named diseases in the Caribbean basin affecting 45 zooxanthellate 

scleractinian corals, three hydrozoan corals, ten octocorals, two zoanthids, nine sponges 

and two crustose coralline algae (Green and Bruckner, 2000; Weil et al., 2006), and at 

least seven major diseases from the IndoPacific, along with about 30 additional 

conditions that are associated with compromised health in scleractinian corals. While an 

apparently unprecedented increase in disease occurred in the Caribbean since the 1980s, 

much less is known about the status of disease in the IndoPacific and Red Sea. Surveys 

over the last decade in Australia, Palau, East Africa, the Philippines and other locations 

have revealed new diseases, suggesting a rapid emergence of disease, or at least a 

realization of their presence, throughout the Indo-Pacific. Between 1972 and 2005 coral 

diseases were reported on 39 genera and 148 species worldwide, with observations in 63 

countries. Although Pacific reefs have a higher diversity of reef-building corals than the 

Atlantic and harbor 92% of the world’s coral reefs (Spalding and Greenfell, 1997), only 

14% of the global observations of coral disease were from the Indo-Pacific during this 

period (Green and Bruckner, 2000, Sutherland et al., 2004, GCDD, 2007), and 58% of all 

coral disease records are for BBD, WBD and WP. The Caribbean has historically been 

referred to as a “hotspot” for disease, largely because of the rapid emergence, high 

prevalence, wide distribution, large numbers of host species, and virulence of diseases in 

this region. 

There are eight major diseases (BBD, WP, WBD, YBD, DSD, WPX, ASP and 

tumours) that have been reported from throughout the western Atlantic along with 

another 32 conditions (including different “types” of the major diseases) that have been 

reported since 1972. WBD, BBD and WP were first reported from the Caribbean in the 

1970s from a small number of countries, with observations expanding to new locations 

during the 1980s including reports of WBD from about half of the Caribbean nations. 

During this period, BBD and WP caused localized mortality, while WBD contributed to a 
 

91 

regional decline of Acropora. Reports of WBD decreased dramatically during the 1990s, 

and then increased again since 2000, with most reports on A. cervicornis. Reports of WP 

and BBD have also escalated since 1998, with recent observations from 24 countries. 

While low level chronic infections of BBD have been observed on the same reef for years 

to decades, WP prevalence has dramatically increased since 1998, with outbreaks 

occurring over an expanding range. Many other new diseases have been reported on 

western Atlantic reefs since the mid 1990s, including four (DSD, YBD, WPX and ASP) 

that are widely distributed and four (YBD, WPX, WP-II and ASP) that are causing 

substantial coral mortality. Close to 80% of all western Atlantic corals are affected by 

diseases (41 species of scleractinian corals, 8 gorgonians, 2 hydrozoans), with some 

corals (especially M. annularis complex) being susceptible to as many as 8 diseases and 

corals showing signs of 2-3 diseases at one time. During the 1970s-early 1990s 

acroporids were most severely impacted by disease, while massive and plating corals, and 

in particular the M. annularis complex, are being affected more severly today. WP is the 

most virulent disease and has the widest host range. 

Coral diseases were first reported from the IndoPacific and Red Sea in the late 

1970s. Most observations during the 1970s and 1980s were for BBD and WBD by a 

single researcher working in three countries (Philippines, Egypt and Saudi Arabia), along 

with additional reports of abnormal skeletal development (tumors). By 1994, diseases 

had only been reported from six countries, including several new conditions first 

observed on reefs in Australia. In the mid to late 1990s, several new diseases emerged 

(YBD, SEB, PUWS), but these and other diseases were restricted to a few countries. 

IndoPacific diseases appear to be exhibiting a rapid expansion in range and in the types 

of disease since 2000. This includes reports from new regions that were previously 

unaffected (South Africa, Solitary Islands), a higher percentage of reefs in certain 

locations (e.g., Great Barrier Reef Australia) with diseases, an increasing incidence of 

diseases, and an emergence of several new conditions (fungal disease, WS, BrBD, Pink 

Line). Fast growing corals in the family acroporidae and pocilloporidae in the IndoPacific 

are affected by the largest number of diseases and are observed with disease more 

frequently than all other species. 

Introduction 

Coral reefs have experienced unprecedented losses of live coral cover from 

anthropogenic and natural stressors during the last three decades (Byrant et al., 1998; 

Jackson, 2001; Pandolfi et al., 2003). Coral diseases are one of the major factors 

responsible for this decline, especially in the wider Caribbean (Harvell et al., 1999; 

Aronson et al., 2003; Gardner et al., 2003). The Caribbean has been referred to as a “hot 

spot” for coral diseases, due to the rapid spread, wide distribution, expanding host ranges, 

and increased virulence of these diseases (Rosenberg and Loya, 2004; Weil, 2006). In 

addition to black band disease (BBD), white plague (WP) and white band disease 

(WBD), which have persisted on Caribbean reefs since the 1970s, there has been a recent 

emergence of diseases with new types of pathologies and elevated rates of tissue 

mortality (Richardson and Aronson, 2002; Weil, 2004). 

By the late 1990s, diseases had been observed on 102 coral species in 54 different 

nations, with 27 diseases reported from the Caribbean and 13 from the Indo-Pacific and 

Red Sea (Green and Bruckner, 1999). Over 66% of these reports were for BBD, WBD 
92 

and WP in the western Atlantic (Green and Bruckner, 2000; Sutherland et al., 2004). 

Although western Atlantic reefs exhibit a low diversity of reef-building corals relative to 

the IndoPacific, and they constitute only 8% of the world’s coral reefs (Spalding and 

Grenfell, 1997), this region hosted a disproportionate number of diseases and affected 

corals (>80%) (Sutherland et al., 2004). 

Although coral diseases were reported from the Indo-Pacific in the 1980s 

(Antonius, 1985), the vast majority of these observations were made by one researcher in 

the Red Sea and Gulf of Arabia (Antonius, 1985; 1987; 1988). Recent surveys conducted 

in Australia (Willis et al., 2004), western Indian Ocean (McClanahan, 2004), Philippines 

(Raymundo et al., 2004), and Red Sea (Loya et al., 2004) illustrate the widespread, global 

distribution of coral diseases. Through annual and semi-annual monitoring programs on 

the Great Barrier Reef Australia, the Philippines, and other locations, researchers are 

identifying coral diseases on a greater number of reefs and species, and disease incidence 

appears to have increased since the late 1990s, suggesting that diseases have become 

more prevalent in the IndoPacific over the last five years (Raymundo et al., 2003; Willis 

et al., 2004; Kaczmarsky, 2006). However, it is difficult to determine “baseline” levels 

of coral diseases, and conclusively state that diseases are increasing, as the proliferation 

of reports at least partially reflects an increased monitoring effort. 

Increases in the types of diseases and their abundance and severity may be at least 

partially related to an overall deterioration of the marine environment due to human 

stressors (e.g., land-based pollutants), climate warming, and other changing 

environmental conditions (Harvell et al., 2002; Kuta and Richardson, 2002; Garrison et 

al., 2003; Kaczmarsky et al., 2005). Sediment, sewage, toxic chemicals and other 

pollutants may facilitate disease outbreaks by introducing opportunistic pathogens, 

increasing pathogen virulence, and reducing host resistance (Antonius, 1977, Ducklow 

and Mitchell, 1979; Peters, 1984; Peters, 1993). However, reefs removed from direct 

anthropogenic inputs are also being impacted by disease (Santavy and Peters, 1997; Weil, 

2004; Bruckner and Bruckner, 2006) highlighting potential associations between disease 

and elevated temperatures, light levels and other manifestations of global climate change 

including coral bleaching. Corals live close to their thermal tolerance limits, and a 1-2°C 

increase in SST is sufficient to induce coral bleaching. Recent outbreaks of WP in the 

eastern Caribbean following the 2005 bleaching event (Miller et al., 2006; Weil et al., 

2006), provide additional evidence that bleached corals have a higher susceptibility to 

other diseases. 

 

The Global Coral Disease Database 

To begin gathering more comprehensive data on the global distribution and 

abundance of coral diseases, and quantify relationships between coral disease and various 

environmental stressors, NOAA Fisheries worked with the United Nations Environmental 

Program’s World Conservation Monitoring Centre (WCMC) to develop a Global Coral 

Disease Database (GCDD)4 . The GCDD is a web-accessible GIS database that 

compiles records of disease observations and tracks their spread over time, by georeferencing disease locations and plotting their occurrences onto WCMC coral reef 

 

4 http://development.unep-wcmc.org/GIS/Coraldis/index.cfm 
 

93 

distributional maps. The GCDD includes a new online mapping tool (prototype IMAPS 

tool) that enables users to search and plot data by disease name and year, with zoom 

capabilities and full information sheet for each line of data. For each disease, information 

can be obtained on its global and regional occurrence and abundance, affected locations 

(e.g., country, reef, latitude and longitude) and species, and any available site-specific 

data on prevalence, incidence, and extent of mortality. A summary of all in situ 

observations on the prevalence, range of species affected, global geographic distribution, 

and mortality for reported coral diseases up to 1999 (2076 records of coral disease from 

155 references) are included in the first iteration of the GCDD. The second version of 

the GCDD includes over 7100 data points compiled from information available through 

December, 2005, including peer-reviewed literature, grey literature, regional monitoring 

data from AGRRA (Atlantic and Gulf Rapid Reef Assessment surveys conducted 

between 1998-2000 in 22 countries; Lang, 2003), CARICOMP (survey of 19 reef sites 

from 6 countries in the Caribbean; Weil, 2004), Reef Check, and other programs, and 

reports submitted by researchers. These datasets reflect wider spatial coverage of disease 

surveys, repeat surveys, and increases in the types of diseases and species affected. 

Global diversity and distribution of coral diseases 

The GCDD contains records for over 40 coral diseases from the western Atlantic, 

28 from the IndoPacific and 5 from the Red Sea that were reported between 1972 and 

2005 (Table 1-4). Five coral diseases [BBD, WBD, WP, red band disease (RBD) and 

shut down reaction (SDR)] were first observed in the western Atlantic 20-30 years ago 

and three of these (BBD, WBD, SDR) were also reported from the Red Sea and 

IndoPacific during the 1980s (Antonius, 1977, 1981, 1985). Five other diseases [WP 

type II, white pox (WPX), yellow band disease (YBD), dark spots disease (DSD) and 

Aspergillosis (ASP)] first emerged on Caribbean reefs in the 1990s; all of these diseases 

(with the possible exception of DSD), have caused significant localized mortality and 

they represent continuing major threats to western Atlantic coral reefs. More recently, 

five IndoPacific diseases [white syndrome (WS), YBD, fungal syndrome, Porites 

ulcerative white spot disease (PUWS)] are causing substantial localized mortality and the 

prevalence of two of these (WS and PUWS) appears to be increasing. In addition to 

diseases that are presumed to be caused by bacteria, fungi and cyanobacteria, several 

conditions with rapidly expanding ranges [skeletal eroding band (SEB) and brown band 

disease(BrBD)] are being caused by ciliates and one disease observed so far only in 

Hawaii results from infection by a trematode (Plagioporus). Skeletal anomalies (tumors, 

hyperplasia, neoplasia, calicoblastic epitheliomas) have been reported from the Atlantic, 

Pacific and Indian Oceans and the Red Sea since at least 1965 (Squires, 1965), but few 

data are available on prevalence or impact. Some conditions are visible only with 

microscopy (e.g., coccidian infections, nematopsis spores). Most of the other conditions 

have been observed infrequently or are confined to localized areas. 

A lot of confusion has been created by many reports of new diseases over the last 

ten years. There are also at least 19 other diseases that have been assigned on the basis of 

a few or single observations. These include 1) conditions presumed to be caused by a 

pathogen but later shown to result from predation; 2) conditions that lack details on gross 

signs or photographic documentation, or evidence of coral tissue destruction; 3) 

terminology that has been used interchangeably to describe similar signs, such as the 
94 

various white syndromes; and 4) similar conditions identified in the Caribbean that have 

been split into two or more syndromes (e.g., “Type 1” and “Type II”), based on rates or 

patterns of disease spread or species affected. Because of the difficulty in verifying 

which “type” of disease is present based on single observations (e.g., initial signs of 

infection may look different than later stages and rates of spread may vary over the 

duration of the infection), many researchers do not differentiate between types, or they 

use a different name overall (e.g., “plague-like”). Examples from the Caribbean include 

1) white plague type I, II, II (Richardson and Aronson, 2002); 2) WBD type I and II; 3) 

DSD type I, II, dark band syndrome, purple band syndrome and tissue necrosis (Weil, 

2004); and 4) white pox, patchy necrosis and necrotic patch syndrome. 

1. White syndromes 

There is a proliferation of names for coral diseases that are characterized by white 

lesions with a sharp, distinct line between apparently healthy tissue and exposed skeleton 

and an absence of an obvious microbial community at the disease line. These have been 

separated based on the identification of variable features such as 1) a zone of bleached 

tissue that may or may not be present used to differentiate WBD type I from WBD-II, 

differences in the rates of tissue loss and patterns of spread in WP type I, WP-II and WPIII, or differences in affected species (WP versus WBD). Antonius (1977, 1981) and 

other colleagues reported WBD on acroporids and other massive and plating corals in the 

western Atlantic, as well as corals in the IndoPacific. Other researchers from the 

Caribbean report WBD on Acropora and refer to similar signs in other host species as 

WP (Dustan, 1977; Richardson et al., 1998). 

 
 

95 

Table 1. Diseases, syndromes, abnormal tissue conditions, and parasitic infestations of scleractinian corals 

and gorgonians on coral reefs in the tropical western Atlantic. 

condition geographic range host species source

Black band disease 

(BBD) 

W. Atlantic, 25 

countries 26 scleractinians, 1hydrozoan, 6 

gorgonians: faviids, Agaricia, 

Siderastrea, Meandrina; A. 

palmata2

, P. astreoides, P. 

porites3

, Madracis mirabilis, M. 

decactis4

Antonius, 1972 2

GarzonFerreira et al.. 2001; 3

G. 

Smith4

Sutherland et al., 

2004 

White band 

disease (WBD) 

Caribbean, 27 countries A. palmata, A. cervicornis 1Gladfelter et al., 1977 

WBD type II Bahamas, Puerto Rico A. cervicornis Richie and Smith, 1995; 

Weil, 2006 

White pox (WPX) Bahamas, Florida, Cuba 

Puerto Rico, Jamaica 

A. palmata 

Synonyms: Patchy necrosis2 

Necrotic patch syndrome3

Porter, 1996 Patterson et 

al., 2002; Bruckner and 

Bruckner, 19972 JordanDahlgren and RodríguezMartinez, 20043

Plague (WP) 20 countries 31 species GCDD records 

WP type I Florida and Bahamas Mycetophyllia, Montastraea, 

Colpophyllia, Agaricia, Mussa, 

Stephanocoenia, Porites; 12 

species 

Dustan, 1977; 1984 

WP type II Bermuda, Bonaire, 

Colombia, Florida, 

Jamaica, Mexico, 

USVI, Puerto Rico, 

Venezuela 

D. stokesi and 17 other species1 41 

species2

Richardson et al., 1998 

2

Weil et al., 2006 

WP type III Florida large corals (M. faveolata, C. 

natans) 

Richardson, 2000 

Yellow band 

disease (YBD) 

12 countries M. annularis complex; M. 

cavernosa; C. natans and other 

faviids ; P. astreoides; A. 

agaricites

Reeves, 1994; Cervino et 

al., 2001; Bruckner and 

Bruckner, 2006 

Dark-spots disease 

(DSD) 

Caribbean M. annularis, S. siderea, S. 

radians, S. intersepta; 1 also M. 

franksi, M. faveolata and M. 

cavernosa2

Garzón-Ferreira and GilAgudelo, 1998; 2

GarzonFerreira et al.. 2001 

DSD- II Bermuda, Bonaire, 

Colombia, Puerto Rico, 

Venezuela 

S. intersepta, M. annularis, M. 

faveolata, M. cavernosa, C. 

natans, C. amaranthus, S. siderea

Weil et al., 2002; Weil, 

2004; Weil, 2006 

Dark band 

syndrome (DBS) 

Puerto Rico, Mexico M. annularis, M. faveolata Weil, 2002;2004 

Purple band 

syndrome (PBS) 

Grenada, Venezuela S. siderea, S. intersepta Weil, 2004 

Tissue necrosis Puerto Rico M. faveolata Weil, 2004 
96 

Table.1a. Syndromes reported for scleractinian corals and gorgonians in the tropical western Atlantic 

(continued). 

Red band disease (RBD) 

type I 

Bahamas, Belize, Bonaire, 

Colombia, Costa Rica, 

Curaçao, Dominica, Puerto 

Rico, Jamaica, Mexico, 

Turks and Caicos, Florida 

11 species: Gorgonia, 

Agaricia, Colpophyllia,

Mycetophyllia, Diploria, 

Stephanocoenia Millepora, 

Meandrina, Montastraea, 

Porites, Siderastrea. 

Rützler et al., 1983; 

Santavy and Peters, 

1997 

RBD type II Bahamas, Mexico D. strigosa, M. annularis, M. 

cavernosa, P. astreoides, S. 

radians

Richardson, 1992 

Mottling syndrome Flower Gardens GOM C. natans Borneman, 2005 

Pale ring syndrome Flower Gardens GOM Montastraea, Colpophyllia, 

Diploria 

Borneman, 2005 

Light patch syndrome Flower Gardens GOM D. strigosa Borneman, 2005 

Hyperplasia (accelerated 

growth) 

Bermuda, Puerto Rico, 

USVI, Jamaica, Netherlands 

Antilles, Trinidad, Belize, 

Brazil 

12 species: Porites, Favia, 

Diploria, Montastraea, 

Stephanocoenia, Acropora, 

Siderastrea, Colpophyllia. 

Loya et al., 1984 

Calicoblastic Neoplasm Florida, Bonaire, Puerto 

Rico, Trinidad, Mexico 

A. palmata Peters et al., 1986 

Folliculinid ciliates 

(SEB) 

Venezuela 10 species Croquer et al., 2006 

Shut-down reaction Belize, Florida massive corals, acroporids Antonius, 1977 

Coccidiosis Jamaica, Puerto Rico, USVI A. agaricites, D. cylindicus, 

D. strigosa, M. meandrites, 

M. cavernosa, P. astreoides, 

P. porites 

Upton and Peters, 

1986 

Nematopsis spores USVI Porites spp Peters, 1984 

Stress-related necrosis Puerto Rico Multiple species Peters, 1984 

Blistering necrosis Puerto Rico, USVI S.siderea D. strigosa, D. 

labyrinthiformis M.annularis, 

P.astreoides, S. intersepta, A. 

agaricites

Peters, 1984 

Ring disease Bermuda, Florida, Honduras D. labyrinthiformis Weil, 2001 

Algal tumors Bonaire, Trinidad, Florida Gorgonia Pseudoplexaura 

Plexaura

Morse et al., 1977 

Aspergillosis 18 countries Gorgonia spp. Nagelkerken et al., 

1997 

Fire coral fungal disease Florida Millepora spp. TeStrake et al., 1988 

Epizoism Florida and Belize Acropora, P. porites Antonius, 1998 

Epizootic Cyanobacteria Florida Briareum asbestinum Harvell et al, 2001 
 

97 

In a review article, Sutherland et al. (2004) suggests these all represent a single disease 

which she refers to as “white plague like”, however the term white plague has not been 

reported in the IndoPacific. In contrast recent IndoPacific studies are reporting a disease 

with signs that are similar to WBD as white syndrome (WS) (Willis et al., 2004). To 

avoid confusion, the white diseases are grouped here as 1) WBD for Caribbean 

acroporids; 2) white pox (WPX) for acroporids reported with WPX, patchy necrosis or 

necrotic patch syndrome; 3) white plague (WP type I or WP-II) for all non acroporids 

corals in the western Atlantic with signs similar to WBD; and 3) white syndrome for 

cases identified as WBD, white syndrome, white plague, or plague-like from the Red Sea 

and IndoPacific 

White band disease (WBD) was first observed in the mid 1970s in St. Croix, 

USVI among A. palmata populations (Gladfelter et al., 1977). It subsequently spread 

throughout the Caribbean where it affected A. palmata and A. cervicornis, with reports of 

WBD from 27 countries during the 1980s. WBD has been reported much less frequently 

during the last decade; isolated cases of WBD were identified among A. palmata

populations in 5 countries (Jamaica, Mexico, Cuba, Caymans and Bahamas) with an 

outbreak observed in a single location that spread throughout a population off Mona 

Island, Puerto Rico between 2003-2005 (Bruckner, 2005). Conversely, recent outbreaks 

of WBD on A. cervicornis populations appear to be more prevalent over the last decade. 

This condition may represent a new syndrome (it has also been referred to as WBD-II by 

Weil, 2004 and rapid tissue loss by Williams and Miller, 2005), as rates of tissue loss are 

much more rapid than that reported for WBD and patterns of tissue loss were more 

irregular (Williams and Miller, 2005). 

White pox (WPX) was first observed in Puerto Rico in 1994 (called patchy 

necrosis (PN); Bruckner and Bruckner, 1996) and in Florida in 1996 (Patterson et al., 

2002). WPX has also been reported from the USVI and Puerto Rico, with reports for PN 

from the Bahamas, Cuba, Puerto Rico, Jamaica and necrotic patch syndrome from 

Mexico. WPX is believed to have caused losses of 88% of the remaining acroporids in 

the Florida Keys between 1996-2002 (Porter et al., 2001; Sutherland et al., 2004). 

White plague has been reported from 20 countries in the Caribbean, with few 

reports specifically identifying this as Type I or Type II . WP (type I) was first observed 

in 1975 on reefs off Key Largo Florida among six species, with the highest prevalence in 

Mycetophyllia spp. and C. natans (Dustan, 1977). It was still prevalent throughout the 

Key Largo region ten years later, although M. annularis (complex) colonies were affected 

most severely, along with 11 other species (Dustan, 1987). Since this time, WP-I has 

only been reported from the Bahamas and Puerto Rico. A condition with similar signs, 

but more rapid rates of tissue loss and a wider host range emerged on these reefs in 1995 

(WP type II). The most susceptible species (D. stokesi) was unaffected during WP 

outbreaks in the 1970s and 1980s; it was also observed on 17 other species in Florida, 

including 8 (M. annularis, M. cavernosa, M. faveolata, S. siderea, A. agaricites, C. 

natans, D. labyrinthiformis, S. intersepta) reported during earlier WP outbreaks 

(Richardson et al., 1998). WP type II has been reported from 9 countries, with infections 

documented on 41 species (Weil et al., 2006). A separate condition termed WP Type III 

(based on rates of spread of up to 10 cm/day) was reported to affect the largest massive 

corals including Montastraea spp. and C. natans (Richardson and Aronson, 2001); it is 

unclear whether this is distinct from WP-II and epizootiological data are currently 
98 

unavailable. Outbreaks of WP have been reported more frequently since 2000, including 

offshore locations and deeper reefs (e.g., Sherwood Forest, Dry Tortugas; St Croix; La 

Parguera PR Shelf Edge). A similar condition has also been observed in a remote 

location (Flower Gardens, Texas) that was not previously affected (Hickerson, 2005). 

White syndrome was first reported from the Red Sea in 1996 and Australia in 

2001. This may be the same as WBD, which was first documented in the IndoPacific in 

the 1980s as many of the same species are affected and patterns of tissue loss are similar. 

Antonius (1981; 1985) reported WBD in the Red Sea on 17 genera and 31 species of 

corals, including 11 acroporids (Egypt, Saudi Arabia, United Arab Emirates) and 22 

species in the Philippines, including two new genera (Montipora and Podabacia). 

Additional cases reported over the last ten years in Australia, Guam, Oman, India, 

Malaysia and the Philippines (Coles, 1994; Riegl, 2002; Jeyabaskaran and Raghukumar, 

2004). Willis et al. (2004) observed a 20 fold increase in the number of corals affected by 

white syndrome between 1998 and 2003, with the greatest increases on outer reefs. In 

addition, infections spread from 75% of the regions and 45% of the reefs in 1998 to all 

regions and 89% of the reefs by 2003 (Willis et al., 2004). A disease that is similar to 

white syndrome and white plague was reported in a subtropical location (Solitary Islands) 

off Australia. Six coral genera were affected, with new observations for Turbinaria (2 

species). Disease incidence in the Solitary Islands varied throughout the year but was 

lowest in March (6.2%) and highest in June (13.6%) (Dalton and Smith, 2006). 

Porites ulcerative white spot syndrome (PUWS) was first observed in 1996 in 

the Philippines, where it caused discrete bleached round lesions that may result in 

ulcerations that coalesce and cause tissue loss and colony mortality (Raymundo et al., 

2003). This disease affected >20% of the Porites colonies on 8 out of 10 reefs examined 

in the 1990s (Raymundo et al., 2003). More recently up to 40% of the colonies were 

affected at sites near a populated city (Dumaguete), with prevalence declining with 

increasing distance from the city. The incidence of PUWS also increased between March 

and August, 2003, as water temperatures became elevated. In this study, PUWS was 

identified to affect 6 branching species of Porites and one massive species (Kaczmarsky, 

2006). 

Shutdown reaction (SDR) has been reported in the Caribbean and Red Sea, with 

a single report from Tonga (Chesher, 1985; Antonius, 1988). No information is available 

on the prevalence of this condition. There also was a single report of white blotch 

disease in Australia. 

2. Cyanobacterial mat diseases 

Interactions between cyanobacteria and corals have been documented throughout 

the Caribbean, and on reefs of Guam, Micronesia, NWHI and other locations, and 

cyanobacterial blooms are believed to be becoming more frequent (Thacker and Paul, 

2001; Kuffner and Paul, 2004). A number of cyanobacteria have been identified as the 

primary causative agent of coral diseases (e.g., BBD and RBD) while others that form 

mats on the substrate and may smother corals and other organisms (e.g., Schizothrix). 

 
 

99 

Table 2. Various white syndromes reported to affect stony corals in the tropical Pacific Ocean, Indian Ocean 

and Red Sea. 

Condition Location and Species 

affected

Description Source

White band 

disease 

Australia, Egypt, Guam, 

India, Mauritius, Oman, 

Papua New Guinea, 

Philippines, Saudi Arabia, 

United Arab Emirates 

18 genera; 37 species 

A distinct band of white, recently exposed 

skeleton between healthy tissue and algal 

colonized skeleton. The white band forms a 

moving front that advances a few mm per 

day. It may be triggered by contact to 

cyanobacteria1

Antonius, 1981; 

1985; 1987; 19951 

Coles, 1994; 

Korrubel and Riegl, 

1998; Baird, 2000; 

Riegl, 2002 

White 

syndrome 

Egypt2, Australia, Solitary 

Islands, 4 

38 species1 2, 3Turbinaria, 

Acropora, Goniastrea, 

Pocillopora, Stylophora

and Porites4 

A distinct band of white, recently exposed 

skeleton between apparently healthy tissue 

and algal colonized skeleton that advances 

several mm/day

1

Willis et al., 205; 

2

Riegl, 1998 3AIMS 

archives 4

Dalton and 

Smith, 2006 

Shutdown 

reaction 

(SDR) 

Saudi Arabia, Egypt, 

Tonga 

Acropora 

Complete and sudden disintegration of 

coral tissue, starting at the margin of an 

injury. Coenosarc sloughs off skeleton in 

thick strands or blobs at rates of 10 cm/hr 

Antonius, 1988 

Chesher, 1984 

Porites

ulcerative 

white spot 

disease 

Philippines 

Porites: 7 species

Ovoid bleached lesions, 3-5 mm diameter, 

affecting 3-4 polyps and surrounding 

coenosteum; discrete margin between 

bleached and apparently healthy tissue. 

Bleaching is followed by tissue mortality. 

Recovery observed in small lesions; larger 

lesions may coalesce and kill the coral 

Raymundo et al., 

2003; Kaczmarsky, 

2006 

White blotch 

disease 

Australia 

Acropora

White blotches associated with infestations 

of polychaetes 

Dinsdale, 1994 

Black band disease (BBD) was first described in 1972 from reefs off Belize, 

Puerto Rico, Florida and Bermuda (Antonius, 1973). BBD is now known to occur in at 

least 25 countries in the western Atlantic, and 11 countries in the Red Sea and IndoPacific, although cyanobacteria differ depending on location (Cooney et al. 2002, FriasLopez et al. 2002, 2003). In the western Atlantic, BBD has been reported on 26 

scleractinian corals, one hydrozoan coral (M. complenata) and six gorgonians (Rützler et 

al. 1983; Feingold 1988; Green and Bruckner 2000). Faviid corals are most susceptible, 

although infections are frequently observed on S. siderea, and occasionally on Agaricia

spp, Mycetophyllia spp., and M. meandrites. Caribbean colonies of Porites spp. and 

Acropora spp. were thought to be resistant to BBD, although BBD was reported on A. 

palmata in Colombia (Garzon-Ferriera et al., 2001), P. astreoides in Cuba (AGRRA 

database), Bermuda (Garret and Ducklow, 1975) and Mexico (Ryan Walker, Coral Cay 

Conservation, pers. Comm.), and P. porites in the Bahamas and Jamaica (AGRRA 

database). Several cases of BBD have also been observed on Solenastrea bournoni in 

Mexico (Ryan Walker). Sutherland et al. (2004) also reports BBD on Madracis mirabilis

and M. decactis, although the source of these records is not provided. 
100 

In the IndoPacific and Red Sea, BBD has been observed on 19 genera and 49 

species, most commonly on faviids and acroporids (Antonius 1988; Miller 1996; Green 

and Bruckner 2000; Dinsdale 2002; Sutherland et al., 2004). BBD was observed on 19% 

of 91 reefs examined in 1993/94 (Miller, 1996). More recent surveys show that BBD is 

widely distributed throughout the GBR Australia, but prevalence remained very low (04-

0.47 colonies per reef on any given year) between 1998 and 2003 (Willis et al., 2004). 

Kaczmarsky (2006) recently identified an outbreak of BBD affecting close to 8% of the 

corals at one site in the Philippines; these observations include 5 new hosts for BBD in 

the Philippines and one new genera overall (Coscinaraea columna). 

Red band disease (RBD type I and RBD-II) are only known from the Caribbean, 

although another disease termed “red band” has also been reported from Palau on 

Pachyseris spp. (Harvell et al., 2004). RBD- I was first identified on gorgonians in Belize 

in the 1980s, and has since been reported from 12 countries in the Caribbean, with 

records from 10 scleractinian corals, Millepora spp., and the sea fan G. ventalina (Rutzler 

et al., 1983). RBD-II has only been observed in a single location in the Bahamas 

(Richardson, 1993). 

Several other cyanobacterial diseases have also been reported from the 

IndoPacific. Black overgrowing cyanobacteria is associated with at least five 

cyanobacteria that overgrow Acropora, Favia, Pocillopora and Porites on reefs in the 

Indian Ocean (Antonius, 1995). Black aggressive band has been observed in a single 

location on branching acroporids (Antonius, 1995), while brown band disease has only 

been recorded on A. formosa on the GBR Australia (Dinesdale, 1994; Antonius, 1999). 

Pink line syndrome, reported on Porites compressa and P. lutea in the Indian Ocean, has 

also been associated with a cyanobacteria (Phormidium valderianum) that is thought to 

induce pink coloration in affected coral tissue (Ravindran & Raghukumar, 2002). 

3. Color change 

In many reported syndromes, color change is an important diagnostic feature used 

to identify and differentiate diseases. Color change may include darker than normal 

tissue, lighter tissues, or a change in color such as the appearance of purple or pink spots 

or bands. Three syndromes associated with lightening of tissue have been reported from 

the Flower Gardens (Texas). This includes: 1) light patch syndrome which is observed 

in D. strigosa and is associated with variably sized, solid patches of uniformly 

contrasting paler tissue on normally pigmented colonies; 2) pale ring syndrome, which 

causes a variably wide ring that occurs singly or in multiples on the corallum surface in 

M. faveolata, M. cavernosa, C. natans and D. strigosa; and 3) mottling syndrome in C. 

natans, in which the tissue appears mottled as a result of total to near-total bleaching 

associated with a focal lesion, with spotty bleaching occurring in a wide band that grades 

towards apparently healthy tissue (Borneman, 2005). 

 
 

101 

Table 3. Diseases associated with cyanobacteria reported to affect stony corals in the tropical Pacific Ocean, 

Indian Ocean and Red Sea. 

Condition Location and

Species affected

Description Source

Black band 

disease 

Australia, Egypt, Fiji, India, 

Jordan, Papua New Guinea, 

Philippines, Saudi Arabia, 

Tonga, South Africa, CNMI, 

Palau 

19 genera, 49 species; 

Pocillopora and Acropora 

most frequently affected 

A darkly pigmented mat/band 1-

30 cm wide on the surface of the 

coral that separates healthy tissue 

from recently denuded white 

skeleton. 

Antonius, 1987; Chesher, 

1985; Glazebrook and 

Steiner, 1994; Littler and 

Littler, 1996; Miller, 1996; 

Korrubel and Riegl, 1998; 

Fenner, 1998; Cervino, 

1998; Jordan and Samways, 

2001; Dinesdale, 2002, 

Willis et al., 2004 

Brown band 

disease 

Australia 

Acropora Formosa

Different condition from above 

associated with cyanobacteria 

Dinsdale, 1994 

Black 

aggressive 

band 

Mauritius 

Acropora (staghorn coral) 

Resembles BBD but the band 

material is thinner and appears 

grey rather than black; possibly 

caused by a cyanobacteria 

(Spirulina) or a spirochete 

Antonius, 1995a 

Black 

overgrowing 

cyanobacteria 

Indian Ocean, Mauritius 

Acropora, Favia Pocillopora, 

Porites, 

Cyanobacteria (Calothrix, 

Hormothamnium, Lyngbia, 

Phormidium, Spirula) cover coral 

tissue and progressively 

overgrow it; may penetrates and 

erodes skeleton 

Antonius, 1995a 

Red band 

disease 

Palau 

Pachyseris speciosa and 

Porites spp. 

A reddish band on the surface of 

the coral that separates healthy 

tissue from recently denuded 

white skeleton. 

Harvell et al., 2004; 

Sussman et al., 2006 

Pink line 

disease 

/syndrome 

Papua New Guinea, 

Sri Lanka, Kavaratti Island, 

Indian Ocean 

Porites compressa, P. lutea

Band of pink pigmented tissue 

separating recently killed 

skeleton and normal tissue; it 

may begin as a small ring and 

progress outward. Associated 

with a cyanobacteria. 

Ravindran et al., 2001; 

Goreau/Cervino, coral list 

server 

Two distinct conditions have been reported as yellow band disease. In the 

Caribbean, YBD (also referred to as yellow blotch disease) was first reported from 

Florida in 1994 (Reef Relief), and subsequently observed in 24 countries throughout the 

Caribbean. It primarily affects M. annularis complex and 4 other massive faviids corals, 

A. agaricites, and P. astreoides. This disease has been reported at an unusually high 

prevalence in a number of countries (18-91%) including Puerto Rico, Mexico, Curacao, 

Bonaire, Grenada, Panama, and USVI (Cervino et al., 2001; Jordan-Dahlgren and 

Rodriguez-Martinez, 2004; Bruckner and Bruckner, 2006). Yellow band disease was 

first reported in 1995 from the Arabian Gulf off Dubai (United Arab Emirates) and in 

1999 and 2003 off Fahr Island and Kish Island (Iran). It affects Turbinaria, Porites, 

Cyphastrea and Acropora (Korrubel and Riegl, 1998). 
102 

Dark spots disease was first observed in Colombia in the mid 1990s, but has 

since been reported from 15 other countries in the Caribbean (Garzon-Ferriera et al., 

2001; Weil 2004). It is most commonly observed on the genera Stephanocoenia, 

Siderastrea and Montastraea, although similar signs are observed on 6 other species. 

Colonies are characterized by darkly pigmented spots or bands within the tissue, and 

occasionally extending into the skeleton, with depressed skeletal features observed in 

Stephanocoenia. Over time these dark spots may increase in size, or the center of the spot 

may die and dark tissue may expand into a band or ring that slowly migrates outward. 

Weil (2002; 2004) reported three additional syndromes that are similar in appearance to 

DSD (DSD-II, dark band disease, purple band disease and tissue necrosis). These 

syndromes could be related, or are a different stage in the progression of dark spots 

disease (Weil, 2004). 

4. Other conditions 

Two conditions have been reported in the GCDD that are associated with ciliates, 

brown band disease (BrBD) and skeletal eroding band (SEB). BrBD has only been 

reported from the GBR, Australia, where it affected a low proportion of corals (0.3%), 

including acroporids, pocilloporids and faviids (Willis et al., 2004). SEB has been 

observed in the Red Sea, Indian Ocean and Pacific (5 countries) on 21 genera of corals 

(Reigl and Antonius, 2003; Willis et al., 2004). In Australia, SEB was the dominant 

disease affecting acroporids and pocilloporids, with a 20 fold increase during summer 

(Willis et al., 2004). A similar condition (folliculinid ciliates) was recently reported from 

the Caribbean (Venezuela) on 10 species of coral (Croquer et al., 2006). 

Tumors (including calicoblastic neoplasms, hyperplasias, abnormal growth) are 

among the most widely reported condition affecting corals with the first observations 

over 40 years ago (Squires, 1965), and subsequent reports from 15 countries in the 

IndoPacific and 13 countries in the Caribbean. Neoplasia has been reported most 

frequently on Acropora, with reports from the Caribbean, Philippines, Guam, Hawaii, 

and Oman. 
 

103 

Conclusions 

1. Diseases occur globally, in most reef habitats and in most locations including 

reefs near human population centers and remote offshore locations. Although 

most of the reports available prior to 1998 were from areas that had a medium to 

high level of human impact, reports of disease from remote locations has 

escalated, and in some cases offshore locations are exhibiting the most dramatic 

increases in diseases incidence and mortality. 

2. Diseases have been observed in 63 countries, a 17% increase since 1999. This 

includes increasing numbers of observations of disease in the IndoPacific, along 

with a number of new diseases and increasing prevalence of these diseases, but 

Caribbean reefs are still disproportionately affected by disease. 

3. There are six major diseases of concern in the Caribbean (BBD, WBD, WP, 

YBD, ASP, WPX) that have caused substantial coral mortality since their 

discovery; two of these remain a major threat to acroporids (WBD, WPX), one is 

impacting a growing number of gorgonian species (ASP), and three (WP, YBD, 

BBD) are of major concern to M. annularis (complex) and other species. Two 

other conditions appear to be widespread (DSD and SEB), but are causing slow 

rates of mortality at this time. 

4. The disease of most concern on IndoPacific reefs is white syndrome, which is 

having the largest impacts on acroporids throughout the region; PUWS is a 

growing threat to Porites, but at this time it appears to be restricted to the 

Philippines. Most other newly emerging IndoPacific diseases have caused 

localized mortality and appear to have a limited distribution. 

5. Although a greater number of corals have been identified with disease in the 

IndoPacific (34 genera and 97 species), a higher percentage of coral species (close 

to 80% of all taxa; 41 species of scleractinian corals, 8 gorgonians, 2 hydrozoans) 

are affected by diseases in the Caribbean. This represents a 25% increase in 

number of genera and 45% increase in number of species and includes 7 new 

genera identified with disease in the IndoPacific since 1999. 

6. Rapidly growing corals in the family acroporidae and pocilloporidae in the 

IndoPacific are affected by the largest number of diseases and are observed with 

disease more frequently than all other species, while the M. annularis complex is 

being affected most severely in the Western Atlantic. 

7. Tumors (hyperplasia, neoplasia etc.) are the oldest known afflictions of corals, 

and are found on most corals in most locations, but their impacts appear to be 

minimal at this time. 

 
104 

Table 4. Other Diseases, syndromes, and anomalies reported to affect stony corals in the tropical Pacific 

Ocean, Indian Ocean and Red Sea. 

Condition Location and

Species affected

Description Source

Yellow band 

disease 

United Arab Emirates; 

Arabian Gulf; Iran2

4 genera, 12 species 

A broad band of denuded skeleton, 

yellow in color, adjacent to decaying and 

sloughing tissue; the band advances 9-20 

mm/week. 

Korrubel and 

Riegl, 1998 

2

Maghsoudlou, 

and Eghtesadi, 

2004 

Brown band 

disease 

Australia 

Acropora Formosa

A brown band of variable width flanked 

by healthy tissue at6 the advancing front 

and exposed white skeleton at the trailing 

edge. The band moves in both directions 

along the branch, destroying coral tissue. 

Dense populations of ciliates, packed 

with zooxanthellae from coral cause 

brown coloration. 

Willis et al., 2004 

Skeleton eroding 

band (SEB) 

Egypt, Jordan1 PNG, 

Mauritius2

, Australia 2

21 genera ; Cyphastrea 

chalcidicum, acroporids2 

13 genera scleractinian, 1 

hydrozoan in Australia 3 

Masses of black loricae of

Halofolliculina corallasia, a colonial 

heterotrich ciliate, that forms a front 

separating live tissue from a white zone; 

the front advances like BBD, causing 

tissue loss and skeletal damage.

1

Antonius, 1999; 

Winkler et al., 

2004 

2

Riegl and 

Antonius, 2003 

3

Willis et al., 

2004 

Plagioporus Hawaii 

Porites compresssa, P. 

lobata 

Metacercaria of the digenetic trematode 

encyst in elevated nodules, causing 

enlarged pink polyps. Cyst wall is 

secreted by parasite, produces distortions 

of gastrovascular cavity and cellular 

alterations within tentacles 

Aeby, 1991 

Patchy necrosis Adaman Islands, Indian 

Ocean 

Porites,Goniastrea 

Goniopora, Montipora, 

Favia, Goniastrea and 

Pocillopora 

Hyphomycetous fungus associated with 

necrotic patches. Top layer of necrotic 

patches consists of epilithic algae, 

followed by a thin black zone of fungal 

growth, a green band containing shellboring algae and a dense black fungal 

layer at the base 

Raghukumar and 

Raghukumar, 

1991; Ravindran 

et al., 2001 

Fungal syndrome East African Coast 

Astreopora, Montipora, 

Echinopora, Acropora, 

Goniopora, Platygyra, 

massive Porites, 

Pocillopra, Goniastrea 

Hydnophora, Cyphastrea 

Corals develop ashy dull color and brittle 

or weak skeleton. Corals become covered 

in mucus, which traps debris. Once this 

clears, a white calcareous dust is left on 

the surface and a black layer forms 

underneath; death occurs in about two 

weeks 

McClanahan et 

al., 2004 

 
 

105 

Table 4 (continued). Other Diseases, syndromes, and anomalies reported to affect stony corals in the 

tropical Pacific Ocean, Indian Ocean and Red Sea.

Condition Location and

Species affected

Description Source

Hyperplasia (and 

other reports of 

tumors) 

Australia, Hawaii, Guam, 

Palau, Enewatak, French 

Polynesia, New 

Caledonia, Maldives, 

Micronesia, Marshall 

Islands, Japan, Oman, 

China, Philippines 

Pocillopora, Pavona, 

Fungia, Madrepora, 

Montipora, Platygyra 

Irregular growths on colonies reported as 

tumors and hyperplasms associated with 

a proliferation of cell types (normal in 

appearance, but larger in size) 

Loya et al. 1984; 

Peters et al., 

1986 ; 

Glazebrook and 

Steiner, 

1994;Yamashiro 

et al., 2000 

Neoplasia CNMI, Oman 

Acropora 

calicoblastic epitheliomas, neoplasms 

associated with a proliferation of cell 

types and white globular masses of 

skeleton with few discernable polyp 

structures. 

Cheney, 1975; 

Coles and Seapy, 

1998 

Stress related 

necrosis 

Hawaii 

Porites lobata 

Gram negative bacterial aggregates in 

gastrodermal cells of tentacles. Tissues 

exhibit lysed nuclei and cell death 

Hunter, 

Pink-blue disease Israel, India, 

Lackshadweep Islands 

Acropora, Porites

Pink to blue coloration adjacent to 

lesions 

Red Sea Marine 

Park, 2001; 

Ravindran et al., 

2001 

Black necrosing 

syndrome 

Australia 

Gorgonians, Isis hippuris

Black necrotic patches appearing on 

10% of the population on one reef 

Morrison 

Gardiner, 2001; 

Willis et al., 2004 

Vibrionic 

Bleaching 

Mediterranean, Israel, 

Tanzania 

Oculina pategonica; 

Pocillopora 

 Rosenberg, 2002 

Atramentous 

necrosis 

Florence Bay and Bright 

Point, Australia 

Montipora 

aequituberculata 

 Jones et al., 2004 

Yellowing 

disease 

Sodwana, South Africa 

Favia pentagona and 

Lobophytum 

 Jordan and 

Samways, 2001 

Red plague 

syndrome 

Kavaratti Island, India 

Montipora spp. and

Porites spp. 

 Jeyabaskaran and 

Raghukumar, 

2004 
106 

Fig. 1. Five major scleractinian coral diseases reported for the wider Caribbean compiled in 

the GCDD. Reports of syndromes with different “types” (e.g., WP type I and WP type II) 

have been pooled.

 

0

1

2

3

4

5

Number of diseases

Anguilla Antigua 

Bahamas

BarbadosBelize

Bermuda

Bonaire

BVICaymans

Colombia

Cuba

Curacao

Dominican Republic

DominicaFloridaGrenadaGrenadines Guadalupe

Haiti

HondurasJamaica MartiniqueMexico

Nicaragua

Panama

Puerto RicoSaba

St. Eustatius

St. LuciaSt. Vincent Trinidad and TobagoTurks and Caicos

Venezuela

USVI

GOM (Flower Gardens)

BBD WBD WP YBD DSD

0

1

2

3

4

5

Number of diseases

0

1

2

3

4

5

Number of diseases

Anguilla Anguilla Antigua Antigua 

Bahamas Bahamas

Barbados BarbadosBelize

Bermuda Bermuda

Bonaire Bonaire

BVICaymans Caymans

Colombia Colombia

Cuba

Curacao Curacao

Dominican Republic Dominican Republic

Dominica DominicaFlorida FloridaGrenada GrenadaGrenadines Grenadines Guadalupe Guadalupe

Haiti

Honduras HondurasJamaica Jamaica Martinique MartiniqueMexico

Nicaragua Nicaragua

Panama

Puerto Rico Puerto RicoSaba

St. Eustatius St. Eustatius

St. Lucia St. LuciaSt. Vincent St. Vincent Trinidad and Tobago Trinidad and TobagoTurks and Caicos Turks and Caicos

Venezuela Venezuela

USVI

GOM (Flower Gardens) GOM (Flower Gardens)

BBD WBD WP YBD DSD
 

107 

Fig. 2 Susceptibility of scleractinian corals to seven major syndromes observed in 

the Indo Pacific.

0

2

4

6

8

10

12

14

Enallopsammia

Echinophyllia

Alveopora Astreopora Coscinarea

Cyphastrea Echinopora

Favia

Favites

Fungia Galaxea

GoniastreaGoniopora Hydnophora Leptoria Leptoseris Lobophyllia Madrepora Montipora, Mycedium, Millepora Oulophyllia Pachyseris Pavona

Platygyra Plerogyra Pocillopora Podabacia

Psammocora

Porites

Seriatopora Sympyllia Stylophora Turbinaria

Number of species

BBD WBD

Skeletal eroding band

YBD

white syndrome

abnormal skeletal development

brown band

0

2

4

6

8

10

12

14

Enallopsammia

Echinophyllia

Alveopora Astreopora Coscinarea

Cyphastrea Echinopora

Favia

Favites

Fungia Galaxea

GoniastreaGoniopora Hydnophora Leptoria Leptoseris Lobophyllia Madrepora Montipora, Mycedium, Millepora Oulophyllia Pachyseris Pavona

Platygyra Plerogyra Pocillopora Podabacia

Psammocora

Porites

Seriatopora Sympyllia

Echinophyllia

Stylophora Turbinaria

Alveopora Astreopora Coscinarea

Cyphastrea Echinopora

Favia

Favites

Fungia Galaxea

GoniastreaGoniopora Hydnophora Leptoria Leptoseris Lobophyllia Madrepora Montipora, Mycedium, Millepora Oulophyllia Pachyseris Pavona

Platygyra Plerogyra Pocillopora Podabacia

Psammocora

Porites

Seriatopora Sympyllia Stylophora Turbinaria

Number of species

BBD WBD

Skeletal eroding band

YBD

white syndrome

abnormal skeletal development

brown band
108 

0

2

4

6

8

10

12

14

16

1970s 1980s 1990 1995 1998 2000

Number of diseases

other

fungal

brown band

WS

SEB

PUWS

Vibrionic bleaching

YBD

Tumors

WBD

BBD

Fig. 3. Number of diseases observed on IndoPacific Reefs. Only those conditions 

reported in peer-reviewed publications are included

0

2

4

6

8

10

12

14

16

1970s 1980s 1990 1995 1998 2000

0

2

4

6

8

10

12

14

16

1970s 1980s 1990 1995 1998 2000

Number of diseases

other

fungal

brown band

WS

SEB

PUWS

Vibrionic bleaching

YBD

Tumors

WBD

BBD

other

fungal

brown band

WS

SEB

PUWS

Vibrionic bleaching

YBD

Tumors

WBD

BBD

Fig. 3. Number of diseases observed on IndoPacific Reefs. Only those conditions 

reported in peer-reviewed publications are included
 

109 

 

0

5

10

15

20

25

30

BBD WBD WP YBD

Number of Countries

1970s

1980s

early 1990s

1998-2005

Fig. 4. Number of countries reported with BBD, WBD, WP and YBD during

the 1970s, 1980s, 1990s and today

0

5

10

15

20

25

30

BBD WBD WP YBD

Number of Countries

0

5

10

15

20

25

30

BBD WBD WP YBD

Number of Countries

1970s

1980s

early 1990s

1998-2005

Fig. 4. Number of countries reported with BBD, WBD, WP and YBD during

the 1970s, 1980s, 1990s and today
110 

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122 

WORLD BANK PROJECT: CORAL DISEASE WORKING GROUP

Bette Willis 

James Cook University 

School of Marine Biology and Aquaculture 

James Cook University 

Townsville Queensland 4811, Australia 

bette.willis@jcu.edu.au 

CRTR Coral Disease Working Group 

(excerpted from the CRTR webpage - http://www.gefcoral.org/) 

Coral reefs are under increasing stress from a number of causes, including climate 

warming, poor water quality and over fishing. Disease outbreaks cause not only coral 

loss, but they can result in significant changes in community structure, species diversity 

and reef-associated organisms. Coral diseases potentially impact both well-managed and 

unmanaged reefs indiscriminately. However, strategies for dealing with disease 

outbreaks are currently non-existent. The increasing frequency with which diseases 

influence and alter reef communities means they must be considered and incorporated 

into management plans. 

Background: 

The CRTR Program is a partnership between the Global Environment Facility, the World 

Bank, The University of Queensland (Australia), the United States National Oceanic and 

Atmospheric Administration (NOAA), and approximately 50 research institutes and other 

third parties around the world. The CRTR Coral Disease Working Group’s research will 

provide us with a greater understanding of the ways in which coral diseases can alter reef 

function and the conditions under which outbreaks may occur. 

Global impact of coral disease

Coral disease stands out as a primary factor in the deterioration of many coral reefs 

worldwide, with preliminary surveys indicating that significant and damaging new 

diseases are now beginning to appear in all reef regions. The CRTR Program Disease 

Working Group is conducting a global coral disease census across 24 high priority sites. 

This major assessment is designed to catalogue syndromes for the first time, and to reveal 

whether disease outbreaks are correlated with climate warming anomalies. In each 

location the impact and prevalence of coral disease is being measured. 

Global warming and anthropogenic inputs

Increases in disease following warming events may be because corals have lower ability 

to fight disease while under temperature stress, or because bacteria are more virulent. 

While connections between poor water quality (nutrient loading and sedimentation) and 

disease are of increasing concern, evidence of direct links and synergistic effects is 

limited. The CRTR Program Disease Working Group is measuring nitrogen and sediment 

loading at key research sites. The team will use molecular and enzymatic techniques to 

assess differences in microbial communities - in coral mucus, water and sediment 
 

123 

between sites with different loadings, and between healthy and bleached corals. There 

will also be an evaluation of climate and anthropogenic influences on changes within 

microbial communities. 

The causes, reservoirs and vectors of corals disease 

Current research on disease reservoirs and vectors is hampered by a lack of knowledge of 

the pathogens causing the majority of coral diseases. To date there are only five coral 

diseases for which the microbial cause is known. The Disease Working Group is 

developing a suite of techniques to facilitate the identification of pathogens in coral. 

Because only a small percentage of bacteria in nature are culturable, the identity and 

source of pathogens will be confirmed using various molecular fingerprinting techniques. 

Eventually a micro-array chip of global coral disease will be developed. 

Coral resistance to disease 

The microbial communities associated with coral are very complex, existing both inside 

the coral animal and in the surface mucous layers (SML). These normal communities 

protect the coral from disease. When the community structure changes, corals may 

become more susceptible to disease. Both bleaching and disease appear to change the 

microbial community profiles in the SML. The goal of the Disease Working Group’s 

immunological work is to develop assays to determine general antimicrobial activity. 

Once resistant compounds are identified, they will be incorporated into a chip of 

biomarkers for stress. Field sampling will eventually allow the team to quantify and 

estimate the response of corals to different experimental treatments of enhanced nutrients 

and temperature, and map the spatial extent and variation of disease resistance in the 

field. 

Our Research 

Research Activities: 

Over the last 20 years, unprecedented increases in disease on coral reefs have 

contributed significantly to coral reef degradation. Disease-related damage of coral reefs 

has been well documented in the Caribbean, but recent observations of coral disease in 

other regions of the world are just beginning. Disease occurrence in these other regions 

may be a potential harbinger for further outbreaks and impacts associated with increasing 

climate warming. The Disease Working Group is targeting investigations to address the 

causes of this rapid emergence of coral disease, to understand the impacts of the problem 

and to develop tools and responses that can be used for management. 

Research Update: 

The Disease Working Group has answered many pressing questions including 

which disease syndromes are infectious; which reef regions surveyed as part of the the 

CRTR Program have the greatest prevalence of coral disease; which Centres of 

Excellence would be the most suitable for identifying local factors that might impact on 

disease; and whether ocean warming affects coral disease levels. 
124 

Impact of fish farms 

As part of its study of the impact of local environmental factors on coral health, the 

Group has found that the fish pens in Bolinao Bay (Philippines) have a strong influence 

on bacterial communities, nutrient input, primary production and the patterns of energy 

and carbon flux in the surrounding waters. Researchers are working to identity specific 

bacteria from fish farms that reside on the surface of reef corals, and whether aquaculture 

plays a role as an incubator, conveyor and facilitator of disease into natural populations. 

Disease in a warming ocean 

The Group has made significant discoveries in the Caribbean and Great Barrier Reef 

region in Australia regarding the potential impacts of heat stress, associated with climate 

warming events, on the outbreak of coral disease. In collaboration with the Remote 

Sensing Working Group, it is developing new models to predict disease outbreaks using 

satellite monitoring data. The models use predicted sea temperature data and can identify 

the potential efficacy of various management strategies for future scenarios. 

Other causes of coral disease 

The Group continues to survey the prevalence of coral disease in Caribbean, Yucatan and 

Australian coral reefs, and is making progress in determining agents that cause coral 

disease such as skeletal eroding band, brown band and white syndrome. 

Tools for Management: 

The Disease Working Group has developed important new tools for coral reef 

managers and researchers across the Western Atlantic and the Indo-Pacific to identify and 

address coral disease – the Coral Disease Handbook: Guidelines for Assessment, 

Monitoring and Management and two sets of underwater identification cards. These were 

launched at the 11th International Coral Reef Symposium in July 2008. 

Handbook 

Designed for reef managers by international experts in coral disease, the Handbook 

outlines procedures for describing indicators, measuring impacts, monitoring outbreaks, 

assessing causes, and managing reefs to minimize losses due to disease. This handbook 

helps managers not only to document and manage disease on their reefs, but also enables 

them to contribute to our scientific understanding of this grave and increasing threat. 

Underwater Cards Caribbean 

These Underwater Cards for assessing the health of coral reefs have been designed so that 

scientific, professional and recreational divers can all assist with gathering information on 

the occurrence of coral reef diseases in the Caribbean. These cards will assist in the 

identification and monitoring of diseases in Caribbean coral and other reef organisms. 

Underwater Cards Indo-Pacific 

These Underwater Cards for assessing the health of coral reefs have been designed so that 

scientific, professional and recreational divers can all assist with gathering information on 

the occurrence of coral reef diseases in the Indo-Pacific. These cards will assist in the 

identification and monitoring of diseases in Indo-Pacific corals and other reef organisms. 
 

125 

Who we are 

Working Group Members: 

Working Group members bring international expertise and experience to this targeted 

research: C. Drew Harvell (Chair), Garriet W. Smith (Co-Chair, Microbiology), Bette 

Willis (Co-Chair, Ecology), Farooq Azam, Eric Jordan Dahlgren, Eugene Rosenberg, 

Ernesto Weil, Laurie Raymundo. 

Project Partners: 

Working Group partners bring capacity to this research endeavour: 

Section of Ecology and Evolutionary Biology, Cornell University, USA; 

Department of Biology and Geology, University of South Carolina-Aiken, USA; 

Scripps Institution of Oceanography, University of Southern California, USA; 

Unidad Académica de Sistemas Arrecifiales, Instituto de Ciencias del Mar y Limnologia, 

Universidad Nacional Autónoma de México, Mexico; 

Department of Molecular Microbiology and Biotechnology, Faculty of Life Sciences, Tel 

Aviv University, Israel; 

Department of Marine Sciences, Universidad de Puerto Rico Mayagüez, Puerto Rico; 

School of Marine and Tropical Biology, James Cook University & ARC Centre of 

Excellence for Coral Reef Studies, Australia; 

University of Guam Marine Laboratory, University of Guam, USA. 

Contacts - 

CRTR Program Disease Working Group:

Chair: Dr. C. Drew Harvell 

Cornell University 

Co-Chair (Microbiology): Dr Garriet W. Smith 

University of South Carolina 

Co-Chair (Ecology): Dr. Bette Willis 

ARC Centre of Excellence for Coral Reef Studies and James Cook University 

Project Executing Agency:

Global Coral Reef Targeted Research and Capacity Building for Management Program 

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126 

III. HISTORICAL PERSPECTIVE--LESSONS LEARNED 

PROGRESS IN UNDERSTANDING CORAL DISEASES IN THE CARIBBEAN 

Andrew Bruckner 

NOAA Fisheries 

Coral Reef Conservation Program 

Office of Habitat Conservation 

1315 East West Highway 

Silver Spring, MD 20910 

andy.bruckner@noaa.gov 

ABSTRACT

Coral disease research in the Caribbean initiated in 1972 with the discovery of 

black band disease (BDD) by Dr. Arnfred Antonius. Since this time, there has been an 

expansion in the number of researchers working in the Caribbean, including studies to 

document the prevalence and incidence across large spatial scales and at increased 

temporal frequencies, evaluation of the linkages between disease and environmental 

drivers, identification of disease vectors, and laboratory studies to characterize causes, 

physiological responses, histological changes, defense mechanisms and mechanisms of 

resistance and susceptibility. Since 1998, the Caribbean has emerged as a “hot spot” for 

coral diseases due to the large number of named diseases, their wide distribution, 

expanding host ranges, and increasing abundance and severity, with over 30 diseases now 

reported from this region. Localized epizootics of three diseases (BBD, WBD, WP-I) 

were first documented in the 1970s; one of these (WBD) expanded throughout the 

Caribbean to become the most significant factor in the region-wide decline of acroporids. 

Five diseases (WP-II, YBD, WPX, DSD and ASP) emerged in the mid 1990s, and have 

expanded their geographic distribution and host ranges over the last ten years with 

several of the diseases causing substantial coral mortality since the late 1990s. By 2005, 

at least 41 scleractinian corals, 8 gorgonians and two hydrozoans were observed with one 

or more diseases. The most abundant and important group of corals found on Caribbean 

reefs today (M. annularis complex) is susceptible to at least 8 different diseases, and 

individual colonies may show signs of 2-3 diseases at the same time. The average 

prevalence of coral diseases at the community level is generally low, although it is highly 

variable between and within sites, during different years, and seasonally. Disease 

outbreaks have affected up to 91% of certain susceptible populations in localized areas, 

and often (but not always) exhibit a clumped distribution. Disease prevalence and 

severity is generally greater during warm water periods, and recent disease outbreaks 

have been associated with mass bleaching events. Over the last five years, there has been 

an increase in the numbers of studies that have reported a correlation between disease and 

environmental factors, including higher prevalence rates and greater rates of spread in 

areas affected by nutrients, sediments and other pollutants. Causative agents have been 

identified for relatively few diseases, three of which (WP-II, ASP and WPX) have been 

verified through application of Koch’s postulate. In these and other diseases, complex 

microbial communities have been identified using new molecular techniques, including 
127 

biota on diseased tissue that is absent from control samples and suites of microorganisms 

that differ from those identified using traditional (microscopy and culture) techniques. 

Furthermore, pathogens identified using traditional microbiological approaches are no 

longer infective, including the proposed causative agent for white plague type II, 

suggesting 1) the pathogens may have lost their virulence and/or corals have gained 

immunity, or 2) causation was determined based on a relatively small number of corals 

from a single location/event and other microbial agents are capable of causing similar 

signs. In addition to key advances in understanding the coral holobiont, and how 

microbial communities associated with coral tissue and coral mucus change during 

periods of stress, some advances have been made in identifying possible vectors of 

disease, including linkages between a coral eating snail (Coralliophila abbreviata) and a 

white syndrome that affects acroporids as well as three spot damselfish and BBD. Efforts 

have been made to mitigate disease, through removal of the microbial community, 

antibiotic treatments, use of putty and/or clay to cover the affected area, and addition of 

urchins to reduce algal abundance, however these exhibited only limited success and they 

do not appear to be feasible treatments on a larger scale. One of the major limitations in 

advancing our understanding of diseases has been the lack of standardized nomenclature 

and diagnostic criteria for diseases, which has resulted in a proliferation of names and the 

identification of new presumed diseases that later have been shown to be caused by other 

factors. Some of the key needs for the Caribbean include: 1) greater geographic coverage 

and more frequent surveys to characterize prevalence and incidence; 2) more emphasis on 

population dynamics and impacts, including size structure of diseased and healthy corals, 

extent of partial and whole colony mortality and impact to individual corals and coral 

populations; 3) concurrent monitoring and assessment of environmental factors; 4) 

revision of existing disease nomenclature and adoption of standardized terminology and 

diagnostics; 5) application of traditional culture and histopathology techniques in 

combination with new molecular tools to characterize causative agents and sources of 

pathogens and development of molecular probes to facilitate screening of corals; and 6) 

more emphasis on cellular diagnostics, including biomarker characterization, to assess 

stress levels in corals and underlying causes; and 7) a coordinated rapid response 

program to address coral disease outbreaks and unusual mortality events. 

Introduction 

Until the late 1970s, benthic substrates on Caribbean reefs were occupied 

primarily by reef-building corals, turf algae, coralline algae, and other benthic 

invertebrates (sponges). Coral reefs exhibited a generalized zonation pattern with elkhorn 

coral (Acropora palmata) forming large, monospecific stands in the reef crest and 

shallow fore reef (0-5 m depth); stands of staghorn coral (A. cervicornis) at intermediate 

depths (5-25 m depth) on wave exposed reefs and in shallow, protected environments; 

massive corals (dominated by Montastraea annularis complex) throughout the fore reef 

(5-30 m depth) and in back reef and lagoonal areas; and plating agaricids near the base of 

the reef (20-40 m depth) (Goreau, 1959; Adey, 1978). Caribbean reefs have experienced 

significant losses in living coral cover over the last three decades and “classic” zonation 

patterns have disappeared from many locations (Gardner et al., 2003). As corals die, 

exposed benthic substrates are monopolized by fleshy macroalgae, encrusting and 

bioeroding sponges, and other organisms. These “pest” species are outcompeting and 
128 

overgrowing corals, and may prevent new recruitment and regrowth of damaged corals 

(Hughes, 1994; Aronson and Precht, 2001; Weil 2004). 

Coral diseases were first described in the western Atlantic almost 35 years ago 

(Antonius, 1973), but it wasn’t until about ten years ago that diseases were identified as a 

significant factor accelerating the deterioration of coral reefs (Epstein et al., 1998; 

Harvell et al., 1999; Green and Bruckner, 2000; Sutherland et al., 2004; Weil, 2004). 

Black band disease (BBD; Antonius, 1973; Garrett and Ducklow, 1975; Antonius, 1973), 

white band disease (WBD; Gladfelter et al., 1977) and white plague (WP type I; Dustan, 

1977) were first observed in the 1970s from reefs of Belize, Florida, Bermuda, Puerto 

Rico and the USVI and have become chronic afflictions of important reef-building corals. 

Although generally low in prevalence and patchy in distribution, these diseases have 

persisted on the same reefs for many years, and have spread throughout the western 

Atlantic infecting a growing number of host species (Gladfelter, 1982; Rützler et al., 

1983; Dustan, 1987; Peters, 1984; Edmunds, 1991; Kuta and Richardson, 1996; Aronson 

and Precht, 1997; Bruckner et al., 1997). The earliest report of significant coral mortality 

from disease was from the Florida Keys (USA), where an outbreak of WP spread through 

Mycetophyllia spp. and Colpophyllia spp. populations, and was predicted to cause the 

disappearance of M. ferox from some locations (Dustan, 1977). Ten years later a second 

outbreak of WP affected M. annularis and 11 other species. Large numbers intact dead 

skeletons of M. ferox and other species were found on the fore reef, although numerous 

healthy, unaffected colonies were still apparent (Dustan and Halas, 1987), highlighting 

extensive losses of corals from disease as well as the resilience of these species during 

the 1980s. WBD played a dominant role in the precipitous (90-98%) decline of A. 

cervicornis and A. palmata populations during the 1970s and 1980s (Bruckner, 2002; 

Aronson and Precht, 2001; Gardner et al., 2003). It is the only disease to date that has 

caused major changes in composition and structure of reefs over large areas of the 

Caribbean (Williams et al., 1999; Green and Bruckner, 2000). 

Since the mid 1990s, there has been a rapid proliferation of diseases, including a 

recent emergence of new syndromes (Sutherland et al., 2004; Weil, 2004; Weil et al., 

2006). Over 30 diseases have been reported from the Caribbean (Table 1). Some of 

these affect a single species in specific localities, while others have a widespread 

geographic distributions and wide host ranges (Weil, 2004). Epizootic events have been 

associated with six diseases [WP-II, BBD, WBD-I, yellow band disease (YBD), white 

pox (WPX) dark spot disease (DSD) and Aspergillosis (ASP)], and three diseases (WP-II, 

YBD and ASP) are currently causing extensive mortality throughout the region 

(Bruckner, 2002; Weil, 2004). In addition to the region-wide decline of acroporids, there 

has also been a notable degradation of massive reef-framework corals (in particular the 

Montastraea annularis complex). Declining health of M. annularis (complex) has been 

associated with WP-II epizootics of increasing severity, bleaching events (1995, 1998, 

2005), YBD, BBD, DSD, and parrotfish predation (Cervino et al., 1997; Bruckner and 

Bruckner, 2000; Nugues, 2002; Miller et al., 2003; Jordán-Dahlgren and RodríguezMartínez; Weil, 2004; Bruckner and Bruckner, 2006). The recent emergence of diseases 

in the wider Caribbean appears to be an unprecedented event over a millennial time scale 

(i.e. >3800 yr) (Aronson and Precht, 2001). 

While disease has undoubtedly played a major role in shaping the structure and 

ecology of Caribbean reefs over the past few decades, very little is known about many of 
129 

the fundamental aspects of coral diseases, such as their causes, how diseases are 

transmitted, factors conferring resistance and resilience, and the long-term effects of 

diseases on coral populations and coral reef ecosystems (Woodley et al., 2003). 

Researchers have made significant advances in coral disease research through the 

application of new laboratory tools and more detailed epizootiological studies (e.g., 

Edmunds, 1991; Bythell et al., 1993; Carlton and Richardson, 1995; Kuta and 

Richardson, 1996; Bruckner et al., 1997; Richardson et al., 1998; Bruckner, 2002; Downs 

et al., 2005). Unfortunately, large gaps remain in our understanding of coral disease, and 

few strategies and tools have been provided to resource managers to assist in the 

management of diseases and mitigation of disease impacts. Due to a growing number of 

disease reports, and an absence of standardized criteria for naming diseases, much 

confusion surrounds many of the newly emerging diseases. In some cases, scientists do 

not have the appropriate diagnostic tools to characterize disease outbreaks, and resulting 

analyses may be inconclusive or incomplete. Disease studies are being undertaken 

without the use of standardized investigative methodology, making it difficult to 

consistently characterize these events and draw comparisons between disease outbreaks 

in different locations. Other factors limiting progress include 1) a lack of standardized 

nomenclature and diagnostic tools, 2) conflicting reports on causative agents and their 

sources, 3) insufficient data to conclusively identify linkages between disease and 

environmental stressors. Finally, standard operating procedures for sampling, approaches 

to prevent contamination/dispersal of diseases, and other strategies to minimize 

environmental impacts have not been widely applied in the Caribbean. 

This paper reviews recent progress in coral disease research and summarizes our 

current understanding of the major diseases that have impacted Caribbean coral reefs 

over the last several decades. Topics discussed include 1) number and variety of 

diseases, 2) host ranges and geographic distribution, 3) prevalence and impact, 4) causes, 

and 5) role of environmental factors. An effort is made to identify gaps in knowledge, 

factors hindering progress, and contentious issues surrounding specific diseases from the 

western Atlantic. It is hoped that the information and lessons learned in the Caribbean 

can be applied to Pacific coral disease studies. 

How many diseases are there? 

Although over 30 coral diseases have been reported from the wider Caribbean 

since 1972 (Appendix I and II), only a handful of these syndromes (e.g., BBD, WBD, 

WP, YBD, DSD, WPX, ASP, and various skeletal abnormalities) have been observed 

throughout much of the Caribbean and certain aspects of their etiology and ecology have 

been characterized. Much confusion surrounds many of the other described syndromes, 

and few data are available on their distribution and abundance, impact, or cause. Several 

diseases have been subdivided into different “types” based on highly variable features 

(e.g., a zone of bleached tissue; differences in rates of movement, species affected). 

These characteristics often differ temporally and spatially, and may be unreliable, unless 

affected corals are tagged and followed over time. Syndromes have also been identified 

with limited etiological and ecological observations. These may lack a unique 

description of gross signs, disease signs differ among publications, or conditions were 

named on the basis of a single observation (Appendix II). Unsubstantiated causes or 
130 

agents have been proposed for several new syndromes, and information on prevalence, 

patterns of spread, or evidence of tissue mortality may be lacking. One of the difficulties 

in standardizing nomenclature used for coral diseases is that disease signs manifest on 

corals in a limited number of ways, but they may be caused by different pathogens or 

unrelated abiotic factors. 

The major syndromes reported in the literature from the wider Caribbean are 

combined here into six major categories, based on similarities of gross field signs 

(Appendix I). This includes: white syndromes, cyanobacterial mat diseases, tissue 

discoloration, abnormal skeletal development, skeletal damage, and gorgonian 

syndromes. 

White syndromes 

There has been a proliferation of names for coral diseases with virtually identical 

visible signs that reflect the pattern of loss of coral tissue and exposure of skeleton. All 

of these syndromes are characterized by a sharp, distinct line between apparently healthy 

coral tissue and freshly exposed skeleton, with no obvious microbial mat present at the 

disease interface. These conditions have been differentiated based on 1) species affected; 

2) presence of a zone of bleached tissue at the disease boundary; 3) rates of tissue loss; 4) 

location of lesion on colony surface; and 5) patterns of spread. Without microbial 

analysis of these diseases (or use of a molecular probe to confirm proposed causative 

agents), it is difficult to verify that WBD, various forms of WP, and other white 

syndromes are in fact distinct diseases, since disease signs are so similar (Appendix III; 

Bythell et al., 2004). 

Many studies have used various terms interchangeably to describe white 

syndromes, making it difficult to characterize regional patterns of disease occurrence. For 

example, Antonius (1977; 1981) identified 11 species of massive and plating species with 

WBD, while other researchers report this as WP (Dustan, 1977), and only use the term 

WBD for Acropora spp. (Aronson and Precht, 2001). Dustan (1977) suggested that WP 

represents a suite of diseases that result in the death of coral tissue, but he does not 

provide a detailed diagnosis of the macroscopic field signs. He characterized WP as 

“lesions on the colony that expanded at a rate of a few mm per day and often resulted in 

whole colony mortality”, but presents little information on location of lesions or patterns 

of progression. An outbreak of a disease with signs that are similar to Dustan’s “plague” 

(Dustan, 1977) was observed in 1995 on the same reefs (Richardson et al., 1998a). This 

condition was designated WP type II because of 1) a faster rate of progression (up to 2 

cm/day); 2) highest prevalence on Dichocoenia stokesi, a species unaffected during the 

original WP outbreaks; and 3) a unique pattern of tissue loss. WP-II progresses from the 

entire base of the colony to the apex, while WP- I lesions occur more variably across the 

colony (Richardson et al., 1998b). 

Richardson et al. (2001) also reported a third type of plague, WP type III, which 

was characterized by more rapid rates of progression (up to 10 cm/day) and a different 

pattern of tissue loss. Unlike WP-II, lesions start in the center of colonies and radiate out, 

and only the largest colonies of M. annularis (complex) and Colpophyllia natans are 

affected. White plague has also been used to describe tissue loss characterized by random 

patches of denuded skeleton that extend sporadically and do not give rise to a graded 
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algal community (Bythell et al., 2002). Peters (1984) coined the term “stress-related 

necrosis” for another similar condition characterized by sloughing of degenerating tissue, 

with no obvious discernable pathogens at the disease line. 

Since the mid 1990s, several white syndromes with unique diagnostic features 

have been reported on A. palmata, including WPX, patchy necrosis, necrotic patch 

syndrome, and other unnamed conditions (Ritchie and Smith, 1998; Bruckner and 

Bruckner, 1996; Patterson et al., 2002; Sutherland et al., 2004; Jordán-Dahlgren and 

Rodríguez-Martínez, 2004). While some authors have suggested that these syndromes are 

synonymous (Sutherland and Ritchie, 2004; Sutherland et al., 2004), a pathogen has been 

identified only for colonies identified with WPX in the FKNMS (Sutherland et al., 2002), 

and descriptions and photographs of these conditions are highly variable. In some cases, 

WPX has been described as circular, dime-sized lesions, while other descriptions suggest 

these are more irregular in shape. In addition, Weil (2003, 2004) reported “patchy 

necrosis” on A. palmata colonies during doldrums-like conditions, and later indicated that 

these were associated with parrotfish and sea cucumber fecal matter. 

Only two diseases have been identified in A. cervicornis, WBD type I and WBD 

type II. Published descriptions of WBD from A. cervicornis have far less detail on the 

pattern and rates of progression than reports of WBD on A. palmata. For example, 

WBD- II can be confused with both bleaching and WBD-I. Affected colonies have a 

receding margin that progresses at a faster rate than WBD-I, and tissue loss is preceded 

by a band of bleached tissue up to 20 cm in width. The bleaching margin may arrest, 

however, allowing the “peeling” margin to catch up to the pigmented tissue (Ritchie and 

Smith, 1998). Without the presence of a bleached margin, the disease is indistinguishable 

from WBD type I. Williams and Miller (2005) reported an outbreak of disease affecting 

A. cervicornis in Florida. Unlike WBD, tissue loss was characterized by rapid tissue 

sloughing from multifocal lesions and no bleaching was noted. They termed this 

condition rapid tissue loss. 

Further complicating distinctions between various white syndromes, scars from 

predation can be difficult to differentiate from diseases, especially when predators are 

cryptic (e.g., Coralliophila abbreviata) or nocturnal (Hermodice carunculata). Predators 

frequently feed on degrading tissue associated with disease lesions; fireworms and 

corallivorous snails often occur on colonies with BBD, WP, WBD and other white 

syndromes, and they may also serve as vectors for disease (Bruckner, 2002; 2003; 

Williams and Miller, 2005). 

Cyanobacterial mat diseases 

A number of diseases are associated with cyanobacteria. These often exhibit a 

similar identifiable group of signs on the coral and consistent anatomical alterations that 

are visible in the field, making it difficult to separate these conditions without laboratory 

confirmation of the specific cyanobacteria present. Affected colonies have a distinctive 

visible microbial assemblage that forms an advancing band or mat, separating denuded 

coral skeleton from living tissue. The mat is usually dominated by one or several 

cyanobacterial species, although the species of the dominant cyanobacterium may vary 

between large geographic regions, even in the same presumed disease (Cooney et al. 

2002; Frias-Lopez et al. 2002, 2003). The mat may appear black, brown or reddish 

depending on light levels, the species of cyanobacterium, and its complement of 
132 

photosynthesis pigments. This includes diseases referred to as BBD and red band disease 

(RBD type I and RBD-II; Appendix I; III). 

Tissue discoloration 

Corals exhibit wide variations in color depending on species, genotypes, clade of 

zooxanthellae and/or type and concentration of algal pigments, and in response to 

physical and environmental factors. Individual colonies may show changes in coloration 

due to a partial loss of zooxanthellae or their photosynthetic pigments (bleaching), host 

responses to irritants and injuries, or from coral diseases. 

YBD is characterized by lightening of tissue. Affected colonies have small 

circular blotches of pale yellow tissue surrounded by normally pigmented tissue. These 

lesions expand in size over time, with central areas dying and becoming colonized by 

algae. YBD lesions can be confused with bleaching, and during bleaching events it may 

be difficult to determine which corals are affected by YBD (Cervino et al., 2001). 

DSD is characterized by darker than normal coloration. Colonies may have one or 

more small, round spots or patches of darkened tissue (and discolored skeleton in some 

cases) that grow in size over time. The spots may be associated with a depression in the 

coral surface, and spots may expand into a ring surrounding dead coral. Weil (2004) 

recently divided DSD into DSD type I and DSD-II, and also identified three other similar 

syndromes, dark band disease (DBD), purple band syndrome (PBS) and tissue necrosis. 

DSD-II is similar to DSD-I, except the “spots” were larger and a thin, necrotic tissue line 

was apparent at the margin. PBS differs from DSD in that colonies of S. siderea have a 

band of discolored tissue that advances from the outer margin to the inside. It is 

unknown whether these are different diseases, or are later stages in the progression of 

DSD, as a causative agent has not been identified and few studies have followed the 

progression of DSD lesions over time. Some researchers consider these conditions the 

same as DSD (Gil-Agudelo et al., 2004; Appendix I and III). 

Abnormal skeletal growths

Coral colonies often exhibit distinct circumscribed lesions on the surface of a 

coral, composed of the corals tissue and skeleton. These structures are typically raised 

spherical to irregular masses that project above the surrounding corallum. They can be 

subdivided into three categories on scleractinian corals: a) a proliferation of all cell types 

that may be atrophied or normal in appearance (gigantism, area of accelerated growth, 

hyperplasm, growth anomaly); b) white, globular masses with few discernable polyp 

structures and a reduction or absence of zooxanthellae (tumor, neoplasm, calicoblastic 

epithelioma); and c) chaotic polyp development (Peters et al., 1986; Appendix I and 

Table 1). Hyperplasms do not appear to cause significant damage to the colonies, while 

neoplasms damage affected areas, leaves them more susceptible to invasion by boring 

organism, and destroys normal polyps and their functions (e.g., reproduction). 

Skeletal damage or erosion 

Damage to scleractinian corals associated with the disruption of septa or calices, 

or complete loss of the upper skeletal layers may be the result of physical injuries (e.g., 

abrasions during storms, anchor damage, fin damage), various biotic interactions 

(predation by fishes, sponge bioerosion, aggressive interactions among corals) and certain 
133 

coral diseases. Loss of corallites has been reported for WPX lesions, but the skeleton 

remains intact (Sutherland, 2002). Skeletal damage has also been reported in WBD-II 

(Ritchie and Smith, 1998). In skeletal eroding band (SEB), ciliates create a distinct black 

band adjacent to living tissue. The ciliates secrete a lorica (their “house”), which is 

embedded in the coral’s skeleton and can completely destroy the surface layer of the 

skeleton (Antonius, 1999). The ciliates form a distinct black to grey band at the margin 

between exposed skeleton and live tissue, which may be confused with BBD. 

Rapid wasting disease (RWD) and ridge mortality disease (RMD) were reported 

as coral diseases (Abbott, 1979; Cervino et al., 1997; Goreau et al., 1998), but have since 

been found to be associated with predation by fishes and the formation of territorial algal 

lawns (Bruckner and Bruckner; 1998; 2000; Borneman, 2005). RWD was characterized 

as irregularly-shaped white lesions denuded of tissue with the uppermost layers of the 

skeleton etched away; the exposed limestone was unusually brittle and crumbly (Cervino 

et al., 1997). Filamentous fungal hyphae covered and were invading epidermal cells, and 

were proposed as the causative agent. Detailed visual and photographic observations and 

experimental manipulations demonstrated that RWD is caused by focused biting by the 

stoplight parrotfish Sparisoma viride (Bruckner and Bruckner, 2000), a phenomena that 

was documented over 100 years ago. The RWD researchers recently identified a fungus 

in the mouth and fecal matter of S. viride, and proposed that parrotfish were a vector for 

RWD (Richardson, 2000). While linkages between a fish and a fungal pathogen have not 

been conclusively verified, the major damage to affected colonies has been shown to 

result directly from predation: 1) lesions advance only during daylight; 2) no further 

tissue or skeletal loss occurs once the parrotfish were excluded; and 3) lesions rapidly 

heal in absence of further biting (Bruckner and Bruckner, 2000). 

Ridge mortality disease is associated with the loss of tissue and skeletal structures 

along elevated ridges of brain corals, with tissue remaining in the valleys (Abbott, 1979). 

Lesions initiate at a single point within the colony surface (or at the margin) and expand 

outward, following the meanders of the colony. The ridges typically are not completely 

destroyed; skeletal damage is largely restricted to the loss of septa. This condition is 

associated with the development and expansion of Stegastes planifrons algal lawns 

(Bruckner, 2002, 2003; Borneman, 2005). However, it is unclear whether fish bites are 

the sole cause of tissue loss. Biting may cause a stress response that triggers tissue 

sloughing, or the fish may introduce a pathogen that causes advancing tissue loss. 

Interestingly, only ridges are affected, and tissue remains in the valleys (and around 

polyp mouths) until it is overwhelmed by algae. Similar biting by damselfish can create 

multiple focal lesions that affect individual circular polyps (on M. annularis and S. 

siderea), or result in the development of “chimneys” in acroporids (as the coral attempts 

to contain the algae). 

Gorgonian syndromes 

Gorgonians have been observed with BBD, RBD, Aspergillosis, predation by 

gastropods and polychaetes, tumors, and other conditions (Morse et al., 1977; Rützler et 

al., 1983; Nagelkerken et al., 1997). Abnormal growths often develop on the branches of 

gorgonian corals (algal tumor, algal gall, or nodules) in response to endolithic algae, 

fungi and other epibionts (Morse et al., 1977). These are hard concretions of fibers of 

gorgonin that form spherical or irregular, but may be irregular shaped masses. They are 
134 

located predominantly at the axial bases of the colony, but often extend the overall length 

of the colony. 

Aspergillosis is an extremely virulent fungal disease that affects sea fans and 

branching gorgonians, causing tissue loss and destruction of the skeleton (Nagelkerken et 

al., 1997). ASP is characterized by degradation and recession of coenenchyme, purpling 

of adjacent tissue, production of galls, and secondary colonization of exposed axial 

skeleton. Field identification of ASP may be difficult, as similar lesions, purpling of 

tissue and nodules, and skeletal and tissue loss occur in response to predation, abrasions, 

algal interactions and other factors. Confirmation of ASP requires identification of A. 

sydowii, which may not be visible without microscopy. 

What corals are affected by disease and what are the impacts? 

Records in the Global Coral Disease Database (GCDD) show that 33 species of 

stony corals, 8 gorgonians and two hydrozoans are affected by at least one disease. This 

list may not be comprehensive, as Weil (2004) indicates that at least 41 scleractinian 

corals have been affected by diseases. Some of these differences may be related to the 

taxonomy used (i.e. whether species are combined or split), or may reflect unpublished 

observations. Some conditions show geographic variability in occurrence, and 

susceptibility may vary among species for the different “types” reported (Richardson and 

Aronson, 2002; Weil 2004). Montastraea annularis (complex) is currently most severely 

impacted by coral diseases, being susceptible to at least eight syndromes (Weil, 2004), 

with single colonies showing signs of two or more diseases simultaneously (Bruckner and 

Bruckner, 2006). White plague (type I and II), the most virulent disease observed to date, 

affects 39 scleractinian corals (Weil, 2004). BBD has been reported on 25 scleractinian 

corals, 6 branching gorgonians and sea fans (Green and Bruckner, 2000). YBD primarily 

affects M. annularis complex, although other faviids, A. agaricites, and P. astreoides are 

reported with this condition (Gil-Agudelo et al., 2004). The various dark spot/band 

diseases (Appendix I) collectively affect 14 species (Gil-Agudelo et al., 2004; Weil, 

2004). Skeletal anomalies affect at least 16 Caribbean scleractinian corals, one hydrozoan 

and five gorgonians, with acroporids being most susceptible to neoplasms, and faviids 

commonly exhibiting hyperplasms (Sutherland et al., 2004). Susceptibility of the major 

genera of reef building corals to the 7 most significant scleractinian coral diseases are 

shown in Fig. 1. 
135 

Table 1. Existing descriptions of gross signs of the primary Caribbean diseases 

Syndrome Diagnostics Reference 

WP type I Lesions that expand at a rate of a few mm/day and often result in colony mortality. 

Lesions occur more variably across the colony surface including the edges and 

sides. Edges of lesions show a sharp boundary between apparently healthy tissue 

and freshly exposed skeleton with no build up of microorganisms or necrotic tissue 

visible to the naked eye. Mean rate of loss= 3 mm/day 

Dustan 1977 

WP type II Freshly exposed coral skeleton with a sharp line between skeleton and apparently 

healthy coral tissue. No evident microbial community; a narrow (2-3 mm) zone of 

bleached tissue at the disease line. No skeletal damage. Similar to type I but faster 

progression and lesions always start at the base of the colony and advances to the 

apex. Max loss=2cm/day 

Richardson 

et al., 1998 

WP Type III Lesions start in the center of the colony and expand outward. Tissue loss occurs as 

large patches on the sides of large (>2m) colonies. Rates of loss can exceed 10 

cm/day 

Richardson 

et al., 2001 

WBD A distinct band of white exposed skeleton separates live tissue and algal colonized 

dead coral. Tissue adjacent to lesion may appear healthy or form a narrow band of 

disintegrating coral tissue that is peeling off the skeleton. Tissue mortality starts 

near the base of a colony and where branches furcated, advancing towards branch 

tips at a rate of 1-21 mm/day (mean = 5.5 mm/day)2

; it sometimes but not always 

encircles the entire branch. .No skeletal damage. The width of exposed skeleton 

varies depending on spreading rates, with older areas becoming progressively 

colonized by filamentous, turf, macro and coralline algae. 

Gladfelter, 

1982 

2

Davis et al., 

1986 

WBD II A distinct band of white exposed skeleton separates live tissue and algal colonized 

dead coral. The lesion boundary is preceded by a 2-20 cm band of bleached tissue. 

The advancing lesion may “catch up” to the bleached margin, making the disease 

indistinguishable from WBD I. The disease progresses from the base to the branch 

tips, but can also progress from branch tips towards the base. Some dissolution of 

the skeleton may occur. Advance of up to 10 cm per day. 

Ritchie and 

Smith,1998 

WPX Irregularly shaped distinct white patches devoid of coral tissue. Most lesions are 

small but can be > 80 cm2 and can develop simultaneously on all surfaces of the 

coral colony. Lesions can merge, resulting in tissue loss that spans the entire 

colony. The denuded coral skeleton remains intact, but loss of corallites is 

common. Lesions enlarge along the perimeter at a rate of 2.5 (max= 10.5) cm2

/d 

Patterson et 

al., 2002; 

Sutherland 

and Ritchie, 

2004 

BBD Black mat/band on the surface of the coral that separates healthy tissue and white, 

tissue-denuded skeleton. The band consists of a microbial community (black, 

chocolate brown or reddish rust colored with white filaments) a few mms to cms in 

width, and 1 mm thick. The width of exposed skeleton varies with spreading rates, 

with older areas progressively colonized by algae. BBD progresses from single 

point (at the margin of the colony, or within the colony surface at the interface 

between previously killed skeleton and live tissue) and radiates outward in a 

circular or semicircular pattern The microbial consortium functions together to 

generate and maintain an environment of anoxia adjacent to living coral tissue, 

possibly causing tissue necrosis through a lack of oxygen and exposure to 

hydrogen sulfide. Tissue loss of up to 1 cm/day (mean=3 mm/day) 

Rützler and 

Santavy 

1983, 

Edmunds 

1991, 

Richardson 

et al. 1997; 

Bruckner et 

al., 1997. 

RBD-II Small (2-3 cm) lesions on scleractinian coral colonies. Cyanobacterial filaments 

form a loose biofilm, or matrix, that is spread out over the lesion and onto adjacent 

healthy coral tissue during the day. At night, the filaments contract to form a 

tightly compacted band less than 1 mm wide that is closely associated with the 

edges of the lesion at the interface with apparently healthy coral tissue. Tissue 

loss= 1 mm/day 

Richardson, 

1992 

RBD-I A band or mat of filamentous cyanobacteria, 0.5-2.5 cm wide, that separate coral 

skeleton from live tissue; the band moves typically from the base to the tips. 

Rützler et 

al., 1983 
136 

Syndrome Diagnostics Reference 

YBD Small circular area (s) of translucent light yellow tissue surrounded by fully 

pigmented tissue, or a narrow band of pale tissue at the colony margin that slowly 

expands in size. Tissue first affected (e.g., in the center of the blotch) gradually 

darkens and dies and these areas become colonized by algae. Recently exposed 

white skeleton may be absent or confined to small (<2 cm) irregular patches within 

the yellow band. Lesions expand 0.3-2 cm per month; multiple lesions appear on 

individual corals; these coalesce and continue spreading. Colonies show YBD 

signs for multiple years. 

Bruckner 

and 

Bruckner, 

2006 

DSD Small, round, dark spots that grow in size over time. Affected tissue may be 

depressed relative to the rest of the coral. Spots may expand into a ring 

surrounding dead coral1

 Rates of tissue loss for S. siderea were 0.51 cm2/month 

and 1.33 cm2

/month for M. annularis2

1

GarzónFerreira and 

GilAgudelo, 

1998; 

DSD-II Similar to DSD-I except the “spots” were larger and may cover 90 % of the 

colony; Dark but healthy looking tissue up to 45 cm (diameter) associated with 

depressed skeletal areas. Darkened tissue eventually dies. Dead areas are usually 

associated with thin, necrotic tissue at the margin. The syndrome advances slowly 

but faster than DSS-I. 

Weil 2004 

DBS Round or elongated bands of pale to dark, live tissue that is sometimes associated 

with depressed skeletal areas in the corallum. Starts as spots and develops into 

wide dark bands (1 – 2 cm) of ill-looking tissue. The bands advance from areas in 

the center or side of the colony towards the edge of the colony in most cases. In S. 

siderea, the syndrome advances from the edge to the center of the colony, or from 

one side to the other. Rates of advance are faster than those in DSS-I and DSS-II. 

Weil 2004 

PBS Colonies have several purple spots over the surface, or a purple band that develops 

at the edge and moves to the center, leaving clean skeleton behind that is quickly 

colonized by turf algae. The width of the purple band is variable, but generally 

over 1 cm. The rate of advance is approx. 1 cm/month 

Weil 2004 

Tissue 

Necrosis 

Similar to PBS, except colonies lack spots, band is wider and more irregular and 

tissue looks necrotic and peels off skeleton 

Weil 2004 

Calicoblastic 

Neoplasm 

Raised (up to 1 cm) whitened, irregularly shaped lumps on upper or lower branch 

surfaces in any region of the coral colony, sometimes extending from one side of 

the branch to the other. Normal polyps absent from the center of the mass. 

Coenosteal skeletal material spreading upward between polyps at the margins, or 

over polyps toward the middle; coral tissue at the edges appears slightly swollen, 

ruffled, and lifted above the skeleton. Mean growth rate of 0.12 mm/d 

Peters et al., 

1986 

Hyperplasm Protuberant circular to ovoid lesions with enlarged skeletal elements relative to 

adjacent surfaces. Normal tissue features such as polyps and tentacles are present 

but enlarged. Pattern of the polyps, valleys, ridges may differ from the rest of the 

colony but tissue is usually similar in coloration to the rest of the colony. 

Peters et al., 

1986 
137 

Fig. 1. Number of diseases affecting different genera of western Atlantic 

scleractinian corals. 

0

2

4

6

8

10

12

14

16

18

20

Acropora

Montastraea

Colpophyllia

Diploria

Siderastrea

Stephanocoenia

Meandrina

Porites

Madracis

Agaricia

Mycetophyllia

Dichocoenia

Number of species

hyperplasia

DSD

YBD

RBD

BBD

WP

WBD
138 

The average prevalence of coral diseases at the community level is generally low, 

although it is highly variable between and within sites, during different years, and 

seasonally. Outbreaks of BBD, WP and WBD were identified during the 1970s and 

1980s in Florida, Belize, Jamaica, USVI, Netherlands Antilles (Dustan, 1977; Rützler et 

al., 1983; Peters 1984; Rogers, 1985). In some locations, these diseases affected 50-80% 

or more of the corals, although outbreaks were largely confined to specific reefs or zones 

(e.g., the palmata zone). Over the last ten years, there has been an increase in monitoring 

efforts targeted at disease, and many of these report an increase in the prevalence and 

incidence of disease throughout the region over time, including outbreaks of WP-II, 

YBD, WPX and other emerging acroporids syndromes (Porter et al., 2001; Nugues, 2002; 

Miller et al., 2003; Weil, 2004; Bruckner and Bruckner, 2006). In one of the first 

Caribbean-wide surveys, prevalence rates in 9 locations ranged from 0.9% in Bermuda to 

16% in Jamaica during 1999, with a higher number of diseased gorgonians (compared to 

scleractinian corals) and a significant increase in prevalence between 1999-2001 in 

Bermuda (4.3% in 2001), Puerto Rico (from 2.1% in1999 to 6.6% in 2001) and 

Venezuela (3% to 5.8%) (Weil, 2004). In contrast, more recent studies near Lee Stocking 

Island, Bahamas found very low levels of disease (<0.7% in 2002 and 2003; Voss and 

Richardson, 2006). 

White band disease and other syndromes affecting acroporids 

WBD was first documented on reefs around St. Croix, USVI, and later throughout 

the Caribbean. During the 1970s and 1980s, the prevalence of WBD varied from 1-2% to 

26% in the British Virgin Islands (Davis et al., 1986), 33% in Parguera, Puerto Rico 

(Goenaga and Boulon, 1992), 40% in Florida and Belize (Antonius, 1981), 64% in the 

USVI (Gladfelter et al., 1977) and as high as 80% in Jamaica and the Netherlands 

Antilles (Rogers, 1985). Epizootics of WBD significantly reduced populations of 

acroporids throughout the region. 

Although WBD was reported from 9 countries in the last ten years, most 

observations of WBD on A. palmata are for isolated colonies, with only one outbreak 

reported (Mona Island, Puerto Rico; Bruckner and Bruckner, 2005). In contrast, recent 

outbreaks of a more virulent disease (possibly a form of WBD, WBD-II, or some other 

syndrome) have been noted among A. cervicornis in Puerto Rico, Bahamas, Florida and 

other locations (Weil, 2004; Williams and Miller, 2005). Other conditions (WPX and 

other emerging syndromes) are also being observed more frequently on A. palmata since 

1994. These are causing much more rapid rates of tissue loss (cm/day) than that reported 

for WBD in the 1970s and 1980s (5 mm/day). For instance, WPX lesions expand 

radially at their perimeters at an average rate of 2.5 cm2

/day and individual lesions may 

be greater than 80 cm2 in area; lesions can develop simultaneously on all surfaces, and 

individual lesions often coalesce, resulting in tissue loss that spans the entire colony 

(Sutherland and Ritchie, 2004). In the Florida Keys populations of A. palmata sustained 

losses averaging 88% between 1996-2002, which was attributed primarily to WPX 

(Porter et al., 2001; Sutherland et al., 2004). 

Black band disease 

BBD is widely distributed throughout the Caribbean, with reports from 25 

countries. BBD generally affects a low percentage of corals (<1%) at the community 
139 

level (Edmunds, 1991; Kuta and Richardson, 1996), but it occurs in most reef 

environments, and localized epizootics have been observed in the USVI, Jamaica, Florida 

and Puerto Rico (Peters, 1984; Bruckner and Bruckner, 1997; Bruckner, 1999 Bruckner, 

2002). The disease may exhibit a clumped distribution (Kuta and Richardson, 1996; 

Bruckner et al., 1997), affecting up to 10 corals within a 2 m radius area (Peters, 1984). 

A greater percent of the corals may be affected by BBD in areas with high coral cover, 

and in habitats with a high density of colonies or dominance by susceptible species. For 

example, prevalence of BBD in St. John was low at the community level (0.2%), but 

much higher at the species level (5.5% of the D. strigosa); these sites had a high density 

of colonies, but susceptible species accounted for only 24% of the total coral composition 

(Edmunds, 1991). Florida reefs examined by Kuta and Richardson (1996) had a low 

density of corals (0.15 colonies/m2

) and relatively few infections (0.72%). Other sites 

examined in the Florida Keys ten years earlier (when they had 50-60% cover) had a mean 

prevalence of BBD of 6% (Dustan, 1987). Bruckner and Bruckner (1997) observed a 

maximum prevalence of 1.2% in Jamaica, although 5.2% of the corals became infected 

over 20 months. These sites had an intermediate density of corals (0.9 colonies/m2

), 

although over 90% of the corals were susceptible to BBD (Bruckner et al., 1997). 

BBD typically advances at rates of about 3 mm/day (Rützler et al., 1983), and 

occasionally increases to a maximum of 1 cm/day (Antonius, 1981). Considerable 

variation in spreading rates is observed over the duration of individual infections (Rützler 

et al., 1983) and also between species, depths, seasons and locations (Bruckner, 2002). 

BBD occurs year round on tropical Caribbean reefs, while infections often disappear in 

winter months in Florida and other northern reefs, when temperatures decline below 

20oC. BBD can kill small (<50 cm2

) corals in several days while larger corals experience 

partial mortality before signs of BBD disappear (Bruckner, 2002). However, BBD may 

reappear later that season or the following year, and individual colonies can be affected 

by BBD for multiple years (Feingold, 1988; Kuta and Richardson, 1997; Bruckner and 

Bruckner, 1997). While BBD does not appear to have caused large die-offs of important 

reef-building corals, individual colonies lose substantial amounts of tissue that may affect 

their reproductive potential or their ability to resist other stresses (Edmunds, 1991; 2000). 

Kuta and Richardson (1997) noted that corals continue to lose tissue after signs of BBD 

disappear. In the USVI, 28 colonies identified with BBD in 1988 were tagged and 

followed for ten years; 50% of these were subsequently killed during a hurricane or died 

of unknown causes, 36% died from BBD, and 14% were still alive 10 years later 

(Edmunds, 2000). Regrowth of corals affected by BBD has been observed (especially in 

D. strigosa), although larger lesions in M. annularis and other species fail to completely 

regenerate (Bruckner, 2002; Weil, 2004). 

White plague 

White plague was first observed in Key Largo, Florida in the 1975, where it 

affected up to 7% of S. siderea colonies and 24-73% of M. ferox colonies at Carysfort 

Reef (Dustan, 1977). WP was still prevalent in 1984 on Carysfort Reef, and was also 

documented throughout the entire Key Largo region (inner, middle and outer reefs) at a 

mean prevalence of about 3.7% (Dustan, 1993). WP caused rates of tissue loss of up to 

3.1 mm/day, and was estimated to have killed 20-30% of M. ferox population (Dustan 

1977, 1987). 
140 

A more virulent form of WP (WP-II) was observed on reefs of the middle and 

northern Florida Keys in 1995. It initially affected 9-38% of D. stokesi colonies, and 

subsequently spread to 16 other species (Richardson et al., 1998a). The epizootic 

recurred in 1996 in the lower Keys and Dry Tortugas (although sites with outbreaks in 

1995 had few infections in 1996) and in 1997 emerged on reefs north of the Florida Keys 

reef tract (Richardson et al . 1998b). 

WP (type I and type II) has continued to spread throughout the region over the 

last 10 years, with reports from 21 countries. In La Parguera, Puerto Rico, WP first 

appeared in 1996 on inner middle and shelf edge reefs; it affected 5 genera, but was most 

severe on one inner reef where 47% of the D. labyrinthiformis colonies contracted WP 

between August and December (Bruckner and Bruckner, 1997). Subsequent outbreaks 

were observed in Puerto Rico in 1998, 2000, 2002 and 2006 (Bruckner, pers. Obs., Weil 

2004; Hernandez, coral list posting). 

WP-II first appeared on reefs around St. John, USVI in 1997, and has been since 

observed on most back reef (< 3m depth), fore reef slope (6-12 m) and deeper offshore 

habitats (24-32 m). It primarily affects M. annularis (over 90% of infections) but also M. 

cavernosa, C. natans, S. siderea and Diploria spp. are susceptible (Miller et al., 2003). 

New infections were observed every month over 4 years at Tektite Reef, although the 

incidence varied substantially (3-58%) over the duration of the study and was highest 

during the first year (Miller et al., 2003). An outbreak occurred on these and other reefs 

in St. John following the 2005 bleaching event (J. Miller, unpubl obs). 

An outbreak of WP was also first observed on reefs near Soufriere, St. Lucia in 

July 1997 (Nugues, 2002). Eleven percent (range=7-14%) of the six dominant coral 

species were infected with WP on three reefs in March 1998. Over 8 months, WP was 

estimated to have killed 6.6% of the living coral tissue at the most affected site, with most 

of the tissue loss occurring on the two dominant species (M. faveolata and C. natans)

(Nugues, 2002). 

Yellow band disease 

YBD was first reported from the Florida Keys in 1994 (Cervino et al., 2001), with 

subsequent observations from 24 countries. The incidence of YBD increased between 

1996-2000 in Colombia, Mexico, the Netherland Antilles, Panama, Puerto Rico, Grenada, 

St. John, Turks and Caicos, USVI and Venezuela, where 18-91% of M. annularis

(complex) colonies were affected (Santavy et al 1999; Cervino et al 2001; Bruckner and 

Bruckner 2003; Gil-Agudelo et al. 2004; Jordán-Dahlgren and Rodríguez-Martínez 2004; 

Bruckner and Bruckner, 2006). YBD currently appears to be most abundant in remote, 

offshore locations removed from human population centers (Bruckner and Bruckner, 

2003; 2006; Weil, 2004). 

Rates of mortality from YBD are generally slow (5-15 cm/yr), although colonies 

with single YBD lesions become infected in multiple locations, and infections can persist 

for over 5 years (Bruckner and Bruckner, 2006). In both Curacao and Puerto Rico, YBD 

appeared to preferentially target the larger corals in the population; over several years, 

live tissue area is progressively reduced in size, with infections persisting until the coral 

dies (Bruckner and Bruckner, 2006; Bruckner and Bruckner, in press). 
141 

Dark spots disease 

DSD was first noticed in Colombian reefs in 1992 during a bleaching event 

(Solano et al., 1993), with the first quantitative study conducted in 1997 (Garzón-Ferriera 

and Gil, 1998). In this study, DSD affected > 16% of six species (over 1545 colonies); 

the two most abundant species (M. annularis and S. siderea) had the highest number of 

infections (Gil-Agudelo and Garzón-Ferreira, 2001). Cervino et al., (2001) reported 

prevalence rates of 42-56% for S. intersepta and S. siderea in Bonaire, Turks and Caicos, 

and Grenada. Gochfeld et al. (2006) reported a mean prevalence of 31.5% on St. Thomas, 

USVI, 50.3% on Culebra, Puerto Rico, and up to 80% in the Bahamas for S. siderea, with 

the highest incidence during August and sudden declines each year in October. 

Spreading rates of DSD are generally low. In Colombia, loss was 0.51 cm2

/day 

for S. siderea and 1.33 cm2

/month for M. annularis. Recovery of lesions was not 

observed, and signs of the syndrome persisted for several years (Garcés-Baquero, 2000). 

Cervino et al., (2001) reported rates of tissue die back of 3.99 cm/month for 2 colonies of 

S. siderea. In the Bahamas, Gochfeld et al., (2006) did not observe any colony mortality 

from DSD over two years; small areas of necrosis were noted, but these areas regenerated 

relatively rapidly. In addition, dark spots disappeared from affected colonies in October, 

but they also often reappeared the following year in the same or different location 

(Gochfeld et al., 2006). 

Aspergillosis 

Aspergillosis is thought to have emerged in the 1980s along the coast of Costa 

Rica, Panama and Trinidad (Guzman and Cortes, 1984, Garzón-Ferreira and Zea, 1992, 

Laydoo, 1983), where it caused localized mass mortalities. Sea fans showing similar 

signs to the 1980s epizootics were reported from 22 locations throughout the Caribbean 

in 1995 (Nagelkerken et al., 1997). In the Bahamas, disease incidence and virulence 

increased between 1995-1998 (Smith and Weil, 2004). By 1999, Aspergillosis was 

identified on branching gorgonians (Pseudoterigorgia, Plexaura, Pseudoplexaura and 

Plexaurella spp.) in Puerto Rico and the Bahamas. Over the last 5 years ASP infections 

have been observed in 17 countries. 

Prevalence of ASP appears to be greater in protected sites and in deeper areas on 

exposed reefs (Nagelkerken, 1997). In the Florida Keys, 31% of sea fans were affected in 

August 1997; declining numbers of infections were observed over the next seven years in 

all sites, except for three localized outbreaks during the summers of 1998, 2000 and 2002 

(Kim and Harvell, 2004). Aspergillosis does not appear to have impacted the abundance 

of sea fans in Florida, although partial and complete mortality altered the size-class 

structure of the population by removing the large colonies (Kim and Harvell, 2004). 
142 

Table 2. Prevalence, incidence and impact of the major western Atlantic coral diseases. 

Disease Spatial distribution and 

prevalence 

Temporal/ Spatial 

variations 

Impact 

WP 7% of S. siderea, 24-73% of M. 

ferox in Florida1

; 20.1% of D. 

stokesi colonies in Florida2

 11% of 

all species, 19% M. faveolata and 

13% C.natans in St. Lucia3

Highest prevalence in late 

summer and early fall at 

temps of 29-30° C 1 In St. 

Croix, prevalence of 3.1% in 

clean site and 11.4% in 

polluted site5

20-30% mortality of M. ferox

populations1 0.1-5% tissue 

loss over 26 months in the 

USVI during the 1980s 4 9.4% 

of affected D. stokesi colonies 

died in 2 months5

WBD 2-5%; up to 40% in Florida, USVI, 

Belize1

; 5-26% in BVI2; up to 64% 

in USVI3

; 20-33% in Puerto Rico4

 Contributed to a regional 

decline of Caribbean 

acroporids 

WPX Contagious; Clumped distribution1, 

up to 100% of colonies may be 

affected2

 35-73% affected in PR3

Greatest rate of tissue loss 

during warm water1

Rapid spread within and 

between reefs during the 

1990s; killed 50-80% of 

elkhorn coral in certain areas 

in FKNMS1

Average loss of 

tissue over 10 days was 17%3

BBD Up to 8% of gorgonians at one time, 

13.8% of all colonies over 26 

months in Florida1 0.2% of all 

corals; 5.5% of D. strigosa2 5.2% 

total over 20 months; max 1.2% at 

one time3

Highest prevalence in summer 

in shallow locations; 

disappears in winter in 

Florida1

 and when temps drop 

below 27.5 C in the Bahamas5

Temperature and light affect 

growth and spreading rates of 

BBD3

 In USVI higher 

prevalence (1% vs. 2.7%) in a 

polluted site 4 Sites with BBD 

had higher sedimentation 

rates5

Mean rate if tissue loss is 3 

mm/day; in St. Croix, rates 

were 1.45 mm/day4

 58% of D. 

strigosa colonies lost >75% of 

their tissue; overall loss of 

3.9% of D. strigosa tissue per 

year2

YBD Up to 12.5% M. annularis and 7.8% 

D. strigosa affected in Colombia in 

19991 35% of M. annularis in 

Mexico during 20012 up to 52% in 

Puerto Rico3 

Higher spreading rates in 

summer. Sites affected 

between 1997-2002 shows a 

declining trend of new 

infections; older infections 

have persisted and new areas 

are being impacted. 

Colonies affected with YBD 

in 1999 and 2000 lost 60% of 

their tissue by 2003 and most 

were still affected by YBD3

DSD 16% of six species; 1; 42-56% of S. 

intersepta and S. siderea2

 Incidence 

on S. siderea varied from 81% on 

the deepest reef in May 2002 to 

67% in a shallow site in Jan 20033

Highest incidence July-Oct.; 

more infections in shallow 

water 1 In the Bahamas 

dramatic decrease in October, 

unrelated to temperature and 

depth 3

Tissue loss of 4 cm/month in 

S. siderea2

 No significant loss 

over two years; small lesions 

recover3

ASP 39% of sea fans in Caribbean in 

1995-19961

; 31% in Florida in 1997, 

declining to 5.9% by August 20032

In Mexico prevalence declined from 

12.9% in 2002 to 5.3% in 2004 

Prevalence higher in protected 

sites and deep water 1

Sea fan density has remain 

constant; Keys-wide reduction 

in height of sea fans (40 cm – 

26 cm) and >50% of the tissue 

area over six years 2

WP: 1

Dustan, 1977; 2Richardson, 1995; 3Nugues, 2002; 4Bythell et al.,1993; 5 Kaczmarsky et al., 2005. 

WBD: 1

Antonius, 1981 2Davis et al., 1986 3Gladfelter et al., 1977 4Goenaga and Boulon, 1992 5Rogers, 1985 

WPX: 1

Patterson et al., 2002; 2Sutherland and Ritchie, 2004 3Weil, 2004 4 Kaczmarsky et al., 2005. 

BBD: 1

 Feingold, 1988. 2Edmunds, 1991; 3Rützler et al., 1983 ; 4 Bruckner et al., 1997 

YBD: Cervino et al., 2001 Gil-Agudelo et al., 2004; Bruckner and Bruckner 2003; Bruckner and Bruckner, 2006 

DSD: 1

Gil-Agudelo and Garzón-Ferreira, 2001; 2Cervino et al., 20013 Gochfeld et al., 2006 

ASP: 1

Nagelkerkin et al., 1997; 2Kim and Harvell, 2004 
143 

What is causing these diseases and where are they coming from? 

Proving disease causation has been one of the largest challenges in coral disease 

research. Because diseases manifest on corals in a limited number ways, corals that 

exhibit specific disease signs in the field may be affected by a variety of pathogens that 

differ spatially or temporally (e.g., the pathogen for WP-II may differ depending on the 

location, affected species, or other factors). To date, causative agents have been 

identified for four of the most common diseases found on Caribbean reefs (BBD, WP-II, 

ASP, and WPX). Three of these (WP-II, ASP, WPX) were verified through inoculation 

experiments with cultured bacterial isolates (through fulfillment of Koch’s postulate), 

while the cause of BBD was identified using microscopy. In other diseases (YBD, DSD, 

WBD-II) screening of microbial communities of healthy and diseased tissue (and mucus 

layer) using traditional culture methods illustrates a high diversity of microorganisms, 

along with several bacteria (especially Vibrio spp.) that appear to be more prevalent in 

diseased samples (Cervino et al., 2001; Gil-Agudelo et al., 2004; Weil, 2006) . Molecular 

studies (16S and 18S rRNA/DNA gene sequence amplification of microbial 

communities) have identified complex multi-species microbial communities in corals 

(including microorganism that may be unculturable) that appear to vary spatially, 

seasonally, between species, and also between diseased and apparently healthy parts of 

the colony (Rohwer et al., 2002; Pantos et al., 2003; Pantos and Bythell, 2006). In many 

cases (e.g., WP-II, BBD and WBD) these molecular studies have identified a different 

suite of organisms as potential causative agents than that observed in earlier studies. 

Black band disease 

The causative agent of BBD was originally described as the cyanobacteria 

Oscillatoria submembranaceae and then Phormidium corallyticum based exclusively on 

filament morphology, pigmentation and motility determined using light microscopy 

(Antonius, 1981; Rützler et al., 1983). Other heterotrophic bacteria (Garrett and 

Ducklow, 1975), the sulfide oxidizing bacterium Beggiatoa spp. (Ducklow and Mitchell, 

1979) and marine fungi (Ramos-Flores, 1983) have also been suggested as the primary 

pathogen. Richardson and colleagues described BBD as a consortium of microorganisms 

dominated by a gliding filamentous cyanobacteria (P. corallyticum) that functions 

together with sulfur oxidizing bacteria (Beggiatoa spp.) and sulfur reducing bacteria 

(Desulfovibrio spp.) to produce anoxia and high levels of sulfide adjacent to the coral, 

conditions that are lethal to the coral (Carlton and Richardson, 1995; Viehman et al., 

2006). More recent work using 16S rRNA gene sequencing identified a complex and 

variable assemblage of heterotrophic organisms that includes over 500 species of bacteria 

as well as cyanobacteria (Cooney et al. 2002, Frias-Lopez et al. 2002, 2003). These 

molecular studies identified anomalies in the identification of the cyanobacteria: three 

unique taxa of cyanobacteria have been isolated, with differences noted between the 

Caribbean and IndoPacific. Interestingly, P. corallyticum was not detected in the clone 

libraries or evident in the DGGEs (Cooney et al. 2002, Frias-Lopez et al. 2002, 2003). 

White plague 

The disease pathogen for WP II was identified as a gram negative -

proteobacterium (a new species of Sphingomonas later renamed Aurantimonas 
144 

coralicida; Denner et al., 2003) based on culture of a bacterial isolate obtained from a 

single diseased D. stokesi colony and subsequent inoculation on two healthy colonies of 

D. stokesi (Richardson et al., 1998a). This same microbial pathogen was subsequently 

reisolated from another affected colony at a later date. Although both strains are in 

culture, apparently healthy colonies no longer appear to be susceptible to either the 

original or newly isolated strains of the pathogen. This suggests that bacteria may lose 

virulence when in culture or A. coralicida is not in fact the causative agent. Another 

study examining a plague-like disease on M. annularis colonies from the USVI and 

Barbados (using bacterial 16s rDNA genes) identified a high diversity of bacteria in 

diseased samples, and differences between diseased and healthy tissue (Pantos et al., 

2003). While Sphingomonas spp. was detected in healthy corals and control areas on 

diseased colonies, it was absent from diseased areas. Instead, an -proteobacterium most 

closely related to the causative agent of juvenile oyster disease was present in diseased 

tissues, but consistently absent from healthy tissue (Pantos et al., 2003). 

A fluorescent probe specific for A. coralicida has tested positive on colonies with 

signs of WP-I and WP-II in a number of locations including the USVI, Puerto Rico 

(Miller et al., 2003; Weil, 2004), suggesting that this bacterium is widely distributed 

throughout the region. 

White band disease 

A causative agent for WBD type I has not been identified. Using histology, 

Peters et al., (1983) identified gram negative rod-shaped bacterial aggregates in the 

calicoblastic epidermal tissue of A. palmata colonies with WBD from the USVI and 

Bonaire. These bacterial bodies were also found in acroporids without signs of WBD, 

although the counts of bacteria per area were significantly less (Peters, 1984). Santavy et 

al., (1995) found bacterial aggregates in some but not all colonies of A. cervicornis with 

WBD on one reef in the Bahamas, while corals on a neighboring reef did not contain 

bacterial aggregates (Santavy and Peters, 1997). Bacteria were absent from WBDaffected A. cervicornis colonies in Florida (Kozlowski, 1996). 

Studies of the bacterial community of WBD-II has concentrated on the surface 

mucopolysaccharide layer and the use of preferential carbon utilization methods. A 

bacterium most closely related to Vibrio carchariae was identified as a possible cause, 

and these were found to increase in number with the onset of disease WBD II (Ritchie 

and Smith, 1995). 

Microbial communities identified using 16s RNA techniques were found to differ 

substantially (only 10% similarity) between healthy and WBD A. palmata colonies. 

Healthy and diseased tissues both contained similar proportions of four predominant 

bacterial groups, although planctomycetes, cyanobacteria and Cytophaga-FlexibacterBacteroides group were found only in diseased samples (Pantos and Bythell, 2006). 

Yellow band disease 

The causative agent for YBD is unknown. Cervino et al. (2001) proposed that 

YBD is a zooxanthellae disease which can kill coral by damage produced by the 

symbiont, based on a finding of a reduction of the number of zooxanthellae (41 to 97%) 

and reduction in the mitotic index of zooxanthellae (2.5% to 0%). Several bacterial 
145 

strains metabolically related to the genus Vibrio have been found in the mucus associated 

with diseased tissue (Gil-Agudelo et al., 2004). 

Dark spots disease 

The causative agent for DSD is not known. Differences in the structure of the 

microbial community from the mucus of healthy and diseased M. annularis and S. 

siderea colonies were identified based on the metabolic profile of culturable bacteria 

(Gil-Agudelo et al., 2004). A total of 17 groups of bacteria were identified, 16 of which 

were found in both diseased and healthy tissue, and one (V. carchariae) that was only 

observed in diseased samples. Healthy colonies inoculated with this bacterium failed to 

manifest signs of DSD (Gil-Agudelo et al., 2004). 

Aspergillosis 

Perhaps one of the most comprehensive etiologic studies of a coral disease in the 

Caribbean involves Aspergillosis. The fungus Aspergillus sydowii was identified as the 

cause of this disease through the use of transfection experiments, fungal cultures, 

morphologic and metabolic characteristics and 18s rDNA gene sequencing (Smith et al., 

1998; Alker et al., 2001). A sydowii has been isolated from benthic environments near the 

Orinoco River, and pathogenic strains have also been collected in the USVI during 

African dust events (Smith and Weil, 2004). 
146 

Table 3. Causative agents and associated microorganisms reported for western 

Atlantic coral diseases. 

Disease Reported causes and associated organisms 

WBD unknown ; gram negative rod-shaped bacterial aggregates in the calicoblastic epidermal tissue1; blue 

green algae, ciliates, turbellarian flatworms, copepods, amphipods, nematodes 2

WBD II Vibrio harveyi/carchariaea

WPX Serratia marcescensa , a common gram-negative bacterium classified as a coliform and a member of 

the Enterobacteriaceae family; fish feces proposed as a vector2

 

WP I Unknown, Gram negative bacteria 

WP II Aurantimonas coralicidaa , an obligately aerobic,polarly flagellated gram negative bacterium1; -

proteobacterium closely related to the causative agent of juvenile oyster disease2

 

BBD Oscillatoria submembranopora1 The cyanobacteria Phormidium corallyticum2 in association with 

sulfate reducing bacterium Desulfovibrio spp, and sulfide oxidizing bacterium Beggiatoa2

 

Oscillatoria spp and Trichodesmium tenue3

 Other cyanobacteria (Oscillatoria, Spirulina, Lyngbya, 

Arthrospira and other Phormidium species), pennate diatoms, ciliates, flagellates, and marine fungi 

occur in the band

RBD-I Cyanobacteria Schizothrix mexicana and S. calcicola

RBD-II Cyanobacteria; Two species of Oscillatoria characterized by filaments that are wider than they are 

long; filaments have two rounded tips 

YBD Undescribed Vibrio

DSD Unknown; Over 250 bacteria were isolated from mucus of healthy and diseased M. annularis and S. 

siderea colonies; A bacterium most closely related to V. carchariae was isolated from diseased 

corals. 

Tumors Unknown. May be mutations of the genome or programmative changes in gene expression of the 

coral cells. The role of environmental parameters (e.g., UV radiation) has not been determined. 

ASPa Aspergillus sydowii1

A. terreus, A. niger and A. flavus2

WBD: 1

Peters et al.,1983 2Gladfelter et al., 1977 WBD II: Ritchie and Smith, 1998; Weil, 2006 

WPX: 1

Patterson et al., 2002. 2 Weil, 2004 

WP: Dustan, 1977 

WP-II: 1

Denner et al., 2003 2Pantos et al., 2003 

BBD: 1Antonius, 1973; 2

Rutzler and Santavy, 1983; Richardson et al., 1995; 3Cooney et al. 2002, Frias-Lopez et al. 

2002, 2003 

RBD-I: Santavy and Peters, 1997 

RBD-II Richardson, 1993 

YBD: 1

Cervino et al., 2004; 2Gil-Agudelo et al., 2004 

DSD : 1

Gil-Agudelo et al., 2004 2Jordan-Dahlgren and Rodríguez-Martínez, 2004, 

ASP : 1

Smith et al. 1996, Geiser et al. 1998, Alker et al. 2001 2Toledo-Hernandez et al., 2004 

a

Causative agent identified through fulfillment of Koch’s postulate 
147 

Where are these pathogens coming from? 

External sources of pathogens that have been proposed include terrestrial runoff 

(Aspergillus), sewage (Serratia marcescens), and African dust events (Aspergillus). 

Pathogens may also already be present in the marine environment. Reservoirs of P. 

corallyticum (along with other cyanobacteria) occurred as biofilms on the surface of 

sediment patches present in depressions on healthy M. annularis, M. cavernosa and C. 

natans colonies (Richardson, 1996). These may be dispersed via movement of water 

masses, especially during storms (Bruckner and Bruckner, 1997), and transmitted through 

various vectors like damselfish, parrotfish, fireworms and coral-eating snails (Williams 

and Miller, 2005; Aeby and Santavy, 2006). 

Bacteria also occur on corals in a non-infectious state. Coral mucus is a rich 

protein-carbohydrate complex that harbors a diverse community of bacteria and other 

microbiota, and these communities are known to be distinct from the surrounding water 

(Rohwer and Kelley, 2004). Bacterial diversity varies between healthy corals, healthy 

parts of diseased corals, and diseased tissue (Rohwer et al., 2002; Pantos et al., 2003). 

Environmental changes can affect the physiological equilibrium between bacteria 

associated with the corals and their hosts, or stimulate the growth of other bacteria 

(Pantos et al., 2003). The coral-microbe relationship can be disrupted by nutrient and 

organic carbon loading by overstimulating the growth of these microbes, which may 

result in coral mortality (Kuntz et al., 2005). Under stressful conditions one or more of 

these microbes may become virulent or affect the resistance of the host, and subsequently 

trigger onset of an infectious disease. 

Are disease outbreaks associated with changing environmental conditions? 

Diseases may be infectious (produced by parasites and pathogens) or noninfectious (genetic mutations, produced by environmental factors). The frequency and 

severity of infectious diseases may affected by changing environmental conditions 

(elevated SST, declining water quality), human induced alterations of the marine 

environment (e.g., input of land-based pollutants; dredging, coastal development), and 

hurricanes and other natural disturbances. Increased temperatures may cause 

physiological stress and/or trigger the development of pathogenic agents that otherwise 

would remain non virulent. 

Increased abundance and virulence of at least five diseases (BBD, WPX, DSD, 

ASP and YBD) has been associated with elevated seawater temperatures, with declines in 

these conditions reported during winter months (Kuta and Richardson, 2002, Alker et al., 

2001; Patterson et al., 2002, Gil-Agudelo and Garzón-Ferreira, 1999 and Weil, 2004). 

Disease outbreaks may also be more severe during or immediately following bleaching 

events due to a lower resistance of host corals. Widespread and severe outbreaks of WPII were observed in Puerto Rico, USVI and the eastern Caribbean following the 2005 

Caribbean bleaching events (J. Miller, coral list posting; Weil, 2006). Other natural 

factors, such as habitat characteristics, composition, cover and abundance of susceptible 

corals, the amount of macroalgae, and presence/absence of certain key indicator species 

such as Diadema may also influence the occurrence and severity of coral diseases. 

Patterns of disease distribution obtained from the Global Coral Disease Database have 

shown that 97% of the areas affected by disease in the Caribbean prior to 2000 correlate 
148 

to areas where human activities have medium to high impact (Green and Bruckner, 

2000). Despite the contention that deteriorating water quality associated with land-based 

inputs of pollutants and sediments and other human impacts is linked to disease 

outbreaks, there is minimal quantitative data to support this hypothesis, and links to 

specific disturbances are unclear (Bruckner, 2002). 

Black band disease 

Goreau et al. (1998) reported that BBD often first appeared in polluted areas and 

infections spread radially outward. They suggest that the abundance of BBD mimics the 

distribution of human influenced areas, with the largest impacts near sewage outflows 

and areas of high turbidity. Peters (1993) also noted that BBD prevalence is related to 

adverse environmental conditions, including warmer than normal temperatures, nutrient 

loading, increased sedimentation and turbidity, predation, and toxics. In Jamaica, the 

incidence of BBD progressively increased over 19 months, with the largest increase 

during or just after a period of unusual rainfall and run-off (Bruckner et al., 1997a). In 

this study, one species that is generally resistant to BBD (S. siderea) exhibited few 

infections prior to the rainfall event, with a dramatic increase in bleaching, WP and BBD 

in the second year of the study, corresponding to periods of high rainfall and run-off 

(Bruckner, et al., 1997). 

An extensive, multi-year study evaluating BBD incidence on reefs off southern 

and western Puerto Rico failed to identify direct relationships between BBD prevalence 

and poor water quality (Bruckner, 1999). The lowest prevalence of BBD overall was 

found near Mayaguez and Ponce, which are the most polluted and turbid sites in Puerto 

Rico due to high sedimentation and nutrification associated with river discharge, 

agricultural runoff, and direct input of untreated sewage. On a fringing reef off the west 

coast (Rincon), BBD incidence was highest in spring (May-June) when water clarity was 

high, with infections disappearing during the rainy period (July-August) when run-off 

increased and visibility declined, even though temperatures were approaching their 

annual maxima. High turbidity also appears to limit the spatial distribution of BBD in 

southwest Puerto Rico (La Parguera). Infections were restricted to shallow water (<8 m 

depth) on turbid inshore reefs, even though species susceptible to BBD occurred in 

shallow and deep water, while BBD occurred to depths of 30 m on offshore shelf edge 

reefs with high water clarity. The disease was also common in remote locations around 

Mona Island, which is 70 km from the mainland of Puerto Rico and lacks permanent 

inhabitants, industry, agriculture or river discharge (Bruckner, 1999). 

In contrast to Bruckner (1999), Voss and Richardson (2006) reported higher 

sedimentation rates on sites with BBD in the Bahamas. Some of the differences between 

this study and Bruckner (1999) may be related to the scale of inputs: sites near LSI 

Bahamas described as having high rates of sedimentation have relatively low levels of 

sedimentation and high water clarity, when compared to coastal reefs near Puerto Rico. 

Kaczmarsky et al., (2005) also observed a significantly higher prevalence of BBD in a 

site off St. Croix, USVI exposed to sewage discharge, as compared to an ecologically 

similar location upstream from the pollution effluent. 
149 

White plague 

WP is reported to be seasonal on some northern reefs (Bahamas and Florida), 

while infections occur year round in USVI, Puerto Rico, Curacao and other locations 

(Richardson et al., 1998a; Miller et al., 2003; Weil, 2004; Bruckner and Bruckner, in 

press) and outbreaks have been observed during the coldest time of the year in the Flower 

Gardens (Hickerson, coral list posting) and in St. John (J. Miller, pers. Comm.). In St. 

Croix, USVI, Kaczmarsky et al. (2005) observed a much higher prevalence of WP 

(11.4% in a site affected by sewage discharge, when compared to a site located upstream 

from the effluent (3.1%). 

White band disease 

Few data are available to verify the role of environmental factors on WBD 

prevalence or severity. Outbreaks of WBD have been reported from throughout the 

region which has spread through acroporids reefs in both nearshore areas impacted by 

human settlement as well as remote locations and protected watersheds. 

White pox 

The prevalence and rates of tissue mortality are greater during warm water 

months (Sutherland et al., 2002). Sewage effluent is the proposed source of the WPX 

pathogen (Patterson et al., 2002), but no information is available on the prevalence and/or 

severity of WPX in polluted versus unpolluted sites. 

Yellow band disease 

YBD progresses more rapidly during warm water periods (Gil Agudelo et al. 

2004). Although nutrient enrichment has been shown to increase the rate of tissue loss 

from YBD (Bruno et al., 2003), YBD is currently most abundant in remote locations or 

reefs subjected to low levels of human impact (Bruckner and Bruckner, 2006). 

Dark Spots Disease 

DSD was found to be more prevalent when water temperatures are over 28oC and 

in shallow (<10 m depth) reef habitats in Colombia (Gil-Agudelo et al., 2004). In 

contrast, Gochfeld et al. (2006) did not find a correlation between DSD and water 

temperature; infections dramatically declined each year in October (which is just after the 

warmest time of year) and new infections emerged beginning in January of each year 

(close to the coldest water temperatures of the year). There also was no relationship with 

depth and DSD prevalence in the Bahamas. In 2002, the highest prevalence was observed 

at the deepest site (81.25%), while the highest prevalence was in a shallow (<5 m) site 

(67%) in January, 2003 (Gochfeld et al., 2006). Nutrient enrichment also did not appear 

to affect the prevalence or severity of dark spots disease in laboratory studies, although 

increased nutrients did induce bleaching (Gochfeld et al., 2006). 

Aspergillosis 

Aspergillus sydowii exhibits maximal growth at 30°C and is less affected by the 

hosts defenses at 30oC than at 25oC (Kim and Harvell, 2004). Nutrient enrichment 

(Nitrates) was shown to increase the progression of Aspergillosis (Bruno et al., 2003). 
150 

What have we learned from Caribbean coral disease research? 

Research on coral diseases requires an approach that combines ecological 

monitoring with biochemistry, molecular biology, histology, toxicology, physical 

oceanography, ecology, taxonomy and other laboratory and field methods. An 

interdisciplinary approach is necessary to identify, differentiate and characterize coral 

diseases and their consequences, and understand relationships among diseases and other 

biotic and abiotic factors. 

 Epizootiology: To understand the spatial extent of diseases at local to global scales, 

large areas of reef must be examined at the same time. Surveys must also be 

conducted at frequencies that are sufficient to document the duration of the condition, 

and identify seasonal patterns or chronic effects. Monitoring programs should include 

size measurements and colony condition (amount of recent and old mortality), and 

follow individual colonies over time to determine the severity of disease and potential 

population level impacts. Efforts should be made to standardize monitoring 

approaches. 

 Relationships between disease outbreaks and environmental factors:

Epizootiological studies must be combined with an examination of climate 

parameters (e.g., temperature and light levels), water quality measures (levels and 

types of nutrients and contaminants, turbidity, and rates of sedimentation), and 

impacts of other natural disturbances (e.g., predator outbreaks and hurricanes). 

 Rapid response program: A coordinated rapid response to disease outbreaks can 

allow for the timely recognition, characterization, and reporting of disease outbreaks. 

This information is necessary so managers can 1) quickly direct resources to 

additional studies that are needed to identify appropriate management responses; 2) 

identify possible responses to control or mitigate the outbreak and 3) educate local 

and regional stakeholders on the condition of the corals. 

 Coral disease diagnostics and nomenclature. There is a need to review and refine 

existing terminology and develop an approach for naming new diseases to reduce 

confusion. Disease nomenclature must include descriptive terminology of the gross 

signs (visible by an unaided eye, underwater) that could be applied by all scientists 

conducting epizootiological studies. Lesions should first be categorized as tissue 

loss, growth anomaly, and/or change in coloration. For each lesion, relevant 

information on the distribution of the lesions (e.g., focal or multifocal), location on 

colony, lesion shape, relief, texture, color, and size, and structures affected (e.g. 

tissue, individual polyps, coenosarc, skeleton) should be included in the morphologic 

diagnosis. By following affected colonies over time, more detailed information on 

patterns and rate of spread and extent of tissue loss can be compiled. This field 

terminology can be further refined once a causative agent is identified. 

 Identification of the causative agents Molecular approaches should be combined 

with traditional culture techniques to identify and verify coral associated microbes, 

including spatial and temporal fluctuations, variations among species, and differences 

between healthy and diseased corals. Screening must include larger sample sizes 

(especially when isolating a putative pathogen and testing infectivity of proposed 

pathogens), multiple species (if they show similar signs), and multiple locations. 

There is an urgent need for molecular probes that will allow rapid screening of corals. 
151 

 Application of new approaches and tools. More emphasis needs to be placed on 

understanding processes and factors that may improve the resistance and resilience of 

the coral hosts, such as antimicrobial activities, immune responses, and regeneration 

processes. Efforts should also include a cellular diagnostics approach to identify 

stress and its underlying causes, and identify biomarkers that can characterize the 

condition of the coral and normal ranges of these biomarkers. 

Appendix 1. Diseases reported to affect scleractinian corals and gorgonians on 

coral reefs in the tropical western Atlantic. The terminology highlighted in bold 

represents the proposed nomenclature identified at the 2004 CDHC workshop in 

Madison, Wisconsin. 

Condition Synonyms Host range Source

White syndromes 

White band 

disease (WBD) 

White line disease; white 

death; white plague 

Acropora palmata 

A. cervicornis

Gladfelter et al., 1977 

WBD type II White band disease A. cervicornis Ritchie and Smith, 1995; Weil 

2004 

Plague type I White plague, white band 

disease; plague-like2

 Stressrelated necrosis3

12 species of massive 

and plating corals 

Dustan, 1977; 2

Pantos et al., 

2003 3

Peters, 1984 

Plague type II White plague, white band 

disease, white line disease 

D. stokesi; 40 other 

species of plating and 

massive corals 

Richardson et al., 1995; Weil, 

2006 

Plague type III Plague type II large massive corals (M. 

faveolata, C. natans) 

Richardson and Aronson, 2001 

Shut-down 

reaction (SDR) 

Rapid tissue necrosis (in 

aquaria) 

massive corals, 

acroporids 

Antonius, 1977 

White pox (WPX) White patch disease; 

acroporid serratiosis; 

white pox serratiosis, 

patchy necrosis 

A. palmata Porter, 1996; Patterson et al., 

2002; Sutherland and Ritchie, 

2004 

Patchy necrosis1 White patch disease; white 

pox, necrotic patch 

syndrome2

A. palmata 1

Bruckner and Bruckner, 1997;

2

Rodríguez-Martínez et al., 2001 

Cyanobacterial mat diseases 

Black band 

disease (BBD) Black line disease 

24 scleractinian corals, 1 

hydrozoan, 6 gorgonians 

Antonius, 1973 

Red band disease 

type I (RBD) 

Red band disease Gorgonia, Colpophyllia,

Agaricia, Mycetophyllia 

Stephanocoenia

Rützler et al., 1983 

Santavy and Peters, 1997 

RBD type II Red band disease D. stigosa, M. annularis, 

M. cavernosa S. radians, 

P. astreoides 

Richardson, 1992 

 
152 

Condition Synonyms Host range Source

Tissue Discoloration

Yellow band 

disease (YBD) 

Yellow blotch disease; ring 

bleaching1

, yellow pox 

disease2

; yellow band 

syndrome3

M. annularis complex, other 

faviids ; A. agaricites 4 ; P. 

astreoides5

Reeves, 1994;1Dustan 1977; 2

Garriet Smith; 3Foley et al., 

2004; 4

Gil Agudelo et al., 

2004; 5

 Sutherland et al., 

2004 

Dark spots disease

(DSD) 

Dark spot disease, dark spot 

syndrome, Ring disease 2

M. annularis (complex), S. 

siderea, S. intersepta and 

Agaricia agaricites

Gil-Agudelo and GarzónFerreira, 2001; 2

Agudelo et 

al., 2004; Gochfeld et al., 

2006 

Dark spots disease 

Type II (DSD- II) 

Dark spots disease S. intersepta; M. annularis; 

M. faveolata; M. cavernosa; 

C. natans; C. amaranthus; S. 

siderea

Weil, 2004 

Dark band syndrome 

(DBS) 

Dark spots disease M. annularis; M. faveolata Weil, 2004 

Purple band 

syndrome (PBS) 

Dark band syndrome S. siderea, S. intersepta Weil 2004 

Tissue necrosis Dark spots disease M. faveolata Weil 2004 

Mottling syndrome bleaching C. natans Borneman, 2005 

Pale ring syndrome 

bleaching 

Montastraea, Colpophyllia, 

Diploria 

Borneman, 2005 

Light patch 

syndrome 

bleaching D. strigosa Borneman, 2005 

Bleaching Blanching All zooxanthellate corals 

Abnormal growth 

Hyperplasia Growth anomaly, tumors, 

Gigantism, area of 

accelerated growth, chaotic 

polyp development 

Diploria, Colpophyllia, 

Montastraea, Agaricia, 

Porites, Dichocoenia, 

Madracis

Loya et al., 1984 

Calicoblastic 

epithelioma 

Growth anomaly, tumor, 

neoplasm, 

A. palmata Peters et al., 1986 

Algal tumors Tumor-like growth, tumor, 

algal tumor, gorgonin pearl, 

nodule, galls 

Gorgonia spp. 

Pseudoplexaura; Plexaura

Morse et al., 1977 

Skeletal damage 

Skeletal eroding 

band 

Follicullinid ciliates 10 species: Dichocoenia, 

Montastraea, Acropora, 

Croquer et al., 2006; Weil et 

al., 2006 

Rapid wasting 

disease (RWD)1 

(Rapid wasting 

syndrome) 

parrotfish white spot 

biting2

; parrotfish spot 

biting; parrotfish focused 

biting3 Rhodotorulosis 4

Montastraea spp., 

C. natans

1

Cervino et al., 1997; 

2

Bruggeman et al., 1994 3 

Bruckner and Bruckner, 

2000; 4 Richardson, 2000 

Ridge mortality 

disease (RMD) 

Damselfish ridge denuding 

syndrome2

C. natans, 

D. strigosa

Abbott, 1979, 1

Zimmerman 

1994 2

Williams et al., 2000 

Tissue and skeletal loss, discoloration of tissue and abnormal growth 

Aspergillosis Sea fan disease Gorgonia spp. Nagelkerken et al., 1997 

 
153 

Appendix II. Other abnormal conditions observed infrequently in scleractinian corals and 

gorgonians in the tropical western Atlantic. Some of these require histological analysis for 

confirmation (Coccidiosis and Nematopsis spores), while others are unconfirmed 

syndromes. 

Syndrome Synonyms Host species Description 

Coccidiosis Coccidian 

infection 

8 species: Agaricia, 

Dendrogyra, Diploria, 

Montastraea, Meandrites, 

Porites 

Parasite infection: Oocysts found in 

mesentarial filaments; causes loss of 

zooxanthellae, patchy bleaching and 

tissue necrosis 

Upton and 

Peters, 1986 

Nematopsis 

spores 

Sporozoan 

(protozoan) 

infection 

Porites spp. Thick walled ovoid ovoid capsules in 

calicoblastic epithelium 

Peters, 1984 

Ring syndrome hyperplasia D. labyrinthiformis Fast growth of tissue and skeleton at 

ridge areas produces high, pale and 

thin ridges over the colony. Tissue 

inside ridges slowly dies 

Weil, 2004 

Fire coral fungal 

disease 

Millepora spp. Associated with bleaching TeStrake et al., 

1988 

Thin dark line Blistering 

necrosis 2 8 species: Diploria. 

Montastraea, Porites, 

Siderastrea

Thin dark line at the boundary of 

living tissue that advances <1 cm/year Jordan-Dahlgren 

and RodriguezMartinez, 2004;

2

Peters, 1984 

White spot 

syndrome 

Spot biting massive corals Predation by parrotfish referred to as 

“spot biting 1

” 

Global Coral 

Reef Alliance ; 

1

Bruckner and 

Bruckner., 2002 

Star coral polyp 

necrosis (SCPN) 

M. cavernosa No further information presented Williams and 

BunkleyWilliams, 2000 
154 

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162 

IV. STATE OF KNOWLEDGE IN THE PACIFIC—WHAT DO WE 

KNOW AND WHAT HAVE WE LEARNED?

OVERVIEW OF ISSUES UNIQUE TO THE PACIFIC: BIOLOGICAL & 

SOCIAL PERSPECTIVES

Michael J. Gawel 

Guam EPA 

120 Bengbing St. 

Y-Papao 

Dededo, GU 96929 

Mike.Gawel@guamepa.net 

Pacific Islands

The term “Pacific Islands” in the context of this paper arbitrarily refers to those tropical 

islands of the central and western Pacific Ocean which support shallow hermatypic coral 

reefs, but excluding the Hawaiian Archipelago, which is covered in other papers. The 

tropical Pacific Island nations and territories all support coral reefs and, no doubt, harbor 

coral diseases, although these have not been scientifically documented in many of the 

islands. In fact, as part of the U.S. National Action Plan to Conserve Coral Reefs, 

surveys in 2002 and 2004 of coral reef academic scientists, resource managers, 

government agencies and NGOs recorded that in the U.S. Pacific islands they perceived 

“no threat” from coral disease, although American Samoa registered an increase to 

perception of “moderate threat” in the 2004 survey (Waddell, 2005). This lack of 

concern partially reflects a lack of information on the status of diseases in many islands. 

Wilkinson (2004, p. 405) notes that in American Samoa and Micronesia “Coral bleaching 

and disease were either rare or undocumented in 1994, but are now clearly evident and 

considered a serious threat to many reefs in the region.” 

The Pacific island coral reefs range from veneers on newly emergent volcanic islands, to 

platform-like fringing reefs, to barrier reefs with lagoons, to atolls, and include nonemergent isolated banks. 

The islands associated with the reefs vary from large high islands, such as in Fiji and 

New Caledonia, to small low atoll islands rising less than two meters above sea level, as 

in the entire nations of Tuvalu and the Republic of the Marshall Islands. Although the 

availability of land resources has limited human settlement and development in these 

islands, even some of the small atoll areas have been inhabited continuously for 

thousands of years. The long term and current native residents of the islands are 

generally defined as Polynesian, Melanesian and Micronesian, based upon their ancestry, 

culture and languages and their geographic association within these island archipelagoes. 

 
163 

Similarities to Atlantic Areas

Before European contact, the Atlantic and Pacific coastal residents and islanders (except 

for those far in the interior of high islands), depended on coral reef resources for survival 

and managed these resources in a sustainable way. But Western development brought 

major changes to land use, which impacted on surrounding reefs. As in the Western 

Atlantic area of coral reefs, the Pacific Islands have had similar political histories of 

colonialism and plantation agriculture exploitation over the last few centuries. Both areas 

were colonized by European nations from the Sixteenth Century to the present, although 

most island states have become independent countries in the decades since World War II. 

During the early periods of colonization, diseases, warfare and forced relocation 

decimated local populations. During the last century, populations have re-established or 

been replaced by immigrants and are in many cases exceeding the traditional selfsustainable carrying capacities. Economic development bases have been shifting from 

plantation monoculture agriculture to tourism and, to a limited degree, mining, fisheries, 

and logging (which is typically not sustainable). Impacts of related coastal pollution are 

similar world-wide. 

Atlantic and Pacific reefs are influenced by similar weathers patterns with the same water 

temperature ranges, variable annual precipitation from very dry to some of the wettest 

places on earth and frequent violent tropical storms (hurricanes, typhoons or cyclones). 

Trans-oceanic wind-driven continental dust may be reaching parts of the North Pacific 

from Asia, but this is not as apparent as African wind driven pollutants entering the 

Caribbean. 

Differences between the Pacific and Atlantic

Island and Reef Numbers: 

Although both oceans have atolls and barrier reefs, the numbers of islands and atolls and 

the lengths and areas of their reefs are much greater in the Pacific (Wilkinson, 2004). 

Although they are relatively small, the islands of Micronesia alone number over one 

thousand. Compared to the few atolls in the Caribbean, the Pacific has over fifty. The 

barrier reefs of Fiji, New Caledonia, Papua New Guinea and other Pacific islands 

together exceed the extent of the Mesoamerican Barrier Reef System, without 

considering the world’s largest barrier reef in Australia. 

Ocean Size: 

Distances across the vast Pacific and between its far-spread reefs dwarf those of the 

Caribbean. The entire Caribbean, if it could be moved over the Pacific, would be lost 

between Hawaii and Guam without even overlapping the larger and broader tropical 

Pacific waters south of the equator. 
164 

Fisheries: 

These great expanses of the Pacific support industrial fisheries fleets supplying over one 

third of the annual worldwide catch of tropical tuna. And the artisanal and subsistence 

catches of reef fishes continue to supply the basic protein needs of hundreds of thousands 

of Pacific islanders. 

Biodiversity: 

The greatest marine bio-diversity lies in the western Pacific. This diversity diminishes 

from island to island, crossing the Pacific to the east. For example, the corals of the 

Hawaii Islands have been intensively studied and found to have similar species numbers 

to the Caribbean (approximately 60 and 2 massive soft corals) (Waddell, 2005). But the 

Hawaiian Island Archipelago is isolated from the central triangle of highest marine 

diversity among western Melanesia, Indonesia and the Philippines (Carpenter and 

Springer, 2005). The Marianas including Guam, also fairly well studied, lie closer to this 

center, and typical of many Pacific islands, have recorded over 400 species in 108 genera 

and 21 families of hard corals and over 30 species of massive soft corals (Paulay, 2003). 

Higher diversity progresses towards this center through Fiji, Palau and the Great Barrier 

Reef of Australia. 

Traditional Knowledge: 

The ancient pre-colonial knowledge of coral reef resources, which must have resided 

with the aboriginal Caribbean residents, apparently has been lost through most of those 

islands. But the descendents of Pacific island fishermen have retained much of their 

ancestors’ knowledge of their reefs, which has been accumulated and passed down over 

thousands of years. The sustainable management practices for reef resources that 

evolved over these thousands of years remain active in some of the islands, although 

western ideas and their misplaced or unsuccessful management approaches have replaced 

traditional controls in many islands. Traditional knowledge retained by Palauan 

fishermen has been partially recorded in the book “Words of the Lagoon” compiled by 

Robert Johannes (1981), after residing in Palauan villages for over a year to seek out this 

knowledge. This gives an example of the actual scientific knowledge base that exists 

among island fisherfolk. Although their knowledge is usually focused on edible or 

harvestable species, it includes ecological information that can relate directly to coral 

health. 

Many traditions regarding coral reefs still strongly influence the daily lives of islanders 

and must be recognized and respected by scientists wanting to study the reefs. For 

example, in many islands, submerged reef resources are privately owned or are strictly 

managed by chiefs or families (Gawel, 1984). This ownership and control is not simple 

in any case and involves complicated overlapping and changing rights to use various 

resources. These systems have succeeded in managing many of the key reef resources 

for centuries, but are being eroded often because of modern aspirations for commercial 

development of marine and coastal resources. Entry to some reef areas or taking of 

scientific samples may sometimes not be allowed. Even taking of a dead coral or piece 

of rock may be taboo at times in certain places. Gender distinctions separating how men 

and women relate to coral reef activities strongly persist in many islands, especially 
165 

related to subsistence uses. And diving on Sunday may be offensive or prohibited in 

some islands due to European derived religious beliefs, which are treated as strong 

tradition in many islands. Consequences of violating traditional laws can be very severe 

in certain island communities. Value of conservation or research efforts to the traditional 

users and to the health of the reefs may not always be recognized in decisions by 

traditional leaders. But their authority can remain unchallenged because of broader 

aspects of custom and traditional life. 

War: 

The impacts of World War II and pre-war activities in the Pacific islands contrast with 

that war’s impacts on Atlantic reefs. American, European colonial and Japanese harbors 

and fleets were developed and destroyed across the coral reef islands. Serious damage 

was caused and, although most coral reefs have recovered over the last sixty tears, 

millions of pounds of explosives, fuel and toxic chemicals remain in the ships sunk in 

coral reef areas. An unfortunate result of war practices is the use of old recycled 

explosives to illegally harvest fishes by blasting coral reef areas. 

Current Political Ties: 

Although Guam and parts of Micronesia had been Spanish colonies for hundreds of 

years, and subsequently these islands (excluding Guam) were German and then Japanese 

owned, their ties with these mother countries have been greatly over-shadowed by the 

American influence since WWII. This has led to English being the most widespread 

language of Micronesia. South of the equator, France has retained three island groups 

within its nation and Australia and New Zealand have replaced former European nations 

as having the greatest alliances with the former colonies. (Note: the three Tongan 

archipelagoes had never been colonized and retain their traditional king.) The recently 

independent Pacific island countries are members of the United Nations and have 

attracted assistance and attention from East Asian neighbors including Japan, China, 

Taiwan and South Korea (Crocombe, 2001). 

Authorities for Management: 

Under modern laws in force in the Pacific islands, regulations and permit systems to 

manage marine resources uses and activities that impact coral reefs exist at national 

levels. For example, taking of endangered species like turtles may be prohibited and 

dredging for a new reef passage or harbor may require environmental impact assessments 

and permits with conditions. But these legal controls apply mostly to centers of 

population where more damaging impacts to the reefs tend to occur (Birkeland, 1997). 

Fortunately, the more remote reef areas remain more pristine although modern legal 

controls are less recognized by outer island populations. Traditional and local 

community controls continue to function more in areas of low development and 

population pressure. Even in national centers and developed areas, the approach of 

involving communities in coral reef conservation is proving to be the best approach. The 

U.S. Coral Reef Task Force is pursuing support of “Local Action Strategies” to locally 

develop strategies and projects at more of a community level for coral reef conservation, 

to be implemented with federal funding (Wilkinson, 2004). One of the nationally 

applied LAS issue areas is Coral Bleaching and Disease (Waddell, 2005). Those islands 
166 

not under the U.S. flag have other sources of support for coral reef conservation such as 

the Global Environment Facility and non-governmental organizations such as TNC. 

Scientific Resources in the Pacific

A number of centers of coral reef scientific expertise have developed in the Pacific and 

new ones are arising. The following tables list some of the major academic, research and 

data centers in the tropical Pacific, excluding many from Hawaii and Australia. 

Universities and Colleges:

• University of the South Pacific 

• University of French Polynesia 

• University of New Caledonia 

• University of Papua New Guinea 

• Community College of Micronesia 

• College of the Northern Marianas 

• College of the Marshall Islands 

• Palau Community College 

• University of Guam 

Regional Institutions and Centers:

• Secretariat of the Pacific Regional Environmental Programme (SPREP) 

• South Pacific Applied Geoscience Commission (SOPAC) 

• Secretariat of the Pacific Community (SPC) 

• Coral Reef Initiative for the South Pacific (CRISP) 

• University of the South Pacific (USP) 

• University of Guam (UOG) 

• US Coral Reef Task Force: All Islands Group 

• Marine Resources Pacific Consortium (MAREPAC) 

– American Samoa 

– Republic of the Marshall Islands 

– Federated States of Micronesia 

– Republic of Palau (Palau International Coral Reef Center) 

– Commonwealth of the Northern Marianas 

– University of Guam 

Global and Regional Research and Data Organizations: 

• Australian Institute for Marine Sciences 

• The Global Coral Reef Monitoring Network 

• ReefBase 

• Reef Check 

• Hawaii Institute of Marine Biology, University of Hawaii 

• Institute of Marine Resources, University of the South Pacific 

• University of Guam Marine Lab 

• Palau International Coral Reef Center 

• CRIOBE Research Center Moorea 
167 

References: 

Birkeland, C. 1997. Life and Death of Coral Reefs. Chapman and Hall, N.Y. 536 pp. 

Carpenter, K.E. and V.G. Springer 2005. The center of the center of marine shore fish 

biodiversity: the Philippine Islands. Environmental Biol. of Fishes: 72, pp. 467-480. 

Crocombe, R. 2001. The South Pacific. Univ. of the South Pacific Press. 

Gawel, M.J. 1984. Involvement of the users of coral reef resources in management plans. 

IN: Coral Reef Management Handbook, Kenchington and Hudson (Eds). UNESCO. 

pp. 99-109. 

Johannes, R.E. 1981. Words of the Lagoon. Univ. Cal. Press, Berkeley, CA. 320 pp. 

Paulay, G. (Ed.) 2003. The marine biodiversity of Guam and the Marianas. 

Micronesica: 35 & 36. Univ. of Guam Press. 682 pp. 

Waddell, J.E. (Ed.) 2005. The state of coral reef ecosystems of the United States and 

Pacific Freely Associated States: 2005. NOAA Technical Memorandum NOS 

NCCOS 11. Wash. D.C. 

Wilkinson, C.R. (Ed.) 2004. Status of coral reefs of the world: 2004 (Vol. 1&2). Global 

Coral Reef Monitoring Network and Australian Institute of Marine Science. 
168 

BASELINE LEVELS OF CORAL DISEASE IN THE NORTHWESTERN 

HAWAIIAN ISLANDS

Greta Smith Aeby 

Hawaii Institute of Marine Biology 

PO Box 1346 

Kaneohe, HI 96744 

greta@hawaii.edu 

ABSTRACT 

There has been a worldwide increase in the reports of diseases affecting marine 

organisms. In the Caribbean, mass mortalities among organisms in reef ecosystems have 

resulted in major shifts in community structure. However, our ability to fully understand 

recent disease outbreaks is hampered by the paucity of baseline and epidemiological 

information on the normal disease levels in the ocean. The Northwestern Hawaiian 

Islands (NWHI) is considered one of the last relatively pristine coral reef ecosystems 

remaining in the world. As such, it provides the unique opportunity to document the 

normal levels of disease in a coral reef system exposed to limited human influence. 

In July 2003, baseline surveys were conducted at 73sites throughout the NWHI to 

quantify and characterize coral disease. Ten disease states were documented with the 

most common disease found to be Porites trematodiasis. This disease was widespread 

and is known to exclusively affect Porites sp. coral. Numerous other conditions were 

observed but at much lower levels of occurrence. Numbers of colonies affected by 

Porites trematodiasis were not enumerated but other types of conditions were counted 

with the average prevalence of disease estimated at 0.5%. Several of the observed disease 

states were distinct from what has been described from other coral reef systems. Coral 

genera exhibited differences in types of syndromes and prevalence of disease. 

Pocilloporids, common corals on the reefs of the NWHI, were comparatively resistant to 

disease. In contrast, acroporids showed the greatest damage from disease and the highest 

estimated prevalence of disease. 

Report 1: Published in Atoll Research Bulletin online: 

http://www.botany.hawaii.edu/faculty/duffy/arb/543/29.pdf 

Aeby, GS (2006). Baseline levels of coral disease in the Northwestern Hawaiian Islands, 

Atoll Res. Bull. No. 543:471-488. 

Report 2: French Frigate Shoals Reef Health Survey, included in this document 

below. 
169 

Report 2. French Frigate Shoals Reef Health Survey

Thierry M. Work1

, Steve L. Coles2, Robert A. Rameyer1

1. USGS-National Wildlife Health Center-Hawaii Field Station, PO Box 50167, Honolulu, HI 

96850. 

2. Bishop Museum, Dept. Invertebrate Zoology, 1525 Bernice Street, Honolulu, HI 96817 

Submitted 18 June, 2002 
170 

INTRODUCTION 

French Frigate Shoals (FFS) is one of the refugia comprising the Northwest Hawaiian 

Islands National Wildlife Refuge (NWHINWR). French Frigate Shoals was discovered 

by La Perouse in the late 18th century; however, the atoll was most notable as a naval air 

station during World War II when the US Navy dredged Tern Island into an airstrip, and 

the US Coast guard established a LORAN station on East Island. After the war, the 

LORAN station was moved to Tern Island where it remained until the Coast Guard 

vacated in 1979. Since then, the US Fish and Wildlife Service (USFWS) has managed 

Tern Island-FFS as a wildlife refuge with a full time staff presence (USFWS, 2001). 

French Frigate Shoals consists of a large (31 nm) fringing reef partially enclosing a 

lagoon. A basalt pinnacle (La Perouse Pinnacle) arises approximately halfway between 

the two ends of the arcs of the fringing reefs. Tern Island is situated at the northern end 

of the lagoon and is surrounded by a dredged ship channel. The lagoon becomes 

progressively shallower from west to east and harbors a variety of marine life including 

corals, fish, marine mammals, and sea turtles (Amerson 1971). In 2000, an interagency 

survey of the northwestern Hawaiian Islands was done to document the fauna and flora in 

FFS (Maragos and Gulko, 2002). During that survey, 38 stations were examined, and 41 

species of stony corals were documented, the most of any of the NW Hawaiian islands 

(Maragos and Gulko 2002). In some of these stations, corals with abnormalities were 

observed. The present study aimed to expand on the 2000 survey to evaluate the lesions 

in areas where they were documented. 

METHODS 

Survey areas: 

Because of the ocean conditions, patchy distibution of corals, and lack of water clarity, 

all surveys were done using SCUBA. Survey locations were chosen based on 

observations of Jim Maragos during the 2001 NOWRAMP surveys (Fig. 1). Specifically, 

he had noted bulbous white tumors in Montipora patula on site R31 and Porites lobata

with dead lesions in sites R33 and 39. Emphasis was placed on these locations and those 

areas where coral cover was substantial (>40%) and that were accessible by boat. 

Corals were photographed using a Nikonos V underwater camera with a 20 mm lens and 

twin Ikelite 50 strobes or a digital camera in an underwater housing. Close-up photos 

were taken with a Nikonos V camera with a single Ikelite 50 strobe and a 2:1 extension 

tube. Coral samples were taken using bone shears, or hammer and chisel, and placed 

into labeled plastic bags in seawater. Gross lesions were broadly characterized as growth 

anomaly, tissue necrosis, algal infiltration, trauma, or a combination thereof. 

Corals were preserved in Helleys fixative (Barszcz and Yevich, 1975) with added salt and 

allowed to fix for 24 hr. The fixative was decanted and the coral rinsed with fresh water 

once every 12 hr for 24 hr. Subsequently, coral was stored in 70% ethanol, decalcified 
171 

with Cal-ex II (Fisher Scientific), placed in cassettes, processed for paraffin embedding, 

trimmed at 5 um, and stained with hematoxylin and eosin. Slides were examined using 

light microscopy at magnifications ranging from 20-1000X. Normal histology of species 

of corals not yet in USGS-Hawaii Field Station archives was described. Lesions were 

classified as neoplasia, algal infiltration, necrosis, inflammation, atrophy or parasites. 

RESULTS 

For some of our survey, we were limited to doing shore dives from Tern Island because 

of wind conditions that rendered small boat operations in the lagoon unsafe. A review 

of available wind speed data for 1989-93 and 2000-1 revealed that the best times to 

conduct open water operations on Tern Island was late March-early April, late May-early 

June, late July mid-August, and early September-mid October (Fig. 2). We did a total of 

16 dives half of which were shore dives from 18-28 March, 2002. Coral cover was 

generally patchy throughout all dive sites but seemed most sparse around the ship 

channel and most rich near La Perouse Pinnacle. 

Lesions 

Of 44 coral samples examined, 34 had lesions. Of the samples with lesions, algal 

infiltration of coral tissue was the predominant diagnosis (26) followed by bleaching (4), 

tumors (2), and parasites (1). The remainder of corals was healthy individuals used for 

reference purposes. 

Algae-coral interactions: 

Invasion of coral tissue by marine algae was seen in Acropora cytherea, Porites lobata, 

P. evarmanni, P. compressa, Leptastrea purpurea, Montipora capitata, and Pavona 

duerdeni. In P. duerdeni and L. purpurea, algal infiltrates had a distinct border with 

presence of macro-algae within the algal mats (Figs. 3A-B). Algal infiltrates in A. 

cytherea were characterized by ill-defined discolored areas with occasional greenish or 

yellow tinge or complete bleaching (Figs. 3C-D). In some instances, algal infiltrates 

were accompanied by exuberant skeletal growth (Figs. 3E-F). In P. lobata and P. 

evarmanni, algal infiltrates had less distinct borders, and coral tissues adjacent to 

infiltrates were bleached or tinged with pink coloration (Figs. 3G-H). Gross lesions of 

algal infiltration in M. capitata consisted of firm, smooth to rugose raised areas (Figs. 

4A-D). 

On microscopy, a mixed assemblage of algal organisms infiltrated coral tissue. In A. 

cytherea, reaction to algal infiltration was much less marked and generally characterized 

by focal tissue death and focal thickening of the gastrodermis of the gastrovascular canal 

near the algal infiltrates (Figs. 4E-F). In Porites sp. and P. duerdeni, within 

gastrovascular canals, gastrodermal cells formed rosettes and clumps among algal 

filaments. In many instances, there was localized thickening of calicoblast layer adjacent 

to algae. Clumps of sloughing and necrotic gastrodermal cells appeared constricted by 
172 

linear bands of unidentified granular grey material. In many cases, there were clumps of 

necrotic debris associated with algae (Figs 4G-H; 5A-D). In Montipora sp., algal 

infiltrates were often accompanied by necrosis and a prominent cellular response 

comprising calicoblast and pigment cells (Figs. 5E-H). 

Parasites: 

The only instance of parasitism was in P. lobata. Grossly parasites were manifested by 

multiple small bumps scattered throughout the surface (Figs. 6A-B). On histology, these 

foci were characterized by necrosis of epithelium (Fig. 6C). Within the gastrovascular 

canal network, there was erosion of epithelium and proliferation of calicoblast and 

pigment cells around putative coccidia (Figs. 6C-F). As the lesion progressed, it 

appeared that these coccidia became encapsulated leading to eventual loss of sporozoites 

(Figs. 6G-H). In many cases, parasite-induced lesions were accompanied by algal 

infiltrates (Fig. 6H). 

Tumors: 

Tumors were seen only in A. cytherea. One type of tumor was cauliflower-like and had 

focal distribution on the coral (Fig. 7A). Another type of tumor was also localized but 

appeared vermiform (Fig. 7B). On histology, both tumors revealed a marked disorganized 

proliferation of gastrodermal cells with no mitotic figures and no necrosis (Figs. 7C-D). 

Miscellaneous: 

Other lesions included the burrows of the skeleton-dwelling symbiotic crab 

Pseudocryptochirus kahe McCain and Coles (1979) (Fig. 7E) and bleaching (Fig. 7F) in

P. eydouxi and trauma of P. evermani due to fish bites. Bleaching of P. eydouxi was 

characterized by lack of pigmentation of tissues, and on histology, bleached tissue was 

markedly atrophied with loss of mesoglea and zooxanthellae (Fig. 7H). Lesions caused 

by P. kahe consisted of distinct holes within coral skeleton surrounded by 

hyperpigmented tissue. On microscopy, each hole contained a single crab surrounded by 

mats of algae. Fish bites in P. evarmanni consisted of localized areas of tissue ablation 

revealing white skeleton beneath. 

Normal histology:

Palythoa tuberculosa (Figs. 8A-D) 

Colonies consisted of closely apposed large polyps encrusting on the substratum. 

Coenosarc epithelium was composed of columnar cells mixed with holotrichous 

isorhizas, clusters of eosinophilic granular cells, scarce zooxanthella, and large vacuoles. 

Tentacle epithelium consists of closely apposed columnar cells mixed with spirocysts, 

granular pigment cells, and zooxanthella. Deeper down, near the mesoglea, there was a 

mesh-like filigree of cells and delicate filaments. Pharyngeal epithelium was composed 
173 

of closely apposed ciliated columnar cells with aggregates of granular eosinophilic and 

brown pigment cells at the base. 

Tentacle gastrodemis was composed of cuboidal cells replete with zooxanthellae. 

Gastrovascular canals course through the large mesoglea in a haphazard manner and are 

lined by similar cells as those found in tentacles. Mesenteric filaments was composed of 

a cnidoglandular cap consisting of closely apposed columnar cells, eosinophilic granular 

cells, few holotrichous isorhizas, and a base consisting of columnar cells mixed with 

large numbers of zooxanthella and granular eosinophilic cells. 

Mesoglea consisted of a large network of connective tissue enveloping a mesh of 

skeleton. Gastrovascular canals course through the mesoglea that forms the structural 

matrix. Several different types of cells were noted within the mesoglea including 

eosinophilic granular cells, stellate cells with basophilic cytoplasm, denegerating 

zooxanthella, and small amphophilic cells with small dark granules in a clear cytoplasm. 

At the base where the zooxanthid contacted the substrate, the mesoglea was composed of 

eosinophilic debris mixed with branching septated organisms. 

Trabeculae of skeleton coursed through mesoglea. Calicoblast layer was almost not 

discernable and consisted of a single layer of eosinophilic granular cells. Occasional 

hyphae and filamentous organisms were seen in the skeletal space. 

Cyphastrea ocellina (Figs. 8E-F) 

Large brown encrusting colony with large calices. Coenosarc epithelium consisted of 

columnar cells mixed with vacuoles and pigment cells. Epithelium of polyps consisted of 

closely apposed columnar cells mixed with vacuoles and batteries of spirocysts. Pharynx 

epithelium consisted of closely apposed ciliated columnar cells. Mesoglea of coenosarc 

was thin and somewhat thickened with mesogleal pleats within mesenteric filaments. 

Gastrodermis of coenosarc was vacuolated and contained moderate numbers of 

zooxanthella and granular brown pigment cells. Gastrodermis of polyps was massively 

distended with zooxanthella. Gastrodermis of gastrovascular canals contained granular 

brown pigment cells. Cnidoglandular cap of mesenteric filaments consisted of closely 

apposed columnar cells with spirocysts. Occasional planula were noted within 

gastrovascular canals. Calicoblast consisted of single squamous layer of cells. 

Leptastrea purpurea 

Coral was encrusting, brown, and has large contiguous calices reminiscent of brain coral. 

Epithelium consisted of columnar ciliated cells underlaid focally by larger supporting 

cells. Spirocysts were scattered throughout although these were clumped and more 

numerous within tentacles. Occasional gray vacuolar cells are noted. Pharyngeal 

epithelium consists of closely apposed columnar ciliated cells mixed with larger dark 

globular cells. 
174 

The mesoglea formed an arching structure that was overlaid externally by epithelium and 

internally by gastrodermis forming a single layer canal network. Mesogleal pleats were 

prominent. The gatrodermis underlying epithelium was composed of pseudostratified 

columnar epithelium containing numerous zooxanthellae. Mesenteric filaments contained 

typical closely clumped columnar cells with prominent eosinophilic granular cells at 

cnidoglandular cap. Some mesenteric filaments contained batteries of holotrichous 

isorhizas. Gastrodermis of gastrovascular canal contained numerous mucous and 

pigment cells. The calicoblast consisted of a single layer of squamous cells that were 

focally hyperplastic. 

DISCUSSION 

Algal-coral interactions made up the preponderance of lesions encountered in corals at 

FFS. It is likely that some of the necrotic lesions in Porites sp. and the tumor-like lesions 

in Montipora observed by Maragos during the 2000 NOWRAMP survey were due to 

invasion of coral tissue by algae. Insufficient time and weather conditions precluded our 

doing manta-tows to assess spatial distribution of lesions. As such, we were unable to 

determine if certain sites had higher incidence of coral-algal interactions than others. 

However, cursory observations did not indicate a particular site having unusual numbers 

of lesions. 

Different species of corals appeared to respond to algal invasion differently. All species 

responded by increasing thickness of gastrodermis and calicoblast layers adjacent to 

algae. Peters (1984) described blistering necrosis of cells in Caribbean corals infiltrated 

by algae. The appearance of sloughing rosettes of gastrodermis appeared to be a 

response limited to Porites sp. and P. duerdeni. Exuberant growth of skeleton in 

response to algae was characteristic of Montipora sp. giving them a gross appearance of a 

tumor-like growth. Although similar responses were seen in some A. cytherea, this was 

far less common. A similar manifestation to coral invasion was seen in Montipora from 

Johnston Atoll (Work et al., 2001). Montipora sp. were one of the few species that also 

showed microscopic evidence of a distinct cellular inflammatory response to algal 

invasion. Most studies of coral immunity have involved grafting experiments (Jokiel and 

Bigger 1994, Hildeman et al. 1975). Microscopic evidence of inflammation in corals is a 

rarely documented phenomenon that merits further study. Likewise, the algal assemblage 

infiltrating coral tissues appeared to be a mix of different species. There is a need to 

elucidate what species of algae are associated with these lesions. 

The manifestation of parasitism in P.lobata was markedly different than that observed in 

the main Hawaiian Islands. In the latter case, the parasite was a trematode that is 

common in the main Hawaiian Islands (Aeby 1991). In this study, the parasites were 

compatible in morphology to coccidia and were similar in appearance to Gemmocystis sp. 

recorded by Upton and Peters (1986) in Porites sp., Montastrea sp., Diploria sp. and 

Meandrina sp. from the Caribbean. The coccidia seen here contained a single sporozoite, 

and the coral appeared to mount a response to these parasites via proliferation of 

calicoblast cells. In later infections, there appeared to be encapsulation of coccidia 
175 

suggesting a possible mechanism of parasite clearance by the coral. Other parasites that 

have been documented from corals elsewhere in the Caribbean include ciliates, 

nematodes, and amoeba (Peters 1984). 

The tumors in A. cytherea were both gastrodermomas based on tissue morphology and 

location of cell proliferation. Criteria used to define these lesions as tumors were similar 

to those used by Work et al. (2001). One type of tumor was identical to that seen in A. 

cytherea from Johnston Atoll and classifed as type 1 tumor (Work et al., 2001). The 

second type of tumor was also a gastrodermoma but manifested as a vermiform rather 

than a cauliflower-type growth. Two coral heads were seen with a type 1 tumor whereas 

only one coral was noted with the vermiform tumor. The paucity of tumors on A. 

cytherea suggests that they did not appear to pose a major threat to this species. 

Remaining lesions were incidental findings. The crab-induced lesions in P. eydouxi were 

similar to those observed on the main Hawaiian Islands (Work and Rameyer, 2001). The 

numbers of corals affected with this lesion appeared small, and interestingly, corals that 

were infested with crabs appeared to have high numbers with tissue that appeared paler 

than normal. The crab-induced lesions are common on thick-branched Pocillopora corals 

in the Hawaiian Islands (McCain and Coles, 1979) and Johnston Atoll (Work et al., 

2001). Fish bites in Porites sp. were also similar to those observed in the island of 

Hawaii. 

References: 

Aeby GS (1991) Behavioral and ecological relationships of a parasite and its hosts within 

a coral reef system. Pac Sci 45: 263-269 

Barszcz CA, Yevich PP (1975) The use of Helly’s fixative for marine invertebrate 

Histopathology. Comp Path Bull 7:4 

US Fish and Wildlife Service (2001) Draft environmental assessment. Reconstruction of 

the shore protection for Tern Island, Hawaiian Islands National Wildlife Refuge, 

134 pp. 

Amerson AB Jr (1971) The natural history of French Frigate Shoals, Northwestern 

Hawaiian Islands. Atoll Res Bull 150, 383 pp 

HildemannWH, Linthicum DS, Vann DC (1975) Immunoincompatibility reactions in 

corals (Coelenterata). Adv Exp Med Biol 64: 105-114 

Jokiel PL, Bigger CH (1994) Aspects of histocompatibility and regeneration in the 

solitary reef coral Fungia scutaria. Biol. Bull 186, 72-80. 

Maragos J, Gulko D (2002) Coral reef ecosystems of the northwestern Hawaiian islands: Interim 

results emphasizing the 2000 surveys. US Fish and Wildlife Service and the Hawaii 

Dept. Land and Natural Resources, Honolulu, Hawaii, 46 pp 

McCain JC, SL Coles (1979) Pseudocryptichirus kahe. A new species of crab (Brachyura, 

Hapalocarcinidae) inhabiting pocilloporid corals in Hawaii. Crustacea 36:81-89. 

Peters EC (1984) A survey of cellular reactions to environmental stress and disease in Carribean 

scleractinian corals. Helgo Meere 37: 113-137 

Work TM, Coles SL, Rameyer RA (2001) Johnston Atoll Reef Health Survey. US Geological 

Survey, National Wildlife Health Center, Hawaii Field Station, 28 pp. 
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Wind speed (Knots)

Daily

10 d avg

Figure 2. Daily average wind speed (orange) and 10 day running average 

wind speed for 1989-93; 2000-11, FFS.

Figure 1. NOWRAMP 2001 survey locations for FFS. Survey sites for this 

study in red 
177 

 
178 

Figure 3. P. duerdeni. Note clear demarcation between normal tissue (right) 

and alga (left) (A). L. purpurea. Note clearly defined patches of algal growth 

(arrow) (B). A. cytherea (C-F). Note algal infiltration with bleaching (C) and 

pigmentation (D). Note algal growth (arrow) accompanied by skeletal 

proliferation (E). Close up of C (F). P. lobata (G-H). Note ill defined areas of 

depigmentation (G) and raised pigmented areas on edge of lesion (H). 
179 

B

E F

A

G H

C D
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Figure 4. M. capitata, note growth anomalies (arrows) (A-D). A. cytherea (E-F). 

Note focus of necrotic tissue (arrow) and algal filaments (arrowhead), bar=50 μm 

(E). Hyperplastic gastrodermis (arrow) and algal filaments (arrowhead), bar=100 

μm (F). P. lobata (G-H). Polyp being invaded by algae (arrowhead), bar=100 μm 

(G). Sloughing gastrodermal cells forming rosettes (arrowhead), bar=50 μm (H).
181 

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182 

Figure 5. P. lobata (A-D). Note clump of alga surrounded by red capsule (arrow) 

and reactive calicoblast cells (arrowhead), bar=50 μm (A). Note alga (arrowhead) 

and reactive calicoblast (arrow), bar=100 μm (B). Clump of necrotic gastrodermal 

cells among algal filaments. Note bands of grey material (arrow), bar=100 μm (C). 

Close of of band of grey material (arrow) and algal filament (arrowhead), bar=100 

μm (D). M. capitata (E-H). Note thickened gastrodermis in area of algal infiltration 

(arrowhead), bar=200 μm (E). Note sparse algal infiltrates in skeletal matrix 

(arrowhead) overlaid by thin squamous membrane (arrow), bar=200 μm (F). Note 

thickened gastrodermis in gastrovascular canal (arrowhead) and granular red 

inflammatory cells (arrow), bar=50 μm (G). Granular red cells (arrow) among 

thickened gastrodermal cells and algal filaments (arrowhead), bar= 50 μm (H).
183 

B

C D

E F

A

G H
184 

Figure 6. P. lobata (A-H). Coral with focal lesions pan view (A) and macro (B). 

Coenosarc epithelium. Note necrosis (arrow), bar=100 μm (C). Reactive calicoblast 

(arrowhead) and pigment cells (arrow), bar=10 μm (D). Clump of gastrodermal 

cells, loose zooxanthella and pigment cells (arrow), bar=20 μm (E). Coccidia 

containing single sporozoite (arrow) surrounded by reactive calicoblast cells, bar=20 

μm (F). Similar coccidian as in F (arrow) surrounded by laminar capsule 

(arrowhead), bar=20 μm (G). Encapsulated coccidian minus sporozoites. 

Note algal filaments (double arrow), bar=20 μm (H). 
185 B

C

D

E

F

AG

H
186 

Figure 7. A. cytherea (A-D). Type 1 tumor (A) and vermiform tumor (B). Note 

proliferation of gastrodermis, bar=100 μm (C-D). P.eydouxi (E-H). Note holes with 

pigmented rim of tissue (arrow) (E). Note areas of bleaching (arrow) (F). Normal 

epithelium (arrow) and gastrodermis (arrowhead), bar=50 μm (G) and atrophied 

epithelium (arrow) and gastrodermis (arrowhead), bar=50 μm (H).

 
187 

G

FG

A B

E F

C D

FH
188 

Figure 8. Blue-gray zooanthid (A-D). Epithelium (bottom) and mesoglea (top). 

Note holotrichous isorhizas (arrow) and red granular cells (arrowhead) in 

epithelium, bar=100 μm (B). Mesenteric filament. Note the base replete with 

zooxanthella and red granular cells (arrow), bar=100 μm (C). Mesoglea. Note 

gastrovascular canal (arrowhead) and mesogleal cells (arrow), bar=100 μm (D). 

Cyphastrea ocellina (E-F). Note planula (arrow) in gastrovascular canal, bar=100 

μm (F). 

B

C D

E F

A
189 

CURRENT KNOWLEDGE OF DISEASES IN US TERRITORIES/FREELY 

ASSOC. STATES

Thierry Work 

US Geological Survey 

PO Box 50167 

Honolulu, HI 96850 

Report 1: CORAL AND CRUSTOSE CORALLINE ALGAE DISEASE ON THE 

REEFS OF AMERICAN SAMOA 

Greta Aeby, Thierry Work, Eva Didonato 

Report 2: JOHNSTON ATOLL REEF HEALTH SURVEY 

Thierry M. Work, Steve L. Coles, Robert A. Rameyer 
190 

Report 1. CORAL AND CRUSTOSE CORALLINE ALGAE DISEASE ON THE 

REEFS OF AMERICAN SAMOA 

Greta Aeby, Hawaii Institute of Marine Biology 

Thierry Work, USGS, National Wildlife Health Center, Hawaii Field Station 

Eva Didonato, National Park Service, American Samoa 

Submitted October, 2005 

INTRODUCTION 

The world’s coral reefs are in serious decline (Wilkinson 2004). The effects of 

overfishing and pollution from agriculture and land development have been a major force 

accelerating decreases in abundance of coral reef species (Hughes et al. 2003, Pandolfi et 

al., 2003). With increased human populations the scale of human impacts on reefs has 

grown exponentially. Within American Samoa, alone, the population has risen 22% in 

the last ten years (Turgeon et al., 2002) and thus so has the potential for damage to the 

near shore resources. Compounding these anthropogenic stressors are the impacts of 

global climate change which is predicted to result in more frequent bleaching episodes 

and higher levels of disease (Hughes et al., 2003). As such, reef managers are faced with 

the challenge of developing strategies to maintain these reefs in the face of these 

changing conditions and it becomes clear that research in support of management is 

urgently needed. 

The reefs of American Samoa support more than 200 species of corals and their 

conditions have been affected by both natural disturbances (crown-of-thorns starfish 

invasion, hurricanes and mass bleaching events) and human-induced impacts (pollution 

and over fishing) (Turgeon et al., 2002). The reefs of American Samoa suffered mass 

bleaching in 1994 (Birkeland et al., 2000) with reports of bleaching also occurring in both 

2002 and 2003 (Peter Craig, pers. comm.). Coral disease has been reported from these 

reefs (Work & Rameyer 2002) but no surveys to quantify disease on a spatial scale had 

been conducted. An important component of monitoring the health of reefs is to have 

baseline ‘before’ data with which to compare ‘after’ conditions (Porter et al. 2001; 

Santavy et al. 2001). Unfortunately, investigations on the role of disease in animal 

populations are often done only after problems are noticed and out of control. However, 

American Samoa is in the unique position of not having suffered major catastrophic 

declines of reefs due to disease. Furthermore, significant effort is planned by American 

Samoa Department of Marine and Wildlife Resources to conduct monitoring programs on 

reefs throughout Manua and Tutuila. As such, American Samoa is well placed to develop 

a baseline assessment of the health of their reefs. The objectives of this study were to: 1) 

document the baseline levels of bleaching and disease in the major genera of corals and 

coralline algae; 2) compare incidence of disease in coral and coralline algae across a 

gradient of levels of reduced water quality based on watershed population; 3) 

systematically describe gross and microscopic morphology of lesions in reef corals and 

develop a standardized nomenclature for identifying and designating coral disease. 
191 

METHODS 

The first task of the proposed research was to conduct a baseline assessment of 

the abundance and distribution of bleached and diseased corals and crustose coralline 

algae at seven sites in American Samoa (Vatia (National park), Tafeu Cove (National 

park), Fagaitua, Faga’alu, Fagatele Bay (National marine sanctuary), Leone and Maloata 

(see Table 1, GPS coordinates, and Fig. 1, map). 

Figure 1. Map showing the seven sites surveyed for bleaching and disease in corals 

and crustose coralline algae in June, 2004. 
192 

A project funded by the World Wildlife Federation (WWF) has been documenting 

water quality parameters at these sites, providing a gradient of sites with presumed 

anthropogenic impacts (Lara Hansen, personal communication). We documented baseline 

levels of coral bleaching and disease at each of the sites using two 25 m x 2 m belt 

transects with visual counts (total 100 m2

 area of reef). The two transect lines were laid 

end to end along depth contours (20-30 ft) separated by approximately 5 meters. A team 

of two divers swam along the transect, with one diver identifying and enumerating coral 

colonies, while the other diver recorded incidence of bleaching and disease. Corals were 

identified to the genus level and assigned to one of seven size classes (0-5cm, 6-10cm, 

11-20cm, 21-40cm, 41-80cm, 81-160cm and > 160cm). These size classes and protocols 

were adapted from Mundy (1996) who used them for broad-scale surveys in American 

Samoa. They have also been used to examine coral community structure in the NWHI 

(Maragos et al., 2004). Diseased corals and coralline algae were photographed and a 

general description of the condition was recorded. Samples of diseased coral (and 

healthy portions for controls) were collected for laboratory investigations using standard 

histopathological techniques. Substrate characteristics were documented by line-intercept 

method whereby the substratum underlying the tape measure was recorded at 10 cm 

intervals. At some of the sites (Vatia, Tafeu, Fagatele, Faga’itua) a 2nd station was 

surveyed as described above. Surveys from both stations were combined at these sites 

for analysis. Surveys were conducted June, 8-16, 2004. 

Another task of the proposed research was to systematically describe gross and 

microscopic morphology of lesions in corals and crustose coralline algae and develop a 

standardized nomenclature for identifying and designating disease. For characterization 

of gross lesions, corals with abnormalities were photographed with a digital camera 

(Olympus C5050) contained in an Ikelite® housing, and attached to an Ikelite® 50 

substrobe. Lesions were photographed from two aspects. A pan photograph encompassed 

the larger colony to gauge the extent of the lesion. Close-up photos were done of the 

same lesion to gain detail on polyp morphology. The following data were recorded: date, 

location, and depth of collection. 

Grossly, lesions were classified by distribution as focal, locally extensive, or 

diffuse. Lesions were further classified as tissue loss, discoloration, or growth anomaly. 

Table 1. Coordinates of sites surveyed for bleaching and disease of coral and coralline algae on Tutuila in June, 2004.

Coordinates were taken by GPS unit onboard boat at start of transect 1

Site Date Depth (ft)

Latitude 

(S)

Longitude 

(W) Notes

Fagaitua1 6/8/04 27 14 16.342' 170 36.728' fringing reef off Fagaitua village- WWF site

Fagaitua 2 6/8/04 22 14 17.005' 170 36.393' fringing reef off Alofau village

Fagatele Bay 1 6/9/04 18 14 21.944' 170 45.736' Fagatele Bay National Marine Sanctuary-WWF site

Fagatele Bay 2 6/9/04 22 14 21.817' 170 45.708' other side of the Bay from WWF 

Tafeu 1 6/10/04 20 14 15.142' 170 41.338' fringing reef- WWF site

Tafeu 2 6/10/04 21 14 15.158' 170 41.498' other side of the embayment from WWF

Vatia 1 6/14/04 20 14 14.774' 170 40.076' fringing reef- WWF site

Vatia 2 6/14/04 26 14 14.704' 170 40.262' fringing reef other side of the embayment from WWF 

Leone 6/15/04 32 14 20.592 170 47.328 fringing reef- WWF site

Maloata 6/15/04 25 n/a n/a fringing reef- WWF site

Faga'alu 6/16/04 19 n/a n/a fringing reef- WWF site
193 

Tissue loss included those cases where tissue was missing leaving exposed skeleton. In 

such cases, we recorded if the skeleton was intact or damaged (eroded) and characterized 

as acute, subacute, and chronic. Acute tissue loss was those cases where skeleton was 

bare (eroded or intact). Subacute tissue loss included cases of algal growth on skeleton 

separated from intact tissue by bare skeleton. Chronic tissue losses were those cases 

where skeleton was completely covered by algae or sediment. Discoloration included 

those lesions where tissues were abnormally colored and was further subdivided into 

bleaching and non-bleaching discoloration. Growth anomaly included those lesions 

exhibiting anomalous growth of coral skeleton. 

For histopathology, sections of corals were fixed in Z-Fix (Anatech Ltd.) 

according to manufacturer instructions. Briefly, Z-fix was diluted 1:5 with seawater and 

placed in 100 cc plastic jars. Coral were placed in the fixative and allowed to fix for at 

least 24 h. Corals were decalcified in dilute formic acid/formaldehyde solution (CalExII, 

Fisher Scientific) until the skeleton was completely dissolved. Tissues were dehydrated 

in alcohol series, embedded in paraffin, sectioned at 5 μm, placed on microscope slides 

and stained with hematoxylin and eosin. Special stains were used as appropriate to 

identify fungi, bacteria, algal filaments, or protozoa. Tissues were examined using light 

microscopy at magnifications ranging from 40X-1000X. 

On histology, lesions were classified as depletion of zooxanthella, atrophy, 

uncomplicated necrosis, necrosis associated with fungi, algae, protozoa, or metazoa, and 

hyperplasia of gastrovascular canals. Depletion of zooxanthella included cases where 

gastrodermis was depleted of zooxanthella. Uncomplicated necrosis included evidence 

of cytoplasmic fragmentation and hypereosinophilia, pyknosis, or karyorrhexis. 

Organisms were classified as algae if they were filamentous and stained negative with 

silver or if cell walls were present or fungi if they stained positive with silver (Prophet et 

al. 1992). 

RESULTS 

Surveys 

Coral community structure 
194 

Based on colony counts within transects, the four dominant coral genera on the reefs of 

Tutuila were Montipora (39.9% of the total colonies), Galaxea (12.9%), Pocillopora

(11.4%) and Acropora (10.1%). Coral community structure varied among the seven sites 

as did the coral cover (Table 2). 

Overall occurrence of bleaching and disease 

Within belt transects an estimated 16,824 coral colonies from 24 different genera 

were examined for bleaching and disease. Bleaching was found at very low levels 

affecting less than one percent of the overall colonies. Six different coral disease states 

as well as a number of lesions not associated with disease were documented from four 

coral genera on the reefs of Tutuila (Appendix I). Three diseases affected Acropora: 

Acropora white syndrome, Acropora ciliate disease, and Acropora growth anomalies. 

Montipora was affected by one disease: Montipora growth anomalies. Porites was 

affected by one disease: Porites tissue loss syndrome. Lobophyllia was affected by one 

disease: Lobophyllia tissue loss syndrome. Coral disease was found at all seven sites but 

the overall proportion of colonies examined that had signs of disease (prevalence) was 

low (0.143%) (range = 0.029-0.40%). The crustose coralline algae (CCA) disease, 

Table 2 . Coral community structure at seven sites around Tutuila surveyed for bleaching and disease in 

June, 2004. Percent coral cover was estimated using line-intercept. Coral community was calculated from 

colony counts along belt transects. Data show the percentage of colony counts along the transect represented 

by each coral genera. Dominant coral genera shown in bold for each site.

Fagatele Maloata Tafeu Vatia Faga'itua Leone Faga'alu

coral community (%)

Acropora 8.7 4.6 3.1 19.7 10.7 15.3 10.6

Astreopora 0 0.57 0.77 0.24 0.39 0 0

Coscinaraea 0 0.57 2.3 0.72 0.65 0.4 0

Cyphastrea 0 0 0 0 0.13 0 0

Diploastrea 00 0 0 00 0

Echinophyllia/Oxypora 0.25 0 0 0 0.65 0 0

Echinopora 0.13 0 0 0 0.91 0 0

Favia/Favites 4.9 4.6 3.8 3.6 1.7 1.2 0.33

Fungiidae 1.6 0.57 0.38 2.2 0.78 0 0.66

Galaxea 38.6 9.7 1.2 1.9 10.5 0 0

Goniastrea 0.5 0 0 0.24 2.2 0 0

Goniopora/Alveopora 0.13 0 0 0.24 0 0.4 0

Hydnophora 0 0 0.19 0 0.52 0 0

Leptastrea 0.38 2.3 11.2 0.48 0.65 1.2 0.33

Leptoseris/Pachyseris/Coe 0.63 0 0 0 0 0 0

Lobophyllia 0.25 0 0 0.24 3.8 0 0

Merulina/Scapophyllia 0 0 0 0 0 0.8 0

Millepora 0 0 0 0.24 0 0 0

Montastrea 0 4.6 0.77 0.96 0.26 0.4 1.3

Montipora 20.8 39.4 51.9 41 39.7 70.7 46.4

Pavona 2.4 10.3 14 13.4 11.2 2.4 5.6

Pocillopora 7.8 21.7 4 9.4 12.9 3.6 33.4

Porites 12.9 1.1 6.3 5.5 2.5 3.6 0.66

Psammocora 0 0 0 0 0 0 0.66

avg. coral cover (%) 46.3 22.8 45.7 48.2 28.4 40.9 32.6
195 

coralline lethal orange disease (CLOD) was found at 4 of the 7 sites (57% of the sites). 

The number of CLOD infections per m2

 of CCA ranged from 0 to 0.24 (Table 3). 

Distribution and prevalence of each disease state 

Distribution of the different coral diseases varied (Table 3). Acropora white 

syndrome was found to be the most widespread disease occurring at 5 of the 7 sites 

(71.4%). Acropora growth anomalies occurred at 4 of the 7 sites (57.1%) with the other 

diseases only occurring at one site each (14.3%). The proportion of coral colonies 

affected by each disease (prevalence) also varied with both Acropora white syndrome 

and growth anomalies being the highest (0.624% each). Prevalence of the other diseases 

was lower; Acropora ciliate disease (0.07%), Porites tissue loss syndrome (0.095%), and 

Montipora growth anomalies (0.031%). Prevalence of Lobophyllia tissue loss syndrome 

was not calculated as the diseased colony was not found within the transect area. 

Prevalence of disease differed among the affected genera with Acropora having 

the highest overall prevalence (1.2%) compared to the other genera; Montipora (0.031%), 

Porites (0.095%). 

Relationship between disease and watershed usage 

The seven sites were originally selected based on a population gradient within 

each watershed used as an indicator of anthropogenic stress. The number of different 

diseases present within each site varied as did the overall prevalence of disease (Table 3). 

However, no patterns emerged suggesting that disease levels were directly related to 

anthropogenic watershed stress. 

Table 3. Distribution and prevalence of different coral diseases and density of coralline algae diseases 

around Tutuila in June, 2004. Coral disease prevalence=(# diseased colonies/# colonies examined)*100

Coralline lethal orange disease (CLOD) density =# CLOD infections/est. m^2 of CCA at site

X* Disease present at site but prevalence not calculated as affected colony was not within belt transect

Human usage rating based on watershed populations. 

human usage pristine pristine pristine minimal intermediate extensive extensive

site Fagatele Maloata Tafeu Vatia Faga'itua Leone Faga'alu

Acropora white syndrome 0.24 2.08 1.08 0.54 0.52

Acropora ciliate disease 0.27

Acropora growth anomalies X* 4.2 1.6 5.3

Montipora growth anomalies 0.48

Porites tissue loss syndrome 0.16

Lobophyllia tissue loss syndrome X*

# CLOD/m^2 CCA 0.24 0.02 0 0.009 0 0.004 0

overall coral disease prevalence 0.031 0.286 0.032 0.266 0.029 0.402 0.055
196 

Histology (gross and microscopic findings) 

 We examined tissue specimens from 8 sites comprising 67 samples from 59 

colonies comprising at least 20 species of corals (Table 4). Of these, 10 were from 

apparently normal coral and the remainder from lesions. The most common gross lesions 

included tissue loss and growth anomalies, and for these, Acropora sp. and Montipora sp. 

were over-represented (Table 5). 

Table 4. Number of coral samples collected for histopathology at various sites around

Tutuila, June 2004.

Species Faga’itua2 Faga’alu Fagatele Faga’itua1 Leone Malato Tafeu1 Vatia1 Total

Acropora

abrotenoides

1 23

A. cytherea 1 78

Acropora sp. 1 1

plate

Acropora

1 2 7 10

corymbose

Acropora

1 3 15

encrusting

Acropora sp.

21 1 4

Astreopora

sp.

1 1

Favia sp. 1 1 2 4

Galaxea sp. 2 2

Goniastrea

sp.

1 1

Leptoria

phrygia

1 1

Lobophyllia

corymbosa

2 2

Lobophyllia

sp.

22 4

massive

Porites sp.

1 23

Porites rus 2 2

Montastrea

sp.

1 1

Montipora

sp.

1 1 2 3 1 1 1 1 11

Pocillopora

eydouxi

2 2

Pocillopora

meandrina

1 1

Pavona sp. 1 1

Total 7 3 14 8 5 2 9 19 67
197 

Tissue loss: 

The following patterns were seen for tissue loss: 

Barnacle infestation: This was seen in Goniastrea only and was characterized by small white 

foci encompassing approximately the diameter of one polyp (Fig. 2A). The center of the area 

contained a barnacle with bleaching of tissues immediately around the barnacle (Fig. 2B). 

Microscopy revealed a crustacean surrounded by normal coral tissue (Fig. 2C). In some cases, a 

mix of algae and sponges infiltrated into the coral tissue leading to cell fragmentation and 

necrosis. 

Table 5. Gross lesions found in various genera of corals in Tutuila, June 2004.

Genus Discoloration Growth anomaly Tissue Loss Normal Total

Acropora 1 11 14 5 31

Astreopora 1 1

Favia 4 4

Galaxea 1 12

Goniastrea 1 1

Leptoria 1 1

Lobophyllia 1 2 36

Montastrea 1 1

Montipora 3 8 11

Pavona 1 1

Pocillopora 1 1 13

Porites 4 15

Total 15 14 28 10 67
198 

Figure 2. A) Goniastrea sp. with barnacles. B) Note barnacles (arrowhead) 

surrounded by bleached tissue. C) Photomicrograph of barnacle (arrowhead) 

among coral tissue. 

A B 

C
199 

Chronic tissue loss and excessive skeletal growth: This was seen in massive Porites sp. 

and Acropora cytherea and was characterized by a focus of coralline or turf algae 

surrounded by exuberant skeletal growth. On microscopy, these lesions manifested as 

full thickness necrosis of coral tissue associated with marine algae with some depletion of 

zooxanthella (Fig. 3). 

Fig. 3. A) Massive Porites. B) Acropora cytherea. A-B) note central area of coralline 

algae infiltration with exuberant skeletal growth surrounding lesion. C) 

Photomicrograph of E. Note, mass of algae and sponges and clumps of necrotic 

coral tissue. 

 

C

A B
200 

Fish bites: This was manifested by wellcircumscribed localized loss of tissue 

accompanied by bare eroded skeleton (Fig. 

4). On histology, these lesions were 

characterized by fragmentation of coral 

tissue with depletion of zooxanthella from 

gastrodermis. 

Figure 4. Montipora sp. fish bite. Note 

characteristic erosion of skeleton and 

loss of tissue.

Subacute tissue loss: This was manifested 

by complete tissue loss of single polyps 

revealing bare intact skeleton completely 

covered with algae. Only Lobophyllia sp. 

was sampled with this lesion (Figure 5). 

Figure 5. Lobophyllia tissue loss 

Acute tissue loss: This was manifested by a well-circumscribed diffuse area of tissue 

loss revealing intact white skeleton. The tissue loss usually encompassed the edge of the 

colony. On histology, the major changes seen included no lesions, tissue fragmentation, 

or hypertrophy of calicoblastic epithelium. In some cases, this tissue loss was associated 

with presence of corallivorous snails. Tissue loss in P. rus was attributed, on microscopy, 

to infestation with sponges associated with necrosis. (Fig. 6). 

 
201 

Figure 6. A-B) Acute tissue loss in encrusting Montipora sp., note bare white 

skeleton bereft of tissue and lesion predominantly on the edge of the colony. B) 

Snail (arrowhead) associated with acute tissue loss in Montipora sp. C) P. rus acute 

tissue loss. D) Photomicrograph of D. Note invasion of coral tissue with sponge 

(white arrowhead) and necrosis of tissue (black arrowhead). 

Acute to subacute tissue loss: This was manifested by well circumscribed diffuse areas 

of tissue loss revealing intact skeleton with presence of recent algal growth in the center 

and bare intact white skeleton at the interface between tissue and algae. This was found 

mainly in plating Acropora. On microscopy, findings ranged from simple uncomplicated 

tissue loss to infection with microparasites (ciliates) (Fig. 7). 

A

C

B

D
202 

Figure 7. A-B) Plating Acropora sp. with subacute tissue loss. A) note distinct band 

of white skeleton bereft of algae separting intact tissue and skeleton covered by 

algae. B) Note presence of algae covered intact skeleton (black arrowhead) 

separated from intact tissue by intact skeleton bereft of algae (white arrowhead). C) 

Photomicrograph of B, Acropora with ciliate infection. Note invasion of ciliates 

(white arrowhead) associated with necrotic tissue (black arrowhead). 

Discoloration: 

Bleaching: We saw 10 cases of bleaching in 7 genera of corals. Grossly, bleaching was 

characterized by a diffuse white discoloration. Bleaching in corals is typically attributed 

to loss of symbiotic zooxanthellae from coral tissues, and on microscopic examination, 

this was seen in all cases. In 3 cases, additional microscopic lesions were seen including 

necrosis of tissue associated with infiltrates of sponges or algae. In those cases, the 

sponge/algae complex was seen invading tissue from below and overlying epidermis and 

gastrodermis were intact but atrophied and bereft of zooxanthella (Fig 8). 

A B

C
203 

C

AA B

Figure 8. A) Astreopora sp. with diffuse bleaching. B) Favia sp. with diffuse 

bleaching. C) Photomicrograph of B. Note infiltration of sponges and algae (black 

arrow) below the intact epidermis (white arrowhead) with gastrodermis bereft of 

zooxanthella. 

Non-bleaching discoloration: Other cases of discoloration did not fit the bleaching 

pattern. Discoloration in Favia/Favites was, on microscopy, attributed to mucus 

sheathing and not considered abnormal. No microscopic lesions associated with 

discoloration were seen in Lobophyllia (Fig. 9). 
204 

A B

Figure 9. A-B) Mucus sheathing in Favia sp., note well-defined areas of 

discoloration. 

Growth Anomaly

Acropora spp. were the most common genera see with this lesion although Montipora spp., also 

had growth anomalies. These ranged from smooth to more rugose and cauliflower shapes and 

was found in branching, corymbose, and plating Acropora (Figure 10). On microscopy, the most 

common finding was hyperplasia of gastrovascular canals; however, there were not the classic 

hallmarks of cancer as seen in other animals making it difficult to conclude that these are true 

neoplasia sensu stricto. In two cases, growth anomalies were, on microscopy, associated with 

necrosis of tissues associated with marine algae. 

 

A B 
205 

Figure 10. Growth anomalies in Acropora species. A) Corymbose colonies; B) 

Branching colonies; C-D) plating colonies. 

Summary of Survey Findings 

1. The overall prevalence of coral disease was found to be low (0.143%) as compared to 

other regions in the Indo-Pacific. Overall disease prevalence in the Northwestern 

Hawaiian Islands was found to be 0.5% (Aeby, in press). Willis et al. (2004) surveyed 

eight sites along the Great Barrier Reef (GBR) and found the prevalence of disease in 

hard corals to range from 7.2-10.7%. Raymundo et al. (in press) surveyed eight sites 

in the Philippines and reported an overall prevalence of disease of 14.2%. 

2. Six coral disease states and one disease of CCA were documented from the reefs of 

Tutuila. Bleaching was found at low levels. 

3. Five of the six coral disease states have been reported from other areas of the IndoPacific. Porites tissue loss syndrome is reported from the NWHI (Aeby, in press) 

Australia (Willis et al., 2004) and the Philippines (Raymundo et al., in press). 

Acropora white syndrome is reported from the NWHI (Aeby, in press) and Australia 

(Willis et al., 2004). Growth anomalies in both Acropora and Montipora have been 

recorded from Australia (Willis et al., 2004), Johnston Atoll (Work et al., 2001) and 

Okinawa (Yamashiro et al., 2000, 2001; Yamashiro 2004). Lobophyllia tissue loss 

syndrome has not yet been reported elsewhere. It must be noted that there are 

regional differences in names assigned each set of field disease signs but through the 

efforts of the Coral Disease and Health Consortium 

(www.coral.noaa.gov/coral_disease/cdhc.shtml) this nomenclature problem will 

eventually be resolved. It should also be noted that any similarities in field signs of 

disease between regions does not necessarily imply the diseases have the same 

etiology. 

4. After histopathological analysis it was found that a number of coral lesions found 

during surveys were not associated with infectious agents or underlying pathologic 

process. These include lesions due to predation, barnacle infestation and mucous 

sheathing. This confirms the critical component histology plays in understanding 

disease processes. 

C D
206 

5. There were differences in prevalence of disease among coral genera with Acropora

having the highest prevalence. Acropora comprised only 10.1% of the overall coral 

community along the transects yet showed the highest overall prevalence of disease 

(1.2%). In contrast, Montipora comprised 40% of the coral community but had a 

disease prevalence of 0.031%. This suggests that there may differences in disease 

susceptibility among coral genera and that pathogens do not necessarily affect the 

most common or abundant corals. Acropora have also been found to have the highest 

levels of disease in the NWHI (Aeby, in press). The sites surveyed had differences in 

coral community which would be a factor in what diseases and what levels of disease 

would be found at a particular reef. 

6. No pattern emerged suggesting that disease levels were directly related to anthropogenic watershed stress. 

Summary of Histological Findings

1. Some cases of acute tissue loss are probably due to snail predation. We opted to be 

conservative and to include only those cases where snails were visible, however, this 

is probably an underestimate. Lesions presumably attributable to snails were 

generally peripheral on encrusting colonies and this pattern was more prevalent in 

certain sites versus others. Quantifying populations of corallivores in conjunction 

with measurement of lesions would be helpful in evaluating their effects on reefs. 

2. Certain gross lesions have clear causes. For example, patchy tissue loss and 

discoloration with presence of a crustacean in the center of the lesion is indicative of 

barnacle infestations. Likewise, focal erosion of tissues and skeleton are indicative of 

fish bites. Determining the species of barnacles affected and the types of bites 

produced by particular fish may be useful in the future. 

3. Not all discolorations are disease processes. In the case of faviids, mottled 

discoloration is probably indicative of mucus shedding. 

4. Growth anomalies are more common in acroporids. Determining how fast these grow 

and what effect they have on the health of the corals should be the focus of future 

investigations. 

5. There is a need to refine the description of gross lesions in corals in order to better 

understand whether certain gross lesions can be related to microscopic findings in a 

more consistent manner. 

References: 

Aeby, G.S. In press. Baseline levels of coral disease in the Northwestern Hawaiian 

Islands. Proc. 3rd. Symp. Northwestern Hawaiian Islands. 

Birkeland, C.E., Craig P., Davis G., Edward A., Golbuu Y., Higgins J., Gutierrez J., 

Idechong N., Maragos J., Miller K., Paulay G., Richmond R., Tafileichig A., and D. 

Turgeon. 2000. Status of coral reefs of American Samoa and Micronesia: USaffiliated and freely associated islands of the Pacific. In: C. Wilkinson (ed.), Status of 

coral reefs of the world: 2000. Australian Institute of Marine Science. Pp. 199-217. 

Hughes, T., Baird, A., Bellwood, D., Card, M., Connolly, S., Folke, C. Grosberg, R., 

Hoegh-Guldberg, O., Jackson, J., Kleypas, J., Lough, J., Marshall, P., Nystrom, M., 
207 

Palumbi, S., Pandolfi, J., Rosen, B., and J. Roughgarden. 2003. Climate Change, 

human impacts and the resilience of coral reefs. Science 301:929-933. 

Maragos J., Potts D., Aeby G., Gulko D., Kenyon J., Siciliano D., VanRavenswaay D. 

2004. 2000-2002 Rapid Ecological Assessment of Corals (Anthozoa) on Shallow 

Reefs of the Northwestern Hawaiian Islands. Part 1: Species and Distribution. Pac. 

Sci. 58(2): 211-230. 

Mundy, C. 1996. A quantitative survey of the corals of American Samoa. Dept. of 

Marine and Wildlife Resources, American Samoa Government, Pago Pago, 25 pp. 

Pandolfi, J., Bradbury, R., Sala, E., Hughes, T., Bjorndal, K., Cooke, R., McArdle, D., 

McClenachan, L., Newman, M., Paredes, G., Warner, R., and J. Jackson. 2003. 

Global trajectories of the long-term decline of coral reef ecosystems. Science 

301:955-958. 

Porter, J., P. Dustan, W. Jaap, K. Patterson, V. Kosmynin, O. Meier, M. Patterson and M. 

Parsons. 2001. Patterns of spread of coral disease in the Florida Keys. Hydrobiologia 

460:1-14. 

Prophet E, Mills B, Arrington J, Sobin L (1992) Laboratory methods in histotechnology, 

Vol. Armed Forces Institute of Pathology, Washington 

Raymundo, L., Rosell, K., Reboton, C., and L. Kaczmarsky. In press. Coral diseases on 

Philippine reefs: Genus Porites is a dominant host. Dis. Aquatic Org. 

Santavy D, Mueller E, Peters E, MacLaughlin L, Porter J, Patterson K, Campbell J (2001) 

Quantitative assessment of coral diseases in the Florida Keys: strategy and methodology. 

Hydrobiologia 460:39-52 

Turgeon, D., Asch, R., Causey, B., Dodge, R., Jaap, W., Banks, K., Delaney, J., Keller, 

B., Speiler R., Matos, C., Garcia, J., Diaz, E., Catanzaro, D., Rogers, C., Hillis-Starr, 

Z., Nemeth, R., Taylor, M., Schmahl, G., Miller, M., Gulko, D., Maragos, J., 

Friedlander, A., Hunter, C., Brainard, R., Craig, P., Richmond, R., Davis, G., 

Starmer, J., Trianni, M., Houk, P., Birkeland, C., Edward, A, Golbuu, Y., Gutierrez, 

J., Idechong, N., Paulay, G., Tafileichig, A. and N. Vander Velde. 2002. The state of 

coral reef ecosystems of the United States and Pacific freely associated states: 2002. 

National Oceanic and Atmospheric Administration, Silver Spring, MD. 265 pp. 

Wilkinson, C. 2004. Status of coral reefs of the world: 2004. Australian Institute of 

Marine Science. 301pp. 

Willis, B., Page, C. and E. Dinsdale. 2004. Coral disease on the Great Barrier Reef. 

Pages 69-104 in E. Rosenberg and Y. Loya, eds. Coral Health and Disease. SpringerVerlag, Germany. 

Work, T., Coles, S. and R. Rameyer. 2001. Johnston atoll reef health survey. 

Geological Survey, National Wildlife Health Center, Hawaii Field Station, 28 pp. 

Work, T. and R. Rameyer. 2002. American Samoa reef health survey. Geological 

Survey, National Wildlife Health Center, Hawaii Field Station, 42 pp. 

Yamashiro, H., M. Yamamoto, and R. van Woesik. 2000. Tumor formation on the coral 

Montipora informis. Dis. Aquat. Org. 41:211-217. 

Yamashiro, H., H. Oku, K. Onaga, H. Iwasaki, and K. Takara. 2001. Coral tumors store 

reduced level of lipids. J. Exp. Mar. Bio. Ecol. 265:171-179. 

Yamashiro, H. 2004. Coral disease. Pp. 56-60 in Coral Reefs of Japan. Ministry of the 

Environment, Japanese Coral Reef Society. 
208 

Appendix I. Summary of coral lesions found in American Samoa in June 2004. 

A. CORAL DISEASES

Acropora ciliate disease

Histology: ciliates associated with necrotic tissue

Location: Vatia 

Frequency of occurrence (# sites w/ disease/tot sites surveyed): 9.1% 

 
209 

Acropora white syndrome

Histology: subacute tissue loss and necrotic tissue consistent with disease

Location: Fagatele, Tafeu, Vatia, Faga’itua, Faga’alu 

Frequency of occurrence: 45.5% 

 
210 

Acropora Growth Anomalies

Histology: hyperplasia (overgrowth) of gastrovascular canals.

Location: Fagatele, Maloata, Vatia, Leone 

Frequency of occurrence: 27.3% 

 
211 

Montipora growth anomalies

Histology: hyperplasia (overgrowth) of gastrovascular canals.

Location: Maloata 

Frequency of occurrence: 9.1% 

Porites tissue loss syndrome 

Histology: tissue necrosis and sponge invasion

Location: Fagatele 

Frequency of occurrence: 9.1% 

 
212 

Lobophyllia tissue loss syndrome 

Histology: chronic tissue loss

Location: Fagaitua 

Frequency of occurrence: 9.1% 
213 

Coralline lethal orange disease (CLOD)

Location: Fagatele Bay, Maloata, Vatia, Leone 

Frequency of occurrence: 45.5% 
214 

Report 2. JOHNSTON ATOLL REEF HEALTH SURVEY

Thierry M. Work1

, Steve L. Coles2, Robert A. Rameyer1

1. USGS-National Wildlife Health Center-Hawaii Field Station, PO Box 50167, Honolulu, 

HI 96850. 

2. Bishop Museum, Dept. Invertebrate Zoology, 1525 Bernice Street, Honolulu, HI 96817 

Submitted 4 September, 2001 

In partial fulfillment of USFWS Interagency Agreement No.: 122000N004 
215 

INTRODUCTION 

Johnston Atoll is an overlay U. S. Fish and Wildlife Service (USFWS) National 

Wildlife Refuge located ~1300 km southwest of Honolulu, Hawaii. Johnston Atoll is not 

part of the Hawaiian Islands, but is more closely associated with a subsurface mountain 

range called the Marcus-Necker Rise (Amerson and Shelton, 1976). The atoll was 

discovered in 1796, used in the early 19th century for guano extraction, and during WWII, 

the US Navy used it for aerial and submarine operations. Subsequent activities included 

establishment of LORAN towers by the US Coast Guard, and use of the atoll for atomic 

weapons tests (Amerson and Shelton, 1976). Since 1976, the USFWS and the Defense 

Nuclear Agency have an agreement whereby USFWS manages the natural resources of 

the atoll. In 1985, a chemical weapons disposal plant (Johnston Atoll Chemical Agents 

Disposal System) was built on the Western end of the main island (Johnston). This plant 

is soon to be decommissioned, and Johnston Atoll will revert back to the USFWS in 

~2003. 

Johnston Atoll is composed of a fringing reef surrounding 4 islands, two of which 

(Haukau and Hikinau) are man made (Fig. 1). The lagoon becomes progressively deeper 

from northwest to southeast and supports a variety of corals, reef fish, sea turtles, and 

seabirds (see Coles et al., 2001, Appendix A for full listing of recent and previous 

reports). Compared to other atolls and reef environments, the marine fauna of Johston 

Atoll is depauperate by species, although coral coverage is high. The dominant species 

of corals include Acropora cytherea, A. humilis, A. valida, Montipora patula, Pocillopora

eydouxi and P. meandrina. Maragos and Jokiel (1986) classified the lagoon into 4 area 

with the northwest portion harboring the greatest abundance of corals. During and after 

WWII, much of the coral in that area was destroyed during extensive dredging and filling 

of the reef and lagoon (Brock et al 1965, 1966). 

Much work has been done to identify the identity and extent of organisms at 

Johnston Atoll (see Coles et al., 2001 for review). However, relatively little effort has 

been spent looking at health parameters of marine fauna. Cohen et al. (1997) observed 

bleaching of corals, and Coles et al. (2001) observed growth anomalies in Acropora

cytherea. The USFWS sponsored the USGS National Wildlife Health Center to further 

investigate growth anomalies of corals in Johnston Atoll. From 29 March to 2 April, 

2001, a team from the US Geological Survey Hawaii Field Station (Work, Rameyer) and 

the Bishop Museum (Coles) surveyed coral reefs at Johnston Atoll for lesions. The trip 

had the following objectives: 

1) Conduct manta tow and spot surveys for lesions in dominant coral species in the 

northern lagoon and sites off Johnston and East islands. 

2) Describe gross and microscopic anatomy of lesions in corals. 

3) Obtain pigment profiles of the dominant coral (Acropora cytherea). 

METHODS 

Survey areas: 

Broad-scale manta tow surveys were done using flat-bottom boats with an 

outboard motor focusing on the northwestern portion of the lagoon because it had the 

highest density of coral (Maragos and Jokiel, 1997), and because it encompassed the area 

where growth anomalies in A. cytherea were previously noted by Coles et al. (2001). 
216 

Six locations were selected for spot dives. Site 1 was where Coles et al. (2001) observed 

growth abnormalities in Acropora cytherea. Site 2 (Agent Orange) was immediately 

offshore the northwestern portion of Johnston Island where the herbicide Agent Orange 

had been stored during the Vietnam war. Site 3 (Mt. Pluto) was directly offshore the 

middle of north Johnston Island where an aborted launch of a nuclear warhead caused 

localized contamination with plutonium during the 1960s. Site 4 (Burn pit) was north of 

Eastern Island and was adjacent to an old burn pit where plastics and other materials were 

incinerated in open air. Sites 5 and 6 (Signal Tower and Donovan’s reef, respectively) 

were “control” areas (Fig. 1). 

Manta tows were done according to methods of English et al. (1994). Briefly, a 

diver was towed at low speeds ca. 30-40 feet behind a boat for 2 minute intervals at the 

end of which the diver recorded the bottom type (rubble, sand, coral), estimated percent 

coral cover by category (0-10%, 10-25%, 26-50%, >50%), and dominant coral genera 

(Acropora sp., Montipora sp. or Pocillopora sp.). For Acropora sp., the diver 

categorized lesions into 5 groups (see results). After each two-minute manta tow 

interval, the diver recorded the number of each type of lesion. Manta tows proceeded 

perpendicular to the long axis of Johnston Island and coordinates of way points were 

collected at the start and end of every 2 minute tow using a Garmin GPS 12 unit. Spot 

dives were done using SCUBA in Sites 1, 3, 5 and 6 and snorkel for the remaining sites. 

For areas 2 and 4, we snorkeled a network of parallel lines close to shore. Scuba surveys 

consisted of swimming in a haphazard pattern looking for lesions. 

Corals were photographed using a Nikonos V underwater camera with a 20 mm 

lens and twin Ikelite 50 strobes or a digital camera in an underwater housing. Close-up 

photos were taken with a Nikonos V camera with a single Ikelite 50 strobe and a 2:1 

extension tube. Coral samples were taken using bone shears, or hammer and chisel, and 

placed into labeled plastic bags in seawater. Corals were preserved in Helleys fixative 

(Barszcz and Yevich, 1975) with added salt and allowed to fix for 24 hr. The fixative 

was decanted and the coral rinsed with fresh water once every 12 hr for 24 hr. 

Subsequently coral was stored in 70% ethanol, decalcified with Cal-ex II (Fisher 

Scientific), placed in cassettes, processed for paraffin embedding, trimmed at 5 um, and 

stained with hematoxylin and eosin. Slides were examined using light microscopy at 

magnifications ranging from 20-1000X. 

Twenty fragments of normal A. cytherea were collected for pigment analyses. 

Coral fragments were weighed (nearest 0.001 g), placed in 50 ml of 100% methanol 

(n=10) or 0.6M phosphate buffer pH 8 (n=10), and extracted in the dark at 4C for 24 hr. 

The supernatant was decanted, centrifuged (14000g) for 5 minutes, and stored at –190C. 

The extract was filtered using 0.45  syringe filters and scanned from 200-700 nm using 

a Spectronic Genesys 8 Spectrometer. Methanol extracts were for chlorophyll pigments, 

and phosphate buffer extracts for pigments insoluble in methanol. 

RESULTS 

Surveys

Coral cover seemed uniform over most of the lagoon but appeared denser away from the 

dredge channel (Fig. 2). Coral cover was relatively sparse east of Johnston Island. Acropora 

(mostly A. cytherea) was more dominant towards the reef edge, and Montipora sp. was more 
217 

dominant near the ship channel. Pocillopora sp. appeared more numerous east of Johnston Island 

(Fig. 3.). 

Normal morphology

Acropora cytherea 

Normal A. cytherea colonies formed wide flat tables (Fig. 4A) with small 

branches containing numerous tan-brown to tan-pink exsert axial corallites (Fig. 4B). On 

microscopy, the epithelium overlying was composed of an intact continuous layer of 

columnar cells with basally located nuclei. These were interspersed with occasional 

intracytoplasmic basophilic granular cells, mucus cells, and rare isolated spirocysts (a 

type of nematocyst) (Fig. 4C). Epithelium overlying tentacles contained numerous 

batteries of spirocysts mixed with barely visible holotrichous isorhizas. Spirocysts 

became less numerous and eventually absent in the stomodeum, the epithelium of which 

was lined by closely apposed ciliated columnar epithelium. Mesoglea was uniformly thin 

except near the base of tentacles where it thickened and contained prominent mesogleal 

pleats; within the gastrovascular canal, mesoglea was not discernable. 

Coenosarc gastrodermis was composed of columnar and mucus cells mixed with 

focally aggregated zooxanthella. In tentacles, gastrodermis was thickened and contained 

clusters of zooxanthella. Within the gastrovascular canal, gastrodermis was focally 

hyperplastic and contained rare zooxanthella. The gastrodermis was either closely 

apposed to calicoblast or contained prominent mucus cells, giving it a foamy appearance. 

Mesenteric filaments were of two types. One consisted of densely packed columnar cells 

with closely apposed nuclei just below the cnidoglandular cap, giving the filament a 

distinct pattern (Fig. 4D). Other filaments contained prominent mesogleal pleats, 

scattered eosinophilic granular cells, and mucous cells giving them a moth-eaten 

appearance. Occasional filaments at the base of the branch contained ovarian tissue. 

Cnidoglandular caps of all filaments contained eosinophilic granular cells. The 

calicoblast was uniformly cuboidal to squamous, closely apposed to gastrodermis, and 

contained scattered desmoid processes. 

Montipora patula 

Colonies were plate-like to encrusting, with purple polyps interspersed among a 

network of yellow trabeculae (Fig. 4E). Epithelium overlying coenosarc was composed 

of a single layer of columnar cells with basal nuclei and interspersed with occasional 

mucus cells. Epithelium overlying tentacles contained localized batteries of spirocysts 

(Fig. 4F), which gave way to small clusters of eosinophilic granular cells in the 

stomodeum. 

The mesoglea was barely visible in the coenosarc and tentacles, but became more 

prominent along with mesogleal pleats within gastrovascular canals at the base of polyps. 

Occasional eosinophilic granulocytes characterized by cells with an eccentric nucleus and 

distended by intracytoplasmic accumulations of brightly eosinophilic granules were seen 

within the mesoglea of the gastrovascular canal. 

The coenosarc gastrodermis was cuboidal, contained numerous zooxanthella, and 

was closely apposed to squamous calicoblast layer. Within gastrovascular canals, 

gastrodermal cells were cuboidal or focally hyperplastic and apposed to squamous 

calicoblastic cells. The gastrodermis contained scattered zooxanthellae. Mesenteric 

filaments deep within canals contained batteries of macrobasic mastigophores (a type of 
218 

nematocyst). Other mesenteric filaments were composed of closely apposed columnar 

cells mixed with mucus cells and eosinophilic granular cells. Occasional ova were noted 

within filaments. The skeleton contained mats of gray to amphophilic branching 

filaments (probable endolithic algae). 

Montipora capitata 

Colonies were placoid to branching, brown, with a verrucose surface containing 

polyps interspersed among a network of trabeculae. Epithelium overlying coenosarc was 

simple columnar interspersed with occasional clear mucus cells. Epithelium overlying 

tentacles was pseudostratified columnar with numerous large glandular cells giving it a 

vacuolated appearance. Batteries of spirocysts were noted near the base of tentacles, and 

these disappeared in the stomodeum and were replaced by closely packed columnar cells 

with a ciliated surface. Deeper into the stomodeum, there were clumps of eosinophilic 

granular cells near the central lumen. Mesoglea was uniformly thin and bereft of cells 

except near base of polyps or near mesenteric filaments where mesogleal pleats were 

noted. 

The coenosarc gastrodermis was simple to pseudostratified cuboidal and contained few 

zooxanthellae. Zooxanthellae were much more numerous within gastrodermis of tentacles. 

Within gastrovascular canals, gastrodermis was squamous and focally hyperplastic with few 

zooxanthella and occasional ovarian tissue. Mesenteric filaments were composed of closely 

apposed columnar cells interspersed with aggregates of red granular cells at cnidoglandular caps, 

and occasional mucus cells giving the filament a moth-eaten appearance. Batteries of macrobasic 

mastigophores were occasionally noted within the gastrodermis. Planulae, characterized by three 

layers of cells (ciliated columnar cells, mesoglea, and gastrodermis) surrounding a lumen were 

sometimes seen in the gastrovascular canal. Calicoblastic epithelium was uniformly squamous. 

Pocillopora eydouxi 

Colonies were composed of tan to cream upright flattened branches with a 

verrucous surface containing haphazardly arranged corallites (Fig. 7 C-D). Coenosarc 

epithelium was composed of a single layer of ciliated columnar cells. Over the tentacles, 

columnar cells were prominent and mixed with batteries of spirocysts, which disappeared 

within the stomodeum and were replaced by closely apposed ciliated columnar cells. 

Coenosarc mesoglea was thin and not discernable but widened and contained mesogleal 

pleats, particularly around polyps and within tentacles. 

Gastrodermis was squamous to cuboidal and contained focally aggregated 

zooxanthellae, which were more numerous within tentacles. Gastrovascular canals 

formed a single layered parallel network below the external epithelium. Mesenteric 

filaments consisted of closely apposed columnar cells mixed with eosinophilic granular 

and mucus cells with rare zooxanthella. The calicoblast was squamous with focal 

hypertrophy where cells took on a columnar appearance. 

Lesions: 

Any anomaly in gross skeletal or tissue morphology was classified as a lesion. 

Lesions in A. cytherea were categorized into five groups (Fig. 5): purple bleaching, 

yellow bleaching, brown blotch, growth anomalies, and brown band. Purple bleaching 

(Fig. 5A-B) referred to areas of coral that were bleached with a raised light to dark purple 

margin, giving the entire lesion a bluish hue. This lesion usually surrounded a variably 
219 

sized central area of dead coral overgrown by algae. Polyps near the edge of these 

lesions appeared atrophied or entirely missing. Yellow bleachings (Fig. 5C-D) 

designated dwell-defined areas of bleached coral with a yellow hue and no distinct raised 

margin. These areas were separated from live coral and often had incipient algal growth 

on coral tissue. Brown blotch corresponded to single well-defined circular dark brown 

lesions on coral tables, usually near the middle of the plate, and was characterized by a 

film of brown mucoid material surrounded by apparently normal coral tissue. Growth 

anomalies (Figs. 5E, 6, 7A-B) included any abnormal growths of the coral skeleton. 

Brown bands (Fig. 5F) were slice-shaped areas of dead coral overgrown with algae 

demarcated from adjacent normal coral by a distinct band of bleached tissue 

Growth anomalies in A. cytherea were of 3 types: Grossly, type 1 (Figs. 5E, 6AB) growths were focal to coalescing, white to pink, and rugose, and tissue covering these 

masses was smooth and bereft of polyps. On histology (Fig. 6C), coenosarc epithelium 

was markedly hyperplastic and characterized by numerous pseudostratified columnar 

cells. Polyps were absent or manifested by rare batteries of spirocysts. The mesoglea 

was enlarged, and gastrodermal cells adjacent to epithelium were markedly hyperplastic 

to anaplastic, pleomorphic, and characterized by stellate nuclei, and widened intercellular 

spaces. Gastrodermis of gastrovascular canals was focally hyperplastic with clumps of 

proliferating cells free or projecting within the lumen of canals. Based on these 

characteristics, this lesion was considered neoplastic and classified as a gastrodermal 

neoplasm. Zooxanthellae were rarely seen. In some instances, calicoblast cells appeared 

enlarged and hypereosinophilic with swollen nuclei. Rare mesenteric filaments 

containing macrobasic mastigophores were noted. 

Type 2 growths (Fig. 6D-E) were focal to coalescing, pink, with numerous 

cylindrical tubercles with an apical indentation. Tissue overlying these growths was 

generally bereft of polyps save for occasional single tentacles. On histology, (Fig. 6F) 

there was marked hyperplasia of coenosarc epithelium with cleft formation and 

thickening of mesoglea. Coenosarc gastrodermis was composed of simple columnar cells 

and that of gastrovascular canals was cuboidal and focally hyperplastic. Zooxanthella 

and mesenteric filaments were rarely seen. Calicoblast layer was uniformly squamous. 

Type 3 growths (Fig. 7A) consisted of smooth, well-defined, sessile white firm 

growth arising from normal skeleton. Tissue overlying these growths lacked 

zooxanthella. On histology, tumor tissue was characterized by a markedly hyperplastic 

epithelium bereft of polyps. Coenosarc gastrodermis was largely bereft of zooxanthella 

and focally hyperplastic with stellate nuclei. Within gastrovascular canal, gastrodermal 

cells, particularly those associated with mesenteric filaments, were hyperplastic, 

fibroblast-like and pleomorphic forming papillary projections into the gastrodermal 

cavity. Myonemes within occasional mesenteric filaments were enlarged and 

occasionally diffusely necrotic. Diffusely, calicoblast was squamous and focally 

hyperplastic. Based on pleomorphic appearance of gastrodermal cells and cellular 

necrosis, these growths were classified as gastrodermal neoplasms. 

Pocillopora eydouxi 

Grossly, lesions were characterized by exuberant growth of skeleton overlaid by 

apparently normal tissue (Figs. 7D-E). These were seen in one location on the north 

lagoon and Site 3. On histology, no significant lesions were noted save for markedly 
220 

atrophied epithelium and absence of polyps and zooxanthella within coenosarc. One 

normal appearing colony from the northern lagoon that contained variably sized, well 

defined, round aggregates of deeply basophilic filamentous organisms (probable bacteria) 

within tentacular epithelium (Fig. 7F). 

Montipora patula, Montipora capitata 

Grossly, lesions were characterized by single to coalescing well-defined firm 

smooth to rugose white nodules ranging in size from ca. 0.5-5 cm diameter. In some 

instances, the center of the lesion was ulcerated and colonized by filamentous algae. 

These lesions were seen sites 1-4 and did not appear particularly numerous at any one site 

(Fig. 8A-B, D-E). 

On histology, large mats of variably sized eosinophilic filamentous organisms 

displaced coral tissue. Epithelium of adjacent coral was cuboidal to simple columnar, 

and gastrodermal cells were hyperchromatic with shrunken cytoplasm. The mixed 

population of filamentous branching structures was largely limited to the skeleton and 

ranged in invasiveness from localized penetration into gastrovascular canals to complete 

invasion and effacement of tissue architecture. In some cases, the filamentous material 

encompassed fragments of degenerating gastrodermis. In other cases, these nodules were 

composed of granular gray material overlaid by cells with cell walls (plant material) (Fig. 

8C). The center of the nodule occasionally contained an invertebrate (metazoan) of 

unknown identity (Fig. 8F). 

Distribution: 

Lesions (all types) in Acropora cytherea were more numerous in the areas where this 

species was dominant (Fig. 9). Purple bleaching, yellow bleaching, brown band, growth 

anomalies, and brown blotch made up 57%, 38%, 2%, 2%, and 0.5%, respectively of the total 

(555) number of lesions seen. There did not appear to be a pattern to the distribution of the major 

types of lesions (Figs. 10-12). In addition to manta tow survey areas, purple and yellow 

bleaching was seen during spot dives in sites 1-5 and growth anomalies were noted in sites 1 and 

2 (Fig. 1) 

Pigment profiles

A. cytherea (n=10)

0

0.5

1

1.5

2

2.5

3

3.5

4

200244288332376420464508552596640684

nm

Mean OD

MeOH

Buffer
221 

Peaks at ~230, 290, and 325 nm were seen for both methanol and buffer soluble 

pigments while peaks at 441 and 665 (Chlorophyll) were seen in methanol extracts only. 

DISCUSSION 

Distribution of corals and lesions 

Distribution of corals in our survey area appeared similar to that observed by 

Maragos and Jokiel (1986). Although a variety of lesions were seen in different coral 

species, no distinct distributional pattern was recognized. The distribution and extent of 

lesions in A. cytherea was a function of coral abundance, and the most widespread lesion 

(purple bleaching), appeared to be a normal process ofsenescence, because this lesion 

was usually located adjacent to dead coral near the center of the plates. This area of dead 

coral seemed to expand as the plates became larger, whereupon they would collapse. 

Diffuse purple bleaching was noted on the underside of many collapsed colonies. 

Yellow bleaching was associated with incipient algal overgrowth and was noted 

wherever A. cytherea was present, including deep (80 ft.) habitats such as Donovan’s 

reef. Contrary to expectations, skeletal growth anomalies in A. cytherea and other 

species of corals did not appear concentrated in areas contaminated with tumor-inducing 

compounds such as organohalogens (Site 2) or plutonium (Site 3). Although rare growth 

anomalies in A. cytherea were seen in Site 2, coral in the general area appeared 

particularly healthy. 

Growth anomalies were noted in 4 species of corals (A. cytherea, P. eydouxi, M. 

patula, and M. capitata), however, in only two instance were these growth considered 

neoplastic (cancerous). Documented instances of neoplasms in corals are rare, and those 

that are documented mostly involve description of skeletal growth anomalies in absence 

of histology (Peters et al., 1986). In the most complete description of growth anomalies 

in a coral, Peters et al. (1986) concluded that growths in A. palmata were calicoblastic 

epitheliomas based on locally invasive skeletal protuberances with associated 

proliferation of calicoblast and associated tissues. In vertebrates, neoplasms are defined 

by uncontrolled proliferation of tissue with cells that exhibit abnormal morphology 

including nuclear or cytoplasmic polymorphism and, on occasion, mitotic figures and 

tissue necrosis (indicating rapid cell division) (Cheville, 1988). This is opposed to 

hyperplasia where cell growth is excessive but controlled, and where cell morphology is 

not abnormal. The definition of neoplasias in invertebrates is less clear, and some cases 

of neoplasia in invertebrates could also be interpreted as hyperplasia (Sparks, 1985). 

In this study, growth anomalies needed to fulfill two criteria to warrant a 

diagnosis of neoplasia: 1) abnormal and excessive growth of skeleton and 2) cellular 

proliferation accompanied by cell anaplasia and polymorphism. In A. cytherea, only two 

growth anomalies (Type 1 and 3, Figs. 11 A-B) were neoplastic. The other growth 

anomalies (Type 2) were classified as hyperplasia. No organisms were seen in tissue 

associated with growth anomalies in A. cytherea, and the cause of such lesions remains 

unknown. Interestingly, tumors that appeared different in gross appearance (Types 1 and 

3) were both considered neoplasm of the same tissue type (gastrodermis). Tumors 

similar in appearance to Type 3 growths were seen in a tabular Acropora from a shallow 

site in an embayment in Oman and were classified as calicoblastic neoplasms (Coles and 
222 

Seapy 1998). Given the simple anatomic plan of corals (4 tissue layers), it is perhaps not 

surprising that the same tissue type would give rise to different tumor morphs. There is, 

however, a clear need for continued refinement of classification of coral neoplasms. 

Future investigations might focus on molecular markers for different tissue types in 

corals to better differentiate the tissue origin of tumors. Given the uncertain state of 

classification of coral neoplasia, speculation as to potential causes of these lesions seems 

unwarranted. In higher organisms, causes of neoplasia typically include viruses, ongoing 

damage to DNA from chronic trauma or senescence, and certain environmental 

contaminants. 

Skeletal growth anomalies in Montipora sp. were responses to foreign agents 

including fungi, algae, and intra-skeletal metazoans (invertebrates). The coral skeleton 

harbors a variety of metazoans, filamentous algae, and fungi, and in most cases, these do 

not invade coral tissue. Le Campion-Alsumard et al. (1995) demonstrated that invasion 

of tissue by these organism is kept in check by a continuous process of mineralization. In 

some cases, however, this process fails and algae and fungi colonize live tissue. 

Interestingly, tissue reaction (necrosis) was minimal in spite of invasion of the 

gastrovascular canal by algae. Colonies of bacteria were seen in tissue associated with 

skeletal anomalies in P. eydouxi , however, this was not consistent. Thus, the cause of 

such anomalies in this species remains unknown. 

In the pigment profiles for A. cytherea, peaks in the methanol extracts at 441 and 

665 nm corresponded to chlorophyll (Dustan, 1979). Various coral proteins (UV 

pigments)were probably responsible for the peaks below 400 nm (Dove et al. 1995). 

Fluorescent pigments have been shown to be protective against sunlight for several 

species of Australian corals (Salih et al. 1998; 2000) and determination of fluorescent 

pigment properties may prove useful in future investigations of coral health. This 

pigment profile should provide a baseline to investigate future events of bleaching or 

pigment abnormalities in A. cytherea. 

RECOMMENDATIONS 

1. There needs to be a better method to quantify lesions on reefs during broad scale 

surveys. Surveys of lesions are complicated by the three dimensional nature of 

coral reefs and the intermixing of species. Ideally, it would be useful to have 

percent coverage of different species. Surveys would be targeted in such a way as 

to calculate percent of area of coral x covered by lesion y. Possible tools to 

consider for this include quadrats or video transects. 

2. Pigment profiles of corals with lesions, particularly growth anomalies, should be 

evaluated to further define whether pigments or their absence plays a role in 

genesis of these anomalies. 

3. Consider measuring growth anomalies using manual methods or photogrametry 

and following growth through time (months, years) to determine whether or not 

they are growing uncontrollably or remain unchanged. 

4. Additional criteria are needed to determine exactly what constitutes neoplasia in 

corals. 
223 

5. Most efforts on this trip focused on growth anomalies. It would be useful to 

examine other lesions in Acropora (brown blotch, yellow bleach, purple bleach, 

brown band) in more detail to evaluate potential causative factors. 

References: 

Amerson, A. B. and P. C. Shelton. 1976. The natural history of Johnston Atoll, Central 

Pacific Ocean. Atoll Research Bulletin 192: 1-480. 

Barszcz, C. A. and P. P. Yevich. 1975. The use of Helly’s fixative for marine 

invertebrate Histopathology. Comparative Pathology Bulletin. 7:4. 

Brock, V. E., R. S. Jones and P. Helfrich. 1965. An ecological reconnaissance of 

Johnston Island and the effects of dredging. Annual report. Univ. of Hawaii, Haw. 

Inst. Mar. Biol., HIMB Tech. Rep. No. 5, Honolulu. 

Brock, V. E., W. van Heukelem and P. Helfrich. 1966. An ecological reconnaissance of 

Johnston Island and the effects of dredging. Second annual report. Univ. of 

Hawaii, Hawaii Inst. Mar. Biol., HIMB Tech. Rep. No. 11, Honolulu. 

Cheville, N. F. 1988. Introduction to veterinary pathology. Iowa State University Press, 

537 pp. 

Cohen, A. L., P. S. Lobel, and G. L. Tomasky. 1997. Coral bleaching on Johnston 

Atoll, Central Pacific Ocean. Biological Bulletin 193:276-279. 

Coles, S. L. and D. G. Seapy. 1998. Ultra-violet absorbing compounds and tumorous 

growths on acroporid corals from Bandar Khayran, Gulf of Oman, Indian Ocean. 

Coral Reefs 17: 195-198. 

Coles, S. L., R. C. DeFelice, and D. Minton. 2001. Marine Species Survey of Johnson 

Atoll, Central Pacific Ocean, June 2000. Bishop Museum Technical Report No. 

19, 58 pp. 

Dove, S. G., M. Takabayashi, and O. Hoegh-Guldberg. 1995. Isolation and partial 

characterization of the pink and blue pigments of pocilloporid and acroporid 

corals. Biological Bulletin. 189:288-297. 

Dustan, P. 1979. Distribution of zooxanthellae and photosynthetic chloroplast pigment 

in the reef building coral Montastrea annularis Ellis and Solander in relationship 

to depth in a West Indian coral reef. Bulletin of Marine Science 29:79-95. 

English, S., C. Wilkinson, and V. Baker. 1994. Coral Reefs. In. Survey manual for 

tropical marine resources, Chapter 2. Australian Institute of Marine Science, 

Townsville, Australia, pp. 5-117. 

Le Campion-Alsumard, T., S. Golubic, and K. Priess. 1995. Fungi in corals: a 

symbyosis or disease? Interaction between polyps and fungi causes pearl-like 

skeleton biomineralization. Marine Ecology Progress Series. 117:137-147. 

Maragos, J. E. and P. L. Jokiel. 1986. Reef corals of Johnston Atoll: One of the world’s 

most isolated reefs. Coral Reefs 4:141-150. 

Peters, E. C., J. C. Halas, and H. B. McCarty. 1986. Calicoblastic neoplasms in 

Acropora palmata, with a review of reports on anomalies of growth and form in 

corals. Journal of the National Cancer Institute. 76:895-912. 

Salih A., O. Hoegh-Guldberg and G. Cox. 1998. Photoprotection of symbiotic 

dinoflagellates by fluorescent pigments in reef corals. In: Greenwood, J.G. and N. 

J. Hall, (eds.) Proceedings of the Australian Coral Reef Society 75th Anniversary 
224 

Conference, Heron Island October. School of Marine Science, The University of 

Queensland, Brisbane, Brisbane, Australia, 

Salih, A., A. Larkum, G. Cox. M. Kuhl, and O. Hoegh-Guldberg. 2000. Fluorescent 

pigments in corals are photoprotective. Nature. 850-853. 

Sparks, A. K. 1985. Synopsis of invertebrate pathology. Elsiever Science Company, 

423 pp. 

 
225 

 

Figure 1. Johnston Atoll: Location of spot dives (see methods for details). 

Figure 2. Percent coral cover observed during manta tows of North lagoon, 

Johnston Atoll. 

 
226 

Figure 3: Dominant species of corals seen during manta tows of north lagoon. 

 
227 

Figure 4. A-D) A. Cytherea; C) Coenosarc, bar= 50 μm; D) Gastrovascular canal (v) 

and mesenteric filaments (m), bar=100 μm; E-F) M. Patula; F) Polyp, bar= 100 μm. 

Epithelium (e), gastrodermis (g), calicoblast (c), zooxanthella (z), mesenteric 

filaments (m), tentacle (t), spirocysts (s), eosinophilic granulocyte (r). 

 B

 

m

e 

v 

s 

t

r 

c 

g 

v 

z 

A

C D

E F 
228 

Figure 5. A. cytherea. A) Purple bleaching; B); Purple bleaching-note atrophied 

polyps; C) Yellow bleaching; D) Yellow bleaching-note algal filaments; E) Growth 

anomalies; F) Brown band. 

 

 

 

D 

F 

A B 

C

E 
229 

Figure 6. A. cytherea. A-B) Type 1 growths, note absence of polyps; C) Note 

markedly hyperplastic epithelium and pleomorphic and hyperplastic gastrodermis 

(arrows), bar = 50 μm. D) type 2 growths (arrows); E) note malformed polyps with 

single tentacle (arrows); F) Note markedly hyperplastic epithelium with cleft 

formation (arrow) bar=200 μm. Epithelium (e), gastrodermis (g). 

 

D

A B

e 

e 

g 

C

E F 
230 

Figure 7. A-B) A. cytherea; D-F), P. eydouxi; A) Type 3 growth; B) Note marked 

pleomorphism of gastrodermal cells in tumor tissue (arrow), bar= 100 μm. C, E) 

growth anomalies (arrow) and normal coral (D); F) Polyp of normal appearing P. 

eydouxi, note bacterial colonies in epithelium (arrows) bar=50 μm. 

D 

E F 

A B 

C 
231 

Figure 8. A-C) M. patula, D-F) M. capitata; A-B) growth anomalies (arrow); C) 

note invasion of skeleton and tissue with filamentous organisms (algae and fungi) 

arrow, bar= 200 μm; D-E) growth anomalies; F) note cross section of metazoan 

(arrow), bar=200 μm. 

F

A

B

D

C

E
232 

Figure 9. Number of lesions in A. cytherea observed during each manta tow interval. 

Figure 10. Number of instances of purple bleaching during each manta tow 

interval. 

 
233 

Figure 11. Number of instances of yellow bleaching seen during each 

manta tow interval 

Fig 12. Number of instances of aberrant growth (blue) or brown band 

(violet) seen during each manta tow interval. Large dots=2, small dots=1. 
234 

CORAL DISEASE ON THE GREAT BARRIER REEF AND IN THE WESTERN 

PACIFIC

1

Bette L. Willis, 1Cathie Page, 2David Bourne, 3Leigh Owens, 1Shelley Anthony,

1

Holly Boyett, 1Elizabeth Dinsdale, 4Drew Harvell, 4Dean Jacobson, 1,3Carole 

Lonergan, 1,2Stephan Neale, 1

Caroline Palmer, 6Laurie Raymundo, 1,2Meir Sussman 

1

ARC Centre of Excellence for Coral Reef Studies, School of Marine Biology and Aquaculture, 

James Cook University, Townsville, Qld, 4811, Australia. 

2

Australian Institute of Marine Science, PMB No 3, Townsville, Qld 4180, Australia. 

3 School of Microbiology and Biomedical Sciences, James Cook University, Australia 

4

Cornell University, USA; 5College of the Marshall Islands; 6University of Guam, USA 

Background 

Until recently, it was assumed that disease has had little impact on the population 

dynamics or community structure of coral assemblages on the Great Barrier Reef (GBR). 

However, prior to 2000 there were only two studies of coral disease in the region, one 

focused on black band disease (BBD; Dinsdale 2002) and the other on skeletal eroding 

band (SEB; Antonius 1999; Antonius and Lipscomb 2001), both undertaken at Lizard 

Island in the northern sector of the GBR. Further anecdotal reports of BBD (Miller 1996) 

and a white disease (Baird 2000), plus increasing abundance of white syndrome 

(described below) detected in a Long Term Monitoring Program begun in the early 

1990’s by the Australian Institute of Marine Sciences (AIMS) (Willis et al. 2004), 

highlighted the need for a more in-depth study of coral disease on the GBR. 

As an initiative of the GEF Coral Disease Working Group (DWG), surveys of 

coral disease were commenced in 2002 to more systematically assess the types and 

prevalence of coral disease on the GBR (Willis et al. 2004). Detection of some of the 

more common and infectious Caribbean diseases, in combination with discovery of 

diseases unique to the region (brown band disease: BrBD; Willis et al. 2004), suggested 

that coral disease occurs commonly on Indo-Pacific reefs and may have a greater role in 

structuring coral communities in the region than previously thought. Accordingly, a 7 

year program to assess the ecological significance of coral disease on the GBR has been 

funded by the Australian Research Council (ARC). Results summarized below describe 

progress 2.5 years into the program. In collaboration with the GEF DWG, survey 

protocols and knowledge gained on the GBR have been applied to reefs throughout the 

Western Indo-Pacific, including Palau, the Philippines, Marshall Islands, Papua New 

Guinea and Indonesia, plus imminently Zanzibar, Tanzania, Kenya, Mauritius, 

Madagascar, Seychelles and the Comoros as a consequence of a recent GEF Workshop 

on Coral Disease for local reef scientists and marine park managers (Zanzibar, April 

2006). 

Survey design, transect protocols and targeted disease studies 

Given the lack of baseline knowledge of coral disease on the GBR and the 

vastness of a reef system spanning north-south gradients more than 2000 km in length 

and cross-shelf (east-west) gradients in terrestrial influences up to 100 km across the 
235 

continental shelf, the region was divided into 3 sectors (northern, central and southern 

GBR) to optimize sampling a range of habitats and reef types. The sampling design 

comprises 3 belt and line intercept transects, at each of 2 sites, on each of 3 replicate 

reefs, in surveys at each of 3 cross-shelf positions (inner-, mid- and outer-reef positions) 

in the northern and central sectors, and at 1 cross-shelf (outer-reef) position in the 

southern sector. Transects are surveyed in summer, on the upper reef slope (typically 4-6 

metres) where species diversity tends to be highest. In total, 19 reefs have been surveyed 

annually since 2004 and 21 reefs since the full design was inaugurated in 2005. Surveys 

of 2 reefs in the northern sector in both summer and winter since 2002-03 have shown a 

clear pattern of increased disease prevalence in summer (Willis et al. 2004). 

The survey protocol developed to cope with species-rich, high-cover coral 

communities characteristic of Indo-Pacific reefs is based on a 20m x 2m belt transect 

combined with a 20m line intercept transect (LIT) to produce a concurrent estimate of 

percent coral cover. Belt transects of this size represent an efficient compromise between 

the need to survey a representative proportion of the species diversity and time 

constraints imposed by SCUBA surveys. Three replicate belt and LIT transects are 

typically completed within 1-2 dives (depending on percent cover) by a team of 2-3 

experienced divers. All colonies within the belt are examined, recorded as healthy, 

diseased or showing signs of compromised health (see final section below) based on 

macroscopic field signs, and identified to genus (plus growth form for the genus 

Acropora) or family for less common groups. Diseased colonies are identified to species, 

photographed, and samples collected for microscopic examination and histological 

investigation as appropriate. In selected cases, typically when disease outbreaks are 

encountered, samples for microbiological and molecular studies are collected to isolate 

and identify pathogens. As evidence identifying the most common and virulent disease 

types has accumulated, more in-depth studies of selected disease types (SEB, WS, BBD, 

BrBD, AtN) have been initiated to quantify rates of progression across colonies, impacts 

on coral growth and reproduction, spread throughout populations and the effect of 

elevated temperature on these rates. 

Broad ecological surveys inform detailed studies of lesions, pathogens and 

population impacts

The focus of the ARC-funded program is changing from its current emphasis on 

broad ecological surveys to more in-depth manipulative, microbiological and molecular 

studies of selected disease types as the research progresses. The objective is to use 

ecological surveys to provide the context for selection of disease types for more focused 

research. his overarching research plan recognizes the need to start with imperfect tools, 

i.e. observations of macroscopic disease signs underwater, as the first step in progressing 

research on under-studied Indo-Pacific coral diseases. Through extensive field surveys at 

diverse sites and through time, experienced coral biologists are well-placed to make 

informed decisions about the most prevalent and/or virulent disease types that should be 

targeted for further study. To carry this research to the next level, collaboration with 

biomedical histologists, microbiologists and molecular biologists have been developed. 

As knowledge of disease types is refined, diagnostic tools can be developed that will, in 

turn, refine ecological surveys. The importance of maintaining long-term monitoring 

programs cannot be over-stated, as these are the key to determining whether disease 
236 

incidence is changing through time and for developing hypotheses in relation to potential 

drivers. 

In recognition of the early stage of Indo-Pacific coral disease research, we 

advocate the use of this integrated, collaborative approach to advance current 

understanding of coral diseases in the region. It is hoped that this meeting will be 

instrumental in developing further collaborations and a unified approach among research 

teams throughout the Indo-Pacific to strengthen and coherently build current 

understanding of coral disease in the region. 

Recognizing and standardizing the naming of Indo-Pacific disease types 

The issue of naming diseases when little is known apart from macroscopic and 

microscopic signs of disease is problematic. We support schemes under development to 

apply a structured approach to the description of gross lesions and the naming IndoPacific coral diseases (T. Work, G. Aeby, pers. comm.), with one additional pragmatic 

consideration. Whilst it would be ideal to incorporate the host species or genus of coral 

into each disease name, this approach becomes cumbersome when dealing with the more 

than 580 species and 200 genera of Indo-Pacific corals. An approach whereby disease 

names, at least initially, are applied to all corals exhibiting the same signs, avoids an 

unwieldy system for field surveys and researcher training purposes. Recording the names 

of coral species plus detailed descriptions for all records of disease retains species-level 

information in the event that diseases are later found to be specific to coral species. 

Refinement of disease names as histological, microbiological and molecular studies link 

pathogens to macroscopic field signs provides the foundation for an iterative approach to 

the development of definitive disease names. Figure 1 shows results for surveys of 

disease prevalence in the central and northern GBR using the above naming protocol. It 

is based on recognition of the following disease types in surveys on the GBR. All disease 

types have been detected in surveys on other western Indo-Pacific reefs. 

Black Band Disease (BBD): BBD is widespread throughout the GBR, occurring on more 

than 70% of reefs surveyed (n=19) and in all 3 sectors, although its prevalence is 

typically low (~0.1% of scleractinian corals) (Page and Willis 2006). It has been 

recorded on at least 32 coral species in 10 families, with branching pocilloporid and 

acroporid corals being important hosts on the GBR (Willis et al. 2004). On reefs in 

Palau, a reddish band of cyanobacteria on Pachyseris speciosa and Porites sp. has been 

identified as having the same ribotype as cyanobacteria producing macroscopic signs of 

BBD on Montipora sp. (Sussman et al. 2006). Further evidence is required before the 

potential status of red band as a separate syndrome can be assessed (Sussman et al. 2006). 

Skeletal Eroding Band (SEB): SEB, caused by the protozoan, Halofolliculina 

corallasia, erodes the tissue and skeleton of corals as it produces a black lorica or test 

(Antonius 1999). Clusters of ciliates along the tissue-skeleton interface produce a black 

band similar in appearance to black band disease, but, unlike the uniformly white 

skeleton exposed as BBD advances, the skeleton behind the advancing SEB is speckled 

with the remains of empty black loricae (Antonius and Lipscomb 2001). Progression of 

SEB can be relatively slow, approximately 1 mm per week, further distinguishing it from 

BBD, but it may also advance at rates up to 1 mm per day, comparable to BBD (Antonius 
237 

and Lipscomb 2001). SEB affects at least 31 species of corals in 6 families on the GBR. 

Recent records of a different species of Halofolliculina causing similar signs on 25 corals 

in 6 families from the Caribbean suggest that halofolliculinid infections affect corals on 

reefs globally (Croquer et al. 2006). 

White Syndrome (WS): WS is a collective term for conditions producing white signs on 

corals from the GBR and Indo-Pacific reefs (Willis et al. 2004). Given the difficulty of 

consistently identifying features such as the variable zone of bleached tissue that 

distinguishes white band II (WBII) from white band I (WBI) or differences in the rates of 

movement that distinguish the faster moving white plague II (WPII) from white plague I 

(WPI; reviewed in Richardson 1998), we have elected to use the term white syndrome to 

describe conditions resulting in progressive loss of tissues to expose skeleton in white 

bands behind a moving front of tissue loss (Willis et al. 2004). A band of white bleached 

tissue may be present at the tissue-skeleton interface. The role of potentially secondary 

pathogens, like ciliates (see brown band description below), in possibly obscuring 

bleached zones as rates of tissue loss escalate, requires further investigation. 14C studies 

near lesion boundaries on tabular Acropora’s in the southern GBR suggest that 

photoassimilates are preferentially translocated away from lesions in an apparent shutdown reaction, potentially as a result of abiotic factors or pathogens triggering an 

apoptotic reaction in the host (Roff et al. 2006). 

In addition to WBI/II and WPI/II, white syndrome could potentially encompass 

white pox (Patterson et al. 2002) and even shut down reaction (Antonius 1977). However, 

WS is distinguished from feeding scars by the narrow width of the zone of recently 

exposed, white skeleton and the relatively regular appearance of the tissue front. These 

features are in contrast to the wide zone of white skeleton commonly exposed following 

Acanthaster planci predation and the scalloped or wavy tissue front produced by 

Drupella spp. Determining the relationship(s) between the Caribbean white diseases and 

WS and applying the appropriate name(s) will not be possible until potential pathogens 

are isolated and compared to those producing white symptoms in Caribbean corals 

(Sussman et al. in prep.). 

WS has been recorded for 17 species of corals in 4 families on the GBR, with 

species of Acropora being important hosts (Willis et al. 2004). Dramatic increases in 

abundance of WS on the GBR, by up to 20-fold on some outer-shelf reefs in the northern 

and southern sectors in 2002/03, suggest that the prevalence of WS may be increased by 

elevated temperatures when host densities are high (Selig et al. in press). Reports of a 

more than 50% increase in the prevalence of WS (from 8.55% to 13.58%) at a subtropical reef south of the GBR in 3 months following the summer of 2003 (Dalton and 

Smith 2006) provide further evidence of a correlation between aggregated distributions 

and high densities of hosts and WS prevalence. 

Brown Band Disease (BrBD): BrBD is a new syndrome and has been recorded on corals 

in all 3 sectors of the GBR (Willis et al. 2004, unpubl. data). The distinctive macroscopic 

field symptom is a brown zone of variable width, flanked by healthy tissue at the 

advancing front and exposed white skeleton at the trailing edge as the band progresses 

over the surface of the colony. There is often a white zone between the healthy tissue and 

brown band, which may comprise bleached tissue and/or denuded skeleton. Dense 
238 

populations of ciliates, packed with zooxanthellae from engulfed coral tissue, cause the 

brown coloration of the band. As densities of ciliates decrease, the zone becomes lighter 

and may appear white at very low ciliate densities. In these latter cases, the condition 

would be assigned to the WS category based solely on field observations. The possibility 

that BrBD ciliates represent a secondary infection following tissue necrosis induced by a 

primary pathogen requires further investigation. At high densities, however, the ciliates 

become the primary agent of tissue loss. BrBD has been reported on 16 species from 3 

families on the GBR, with acroporid corals being important hosts (Willis et al. 2004). 

Note that an earlier report of a brown band on a colony of Acropora formosa

(Dinsdale 1994) referred to a different, but unknown syndrome, and has subsequently 

been mistakenly quoted as affecting 20 coral species on the GBR (Santavy and Peters 

1997; Borneman 2001). While it is possible that the unknown syndrome was caused by a 

cyanobacterium similar to the one causing red-band disease in the Caribbean as suggested 

by Santavy and Peters (1997), in the absence of the specimen it is not useful to speculate 

further about this isolated observation; it is not to be considered a record of BrB as 

described here. 

Coral Tumors: Hyperplasia’s, manifesting as raised masses projecting about 4.5 cm 

above the surface of the colony, were reported to affect 18-24% of populations of 

Platygyra pini and P. sinensis on Magnetic Island, central GBR (Loya et al. 1984). 

Tumors were associated with increased growth rates of polyps and a general proliferation 

of all cell types, some atrophied and others normal, but in all cases macroscopic polyp 

structures were discernible and tissues remained pigmented (Loya et al. 1984). Bleached 

neoplasms, manifesting as white, globular masses of skeleton raised above the surface of 

the colony with few discernible polyp structures, are most common on acroporid corals 

on the GBR (Willis et al. 2004). Bleached neoplasms, mainly on corals in the family 

Acroporidae, have been reported from throughout the Indo-Pacific, i.e. from Guam and 

Enewetak (Cheney 1975), French Polynesia (Le Champion-Alsumard et al. 1995), Japan 

(Yamashiro et al. 2001) and the Gulf of Oman (Coles and Seapy 1998). 

Porites ulcerative white spots (PUWS): PUWS is characterized by discrete bleached 

round foci, 3-5mm in diameter, that may either regress or progress to full tissue 

ulcerations that coalesce, occasionally resulting in colony mortality (Raymundo et al. 

2003). Definitive cases have not yet been identified from the GBR. 

Atramentous Necrosis (AtN): AtN is characterized by spreading lesions of blackened, 

dead tissues and has primarily been recorded on a Montipora species in the central GBR 

(Jones et al. 2004). Further observations indicate that there are 4 stages in the progression 

of the disease (Anthony et al. in prep). The first stage involves multi-focal areas of 

bleached tissue, 1-2 cm in diameter, often in depressions on the colony surface. In phase 

2, the bleached tissue degenerates, leaving an area of bare, white skeleton. In phase 3, 

areas of bare skeleton are covered with a white, anoxic bacterial film. In phase 4, a black 

deposit accumulates under the white film, giving the lesion a grayish appearance (the 

stage described by Jones et al. 2004). 
239 

Cyanobacterial Syndromes (other than BBD): These include cases of unidentified 

cyanobacteria that appear distinct, both in colour and morphological dimensions, from 

BBD-associated cyanobacterial filaments. Cyanobacteria aggregate along fronts at the 

interface between exposed skeleton and tissue and are associated with tissue mortality 

(Willis et al. 20004). 

Gorgonian Black Necrosing Syndrome: Little is known about gorgonian diseases on the 

GBR. The only study of GBR gorgonians to date reports that 10% of populations of Isis 

hippuris on Davies Reef were infected with a fungal disease that manifested as black 

necrotic areas and led to loss of both tissues and skeleton (Morrison-Gardiner 2001). 

Although two species of Penicillium isolated from infected gorgonians were able to infect 

healthy colonies of I. hippuris and Pinnigorgia sp., and could be re-isolated, they did not 

produce the typical symptoms of the disease (Morrison-Gardiner 2001). Black necrotic 

patches have also been observed on gorgonians at Lizard Island and have been referred to 

as black necrosing syndrome (Willis et al. 2004). 

Indicators of Compromised Health 

Pigmentation responses: Species of Porites, in particular, appear to respond to a variety 

of competitive, invasive and parasitic challenges by producing pink or purple 

pigmentation in coenosarc and polyps adjacent to sites of competitive interactions and 

lesions. Hence pink lines, rings, patches or spots are often visible in coral tissue 

bordering the margins of competing or boring organisms (Willis et al. 2004). The 

pigmentation appears to be part of a generalized response mounted by the coral to contain 

invading or competing organisms such as cyanobacteria (Ravindran and Raghukumar 

2002), polychaetes, molluscs, and the intermediate metacercariae stage of the digenetic 

trematode, Podocotyloides stenometra (Aeby 1998). Although most commonly observed 

on Porites, pigmentation responses have been observed on most genera. 

Algal overgrowth: Algal filaments growing directly on live coral tissue may result in 

small areas of bleaching and subsequent coral mortality or sediment may accumulate 

under the algae leading to small areas of bleaching and subsequent tissue loss (Willis et 

al. 2004). Such cases are differentiated from coral-algal competitive interactions where 

only occasional contact is made between the coral and algae. On reefs in the central 

GBR, examples that appear to cross the boundary between competitive interactions and 

disease include overgrowth of coral by (1) the filamentous algae, Coralliophila 

hurysmansii causing tissue swelling, and (2) by Anotrichium tenue, which traps mucus, 

sediments and possibly microbes damaging the underlying tissues (McCook et al. 2001). 

It is unclear at this stage whether some other stress or pathogen has previously weakened 

the corals’ resistance allowing algae to invade their tissues; hence such cases are 

categorized as an indication of compromised health (Willis et al. 2004). 
240 

Unusual bleaching patterns: Distinct and unusual patches, spots, stripes etc. of bleached 

tissue differ from typical patterns of whole colony bleaching or paling seen during 

thermal anomalies. The causes of these unusual bleaching patterns are unknown and it is 

unclear whether they are caused by specific stressors or pathogens, or if they represent 

more generalized stress responses. At present they are recorded as another indicator of 

compromised health. 

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Roff G, Hoegh-Guldberg O, Fine M (2006) Intra-colonial response to Acroporid “white 

syndrome” lesions in tabular Acropora spp. (Scleractinia). Coral Reefs 25:255-64 

Santavy D, Peters E (1997) Microbial pests: coral disease in the Western Atlantic. Proc 

8th Int Coral Reef Symp 1:607—612 

Sussman M, Bourne DG, Willis BL (2006) A single cyanobacterial ribotype is associated 

with both red and black bands on disease corals from Palau. Dis Aquat Org 69:111-

118 

Sweatman H, Cheal A, Coleman G, Delean S, Fitzpatrick B, Miller I, Ninio R, Osborne 

K, Page C, Thompson A (2001) Long-term monitoring of the Great Barrier Reef. 

Status report no 5, 106 pp 

Willis BL, Page CA, Dinsdale EA (2004) Coral disease on the Great Barrier Reef. In: 

Rosenberg E, Loya Y (eds) Coral health and disease. Springer, Berlin 
242 

V. PATHOLOGY AND EPIDEMIOLOGY

DISEASE AND THE DIAGNOSTIC PROCESS 

Gary Wobeser 

Canadian Cooperative Wildlife Health Centre, Department of Veterinary Pathology, Western 

College of Veterinary Medicine, University of Saskatchewan, Canada 

gary.wobeser@usask.ca 

It often is difficult to define health and disease, or to determine where one ends 

and the other begins. Definitions for these in humans are usually inappropriate for wild 

species, and death is a rather extreme endpoint to define disease in any species. One way 

of defining disease is on the basis of impairment of function. This allows consideration 

of effects on growth, behavior, reproduction, defense and survival as disease. Mild 

dysfunction, for which the organism can compensate, may fall within relative health, 

while more severe dysfunction represents disease. Dysfunction can be related to 

ecological fitness, and the concept can be extended to population effects. 

Disease, regardless of cause, begins with injury to individual cells. However, it is 

the reaction by the organism to cellular injury that results in the dysfunction that we 

recognize as disease. Disease is not synonymous with infection or exposure to an 

agent; an organism may be exposed or infected but if there is no reaction there will be no 

disease. 

Each organism has only a limited numbers of ways in which it can react to injury. 

Certain agents elicit a distinct pattern of reaction, but more than one agent may produce 

the same reaction. Diagnosis is the process of defining those features that distinguish a 

particular process from all others, i.e. distinguishing disease caused by agent A from that 

caused by agent B. Recognition of the pattern of reaction to injury is the basic 

feature for making a diagnosis in the case of disease. 

The first step in the diagnostic process is to form a working description or case 

definition of the condition. This definition represents the state of knowledge at the time; 

it is usually crude at the outset, and it becomes progressively refined as information is 

collected. It is not necessary to know the cause to make a case definition. A critical part 

of the case definition is characterization of the reaction of the organism to injury. This is 

the purview of the diagnostic pathologist. While there may be very few “coral 

pathologists”, there is no reason why description and analysis of the reaction to injury 

should be fundamentally different in coral than in other organisms. The case definition is 

the touchstone (“a criterion for the quality of a thing”) against which all subsequent 

portions of an investigation must be tested. For instance, if a condition in another location 

has a different reaction pattern, or a putative cause results in a different pattern of 

reaction, one should suspect that the conditions are not the same entity. 
243 

A small proportion of diseases are caused by a single agent that is both necessary 

and sufficient in itself to cause a clearly defined disease. A set of rules (Koch’s 

Postulates) often can be used to establish a cause–effect relationship in this type of 

disease. However, the great majority of diseases, in all species, are of more complex 

causation. Agents may cause disease under certain conditions but not under others, 

multiple agents may be required to produce disease, or several agents may independently 

cause similar disease. In many diseases there is a complex web of causation that may 

involve many inter-related factors. Disease must be considered in the context in which it 

occurs. Koch’s Postulates are generally inadequate for establishing cause-effect 

relationships, and other criteria that include epidemiological information are more 

appropriate. 

Investigation of disease involves answering five basic questions: Who? Where? 

When? What? and Why? It is impossible to predict in advance which disciplines or 

diagnostic techniques will be required to solve a problem and no one discipline is 

omnipotent. However, field and laboratory studies must be related back to the case 

definition (i.e., Are we looking at the same disease?) and the results should be used to 

refine the definition of the touchstone. 
244 

EVOLUTIONARY ECOLOGY AND DISEASE EMERGENCE: THE BIG 

PICTURE

Bruce Wilcox 

University of Hawaii 

Dept. Tropical Medicine 

561 Ilalo St. BSB 320 

Honolulu, HI 96813 

bwilcox@hawaii.edu 

Refer to: 

Wilcox, BA and Colwell, RR (2005). Emerging and Re-emerging Infectious 

Diseases: Biocomplexity as an Interdisciplinary Paradigm, EcoHealth 2: 1–14. 

http://www.springerlink.com.nuncio.cofc.edu/content/u318222415449460/fulltext.pdf 

ABSTRACT: Understanding factors responsible for reemergence of diseases 

believed to have been controlled and outbreaks of previously unknown infectious 

diseases is one of the most difficult scientific problems facing society today. 

Significant knowledge gaps exist for even the most studied emerging infectious 

diseases. Coupled with failures in the response to the resurgence of infectious 

diseases, this lack of information is embedded in a simplistic view of pathogens and 

disconnected from a social and ecological context, and assumes a linear response of 

pathogens to environmental change. In fact, the natural reservoirs and transmission 

rates of most emerging infectious diseases primarily are affected by environmental 

factors, such as seasonality or meteorological events, typically producing nonlinear 

responses that are inherently unpredictable. A more realistic view of emerging 

infectious diseases requires a holistic perspective that incorporates social as well as 

physical, chemical, and biological dimensions of our planet’s systems. The notion of 

biocomplexity captures this depth and richness, and most importantly, the interactions 

of human and natural systems. This article provides a brief review and a synthesis of 

interdisciplinary approaches and insights employing the biocomplexity paradigm and 

offers a social–ecological approach for addressing and garnering an improved 

understanding of emerging infectious diseases. Drawing on findings from studies of 

cholera and other examples of emerging waterborne, zoonotic, and vectorborne 

diseases, a ‘‘blueprint’’ for the proposed interdisciplinary research framework is 

offered which integrates biological processes from the molecular level to that of 

communities and regional systems, incorporating public health infrastructure and 

climate aspects. 
245 

EMERGING INFECTIOUS DISEASES

Stephanie Venn-Watson, D.V.M., M.P.H. 

U.S. Navy Marine Mammal Program, San Diego, California. Ph: 619.767.4335, stephanie 

@epitracker.com 

1.0 Background 

Newly emerging and re-emerging infectious diseases have been of increasing concern 

over the past 20 years (1-3). Global transportation of people, animals, and food supplies; 

increased interactions between wildlife, domestic animals and people; high-concentration 

populations; and the increase in the number people with compromised immune systems 

(AIDS/HIV and growing elderly populations) have all been identified as risk factors for 

emerging infectious diseases. This paper summarizes what has been learned from 

emerging infectious diseases in human and non-human animal populations; and provides 

preliminary recommendations for responding to emerging infectious diseases in Pacific 

coral reefs. 

2.0 Unique profiles of emerging diseases 

Emerging infectious diseases, by their nature, affect populations differently than nonemerging diseases. These differences may be considered when developing a strategy to 

prevent or respond to a population health event involving an emerging disease. The 

emergence of infectious diseases is most often due to 1) new pathogens, 2) changed 

indigenous pathogens, or 3) a compromised animal population. When a newly emerging 

infectious disease is introduced to a population, a large percentage of animals (if not all) 

may be immunologically naïve to the pathogen. As such, this pathogen is likely to cause 

rapid morbidity and/or mortality throughout the entire population. The rapid spread of 

the coronavirus causing Severe Acute Respiratory Syndrome (SARS) in China and other 

countries in 2003 demonstrates what can happen when a new disease affects an 

immunologically naïve human population (4). Newly emerging diseases may also affect 

multiple animal species concurrently; for example, during the Ebola virus outbreak in the 

Congo Republic in 2003, mortalities were reported in both gorilla and human populations 

(5); as another example, West Nile virus continues to cause concurrent morbidity and 

mortality in bird and human populations (6). Compared to newly emerging infectious 

diseases, re-emerging infectious diseases often occur due 1) a change in underlying 

factors within a population, or 2) acquired resistance of a pathogen to treatment. Both 

tuberculosis and toxoplasmosis became emerging infectious diseases due to the increased 

number of people with compromised immune systems from the AIDS/HIV pandemic. 

Methicillin-resistant Staphylococcus aureus (MRSA) emerged as a pathogen of concern 

due to its acquired resistance to multiple antibiotics. As such, re-emergence of a 

previously ‘quiet’ pathogen may indicate a more susceptible animal population or a new 

ability for the pathogen to resist natural or medical treatments. 
246 

For the reasons outlined above, emerging infectious pathogens are more likely to cause 

more severe disease in larger percentages of animal populations compared to established 

infectious diseases. Additionally, re-emerging diseases may indicate an 

immunocompromised population or an old pathogen with ‘new tricks’ to overcome 

natural or medical treatments. 

Challenges of emerging diseases 

There are four primary challenges to addressing the emerging disease issue. The first is 

the need to assess whether a disease is truly emerging or if case numbers are increasing 

simply due to improved detection and reporting capabilities. The second challenge is 

detection and characterization of a novel pathogen; if a pathogen is truly novel, 

identifying the appropriate diagnostic tools for detection can be difficult. Third, initial 

treatments for emerging diseases may be limited to supportive care and quarantine until 

the pathogen can be found; if the pathogen is a virus, treatment options will be limited, 

and a vaccine will not be readily available to prevent a pandemic. Finally, even if a 

disease is determined to be emerging, the etiological agent is found, and a treatment is 

identified, there remains a need to assess whether or not the emerging disease is a truly 

primary disease or if it is secondary to an underlying factor in the animal population. 

Responses to these challenges are outlined below. 

3.0 Addressing the challenges of emerging diseases 

Public and animal health agencies throughout the world have implemented targeted 

mitigation strategies to address the challenges of emerging diseases. Below are five 

activities that are commonly implemented to detect, track, prevent, and respond to 

emerging diseases. Any combination of these actions, if not already implemented, may be 

considered to help protect global and regional coral reef populations. 

3.1 Determine the baseline for population health. In order to determine if a 

disease is truly emerging, there is a need to determine the baseline for a 

population’s health. This baseline provides a statistical means of assessing 

significant differences in populations before, during, and after a potentially 

emerging disease. Determination of a population health baseline requires 

long-term collection of standardized health metrics in a population. 

3.2 Establish a standardized disease surveillance system that includes both 

pathogen-specific and syndromic surveillance. The surveillance system should 

routinely collect and report standardized data related to known diseases of 

concern. Additionally, it should enable detection and reporting of an emerging 

disease event in which the cause (etiology) is unknown; many countries use 

syndromic surveillance (e.g., incidence of respiratory illness or skin lesions) 

to detect and track emerging diseases. International, centralized surveillance 

systems are better at detecting emerging diseases compared to multiple, 

fragmented surveillance systems. 

3.3 Implement a robust disease diagnostics program. The more quickly the 

definitive diagnosis of an emerging disease can be acquired, the better chance 
247 

one has to target appropriate mitigation strategies to prevent a catastrophic 

event. Use of molecular diagnostics (e.g., polymerase chain reaction) has 

greatly enhanced the ability to rapidly identify and characterize infectious 

pathogens from clinical samples. 

3.4 Conduct formal epidemiological risk assessments. Using the standardized 

health and disease data collected through a central surveillance system, formal 

epidemiological risk assessments can be conducted to 1) determine risk 

factors for an emerging disease, 2) identify appropriate mitigation strategies 

for specific disease events, and 3) assess the effectiveness of mitigation 

strategies on population health. These assessments can help determine if a 

disease is emerging due to a novel pathogen or a compromised animal 

population. 

3.5 Develop a general emergency response plan. In the event that an emerging 

disease leads to an epizootic of high mortality, an emergency response plan 

may help to minimize the global impact of the event. Response plans may be 

more useful if emerging disease events are categorized (e.g., mild, moderate, 

severe) with corresponding response plans. 

4.0 Potential action items for discussion 

Determine standardized health metrics that can be routinely collected and 

reported for coral populations 

Consider where a centralized coral health & disease surveillance system may 

reside 

Implement a robust molecular diagnostic program based upon polymerase chain 

reaction (PCR) 

Determine study questions for future epidemiologic risk assessments 

Create emerging disease event categories (e.g., Code Red, Yellow, Green) with 

corresponding response plans 

5.0 References 

1. Cunningham AA. A walk on the wild side—emerging wildlife diseases: They 

increasingly threaten human and animal health. BMJ. 2005 Nov 26; 331(7527): 

1214-1215. 

2. Fleck F. Experts urge action to stop animal diseases infecting humans. BMJ. 2004 

May 15; 328(7449): 1158. 

3. Hughes JM. Emerging pathogens. An epidemiologist's perspective on the problem 

and priorities for the future. West J Med. 1996 Jan; 164(1): 21-22. 

4. Holmes KV. SARS coronavirus: a new challenge for prevention and therapy. J 

Clin Invest. 2003 Jun 1; 111(11): 1605-1609. 

5. Walsh PD, Biek R, Real LA. Wave-Like Spread of Ebola Zaire. PLoS Biol. 2005 

Nov; 3(11): e371. 

6. Sutherst RW.Global Change and Human Vulnerability to Vector-Borne Diseases. 

Clin Microbiol Rev. 2004 Jan; 17(1): 136-173. 
248 

WILDLIFE DISEASE INVESTIGATIONS 101 

David A. Jessup, DVM MPVM Dipl. ACZM, Senior Wildlife Veterinarian 

California Department of Fish and Game, 1451 Shaffer Rd., Santa Cruz, CA 95060 

DJESSUP@OSPR.DFG.CA.GOV 

ABSTRACT 

Worldwide we are seeing an increased interest in the ecology of disease in wild 

plants and animals and a concern over whether anthropogenic environmental changes are 

significantly influencing disease to the detriment of important species. This seems to be 

occurring across ecosystem boundaries (ie. in cloud forests, woodlands, savannas, 

deserts, lakes, rivers, and oceans) and with a wide variety of prominent examples (ie. 

distemper and TB in African lions, chytrid fungus in many species of amphibians, CWD 

in deer and elk, mycoplasmosis in tortoise, several viruses and whirling disease in 

salmonids, toxoplasmosis in sea otters, morbiliviruses in seals and dolphins, rickettsial 

wasting disease in abalone). Although none of these are the subject of this workshop on 

Coral Disease and Health; the problems, field methods, concepts and lessons learned 

from investigations of other wildlife diseases were deemed to be useful as an 

introduction. This paper will provide descriptions of actual wildlife disease investigations 

in several wildlife species that illustrate the logistical and physical challenges of trying to 

determine what causes disease process, how basic field information can be refined and 

approaches refined and rudimentary methods for management developed. Much of the 

information is drawn from the author’s experience, various sources in the wildlife disease 

and health literature, and Wobeser, 1994. 

INTRODUCTION: Investigations of wildlife diseases are not really new, they have 

been conducted for at least a century in North America and longer in Europe and Africa. 

However, the frequency of investigations, their complexity and importance attached to 

this area of research and service has increased greatly, particularly in the last decade. 

Wildlife disease investigations are conducted by State, Federal and tribal governments as 

part of their stewardship responsibilities for wildlife, by universities and institutes as part 

of academic or teaching responsibilities, by NGO’s and conservation groups attempting 

to foster species recovery or health, and by cooperatives which are usually hybrids of the 

proceeding 3 institutional types. Examples of the government agencies might include 

USFWS and USGS under Department of Interior, NOAA-NMFS and NOS under 

Commerce, USDA-WS and USDA-APHIS under Agriculture; the Fish and Wildlife 

Agencies of the 50 States and the Canadian provinces; and some of the larger native 

American tribes such the Navaho and Yakima. A number of universities in North 

America have been involved in wildlife health and disease research and many of the first 

host/agent case descriptions, recognitions of environmental influence on disease and 

recognition parasite life cycles come out of academic research. In the last few decades 

nongovernmental organizations like the Wistar, Scripps and Hubbs Institutes, Wildlife 

Conservation Society, the Morris Animal Foundation and others have funded and 

supported wildlife disease research. Several large cooperative efforts, notably the 
249 

Southeastern Wildlife Disease Cooperative and the Canadian Wildlife Health 

Cooperative have successfully combined university, government and other resources, 

mandates and personnel to provide wildlife health research and services. 

Scenario 1: In February of 1995 a California wildlife veterinarian got a call from the 

manager of Grizzly Island wildlife area in the Suisun Marsh just north of San Francisco 

concerning tule elk (Cervus elaphus nannodes) dying. These elk, a subspecies that had 

adapted to the swamps and fens of the central valley and coastal areas of California, had 

been hunted to near extinction in the 19th century and only remnant populations survived 

into the mid 20th century. In the 1970’s and 1980’s groups of tule elk were captured and 

translocated to a number of State, Federal and privately owned properties. The elk had 

done very well at this refuge and had surpassed 120 animals on 500 hectares. Several elk 

had been found down and others were dead. The downed animals appeared to be 

seizuring, paddling and those that had recovered appeared drunk and disoriented. In all it 

was estimated that at least 10-12 of the elk were affected and assistance was requested. 

Analysis: This is a State managed species, on a State refuge, with the contacted 

person being a State Game and Fish Veterinarian responsible for health and disease in 

living and dead free-ranging species. No jurisdiction crossed, no permits or plans needed, 

no significant permission to request either for work on dead animals, handling or “take” 

of sick. It is an acute unexpected, previously undescribed event or phenomenon, a 

significant proportion of the population is affected, and immediate response is probably 

appropriate, although research, planning and sampling gear preparation are limited. 

Response: Load up the necropsy kit, a rifle, sampling gear, immobilization 

equipment, leave the wife a note, (that’s something people did before cell phones) and hit 

the road. 

Findings: Eleven dead animals were located, all of them very fresh having died 

within the last day or two. All were yearlings, 6 male, 5 female. Several had been 

paddling around for several hours working up the ground around them, no external 

lesions of signs other than minor contusions and abrasions noted. Several live animals 

including at least one adult male were seen showing signs of incoordination, stiff high 

gait, opisthotonus (neck arched and head held high). Two live elk were down and could 

not rise. Treatment with steroids, antibiotics (penicillin) and atropine were tried with no 

results. 

Postmortem examinations were done on 5 of the dead elk. 

Dead elk were in fair to good body condition, no significant lesions were noted in 

the eyes, ears, nose, or mouth. Brains were not examined in the field. The lungs, heart, 

liver, kidneys, spleen, adrenals, reproductive organs, intestinal tract also appeared 

normal. The rumen contained bright green, somewhat frothy contents and some pale 

carrot like tubers. The smell of the rumen contents was unusual. 

There had been many days of fog and rain and most grasses and forbs were buried 

under a think thatch of dead grasses. The primary green plant available was poison 

hemlock (Conium maculatum) and areas of heavy grazing and pawing to unearth roots 

were evident. Animals with CNS signs were actually seen returning to hemlock patches 

to graze. The roots of the hemlock looked very similar to those seen in the rumen of dead 
250 

animals, the leaves were the same bright green and the smell of roots and leaves were 

similar to that unusual small coming from the rumen. Diagnosis of acute hemlock 

poisoning was confirmed by isolation of conine toxin from rumen contents. 

The following management actions were recommended: provide attractive 

grain and alfalfa hay feed it areas away from hemlock. Spray hemlock patches with 

carrot oil and disk it under ASAP, set up zone guns to scare elk away from hemlock areas 

where they were eating it, provide more diverse feed, reduce the numbers of elk on the 

refuge. 

Scenario 2: In September of 2002 SCWDS gets a call about white-tailed deer 

(Odocoileus virginianus) that are dying around campgrounds in Great Smokey Mountains 

National Park. The person calling was camping there and describes depressed animals 

with foam coming from their mouths and bleeding from the rectums. They had described 

the deer to a NPS Ranger who didn’t seem too excited about it and the person, a citizen 

of Athens, GA., was aware that SCWDS does a lot of wildlife health work all around the 

southeastern USA. 

Analysis: SCWDS works with NPS and a call to offer diagnostic assistance and 

to discuss the need to deal with park visitor concerns is warranted. The description 

sounds a lot like EHD or bluetongue, an endemic orbiviral disease of deer, which is fairly 

common in the summer and fall but could be the start of a die off. Call the chief ranger 

of Great Smokey Mtns., it’s their call. They may want to collect and ship the animals or 

take samples as they have been part of previous sampling programs. 

Response: NPS personnel took blood samples from fresh dead deer and sent 

them to SCWDS. SCWDS personnel visited the park a week later and collected 4 deer, 

and examined 2 of which had died recently. 

Findings: EHD 1 virus was isolated from tissues of one deer examined by 

SCWDS and blood of 1 animal sampled by NPS. Lesions in the 2 dead deer were 

compatible with hemorrhagic disease, these were confirmed by histopathology. Serology 

showed high antibody titers to EHD 1 and BT 10 viruses. 

Comment: Although the initial observations (deer dying near campgrounds, 

frothing at the mouth and bleeding) were somewhat alarming, the syndrome is relatively 

common in the southeastern USA, particularly in the late summer and fall. The disease is 

a relatively natural process little influenced by human activities, but the epidemiology is 

followed closely by SCWDS in hopes of identifying predictors. Few if any actions are 

recommended for management despite the fact that dieoffs can involve many animals. 

The above scenarios illustrate some reasons why wildlife disease investigations are 

done. Basic reasons for studying any disease (from Wobeser 1994) are to: 

1) determine its nature and cause, 

2) to determine the effects on individuals, populations and ecosystems (to assess 

its significance), 

3) to identify methods to prevent, control or reduce the disease or its effects. 
251 

In addition, with regard to wild species the reasons may also include: 

1) curiosity about the disease as a biological phenomenon, 

2) concern over its impact on wild populations and ecosystem integrity, 

3) public concern over highly visible die offs or unsightly conditions, 

4) concern that disease in a wild species may be transmissible to humans or 

domestic species, and 

5) concern that diseases in wild species are indicators of undesirable changes in 

the environment. 

Scenario 3: In April of 1989 California bighorn sheep (Ovis canadensis californiana) in 

the Warner Mountains of the northeastern corner of California are reported to be dying, 

only few living animals and several bodies were spotted in a recent aerial survey. Mule 

deer (Odocoileus hemionus) in the area are also reported to be dying in large numbers in 

the valley bottom adjacent to a north-south highway and valley ranch lands. 

Background: This bighorn population had started from a nucleus 12 animals 

released into a vast mountain range 10 years previously and was thought to now number 

approximately 70 individuals. Only about 600 of this subspecies live in California and 

they are State listed as “threatened”. Bighorn sheep have a history of dying in large 

numbers due to fibrinopurulent (Pasteurella) broncho- pneumonia. Previous dieoffs in 

other locations have resulted in local extinctions. There are serious conservation and 

political implications (previous dieoffs have been associated with contact between 

domestic sheep and bighorn). The area is vast and steep, it is a late winter and only the 

valley areas thaw during sunny days. 

Analysis: Investigation needs to proceed immediately as decomposition and 

scavenging will obliterate destroy all evidence quickly. The entire heard of bighorn 

could be in jeopardy. The deer and bighorn dieoffs may be linked or entirely separate 

events. 

Response: Load up the necropsy kit, a rifle, sampling gear, arrange for a 

helicopter that can do both survey and capture (net-gunning) for sampling, arrange for the 

ex-wife to care for your dog (divorce is one hazard of lots of field work). Discuss the 

situation in detail with the local biologist, make arrangements to meet with ranchers in 

the area who may be cooperative and who control ground access. 

Findings: Many deer carcasses in various states of preservation (those that die in 

the shadows have probably been frozen for weeks). Quick field postmortem examinations 

are done on 5. All the deer (about 10 observed grossly, 5 necropsies) are extremely 

emaciated. None show significant parasite loads, evidence of infectious disease processes 

including but not limited to respiratory disease, gastrointestinal disease, systemic 

lymphoid or hemorrhagic disease. Stomach contents are minimal but often straw or old 

alfalfa from hay bales. No significant natural browse or forage is available due to 

prolonged cold winter. General impression is one of starvation/malnutrition. 

While doing post mortem examinations of deer at one of the cooperating ranches, 

the rancher mentioned that he had lost a number of sheep that he grazed in the adjacent 

range and had only recently found them as they were driven down by harsh weather. He 

had killed them and allowed access to the reasonably fresh carcass of one. Histological 
252 

examination by a state diagnostic lab pathologist revealed chronic bronchitis and low 

grade bacterial pneumonia. Cultures grew no bacteria of note. 

Relatively few bighorn sheep carcasses are found and these have been dead for 

weeks and are badly scavenged. There are some sites of subcutaneous fat and bone 

marrow fat is evident when long bones are broken. Mats of yellow fibrin and black 

discoloration of the pleural lining suggest and portions of one lung suggest 

fibrinopurulent bacterial pneumonia. A small herd (3) feral goats are spotted in the area 

and one live bighorn ram is seen running and behaving in ways that suggest it is 

reasonably healthy. It was captured and sampled (blood, feces, nasal and tonsular 

swabs), tagged and collared and released. These samples reveal no lungworm 

(Protostrongylus spp.), no evidence of systemic infection (from CBC and chem.), no 

significant pathogenic bacteria isolated. The three feral goats were shot and postmortem 

examination was unremarkable. A Pasteurella multocida was isolated from tonsil of two 

animals. 

Summary: The case described is not unusual in wildlife mortality events. Time, 

space, terrain, weather and other factors make it very hard to establish a cause of death or 

to sort out potential causes from coincidental events. The bighorn sheep dieoff pattern is 

typical of that seen in many western states when bighorn have contact with domestic 

sheep or goats that may carry pathogenic Pasteurella or Manheimia bacteria in their 

upper respiratory tracts. A few shreds of evidence suggest that either the feral goats or 

the feral sheep may have been involved, as both were in the same general area as the 

bighorn and both had some evidence of some potentially virulent bacterial respiratory 

flora, but certainly no cause and effect conclusions can be drawn. Under some 

circumstances bighorn may develop bacterial pneumonia without contact with domestic 

sheep or goats. A very few sightings of bighorn sheep in the range persisted for a few 

years, but all lambs born died before weaned and the herd slipped into extinction within 3 

years of the outbreak. The deer dieoff appeared to have nothing to do with the bighorn 

dieoff but indicated harsh weather conditions that may have impacted other species as 

well. Without solid evidence on which to base land use policy decisions, enforcement 

actions, and wildlife management programs it is impossible to manage disease related 

conflicts between land and resource users. 

Understanding causation is extremely important: In its simplest form disease may be 

seen a single agent infecting one species of hosts, relatively uninfluenced by the 

environment, with clear and decisive outcomes (recovery or death). Clear biological, 

pathological and pathogen isolation information clarifying the role of host(s), agent and 

environment make understanding causation much easier. Unfortunately, those kind of 

simple, straight forward situations are not common. 

(From Wobeser 1994) With the discovery of microbial pathogens at the turn of the 20th

century, human and veterinary medicine was concerned with identification of specific 

agents responsible for acute infectious diseases. A set of rules (Koch’s postulates) were 

developed for establishing cause and effect relationships that were generally widely 

accepted. These were: 

 
253 

1) the agent must be shown to be present in every case of disease through 

isolation in pure culture, 

2) the agent must not be found in cases of other diseases, 

3) the agent must be capable of experimentally reproducing the disease, and 

4) the agent must be recovered from the experimental host. 

But, Robert Koch is dead and our simple concepts of disease have become 

considerably more complex and encompassing of a much wider array of 

processes. Perhaps the broadest view yet is that one can see whole ecosystems as 

“healthy” or “unhealthy” and perhaps identify the reasons why. 

A broader set of criteria for establishing causation, reflecting the multifactorial nature of 

most disease (adapted from Kelly, Thompson and Evans (1986)) is: 

1) the hypothesized cause should be distributed in the population or in nature in the 

same manner as the disease, 

2) the occurrence of the disease should be significantly greater in those exposed to 

the hypothesized cause than in those not exposed, 

3) exposure to the hypothesized cause should be more frequent among those with 

disease than those without , if risk factors are constant, 

4) disease should temporally follow exposure to the cause 

5) higher doses or longer exposure to the cause should increase disease occurrence 

6) for many diseases a spectrum of host responses along a biological gradient from 

mild to severe should follow exposure 

7) other explanations and associations should be eliminated 

8) the association between cause and disease should be evident in various 

populations studied by different methods 

9) elimination or modification of exposure to the cause should decrease occurrence 

of the disease 

10) prevention of exposure or modification of the host response (as by vaccination) 

should decrease or eliminate the disease 

11) disease should occur more frequently in experimentally exposed animals than in 

controls, and 

12) all the relationships and findings should make biological sense. 

Scenario 4: When diseases occur regularly and are a serious threat to the survival of a 

species the efforts put into diagnosis and management may be larger and more prolonged 

than outbreak investigations. Biologists have been studying the diseases and causes of 

death in southern sea otters for over 35 years and for the last 14 years professional 

veterinary postmortem examinations have been done on all essentially all fresh dead 

(from 40-100 animals per year). This effort is seen as vital to sea otter recovery and it 

has allowed the clear description of a number of previously unrecognized or 

underappreciated disease processes. With an extensive dataset for comparison, mortality 

events that exceed average can be recognized and quantified and compared to previous 

years and events. The goal of these efforts is to identify relationships and associations 

that might lead to improvements in management that benefit the effected populations. 
254 

In the spring of 2003 large numbers of dead southern sea otters were picked up 

along the California coast. Record or near record carcass pickups occurred for several 

months and an unusual mortality event was declared by USFWS and NOAA. By the end 

of 2003 the number of sea otters recovered exceeded any previous year, even when 

numbers were indexed to population growth. No unusual spatial or temporal clusters of 

mortality were evident. The causes of death found by pathologists were not “unusual” in 

the sense that the agents and causes were similar in type and proportion to previous years, 

just greater, in magnitude with the exception that some animals had evidence of domoic 

acid (amnesic shellfish poisoning) intoxication. In the end it was felt that DA was an 

additive mortality factor that was behind the record losses. 

In the spring of 2004 another dieoff of even greater magnitude occurred. This 

time the mortalities were clustered in both space and time, occurring around Morro Bay, 

CA in mid-April to mid-May. Eventually nearly 50 otters, some of which were initially 

recovered while still alive were collected. All live animals showed severe central nervous 

system signs including tremors, coma and seizures, and all but one died within a day of 

stranding. The majority of dead and dying animals had severe generalized 

lympadenopathy (swollen lymph nodes), multiorgan congestion, pericardial effusion, 

cardiac mottling and spleenomegaly. Serology suggested some otters had antibodies to 

Toxoplasma gondii but that many more had very high antibody titers to Sarcocystis 

neurona, both of which are protozoal parasites known to kill sea otters. H&E stained 

sections of effected otters showed severe meningoencephalitis (infection of the brain) 

classic rosette formations of schizonts typical of S. neurona and immunohistochemistry 

stains were positive. Although it had been known that S. neurona could and would kill 

sea otters previously, cases had been few in number, sporadic and with no particular 

spatial or temporal pattern that might implicate a source or cause. 

The above should illustrate the importance of establishing a case description: 

(From Wobeser 1994) Identifying and defining a disease or disease process: Defining the 

cause or nature of a disease, or formulating a working hypothesis should be a very early 

step in every investigation. This is equivalent to a clinician arriving at a tentative 

diagnosis after examination of a patient (the “what” questions). This definition, often 

called a “case description” or “case definition” can be dynamic and is very likely to be 

modified by subsequent information and/or field work. The patterns of temporal and 

spatial disease occurrence (the “when” and “where” questions) are very important in 

understanding disease/health conditions in wild species. The disease or disease process is 

further defined by answering the “who” is questions by defining the population and 

parameters affected and the “why” question by defining the consistent cycle of the 

disease (pathogenesis) in the host and the causation. 

SUMMARY: Although it has been customary to believe that wild animals are generally 

very healthy and that health is maintained by natural selection, we are beginning to 

understand that this is perhaps a very simplistic notion. More importantly there are few 

places on earth where human activities have not upset whatever natural balance existed 

and/or where human induced changes are not associated with disease in wild animals, 

wildlife populations and their ecosystems. Although wild animal populations and 

ecosystems have the ability to respond and to heal themselves, we must understand and in 
255 

many cases correct or mitigate the conditions that caused unbalance and/or disease if 

healthy populations and the be restored. 

References: 

Jessup D.A. 2005. Disease of wild ruminant in arid environments. In: 5 Minute 

Veterinary Consult, S. Haskel (Ed). 

Jessup D.A., J.H. Boermans, N.D. Kock. 1986. Toxicosis in tule elk caused by 

ingestion of poison hemlock. JAVMA 189 (9):1173-1175. 

Jessup, D.A., M. Miller, J. Ames, M. Harris, P. Conrad C. Kreuder and J.A.K. 

Mazet. 2004. The southern sea otter (Enhydra lutris nereis) as a sentinel of 

marine ecosystem health. Ecohealth. 1(3):239-245. 

Kreuder C.K., M. Miller, P. Conrad, L. Lowenstine, T. Carpenter, D.A.Jessup J.K. 

Mazet. 2005. Evaluation of cardiac lesions and risk factors associated with 

myocarditis and dilated cardiomyopathy in southern sea otters (Enhydra lutris 

nereis). AJVR, 66(2):289-299. 

Kreuder, C., M. Miller, D. Jessup, L. Lowenstine M.D. Harris, J. Ames, T.E. 

Carpenter, P.A. Conrad, J.K. Mazet. 2003. Patterns of mortality in the southern 

sea otter (Enhydra lutris) from 1998-2001. J Wildl. Dis. 39(3): 495-509. 

Miller, M.A.,I.A. Gardner, D. Paradies, K. Worcester, D. Jessup, E. Dodd, M. Harris, 

J.. Ames, A. Packham, P.A. Conrad 2002. Coastal freshwater runoff is a risk 

factor for Toxoplasma gondii infection of southern sea otters (Enhydra lutris 

nereis). International Jour. Parasit. 32:997-1006. 

Wobeser, G.A. 1994. Investigation and management of diseases of wild animals. 

Plenum Press. New York. 263pp. 
256 

VI. COMMUNICATION TO MAKE A DIFFERENCE

SCIENTISTS, THE PUBLIC AND THE POLITICIANS: HOW DO WE 

CONNECT FOR REEF’S SAKE?

Jeffery Allen 

Clemson University 

Silas Pearman Blvd. 

Strom Thurmond Institute 

Clemson, SC 29634 

jeff@strom.clemson.edu

Two Examples

 

1 - Coastal Land Use and Policy 

2 - Integrating Science & Values to Inform Ecosystem Management 

First Example - Coastal Growth and Sustainability 

South Carolina’s population expected to increase by 24% by the year 2030 according to 

U.S. Census Bureau. 

Rusk and many others have shown that corresponding land development occurs at much 

higher percentages. 

Tools are needed to help policy and decision makers understand patterns of urban growth 

and potential impacts - economic, social/cultural, and ecological. 

Modeling Land Use Change and Urban Growth 

Transportation Models - TRANUS - (Johnston and Shabazian) 

Deterministic Land Use Models - SACMET, UPLAN (Sui) 

Cellular Automaton Models - SLEUTH (Jantz & Goetz, Clarke) 

Rule-based Models (Pijanowski) 

Logistic Regression Models - CUF (Landis) 

Charleston, SC Region Growth Prediction Summary 

Under the current modeling scenario, there are two assumptions involved. The ratio of 

overall urban land use change (255%) to overall population growth (41%) from 1973 to 

1994 occurred at a ratio of about 6:1. Secondly, it is assumed that population for the three 

county area will grow to 795,879 by the year 2030 as predicted by projections of the 
257 

BCD COG compiled with information from the U.S. Census Bureau, SC Department of 

Commerce and the BCD COG. The predicted urban growth mainly takes the pattern of 

urban sprawl and by the year 2030 consumes 868 square miles within the BCD area. If 

the current growth trends continue and the predictions hold true, the future urban growth 

will sprawl considerably outward from the current urban boundaries. This has several 

significant economic, environmental, and social implications in policy-making and urban 

planning. 

Regional Policy Considerations 

Local - majority of land use decisions made at this level - municipalities must work 

closer with developers to balance growth and fiscal responsibilities - work with other 

municipalities to coordinate growth impacts. 

County and State - policies affect how growth spreads into rural areas - have a certain 

amount of regulatory authority which must be carefully used to protect environment and 

influence developer decisions. 

Federal - many programs indirectly influence development (DOT, NFIP, EPA) - can help 

by providing expertise to state and local entities through research/information as well as 

direct funding (community grants, etc.). 

Planning and management - NOAA scientists utilizing growth predictions through LUCES program. SCDNR officials incorporating growth models into coastal habitat 

management. SCDHEC officials considered growth models in Coastal Futures planning. 

TNC, SCCCL use models for open space planning. 

Second Example - Integrating Science & Values to Inform Ecosystem Management 

Will Focht, Director, Environmental Institute 

 Oklahoma State University 

Marty Matlock, Assoc Prof, Bio/Ag Engr 

University of Arkansas 

Ecosystem Management Challenge 

Management of ecosystems involves: 

Factual uncertainty 

Value saliency 

Social controversy 

High stakes 

Distrust 

How should decisions be made in such contexts? How can both facts and values be 

accommodated? 

Four points to consider: 
258 

An “Ecoplex” conceptual framework that sustainably links natural and social 

systems 

An “analysis and deliberation” protocol that recursively integrates science and 

values in ecosystem management decision-making 

A trust-based guide to stakeholder participation in ecosystem management 

Summary 

Part I - Ecoplex and Sustainability 

The Ecoplex framework is a conceptual aid to understanding sustainable 

ecosystem mgt 

Sustainability Definition 

Development that is environmentally, economically, and socially sustainable

Sustainable development requires balanced conversion of resources to improve 

quality of life (welfare) 

Sustainable Capital Conversion

Conversion of natural and human capital (resources) to economic and social 

capital (welfare), and vice versa 

o Resources Conversion Welfare 

Natural Capital + Human Capital Economic Capital + Social Capital

Legend: 

Natural capital = ecosystem goods and services 

Human capital = labor, intelligence, technology 

Economic capital = wealth (currency, property, investments) 

Social capital = order, stability, fairness (social networks, security, trust, justice, 

laws) 

Coupling of Social & Natural Systems 

Sustainability (a balanced conversion of resources to welfare) requires a carefully 

integrated coupling of social and natural systems 

We have developed a framework that provides a conceptualization of how this 

coupling can be accomplished 

Part II - Analysis and Deliberation 

A&D protocol was proposed by National Research Council in its 1996 report, 

Understanding Risk: Informing Decisions in a Democratic Society

A&D is an alternative to the 1983 NRC protocol that envisioned a top-down 

process of scientific impact assessment followed by a political process of impact 

management 

1983 approach has been criticized for failing to recognize the importance of 

involving stakeholders in framing analyses to inform eco-mgt decisions 

Recursive relationship between analysis and deliberation 
259 

Analysis is used to gather information about the social and natural systems to 

inform decision-making 

“Getting the science right” 

Deliberation is used to frame analysis and to make ecosystem management 

decisions 

“Getting the right science” 

A&D in Ecosystem Management 

The 1983 protocol dictated that scientists alone define ecosystem management 

problems and decide what analyses are pertinent and whether fixes are necessary 

The A&D protocol places analysis in the service of deliberation and provides an 

opportunity for deliberants to help frame analysis 

However, the intensity of A&D should vary with context – specifically trust

Part III - Relationship of Trust to Participation 

Trust: the willingness to accept the risk of deferring to the judgments of others 

based on judgments of expertise and value similarity 

High trust: deference 

Low trust: vigilance 

The participation strategy that is most appropriate depends on stakeholders’ trust 

of other policy actors 

Policy actors include experts, fellow stakeholders, and government decisionmakers 

Expert Trust 

Stakeholders’ expert trust judgments based on: 

Perceived expertise 

Factual certainty and salience 

Subject matter and analytical competence 

Objective (unbiased) interpretation 

Perceived value similarity 

Responsiveness to stakeholder concerns (framing), caring attitude, openness, 

honesty, and forthrightness 

High expert trust: evidentiary participation 

Low expert trust: constitutive participation 

Social Trust (of stakeholders) 

Stakeholders’ social trust judgments based on: 

Perceived expertise 

Familiarity 

Perceived value similarity 

History of social interaction 

Conformance to dominant culture and traditions 

Civic mindedness 

High stakeholder trust: cooperative participation 
260 

Low stakeholder trust: defensive participation 

Government Trust 

Stakeholders’ government trust judgments based on: 

Perceived expertise 

Technical competence 

Perceived value similarity 

Fiduciary responsibility 

High government trust: trustee (leader) role 

Low government trust: delegate (follower) role 

Part IV - Summary 

Ecosystem management policy must recognize the relationship between natural & 

social systems 

We endorse sustainability as a guiding principle in this relationship 

Analysis and deliberation is the preferred mechanism by which to integrate facts 

and values 

The intensity of analysis and deliberation depends on the level of trust that 

stakeholders have of other policy actors (“one size does not fit all”) 
261 

VII. TECHNOLOGIES FOR THE FUTURE OF CORAL HEALTH 

POTENTIAL TECHNOLOGICAL DEVELOPMENTS FOR CORAL DISEASE 

MONITORING

Melissa Bos 

Hawaii-Pacific Coordinator of the Alliance for Coastal Technologies 

The Alliance for Coastal Technologies (ACT) is a NOAA-funded partnership of research 

institutions, state and regional resource managers, and private sector companies interested 

in developing and applying technologies for monitoring and studying coastal 

environments. The long term goal of ACT is to be a national resource for facilitating the 

transition of sensor technologies to routine use in monitoring and studying coastal 

environments. ACT was established to serve as a comprehensive information 

clearinghouse on technology performance, a forum for capacity building, and an 

unbiased, third-party testbed for evaluating coastal sensor technologies. ACT strives to 

provide products such that the coastal observing community is able to identify and select 

technologies that are appropriate for their needs and capacities, technology developers 

have tools for trend identification and targeted marketing, and that the latest, innovative, 

and most effective technologies are continuously integrated into observing capabilities. 

ACT is organized to ensure geographic and sector involvement. The program is 

headquartered at the University of Maryland’s Chesapeake Biological Laboratory, and 

there are currently eight ACT Partner institutions around the country with coastal 

technology expertise that represent a broad range of environmental conditions for testing. 

The ACT Stakeholder Council is comprised of resource managers and industry 

representatives who ensure that ACT focuses on service-oriented activities. Regional 

chapter Alliance Members provide advice to ACT and are kept abreast of ACT activities. 

The Hawaii-Pacific Partnership is housed at the University of Hawaii, Hawaii Institute of 

Marine Biology. This relatively new partnership is striving to assess the needs of the 

region before full-scale implementation throughout the entire region. More information 

on current ACT activities throughout the nation can be found at www.act-us.info. 

Preliminary ACT assessments revealed that coral disease monitoring is emerging as a 

critical issue in Hawaii and the broader Pacific. Current monitoring programs are often 

limited by the number of trained professionals who can do in situ assessments of coral 

disease status. In situ assessments require skilled personnel and are time consuming. 

Technological advancements have allowed many types of coastal monitoring programs to 

increase precision and efficiency, and to decrease the number of people, training of those 

people, and overall program expense. Tools can increase the number of lesser-trained 

personnel who can be involved in a program, often enabling community participation, 

and can decrease the number of experts who have to be involved in the entire monitoring 

effort. This is especially true for a parameter like coral disease which requires a very high 
262 

skill level for in situ determination. Monitoring technologies tend to increase precision, 

allowing measurements to be taken by multiple individuals with reduced observer error. 

Accuracy may be increased or decreased by switching to or adding in technology-based 

monitoring, so program managers should be aware of the level of accuracy needed to 

meet their goals, such as to establish a baseline or temporal trend, or to trigger 

management actions. Program managers should also consider what factors are limiting to 

them in developing a monitoring program: number of people, training level of people, 

operating budget, capital expense budget, equipment, analysis abilities, etc. Evaluating 

these limits can assist in the determination of what tools are best for their situation. 

ACT Hawaii-Pacific is not aware of any existing technologies that have been specifically 

designed for coral disease monitoring. Many tools used in other coastal monitoring 

programs may be useful to coral disease monitoring, and many existing technologies used 

in diverse applications may be adapted for specific coral disease use. The best strategy is 

to build upon existing technologies and identify what adaptations are necessary for coral 

disease monitoring needs. 

The first four things that coral disease experts and managers should work together to 

identify are 1) the best set of parameters to be measured, 2) sampling frequency, and 3) 

preferred method of deployment (in-situ mooring, hand-held, etc.), and 4) level of 

accuracy required. For the parameters that are proxies or indicators for disease, e.g. a 

water quality parameter, determine if an existing tool is able to sample at your required 

frequency, deployment type, and accuracy. A comprehensive database of existing sensors 

can be found at www.act-us.info. 

For parameters that do not have adequate existing sensors, the next phase is to determine 

if any sensors exist that could be easily adapted to coral disease monitoring needs. If a 

tool already exists for the parameter, but the frequency, deployment type, or accuracy is 

not satisfactory, scientists and managers can collectively voice their needs to industry and 

ask for a modification. ACT was created to be a liaison between these communities and 

can assist in these discussions and negotiations. 

If no sensors exist for a chosen parameter, an analysis of tools used in related fields may 

identify places to start. For example, if a manager needs to be able to spot-check for the 

presence of a particular bacterium, one can ask, what other fields are interested in spotchecking bacteria levels? Public health and bioterrorism experts come to mind. Perhaps 

tools that have been developed in those fields could be adapted by changing the 

bacterium of interest. Once a similar sensor is identified, the process of negotiating with 

industry begins. 

This likelihood of success for convincing a company to modify a tool or create a new one 

depends on the collective finances available to purchase the tool. If only a few 

individuals would be able to purchase the tool, it is not likely that industry could justify 

the expense. This is one key reason that the global coral disease monitoring community 

would benefit from standardized protocols. If, however, this approach does not work, a 
263 

researcher may be able to create a tool and produce it on small scale using a federal grant 

for technology development. Several of these opportunities exist. 

Consideration should be given not only to identifying the correct sensors, but also to data 

analysis protocols/tools and personnel training. ACT Hawaii-Pacific is poised to assist 

will all of these questions and hopes to facilitate some of the necessary discussions. 
264 

LEVERAGING POST-GENOMIC TOOLS AND SYSTEMS BIOLOGY 

APPROACHES TO ACCELERATE THE UNDERSTANDING OF CORAL 

DISEASE AND EFFECTIVELY MONITOR THE HEALTH OF TROPICAL 

REEF ECOSYSTEMS

Eric J. Mathur 

Consultant, J Craig Venter Institute & Synthetic Genomics Inc; Delegate, EO Wilson 

Biodiversity Foundation; Founder, Diversa Corporation 

Biotechnology can no longer be considered a new scientific discipline; molecular and 

genomic innovations have progressed dramatically and continue to advance at 

unprecedented rates. No longer is there simply the promise of how these new 

technologies will one day help solve biological problems; already there exists many 

tangible examples of biotechnological success stories in fields ranging from aquaculture 

to transgenic plants, from fermentation sciences to animal health, and from biocatalysis to 

solutions for alternative energy. 

Moreover, the development and refinement of molecular methods is beginning to impact 

our understanding of basic biological processes, including coral bleaching and the health 

of tropical reef ecosystems. In the context of genomics, DNA sequencing costs have 

plummeted more than three orders of magnitude resulting in the availability of complete 

genome sequences for over 300 microorganisms and representative genome sequences 

available for most eukaryote lineages. Furthermore, the dramatic reduction in sequencing 

costs has catalyzed the development of a new method which involves direct sequencing 

of uncultured microbial communities and organismal consortia. This environmental 

sequencing strategy, also known as metagenomics, utilizes genomic principles to glean 

information and understanding from such complex biological processes as symbioses and 

host:pathogen relationships. Metagenomics can also be used to evaluate and quantify the 

metabolic potential of a given environment and even serve to identify nucleic acid, 

protein and small molecule-based probes which can monitor spatial and temporal 

metabolic changes within a defined ecosystem. 

In addition and complementary to genomics, improvements and recent progress in 

proteomics and metabolomics now enable one to pose scientific questions which utilize 

genomic and metagenomic sequence data sets as reagents to help understand and unravel 

the physiological and biological consequences of an ecological perturbation, such as coral 

bleaching. Collectively, these strategies make use of extremely sophisticated molecular 

tools to revisit the age old concept of gestalt biology, which views biological systems as 

complex, multi-organism, complete ecosystems which respond cooperatively to given 

environmental circumstances. Improvements and advancements of these genomic and 

systems biology tools will be reviewed and the ramifications toward understanding of 

coral disease and monitoring ecosystem health will be discussed. 
265 

References: 

Brennan Y., Callen W.N., Christoffersen L., Dupree P., Goubet F., Healey S., Hernandez 

M., Keller M., Li K., Palackai N., Sittenfeld A., Tamayo G., Wells S., Hazlewood 

G.P., Mathur E.J., Short J.M., Robertson D.E., Steer B.A. Unusual microbial 

xylanases from insect guts. (2004) Appl and Environl Microbiol 70(6):3609-17. 

Giovannoni S.J., Bibbs L., Cho J., Stapels M.D., Desiderio K.L., Vergin K.L., Rappe 

M.S., Laney S., Wilhelm L., Tripp J.H., Mathur E.J., Barofsky D.F. Proteorhodopsin 

in the Ubiquitous Marine Bacterium SAR 11. (2005) Nature 438: 82-85. 

Giovannoni S.J., Tripp J., Givan S., Podar M., Vergin K.L., Bibbs L., Eads J., Richardson 

T.H., Noordeweir M., Rappe M.S., Short J.M., Mathur E.J. Genome streamlining in 

an oceanic bacterium. (2005) Science 309:1242-45. 

Mathur E.J., Toledo G., Green B.D., Podar M., Richardson T.H., Kulwiec M., Chang 

H.W. A biodiversity-based approach to development of performance enzymes: 

applied metagenomics and directed evolution. (2005) Industrial Biotechnology

(1)4:283-287. 

Toledo G., Green W., Gonzalez R., Christoffersen L., Podar M., Chang C., Hemscheidt 

T., Trapido-Rosenthal H.G., Short J.M., Bidigare R.R., Mathur E.J. High throughput 

cultivation for isolation of novel marine microorganisms. (2006) Oceanography

(19)2:120-5. 

Tringe S.G., von Mering C., Kobayashi A., Salamov A., Chen K., Chang H.W., Podar 

M., Short J.M., Mathur E.J.; Detter J.C., Bork P., Hugenholtz P., Rubin E.M. 

Comparative metagenomics of microbial communities. (2005) Science 308 (5721), 

554-557. 

 Waters E., Hohn M.J., Ahel I., Adams M.D., Barnstead M., Beeson K.Y., Bibbs L., 

Bolanos R., Keller M., Kretz K., Lin X., Mathur E. J, Ni J., Podar M., Richardson T., 

Sutton G.G., Simon M., Soll D., Stetter K.O., Short J.M. The genome of 

Nanoarchaeum equitans: insights into early archaeal evolution and derived 

parasitism. (2003) Proc Natl Acad Sci USA. 100(22):12984-8. 

Zengler K., Toledo G., Rappe M., Elkins J., Mathur E.J., Short J.M., Keller M. 

Cultivating the uncultured. (2002) Proc Natl Acad Sci USA. 99(24):15681-86. 
266 

ACKNOWLEDGEMENTS

We would like to acknowledge the Workshop Organizing Committee composed of Dr. 

Kay Briggs (U.S.G.S); Dr. Andy Bruckner (NOAA); Ms. Athline Clark (Hawaii Division 

of Aquatic Resources); Dr. Sylvia B. Galloway; Ms Jennifer Kozlowski (NOAA); Dr. JoAnn Leong (HIMB, Univ. Hawaii); Ms. Betsy Mordecai (MorEvents); and Dr. Cheryl 

Woodley, Chair (NOAA) for their collective efforts in the weeks prior to the workshop. 

This team set the vision and goals for the workshop, developed the agenda and identified 

experts to represent key disciplines in the deliberations. 

We would like to thank Ms. Athline Clark for her opening remarks that introduced us to 

the customs and traditions of the Pacific Islands which helped us understand a bit of the 

culture, their dependence on, yet love for coral reef ecosystems and their unique approach 

to stewardship of this resource. 

We are grateful to Dr. Gary Ostrander for his time and welcome presentation. His candid 

insightful remarks called each of us in the coral disease community to action, action for 

change and action to work together as a cohesive research community that rallies around 

common goals and collaborating on common objectives. This moving presentation was 

transcribed and is the Forward to this document. 

Background information that created a context for the workshop participants was 

generously provided by a series of 16 white papers and oral presentations. 

Mr. Mike Gawel provided a context for the unique nature of the Pacific culture and 

biology in his presentation titled: Overview of issues unique to the Pacific Biological & 

Social perspectives. 

Dr. Cheryl Woodley then provided an introduction for the Coral Disease and Health 

Consortium and shared some of the CDHC’s progress over the last 4 years in her talk 

titled: Introduction to the CDHC and Progress on the National Plan. 

Dr. Esti Winter provided introductory remarks that helped define the topic and scope for 

coral disease with her presentation titled: Definition of Disease and Various 

Presentations of Disease in Coral. 

In his two white papers, Dr. Andy Bruckner provided insights from experiences with 

Caribbean coral diseases and a perspective of the global pervasiveness of coral disease. 

His presentations were titled: Lessons learned in the Caribbean (Historical perspective)

and Global perspective of Incidence & Prevalence of Coral Disease. 

Dr. Bette Willis updated the group on the international coral disease work of the Coral 

Reef Targeted Research & Capacity Building for Management Program, a partnership 

between the Global Environmental Facility, the World Bank, The University of 

Queensland, NOAA, research institutes and third-parties globally and she also provided a 
267 

report specifically addressing coral disease in the Western Pacific with her presentation 

titled: Current knowledge of diseases in Western Pacific. 

Dr. Greta Aeby began focusing on the Pacific issues with her white paper and 

presentation: Current knowledge of diseases in Hawaii & Northwest Hawaiian Islands. 

Dr. Thierry Work is a veterinary diagnostician that has worked on coral disease 

throughout the Pacific. His presentation and white papers were titled: Current knowledge 

of diseases in U.S. Territories and Freely Assoc States. 

Dr. Gary Wobeser, a prominent wildlife veterinarian and professor of wildlife diseases 

provided the participants with a basic primer outlining fundamentals that need to be 

considered when studying diseases in wildlife. His presentation was entitled: Basic 

Concepts in Diseases of Wildlife: The Diagnostic Method. 

Dr. Dave Jessup helped provide some practical guidelines responding to outbreaks of 

disease in the wild with his presentation: Disease Outbreak Investigation: The Process - 

What elements are critical? 

Dr. Stephanie Venn-Watson is a veterinarian and wildlife epidemiologist. She shared 

with the group insights into preparing for diseases in corals with her talk: Emerging 

Disease – How do we identify it? 

Dr. Bruce Wilcox is a leader in exploring human-ecosystem interactions as it relates to 

human health and environmental change. He provided context for coral disease and as an 

emerging issue with ocean health in his presentation: Evolutionary Ecology, and Disease 

Emergence: The Big Picture. 

Dr. Jeffery Allen explored the inter-relatedness of good science with politicians and the 

public and the importance of these interactions to actually identify and make changes to 

save reefs in his presentation: Scientists, the Public and the Politicians: How do we 

connect for reef’s sake? 

Ms Melissa Bos shared with the group, advances in marine science technologies in her 

presentation: Technologies for Disease Monitoring and Assessment and asked the group 

for specific needs that with improved technology the field of coral disease research would 

be enhanced. 

Mr. Eric Mathur presented a stimulating talk titled: Technologies for Diagnostics: 

Leveraging Post Genomic Tools and Systems Biology to Accelerate the Understanding of 

Coral Disease and Effectively Monitor Tropical Reef Ecosystems, in which he showed 

the power and possibilities provided with post-genomic information and new platforms 

for that information that could directly impact coral health and disease research. 

We would like to thank all of the participants that served in working groups whose 

experience and knowledge laid the foundation for this document. We are especially 
268 

grateful to the Working Group Chairs and their Rapporteurs that not only presided over 

the deliberations during the workshop but also provided draft reports for each group that 

were used for preparing this document. The Cellular Physiology and Pathology group 

was chaired by Dr. JoAnn Leong and rapporteur, Dr. Sylvia Galloway. The Toxicology 

and Ecological Epidemiology was chaired by Dr. Stephanie Venn-Watson with 

rapporteur, Dr. Katie Tucker-Mohl. The Pathology of Infectious Disease working group 

was chaired by Dr. Thierry Work with Ms. Julie Higgins serving as rapporteur. The 

working group Preventing and Responding to Coral Disease in the Pacific: Management 

Perspectives was chaired by Ms. Jennifer Kozlowski with rapporteur, Ms. Amanda 

McLenon. 

 

A special thanks go to members of the Woodley Lab that assisted in preparing the 

Workshop Briefing Book, in particular, Sara Polson for artwork and Julie Higgins and 

Amanda McLenon for copying and organizing the materials into the briefing book. 

Many thanks go to the Alliance for Coastal Technologies and the Khaled bin SultanLiving Oceans Foundation for hosting a reception for the meeting at the Waikiki 

Aquarium. We would also like to acknowledge our meeting organizer, MorEvents and 

give a special thanks to our onsite meeting liaison, Ms. Kay Luzaich who worked 

tirelessly to resolve problems from transportation to desserts so the organizer could focus 

on the science. 

We very much appreciate the financial support for this workshop and this document 

which was provided by NOAA through the Coral Reef Conservation Program in support 

of the Coral Disease and Health Consortium project.
269 

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Appendix I. Meeting Agenda 

CORAL HEALTH AND DISEASEIN THE PACIFIC:

VISION FOR ACTION

 AGENDA 

Monday June 19, 2006 

Sheraton Moana Surfrider 

Ballroom I 

8:00 Call Meeting to Order - Opening Ceremony & OLI 

Athline Clark 

8:15 Welcome Address 

Athline Clark 

 Gary Ostrander

8:40 Overview of Pacific Issues: Biological & Social Perspectives 

Mike Gawel 

9:00 Introduction to the CDHC and progress on the National Plan 

Cheryl Woodley 

9:15 Definition of Coral Disease and Its Various Presentations 

Esti Winter 

9:45 Lessons learned in the Caribbean (Historical perspective) 

Andy Bruckner 

10:00 BREAK 

10: 20 Global perspective of Incidence & Prevalence of Coral Disease 

Andy Bruckner 

10:45 World Bank Project: Coral Disease Working Group

Bette Willis 

11:00 Current knowledge of diseases in Hawaii & Northwest Hawaiian Islands 

Greta Aeby 

11:20 Current knowledge of diseases in US Territories/Freely Assoc States 

Thierry Work 

11:40 Current knowledge of diseases in Western Pacific 

Bette Willis 

12 NOON LUNCH – Parlor Room 

1:15 Basic Concepts in Diseases of Wildlife: The Diagnostic Method 

 Gary Wobeser 
285 

1:45 Emerging Disease – How do we identify it? 

 Stephanie Venn-Watson 

2:15 Leveraging Post Genomic Tools and Systems Biology to Accelerate the 

Understanding of Coral Disease and Effectively Monitor Tropical Reef 

Ecosystems 

Eric Mathur 

2:45 Disease Outbreak Investigation: The Process - What elements are critical? 

Dave Jessup 

3:15 BREAK 

3:45 Evolutionary Ecology, and Disease Emergence: The Big Picture 

Bruce Wilcox 

4:15 Scientists, the Public and the Politicians: How do we connect for reef’s sake? 

Jeffery Allen 

4:45 Technologies for Disease Monitoring and Assessment 

Melissa Bos 

5:15 Adjourn for the day 

6:00-8:00 Reception – Waikiki Aquarium 

Many thanks to the Alliance for Coastal Technologies and 

Kahaled bin Sultan-Living Oceans Foundation for hosting this event

Tuesday, June 20, 2006 

8:00-12:30 Breakout Groups I-IV 

 Group I – Coral Cellular Physiology & Pathology 

 Ship’s Tavern 

 Group II – Coral Toxicology & Ecological Epidemiology 

 Ship’s Tavern – Captain’s Quarters 

 Group III – Pathology of Infectious Disease 

 Board Room 

Group IV - Preventing and Responding to Coral Disease in the Pacific 

Region: Management Perspectives 

 Admirals Room 

12:30-1:30 LUNCH – Ballroom I 

2:00-5:00 Resume Breakout Group Deliberations 

5:30 Adjourn for the Day 

6:30 Reception – Terrace Moana Surfrider 
286 

7:30 Dinner – Grand Salon Moana Surfrider 

Wednesday, June 21, 2006 

8:00 General Session – Ballroom I 

Group I and II Preliminary Report & Discussion

10:00 Break 

10:20 General Session – Ballroom I 

Group III and IV Preliminary Report & Discussion

11:30 Open Discussion on Needs for Technological Advances 

Melissa Bos 

12:00 – 1:00 Lunch – Parlor Room 

1:30 – 5:00 Finalize Breakout Group Reports 

 Dinner on Your Own 

Thursday, June 22, 2006 

8:00 General Session – Parlor Room 

Final Presentations of Breakout Groups 

12 NOON Workshop Adjourned 
287 

Appendix II. Previously recommended cnidarian ‘model species’ and their 

justification from peer-reviewed literature. 

Anthozoans 

 

Plesiastrea versipora was recommended by (Ritchie et al. 1997): “Plesiastrea versipora

(Lamarck, 1816) is a hardy scleractinian coral that can be maintained for long periods in 

the laboratory even without feeding. After removal of tissue, it shows considerable 

powers of regeneration and, following recovery, can be reused in later experiments. The 

rates of respiration, photosynthesis and translocation of photosynthate from algae to 

animal recover to normal levels and the regenerated animal tissue has host release factor 

activity. We have also shown that small pieces broken off the colony will survive and 

grow slowly to form clones of the parent colony.” 

Acropora spp. was recommended by Miller and Ball (2000): “The diploblastic Cnidaria 

form one of the most ancient metazoan phyla and thus provide a useful outgroup for 

comparative studies of the molecular control of development in the more complex, and 

more often studied, triploblasts. Among cnidarians, the reef building coral Acropora is a 

particularly appropriate choice for study. Acropora belongs to the Anthozoa, which 

several lines of evidence now indicate is the basal class within the phylum Cnidaria, and 

has the practical advantages that its reproduction is predictable, external and accessible 

and that the base content of its genome is not strongly biased. The Acropora system has 

already provided insights into ancestral linkages of homeobox genes and the evolution of 

the Pax genes, and has the potential to provide further new perspectives on the age, role 

in development, and evolution of these and other gene families.” 

Frank et al. (2001) also recommended Acropora as a model scleractinian species: 

“Scleractinians are of great value in various ecological studies, in particular those related 

to bleaching, global warmth, CO2 household, etc. In addition, they may serve as a model 

system for certain questions in evolutionary developmental biology, given their basal 

position within the Cnidaria. Scleractinians are also good model organisms to study 

biomineralization. However, the cultivation of reef corals outside their natural habitats 

(which is inaccessible for most researchers outside the tropics) is very difficult. The 

generation time of corals is measured in years and their growth rate is extremely low. 

Embryos are available only a few days a year in Acropora, or a few months in other 

genera. Finally, reef corals are all protected by international law and the exchange of 

samples between laboratories is likely to be associated with legal problems.” 

The anemone Nematostella vectensis was recommended by Darling et al. (2005): N. 

vectensis is a gonochoric anemone that has been cultured through its entire life cycle 

(Fautin 2002; Hand and Uhlinger 1992). “In recent years, a handful of model systems 

from the basal metazoan phylum Cnidaria have emerged to challenge long-held views on 

the evolution of animal complexity. The most-recent, and in many ways most-promising 

addition to this group is the starlet sea anemone, Nematostella vectensis. The remarkable 

amenability of this species to laboratory manipulation has already made it a productive 

system for exploring cnidarian development, and a proliferation of molecular and 
288 

genomic tools, including the currently ongoing Nematostella genome project, further 

enhances the promise of this species. In addition, the facility with which Nematostella

populations can be investigated within their natural ecological context suggests that this 

model may be profitably expanded to address important questions in molecular and 

evolutionary ecology. In this review, we explore the traits that make Nematostella

exceptionally attractive as a model organism, summarize recent research demonstrating 

the utility of Nematostella in several different contexts, and highlight a number of 

developments likely to further increase that utility in the near future.” 

Hydrozoans 

 

Frank et al. (2001) recommended Hydractinia echinata and H. symbiolongicarpus: “The 

Cnidaria represent the most ancient eumetazoan phylum. Members of this group possess 

typical animal cells and tissues such as sensory cells, nerve cells, muscle cells and 

epithelia. Due to their unique phylogenetic position, cnidarians have traditionally been 

used as a reference group in various comparative studies. We propose the colonial marine 

hydroid, Hydractinia, as a convenient, versatile platform for basic and applied research in 

developmental biology, reproduction, immunology, environmental studies and more. In 

addition to being a typical cnidarian representative, Hydractinia offers many practical 

and theoretical advantages: studies that are feasible in Hydra like regeneration, pattern 

regulation, and cell renewal from stem cells, can be supplemented by genetic analyses 

and classical embryology in Hydractinia. Metamorphosis of the planula larva of 

Hydractinia can be used as a model for cell activation and communication and the 

presence of a genetically controlled allorecognition system makes it a suitable model for 

comparative immunology. Most importantly, Hydractinia may be manipulated at most 

aspects of its (short) life cycle. It has already been the subject of many studies in various 

disciplines, some of which are discussed in this essay.” 

Day and Lenhoff (1981), Koizumi (2002) and Shimizu and Fujisawa (2003) also 

recommended Hydra as a model animal of cnidarians: 

As a model of developmental neurobiology (Koizumi 2002): “Hydra belongs to the 

class Hydrozoa in the phylum Cnidaria. Hydra, is a model animal, who’s cellular and 

developmental data are the most abundant among cnidarians. The hydra nerve net is a 

mosaic of neural subsets expressing a specific neural phenotype. The developmental 

dynamics of the nerve cells are unique. Neurons are produced continuously by 

differentiation from interstitial multi-potent stem cells. These neurons are 

continuously displaced outwards along with epithelial cells and are sloughed off at 

the extremities. However, the spatial distribution of each neural subset is maintained. 

Mechanisms related to these phenomena, i.e., the position-dependent changes in 

neural phenotypes, are proposed... By large-scale screening of peptide signal 

molecules, peptide molecules related to nerve-cell differentiation have been 

identified... The neurons in the nerve ring show little turnover, although nerve cells in 

all other regions turn over continuously. These associations and quiet dynamics lead 

me to think that the nerve ring has features similar to those of the central nervous 

system in higher animals.” 
289 

As a classical model in evolutionary developmental biology (Hemmrich et al. 2007): 

Hydra phylogenetic relationships “reveal fundamental principles that underlie 

development, differentiation, regeneration and also symbiosis.” 

As receptor-based models with hysteresis for pattern formation (Marciniak-Czochra 

2006): “The properties of the model demonstrate a range of stationary and oscillatory 

spatially heterogeneous patterns, arising from multiple spatially homogeneous steady 

states and switches in the production rates” of diffusible biochemical molecules. 

As a model of stem cell morphogenesis (Wittlieb et al. 2006): “Transgenic Hydra

allow in vivo tracking of individual stem cells during morphogenesis.” 

As an evolutionarily conserved model system for regeneration (Holstein et al. 2003): 

 “They (Hydra) can regenerate any amputated head or foot, and when dissociated 

into single cells, even intact animals will regenerate from reaggregates. This 

extensive regeneration capacity is mediated by epithelial stem cells, and it is based on 

the restoration of a signaling center, i.e., an organizer. Organizers secrete growth 

factors that act as long-range regulators in axis formation and cell differentiation.” 

As a model of heart formation (Shimizu and Fujisawa 2003): The “peduncle of Hydra

and the heart of higher organisms share a common ancestral origin. The heart is 

assumed to have evolved as the organ for pumping blood. Here we report a pumping 

phenomenon in Hydra, a member of the phylum Cnidaria. We find that the peduncle, 

lower quarter of the body column, stores most of the gastrovascular fluid when the 

animal is an elongate form. Upon contraction of the polyp, the peduncle contracts and 

transfers the fluid into the rest of the cavity. We also find that Hydra RFamide III, a 

homolog of cardioexcitatory RFamide neuropeptides in higher organisms, elevates 

this transfer activity. Further, CnNk-2, a homolog of a cardiomuscular tissue marker 

Nkx-2.5, is expressed in the endodermal tissue of the peduncle. These observations 

indicate that the transfer of fluid by the peduncle has a similar neurological and 

genetic basis to the pumping of blood by the heart, suggesting that the Hydra 

peduncle and the heart of higher organisms share a common ancestral origin.” 

As a model for investigating epithelial cell--basement membrane interactions (Day 

and Lenhoff 1981): “Hydra mesoglea served as a suitable substrate for the 

attachment and spreading of hydra cells in vitro, irrespective of the species tested.” 
290 

Appendix III. Coral Model Species Supplementary Information 

The CoralZoo Project (for further information see the following web site: http://www.istworld.org/ProjectDetails.aspx?ProjectId=cd19d34b169247f4a3e907f1a178b772) claims 

to be the first comprehensive approach that makes use of molecular biology, 

mathematical, toxicological and nutritional tools for the development of unique breeding 

protocol for corals in captivity. The goal is to enable the SMEs to establish large stocks 

of coral colonies (the asexual approach) that represent a high genetic variability (the 

sexual approach) and exhibit natural growth forms. 

In order to achieve the main deliverables, research will focus on the following topics: 

(1) sexual and asexual breeding of corals in captivity, including breeding and feeding 

techniques and induction of natural coral colony morphogenesis 

(2) coral husbandry: development of generic bioassays to evaluate biotic and abiotic 

husbandry parameters and to monitor coral health, elaboration of methods for 

identification and treatment of coral diseases and optimization of transport and 

acclimation procedures. 

The consortium members bring complementary expertise to the project. Researchers at 

Wageningen University have experience in water recirculation systems and the culturing 

of marine organisms. Microbiologists specializing in coral diseases are based at the 

Italian Consortium for Marine Sciences, while coral biologists at the Israel Oceanography 

and Limnology Research Institute are primarily investigating nutritional aspects. Finally, 

a group at the Technical University of Dresden is modeling the data obtained from the 

other research partners, to predict how corals will perform under particular aquarium 

conditions. The academic competences are complemented by the applied aquarist’s 

research skills of the SME partners. 
291 

Appendix IV. Biographical Sketches of Workshop Participants 

Greta Aeby 

Greta is a coral biologist at the Hawaii Institute of Marine Biology (HIMB). She 

obtained her Ph.D. at the University of Hawaii where she studied the evolution and 

ecology of the coral disease, Porites trematodiasis. She then completed post-doctoral 

training at the University of West Florida examining factors affecting the susceptibility of 

coral to black band disease. She returned to Hawaii and has been investigating coral and 

fish disease in the main and northwestern Hawaiian Islands as well as in other areas of 

the Indo-Pacific. 

Email: greta@hawaii.edu 

Jeff Allen 

Jeff received his BS degree in Wildlife Biology from Michigan State University and his 

MS degree in Geography from the University of South Carolina. He received a Ph.D. in 

Policy Studies from Clemson University with an emphasis in natural resources policy. 

Prior to coming to the Thurmond Institute, he worked for the S.C. Wildlife and Marine 

Resources Department as a cartographic database manager; Clemson University and the 

National Park Service as an outdoor recreation planner for military installations across 

the U.S.; and the Regional Resources Development Institute at Clemson University as its 

program administrator. Currently, Jeff is the Director of the South Carolina Water 

Resources Center as well as Research Coordinator at the Strom Thurmond Institute of 

Government and Public Affairs (STI) at Clemson University. He oversees all projects 

within the Water Center (SCWRC), Regional Development Group (RDG), and Decision 

and Communication Technologies Group (DCTG). His work with the SCWRC involves 

administering grant money from USGS, coordinating water research with a national 

network of water research institutes and identifying and pursuing critical water research 

needs for South Carolina. His duties associated with other research groups include 

facilitating graduate student and faculty research, supervising STI's involvement with 

regional development issues, and initiating new endeavors that blend the needs and 

expertise of STI and various academic departments. Jeff has been actively involved in 

community development projects as well as natural resource policy and coastal research 

issues. Recent projects have included developing spatial models for predicting urban 

growth patterns as well as collaborating with a private company (SpectroTech) to bring 

hyperspectral remote sensing technology to Clemson University. Additionally, Jeff’s 

work includes project design and administration of research within the Institute’s Spatial 

Analysis Laboratory. This facility houses computers used for geographic information 

systems research and remote sensing image analysis. Projects within the facility focus on 

providing better spatial information to decision-makers and stake-holders regarding 

South Carolina and the Southeast. 

Email: jeff@strom.clemson.edu 
292 

Melissa Bos 

Melissa joined the Alliance for Coastal Technologies several months ago as the HawaiiPacific Coordinator based at the Hawaii Institute of Marine Biology. Prior to this, 

Melissa was the Coral Reef Specialist for the Hawaii Division of Aquatic Resources 

where she worked on six local action strategies for coral reef management in the Main 

Hawaiian Islands and with the US All Islands Group of the US Coral Reef Task Force. 

Nutrient uptake of coral reef communities under varying flow conditions was the topic of 

Melissa’s MS thesis at the University of Hawaii Oceanography Department. Melissa 

worked as an environmental consultant in Hawaii and Texas after she received a BS in 

Chemistry and Marine Science from the University of Miami. 

Email: mbos@hawaii.edu 

Andy Bruckner 

Andy is a coral reef ecologist with the NOAA Fisheries Office of Habitat Conservation. 

He received his MS in marine biology from Northeastern University, Boston MA in 

1988, and his Ph.D. from the University of Puerto Rico in 1999. His Ph.D. dissertation 

involved a study on the occurrence, impact and treatment of black-band disease. During 

the 1990s he devoted much of his time to Caribbean coral reef research, focusing on the 

effects of coral predators and coral diseases on the survival of important reef-building 

corals. Andy has also been involved in the development, implementation and training in 

coral health monitoring protocols. 

Most recently, Andy works on the NOAA Coral Reef Conservation Program and the U.S. 

Coral Reef Task Force on international and domestic coral reef conservation activities. 

Through the Coral Disease and Health Consortium (CDHC) he has been working with 

partners to develop diagnostic criteria for coral diseases, implement a rapid response 

protocol to address coral disease outbreaks; and improve our understanding of the global 

distribution and abundance of coral diseases and relationships with environmental 

factors. He recently developed a coral disease identification CD for western Atlantic 

reefs and partnered with UNEPs World Conservation Monitoring Center to implement 

the Global Coral Disease Database. He also continues his research on coral diseases and 

predators in Bonaire, Curaçao, Puerto Rico, Jamaica and the Flower Gardens. His recent 

efforts on the international trade in coral reef species include analyses of the volume, 

sources and types of coral reef species collected for marine aquaria and curios; an 

identification guides for corals in trade; assistance to developing countries in the 

development of sustainable management guidelines for ornamental coral reef fisheries; 

use of CITES Appendix II listings to prevent unsustainable trade in seahorses, humphead 

wrasse, corals, and other species on of CITES; the development of conservation strategies 

for sea cucumbers, and collection and mariculture guidelines for stony corals. In addition 

to his coral reef research, Andy manages two parts of the NOAA coral grants program 

and helps coordinate NOAAs Coral Reef Conservation Programs coral reef research, 

monitoring and management efforts. Recent awards include a 2004 Presidential Early 

Career Award for Scientists and Engineers (PECASE), and a 2003 NOAA Administrators 

Award. 

Email: Andy.Bruckner@noaa.gov 
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Athline Clark 

Athline was one of the first to merge science and policy together in Hawaii during her 

Master's Thesis in Urban and Regional Planning at the UH Manoa. She now uses her 

training and experience as a Special Projects Program Manager for the Hawaii Division 

of Aquatic Resources. In this role she is the Hawaii Point of Contact to the US Coral Reef 

Task Force and oversees all the projects and programs that Hawaii has initiated in 

response to the Task Force. This includes the creation of six Local Action Strategies to 

address threats to coral reefs. She is also the State lead for the Northwestern Hawaiian 

Islands Sanctuary designation process. 

Email: Athline.M.Clark@hawaii.gov 

Craig Downs 

Craig received his B.A in philosophy and a B.S. in biological science from Hiram 

College and his M.Sc. from Syracuse University, examining the relationship of 

biochemical/biophysical properties of photosynthesis to physiological/ecological 

phenomena. He is the founder and Executive Director of Haereticus Environmental 

Laboratory, a tax-exempt, non-profit organization whose purpose is to build scientific 

and technological capacities to address environmental health concerns. This concept was 

inspired during his time as Chief Executive Officer of the for-profit company, EnVirtue 

Biotechnologies, Inc., which provided financial and technological services pro bono to 

organizations, communities, and governments whose environmental issues could, in part, 

be resolved by the technologies provided by EnVirtue. Craig has almost 40 peerreviewed scientific publications and leads scientific research and environmental 

assessment efforts at a number of universities, including University of Hawaii and Tel 

Aviv University (Israel). Craig founded Haereticus in 2004, and to date, and has built 

numerous partnerships and collaborations with U.S. and international national, state, and 

city agencies, non-governmental organizations, and academic institutions throughout the 

world (Micronesia, Polynesia, Central America, Caribbean Islands, New Zealand, the 

Middle East and the Arctic). He has helped establish or expand several environmental 

laboratories. Craig has taught accredited courses in the fields of environmental risk 

assessment, ecotoxicology, cellular diagnostics, and biochemistry and as part of 

Haereticus’ educational effort, trains NGOs and governments in the area of 

environmental forensics and monitoring. He also remains active in the biotechnology 

industry, working with industry and governments to establish new biotech/economic 

zones in a number of countries, as well as encouraging new biotechnology start-up 

companies. 

Email: cadowns@gmail.com 

Sylvia Galloway 

Sylvia is a senior research scientist for NOAA working on assignment with the Marine 

Biomedical and Environmental Sciences Program, Medical University of SC. She 

received a BS in Foods and Nutrition from Syracuse University, a MS in Chemistry from 
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SUNY College of Environmental Science & Forestry and her Ph.D. in biochemistry 

Medical University of South Carolina. Her research focus is in the biochemistry of 

marine animals with particular reference to coral health/disease and to forensics issues. 

Currently she is studying molecular indicators of coral disease in relationship to 

environmental and anthropogenic stressors utilizing a genomic/proteomic approach. Past 

areas of research have included: (1) the measurement of environmental contaminants in 

marine mammal and sea turtle tissues, with special emphasis on the relationship of 

environmental contaminants to disease and death in these species; (2) the study of the 

metabolism of contaminant metals with special emphasis on the interaction of Se and 

CH3Hg; (3) the use of species identification techniques (including PAG-IEF, marine fatty 

acid analysis, DNA sequencing and RFLP) for the forensic identification of unknowns in 

law enforcement cases related to managed or protected marine species; (4) marine 

biotoxin assessment as related to human consumers of marine fishery products; particular 

emphasis on program management at the national level.

Email: sylvia.galloway@noaa.gov 

Mike Gawel 

Mike is the Senior Planner of Guam Environmental Protection Agency and former 

Administrator of the Guam Coastal Management Program, has worked with coral reef 

resources and environmental management issues while residing in the tropical Pacific 

Islands since 1969. After graduating in Biology from Yale in 1968 and studying 

Ecology at the Yale School of Forestry and Environmental Studies, he served in the 

Peace Corps in Fiji as a researcher and lecturer at the University of the South Pacific. He 

moved to Guam in 1973, where he completed a M.Sc. on coral taxonomy and was able to 

discover and describe coral species and coral reef fish species new to science. He has 

worked as an environmental planner and Chief Planner in Guam and other islands of 

Micronesia and Chief of Marine Resources in the Federated States of Micronesia, where 

he was married in Chuuk and his son and daughter were born in Pohnpei. During the 

1980's he studied at the East West Center and University of Hawaii’s Urban and Regional 

Planning Program. In 1989 he was hired as an evaluator of the US AID World-Wide 

Coastal Resources Management Project in Sri Lanka, Thailand and Ecuador. He has 

documented impacts of disastrous typhoons, Acanthaster planci outbreaks, and ship 

groundings on coral reefs and has worked on coral reef conservation and management 

planning and the development of coral reef assessment and monitoring plans for Guam. 

Email: Mike.Gawel@guamepa.net 

Marion Henry 

Marion represents The Federated States of Micronesia (FSM) which are Kosrae, Pohnpei, 

Chuuk (formerly Truk) and Yap, stretching over a vast expanse of Pacific Ocean just 

north of the equator. Geographically, these four small states are part of the Caroline 

Islands, consisting between them of over 600 islands, of which only 65 are inhabited. 

Marion is the Assistant Secretary for the Division of Resource Management & 

Development in the Department of Economic Affairs. The Division responsibilities 
295 

include agriculture, marine resources, tourism, and environment. He has been at this 

position for one year after serving as the Deputy Assistant Secretary responsible for 

marine resources for one year. He was Vice President of the National Fisheries 

Corporation for six year, prior to that served as Director of the Department of Resources 

and Development for the Government of Chuuk State after serving as the Deputy 

Director for 4 years. Prior to that Marion was Chief of Marine Resources for Chuuk 

State, serving in that capacity for more than five years.

Email: marionh@mail.fm 

Julie Higgins 

Julie received her B.S. in Ecology and Evolutionary Biology and her Master’s in 

Microbiology from the University of Tennessee. Her Master’s research investigated viral 

dynamics in high-nutrient, low-chlorophyll marine surface waters. Last year, Julie 

accepted a position with Dr. Cheryl Woodley’s lab, where she is pursuing molecular 

approaches to studying marine diseases. Her current projects involve using PCR and 

DNA sequencing to conduct surveillance screening of Caribbean corals for known and 

suspected coral pathogens. Julie also just received her working diver certification from 

NOAA’s Diving Center in Seattle, WA. 

Email: julie.higgins@noaa.gov 

Dave Jessup 

David Jessup was the first wildlife veterinarian hired by the California Department of 

Fish and Game. He spent 15 years working on terrestrial species including elk, deer, 

bighorn sheep, wild pigs, bear, cougar and waterfowl, primarily their diseases, anesthesia, 

capture and translocation. He has spent the last 15 years working on the health and 

welfare of marine mammals and birds and marine ecosystems. Dave has authored or coauthored over 230 scientific and popular publications, book chapters or monographs from 

1975-2006. He has also worked in Mexico, India and Africa on wildlife health and 

conservation problems. Dave currently supervises the Marine Wildlife Health and 

Research Center in Santa Cruz, CA for the OSPR division of CDFG. 

Email: DJESSUP@OSPR.DFG.CA.GOV 

Bob Jonas

Bob received his Ph.D. in Environmental Microbiology (1981) from University of North 

Carolina, Dept. of Environmental Sciences and Engineering as well as a Master’s of 

Science in Public Health also from UNC. He is Associate Professor of Environmental 

Science and Public Policy at George Mason University and former Director of Graduate 

Programs in Environmental Science and Public Policy. Bob’s research focuses on 

microbial responses in stressed ecosystems (e.g. the Chesapeake Bay, coral disease). 

Along with Dr. Esther Peters he has taught a course in Diseases of Corals and Other 

Marine Organisms through Mote Marine Laboratory each summer since 1996. In a 
296 

collaboration between the College of the Bahamas and George Mason University he has 

been investigating white plague type II as well as black-band disease affecting corals 

along the barrier reef east of Andros Island. Currently he and his collaborators (Drs. 

Gillevet and Peters) (and of course the graduate students) are working on white plague 

(or white plague-like disease) from reefs around Lee Stocking Island, The Bahamas, and 

St Croix, USVI and a white syndrome (white plague-like) at the Flower Garden Banks 

National Marine Sanctuary. 

Email: rjonas@gmu.edu 

Eugene Joseph 

After graduating from the College of Micronesia – Federated States of Micronesia 

(COM-FSM) in 1999 with an Associate’s Degree in Marine Biology, Eugene was already 

motivated to work on protecting Pohnpei’s coral reef, so in early 2001, he started 

working with the Conservation Society of Pohnpei (CSP). CSP Marine Program 

combines elements of traditional marine resource management with modern science to 

empower local communities to protect Pohnpei’s marine biodiversity. Currently, the 

program’s main focuses are MPA establishment, management and networking, spawning 

and aggregations, fish and coral monitoring, and income generating activities for MPA 

communities. Long before Eugene started at CSP, Pohnpei State Division of Marine 

Resources (DMR) has been exercising marine biophysical monitoring and data 

collection. However, there was no monitoring plan in place to keep the program running. 

Fortunately, a biophysical monitoring plan was successfully established in 2004 through 

a firm partnership between Palau International Coral Reef Center (PICRC), The Nature 

Conservancy (TNC), Pohnpei Marine Development and CSP. Two monitoring protocols 

were developed in the plan; a simple community based monitoring exercise and a more 

rigorous/science-based program to help monitor the changes in fish populations and coral 

reef cover and health. Eugene is currently a Marine Program Manager and as the 

monitoring team leader, aims to continue improving CSP marine program by enhancing 

project partnership both nationally and internationally. He is representing the 

Conservation Society of Pohnpei, Federated States of Micronesia at this workshop. 

Email: cspmarine@mail.fm Web: www.serehd.org 

Esti Kramarsky-Winter 

Esti received her Ph.D. from Tel Aviv University. She conducted her studies in the 

laboratory of Professor Yossi Loya where she studied strategies in the survival of corals 

from stressed environments, with an emphasis on reproduction and regeneration. She has 

continued her work in corals, merging coral ecology with cellular physiology and 

microscopic anatomy and physiology. Her interests lie in understanding processes of 

coral tissue repair particularly as they pertain to the ability to resist and recover from 

disease. In addition, in collaboration with Dr. Ariel Kushmaro of Ben Gurion University, 

she is currently investigating the role that symbiotic microorganisms (bacteria and 

protists) may have in coral holobiont physiology. Esti is a leader in light and electron 
297 

microscopy of corals and is an active participant with other CDHC members in 

developing the field of coral pathology. 

Email: wintere@post.tau.ac.il 

Jennifer Kozlowski 

Jennifer is a Coral Reef Program Specialist for NOAA’s National Ocean Service Coastal 

Programs Division where she directly works with the state of Florida on their Local 

Action Strategy activities and is the Program Officer for Florida’s annual Coral Reef 

Management Grant. She also serves as the lead for her office on coastal watershed 

management, land-based pollution, and coral disease-related issues in the states and 

Territories with coral resources and the U.S. Freely Associated States. Prior to joining 

NOAA, she worked with the EPA Chesapeake Bay Program as a coordinator of their 

Community-based Watershed Initiative. Jennifer has significant field experience during 

her Master’s thesis where she studied white and black band diseases in the Florida Keys 

and Bahamas, she then spent 6 years conducting pharmaceutical research and 

development, and analytical development for both veterinary and pediatric vaccines. 

Among her other interests Jennifer volunteered at the University of Maryland Center for 

Marine Biotechnology investigating microbial communities in marine sponges as 

possible sources of medically important anti-viral, anti-bacterial or anti-cancer 

compounds, and worked in a research lab at Aberdeen Proving grounds developing a 

molecular-based rapid test methodology for detecting waterborne pathogens in drinking 

water sources. 

Email: Jennifer.Kozlowski@noaa.gov 

Ariel Kushmaro 

Ariel is the head of the Environmental Biotechnology lab at Ben-Gurion University, 

Israel. Research activity includes investigation of the diversity, and distribution of 

microorganisms through approaches based on molecular (e.g. 16S rRNA analysis, FISH 

and DGGE) and novel culturing techniques. In addition his research work is aimed at 

understanding the structure and function of microbial communities and their dynamics 

with regard to the environment. Research projects include; coral diseases (e.g. bacterial 

bleaching and black band disease), novel antibiotics from cultured and uncultured 

microorganisms, characterizing microorganisms from coral surfaces and their potential 

roles in the marine ecosystem. 

E-mail: arielkus@bgumail.bgu.ac.il 
298 

Jo-Ann Leong 

Jo-Ann is Director of the Hawaii Institute of Marine Biology at Coconut Island. She 

received her Ph.D. in Microbiology from the University of California, School of 

Medicine and her A.B. in Zoology at the University of California at Berkeley. Her 

research interests are in molecular virology, vaccine development and phylogeography. 

Viruses that infect aquatic organisms are important disease pathogens and their impact on 

aquacultured species such as salmon and trout can be devastating. These viruses, 

particularly infectious hematopoietic necrosis virus (IHNV), a rhabdovirus, and 

infectious pancreatic necrosis virus (IPNV), a birnavirus, are so lethal that 90% of salmon 

production at a hatchery can be lost to these diseases. Her laboratory is developing 

vaccines and other treatments to control these diseases in fish. After her arrival in Hawaii, 

Jo-Ann has become intrigued by the devastating diseases in corals and tropical fish and 

expanded her research into these research arenas. Jo-Ann helped in the formulation of 

the current CDHC National Research Plan and has been an active member in the 

Consortium since 2001. 

Email: joannleo@hawaii.edu 

Qing Xiao Li 

Qing is a professor in the Department of Molecular Biosciences and Bioengineering, 

University of Hawaii at Manoa. He is also the director of the Pesticide Residue Research 

Laboratory at UH Manoa. Qing received his Ph.D. from the University of California at 

Davis, California, in 1990, and his post-doctoral training in the University of California at 

Berkeley from 1991 to 1994. His current research is in the areas of analytical and 

environmental chemistry; marine pollution and toxicology, immunochemistry and 

antibody-based assays for environmental applications, phyto-remediation, 

bioremediation, microbial degradation, environmental metabolomics and proteomics. He 

has more than 100 peer-reviewed publications in these research areas and is interested in 

effects of pollutants on coral, particularly persistent organic pollutants. 

Email: qingl@hawaii.edu 

Kay Marano-Briggs 

Kay received her Ph.D. from George Mason University where she studied the highly 

sulfidic Bahamian Blue Holes, characterizing the chemistry of this extreme environment 

and identifying novel microbial species. Kay is currently employed by the US 

Geological Survey and coordinates their biological research in the international arena. 

As an Affiliate Professor in the Department of Environmental Science and Policy at 

George Mason University, Kay collaborates with several GMU faculty on applied 

research topics related to coral disease and the marine environment. Her current research 

interest addresses the question of whether diver wetsuits can serve as a possible vector of 

disease, both for coral and humans. Kay has two daughters and five Thoroughbred 

horses, all of which necessitate her continued employment. 

Email: kmbriggs@usgs.gov 
299 

Eric Mathur 

In May 2006, Eric accepted a position as a scientific consultant (Animales, LLC) for the 

J. Craig Venter Institute and Synthetic Genomics, Inc. In addition, earlier this year, he 

became a delegate of the EO Wilson Biodiversity Foundation. Prior to these recent 

positions, he was the first employee and one of the scientific founders of Diversa 

Corporation. During his 12 year tenure at Diversa, he assembled the research 

organization, was instrumental in the development of their intellectual property portfolio 

and one of the lead technical scientists for business development. At various times he 

was responsible and had direct oversight for most of the research and development 

organization, including enzyme discovery, gene evolution, gene expression, cell 

engineering, sequencing, bioinformatics, subcloning and manufacturing. He eventually 

served as Vice President of Scientific Affairs and Molecular Diversity at Diversa 

Corporation. His Scientific Affairs responsibilities included external scientific 

spokesperson for Diversa Corporation, public relations officer and of Diversa’s 

Biodiversity Access Program involving management of relationships with over 20 

Countries and Institutions. Eric is the principle investigator on four separate DOE 

Initiatives for Proliferation Prevention (IPP) grants and has directed research in five 

former bioweapons laboratories in Russia. He also had oversight and directed Diversa’s 

Molecular Diversity Program, which involved recovery and isolation of environmental 

nucleic acids, metagenomics, high throughput microbial cultivation and sequence-based 

gene and pathway discovery. Prior to Diversa, Eric was a founding Senior Scientist at 

Stratagene Cloning System, a La Jolla based biotechnology company where he was 

responsible for the discovery of Pfu DNA polymerase, Stratagene’s current largest selling 

product. Eric also performed research at Scripps Research Foundation and at the 

University of California, where he received his BS degree in Biology with Highest 

Honors in 1977. Eric is an National Fellow of the Explorer’s Club, he sits on the 

Scientific Advisory Boards of Synthetic Genomics, Inc., The Explorer’s Club, 

Department of Energy’s Joint Genome Institute, the Monterrey Biotechnology Institute 

and the Thermal Biology Institute at Montana State University; he has been a member of 

the SETI Life in the Universe Working Group, the PREVCON (Prevention of Forward 

Contamination of Mars) Space Studies Board of the National Academy of Science and 

served on the Sloan Foundation’s International Census For Marine Microorganisms 

Technology Working Group. Additionally, Eric is an adjunct professor at the University 

of Hawaii’s Institute of Marine Biotechnology and holds Visiting Distinguished Scientist 

positions at both the Institute of Thermal Biology at Montana State University and the 

International Center for Insect Physiology and Ecology in Kenya; sits on the Queensland 

North America Biotechnology Council, Cal State San Marcos Biotechnology Advisory 

Council, and is an Editor of the journal, Extremophiles. Eric has published over 60 

scientific papers, is named inventor on more than 25 issued US patents and has been 

invited to present over 100 scientific lectures. 

Email: eric.mathur@gmail.com 
300 

Amanda McLenon 

Amanda is currently working with the CDHC as an Educational Coordinator, developing 

training materials for conducting Coral Disease Outbreak Investigations. As a recent 

"transplant" from Ann Arbor, MI she will begin the College of Charleston, SC graduate 

program in Marine Biology in the fall. She has seven years of professional experience as 

a high school biology teacher, specializing in science literacy. Her education to date 

includes a Bachelor of Science Education in biology and chemistry from the University 

of Michigan, and a Master of Arts in Teaching from Marygrove College. Her goal in 

returning to graduate school is to gain significant laboratory and field experience. 

Ultimately, she wants to use her strong education background to help change global 

perceptions of the ocean and its importance. Her broad interests include coral ecology 

and disease, anthropogenic influences on marine ecosystems, macroalgae, and symbiotic 

relationships. 

Email: Amanda.mclenon@gmail.com 

Margaret Miller 

Margaret is an Ecologist with the NOAA Fisheries’ Southeast Science Center. She 

received an undergraduate degree from Indiana University and a doctorate in marine 

ecology from the University of North Carolina (Chapel Hill). Her dissertation involved 

ecological studies of non-reef building coral, Oculina spp, off North Carolina and factors 

that determined their growth and distribution. She then moved south to examine some 

“real” corals, in a three years post-doctoral position with the University of Miami. She 

began work for NOAA-Fisheries in 1997 as the sole benthic ecologist at the Miami Lab 

and has served as a foundation for its growing coral reef program. She is an active field 

researcher and diver. Her involvement with coral disease was forced upon her in the 

course of monitoring activities focused on Acropora palmata and A. cervicornis in the 

Florida Keys as massive die-offs were observed. Her disease-related research has mainly 

involved field assessment and transmission experiments and collaborating with the 

CDHC in outbreak investigation and other sample collections. Her additional current 

research foci include coral early life history, population studies of threatened elkhorn and 

staghorn corals and their threats, and area assessments of reef and fisheries status around 

remote Navassa Island. She lives with her husband and 2-year old son in Miami. 

Email: margaret.w.miller@noaa.gov.

Gary Ostrander 

Gary is the Vice Chancellor for Research and Graduate Education at the University of 

Hawai‘i at Manoa. He received his Ph.D. from the University of Washington and 

completed his postdoctoral training in the Department of Pathology at the University of 

Washington Medical School in biochemical oncology. In 1990 he joined the Department 

of Zoology at Oklahoma State University as an Assistant professor and was promoted 

and tenured in 1993. He assumed the role of Directory of the Environmental Institute and 

Associate Dean of the Graduate College in 1995. Gary joined the faculty at Johns 
301 

Hopkins University in 1996. At the time of his departure in 2004 he was the Associate 

Provost for Research and Chair of the Graduate Board. While at Hopkins he held 

academic appointments in the Department of Biology and the Department of 

Comparative Medicine. Gary has authored over 80 technical papers and book chapters, 

edited 4 books and written a field guide. His primary research interest has been 

elucidating mechanisms of chemical carcinogens for which he has employed aquatic, 

rodent and human models. A second aspect of his work has involved both laboratory and 

field studies focused on understanding world-wide deterioration of coral reef ecosystems. 

Email: gko@hawaii.edu 

Pam Parnell 

Pam is a veterinary pathologist, and also serves as Director of the Clemson Veterinary 

Diagnostic Center in Columbia, South Carolina. She received her BS in Biology from 

Wofford College in 1983, Doctor of Veterinary Medicine (1987) and Doctor of 

Philosophy in Veterinary Pathology (1993) from the University of Georgia where she 

also completed her residency in anatomic veterinary pathology. She is a Diplomat of the 

American College of Veterinary Pathologists (1995) and has 13 years experience in 

diagnostic veterinary pathology. Research interests have included isolation and 

characterization of tumor growth factors, and more recently, viral diseases of shrimp and 

effects of environmental estrogens on development of mammary tumors in mice. She has 

participated in the CDHC since 2002. 

E-Mail Address: pgparnell@provetpath.com 

Esther Peters 

Esther received her Ph.D. in biological oceanography from the University of Rhode 

Island, followed by a Postdoc where she studied at the National Museum of Natural 

History and the Registry of Tumors in Lower Animals. She is an internationally 

recognized expert on coral reefs and diseases of coral reef organisms, contributing 

chapters to books (e.g., Life and Death of Coral Reefs) and journal articles, including a 

review (with others) on “Ecotoxicology of Tropical Marine Ecosystems” (Environ. 

Toxicol. Chem. 16(1):12-40). Her research includes the effects of exposures to 

biological, chemical, and physical environmental stressors on a variety of invertebrates 

and fishes, comparative histopathology, and risk assessment. Her experience with 

examining the distribution of diseased corals and histopathological examinations of 

diseased corals includes the Florida Keys, northern and western Caribbean, Gulf of 

Mexico, and Hawaii. Esther is also an adjunct scientist, Mote Marine Laboratory; 

adjunct professor, where she has been teaching the course "Diseases of Corals and Other 

Reef Organisms" at the Tropical Research Laboratory, Summerland Key, Florida, since 

1997. She also holds adjunct positions at Nova Southeastern University, Oceanographic 

Center, collaborating with scientists at the National Coral Reef Institute there; and an 

affiliate professor, Department of Environmental Science and Policy, George Mason 

University. Esther’s involvement with coral issues also includes participating in the 

interagency Coral Disease and Health Consortium, U.S. Coral Reef Task Force, and the 
302 

Technical Advisory Committee on Land-Based Sources of Pollution for the Southeast 

Florida Coral Reef Initiative. In addition to all of these activities she her ‘day job’ is as 

an Environmental Scientist VI (toxicology and pathobiology) and Quality Assurance 

Manager in the Fairfax, Virginia, office of Tetra Tech, Inc. 

Email: esther.peters@verizon.net 

Bob Richmond 

Bob is presently a Research Professor at the University of Hawaii’s Kewalo Marine 

Laboratory. He previously served as a Professor of Marine Biology at the University of 

Guam Marine Laboratory for 18 years, and as Director of the Marine Lab from 1988 - 

1991. He received a B.S. in Biology/Geology with High Distinction from the University 

of Rochester in 1976, an M.S. in Marine Environmental Sciences from the Marine 

Sciences Research Center, SUNY at Stony Brook, in 1982 and a Ph.D. in Biological 

Sciences from the Dept. of Ecology and Evolution, SUNY at Stony Brook, in 1983. 

Following completion of his graduate work, he received two postdoctoral fellowships, 

from the Smithsonian Institution and the Smithsonian Tropical Research Institute in 

Panama. He has spent most of his professional career studying coral reef ecosystems in 

both the Caribbean and the Pacific. He began his studies in the U.S. Virgin Islands and 

the Grenadines, and since 1980, has worked extensively throughout the Pacific Islands, 

from Hawaii to Palau. He served as Chief Scientist for a World Conservation Unionsponsored mission to the Galapagos Islands, and has assisted numerous Pacific Islands in 

dealing with marine resource and related conservation issues. He is the scientific advisor 

to the All-Islands Committee of the U.S. Coral Reef Task Force, and served as a Council 

Member for the International Society for Reef Studies. He was awarded an Aldo 

Leopold Fellowship in Environmental Leadership in 2004, and a Pew Fellowship in 

Marine Conservation in 2006. He works closely with island community-based 

organizations, traditional leaders and stakeholders, and has trained over 35 Pacific 

Islanders in his laboratory over the years. His present interests include coral reef 

ecology, marine conservation biology, ecotoxicology and integration of traditional 

management systems with modern approaches to resource use and protection. 

Email: Richmond@Hawaii.edu 

Mike Risk 

Mike received his BSc (Hon. Geology) U Toronto, MSc Sedimentology U Western 

Ontario, and Ph.D. Marine Biology, with Gerry Bakus. Mike specialises in assessing 

impacts on reefs of land-based sources of pollution, and in climate change as recorded in 

skeletons of shallow and deep-water corals. He has worked in 40 countries, lived in 

seven-speaks five languages equally badly, including English. 

Email: riskmj@univmail.cis.mcmaster.ca 
303 

Emmett Shotts 

Emmett received a BS in Bacteriology, in 1952, from Alabama; CMT, Medical 

Technology in 1953, from the Medical College of Alabama; MS, Medical Microbiology, 

in 1958, from Georgia and a PhD, Medical Microbiology in 1966, from Georgia. His 

specialty certifications include, Medical Technologist (ASCP); Specialist Microbiologist 

(Public Health/Medical), National Registry Microbiology; Diplomate, American College 

of Veterinary Microbiology (ACVM); Diplomate, American Veterinary Epidemiology 

Society (AVES); and a fellow, American Academy of Microbiology (AAM). 

Professionally, Emmett is active in the American Society for Microbiology (Clinical 

Section); American Fisheries Society (AFS; Fish Health Section); Wildlife Disease 

Assoc; International Assoc. Aquatic Animal Medicine; European Assoc. Fish Pathology; 

Epidemic Intelligence Service, Alumni Assoc; American Veterinary Medical Assoc 

(Affiliate); Editorial Board of Journal of Fish Diseases. During his career which has 

spanned some 45 years, he has received much recognition including the Snieszko 

Distinguished Service Award (AFS), the Distinguished Service Award (Wildlife Disease 

Assoc) and a Creative Research Medal from the University of Georgia. He has 

contributed over 250 manuscripts to Scientific Community in the form of articles, book 

chapters and published Abstracts, has two patents and made over 180 presentations. His 

research interests and expertise is varied and includes: Microbial Diseases of aquatic and 

terrestrial animals as well as humans, Zoonoses, Mechanisms of Pathogenesis, Molecular 

Technology, Mycology, Epidemiology, Ecology, Automated Systems, Antimicrobics, 

and Microbial Media development. His career has included affiliations and positions at 

Fort Detrick, MD. US Army (1954-56); Southeastern Wildlife Disease Study, Athens, 

GA (1956-59); Epidemic Intelligence Service officer, CDC; Asst. to the Chief, 

Veterinary Public Health Laboratory, CDC; Asst. to the Chief, National Rabies 

Investigations Laboratory, CDC, Atlanta (1959-64); Asst. Prof., Department of 

Pathology; Assist. Professor, Department of Medical Microbiology and Parasitology, 

Assoc. Prof., Prof., Prof. Emeritus, College of Veterinary Medicine, University of 

Georgia, Athens, GA (1966-97); and Director, National Fish Health Research Laboratory, 

Leetown Science Center USGS/DOI (1997-2000). During his career his research has 

carried him to Germany, England, Scotland, Ireland, Japan, Taiwan and Russia. 

Email: emshotts@alltel.net 

Katie Siegler 

Katie works for the Division of Aquatic Resources (DLNR-DAR) as the NOAA Coral 

Reef Fellow for the State of Hawaii. She is working with Greta Aeby on finalizing the 

Climate Change and Marine Disease Local Action Strategy. She has a Master’s Degree in 

Environmental Science and is interested in pursuing further graduate studies in marine 

disease. 

Email: katiesiegler@yahoo.com 
304 

Meir Sussman 

Meir recently completed his Ph.D. under the mentorship of Drs. Bette Willis (James 

Cook University) and David Bourne (Australian Institute of Marine Science). His Ph.D. 

research investigated coral diseases on the GBR and in the Indo-Pacific where he 

isolated, cultured, and identified causative agents for 4 coral diseases. Meir then 

identified specific proteins and their gene transcripts, actively involved in these diseases 

that are part of bacterial virulence mechanisms expressed during coral infections. He 

plans to continue this line of research with the goal of developing management-applicable 

diagnostic tools for coral diseases. 

Email: sussmanmeir@gmail.com.au 

Mac Terzich 

“Dr. Mac” is a Board certified veterinarian (Diplomate ACPV) that operates Pacific East 

Aquaculture, Inc., one of the nation's largest marine ornamentals captive coral 

propagation facilities, located on Maryland's Eastern shore in Mardela Springs. Pacific 

East Aquaculture is a Maryland State inspected and licensed coral aquaculture facility 

with the capacity to propagate and grow thousands of corals, and marine fishes and 

invertebrates. Mac is also active in sponsoring, setting up, and maintaining coral 

propagation projects in the Solomon Islands, and sponsoring research with local 

universities in coral health and captive propagation of marine ornamentals. 

Email: drmac@dmv.com 

Katherine Tucker-Mohl 

Katherine received her degree from the University of Pennsylvania, School of Veterinary 

Medicine. She received a Veterinary Medicine Fellowship to work with Dr. Patrick Hart,

Biological Resources Division - Pacific Island Ecosystems Research Center on "Avian 

malaria in Hawaii: evaluating prevalence of infection and host resistance in the Common 

Amakihi". Her study seeks to build on recent observations that certain species of native 

birds have returned to lowland habitats and have established successful populations, 

despite high levels of chronic malarial infections. Research will compare the prevalence 

of avian malaria in two previously unstudied lowland populations of Common Amakihi 

near Kona, on the island of Hawaii, with the ultimate goal of improving conservation 

programs for, and the health of, endangered Hawaiian forest birds. She has recently 

accepted an internship with Dr. Thierry Work where she will experience treating and 

studying a variety of diseases in tropical organisms. 

Email: ktmohl@vet.upenn.edu 
305 

Bernardo Vargas 

Bernardo works for NOAA’s Coral Reef Ecosystem Division in Hawaii, leading efforts 

to design and develop methods for identifying and characterizing coral disease in 

shallow-water coral reefs ecosystems of the U.S. Pacific Islands. He holds a Ph. D. from 

the University of Miami, Rosenstiel School of Marine and Atmospheric Science. 

Bernardo’s research interests include coral reef community dynamics, with special 

emphasis on coral health status, disease incidence, prevalence, and development of 

diagnostic criteria based on field observations and histopathological examinations. 

Email: Bernardo.VargasAngel@noaa.gov 

Steven Victor 

Steven is currently Head of the Research Department at the Palau International Coral 

Reef Center (PICRC) and has been a member of the research team since 2002. His main 

research interest is determining the effects of anthropogenic disturbances on coastal and 

marine resources, particularly coral reef habitats. In an effort to protect Palau’s natural 

resources, Steven has worked with local partners such as The Nature Conservancy, Palau 

Conservation Society, local government agencies and international partners such as 

NOAA, the World Bank Targeted Research Group on Remote Sensing, Coral Disease, 

and Remediation, and Restoration Group, and Scientists from Australian Institute of 

Marine Science and University of Hawaii to understand how to best minimize human 

impacts on coral reef resources. Steven completed both his undergraduate and graduate 

degrees in Biology at the University of Guam. He continues to do research on 

mangroves, seagrasses and coral reefs in Palau and Micronesia. 

Email: svictor@picrc.org 

Bruce Wilcox 

Bruce is a Professor of Tropical Medicine, Medical Microbiology and Pharmacology, at 

the John A. Burns School of Medicine, University of Hawaii. He is also the Director of 

the Asia-Pacific Center for Infectious Disease Ecology at the Asia-Pacific Institute for 

Tropical Medicine and Infectious Diseases. His fields of study were population biology, 

ecology and evolutionary biology and biology during his academic career at U. of 

California, San Diego and Yale. In addition, he has served in leadership positions in 

numerous Public Health organizations and as the founding Editor-in-chief of EcoHealth. 

He is an active teacher and researcher. Bruce’s interest in emerging infectious disease, 

ecosystem management and disease ecology has recently synthesized into a research 

focus on social-ecological systems and the relation with emerging infectious disease. 

Email: bwilcox@hawaii.edu 
306 

Dana Williams 

Dana earned her doctorate degree in 2002, at the University of South Florida working 

with Dr. Pam Hallock-Muller on the population dynamics of a reef foraminifer. She then 

began post-doctoral research at the University of Miami Rosenstiel School (RSMAS) 

working with Dr. Margaret Miller (National Marine Fisheries Service) on acroporid coral 

populations in the Florida Keys. In 2003 Dana’s discovery of an atypical disease 

outbreak in Acropora cervicornis in the Florida Keys led to her involvement in the 

CDHC and its first coordinated response and investigation of a coral disease outbreak. 

Since this outbreak investigation, Dana has continued to contribute her time and expertise 

toward refining the field sampling protocols for the CDHC’s overall coral disease 

outbreak investigation response plan. Currently Dana is an assistant scientist at RSMAS 

working on Acropora spp. population monitoring and restoration methods in the Florida 

Keys. 

Email: dana.williams@noaa.gov 

Bette Willis 

Bette is a Professor at the ARC Centre of Excellence for Coral Reef Studies and an 

Associate Professor in the School of Marine Biology and Aquaculture at James Cook 

University (Townsville, Australia). Her research explores questions relating to the 

biology and ecology of scleractinian corals. Current research focuses firstly on the 

prevalence and ecological significance of coral disease on the Great Barrier Reef, and 

secondly on the implications of flexibility in algal endosymbiosis for the physiology of 

the coral host, particularly in relation to thermal tolerance and climate change. She is a 

Co-Chair of the GEF Working Group on Coral Disease (Targeted Research and Capacity 

Building for Management program), a primary goal of which is a global assessment into 

the causes, origins and impacts of coral disease worldwide.

Email: bette.willis@jcu.edu.au 

Wendy Wiltse 

Wendy is an environmental scientist with US EPA Region 9 in Honolulu where she 

works on coral reef, wetlands, and water quality management. Wendy has worked on a 

range of EPA’s water quality management programs, coordinated a watershed 

management project on Maui, and is active in Hawaii’s Local Action Strategy to address 

land-based pollution threats to coral reefs. She’s worked in Hawaii for over 12 years. 

Wendy has a Ph.D. in Marine Ecology from the University of Massachusetts. 

Email: wiltse.wendy@epa.gov 
307 

Gary Wobeser 

Gary is with the Department of Veterinary Pathology, Western College of Veterinary 

Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. He was 

raised on a mixed farm in Saskatchewan and trained initially as a wildlife biologist (BSA, 

MSc) and then entered Veterinary Medicine (DVM) and specialized as a veterinary 

pathologist (my PhD dealt with aquatic mercury poisoning in fish and mink). He has 

been a faculty member of the Department of Veterinary Pathology since 1974 and served 

a stint as Head of the Department. Gary was founding co-director of the Canadian 

Cooperative Wildlife Health Centre, which is a cooperative enterprise among Canada’s 

four veterinary colleges, and serves all federal and provincial wildlife resource agencies. 

He teaches veterinary pathology at the undergraduate and graduate level, and wildlife 

diseases at the graduate level. He also does diagnostic pathology for both domestic and 

wild species. Gary’s research interest includes disease of all types in free-living animals 

and he has worked at one time or another with many different diseases in mammals, birds 

and a few in fish. He has published three books on the subject: Diseases of Wild 

Waterfowl (in its second edition), Investigation and Management of Disease in Wild 

Animals (currently being revised), and Essentials of Disease in Wild Animals (published 

in 2006). 

Email: Wobeser@usask.ca 

Stephanie Venn-Watson 

Stephanie Venn-Watson, D.V.M., M.P.H. received her veterinary degree from Tufts 

University School of Veterinary Medicine (1999) and public health degree from Emory 

University Rollins School of Public Health (2000). During 1999-2001, Stephanie was a 

veterinary epidemiologist at the Centers for Disease Control and Prevention (CDC) and 

served as Project Director for the World Health Organization's Global Salmonella 

Surveillance System (WHO Global Salm-Surv). Stephanie completed a National 

Research Council Associateship at the U.S. Navy Marine Mammal Program (MMP) 

during 2001-2002. She has been a civil servant veterinary epidemiologist at the MMP 

since 2003. Stephanie's primary responsibilities are epidemiological investigations; 

marine mammal infectious diseases; oversight of population health and database 

development; and coordination of clinical research. 

Email: stephanie @epitracker.com 
308 

Cheryl Woodley 

Cheryl received her Ph.D. in Molecular and Cellular Biology and Pathobiology from the 

Medical University of South Carolina. Since 1992, she has served as a research scientist 

with NOAA’s Center for Coastal Environmental Health and Biomolecular Research in 

Charleston, SC and also holds graduate faculty positions at the Medical University of 

South Carolina and the College of Charleston. Over the past five years, her expertise in 

virology, molecular biology and biochemistry has been used in adapting biomedical 

concepts and technologies to investigate the effects of natural and anthropogenic stressors 

on coral heath. Recently her laboratory joined a multi-investigator, multi-agency Marine 

Genomics team at the Hollings Marine Laboratory, providing access to state of the art 

genomic and proteomic technologies to identify diagnostic indicators useful in 

determining the health status of coral reef organisms. In 2002, she helped organize and 

establish the Coral Disease and Health Consortium (CDHC) in response to the US Coral 

Reef Task Force’s National Action Plan to Conserve Coral Reefs. The mission of the 

CDHC is “to understand and address the effects of natural and anthropogenic stressors on 

corals in order to contribute to the preservation and protection of coral reef ecosystems”. 

Cheryl currently serves as Coordinator of the CDHC and together with over 50 CDHC 

members, contributing their time and expertise, they work to unify the coral health and 

disease research community, identify research priorities, develop innovative technologies 

and encourage a new generation of coral researchers through education and outreach. 

Email: cheryl.woodley@noaa.gov 

Thierry Work 

Thierry is project leader for the Honolulu Field Station of the National Wildlife Health 

Center (USGS). He has degrees in entomology, veterinary medicine, and preventive 

veterinary medicine. His interests include diseases of free ranging terrestrial and marine 

wildlife. Current topics of investigations include diseases of reef fish, corals, and marine 

turtles. 

Email: thierry_work@usgs.gov 
309 

Appendix V. List of Participants 

Greta Aeby 

Hawaii Institute of Marine Biology 

PO Box 1346 

Kaneohe, HI 96744 

Jeffery Allen 

Clemson University 

Silas Pearman Blvd. 

Strom Thurmond Institute 

Clemson, SC 29634 

Melissa Bos 

University of Hawaii 

PO Box 1346 

Kaneohe, HI 96744 

Andy Bruckner 

NOAA Fisheries 

Office of Habitat Conservation 

1315 East West Highway 

Silver Spring, MD 20910 

Athline M Clark 

Hawaii Division of Aquatic Resources 

1151 Punchbowl St. Rm. 330 

Honolulu, HI 96813 

Evelyn (Fenny) Cox 

NOAA PIRO 

1601 Kapiolani Blvd. Suite 1110 

Honolulu, HI 96813 

Craig Downs 

Haereticus Environmental Laboratory 

PO Box 92 

Clifford, VA 24533 

Sylvia Galloway 

USDC/NOAA/NOS 

221 Ft. Johnson Rd 

Charleston, SC 29412 

Mike Gawel 

Guam EPA 

120 Bengbing St. 

Y-Papao 

Dededo, GU 96929 

Marion Henry 

Department of Economic Affairs, FSM 

P. O. Box PS12 

Palikir, Pohnpei 96941 

Federated States of Micronesia 

Julie Higgins 

NOAA/NOS 

331 Ft. Johnson Rd. 

Charleston, SC 29412 

Takiora Ingram 

NWHI Policy Specialist, 

Division of Aquatic Resources 

1151 Punchbowl St, Rm 330 

Honolulu, HI 96813 

Dave Jessup 

California Dept. Fish and Game 

1451 Shaffer Rd. 

Santa Cruz, CA 95060 

Robert Jonas 

George Mason University 

Dept Environmental Science and Policy 

George Mason University 

Fairfax, VA 22030 

Eugene Joseph 

Conservation Society of Pohnpei 

P.O.Box 2461 

Kolonia, Pohnpei 96941 

Federated States of Micronesia 

Jennifer Kozlowski 

NOAA 

1305 East West Hwy 

SSMC4, N/ORM3 

Silver Spring, MD 20910 

Esti Kramarksy-Winter 

Tel Aviv University 

25 B Kakal St 

Rehovot 76345 

Israel 

Ariel Kushmaro 

Ben-Gurion University 

Department of Biotechnology Engineering 

P. O. Box 653. 

Be'er-Sheva 84105 

Israel 

Jo-Ann Leong 

University of Hawaii 

Hawaii Institute of Marine Biology 

PO Box 1346 

Kaneohe, HI 96744 
310 

Qing Xiao Li 

University of Hawaii 

1955 East-West Road 

Agricultural Science Building Room 218 

Honolulu, HI 96822 

Kay Marano-Briggs 

US Geological Survey 

12201 Sunrise Valley Dirve 

MS 301 

Reston, VA 20192 

Eric Mathur 

J Craig Venter Institute 

2654 Galicia Way 

Carlsbad, CA 92009 

Amanda McLenon 

NOAA 

331 Fort Johnson Rd 

Charleston, SC 29412 

Margaret Miller 

NOAA-Fisheries 

75 Virginia Beach Dr 

Miami, FL 33149 

Gary K. Ostrander 

University of Hawaii 

2500 Campus Way 

Hawaii Hall 211 

Honolulu, HI 96822 

Pamela Parnell 

Clemson Veterinary Diagnostic Center 

PO Box 102406 

Columbia, SC 29224-2406 

Bob Richmond 

Kewalo Marine Laboratory 

University of Hawaii 

41 Ahui Street 

Honolulu, HI 96813 

Michael Risk 

McMaster University 

PO Box 1195 

Durham Ontario N0G 1R0 

Canada 

Luc Rougee 

Kewalo Marine Laboratory 

41 Ahui Street 

Honolulu, HI 96813 

Emmett Shotts 

Retired (Univ of GA & USGS) 

1112 Logans Ridge Rd 

Cleveland, GA 30528 

Katie Siegler 

Dept of Land and Natural Resources 

202 Getchell St 

Santa Cruz, CA 95060 

Meir Sussman 

James Cook University 

19 McDonald St 

Gulliver QLD 4812 

Australia 

Mac Terzich 

Pacific East Aquaculture 

107 School Street 

Box 217 

Mardela Springs, MD 21837 

Katie Tucker-Mohl 

4408 Pine St. Apt #2R 

Philadelphia, PA 19104 

Bernardo Vargas 

NOAA Fisheries PIFSC 

1125B Ala Moana Blvd 

Honolulu, HI 96814 

Steven Victor 

Palau International Coral Reef Center 

P.O. Box 7086 

Koror, 96940 

Palau 

Bruce Wilcox 

University of Hawaii 

Dept. Tropical Medicine 

561 Ilalo St. BSB 320 

Honolulu, HI 96813 

Dana Williams 

University of Miami 

75 Virginia Beach Dr 

Miami, FL 33149 

Bette Willis 

James Cook University 

c/o - School of Marine Biology and Aquaculture 

James Cook University 

Townsville Queensland 4811 

Australia 
311 

Gary Wobeser 

Canadian Cooperative Wildlife Health Centre 

Department of Veterinary Pathology, 

University of Saskatchewan 

Saskatoon Saskatchewan S7N 5B4 

Canada 

Stephanie Venn-Watson 

Navy Marine Mammal Program 

3812 Park Blvd. #106 

San Diego, CA 92103 

Cheryl Woodley 

NOAA NOS 

Hollings Marine Laboratory 

331 Ft Johnson Rd. 

Charleston, SC 29412 

Thierry Work 

US Geological Survey 

PO Box 50167 

Honolulu, HI 968

 
312 

Appendix VI. 

OPINION PAPER: 

Transmission Experiments in the Field: Ethics, the Law, the Science 

by Cheryl M. Woodley 

“Wildlife disease practitioners determine transmissibility in the field through 

observational studies, not field manipulations. The most valid contribution of field 

studies is to provide detailed observations over time; specifically for coral lesions by 

describing them in very precise detail, determining by the use of specific and 

discriminating characteristics whether the lesions are the same or different among 

affected individual colonies and by recording the movements of the lesion border 

...noting either expansion or contraction.” 

There are three major factors that argue against conducting field activities, presumed to 

be valid transfection or transmission experiments in situ, in a quest to determine whether 

a diseased coral has an infective agent associated with visible lesions. 

The first is an ethical issue. This practice is not condoned in human or veterinary 

medicine and is in direct opposition to the philosophy of conservation medicine, ‘to do no 

harm’. There is a fundamental ethical question related to propagating disease in a ‘wild’ 

population, either within or between populations. When this manipulation is carried out, 

it in essence establishes another focus or node of infection, if the lesion is infectious. For 

example, no veterinarian would think of putting an oyster with Perkinsus into a 

‘healthy’oyster bed nor place a sick deer or bird with their herd/flock in the wild to see if 

members of the herd/flock got sick. A good scientific test of infectivity requires a valid 

statistical design requiring multiple ‘nodes of infection’ thus deliberately spreading the 

disease in an uncontrolled environment. The biologist/scientist unwittingly becomes a 

vector, a totally unacceptable situation. 

The second factor is of a legal nature. Taking into consideration the status of coral 

reefs, and the fact that several species are already listed as threatened, either under the 

ESA or the IUCN’s Red List, the transfection manipulation described presents a 

significant risk of further endangering the reef. This can be interpreted as a deliberate 

natural resource damaging action, and for Acroporids, a violation of the Endangered 

Species Act within U.S. jurisdiction. The IUCN (International Union for the 

Conservation of Nature and Natural Resources)/ The World Conservation Union has 

guidelines on practices related to management and wildlife conservation issues. None 

directly address coral or disease transmission in the wild, however the IUCN Position 

Statement on Translocation of Living Organisms 

(http://www.iucn.org/themes/ssc/publications/policy/transe.htm) points out that any 

movement of organisms (which includes their microbiota) needs to be screened for 
313 

disease and those with disease should not be moved. They further describe penalties that 

may be assessed: “Deliberate introductions without a permit as well as negligence 

resulting in the escape or introduction of species harmful to the environment should be 

considered criminal offences and punished accordingly. The author of a deliberate 

introduction without a permit or the person responsible for an introduction by negligence 

should be legally liable for the damage incurred and should in particular bear the costs of 

eradication measures and of habitat restoration where required.” 

The third factor is scientific considerations. The experimental design is fundamentally 

flawed when conducting a transmission manipulation within the same location/population 

where the disease is observed. This violates the principle of using cohorts in infectious 

disease studies. There are a number of confounding variables that make any results 

obtained from this type of study inconclusive and invalid. These include the fact that it is 

not known: 

1) if the test subjects are already infected and not yet presenting with gross disease signs; 

2) if disease signs appear in the test group whether they are the result of an infectious 

agent as opposed to a toxin or leachate; and 

3) if disease signs appear in the test group whether they are caused by cell signaling 

molecules, chemical compounds released from dying tissue or proteases that propagate 

death (necrosis) from dying tissue. 

In other words, the field studies will not conclusively determine whether an infective 

agent is present or not. Further, a valid statistical design would require exposing at least 

9 individuals from a naïve population to determine infectivity----further deliberately 

spreading disease. 

 Ethical, legal and scientifically sound deliberate disease exposure studies should be 

conducted under containment regimes. A laboratory controlled population that 

consistently has presented with no signs of disease (naïve population) should be used as 

the test subject for exposure to diseased tissue. To meet criteria of evidence, the agent 

(infectious, chemical or toxin) should be isolated and characterized and then used to 

expose the naïve population to determine if the agent does elicit the same disease signs as 

observed in the field. 

 
314 
 

United States Department of Commerce 

Gary Locke

National Oceanic and Atmospheric Administration 

Jane Lubchenco 

Under Secretary of 

Commerce for Oceans and Atmosphere, 

NOAA Administrator 

National Ocean Service 

John (Jack) H. Dunnigan 

 Assistant Administrator for Ocean Service and Coastal Zone Management