Appendix C.1: Review of Published Studies to Characterize Relative Risks 

from Different Sources of Fecal Contamination in Recreational Water, EPA 

822-R-09-001
EPA 822-R-09-001 

REVIEW OF PUBLISHED STUDIES TO CHARACTERIZE 

RELATIVE RISKS FROM DIFFERENT SOURCES OF FECAL 

CONTAMINATION IN RECREATIONAL WATER 

U.S. Environmental Protection Agency 

Office of Water 

Health and Ecological Criteria Division 

February 2009 
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U.S. Environmental Protection Agency

February 2009 i 

DISCLAIMER

This document has been reviewed in accordance with U.S. Environmental Protection Agency 

policy and approved for publication. Mention of trade names or commercial products does not 

constitute endorsement or recommendation for use. 
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February 2009 iii 

ACKNOWLEDGMENTS

Questions concerning this document or its application should be addressed to the EPA Work 

Assignment Manager: 

John Ravenscroft 

USEPA Headquarters 

Office of Science and Technology, Office of Water 

1200 Pennsylvania Avenue, NW 

Mail Code: 4304T 

Washington, DC 20460 

Phone: 202-566-1101 

Email: ravenscroft.john@epa.gov 

This literature review was managed under EPA Contract EP-C-07-036 to Clancy Environmental 

Consultants, Inc. The following individuals contributed to the development of the report: 

Lead Writer: Jeffery Soller Soller Environmental 

Leiran Biton ICF International 

Alexis Castrovinci ICF International 

Jennifer Clancy Clancy Environmental Consultants 

Mary Clark ICF International 

Martha Embrey ICF International 

Mark Gibson ICF International 

Kelly Hammerle ICF International 

Ami Parekh ICF International 

Katherine Sullivan ICF International 

Elizabeth Zelasko ICF International 

Jennifer Welham ICF International 
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February 2009 v 

TABLE OF CONTENTS

ACKNOWLEDGMENTS ................................................................................................................................................. iii

TABLES AND FIGURES ................................................................................................................................................. vii

ACRONYMS ................................................................................................................................................................... ix

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

I. BACKGROUND AND INTRODUCTION .................................................................................................................... 5

I.1 Background: Context and Purpose ............................................................................................................ 5

I.2 Introduction ................................................................................................................................................ 6

II. METHODS ........................................................................................................................................................... 10

III. RESULTS: RECREATIONAL WATER EPIDEMIOLOGICAL STUDIES .................................................................. 12

III.1 Overview of Recreational Water Epidemiological Studies ...................................................................... 12

III.2 Descriptions of Key Recreational Water Epidemiological Studies .......................................................... 14

III.2.1 Selected Recreational Water Epidemiological Studies Based on Human Sources of Fecal 

Contamination ............................................................................................................................. 14

III.2.2 Selected Recreational Water Epidemiology Studies Based on Nonwastewater Effluent 

Sources of Fecal Contamination .................................................................................................. 24

IV. OUTBREAK REPORTS FOR RECREATIONAL AND DRINKING WATERS ............................................................. 31

IV.1 Waterborne Disease Surveillance and Outbreak Reporting in the United States ..................................... 31

IV.2 Summary of CDC Surveillance Reports on Drinking Water ................................................................... 31

IV.3 Summary of Selected Drinking Water Outbreaks Reported in the United States and Internationally ..... 32

IV.4 Descriptions of Drinking Water Outbreaks with Animal Related-Pathogen Sources .............................. 42

IV.5 Summary of Selected Recreational Water Outbreaks .............................................................................. 43

IV.6 Summary of Selected Recreational Water Outbreaks Reported in the United States and 

Internationally .......................................................................................................................................... 57

IV.7 Descriptions of Recreational Water Outbreaks with Animal Related-Pathogen Sources ........................ 57

IV.7.1 Environmental Sampling Including Animal Sources .................................................................. 57

IV.7.2 Environmental Sampling not Including Animal Sources ............................................................ 62

V. COMPILATION OF DATA AND SUMMARY ........................................................................................................... 63

VI. REFERENCES ...................................................................................................................................................... 68

APPENDIX A: LITERATURE SEARCH STRATEGY AND RESULTS ............................................................................. A-1
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February 2009 vii 

TABLES AND FIGURES

Table I.2.1. Representative Fecal Indicator Bacteria and Zoonotic Pathogen Densities in Human and Animal Feces 

and Sewage .................................................................................................................................................................... 8

Table III.1.1. Recreational Water Epidemiology Studies Included in Reviews by Prüss (1998), Wade et al. (2003), 

and Zmirou et al. (2003) .............................................................................................................................................. 13

Table III.1.2a. Recently Completed Recreational Waters Epidemiological Studies—Some of Which Address 

Nonpoint Sources of Fecal Contamination .................................................................................................................. 15

Table III.1.2b. Ongoing Recreational Waters Epidemiological Studies—Some of Which Address Nonpoint Sources 

of Fecal Contamination ............................................................................................................................................... 16

Table IV.2.1. Select Waterborne Disease Outbreaks Associated with Drinking Water in the United States Reported 

by the CDC (1999 to 2004) ......................................................................................................................................... 34

Table IV.3.1. Select Waterborne Disease Outbreaks Associated with Drinking Water ............................................. 38

Table IV.5.1. Select Waterborne Disease Outbreaks Associated with Recreational Water in the United States 

Reported by the CDC (1999 to 2004) .......................................................................................................................... 45

Table IV.6.1. Select Waterborne Disease Outbreaks Associated with Recreational Water ........................................ 58
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February 2009 ix 

ACRONYMS

AWQC 

BEACH Act 

ambient water quality criteria 

Beaches Environmental Assessment and Coastal Health Act 

CCDR 

CDC 

Canada Communicable Disease Report 

U.S. Centers for Disease Control and Prevention 

CFU 

CI 

colony forming unit 

confidence interval 

DNA 

EC 

EEC 

EPA 

GI 

deoxyribonucleic acid 

European Commission 

European Economic Community 

U.S. Environmental Protection Agency 

Gastrointestinal 

HUS 

MMWR 

MPN 

NM 

hemolytic uremic syndrome 

Morbidity and Mortality Weekly Report 

most probably number 

nonmotile 

NOAEL no-observed-adverse-effect-level 

NRC National Research Council 

PCR 

QMRA 

polymerase chain reaction 

Quantitative microbial risk assessment 

SCCWRP 

U.S.

Southern California Coastal Water Research Project 

 United States 

WHO 

WSAA 

World Health Organization (United Nations) 

Water Services Association of Australia 
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EXECUTIVE SUMMARY

Introduction 

The overall goal of the current ambient water quality criteria for bacteria in the United States is 

to provide public health protection from gastroenteritis (gastrointestinal [GI] illness) associated 

with exposure to fecal contamination during water-contact recreation. Because fecal matter can 

be a major source of pathogens in ambient water, and because it is not practical or feasible to 

monitor for the full spectrum of all pathogens that may occur in water, water quality criteria are 

specified throughout the world in terms of fecal indicator organism densities. For decades, these 

fecal indicator organisms have served as surrogates for potential pathogens and subsequent 

health risks in both recreational and drinking waters. 

The U.S. Environmental Protection Agency’s (EPA) recommended recreational water quality 

criteria do not differentiate between fecal sources of pathogens. Thus, EPA’s regulatory premise 

concerning recreational water quality has been that nonhuman-derived human pathogens in 

fecally contaminated waters are as hazardous as their human-derived counterparts. The World 

Health Organization’s (WHO) recommended approach for classifying the water quality of 

recreational waters is based on the premise that the measure of microbiological indicators of 

fecal contamination can be “interpreted” using evidence of the presence or absence of human 

fecal contamination. This approach assumes that in general, sources other than human fecal 

contamination are less of a risk to human health. WHO indicated in their 2003 report Health 

Based Monitoring of Recreational Waters: The Feasibility of a New Approach (The “Annapolis 

Protocol”) that “due to the species barrier, the density of pathogens of public health importance 

is generally assumed to be less in aggregate in animal excreta than in human excreta and may 

therefore represent a significantly lower risk to human health.” 

Ultimately, the critical question is whether exposure to different fecal sources from recreational 

waters translates to significant differences in the risk of human infection or disease severity. The 

purpose of this white paper is to describe the existing knowledgebase available to characterize 

the relative risks of human illness from various sources of fecal contamination in recreational 

waters. Information related to human exposures to pathogens in fecally contaminated 

recreational and drinking waters was obtained by searching the scientific literature for 

epidemiological studies related to exposure to recreational waters and reports of outbreak 

investigations from both recreational and drinking waters. 

Recreational Water Epidemiological Studies 

Numerous epidemiological investigations have been conducted since the 1950s to evaluate the 

association between illness risk to recreational water users and the density of suitable fecal 

indicators. These studies have been conducted in Australia, Canada, Egypt, France, Hong Kong, 

Israel, the Netherlands, New Zealand, Spain, South Africa, United States, and the United 

Kingdom. Importantly, most of these studies investigated waters that were impacted or 

influenced by wastewater effluent. 
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February 2009 2 

Taken as a whole, the weight of evidence from these studies indicates that fecal indicator 

bacteria are able to predict GI and respiratory illnesses from exposure to recreational waters. 

However, as indicated above, most of these studies investigated waters that were impacted or 

influenced by wastewater effluent, and close inspection of this base of information reveals that 

few studies addressed sources of contamination other than wastewater effluent in the investigated 

waters. Prior to 1999, only three peer-reviewed publications addressed this topic substantially 

(Calderon et al., 1991; Cheung et al., 1990; McBride et al., 1998). In the last few years, 

researchers have conducted several additional epidemiological studies focusing on waters not 

predominately impacted by wastewater effluent. Additionally, the Southern California Coastal 

Water Research Project (SCCWRP) is also conducting a series of epidemiological studies that 

investigate recreational water with various contamination sources other than wastewater effluent. 

Review of the epidemiological studies that address recreational water predominantly impacted 

by sources other than wastewater effluent indicates that the results are equivocal. For example, 

Colford et al. (2007) found that the incidence of swimmer illness was not associated with any of 

the traditional fecal indicators at a marine beach with primarily avian contamination. This result 

is substantially different than those studies described above on wastewater impacted waterbodies. 

Whereas, a study from New Zealand (McBride et al., 1998) indicated that illness risks posed by 

animal versus human fecal material were not substantially different. 

Outbreak Reports for Recreational and Drinking Waters 

In the United States, formal surveillance data on the occurrence and causes of waterborne disease 

outbreaks are collected through collaboration between EPA, the Council of State and Territorial 

Epidemiologists, and the U.S. Centers for Disease Control and Prevention (CDC). The goals of 

the surveillance program include characterizing the epidemiology of outbreaks, identifying the 

agents causing outbreaks as well as trends and risk factors, identifying deficiencies in providing 

safe drinking water, encouraging health officials to investigate outbreaks, and fostering 

government and international agency collaboration on waterborne disease prevention. The 

number of outbreaks reported is a significant underestimate of the actual number of outbreaks 

that occur, as the actual numbers reported vary depending on issues such as a lack of laboratory 

capability. Thus, the extent of underestimation is unknown overall. Even with these problems, 

surveillance studies provide the best information available on waterborne disease outbreaks and 

such data are critical to adequately characterizing microbial hazards. 

In reviewing outbreak information for recreational and drinking water waters, several 

overarching points emerged. One is that the pathogen source in the majority of drinking waterrelated outbreaks remains unknown. The source of pathogens in drinking water outbreaks in 

many cases could have been humans or animals. Most reports, however, offered little detail, 

leaving a critical information gap for the purposes of this review. Nevertheless, several outbreak 

investigation studies were able to link pathogens isolated from patients with water samples 

and/or animals using laboratory analysis. Other reports used circumstantial evidence to link 

animal waste to outbreaks; however, although compelling, laboratory results were not available 

to confirm the contamination source. The animal sources linked to outbreaks included beavers, 

cats/cougars, deer, elk, pigs, cattle, and chickens/poultry, and the corresponding animal-related 

human pathogens in these outbreaks were Giardia intestinalis, Cryptosporidium spp., E. coli
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February 2009 3 

O157:H7, Campylobacter spp., Toxoplasma gondii, and S. typhimurium. Given that outbreaks 

are known to be a notoriously poor measure of the actual number of infections and illnesses 

caused by waterborne pathogens, those investigations that link pathogens isolated from patients 

and/or water samples with animals provide unequivocal evidence that human illnesses can and 

do occur from animal-based contamination. Unfortunately, the drinking water outbreak 

literature does not substantially enhance the current ability to quantitatively differentiate risks 

from animal- versus human-related pathogen sources for recreational water exposures. 

The recreational water outbreak literature (Craun et al., 2005) indicates that of the 259 

recreational water outbreaks that occurred in the United States between 1970 and 2000, only 

approximately half included any information about possible sources of the contamination or the 

sources contributing to it. Approximately 18 percent of the total outbreaks were associated with 

animals, likely etiologic agents included E. coli spp., Schistosomes spp., and Leptospira spp. E. 

coli was associated with cattle, deer, or duck feces; Schistosomes spp. were associated with 

snails; and Leptospira spp. were associated with rat urine. Similar to the drinking water outbreak 

compilation, the recreational water outbreak literature does not appear to substantially enhance 

the current state of knowledge on quantitatively characterizing risks from animal-related 

pathogen sources compared with human sources for recreational water exposures. 

Interpretation of Results 

Given that relatively few investigations worldwide have evaluated the risk to human health from 

recreational exposure to waters primarily impacted by sources of contamination other than 

wastewater effluent, and that the potential range of those sources is broad, the findings from this 

literature review are not surprising. 

Although information on differentiating human versus animal sources of pathogens is lacking, 

several research organizations and countries have suggested novel approaches for addressing 

risks from nonhuman sources (e.g., Water Services Association of Australia). For example, New 

Zealand, where about 80 percent of total notified illnesses are zoonotic and potentially 

waterborne, has recently updated its recreational water quality criteria to address the issue of 

animal-source waterborne contamination by basing its freshwater guidelines principally on the 

risks associated with campylobacteriosis using E. coli concentrations as an indicator (Till and 

McBride, 2004). 

In summary, both human and animal feces in recreational waters continue to pose threats to 

human health. Although the public health importance of waterborne zoonotic pathogens is being 

increasingly recognized, it is still not well characterized. Policy makers and researchers have 

often assumed that the human health risk from pathogens associated with domestic and 

agricultural animal and wildlife feces is less than the risk from human feces, in large part 

because viruses are predominately host-specific. This literature review illustrates a lack of 

detailed and unequivocal information concerning the relative risks of human illness resulting 

from exposure to various sources of fecal contamination in recreational waters. Because of their 

retrospective nature, waterborne disease outbreak investigations rarely produce the data needed 

to draw conclusions about the impact of a pathogen source. Finally, the ability to measure how 
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February 2009 4 

the infectivity and virulence of known waterborne zoonotic pathogens are affected when 

passaged through animal hosts remains in its infancy. 
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I. BACKGROUND AND INTRODUCTION

I.1 Background: Context and Purpose 

Since the U.S. Environmental Protection Agency (hereafter EPA or the Agency) last published 

recreational water quality criteria in 1986, significant advances have occurred, particularly in the 

areas of molecular biology, microbiology, and analytical chemistry. EPA believes that these new 

scientific and technical advances need to be considered and evaluated for feasibility and 

applicability in the development of new or revised Clean Water Act (CWA) Section 304(a) 

criteria for recreation. The Beaches Environmental Assessment and Coastal Health (BEACH) 

Act of 2000 (which amended the CWA) required EPA to conduct new studies and issue new or 

revised criteria, specifically for Great Lakes States and coastal marine waters. To this end, EPA 

has been conducting research and assessing relevant information to provide the scientific 

foundation for new or revised criteria. 

To address the BEACH Act requirement, EPA has engaged a range of stakeholders representing 

the general public; public interest groups; state, local, and municipal governments; industry; and 

wastewater treatment professionals. In March 2007, EPA convened 43 national and international 

technical, scientific, and implementation experts from academia, numerous states, public interest 

groups, EPA, and other federal agencies at a formal workshop to discuss the state of the science 

on recreational water quality research and implementation (USEPA, 2007). The workshop 

outcome included a suggestion to incorporate the ability to differentiate sources of fecal 

contamination and determine the relative human health risk from these sources into the new or 

revised criteria. 

Based on the feedback from the larger group of stakeholders and detailed input and 

recommendations from the scientific community, the Agency developed a Critical Path Science 

Plan for Development of New or Revised Recreational Water Quality Criteria. A key question 

the science plan asks is what is the risk to human health from swimming in water contaminated 

with human fecal matter as compared to swimming in water contaminated with nonhuman fecal 

matter? Human and animal feces both can potentially contain pathogens that cause human 

illness. However, while some human pathogens are host-specific (i.e., human enteric viruses), 

other human pathogens can be shed by both humans and animals. In other words, all enteric 

pathogens of humans are infectious to other humans, while relatively few of the enteric 

pathogens of animals are infectious to humans (zoonotic pathogens). Understanding which 

human pathogens are associated with which source of fecal contamination would allow the 

Agency to recommend better (more appropriate) water quality criteria in those situations. 

EPA’s current recommended criteria treat the human health risk from various sources of fecal 

contamination as equivalent based on health risks from fecal contamination originating from 

publicly owned treatment works, which represent the highest relative risks to swimmers. 

Because health risks from other sources (e.g., poorly treated or untreated human waste, 

nonhuman fecal matter, and mixed sources, such as urban stormwater runoff) were not well 

understood at the time the 1986 criteria were developed, the approach was to protect human 

health regardless of the source. However, EPA recognizes that the health risk from fecal sources 

other than publicly owned treatment works may be different and that recent scientific advances 
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February 2009 6 

may now allow the Agency to better characterize the relative risks to human health from 

different sources of fecal contamination. Specifically, the Agency is interested in understanding 

what human illnesses are caused by swimming in waters contaminated with human fecal matter 

from various sources, including human sources (wastewater effluent and untreated human fecal 

matter), nonhuman fecal matter (ranging from wildlife sources to agricultural inputs), and mixed 

sources, such as urban stormwater runoff. 

The purpose of this white paper is to describe the existing knowledge base available to 

characterize the relative risks of human illness from various sources of fecal contamination in 

recreational waters. An overview of recreational water epidemiology studies and results from 

illness outbreak investigations are discussed in an attempt to demonstrate any differential risk to 

human health that may exist from various sources of fecal contamination. 

I.2 Introduction 

The overall goal of the current ambient water quality criteria (AWQC) for bacteria in the United 

States (USEPA, 1986) is to provide public health protection from gastroenteritis (GI illness) 

associated with exposure to fecal contamination during water contact recreation. Because fecal 

matter can be a major source of pathogens in ambient water, and because it is not practical or 

feasible to monitor for the full spectrum of all pathogens that may occur in water, water quality 

criteria are specified throughout the world in terms fecal indicator organism densities (USEPA, 

1986; WHO, 2003). These fecal indicator organisms have been used for decades as surrogates 

for potential pathogens and subsequent health risks in both recreational and drinking waters 

(NRC, 2004). 

The Agency used prospective cohort epidemiological studies of wastewater effluent-impacted 

recreational waters (USEPA, 1986) to develop the 1986 AWQC for recreational water. The 

results of those epidemiological studies provide quantitative relationships between fecal indicator 

density in recreational waters (E. coli and enterococci for freshwaters and enterococci for marine 

waters) and GI illness levels for those individuals exposed to recreational waters (USEPA, 

1986). Using randomized controlled trials, Kay et al. (1994) showed fecal streptococci 

(enterococci1

) to be predictive of gastroenteritis (GI illness) among bathers in the United 

Kingdom. Fleischer et al. (1996) reported that exposure to fecal streptococci also could predict 

acute febrile respiratory illnesses. These studies formed the basis of the guidelines 

recommended by the World Health Organization (WHO, 2003). In addition, detailed reviews 

conducted by Wade et al. (2003) and Prüss (1998) strongly support the findings that increased 

enterococci (or fecal streptococci) concentrations predict GI illness risk (Lepesteur et al., 2006). 

Internationally, many countries still rely on fecal and total coliforms as a basis for their 

recreational water quality criteria, standards, or guidelines (see WHO, 1999). Other countries 

rely on measurements of enterococci, E. coli, or both for their recreational waters, most based on 

criteria recommendations provided by WHO (2003) and/or on EPA’s epidemiological studies 

that led to the 1986 criteria. 

 1

 The terms fecal streptococci, enterococci, intestinal enterococci, and Enterococcus are often used to refer to 

essentially the same environmental and fecal species of bacteria (see NRC, 2004 for further information). Thus, for 

convenience, this white paper uses the term enterococci unless otherwise noted. 
U.S. Environmental Protection Agency

February 2009 7 

EPA’s recommended recreational water quality criteria do not differentiate between fecal 

sources of pathogens. Thus, EPA’s regulatory premise concerning water quality has been that 

nonhuman derived human pathogens when present in fecally contaminated waters are as 

hazardous as their human-derived counterparts (Schaub, 2004). This presumption is supported 

by scientific literature that confirms that there are many waterborne zoonotic bacteria and 

protozoa common to both humans and to various types of animal populations (especially 

mammalian species). The literature also suggests, however, that in certain instances there may 

be attenuation of the infectivity, virulence, and disease severity to humans from animal-derived 

(“passaged”) human pathogens. Moreover, “[w]e must also recognize that more than half the 

bacteria in the human intestine and more than 99 percent of environmental bacteria have not 

been cultured or characterized...This is almost certainly also true for the broad array of domestic 

and wild animals in our environment” (Bolin et al., 2004). 

WHO’s recommended approach for classifying the water quality of recreational waters relies on 

combining microbiological monitoring results for fecal indicators and a sanitary inspection 

(WHO, 2003). This approach is based on the premise that the measure of microbiological 

indicator of fecal contamination can be “interpreted” using evidence of the presence or absence 

of human fecal contamination; the approach also presumes that in general, sources other than 

human fecal contamination present a lesser risk to human health (WSSA, 2003). WHO indicated 

that “due to the species barrier, the density of pathogens of public health importance is generally 

assumed to be less in aggregate in animal excreta than in human excreta and may therefore 

represent a significantly lower risk to human health” (WHO, 1999). 

WHO highlighted this issue of potential differential risks between human and nonhuman sources 

in its recent report on zoonoses (WHO, 2004), which noted that the inability to distinguish 

human from animal fecal contamination has led resource managers and regulators to treat all 

fecal contamination as equally hazardous to human health. The report further indicated the 

following (Till and McBride, 2004): 

• This approach frequently results in the closure of beaches and shellfish harvesting areas 

that are affected by stormwater runoff that carries fecal indicator bacteria of nonhuman 

origin. 

• The true risk of exposure to waters contaminated by animals is not well characterized. 

• Studies that have attempted to define the risk associated with swimming in animalcontaminated water have not given a clear indication that there is an excess illness rate 

related to this type of exposure. 

• These equivocal results do not lead to the conclusion that all fecally contaminated waters 

should be treated alike. 

• New research to define the risk posed by animal fecal wastes to users of water resources 

and indicator systems that identify animal contamination of surface waters are needed. 

Ultimately, the merit of an AWQC approach that treats animal and human sources of pathogens 

and indicators differently or somehow discounts animal sources depends on both the 

characterization of relevant differences between human and animal fecal material and the 

availability of technology that can accurately and reliably differentiate between their sources. 

These issues are of concern to the development of new or revised recreational AWQC because 
U.S. Environmental Protection Agency

February 2009 8 

the normal microbial composition of animal feces is different from human feces and can change 

dramatically over time and space, especially in recreational waters (Table I.2.1) (Boehm et al., 

2002; Dorner et al., 2007; NRC, 2004). Moreover, the critical question is whether these 

differences in fecal sources resulting from recreational water-related exposures translate to 

significant differences in the risk of human infection or disease severity. 

Table I.2.1. Representative Fecal Indicator Bacteria and Zoonotic Pathogen Densities in 

Human and Animal Feces and Sewage* 

Indicator Observed Density Source

Bacteria

Fecal coliforms 108

-109/gram feces Infected person 

Fecal coliforms 4.9 x 1010 organisms/day Canada geese 

Fecal coliforms 1.4 x 108

-2.4 x 109

organisms/day 

Chicken 

Fecal coliforms 5.4 x 109

 organisms/day Cows 

Fecal coliforms 4.2 x 108

 organisms/day Horses 

Fecal coliforms 8.9 x 109

-1.1 x 1010

organisms/day 

Pigs 

Fecal coliforms 1.8 x 109

-1.2 x 1010

organisms/day 

Sheep 

Fecal coliforms 5 × 109

 organisms/day Dogs and cats 

Fecal coliforms 105

-107

(MPN)/100 mL

 most probable number Sewage 

Fecal coliforms 4.2 x 106

 organisms/100 mL Combined sewer overflow 

Fecal coliforms 9.6 x 102

-4.3 x 106

organisms/100 mL 

Urban runoff 

Fecal coliforms 1.2 x 102

-1.3 x 106

organisms/100 mL 

Grazed pasture runoff 

Fecal coliforms 1.35 x 106

-2.4 x 108

organisms/100 mL 

Feedlot runoff 

Fecal coliforms 1.2 x 101

-1.43 x 104

organisms/100 mL 

Cropland runoff 

E. coli 1.7 x 108

 E. coli/gram Pigeons 

E. coli 103

-104 colony forming units 

(CFU)/100 mL 

Stormwater 

Enterococci 4.0 x 105

 enterococci/day Pigeons 

Enterococci 102

-103 enterococci/mL; 

5.4 x 105

 enterococci/100 mL 

Sewage 
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February 2009 9 

Indicator Observed Density Source

Pathogens

Bacteria 

E. coli O157:H7 102

-106 per gram feces Calves 

Pseudomonas aeruginosa 2.3 x 105 MPN/100 mL Sewage 

Salmonella 0.2-11,000 MPN/100 mL Sewage 

Protozoa 

Protozoan parasites 106

-107/gram feces Infected person 

Cryptosporidium oocysts 370 ± 197 oocysts/gram feces 

1.2 x 105

-3.9 x 105 organisms/

day 

Canada geese 

Cryptosporidium oocysts 13.7/mL Slaughterhouse (cattle) 

Cryptosporidium oocysts 1.4 x 104

-3.96 x 104/L Treated effluent (activated sludge) 

Cryptosporidium oocysts 4.0 x 100

-1.6 x 101/L Treated effluent (activated sludge 

and sand filtration) 

Cryptosporidium oocysts 3-13,700/1,000 mL Sewage 

Giardia cysts 450 cysts/gram feces; 3.1 x 105

cysts/day 

Canada geese 

Giardia cysts 2-200,000/1000 mL Sewage 

Viruses 

Enteric viruses 103

-1012/gram feces Infected person 

Adenovirus 1-10,000/100 mL Sewage 

Enterovirus 0.05-100,000/100 mL Sewage 

Reovirus 0.1-125/100 mL Sewage 

Rotavirus 0.1-85,000/100 mL Sewage 

Caliciviruses 106

/gram (1013/day) Gray whales** 

* Although marine mammal caliciviruses are not known to be human pathogens, they have been being 

investigated as potential sources of emerging zoonoses (Smith et al., 1998). 

Source: Adapted from: Protocol for Developing Pathogen TMDLs (USEPA, 2001), Impacts and Control 

of CSOs and SSOs: Report to Congress (USEPA, 2004), and Waterborne Zoonoses: 

Identification, Causes, and Control (WHO, 2004). 
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February 2009 10 

II. METHODS

As indicated previously, the primary purpose of this white paper is to describe the existing 

knowledge base available to characterize the relative risks of human illness from various sources 

of fecal contamination in recreational waters. The paper specifically covers human illness 

resulting from water-related exposures to fecal material from human and nonhuman sources. 

Although the ultimate use of this information is to support the development of new or revised 

water quality criteria and/or standards for recreational waters, this review encompasses both 

recreational and drinking water exposures. 

Information related to human exposures to pathogens in fecally contaminated recreational and 

drinking waters was obtained by searching the scientific literature for epidemiological studies 

related to exposure to recreational waters and reports of outbreak investigations from both 

recreational and drinking waters. Appendix A details the specific search strategies and databases 

employed. 

This literature review combines disparate information to infer potential differences in risk 

between various sources of contamination and the limitations in each class of study are 

important. For example, in epidemiological studies conducted on recreational waters, the 

amount of water ingested during recreation is often not known. In many cases, studies also 

include multiple potential sources of waterbody contamination. Furthermore, outbreaks are a 

notoriously poor measure of the actual number of infections and illnesses caused by waterborne 

pathogens (Craun, 2004). The timely investigation of a waterborne outbreak by the appropriate 

professionals who have access to adequate laboratory resources can provide information about an 

outbreak’s mode of transmission, the etiologic agent, and sources of contamination. However, 

many outbreaks are not recognized or investigated, and even in recognized outbreaks, not all 

cases of disease are reported; the likelihood of reporting is dependent on many factors, including 

pubic awareness of waterborne illnesses (such as media coverage of an event), the local 

requirements for reporting, and the availability of laboratory facilities (Craun et al., 2005). 

Often, gaps in data result in an incomplete picture of the incident—especially in recreational 

water, where water testing may occur days or weeks after the outbreak started. In many 

recreational water outbreaks, by the time an outbreak is discovered and the etiologic agent is 

isolated, it is too late to provide meaningful data regarding the source of disease. 

An example of the difficulty of linking illness with its source in recreational water occurred 

during an outbreak of E. coli-related illness in the Netherlands (Cransberg et al., 1996). Four 

children hospitalized in one town with hemolytic uremic syndrome prompted a search for a 

single source of illness. The results of the investigation pointed to a shallow lake where the ill 

children had all been swimming during a 5-day period. Pulsed-field electrophoresis of E. coli

isolates of patients and family members showed an identical pattern: no E. coli DNA could be 

detected in filter-concentrated lake water samples using polymerase chain reaction (PCR). 

However, water samples were not taken until two weeks after the exposures.
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February 2009 11 

The principal methodology employed for this white paper is provided below: 

• Summarize the recreational water epidemiology studies that have been published 

worldwide. 

• Provide a brief description of the most influential recreational water epidemiology studies 

as well as those that investigated waters impacted with sources other than wastewater and 

wastewater effluent. 

• Summarize waterborne disease outbreaks associated with drinking water in the United 

States reported by the CDC from 1999 to 2004. 

• Summarize select waterborne disease outbreaks associated with drinking water from 

other countries and from the United States before 1999. 

• Summarize waterborne disease outbreaks associated with recreational water in the United 

States reported by the CDC from 1999 to 2004. 

• Summarize select waterborne disease outbreaks associated with recreational water from 

other countries and from the United States before 1999. 

• Provide brief descriptions of reported drinking water and recreational outbreaks with 

animal-related pathogen sources. 

• Compile the information described above and determine the weight of evidence available 

to demonstrate any differential risk to human infection, disease severity, or both resulting 

from exposure to fecal material from human or animal sources in recreational water. 
U.S. Environmental Protection Agency

February 2009 12 

III. RESULTS ECREATIONAL ATER PIDEMIOLOGICAL TUDIES 

III.1 Overview of Recreational Water Epidemiological Studies 

Since the 1950s, numerous epidemiological studies have been conducted throughout the world to 

evaluate the association between recreational water quality and adverse health outcomes, 

including GI symptoms; eye infections; skin complaints; ear, nose, and throat infections; and 

respiratory illness (Prüss, 1998; Sinton et al., 1998; Wade et al., 2003; Zmirou et al., 2003). 

Although most of these studies investigated wastewater effluent-impacted marine and estuarine 

waters alone or in combination with freshwater, several investigated freshwater recreational 

environments or nonwastewater effluent-impacted waters. These studies indicate that the rates 

of some adverse health outcomes are higher in swimmers compared with nonswimmers (Prüss, 

1998). 

Several groups of researchers have compiled information and generated broad and wide-ranging 

inferences from these epidemiological studies. Below is a brief overview of the meta-analyses 

conducted by Prüss (1998), Wade et al. (2003), and Zmirou et al. (2003); Table III.1.1 provides 

an overview of the epidemiological studies included in these reviews. 

• Prüss (1998) conducted a systematic review following discussions between the WHO 

Regional Office for Europe and WHO Headquarters to initiate development of new 

guidelines for recreational use of the water environment. The comprehensive review of 

22 published studies on sewage pollution of recreational water and health outcomes 

concluded that the epidemiological basis had been laid to develop WHO guidelines on 

fecal pollution based on a causal association between GI illness symptoms and increased 

bacterial indicator density (i.e., enterococci for marine, enterococci and E. coli for fresh) 

in recreational waters. 

• A meta-analysis of 18 published studies (Zmirou et al., 2003) was conducted by 

researchers at the National Institute for Public Health Surveillance at the request of the 

French Ministry of Health to help provide a scientific basis for establishing new 

standards for the microbial quality of marine and fresh recreational waters to replace the 

30 year-old European Union bathing water quality guidelines (EEC, 1976). The 

researchers provided four major results: (1) increased concentrations of fecal coliforms 

or E. coli and enterococci in both fresh and marine recreational waters are associated with 

increased risks of acute GI illness, with enterococci eliciting four to eight times greater 

excess risks than fecal coliforms or E. coli at the same concentrations; (2) GI illness risks 

associated with enterococci occur at lower concentration in marine versus fresh 

recreational waters; (3) increased concentrations of total coliforms have little or no 

association with GI illness risk; and (4) no evidence exists of a threshold of indicator 

density below which there would be no GI illness risk to bathers. 

• Wade et al. (2003) conducted a systematic review and meta-analysis of 27 published 

studies was to evaluate the evidence linking specific microbial indicators of recreational 

water quality to specific health outcomes under nonoutbreak (endemic) conditions. 

Secondary goals included identifying and describing critical study design issues and 

: R W E S 
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February 2009 13 

Table III.1.1. Recreational Water Epidemiology Studies Included in Reviews by Prüss 

(1998), Wade et al. (2003), and Zmirou et al. (2003) 

First Author Year Location Water Type Study Design Review Article

Alexander et al. 1992 UK Marine Cohort Wade, Zmirou

Bandaranayake 1995 New Zealand Marine Cohort Prüss

Brown 1987 UK Marine Cohort Zmirou

Cabelli 1983 USA Marine Cohort Wade, Prüss, Zmirou

Cabelli 1983 Egypt Marine Cohort Wade, Prüss

Calderon et al. 1991 USA Fresh Cohort Wade

Cheung et al. 1990 Hong Kong Marine Cohort Wade, Prüss, Zmirou

Corbett et al. 1993 Australia Marine Cohort Wade, Prüss, Zmirou

Dufour 1984 USA Fresh Cohort Wade, Prüss, Zmirou

Fattal et al. 1986 Israel Marine Cohort Wade, Prüss, Zmirou

Ferley et al. 1989 France Fresh Cohort Wade, Prüss, Zmirou

Fewtrell et al. 1992 UK Fresh Event Wade, Zmirou

Fewtrell 1994 UK Marine Cohort Wade, Zmirou

Fleisher et al. 1993 UK Marine Randomized trial Wade

Fleisher et al. 1996 UK Marine Randomized trial Prüss

Foulon et al. 1983 France Marine Cross-sectional Wade

Haile et al. 1996, 1999 USA Marine Cohort Wade, Prüss, Zmirou

Kay et al. 1994 UK Marine Randomized trial Wade, Prüss, Zmirou

Kueh et al. 1995 Hong Kong Marine Cohort Wade, Prüss

Lee et al. 1997 UK Fresh Event Wade

Lightfoot 1989 Canada Fresh Cohort Wade, Prüss

Marino et al. 1995 Spain Marine Cohort Wade

McBride et al. 1998 New Zealand Marine Cohort Wade

Medema et al. 1995 The Netherlands Fresh Event Wade

Medical Research Council 1995 South Africa Marine Cohort Prüss

Mujeriego 1982 Spain Marine Cohort Prüss

Philipp et al. 1985 UK Marine Event Wade, Zmirou

Pike 1994 UK Marine Cohort Wade, Prüss, Zmirou

Prieto et al. 2001 Spain Marine Cohort Wade

Seyfried et al. 1985 Canada Fresh Cohort Wade, Prüss, Zmirou

Stevenson 1953 USA Fresh Cohort Wade, Prüss, Zmirou

UNEP / WHO 1991a Israel Marine Cohort Prüss

UNEP / WHO 1991b Spain Marine Cohort Prüss

van Asperen et al. 1998 The Netherlands Fresh Event Wade, Zmirou

van Dijk 1996 UK Marine Cohort Prüss

von Schirnding et al. 1992 South Africa Marine Cohort Wade, Zmirou

and evaluating the potential for health effects at or below the current regulatory criteria 

(USEPA, 1986). The researchers concluded that (1) enterococci and to a lesser extent E. 

coli are adequate indicators (predictors) of GI illness in marine recreational waters, but 

fecal coliforms are not; (2) the risk of GI illness is considerably lower in studies with 

enterococci and E. coli densities below those established by EPA (1986), thus providing 

support for their regulatory use; (3) E. coli is a more reliable and consistent predictor of 

GI illness than enterococci or other indicators in fresh recreational waters; and (4) based 
U.S. Environmental Protection Agency

February 2009 14 

on heterogeneity analyses, studies that used a nonswimming control group and that 

focused on children found elevated GI illness risks. 

In addition, Sinton et al. (1998) reported on differentiating the relative health risks associated 

with human and animal fecal material. Illness risk associated with bathing in water polluted 

primarily with human fecal material was reviewed based on studies from the United States 

(Cabelli, 1983a; Dufour, 1984), Canada (Seyfried et al., 1985a,b), Israel (Fattal et al., 1983, 

1986, 1987), Egypt (Cabelli, 1983b; El-Sharkawi and Hassan, 1979), Spain (Mujeriego et al., 

1982), France (Ferley et al., 1989; Foulon et al., 1983); the United Kingdom (Brown et al., 1987; 

Jones et al., 1989, 1991), Hong Kong (Holmes, 1989), and Australia (Corbett et al., 1993; 

Harrington et al., 1993). Most of these studies showed a positive correlation between GI illness 

and fecal indicator density; there was little equivalent evidence from waters polluted primarily 

with animal feces. The only study specifically designed to address swimming-associated illness 

in animal-impacted waters was that of Calderon et al. (1991) who found no statistically 

significant association between GI illness and fecal indicator bacteria densities. Based on this 

observation, Sinton and colleagues (1998) concluded that reliable epidemiological evidence was 

lacking, and that other sources of information were needed to identify and apportion human and 

animal fecal inputs to natural waters. 

Since the publication of Sinton’s review article in 1998, a number of additional epidemiological 

studies have been conducted, some of which further address the issue of nonwastewater effluentcontaminated recreational waters. Completed and ongoing studies are summarized in Tables 

III.1.2a and III.1.2b, respectively; however, a comprehensive peer-reviewed summary of that 

information has not, to date, been published. 

The following section provides brief summaries of the epidemiological studies on nonwastewater effluent sources of contamination along with those studies on human sources that 

have most commonly been used as the basis for water quality criteria or standards throughout the 

world. 

III.2 Descriptions of Key Recreational Water Epidemiological Studies 

III.2.1 Selected Recreational Water Epidemiological Studies Based on Human Sources of 

Fecal Contamination 

United States and Egypt (Cabelli, 1983a) 

Cabelli (1983a) conducted epidemiological studies in the following four locations: Coney Island 

and Rockaway beaches in New York, New York; Alexandria beaches in Egypt; Lake 

Pontchartrain in New Orleans, Louisiana; and Boston Harbor in Boston, Massachusetts. The 

goals of the studies were to develop health effects and recreational water quality criteria for EPA. 

The author used similar methods for each location. The studies consisted of two interviews—

one interview at the beach where individuals were recruited and a second phone interview 7 to 

10 days later. Beach interviews occurred only on weekends and were limited to individuals who 

had swam on one or two weekend days. Mid-week swimmers were excluded from the study. 
U.S. Environmental Protection Agency

February 2009 15 Table III.1.2a. Recently Completed Recreational Waters Epidemiological Studies—Some of Which Address NonContamination 

Reference Location Study Design Contamination Source and Indicators Health Effect(s) Health Correlation1 n C

Colford et al., 2005, 2007 

United States 

Cohort Nonpoint source: dominant source 

avian; bacterial indicators via traditional and nontraditional methods, Bacteroides, viruses 

14 health outcomes evaluated including GI and skin rash 

Negative 8,800 Risk of illness was not co

water quality indicators uthe state water quality thr(similar to the 1986 AWQswimming-related illnessefound between increased most nontraditional water study. Diarrhea and skin compared with nonswimm

Wade et al., 2006 

United States 

Cohort Wastewater effluent- impacted 

waters; enterococci and Bacteroides measured via quantitative polymerase chain reaction (qPCR) 

Gastro-enteritis Positive 5,717 Swimmers at two beache

when compared to nonswrelationship was observeillness and enterococci at positive trend for enterocnoted. The association brisk of GI illness was signbeaches were combined. Lake Erie beach for Bactthe Lake Michigan beach

Wiedenmann et al., 2006 

Germany Randomized 

control 

Wastewater-impacted waters and waters impacted by waterfowl and swimmers. E. coli, intestinal 

enterococci, C. perfringens, somatic coliphage, and Pseudomonas aeruginosa

Acute febrile infection, ear, eye, skin, urinary tract, three definitions of GI 

Positive 2,196 Data were not analyzed f

from exposure to animal vAuthors recommended no (NOAELs) for water qualienterococci, 10 somatic c

100 mL. The authors furtapproach would be a morprocess of setting standa

Dwight et al., 2004 

United States 

Crosssectional survey 

Nonpoint source; compared urban to rural runoff 

Diarrhea; vomiting, sore throat 

Positive 1,873 Urban participants report

overall as the rural particimore during the second yrisk increased across almaverage of about 10% for exposure per week. The at the various sites. 

Lepesteur et al., 2006 

Australia Cohort Evaluated for fecal streptococci; 

source recreational users and runoff 

Respiratory illness and GI illness 

Positive 340 Risk of respiratory illness 

age group, where vigorouenergetic swimming was further exposure-related r

1 The health correlation represents the correlation between the health effect observed and the indicator. 
U.S. Environmental Protection Agency

February 2009 16 Table III.1.2b. Ongoing Recreational Waters Epidemiological Studies—Some of Which Address Nonpoint Sourc

Study Location Study Design Pathogen/ Pathogen Source Health Effect(s) Health Correlation1 n Conc

Southern California Coastal Water Research Project (SCCWRP) Studies 

United States 

Cohort, prospective 

30 different microbial indicators including rapid methods and new microbial indicators 

20 different epidemiological outcomes 

Not applicable (N/A) 

N/A SCCWRP is conducting a series 

Southern California to examine from nonpoint source polluted wconducted at three different beathese beaches is estimated to bprimarily nonhuman at the secoand nonhuman at the third beacat multiple locations and times amicrobiological indicators. The traditional fecal indicator bacteriindicators, microbial source trachopes that these studies will helcontracting an illness from swimand whether the risk of illness uwith traditional indicator density 

Virobathe European 

Union 

Laboratory method evaluation 

Adenovirus and norovirus 

Gastroenteritis N/A N/A Virobathe is a project aimed at d

waters and is investigating molepathogen enumeration (adenoviis currently being reviewed by th

Epibathe European 

Union 

Randomized control 

Unknown Unknown N/A N/A Epibathe is a consortium of Euro

out an EC-funded project to expmicrobial indicators and health oguideline levels. The objective irelationships between fecal indicenterococci) and self-reported mgastroenteritis, skin irritation, eyinfections/symptoms) in Mediterfreshwater bathing sites in a new currently being conducted in Spstudy is under consideration in tconsortium is expected to report 

1 The health correlation represents the correlation between the health effect observed and the indicator.
U.S. Environmental Protection Agency

February 2009 17 

Interviews occurred on days with minimal tidal effects and during time periods of peak beach 

usage (from 11 am to 5 pm). For the studies based in the United States, a total of 26,676 

participants were interviewed, while 23,080 participants were interviewed in Egypt. Swimmers 

were defined as individuals whose upper body orifices were exposed to water. Nonswimmers 

who attended the same beach were the control population for the study. 

Water samples were collected at two to three locations along the beach, typically three to four 

samples were collected during the peak beach usage. Water samples were analyzed for 

Salmonella, Enterobacter-Citrobacter, Klebsiella, fecal coliforms, and staphylococci. Results 

were analyzed using regression analysis. 

In the New York study, two beaches were sampled. The Coney Island beach was considered 

“barely acceptable” in terms of pollution levels, whereas the Rockaways beach was deemed 

“relatively unpolluted.” The author found statistically significant differences in the rate of GI 

symptoms in swimmers compared to nonswimmers at the Coney Island, but not Rockaways 

beach. The author also found a higher rate of respiratory symptoms in swimmers at Rockaways 

beach. The symptom rate for GI illness for swimmers at Coney Island was 10 out of 1,000 

swimmers compared to 2 out of 1,000 swimmers for Rockaways beach. There the author 

determined that measurable health effects could occur on beaches that met existing recreational 

guidelines and standards. When examining the relationship of the indicator densities to GI 

symptoms, the author found that enterococci densities provided the best correlation; E. coli was 

the second best indicator. 

The author was unable to find a beach that was both heavily affected with close point-source 

sewage discharges and used by a large number of people. Instead, several beaches with 

combined sewer outfalls in Alexandria, Egypt met those requirements. The author found that 

swimmers in more heavily polluted beaches experienced more symptoms than swimmers at less 

polluted beaches. Rates of GI symptoms appeared to follow Enterococcus and E. coli densities. 

However, the rates of illness were not as high as expected despite higher pollution levels than the 

New York study. 

The author then conducted a focused study on visitors to the beach that were from Cairo. In that 

study, the rates of illness for swimmers was higher than for nonswimmers and there was more 

inverse relationship at the least polluted beach for time spent swimming and rate of illness 

compared to the other beaches. The rate of illness for visitors from Cairo was similar to the New 

York study. 

The Lake Pontchartrain study was located near the mouth of Bayou St. John in a brackish area 

with limited tidal activity. The authors found statistically different rates of illness for swimmers 

versus nonswimmers in symptoms of vomiting, diarrhea, stomachache, earache, and skin 

irritations. In general, the GI symptom rates were higher in children than adults. The authors 

also found that enterococci appeared to be a better indicator of illness than E. coli, stormwater 

runoff appeared to be less harmful than sewage sources, and enterococci and E. coli may 

overstate risks of illness. 
U.S. Environmental Protection Agency

February 2009 18 

The Boston Harbor study took place on two beaches in 1978 and attempted to confirm the 

observation that significant health effects can be observed when there are low indicator densities. 

Although the author did not find statistically different illness in GI symptoms between swimmers 

and nonswimmers, the beach with the most pollution had a greater difference in the rate of 

illness between swimmers and nonswimmers, even if not statistically significant. 

Overall, the Cabelli (1983a) studies found that there was an increased risk in GI illness from 

swimming in waters in increasingly polluted seawater. Enterococci also appeared to be a better 

indicator for illness from swimming in seawater than E. coli or other fecal indicators. 

United States (Dufour, 1984) 

Dufour (1984) conducted a series of epidemiological studies to identify whether a model 

developed by EPA to predict health effects based on marine water quality could also apply to 

freshwater, including identifying a water quality indicator that best describes the relationship 

between health effects and freshwater quality and determining whether the marine water criterion 

was applicable to freshwater. The studies were conducted at two U.S. beaches, Lake Erie in 

Erie, Pennsylvania (29,976 participants) and Keystone Lake in Tulsa, Oklahoma (16,363 

participants). 

The Lake Erie studies were conducted in 1979, 1980, and 1982 on beaches considered to have 

good or excellent microbial water quality. One site was located approximately three-quarters of 

a mile northwest of a sewage outfall for the City of Erie. The Keystone Lake studies were 

conducted in the summers of 1979 and 1980, and the beaches demonstrated variable water 

quality for bacteria. The two beach sites at Keystone Lake were located 3 and 5 miles from an 

outfall for wastewater treatment facility. In 1979, the treatment plant released an average of 

120,000 gallons of unchlorinated sewage per day into the lake. In 1980, this practice was 

discontinued, and sewage passed through a settling lagoon, an aeration basin, and was 

chlorinated before being released into the lake. 

Water samples were tested for E. coli and enterococci (includes Streptococcus faecalis and 

Streptococcus faecium). Fecal coliforms were also monitored for two years during the Keystone 

Lake studies and in two years of the Lake Erie studies. Statistical analyses examined the 

relationship between the occurrence of GI illness in swimmers compared with a nonswimming 

control group. Because of the small population of nonswimmers, the nonswimming control 

group was pooled from an entire season of beachgoers to form a single control population. To 

evaluate their relationship, the incidence of illness between swimmers and nonswimmers and the 

indicator bacteria density at the time of swimming were used. The model controlled for age as a 

confounding factor. A regression analysis determined whether there was a direct relationship 

between swimming-associated GI illness and microbial water quality. A correlation analysis 

determined which water quality indicator showed the strongest relationship to a swimmingrelated illness. 

Researchers conducted surveys at the beaches on weekends when the beaches were more 

crowded and monitored water quality at the time of swimming activity. There were two phases 

of beach interviews—the first as beachgoers were leaving the beach area and a second follow-up 

telephone interview 8 to 10 days after swimming. Follow-up interviews were only conducted on 
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February 2009 19 

beachgoers who had not gone swimming the five days prior to the initial interview. For the 

study, swimming was defined as having all orifices immersed in water. Interviewers asked 

beachgoers during the initial interview about sex, age, race and ethnicity; whether a person 

swam; length of time and time of day in the water; illness symptoms they may have had in the 

previous week; and the reason, if a nonswimmer, why they did not enter the water. Follow-up 

interviewers asked the beachgoers about any illness symptoms that occurred since swimming at 

the beach. 

In the Lake Erie studies, both sites met local and state standards for water quality. In general, 

symptom rates for swimmers were higher than nonswimmers in all categories; however, most 

symptoms were not statistically significant. Statistically significant differences between 

swimmers and nonswimmers were found in symptoms related to enteric diseases and tended to 

occur at the beach with poorer water quality. 

In the Keystone Lake study, symptoms for enteric diseases tended to be higher in swimmers than 

nonswimmers. In 1979, there was only one other group of symptoms (fever, headaches lasting 

greater than three hours, and backache) that showed significant differences between swimmers 

and nonswimmers. In 1980, statistical differences between swimmers and nonswimmers were 

found at one or both sampling locations with symptoms for GI, respiratory, and other illnesses. 

United Kingdom (Fleisher and Kay, 2006; Fleisher et al., 1993, 1996, 1998) 

Fleisher and Kay (2006) and Fleisher et al. (1993, 1996, 1998) reported the results of randomized 

intervention trials at separate marine bathing locations to identify the potential dose-response 

relationships among swimmers exposed to marine waters contaminated with domestic sewage 

and the potential risk of nonenteric illness (e.g., acute febrile respiratory illness, ear, eye, and 

skin ailments). Fleisher et al. (1996, 1998) reported the final results of the four randomized 

intervention trials conducted at four separate marine bathing locations and incorporated the 

results on two of the locations, which were presented preliminarily in Fleisher et al. (1993). 

Fleisher and Kay (2006) analyzed the data presented in Fleisher et al. (1993, 1996, 1998) and 

Kay et al. (1994) to identify and quantify any risk perception biases that may have affected the 

observed association between skin ailments and exposure to marine waters contaminated with 

domestic sewage at one of the study locations. The Fleisher et al. (1998, 1996, 1993) studies are 

included in the meta-analyses of Prüss (1998), Wade et al. (2003), and Zmirou et al. (2003). 

The four separate trials took place at four different locations during the summers of 1989 through 

1992. The study population consisted of 1,216 adults (>18 years of age) that were recruited from 

populations located near the study locations during the 3 weeks prior to the exposure day. No 

recruits participated in more than one study cohort, and study participants were blinded to the 

outcome illness being studied. Study recruits participated in an extensive interview and medical 

examination no more than two days prior to the day of exposure. Researchers gathered data on a 

number of potential confounding factors (e.g., age, sex, general health, illness in previous three 

weeks, medications taken, water contact activities, other confounding factors). 

Study participants were randomized into bathers (548 participants) and nonbathers (668 

participants) who were unaware of their status until they arrived at the study location beach. 

Bathers entered into a defined area in the water, remained in the water for at least 10 minutes, 
U.S. Environmental Protection Agency

February 2009 20 

and completely immersed their heads in the water at least 3 times. Nonbathers remained on the 

beach in a designated area. On the day of exposure, study participants were interviewed again 

about their health and dietary habits and any water contact activities experienced between the 

initial interview and the day of exposure. Furthermore, one week following the exposure period, 

study participants were medically examined and interviewed extensively again for data on their 

health, diet, water contact activity, and other potential risk factors. Lastly, study participants 

were mailed a questionnaire to fill out with any other symptoms of illness and exposure to 

recreational water. 

In addition, the water quality of the bathing area was sampled in 30-minute increments during 

the exposure period at various designated locations (sampled every 20 m at surf, mid [1 m deep], 

chest depth [1.3 to 1.4 m deep], and 30 cm below the surface). These water samples were 

analyzed via standard methods for the following indicators: total and fecal coliforms, fecal 

streptococci, and P. aeruginosa. Total staphylococci were also counted at three of the study 

sites. The sampling results were assigned to each individual bather within 15 minutes of 

exposure and within a maximum of 10 m of the place of exposure. 

Linear trend, chi-square, and multiple logistic regression analyses were used to estimate the 

dose-response relationship between the microbiological water quality results and occurrence of 

gastroenteritis, acute febrile respiratory infection, and eye and ear ailments. The statistical 

analyses controlled for the effects of confounding factors, which included nonexposure-related 

variables associated with the incidence of these outcome illnesses. The results from participants 

who did not take part in the follow-up interviews or who reported illnesses of interest on the 

actual exposure day were excluded. 

Fleisher et al. (1998) indicated that bathers had statistically significant (p<0.05) higher rates of 

gastroenteritis and ear and eye ailments as compared to nonbathers. Moreover, bathers exposed 

to ≥60 fecal streptococci per 100 mL had a statistically significant (p<0.001) higher rate of acute 

febrile respiratory infection relative to nonbathers. In addition, the authors reported that 

approximately 34.4 to 65.8 percent of illnesses reported by the study cohort could be associated 

with bathing in marine waters contaminated with domestic sewage. Fleisher et al. (1996) also 

noted that fecal streptococci exposure of ≥60 per 100 mL was predictive of acute febrile 

respiratory infection and indicated that a fecal coliform exposure of 100/100 mL was predictive 

of ear ailments. No indicator was found to predict eye aliments, although the risk of eye 

ailments was higher for bathers versus nonbathers. There was no statistically significant doseresponse relationship found for skin ailments. Fleisher and Kay (2006) noted that the observed 

difference in skin ailments associated with exposure between bathers and nonbathers at one of 

the four study locations may be attributable to “risk perception bias.” 

Based on the results of these studies, the authors concluded that future epidemiological studies 

should incorporate the same study design to help control for the large disparity observed in risk 

estimates reported in previously published epidemiological studies. Additionally, Fleisher et al. 

(1996) noted that these study results demonstrated that a single indicator would not be sufficient 

to establish water quality standards aimed at protecting public health. Fleisher et al. (1998) 

concluded that illness associated with bathing in contaminated (marine) recreational waters is a 
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February 2009 21 

significant threat to public health, and further studies to assess the severity of illnesses associated 

with bathing in recreational waters contaminated with domestic sewage should be conducted.

United Kingdom (Kay et al., 1994)

Kay et al. (1994) conducted the first randomized control study to evaluate the heath effects 

associated with swimming in coastal waters. This study is included in the meta-analyses of Prüss 

(1998), Wade et al. (2003), and Zmirou et al. (2003). The 4-year study took place at four 

different locations during the summers from 1989 through 1992. This study builds on the 

preliminary results from two of the locations that were published in Fleisher et al. (1993). 

Although this study also uses the same study population that was used in the Fleischer and Kay 

(2006) and Fleisher et al. papers (1996, 1998), it focuses specifically at the dose-response 

relationship between gastroenteritis and exposure to marine water of varying microbial quality. 

Linear trend and multiple logistic regression analyses were used to estimate the dose-response 

relationship between the occurrence of gastroenteritis and microbiological water quality 

(exposure). The statistical analysis controlled for confounding factors, such as nonexposurerelated variables associated with gastroenteritis. 

The results indicated that of the indicators measured, only fecal streptococci demonstrated a 

statistically significant dose-response relationship with gastroenteritis. The model used for 

bathers exposed to more than 32 fecal streptococci/100 mL demonstrated a significant 

relationship with the risk of gastroenteritis, whereas the model utilized for bathers exposed to 

less than 32 fecal streptococci/100 mL did not show a significant relationship. The latter 

relationship was independent of nonwater-related predictors of gastroenteritis. 

Based on their results, the authors concluded that although none of the other microbiological 

indicators illustrated a significant relationship between measured concentrations and occurrence 

of gastroenteritis, the relationship between fecal streptococci concentration measured at chest 

depth and gastroenteritis is robust. However, the biological basis underlying this significant 

relationship is not known. The authors suggested that whatever causes gastroenteritis 

“copartitions” in seawater with fecal streptococci. The authors’ findings also suggest that 

coliforms seem to have little value as indicators of gastroenteritis risk from sewage pollution of 

coastal waters and that fecal streptococci concentrations are a better microbiological indicator. 

Spain (Prieto et al., 2001) 

Prieto et al. (2001) conducted a cohort study to determine whether water polluted with sewage 

posed a danger to a bather’s health and to determine the best microbiological indicator to predict 

illness. The study took place during the summer of 1998 on four beaches in northern Spain and 

included 1,805 participants. Water samples were collected 3 days a week at 10 am in the area of 

the beaches that usually had the highest bather density. Water samples were tested for total 

coliforms, fecal coliforms, fecal streptococci, S. aureus, and P. aeruginosa. 

The epidemiological study consisted of two surveys—one survey at the beach and a follow-up 

survey within seven days of the beach interview. The surveys focused on family groups. Once 

an individual was selected for an interview, all other family members were interviewed. The 

interviews occurred on the same days that water samples were collected and timed so that a daily 
U.S. Environmental Protection Agency

February 2009 22 

average of 15 people were interviewed. During the follow-up interview, individuals were asked 

about a series of symptoms and additional personal information. 

For the statistical analyses, study participants were divided into swimmer and nonswimmer 

categories. The authors conducted a bivariate analysis to examine the relationship of bathing, 

water quality, and illness. A multivariate analysis was carried out to determine the doseresponse relation between indicator bacteria densities and their relation to health problems. 

Water quality at the four beaches exceeded the European Community Directive guide standards 

for total coliforms (39.8 percent of samples), fecal coliforms (57.1 percent of samples), and fecal 

streptococci (in 37.9 percent of the samples). In the follow-up interviews, 7.5 percent of 

participants reported symptoms. The rate of these symptoms was significantly greater (p=0.011) 

for “holidaymakers” (9.9 percent) and “day trippers” (8.4 percent) than for residents (5.8 

percent). The study did not find a significant difference in the incidence rate of each symptom 

between swimmers and nonswimmers, nor did the authors find a difference in the incidence of 

these symptoms between swimmers who submerged their head and those who did not. 

The rate of symptoms did increase with the concentration of total coliforms. Gastrointestinal 

symptom incidence increased with total coliforms and fecal streptococci and was significantly 

higher in swimmers than nonswimmers. 

United States (Wade et al., 2006) 

Wade et al. (2006) conducted a prospective cohort study of beachgoers at two beaches in the 

Great Lakes area—one beach on Lake Michigan in Indiana and the second beach on Lake Erie in 

Cleveland, Ohio. Both beaches were impacted by effluent from wastewater treatment plants. 

First, beachgoers were recruited at beaches on the weekends and holidays during the summer of 

2003. Each participating beachgoer completed and returned the questionnaire prior to leaving 

the beach. The questionnaire asked for information on demographics, swimming and other 

beach activities, consumption of raw or undercooked meat or runny eggs, chronic illnesses, 

allergies, exposure to animals, and other related health symptoms or encounters with sick people 

in the previous 48 hours. Second, following a 10 to 12 day period, a telephone interview was 

conducted to gather information about health symptoms experienced since the beach visit, as 

well as on other water-related activities, contact with animals, and consumption of high-risk 

foods. 

Water samples were also collected three times a day on each study day and analyzed for 

Bacteroides and enterococci. The water samples were analyzed via a modified version of PCR. 

This new method provides a faster assessment of water quality. Respiratory and GI illness and 

ear, eye, and skin rash symptoms were evaluated. The authors only reported the GI illness 

results. Swimmers at both beaches had a higher incidence of GI illness compared to 

nonswimmers. A statistically significant relationship was observed between increased rate of GI 

illness and enterococci at the Lake Michigan beach, while a positive trend for enterococci at the 

Lake Erie beach was noted. The association between enterococci and increased risk of GI illness 

was significant when results for the two beaches were combined. In terms of Bacteroides, a 

positive trend was observed at the Lake Erie beach, but no trend was observed at the Lake 
U.S. Environmental Protection Agency

February 2009 23 

Michigan beach. In addition, the association between enterococci and GI illness strengthened 

with increasing exposure. 

Australia (Lepesteur et al., 2006) 

Lepesteur et al. (2006) conducted an epidemiological study examining the relationship between 

incidence of disease and exposure to fecal contamination in recreational water. The study area 

was the Peel Harvey estuary at Mandurah Bridge beach located 70 km south of Perth in Western 

Australia. Water circulation is influenced by tidal currents, wind, and river flow. The water 

recreational area was relatively small—approximately 500 sq. m. 

The surveys were conducted in the afternoons with water samples collected each day and tested 

for fecal streptococci. Social surveys were conducted at the beach and through follow-up 

interviews by telephone two weeks later. A total of 119 groups or families and 340 individuals 

participated in the study. The interviews included questions related to frequency of beach visits, 

length of stay and days of visit, age of users, and beach activities. Exposure to recreational 

waters consisted of any visit to the estuary over 30 minutes that involved swimming, paddling, 

and playing in wet sand. 

During the initial interview, participants were asked to provide information on their current 

health status. The follow-up interview asked who swam and whether anyone became ill during 

the two-week period since the initial interview. Evidence of GI and respiratory illnesses was 

recorded. Two or more symptoms were considered an incident of illness. Confounding factors 

such as food and drink intake, age, sex, history of diseases, pregnancy, additional bathing, 

jellyfish sting, travel, and period of exposure to sun were identified during the follow-up 

interview. For the analysis, the authors adjusted background illness rates using age-dependent 

probability factors. The odd ratios with 95 percent confidence intervals were used to quantify 

the magnitude of effect of exposure to recreational waters for different age groups. 

The water showed evidence of fecal contamination year-round with increased concentrations 

caused by recreational users during the bathing season. Increased fecal indicator densities were 

also associated with rainfall. Most survey participants conducted a number of recreational 

activities at any visit to the beach, with 76 percent identifying swimming as one of their 

activities. The average number of exposures was 17 per person per season. 

Respiratory illness comprised most of the reported symptoms, with GI illness being less 

common. The authors observed a relationship between excess respiratory illness and exposure to 

fecal streptococci. The highest odds ratio was observed in the 11 to 15 year-old age range. The 

authors attributed this result to greater exposure to water combined with vigorous activity. 
U.S. Environmental Protection Agency

February 2009 24 

III.2.2 Selected Recreational Water Epidemiology Studies Based on Nonwastewater 

Effluent Sources of Fecal Contamination 

United States (Calderon et al., 1991) 

Calderon et al. (1991) followed the health status and swimming activities of volunteer 

participants. This study is included in the meta-analysis of Wade et al. (2003). The study site 

was a small pond (3 ac) located in a semirural and largely forested community in Connecticut. 

An intense sanitary survey of the surrounding watershed indicated that no human sources of fecal 

contamination impacted the stream that fed the pond, and there were no point sources of 

microbial pollution. 

Water samples were analyzed for E. coli, enterococci, fecal coliforms, P. aeruginosa, and 

staphylococci. A total of 104 families participated in the study. Swimming was defined as a day 

in which an individual swam in the pond, and during swimming activity, completely submerged 

their head and body beneath the surface of the water. There were 1,310 exposure-days 

accumulated by swimmers and 8,356 person-days for nonswimmers. 

Water quality data were collected on 49 days of the study. The geometric mean E. coli density 

was 51 CFU/100 mL. Rain occurred on 16 of the 49 days of the study. The geometric mean 

densities of E. coli and fecal coliforms were determined to be over two times greater on rainy 

days than on dry days; levels of enterococci were four times higher on rain days than dry days. 

The densities of staphylococci and Pseudomonas were about the same during rainy and dry 

periods. 

The symptomatic GI illness rate in swimmers was 22.9 per 1,000 person-days, whereas, in 

nonswimmers, the rate was 2.6 per 1,000 person-days. Gastrointestinal illness was also strongly 

associated with swimming when adjusted for age. However, no association was found between 

high fecal indicator bacteria densities and GI illness in swimmers or between swimmer illness 

and high-volume rain days. The authors suggested that swimming-associated illness may have 

been due to etiological agents that were transmitted from swimmer-to-swimmer via bathing 

water. 

The data from this study indicate that illness in swimmers was not statistically associated with 

densities of commonly used fecal indicator bacteria in a recreational water whose source was 

rainwater runoff from a forested watershed. These results led the authors to conclude that 

currently recommended bacterial indicators (i.e., E. coli and enterococci for fresh recreational 

waters per USEPA, 1986) are “...ineffective for predicting potential health effects associated 

with water contaminated by nonpoint sources of fecal pollution.” 

Hong Kong (Cheung et al., 1990; Holmes, 1989)

Cheung et al. (1990) and Holmes (1989) described a prospective cohort study that was conducted 

in two phases in the summers of 1986 and 1987. The first phase involved four popular beaches 

and tested the epidemiological techniques used in the second phase (main study) that 

incorporated results from nine beaches. The main study was undertaken to provide data for 

deriving health-related bathing water quality standard specific to the conditions of Hong Kong. 

Six of the beaches in the main study were predominately impacted by human sewage, two were 
U.S. Environmental Protection Agency

February 2009 25 

impacted by livestock wastes (mainly pig excreta), and one was impacted by a combination of 

sewage and livestock waste. Each phase involved two parts, epidemiological studies using 

beachgoer interviews and follow-up telephone interviews and water testing for microbiological 

quality. Beachgoers (33,083) were recruited to participate in the study during the weekends and 

asked for contact information and any information on potential prestudy illness or swimming 

activities. The following day, telephone interviews were conducted to obtain information from 

these recruits on water exposure and any type of food eaten while at the beach. This information 

allowed the researchers to categorize the participants as swimmers or nonswimmers. 

Additionally, 7 to 10 days after the follow-up telephone interview, the study participants were 

interviewed again via telephone to gather information on any poststudy, mid-week swimming 

activities, any illness, any perceived symptoms, and the duration of any perceived symptoms. 

Water samples were collected on the weekend days from 3 sampling points (50 to 150 m apart 

and 1 m in depth) at each beach in the study and in locations of high bather density. The water 

samples were analyzed for the following microbial indicators: fecal coliforms, E. coli, Klebsiella 

spp., fecal streptococci/enterococci, staphylococci, P. aeruginosa, Candida albicans, and total 

fungi. The beaches were categorized as “relatively unpolluted” and “barely acceptable” for each 

of the microbial indicators analyzed. 

Study results suggest that overall perceived symptom rates were higher for swimmers than 

nonswimmers, and the rates of GI illness, ear, eye, skin symptoms, respiratory illness, fever, and 

total illness were significantly higher for swimmers as compared to nonswimmers. Furthermore, 

swimming-associated symptom rates for GI, skin, and respiratory symptoms, and total illness 

were significantly higher at barely acceptable beaches compared to relatively unpolluted 

beaches, indicating that the perceived symptoms were pollution-related. The authors concluded 

that E. coli is the best indicator of health effects—mainly gastroenteritis and skin symptoms—

associated with swimming at beaches in Hong Kong. Staphylococci was also correlated with ear 

symptoms and respiratory and total illness. A linear relationship was established between the 

geometric mean of E. coli densities and combined gastroenteritis and skin symptom rates for 

individual beaches. However, no significant relationship between E. coli and gastroenteritis or 

skin symptom rates, nor staphylococci and ear or sore throat symptoms, could be established. 

United States (Haile et al., 1999) 

Haile et al. (1999) conducted the first large epidemiological study of persons who swim in 

marine recreational waters contaminated by urban runoff. This study is included in the metaanalyses of Wade et al. (2003) and Zmirou et al. (2003). The exposures of interest were 

swimming distances from storm drains, levels of bacterial indicators (total coliforms, fecal 

coliforms, enterococci, and E. coli) and presence of human enteric viruses. The study assessed 

persons who immersed their heads in ocean water at three beaches in Santa Monica Bay, 

California. 

The study included 15,492 subjects, 13,278 of whom were contacted for follow-up health 

interviews and 10,459 of whom were ultimately included in the analysis. Distance from the 

storm drain where participants swam was noted (0, 1 to 50, 51 to 100, or 400+ yds). During the 

follow-up telephone interview, the occurrence of the following health outcomes was noted: 

fever, chills, eye discharge, earache, ear discharge, skin rash, infected cuts, nausea, vomiting, 
U.S. Environmental Protection Agency

February 2009 26 

diarrhea, diarrhea with blood, stomach pain, coughing, coughing with phlegm, nasal congestion, 

and sore throat. 

The statistical analysis addressed, (1) are there different risks of specific outcomes among 

subjects swimming at different distances from a storm drain? and (2) are risks of specific 

outcomes associated with levels of specific bacterial indicators or enteric viruses? 

The results of the study indicated that the risks of several health outcomes were higher for people 

who swam at storm drain locations compared to those who swam various distances from a drain. 

Other relevant findings include the following: (1) statistically significant increases in fever, 

chills, ear discharge, cough and phlegm, and respiratory disease in people who swam at a storm 

drain than those who swam 400+ yds from a drain; (2) the increase in “highly credible 

gastrointestinal symptoms” (i.e., GI illness with vomiting and fever as used in USEPA, 1986) 

was not statistically significant for those who swam at a drain compared to those who swam 

400+ yds from a drain; and (3) no dose-response relationship was associated with swimming 

closer to a storm drain and illness (one would expect a gradient of increasing risk of illness to 

swimmers the closer they are to a storm drain). Furthermore, swimmers reported adverse health 

outcomes more often on days when the water samples were positive for viruses, suggesting 

assays for viruses may be informative for predicting risk. Notably, the risk of highly credible 

gastrointestinal illness for those swimming at a storm drain location was estimated to be 0.018 

(i.e., 18 in 1,000 bathers), which is effectively identical to the current tolerable GI illness rate of 

0.019 in marine waters (USEPA, 1986). However, Haile and colleagues noted that causal effects 

may be higher than reported because both distance from a storm drain and detections of fecal 

indicator bacteria are proxies for the presence of waterborne pathogens. 

Based on the results, the authors concluded that “there may be increased risk of a broad range of 

adverse health effects associated with swimming in ocean water subject to urban 

runoff....Consequently, the prospect that untreated storm drain runoff poses a health risk to 

swimmers is probably relevant to many beaches subject to such runoff, including areas on the 

East, West, and Gulf coasts of North America, as well as numerous beaches on other continents.” 

Other researchers have concurred with the Haile study conclusions; for example, Grant et al. 

(2004) stated that “contamination of the surf zone by dry weather runoff apparently increases the 

risk that marine recreational bathers will contract diarrhea and other acute illnesses.” 

New Zealand (McBride et al., 1998)

McBride et al. (1998) conducted a cohort study using a modified prospective cohort (“Cabelli 

protocol”) epidemiological study design to ascertain the association, if any, between illness rates 

among beachgoers and the degree of fecal contamination of marine water from either human or 

animal sources. This study is included in the meta-analyses of Wade et al. (2003). It was 

conducted at seven popular bathing beaches during the summer of 1995. Three categories of 

beaches were selected, two control beaches (considered minimal impact), two rural beaches 

(animal waste impacted), and three oxidation pond beaches (human waste-impacted). On each 

of the 107 interview days, groups of bathers and nonbathers were interviewed at each beach 

using a standard questionnaire to obtain basic field data, eligibility, demographic information, 

foods eaten in the past three days that could influence outcome, and contact information. Three 

to five days following the initial interview, study participants were contacted to distinguish beach 
U.S. Environmental Protection Agency

February 2009 27 

swimmers and paddlers from nonswimmers and for information regarding illness and onset of 

symptoms. A swimming-associated illness risk was calculated by comparing illness risks 

between people who swam or paddled in the water (1,577 total) and nonexposed individuals 

(2,307 total). 

Additionally, water quality samples were taken on the same day as the initial interview and 

analyzed for fecal coliforms, E. coli, and enterococci. Samples were taken approximately 10 cm 

below the water surface, twice per day, from the adult chest and knee depth, and generally from 

three locations spaced evenly along the beach. Water samples were collected on days when 

significant bathing occurred, regardless of weather. 

Log-linear modeling of the results demonstrated a statistically significant association between 

illness and enterococci concentration, with the most significant associations observed among 

paddlers and long-duration swimmers (i.e., swimming more than 30 minutes). No significant 

relationships were found between the other fecal indicators and health risks. Furthermore, no 

significant differences in illness risks were found between the human- and animal-impacted 

beaches, although illness risks at both types of beaches were significantly higher than the control 

beaches. 

The researchers concluded that the overall study results were affected by unexpectedly low 

levels of indicator organisms at the impacted beaches. In addition to requiring a greater range of 

fecal contamination at study beaches, the researchers concluded that any future studies designed 

to strengthen the current study conclusions would require larger (sufficient) numbers of bathers 

at the study locations. 

Germany (Wiedenmann et al., 2006) 

Wiedenmann et al. (2006) performed randomized controlled studies at five public freshwater 

bathing sites (four lakes and one river site) in Germany that had complied with current European 

standards for at least the three previous bathing seasons. These studies were conducted to obtain 

a greater scientific basis for the definition of recreational water quality standards. Sources of 

fecal contamination potentially impacting the waterbodies included treated and untreated 

municipal sewage, agricultural runoff, and contamination from water fowl. Data were not 

analyzed for differences in health outcomes from exposure to animal versus human fecal 

contamination. 

A total of 2,196 participants were recruited from the local population. After a pilot study at one 

of the five locations that included only adults, the study was expanded to include children aged 4 

years and up for the other four locations. Approximately two to three days before exposure, 

participants were interviewed and administered a brief medical examination. Volunteers deemed 

unfit for participation were excluded from the study. 

On the day of exposure, study participants were randomized into equal groups of bathers and 

nonbathers. After arriving at their designated locations, study participants were interviewed a 

second time for information on symptoms occurring after the first interview and diet from the 

preceding two to three days. Bathers were exposed for 10 minutes in designated areas and had to 
U.S. Environmental Protection Agency

February 2009 28 

immerse their head at least three times. Following their exit from the water, bathers weres asked 

to report whether they had accidentally swallowed water. 

During the exposure period, water samples for microbiological analysis were collected at 20-

minute intervals and analyzed for E. coli, enterococci, C. perfringens, somatic coliphages, 

aeromonads, and pyocyanine-positive P. aeruginosa. Furthermore, one week following the 

exposure period, study participants were medically examined and interviewed again. Three 

weeks later, study participants were mailed a questionnaire to complete. 

Data were analyzed for the following disease outcomes: acute febrile respiratory infection, 

common cold, ear and eye ailments, skin infections or symptoms, urinary tract infections, and 

three definitions of gastroenteritis that were based on the responses obtained from the 

questionnaires. Dose-response effects with no-observed-adverse-effect-levels (NOAELs) were 

determined for the three different definitions of gastroenteritis and four fecal indicator 

organisms, E. coli, enterococci, C. perfringens, and somatic coliphages. Relative risks for 

bathing in waters with levels above NOAELs compared with nonbathing ranged from 1.8 (95 

percent CI, 1.2 to 2.6) to 4.6 (95 percent CI, 2.1 to10.1), depending on the definition of 

gastroenteritis that was used. Additionally, swallowing water as compared to not swallowing 

water resulted in significantly higher attributable risks above NOAELs than below NOAELs. 

Moreover, swallowing water below NOAELs did not result in any significant effect compared 

with nonbathing, while swallowing water above NOAELs always produced a significant effect. 

Based on the results of this study, the authors concluded that the NOAELs for water quality 

should be as follows: 100 E. coli, 25 enterococci, 10 somatic coliphages, or 10 C. perfringens per 

100 mL. The authors further concluded that a NOAEL approach would be a more robust method 

to the complex process of setting standards. 

United States (Colford et al,. 2005, 2007) 

Colford et al. (2005) conducted an epidemiological study in Mission Bay, California, where 

historically, nearly 20 percent of the routine bacterial samples failed state water quality 

standards, but the dominant fecal source appears to be nonhuman. Microbial source tracking in 

Mission Bay has indicated that human fecal sources are minor contributors to overall microbial 

loading. Moreover, Mission Bay has an unusually long hydraulic residence time compared to 

other coastal systems, which likely affects the age and viability of waterborne fecal material. 

The study focused on whether (1) water contact increased the risk of illness during the two 

weeks following exposure to water, (2) there were associations between illness and measured 

levels of traditional indicators of water quality among those individuals with water contact, and 

(3) there were associations between illness and measured levels of nontraditional (alternative) 

indicators of water quality among those individuals with water contact. 

Nearly 8,800 participants were recruited for this cohort study from the 6 most popular swimming 

beaches in Mission Bay on weekends and holidays during the summer of 2003. Each participant 

provided their current state of health and degree of water exposure during their day at the beach. 

On the same day, water quality was monitored for traditional fecal indicator bacteria 

(enterococci, fecal coliforms, total coliforms). Participants provided their current state of health 

and degree of water exposure during their day at the beach. On the same day, water quality was 
U.S. Environmental Protection Agency

February 2009 29 

monitored for traditional fecal indicator bacteria (enterococci, fecal coliforms, and total 

coliforms). A subset of samples was also measured for nontraditional or alternative indicators, 

such as Bacteroides and viruses (somatic and male-specific phages, adenoviruses, and 

noroviruses). This subset was also tested with new methods for measuring traditional indicators, 

such as chromogenic substrate or quantitative PCR. 

Ten to fourteen days later, the participants were contacted by phone and interviewed about 

symptoms of illness that occurred since their visit to the beach, including GI illnesses (diarrhea, 

nausea, stomach pain, cramps, vomiting, and highly credible GI illness [using two definitions]); 

respiratory illnesses (cough, cough with phlegm, nasal congestion or runny nose, sore throat, and 

significant respiratory illness); dermatologic outcomes (skin rash and infected cuts or scrapes); 

and nonspecific symptoms (fever, chills, eye irritation, earache, ear discharge, and eye irritation 

or redness). Multivariate analyses assessed relationships between health outcomes and degree of 

water contact or levels of water quality indicators. These analyses were adjusted for 

confounding covariates such as age, gender, and ethnicity. 

Of the measured health outcomes, only skin rash and diarrhea consistently were significantly 

elevated in swimmers compared to nonswimmers. For diarrhea, this risk was strongest among 

children 5 to 12 years old. However, illness risk was not correlated with levels of the traditional 

water quality indicators used in the study. Of particular note, the state water quality thresholds 

for bacterial indicators (similar to the 1986 AWQC for bacteria) were not predictive of 

swimming-related illnesses. Similarly, no correlation was found between increased risk of 

illness and increased levels of most nontraditional water quality indicators measured in the study. 

Although a significant association was observed between the levels of male-specific coliphage 

and highly credible GI illness, nausea, cough, and fever, these associations were based on far 

fewer participants. Thus, the researchers urged caution in extrapolating these results. 

The researchers concluded that the results of the study suggest the need for further evaluation of 

traditional indicators in circumstances where nonpoint sources of microbial pollution are the 

dominant fecal contributors to recreational waters. 

United States (Dwight et al., 2004) 

Dwight et al. (2004) compared rates of reported health symptoms among surfers in urban North 

Orange County, California and rural Santa Cruz County, California during the winters of 1998 

and 1999 to determine whether symptoms were associated with exposure to urban runoff. Two 

cross-sectional surveys of 1,873 surfers were conducted. Surfers were selected as the study 

population because of their regular exposure to coastal waters. Data were gathered on reported 

health symptoms (diarrhea, vomiting, and sore throat) experienced during the previous three 

months. 

Logistic regression was used to estimate adjusted odds ratios comparing symptom reporting rates 

between the two counties, stratified by year. The model included county, water exposure, 

gender, age, occupation, educational level, annual income, political outlook, and level of concern 

about water quality. 
U.S. Environmental Protection Agency

February 2009 30 

The results indicate that the urban participants (North Orange County) reported almost twice as 

many symptoms overall compared to the rural participants (Santa Cruz County) during the first 

year and slightly more during the second year. In both study years, risk increased across almost 

every symptom category by an average of about 10 percent for each additional 2.5 hours of water 

exposure per week. The study did not measure water quality at the various sites. 

Based on the results, the authors concluded that discharging untreated urban runoff onto public 

beaches can pose health risks. Furthemore, large-scale epidemiological studies are needed to 

further characterize the health risks of people exposed to urban runoff in coastal waters. 

United States (SCCWRP 2007-ongoing) 

The SCCWRP is conducting a series of epidemiological studies to examine the risk of 

swimming-related illness from waters polluted by nonpoint sources of pollution. The studies are 

being conducted at three diverse beaches with contamination ranging from mostly human 

(untreated or poorly treated), to primarily nonhuman (likely avian), or a mixture of human and 

nonhuman fecal sources. Water samples at the various beaches will be collected at multiple 

locations and times and tested for over 30 different microbiological indicators. These indicators 

are grouped into five categories and include the following: (1) traditional fecal indicator 

bacteria; (2) rapid methods; (3) new, alternative microbial indicators; (4) microbial source 

tracking tools; and (5) viruses. 

The studies are based on a prospective cohort design. Swimmers will be interviewed at the 

beach to determine their eligibility to participate in the study and contacted 10 to 14 days later 

for a follow-up interview. During the second interview, study participants will be asked to 

describe illness symptoms that have occurred since the initial interview. The SCCWRP hopes 

that these studies will help evaluate the relative risk of contracting an illness from swimming at 

beaches polluted with nonpoint sources. Furthermore, the researchers hope to determine whether 

the risk of illness under these conditions correlates with traditional indicator densities and/or new 

indicators or methods. 
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February 2009 31 

IV. OUTBREAK REPORTS FOR RECREATIONAL AND DRINKING 

WATERS

IV.1 Waterborne Disease Surveillance and Outbreak Reporting in the United States 

In the Unites States, formal surveillance data on the occurrence and causes of waterborne disease 

outbreaks are collected through collaboration between EPA, the Council of State and Territorial 

Epidemiologists, and CDC. The goals of the surveillance program include characterizing the 

epidemiology of outbreaks, identifying the agents causing outbreaks as well as trends and risk 

factors, identifying deficiencies in providing safe drinking water, encouraging health officials to 

investigate outbreaks, and fostering government and international agency collaboration on 

waterborne disease prevention (Liang et al., 2006). State, territorial, and local public health 

departments are responsible for investigating and reporting outbreaks to CDC. Because this 

reporting is voluntary and originates with the investigating agency, it is called “passive” 

surveillance. 

The number of outbreaks reported is a significant underestimate of the actual number of 

outbreaks that occur; the actual number reported varies depending on the issues mentioned 

above, and the extent of underestimation is unknown overall. However, CDC is collaborating 

with EPA to prepare an estimate of how many waterborne illnesses occur in the United States 

(Craun and Calderon, 2006; Messner et al., 2006). The adequacy of this approach depends on 

good surveillance data and reasonable estimates for under-reporting cases. 

CDC defines an outbreak as at least two people who are linked by location of exposure to water, 

time, and illness (Liang et al., 2006). Evidence must implicate water as the probable source of 

the outbreak, which is often difficult. CDC uses a classification system to rank the strength of 

the data available based on an outbreak investigation. The classification system is two-pronged, 

based on epidemiological and water quality data, and ranges from Class I, which indicates 

adequate epidemiological and water quality data, to Class IV, which indicates that epidemiologic 

data was available, although limited, but that the water quality data was either absent or 

inadequate. CDC weights epidemiologic data more heavily and will include an outbreak that 

does not include any water quality information, provided the epidemiological evidence is 

sufficient (Liang et al., 2006). 

Despite the problems noted above, surveillance studies provide the best information available on 

waterborne disease outbreaks, and such data are critical to adequately characterizing microbial 

hazards (Embrey, 2002). 

IV.2 Summary of CDC Surveillance Reports on Drinking Water 

CDC systematically tracks the following water-related parameters in their reports: type of water 

system (e.g., community, individual, noncommunity, and bottled); water source (e.g., well, 

spring, and pond); and the water treatment deficiency (e.g., source water contamination, 

treatment deficiency, and distribution deficiency). The classification for deficiencies is further 

broken down by point of contamination and whether or not the water was treated or meant to be 
U.S. Environmental Protection Agency

February 2009 32 

ingested. Although the report narrative occasionally mentions evidence of a sewage leak or other 

pathogen origin, based on standard reporting parameters, it is impossible to determine 

systematically whether the source of contamination was of human or animal origin. 

Craun et al. (2006) summarized CDC statistics on waterborne disease since the first year that 

data were collected in 1920 to 2002, including outbreaks caused by chemical and microbial 

contamination of drinking and recreational water. During that time, over 880,000 illnesses have 

been reported, including over 1,000 deaths—mainly due to typhoid fever before 1940. In terms 

of microbial etiologies, Giardia and Cryptosporidium have been the most frequently identified 

from 1990 to 2002, which the authors attribute to their high infectivity and imperviousness to 

many conventional water treatment practices. Addtionally, reports have identified a wider 

variety of pathogens in recent years, including newly emerging pathogens, such as Cyclospora. 

Although laboratory testing has improved dramatically, many etiologies of outbreaks of 

waterborne disease are still undetermined. 

The deficiencies linked with waterborne disease outlets have also changed. Water treatment 

deficiencies have become a much less important cause (probably due to strengthened regulations 

and better water treatment practices), while distribution system problems have increased in 

importance. Further, the proportion of outbreaks associated with surface water sources of 

drinking water has decreased, while the proportion of outbreaks associated with groundwater has 

stayed constant. Because the predominant pathogens and causes identified in outbreaks have 

changed over the years, it is likely that new regulations or better enforcement of water treatment 

regulations, as well as advances in both treatment and laboratory detection methodologies, will 

affect future surveillance reports. 

Starting in its 2002 report, CDC began disaggregating details of individual outbreaks and 

including data on water quality parameters when available. Table IV.2.1 below summarizes 

CDC data on individual drinking water-related disease outbreaks from the last three reports 

covering outbreaks from 1999 to 2004 (Blackburn et al., 2004; Lee et al., 2002; Liang et al., 

2006). Outbreaks that may have been related to animal contamination are shaded gray. 

IV.3 Summary of Selected Drinking Water Outbreaks Reported in the United States and 

Internationally 

To augment the results reported by CDC, a comprehensive literature search using the U.S. 

National Library of Medicine’s PubMed system was conducted (see Appendix A for further 

information). Search terms included “drinking AND water AND outbreak,” which resulted in 

495 hits and “waterborne AND outbreak,” which produced 448 hits. The results from these 

searches were combined and the result was included in our review if the abstract showed 

evidence that the etiologic agent was detected in the source water (Table IV.3.1). Although this 

is a higher bar than what CDC uses to evaluate outbreak evidence, the large quantity of 

international articles with questionable outbreak investigation methods required a more stringent 

standard for inclusion in the review. 

The summary of reports from outside the United States and U.S. reports older than 1999 that 

may provide useful information, but need to be interpreted within their context. For example, 
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February 2009 33 

countries in Northern Europe (Finland, Norway, and Sweden) often have municipal water supply 

systems that use unchlorinated groundwater in areas of sparse population (Hanninen et al., 2003), 

which makes the water supply susceptible under certain common conditions—every outbreak but 

one reported in Finland between 1998 and 1999 occurred in undisinfected groundwater 

(Miettinen et al., 2001). Also, several giardiasis outbreaks were associated with beavers, but 

none has been reported in the past 15 years. In the 1980s, researchers considered beavers to be a 

primary source of zoonotic Giardia in the environment; however, recent research suggests that 

the importance of animals as a risk factor for human infections is unclear (Hunter and 

Thompson, 2005; Lane and Lloyd, 2002). The outbreaks that are possibly related to animal 

sources are shaded in Table IV.3.1. 
U.S. Environmental Protection Agency

February 2009 34 Table IV.2.1. Select Waterborne Disease Outbreaks Associated with Drinking Water in the United States Report

2004)* 

Reference Location Etiologic Agent Number of Cases Water Source Water Quality/Environmental 

Liang et al., 2006 Montana S. typhimurium 70 Well Coliforms detected; disinfection m

cross-connection 

Liang et al., 2006 Washington Campylobacter

spp. (spp.) 

110 Well Coliforms detected; untreated sou

connection 

Liang et al., 2006 Ohio C. jejuni,

spp. 

Shigella 57 Pond Coliforms and E. coli detected; eti

not detected; untreated source 

Liang et al., 2006 Wisconsin C. jejuni 20 Well Coliforms and E. coli detected; un

Liang et al., 2006 Illinois Unidentified 180 Well E. coli detected; chlorinated sourc

Liang et al., 2006 Pennsylvania Norovirus 70 Pond Coliforms detected; cross-connect

untreated, unpotable water 

Liang et al., 2006 New York C. jejuni,

Entamoeba spp., Giardia spp. 

27 Well Broken sewer line swamped the w

Liang et al., 2006 Ohio C. jejuni, C. lari, 

Cryptospordium spp., and Helicobactercanadensis

82 Well Cryptosporidium spp. detected; cr

with untreated, unpotable water 

Liang et al., 2006 Pennsylvania Unidentified 174 Well Coliforms detected; sewage pipe b

chlorination unit broken 

Blackburn et al., 2004 

Arizona Naegleria fowleri 

(meningoencephalitis) 

2 (2 deaths) 

Well Coliforms and N. fowleri detected; 

source 

Blackburn et al., 2004 

Indiana Cryptosporidium

spp. 

10 Well Filtration system bypassed intentio

located in a high-density septic tan

Blackburn et al., 2004 

New York Giardia intestinalis 6 Well/spring Power outage resulted in negative 

the distribution system 

Blackburn et al., 2004 

Alaska C. jejuni, Yersinia 

enterocolitica

12 Well Coliforms detected; undisinfected 

documented contamination with s
U.S. Environmental Protection Agency

February 2009 35 

Reference Location Etiologic Agent Number of Cases Water Source Water Quality/Environmental 

Blackburn et al., 2004 

Wisconsin C. jejuni 13 Well C. jejuni detected; untreated sourc

contamination with surface water; near a chicken coop 

Blackburn et al., 2004 

Arizona Norovirus 71 

(1 death) 

Well Unsanitary water dispensing and i

documented 

Blackburn et al., 2004 

Connecticut Norovirus 142 Well Coliforms and E. coli detected; he

probably caused surface water infuntreated source 

Blackburn et al., 2004 

Kansas Norovirus 86 Well Coliforms detected; untreated sou

Blackburn et al., 2004; Anderson et al., 2003 

Wyoming Norovirus 230 

(1 hospitalization) 

Well Coliforms and norovirus detected; 

near septic tanks or outhouses; ovseptic system documented 

Blackburn et al., 2004 

Pennsylvania Unknown 19 Well No chlorine residual detected 

Lee et al., 2002 Florida G. intestinalis 2 Well Inadequate chlorine documented; 

maintained near well 

Lee et al., 2002 Minnesota G. intestinalis 12 Well Coliforms detected; cross-connect

sewage pipe documented 

Lee et al., 2002 New Mexico G. intestinalis 4 River Inadequate or nonexistent filtration 

Lee et al., 2002 Colorado G. intestinalis 27 River Giardia detected; treatment malfu

documented 

Lee et al., 2002 Florida G. intestinalis 2 Well Coliforms detected; cross-connect

troughs; inadequate chlorine 

Lee et al., 2002 New Hampshire G. intestinalis 5 Well Filtration system malfunction; non

disinfection 

Lee et al., 2002 Florida C. parvum 5 Well System break documented; low 

residual 

le

Lee et al., 2002 Missouri S. typhimurium 124 

(17 hospitalizations) 

Well Inadequate chlorination 

Lee et al., 2002 New York C. jejuni, E. coli

O157:H7 

781 (71 hospitalizations;2 deaths) 

Well E. coli O157:H7 detected; nonexis

disinfection; heavy rains; cross-coseptic system; possible cross-conmanure storage 

Lee et al., 2002 Texas E. coli O157:H7 22 Well Inadequate chlorination 
U.S. Environmental Protection Agency

February 2009 36 

Reference Location Etiologic Agent Number of Cases Water Source Water Quality/Environmental 

Lee et al., 2002 Idaho E. coli O157:H7 4 Canal Coliforms detected (100/100mL); 

source 

Lee et al., 2002 Idaho C. jejuni 15 Well Coliforms detected; potential surfa

agricultural runoff documented 

Lee et al., 2002 Utah C. jejuni, E. coli 

O157:H7, E. coliO111 

102 Irrigation water C. jejuni detected; nonpotable sou

Lee et al., 2002 California E. coli O157:H7 5 Creek Filtered source 

Lee et al., 2002 Ohio E. coli O157:H7 29 

(9 hospitalizations) 

Surface Coliforms detected; possible cross

with animal-contaminated source 

Lee et al., 2002 Multistate Salmonella Bareilly 84 Spring/well Coliforms and E. coli detected; ad

treatment documented 

Lee et al., 2002 New Mexico Small roundstructured virus 70 Spring Coliforms detected; proximity to la

system documented 

Lee et al., 2002 West Virginia Norwalk-like virus 123 Well Coliforms detected; sewage conta

documented 

Lee et al., 2002 Kansas Norwalk-like virus 86 Well Coliforms detected; improper well 

documented 

Lee et al., 2002 California Norwalk-like virus 147 Well Coliforms detected; untreated sou

Lee et al., 2002 Florida Unknown 4 Well Coliforms detected; improper well 

documented; untreated source 

Lee et al., 2002 Florida Unknown 3 Well Coliforms detected; cross-connect

irrigation well documented 

Lee et al., 2002 Florida Unknown 6 Surface Cross-connection with irrigation w

documented; irrigation well proximcommercial septic system and gar

Lee et al., 2002 Florida Unknown 3 Well No chlorine residual detected; wel

chicken coop 

Lee et al., 2002 California Unknown 31 Well Coliforms detected; untreated sou

Lee et al., 2002 Washington Unknown 46 Creek Untreated source 

Lee et al., 2002 Washington Unknown 68 Well Coliforms detected; horse manure 

the site 
U.S. Environmental Protection Agency

February 2009 37 

Reference Location Etiologic Agent Number of Cases Water Source Water Quality/Environmental 

Lee et al., 2002 Florida Unknown 71 Well Coliforms detected; Cryptosporidiu

detected; well contamination with documented 

Lee et al., 2002 Florida Unknown 2 Well Coliforms detected; heavy rainfall 

well conditions documented; untre

Lee et al., 2002 California Unknown 63 Irrigation Coliforms detected; nonpotable so

* Outbreaks that may have been related to animal contamination are shaded gray. 
U.S. Environmental Protection Agency

February 2009 38 Table IV.3.1. Select Waterborne Disease Outbreaks Associated with Drinking Water* 

Reference Location Etiologic Agent Number of Cases Water Source Water Quality/Environmental Inform

Alamanos et al., 2000 

Greece Shigella sonnei 288 

(91 hospitalizations) 

Well S. sonnei detected with same resistance profi

isolates; coliforms and fecal streptococci detenot regularly disinfected; no structural or functdamaged noted; well situated near a milk facto

Amvrosieva et al., 2001 

Belarus Echovirus 30 

(aseptic meningitis; gastroenteritis) 

460 River and well Echovirus 30 and other enteroviruses detecte

water and source water; 

Amvrosieva et al., 2006 

Belarus Echovirus 30, 

echovirus 6, coxsackievirus B5 (meningitis; encephalitis; herpangina; myocarditis) 

1,351 Surface reservoir Etiologic agents detected in surface and finish

Atherton et al., 1995 

England Cryptosporidium 125 Reservoir Oocysts detected; heavy rain; filter at treatme

received maintenance 

Bell et al., 1995; Bowie et al., 1997; IsaacRenton et al., 1998 

Canada Toxoplasma gondii 

(retinochoroiditis; toxoplasmosis; lymphadenopathy) 

100 (plus 12 congenital cases) 

Well/reservoir T. gondii oocysts undetected; however, sourc

unfiltered and chloraminated, which would not oocysts. Multiple epidemiological measures inmunicipal water supply as the outbreak sourcenear reservoir were seropositive; heavy rain 

Brown et al., 2001 

Bermuda Norwalk-like virus 448 Rainwater catchment Coliforms, Norwalk-like virus, and E. coli dete

supply deficiencies documented 

CCDR, 2000; Bruce-GreyOwen Sound Health Unit, 2000 

Canada E. coli O157:H7, 

Campylobacter spp. 

1,346 (65 hospitalizations, 6 deaths) 

Well Coliforms and E. coli O157:H7 detected; Cam

spp. and E. coli O157:H7 detected in animal madjacent farms (cattle isolates identical to humheavy rain and flooding; chlorinated source 

CDC, 1996 Idaho, U.S. S. sonnei 82 Well Coliforms detected, but S. sonnei tests negati

poorly draining sewage documented 

CDC, 1998a Tajikistan S. typhii 8,901 

(95 deaths) 

River/ground mix 4–400+ CFU/100 mL fecal coliforms detected 

treatment failures; low pressure resulted in crowith wastewater; inadequate chlorination; muldistribution system failures 

Dworkin et al, 1996 

Washington, U.S. 

C. parvum 86 Wells Coliforms and C. parvum presumptive oocysts 

untreated source; treated wastewater from an system leaking into well documented; cattle gwell documented; 

Glaberman et al., 2002 

Northern Ireland 

C. parvum genotype) 

(bovine 129 Municipal supply 

(otherwise unknown) 

Unknown 
U.S. Environmental Protection Agency

February 2009 39 

Reference Location Etiologic Agent Number of Cases Water Source Water Quality/Environmental Inform

Glaberman et al., 2002 

Northern Ireland 

C. parvum (human genotype) 

117 Municipal supply 

(otherwise unknown) 

Unknown 

Glaberman et al., 2002 

Northern Ireland 

C. parvum (human genotype) 

230 Municipal supply 

(otherwise unknown) 

C. parvum detected 

Goldstein et al., 1996 

Nevada, U.S. C. parvum 78 

(20 deaths in immunocompromised patients with cryptosporidiosis) 

River/lake No coliforms or oocysts detected in source or 

during study; presumptive oocysts detected inafter study; municipal supply receives filtration disinfection; no malfunctions detected 

Hafliger et al., 2000 

Switzerland Norwalk-like virus 1,750+ Well Coliforms, enteroviruses, and Norwalk-like vir

detected; identical genotypes of clinical and wdocumented; wastewater system defect docum

Hanninen et al., 2003 

Finland C. jejuni 400 Well Coliforms (1 CFU); C. jejuni; and 

well source and tap water; heavy 

E. coli (1 CF

precipitation 

Hanninen et al., 2003 

Finland C. jejuni 1,000 Well Coliforms (1–66 CFU); E. coli (1–630 CFU); e

1,080 CFU) and C. jejuni detected in well sou

infiltrating surface water; C. coli found in porci

samples; the variety of strains of Campylobacand proximity to a farm indicated animal fecal contamination; heavy precipitation; undisinfec

Hayes et al., 1989 

Georgia, U.S. Cryptospridium 13,000 Surface Cryptosporidium oocysts detected; oocysts de

cattle feces; filtered and chlorinated source; sflocculation and filtration noted; sewage overfldocumented; heavy precipitation 

Howe et al., 2002 

England C. parvum 58 Spring/reservoir C. parvum detected (0.1–0.9 oocysts/L); geno

oocysts suggested animal source; disinfected source; spring collection chambers in poor repfeces on top of spring covers documented; maon field within 5 m of one well head; heavy rai

Isaac-Renton et al., 1994 

Canada G. duodenalis 124 Creek G. duodenalis cysts detected in water and bea

activity noted near water intake; beaver, watecysts of the same karotype; unfiltered source 

Istre et al., 1984 Colorado, U.S. G. lamblia 

(intestinalis) 

20 Creek G. lamblia cysts detected; treatment malfuncti

inadequate chlorination; other treatment deficdocumented; two beaver dams proximate to wheavy snowfall 

Kent et al., 1988 

Massachusetts, U.S. 

G. lamblia (intestinalis) 

703 Surface reservoir Coliforms detected (1–41 CFU/100 mL); G. la

detected (7–80/100 gal); disinfected but unfiltemalfunction in chlorinator documented; beavedocumented; G. lamblia cysts detected in bea

Kukkula et al., 1999 

Finland Norwalk-like virus 1,700–3 ,000 

(estimated) 

Lake Coliforms (38–48 CFU/100mL) in tap water de

Norwalk-like virus detected; filtered and disinfeinadequate chlorination documented 
U.S. Environmental Protection Agency

February 2009 40 

Reference Location Etiologic Agent Number of Cases Water Source Water Quality/Environmental Inform

Kuusi et al, 2004 

Finland C. jejuni 463 

(9 of 113 cases questioned were hospitalized) 

Wells/reservoirs Coliforms and C. jejuni detected; untreated so

precipitation and infiltration of surface water innoted; wells and reservoirs accessible to peopanimals 

Licence et al., 2001 

Scotland E. coli O157:H7 6 Spring Coliforms, E. coli and E. coli O157:H7 detecte

sheep feces; untreated source; sheep and denear source; human, water, and sheep samplindistinguishable 

MacKenzie et al., 1995 

Wisconsin, U.S. C. parvum 403,000 (estimated) Lake C. parvum oocysts detected (0.7–13.2 oocysts

filtered and disinfected source; increased turbprecipitation/runoff 

Maurer and Sturcheler, 2000 

Switzerland C. jejuni, S sonnei, 

enteropathogenic E. coli, small round structured viruses 

1,607–2,213 (estimated) 

Well Enteroviruses, small round structured virus de

sewage pump failure documented 

Melby et al., 1991 

Norway C. jejuni 680 Lake/river Coliforms and C. jejuni detected (different sero

human isolates); untreated source; sheep granoted; sheep infected with campylobacter not

Navin et al., 1985 

Nevada, U.S. G. lamblia 

(intestinalis) 

324 Wells/river/reservoir Giardia cysts detected in source and treated w

cysts/3,800L) supply and a beaver in the resedistribution site; source water disinfected but n

Nygard et al., 2003 

Sweden Norovirus 200 Well Norovirus detected; untreated source; sewage 

documented 

O’Reilly et al, 2007; Fong et al., 2007 

Ohio, USA C. jejuni, norovirus, 

G intestinalis, S. typhimurium

1,450 (21 hospitalizations) 

Well/lake Coliforms (0.1–90 CRI/100 mL); E. coli (0.1–4

mL); enterococci (0.1–6.6 CFU/100 mL); Arco

coliphages; enteric viruses; C. jejuni; Salmone

adenovirus, Cryptosporidium spp., and Giardi

detected (all well water samples); heavy rain; sewage disposal noted; geology noted to be pcontaminate aquifer; possible cross-connectioErie 

Olsen et al., 2002 

Wyoming, USA E. coli O157:H7 157 

(4 hemolytic uremic syndrome cases) 

Spring Coliforms detected; untreated source; surface 

contamination documented; risk of animal connoted; heavy rain and runoff; deer and elk fecdocumented (but negative for E. coli O157:H7

Parshionikar et al., 2003; Gelting et al., 2005; Anderson et al., 2003 

Wyoming, USA Norovirus 84 Well Coliforms and norovirus detected; overloaded 

disposal system noted; heavy precipitation; chmalfunction 

Ramakrishna et al., 1996 

India V. cholerae O139 475 Wells/surface 

reservoirs 

Coliforms (10–1,800 MPN/L) and V. cholerae detected; chlorination had been discontinued 
U.S. Environmental Protection Agency

February 2009 41 

Reference Location Etiologic Agent Number of Cases Water Source Water Quality/Environmental Inform

Stirling et al., 2001 

Canada C. parvum 1,907 

(50 hospitalizations) 

River C. parvum oocysts detected (no coliforms det

disinfected and filtered source water; treatmendocumented which resulted in increased turbidresidual levels normal 

Swerdlow et al., 1992 

Peru V. cholerae O1 16,400 

(6.673 hospitalizations; 71 deaths) 

Wells Coliforms (1–1,800/100 mL), V. cholorae O1 d

untreated source; low water pressure and poointegrity noted

* Outbreaks that may have been related to animal contamination are shaded gray. 
U.S. Environmental Protection Agency

February 2009 42 

IV.4 Descriptions of Drinking Water Outbreaks with Animal Related-Pathogen Sources 

Information in the two outbreak summary tables (Tables IV.2.1 and IV.3.1) indicates that the 

pathogen source in the majority of drinking water-related outbreaks remains unknown. The 

majority of outbreaks in both tables occurred in groundwater sources, and often, surface water 

contamination of the spring or well is the extent of the implication. Although the source of 

pathogens in surface water could be humans or animals, surface water that is subject to 

agricultural runoff would have a closer link to animal pathogens. However, most reports provide 

little detail regarding pathogen source, leaving a critical information gap for the purposes of this 

paper. 

In this review of drinking water outbreaks, several studies have linked pathogens isolated from 

patients with water samples, animals, or both (e.g., CCDR 2000; Howe et al., 2002; Licence et 

al., 2001). The suspected animal sources include beavers, cats/cougars, deer, elk, pigs, cattle, and 

chickens/poultry. The animal-related pathogens in these outbreaks were Giardia intestinalis,

Cryptosporidium spp., E. coli O157:H7, Campylobacter spp., Toxoplasma gondii, and S. 

typhimurium. In addition, Krewski and colleagues (2002) describe waterborne disease outbreaks 

in British Columbia from 1980 to 2000. Of the 24 outbreaks in the records, the suspected source 

of the pathogen (mostly Giardia and Campylobacter) was an animal in 21 outbreaks; however, 

the largest of those outbreaks was caused by Cryptosporidium of human origin. A summary of 

288 Canadian drinking water outbreaks reported between 1974 and 2001 linked 44 (or 15 

percent) with animal sources (Schuster et al., 2005); about half of the 25 outbreaks linked to 

private water supplies in England and Wales listed animals as possible contributing factors (Said 

et al., 2003). 

Furthermore, in some studies, investigators hypothesize about the contamination based on 

circumstantial evidence. For example, Lee et al. (2002) described a Giardia outbreak where pigs 

were housed near a well while Olsen et al. (2002) noted deer and elk feces near a spring that was 

the source of water causing an E. coli O157:H7 outbreak in Wyoming. As laboratory methods 

have become increasingly sophisticated, more investigators are using molecular techniques to 

track pathogen sources. Most investigating agencies do not have the resources to perform such 

in-depth testing. As these techniques become more common and affordable, however, 

investigators will likely use them more often to shed light on outbreak causes. Three studies are 

summarized below to illustrate how advanced laboratory methods can link outbreaks with animal 

sources. 

• An outbreak of E. coli O157 resulted from drinking from an untreated, private supply 

sourced from a spring located in an area where deer and sheep grazed (Licence et al., 

2001). Water samples taken one week before the first illness had elevated coliforms (11 

CFU/100 mL) and E. coli (15 CFU/100 mL) showing fecal contamination. After the 

outbreak, E. coli O157 isolates collected from patient stool, water, and sheep feces were 

all identical based on pulsed field gel electrophoresis analysis. Interestingly, the six cases 

were tourists to the area, while the permanent residents who were also exposed to the 

contaminated water did not experience any GI symptoms. The authors concluded that 

low levels of contamination may have provided some level of immunity. 
U.S. Environmental Protection Agency

February 2009 43 

• Researchers also used pulsed field gel electrophoresis to link Giardia isolates from water, 

beavers, and stool samples from cases from an outbreak in British Columbia (IsaacRenton et al., 1994). A creek used as the drinking water source was chlorinated, but not 

filtered. The source water was found to be heavily contaminated with Giardia cysts, and 

an infected beaver was living near the water intake. When the animal was removed, 

water samples continually tested negative for Giardia cysts. 

• A well documented and highly publicized outbreak that was linked to an animal source 

occurred in Walkerton, Ontario from May to June, 2000. In that municipal water system 

outbreak, E. coli O157:H7 and Campylobacter spp. were implicated in 1,346 reported 

cases of gastroenteritis, including 65 hospitalizations, 27 cases of hemolytic uremic 

syndrome, and six deaths (CCDR, 2000). One particular well was implicated as the 

source of contamination based on microbiological testing and a history of susceptibility 

to surface water influence. In addition, hydrological modeling indicated that the well 

could have been contaminated by an adjacent farm—especially under the record-breaking 

rain conditions present before the outbreak. Subsequent microbiological testing supported 

this model. The Investigative Report of the Walkerton Outbreak of Waterborne 

Gastroenteritis (Bruce-Grey-Owen Sound Health Unit, 2000) reported that “The 

molecular subtyping and phage-typing of the E. coli O157:H7 and the Campylobacter 

spp. isolates from this farm were identical to those found in the majority of the human 

cases. While investigators could not prove the pathogens were present prior to the 

outbreak, the evidence suggested the pathogens likely originated from cattle manure on 

this farm.” Other testing of deer feces was negative for E. coli. 

Finally, in another outbreak in British Columbia, T. gondii was implicated (Bowie et al., 1997). 

The cysts were never detected in the water source; however, the authors concluded that the 

strength of the epidemiological and environmental data was indisputable. Although rarely 

implicated as a waterborne pathogen, T. gondii can have devastating sequelae in fetuses whose 

mothers are infected—especially in the first part of pregnancy. Toxoplasmosis can also be fatal 

in immunocompromised people. Felines are the definitive hosts in the Toxoplasma life cycle, 

and the cysts they excrete are extremely hardy and long-lived in the environment. In this 

outbreak, cats and cougars were implicated as the source of the pathogen. 

IV.5 Summary of Selected Recreational Water Outbreaks 

The CDC tracks waterborne disease and outbreaks from drinking water and recreational water, 

with the latter including recreational water outbreaks since 1978. CDC’s analysis of recreational 

water includes swimming pools, wading pools, spas, waterslides, interactive fountains, wet 

decks, and fresh and marine bodies of water; it does not include recreational waters associated 

with cruise ships. 

A summary by Craun et al. (2005) that analyzed the recreational water outbreaks in the United 

States between 1970 and 2000 illustrates the difficulties associated with addressing all the data 

gaps in an outbreak investigation. During that period, CDC received reports of 259 outbreaks 

associated with recreational water. Over two-thirds were associated with either bacteria or 

protozoa; over 15 percent had unidentified etiologies and only 7 percent were viral. However, 

CDC estimates that approximately 80 percent of the annual illnesses overall in the United States 
U.S. Environmental Protection Agency

February 2009 44 

due to known pathogens are of viral origin (Mead et al., 1999). The trend in the number of 

outbreaks that are reported annually has increased dramatically since 1990, probably due to a 

combination of better reporting practices and the occurrence of more outbreaks. 

Of the 259 recreational water outbreaks reported, only half included any information about 

possible sources of the contamination or contributing factors. In untreated recreational water 

outbreaks, feces or ill bathers in the water, bather overcrowding, and the presence of children in 

diapers accounted for 90 percent of the assumed sources; however, Craun et al. (2005) did not 

indicate that these attributions were anything more than assumptions and were not reinforced by 

laboratory analysis, other than measures of microbial indicators. Further, most of the related 

assumptions were based on eyewitness reports such as adults seen rinsing diapers in the water 

and the measure of bather density was subjective. Craun et al. estimated that 18 percent of the 

outbreaks were associated with animals and 21 percent were associated with sewage 

contamination—although the proportion actually confirmed by laboratory analysis is unknown. 

Some animal-associated outbreaks may have been classified based on the etiological agent itself. 

For example, because the source of Leptospira is animal urine and leptospirosis is not spread 

from person-to-person, any waterborne outbreaks of leptospirosis can be assumed to have an 

animal source (CDC, 2005). Although most cases of leptospirosis occur in Hawaii, a large 

outbreak in 1998 of triathletes in Illinois and Wisconsin caused 375 illnesses and 28 

hospitalizations (CDC, 1998b). 

A summary of the CDC’s surveillance reports since 2000 is provided below: 

• During 2001 to 2002 (Yoder et al., 2004), the largest number of recreational water 

outbreaks occurred since reporting began in 1978. In total, 65 outbreaks were reported, 

with 30 involving gastroenteritis. Fifty percent of the outbreaks involving gastroenteritis 

were associated with Cryptosporidium in treated drinking water, followed by E. coli 

(25 percent) and then norovirus (25 percent) in freshwater. 

• Results from 2003 to 2004 indicate that 26 states and Guam reported a total 62 outbreaks 

associated with recreational water (excluding Vibrio cases) (Dziuban et al., 2006). Of the 

62 cases, 20 were confirmed as bacterial, 15 as parasitic, and 6 as viral. For the 

remaining cases, the etiologic agents were chemical- or toxin-mediated or were not 

identified. Primary illnesses resulting from these outbreaks included gastroenteritis, 

dermatitis, and acute respiratory illness. Other illnesses included amebic 

meningoencephalitis, meningitis, leptospirosis, otitis externa, and mixed illnesses. In 

addition, 16 states reported a total of 142 Vibrio cases associated with recreational water. 

Data for the Vibrio cases were analyzed separately to avoid substantially altering total 

waterborne disease outbreak numbers when compared with previous reports. Of the 

Vibrio cases, 70 resulted in hospitalization and 9 patients died. The most frequently 

isolated Vibrio species was V. vulnificus; others included V. parahaemolyticus, 

V. cholerae, V. damsela, V. fluvialis, nonspeciated Vibrio, and mixed Vibrio. Nearly all 

Vibrio cases were exposed to recreational water in a coastal state. 

CDC data on recreational water-related disease outbreaks from the last three reports covering 

1999 to 2004 (Dziuban et al., 2006; Lee et al., 2002; Yoder et al., 2004) are summarized in 

Table IV.5.1. Individual studies identified in the scientific literature also are included in the 
U.S. Environmental Protection Agency

February 2009 45 Table IV.5.1. Select Waterborne Disease Outbreaks Associated with Recreational Water in the United States Rep2004)* 

Reference Location Year of Outbreak Etiologic Agent Predominant Illness/Symptoms Number of Cases Water Source Water Quality In

Wheeler et al., 20072

California 2004 Cryptosporidium Acute 

gastrointestinal illness (AGI) 

315 Water park Cryptosporidium oo

detected in backwasand filters; Cryptoor Giardia not detecthe county park lakwells; fecal coliform detected in well-wa

Dziuban et al., 20063

California 2004 Cryptosporidium AGI 336 Pool Cryptosporidium oo

detected in backwaCryptosporidium or detected from the clake and three wellcoliform not detectewater 

Dziuban et al., 2006 

Colorado 2004 Cryptosporidium AGI 6 Pool Unknown 

Dziuban et al., 2006 

Florida 2004 Norovirus AGI 42 Waterslide Unknown 

Dziuban et al., 2006 

Georgia 2004 Cryptosporidium AGI 14 Pool Unknown 

Dziuban et al., 2006 

Guam 2004 Leptospira spp. Leptospirosis 3 River Unknown 

Dziuban et al., 2006 

Idaho 2004 Norovirus AGI 140 Pool Unknown 

Dziuban et al., 2006 

Illinois 2004 P. aeruginosa Skin, acute 

respiratory infection (ARI) 

16 Pool, spa Unknown 

Dziuban et al., 2006 

Illinois 2004 P. aeruginosa Skin 5 Spa Unknown 

2 Also referenced in Dziuban et al. (2006) 3 See Wheeler et al. (2007) for additional information 
U.S. Environmental Protection Agency

February 2009 46 

Reference Location Year of Outbreak Etiologic Agent Predominant Illness/Symptoms Number of Cases Water Source Water Quality In

Dziuban et al., 2006 

Illinois 2004 Cryptosporidium AGI 37 Pool, wading 

pool 

Unknown 

Dziuban et al., 2006 

Illinois 2004 Cryptosporidium AGI 8 Pool Unknown 

Dziuban et al., 2006 

Minnesota 2004 Norovirus AGI 9 Lake Unknown 

Dziuban et al., 2006 

Missouri 2004 Giardia intestinalis AGI 9 Lake Unknown 

Dziuban et al., 2006 

North Carolina 

2004 P. aeruginosa Skin 41 Spa Unknown 

Dziuban et al., 2006 

Ohio 2004 C. hominis AGI 160 Pool, wading 

pool, interactive fountain 

Although both Cryptosporidium oo

Giardia cysts were 

the pool water, only 

Cryptosporidium oo

isolated from clinicaspecimens. 

Dziuban et al., 2006 

Ohio 2004 P. aeruginosa Ear, skin 119 Pool, spa Pseudomonas dete

Dziuban et al., 2006 

Oregon 2004 P. aeruginosa Skin 2 Spa Unknown 

Dziuban et al., 20064 Oregon 2004 Norovirus AGI 39 Lake Unknown 

Dziuban et al., 2006 

Vermont 2004 Norovirus AGI 70 Pool Unknown 

Dziuban et al., 2006 

Wisconsin 2004 P. aeruginosa Skin, AGI 22 Pool, spa Unknown 

Dziuban et al., 2006 

Wisconsin 2004 Cryptosporidium AGI 6 Pool Unknown 

Dziuban et al., 2006 

Arkansas 2003 Cryptosporidium AGI 4 Pool Unknown 

Dziuban et al., 2006 

Connecticut 2003 Echovirus 9 Neurological 36 Pool Unknown 

4 See Keen et al. (1994) for additional information 
U.S. Environmental Protection Agency

February 2009 47 

Reference Location Year of Outbreak Etiologic Agent Predominant Illness/Symptoms Number of Cases Water Source Water Quality In

Dziuban et al., 2006 

Connecticut 2003 Microbe-resistant 

Staphylococcusinfection 

Skin 10 Spa Unknown 

Dziuban et al., 2006 

Georgia 2003 S. sonnei AGI 13 Lake Fecal coliform dete

Dziuban et al., 2006 

Idaho 2003 Cryptosporidium AGI 4 Lake Unknown 

Dziuban et al., 2006 

Illinois 2003 P. aeruginosa Skin 52 Spa Pseudomonas dete

Dziuban et al., 2006 

Iowa 2003 Cryptosporidium; G. 

intestinalis

AGI 63 Wading pool Unknown 

Dziuban et al., 2006 

Kansas 2003 C. hominis AGI 617 Pools, wading 

pools 

Unknown 

Dziuban et al., 2006 

Maryland 2003 S. sonnei; P. 

shigelloides

AGI 65 Lake Fecal coliform and 

detected 

Dziuban et al., 20065

Mass. 2003 G. intestinalis AGI 149 Pool Not conducted 

Dziuban et al., 2006 

North Carolina 

2003 N. fowleri Neuro 1 Lake Unknown 

Dziuban et al., 2006 

Ohio 2003 P. aeruginosa Skin 17 Pool, spa Unknown 

Dziuban et al., 2006 

Ohio 2003 P. shigelloides AGI 3 Lake Unknown 

Dziuban et al., 2006 

Oregon 2003 S. sonnei AGI 56 Interactive 

fountain 

Fecal coliform and detected 

Dziuban et al., 2006 

Wyoming 2003 P. shigelloides AGI 2 Reservoir Unknown 

Katz et al., 20066

Mass. 2003 G. intestinalis AGI 149 Pool Not conducted 

5 See Katz et al. (2006) for additional information 6 Also referenced by Dziuban et al. (2006) 
U.S. Environmental Protection Agency

February 2009 48 

Reference Location Year of Outbreak Etiologic Agent Predominant Illness/Symptoms Number of Cases Water Source Water Quality In

Iwamoto et al., 20057 Georgia, 2003 S. sonnei Gastroenteritis 17 Lake Fecal coliform dete

fecal coliform bactemL); Shigella not d

Yoder et al., 2004 

Alaska 2002 P. aeruginosa Skin 110 Pool/spa P. aeruginosa dete

Yoder et al., 2004 

Alaska 2002 P. aeruginosa 

(suspected etiology based on clinical syndrome and setting)

Skin 3 Pool/spa Unknown 

Yoder et al., 2004 

Colorado 2002 P. aeruginosa Skin 12 Pool/spa P. aeruginosa dete

Yoder et al., 2004 

Florida 2002 N. fowleri Meningoencephalitis 1 Lake Unknown 

Yoder et al., 2004 

Florida 2002 N. fowleri Meningoencephalitis 1 Lake Unknown 

Yoder et al., 2004 

Georgia 2002 Cryptosporidium 

spp. 

Gastroenteritis 3 Wading pool Unknown 

Yoder et al., 2004 

Georgia 2002 N. fowleri Meningoencephalitis 1 River Unknown 

Yoder et al., 2004 

Iowa 2002 P. aeruginosa 

(suspected etiology based on clinical syndrome and setting) 

Skin 24 Pool/spa Unknown 

Yoder et al., 2004 

Maine 2002 E. coli O157:H7 Gastroenteritis 9 Wading pool Unknown 

Yoder et al., 2004 

Maryland 2002 P. aeruginosa

(suspected etiology based on clinical syndrome and setting) 

Skin 3 Spa Unknown 

Yoder et al., 2004 

Mass. 2002 Cryptosporidium

spp. 

Gastroenteritis 767 Pool Unknown 

7 Also referenced in Dziuban et al. (2006) 
U.S. Environmental Protection Agency

February 2009 49 

Reference Location Year of Outbreak Etiologic Agent Predominant Illness/Symptoms Number of Cases Water Source Water Quality In

Yoder et al., 2004 

Minnesota 2002 Norovirus Gastroenteritis 11 Lake Unknown 

Yoder et al., 2004 

Minnesota 2002 Norovirus Gastroenteritis 36 Pool Unknown 

Yoder et al., 2004 

Minnesota 2002 Cryptosporidium

spp.

Gastroenteritis 52 Indoor pool Unknown 

Yoder et al., 2004 

Minnesota 2002 Cryptosporidium 

spp.

Gastroenteritis 41 Pool Unknown 

Yoder et al., 2004 

Minnesota 2002 Cryptosporidium

spp.

Gastroenteritis 16 Pool Unknown 

Yoder et al., 2004 

Ohio 2002 P. aeruginosa Skin 18 Spa P. aeruginosa dete

Yoder et al., 2004 

Ohio 2002 P. aeruginosa Skin 31 Pool/spa P. aeruginosa dete

Yoder et al., 2004 

Oregon 2002 Avian schistosomes

(suspected etiology based on clinical syndrome and setting) 

Skin 19 Lake Unknown 

Yoder et al., 2004 

Texas 2002 Cryptosporidium 

hominis

Gastroenteritis 54 Wading pool The species of 

Cryptosporidium thhumans and monke

Yoder et al., 2004 

Wisconsin 2002 Norovirus Gastroenteritis 15 Pool Unknown 

Yoder et al., 2004 

Wisconsin 2002 Norovirus Gastroenteritis 44 Lake E. coli detected 

Yoder et al., 2004 

Wyoming 2002 Cryptosporidium

spp. 

Gastroenteritis 3 Lake Unknown 

Yoder et al., 2004 

Wyoming 2002 G. intestinalis Gastroenteritis 2 River Unknown 

Causer et al., 20058

Illinois 2001 Cryptosporidium Gastroenteritis 358 Pool Cryptosporidium oo

detected 

8 Also referenced in Yoder et al. (2004) 
U.S. Environmental Protection Agency

February 2009 50 

Reference Location Year of Outbreak Etiologic Agent Predominant Illness/Symptoms Number of Cases Water Source Water Quality In

Yoder et al., Colorado 2001 S. sonnei Gastroenteritis 33 Interactive Unknown 

2004 fountain Yoder et al., Florida 2001 P. aeruginosa Skin 34 Pool Unknown 

2004 (suspected etiology 

based on clinical 

syndrome and 

setting)

Yoder et al., 2004 

Florida 2001 P. aeruginosa Skin 53 Spa P. aeruginosa dete

Yoder et al., Florida 2001 P. aeruginosa Skin 7 Spa Unknown 

2004 (suspected etiology 

based on clinical 

syndrome and 

setting)

Yoder et al., 20049

Illinois 2001 Cryptosporidium 

hominis 

Gastroenteritis 358 Pool Cryptosporidium oo

detected; the speciCryptosporidium thhumans and monke

Yoder et al., 2004 

Iowa 2001 S. sonnei Gastroenteritis 45 Wading pool Unknown 

Yoder et al., Maine 2001 P. aeruginosa Skin 21 Spa Unknown 

2004 (suspected etiology 

based on clinical 

syndrome and 

setting)

Yoder et al., Maryland 2001 P. aeruginosa Skin 8 Spa Unknown 2004 (suspected etiology 

based on clinical 

syndrome and 

setting)

Yoder et al., Minnesota 2001 E. coli O157:H7 Gastroenteritis 20 Lake Fecal coliform dete

2004 Yoder et al., Minnesota 2001 Norovirus Gastroenteritis 40 Lake Unknown 2004 

9 See Causer et al. (2005) for additional information 
U.S. Environmental Protection Agency

February 2009 51 

Reference Location Year of Outbreak Etiologic Agent Predominant Illness/Symptoms Number of Cases Water Source Water Quality In

Yoder et al., 2004 

Minnesota 2001 E. coli O26:NM Gastroenteritis 4 Lake Unknown 

Yoder et al., 2004 

Minnesota 2001 P. aeruginosa Skin 6 Spa P. aeruginosa dete

Yoder et al., 2004 

Nebraska 2001 Cryptosporidium

spp.

Gastroenteritis 157 Pools Unknown 

Yoder et al., 2004 

Nebraska 2001 Cryptosporidium

spp.

Gastroenteritis 21 Pool Unknown 

Yoder et al., 2004 

Nebraska 2001 P. aeruginosa

(suspected etiology based on clinical syndrome and setting)

Skin 9 Pool/spa Unknown 

Yoder et al., 2004, 2004 

Oklahoma 2001 N. fowleri Meningoencephalitis 1 Lake Unknown 

Yoder et al., 2004 

Penn. 2001 P. aeruginosa Skin 2 Spa P. aeruginosa dete

Yoder et al., 2004 

Penn. 2001 P. aeruginosa 

(suspected etiology based on clinical syndrome and setting)

Skin 42 Spa Unknown 

Yoder et al., 2004 

Penn. 2001 Bacillus spp. Skin 20 Spa Bacillus detected 

Yoder et al., 2004 

Penn. 2001 Staphylococcus spp. 

(suspected etiology based on clinical syndrome and setting)

Skin 3 Spa Unknown 

Yoder et al., 2004 

South Carolina 

2001 E. coli O157:H7 Gastroenteritis 45 Lake Fecal coliforms det

Yoder et al., 2004, 2004 

Texas 2001 N. fowleri Meningoencephalitis 1 Lake Unknown 

Yoder et al., 2004, 2004 

Texas 2001 N. fowleri Meningoencephalitis 1 Lake Unknown 
U.S. Environmental Protection Agency

February 2009 52 

Reference Location Year of Outbreak Etiologic Agent Predominant Illness/Symptoms Number of Cases Water Source Water Quality In

Yoder et al., 2004, 2004 

Texas 2001 N. fowleri Meningoencephalitis 1 Lake Unknown 

Yoder et al., 2004, 2004 

Texas 2001 N. fowleri Meningoencephalitis 1 Lake Unknown 

Yoder et al., 2004 

Washington 2001 P. aeruginosa Skin 3 Spa P. aeruginosa dete

Yoder et al., 2004 

Wisconsin 2001 P. aeruginosa

(suspected etiology based on clinical syndrome and setting)

Skin 7 Spa Unknown 

Yoder et al., 2004 

Wyoming 2001 Cryptosporidium

spp.

Gastroenteritis 2 Flow-through 

pool/hot spring 

Unknown 

Mathieu et al., 200410

Ohio 2000 C. parvum Gastroenteritis 749 

suspected cases; 144 laboratory confirmed 

Pool C. parvum (both the 

and bovine genotypdetected in water afilter samples 

Lee et al., 2002 

Alaska 2000 P. aeruginosa Skin 29 Pool/hot tub P. aeruginosa dete

Lee et al., 2002 

Arkansas 2000 P. aeruginosa Skin 26 Pool/hot tub Unknown 

Lee et al., 2002 

California 2000 N. fowleri Meningoencephalitis 1 Mudhole Unknown 

Lee et al., 2002 

California 2000 Schistosomes

(suspected etiology based on clinical syndrome and setting)

Skin 6 Pond Unknown 

10 Also referenced in Lee et al. (2002) 
U.S. Environmental Protection Agency

February 2009 53 

Reference Location Year of Outbreak Etiologic Agent Predominant Illness/Symptoms Number of Cases Water Source Water Quality In

Lee et al., 2002 

California 2000 Schistosomes

(suspected etiology based on clinical syndrome and setting)

Skin 4 Pond Unknown 

Lee et al., 2002 

Colorado 2000 C. parvum Gastroenteritis 112 Pool Unknown 

Lee et al., 2002 

Florida 2000 C. parvum Gastroenteritis 3 Pool Unknown 

Lee et al., 2002 

Florida 2000 C. parvum Gastroenteritis 5 Pool Unknown 

Lee et al., 2002 

Florida 2000 C. parvum Gastroenteritis 19 Pool Unknown 

Lee et al., 2002 

Florida 2000 C. parvum Gastroenteritis 5 Pool Unknown 

Lee et al., 2002 

Florida 2000 N. fowleri Meningoencephalitis 1 Unknown Unknown 

Lee et al., 2002 

Florida 2000 P. aeruginosa

(suspected etiology based on clinical syndrome)

Skin 6 Hot tub Unknown 

Lee et al., 2002 

Georgia 2000 C. parvum Gastroenteritis 36 Pool Unknown 

Lee et al., 2002 

Guam 2000 Leptospira 

interrogans 

Leptospirosis 21 Lake Unknown 

Lee et al., 2002 

Maine 2000 P. aeruginosa Skin 9 Hot tub/pool Unknown 

Lee et al., 2002 

Maine 2000 P. aeruginosa Skin 11 Hot tub P. aeruginosa dete

Lee et al., 2002 

Minnesota 2000 C. parvum Gastroenteritis 220 Lake Unknown 

Lee et al., 2002 

Minnesota 2000 S. sonnei Gastroenteritis 15 Lake/pond Unknown 

Lee et al., 2002 

Minnesota 2000 C. parvum Gastroenteritis 7 Pool Unknown 
U.S. Environmental Protection Agency

February 2009 54 

Reference Location Year of Outbreak Etiologic Agent Predominant Illness/Symptoms Number of Cases Water Source Water Quality In

Lee et al., 2002 

Minnesota 2000 C. parvum Gastroenteritis 6 Pool C. parvum not dete

Lee et al., 2002 

Minnesota 2000 S. sonnei Gastroenteritis 25 Lake Shigella not detecte

Lee et al., 2002 

Minnesota 2000 C. parvum Gastroenteritis 4 Pool Unknown 

Lee et al., 2002 

Minnesota 2000 P. aeruginosa Skin 16 Hot tub Unknown 

Lee et al., 2002 

Missouri 2000 Shigella flexneri Gastroenteritis 6 Wading pool Unknown 

Lee et al., 2002 

Nebraska 2000 C. parvum Gastroenteritis 225 Pools Unknown 

Lee et al., 200211

Ohio 2000 C. parvum Gastroenteritis 700 Pool Unknown 

Lee et al., 2002 

South Carolina 

2000 C. parvum Gastroenteritis 26 Pool Coliforms not detec

Lee et al., 2002 

Texas 2000 N. fowleri Meningoencephalitis 1 Lake Unknown 

Lee et al., 2002 

Washington 2000 P. aeruginosa

(suspected etiology based on clinical syndrome)

Skin 10 Pool/hot tub Unknown 

Lee et al., 2002 

Wisconsin 2000 Norwalk-like virus Gastroenteritis 9 Pool Unknown 

Bruce et al., 200312 Washington 1999 E. coli O157:H7 Gastroenteritis, 3 cases of hemolytic 

uremic syndrome 

37 Lake E. coli O157:H7 de

Lee et al., 2002 

Arkansas 1999 P. aeruginosa Skin 10 Pool P. aeruginosa dete

Lee et al., 2002 

Colorado 1999 P. aeruginosa Skin 19 Hot tub P. aeruginosa dete

11 See Mathieu et al. (2004) for additional information 12 Also referenced in Lee et al. (2002) 
U.S. Environmental Protection Agency

February 2009 55 

Reference Location Year of Outbreak Etiologic Agent Predominant Illness/Symptoms Number of Cases Water Source Water Quality In

Lee et al., 2002 

Colorado 1999 P. aeruginosa

(suspected etiology based on clinical syndrome) 

Skin 5 Hot tub Unknown 

Lee et al., 200213

Connecticut 1999 E. coli O121:H19 Gastroenteritis 11 Lake E. coli and shiga to

detected in lake; tofecal coliforms dete(results differ slightstated in McCarthy 

Lee et al., 2002 

Florida 1999 Campylobacter jejuni Gastroenteritis 6 Pool Unknown 

Lee et al., 2002 

Florida 1999 S. sonnei, C. parvum Gastroenteritis 38 Interactive 

fountain 

Coliforms detectedcoliforms not detec

Lee et al., 2002 

Florida 1999 C. parvum Gastroenteritis 6 Pool Unknown 

Lee et al., 2002 

Florida 1999 E. coli O157:H7 Gastroenteritis 2 Ditch water Unknown 

Lee et al., 2002 

Florida 1999 N. fowleri Meningoencephalitis 1 Pond Unknown 

Lee et al., 2002 

Idaho 1999 Norwalk-like virus Gastroenteritis 25 Hot springs Unknown 

Lee et al., 2002 

Mass. 1999 G. intestinalis Gastroenteritis 18 Pond Total coliforms dete

Lee et al., 2002 

Minnesota 1999 C. parvum Gastroenteritis 10 Pool Unknown 

Lee et al., 2002 

Nebraska 1999 E. coli O157:H7 Gastroenteritis 7 Wading pool Unknown 

Lee et al., 2002 

New York 1999 Norwalk-like virus Gastroenteritis 168 Lake Unknown 

13 See McCarthy et al. (2001) for additional information 
U.S. Environmental Protection Agency

February 2009 56 

Reference Location Year of Outbreak Etiologic Agent Predominant Illness/Symptoms Number of Cases Water Source Water Quality In

Lee et al., 2002 

Oregon 1999 Schistosomes 

(suspected etiology based on clinical syndrome and setting) 

Skin 2 Lake Unknown 

Lee et al., 2002 

Vermont 1999 P. aeruginosa

(suspected etiology based on clinical syndrome) 

Skin 9 Hot tub Unknown 

Lee et al., 200214 Washington 1999 E. coli O157:H7 Gastroenteritis 36 Lake E. coli O157:H7 deLee et al., 2002 

Wisconsin 1999 C. parvum Gastroenteritis 10 Pool Unknown 

Lee et al., 2002 

Wisconsin 1999 E. coli O157:H7 Gastroenteritis 5 Lake/pond Total and fecal coli

detected by did not regulatory levels; otested for E. coli O1negative 

Samadpour et al., 200215 Washington 1999 E. coli O157:H7 Gastroenteritis 36 Lake E. coli O157:H7 de

human and duck fe

McCarthy et al., 200116

Connecticut 1999 E. coli O121 Gastroenteritis; 

hemolytic uremic syndrome 

11 Lake E. coli not detected 

water; E. coli detecfrom storm drain; Sproducing strain no(results differ slightthose reported in L2002) 

* Outbreaks that may have been related to animal contamination are shaded gray.

14 See Bruce et al. (2003) and Samadpour et al. (2002) for additional information 15 Also referenced in Lee et al. (2002) 16 Also referenced in Lee et al. (2002) 
U.S. Environmental Protection Agency

February 2009 57 

table (see Appendix A). Outbreaks caused by Legionella spp. were not included in the table 

because they are not relevant to the analysis. Table IV.5.1 is sorted by outbreak year 

(descending order) followed by author and year, and then location (alphabetically). Outbreaks 

that may have been related to animal contamination are shaded gray. 

IV.6 Summary of Selected Recreational Water Outbreaks Reported in the United States 

and Internationally 

To augment the results reported by the CDC, a comprehensive literature search was conducted 

(see Appendix A for further detail). Studies for which the Abstracts from the literature identified 

were reviewed, and studies were included if the abstract showed evidence that the etiologic agent 

was detected in the source water were included in Table IV.6.1. As mentioned previously, this is 

a higher bar than what the CDC uses to evaluate outbreak evidence, but the large number of 

international articles with questionable outbreak investigation methods required a more stringent 

standard for inclusion. The articles are cross-referenced to the CDC table accordingly. The table 

is sorted by outbreak year (descending order) followed by study author (alphabetically) and 

location (alphabetically). Outbreaks that may have been related to animal contamination are 

shaded gray. 

IV.7 Descriptions of Recreational Water Outbreaks with Animal Related-Pathogen 

Sources 

Information from the two outbreak summary tables (Tables IV.5.1 and IV.6.1) indicates that the 

pathogen source in the majority of recreational water-related outbreaks remains unknown. All of 

the outbreak studies that cited an animal source were based in natural water sources that include 

lakes, streams, a swimming area with water fed by a brook, and a canal. The etiologic agents 

were E. coli spp. (n=5), Schistosomes spp. (n=2), and Leptospira spp. (n=1). E. coli was 

associated with cattle, deer, or duck feces; Schistosomes spp. was associated with snails; and 

Leptospira spp. was associated with rat urine. Five studies identified animal sources as part of 

their environmental investigation. Three additional studies cited animal-related pathogens as a 

potential source; however, environmental sampling was not conducted to support this claim. 

Summaries of these studies are provided below. 

IV.7.1 Environmental Sampling Including Animal Sources 

Cornwell, Southwest England (cattle feces) 

In 2004, seven children were infected with E. coli O157:H7 after playing in a stream located in 

Cornwell, southwest England (Ihekweazu et al., 2006). Environmental samples from the stream 

and cattle grazing on the surrounding fields above the stream were analyzed; both the water and 

cattle feces were found to be positive for E. coli O157:H7. Stool samples from all seven cases 

were confirmed E. coli phage type 21/28, though none of the environmental isolates were phage 

type 21/28, including the cattle feces. Regardless, cattle feces, according to the study authors, 

remains the most likes source of stream contamination. Heavy rainfall occurring two days prior 

to the outbreak increased the likelihood that cattle feces were the potential source of 

contamination since the fecal matter could have been washed into the stream. Another potential 

source of contamination was sewage from overflow drains located around the stream. 
U.S. Environmental Protection Agency

February 2009 58 Table IV.6.1. Select Waterborne Disease Outbreaks Associated with Recreational Water 

Reference Location Year of Outbreak Etiologic Agent Predominant Illness Number of Cases Water Source Water Quality Inform

CCDR, 2005 British 

Columbia, Canada 

2004 E. coli 

O157:H7 

Gastroenteritis 10 

(8 (confirmed; 

2 probable) 

Pool Elevated fecal indicators dete

(sample 1: 2,200 fecal colifor1500 E. coli/100 mL; sample fecal coliforms/100 mL, 14,40/100 mL); E. coli O157:H7 no

Ihekweazu et al., 2006 

Cornwall, U.K. 

2004 E. coli O157 Confirmed E. 

coli O157 phage type 21/28 

7 Stream E. coli O157 detected in strea

cattle feces in the catchment stream; none of the environmisolates were phage type 21/

Verma et al., 2007 

Trafford, U.K. 2004 E. coli O157 Gastroenteritis 

and hemolytic uremic syndrome (HUS) 

8 GI and 2 

HUS 

Pool E. coli O157 not detected; blo

chlorine system noted 

Jones et al., 2006 

Southwest England, U.K. 

2003 Cryptosporid

ium

Gastroenteritis 63 Pool Coliform detected (2,100 coli

coli per cu mm) 

Louie et al., 2004 

Surrey, Canada 

2003 C. parvum Cryptosporidiosis 33 Pool C. parvum detected 

Enk et al., 2003 

Minas Gerais, Brazil 

2002 Schistosoma 

mansoni 

Acute schistosomiasis 

17 Pool 

(water provided by nearby brook) 

Schistosoma mansoni detectsnails 

Hoebe et al., 2004 

The Netherlands 

2002 Norovirus Gastroenteritis 90 Pool Coliform bacteria detected (>

organisms/mL); enterococci d(3,500 organisms/100 mL); Edetected (7,700 organisms/10norovirus detected 

Tate et al., 2003 

U.K. 2002 P. 

aeruginosa 

Folliculitis 35 Pool P. aeruginosa not detected in 

detected on inflatable toy 

Bruneau et al., 2004 

MontrealCentre, Canada 

2001 E. coli 

O157:H7 

Gastroenteritis 4 Beach 6-162 fecal coliforms/100mL 

Three strains of E. coli O157
U.S. Environmental Protection Agency

February 2009 59 

Reference Location Year of Outbreak Etiologic Agent Predominant Illness Number of Cases Water Source Water Quality Inform

Hauri et al., 2005 

Kassel, Germany 

2001 Echovirus 30 Aseptic 

meningitis 

215 Pond An echovirus 30 sequence ob

one pond water sample shownucleotide and 100% amino-ahomology with patient isolatetesting for total coliforms, fecenterococci, Staphylococcus never exceed European Unioguidelines 

Maunula et al., 2004 

Helsinki, Finland 

2001 Norovirus; 

astrovirus 

Gastroenteritis 242 Pool Fecal contamination not dete

weeks prior to outbreak; E. cin outlet well 2 weeks after ounorovirus and astrovirus deteNorovirus detected in outlet was 8 months after incident 

Perra et al., 2002 

Rochefort, France 

2001 Leptospira 

spp. 

Leptospirosis 5 

(3 confirmed 

and 2 

possible) 

Canal E. coli detected (between 100 

2,000/100 mL); 130 rats trappprevalence of seropositive ro30.8% 

Feldman et al., 2002 

California, U.S. 

1999 E. coli 

O157:NM 

Gastroenteritis 7 

(3 confirmed 

and 4 

possible) 

Lake Total and fecal coliform coun

weeks prior to outbreak 

Lévesque et al., 2002 

Quebec City, Canada 

1999 Schistosome

s 

Cercarial dermatitis 

53 Lake Fecal coliforms and fecal stre

detected but at very low leveaeruginosa not detected; Staaureus detected by at levels good quality surface water in Ocellate cercaria and non-ocisolated detected in snails 

Fields et al., 2001 

Wisconsin, U.S. 

1998 L. micdadei Pontiac Fever 45 Spa/pool Heterotrophic bacteria detect

micdadei detected 

Fiorillo et al., 2001 

Alberta, Canada 

1998 P. 

aeruginosa 

Pseudomonas hot-foot syndrome 

40 Pool P. aeruginosa detected in inle

and a drain to the pool 

Lim et al., 2004 

Minnesota, U.S. 

1998 Cryptosporid

ium 

Gastroenteritis 26 Pool Cryptosporidium not detected 
U.S. Environmental Protection Agency

February 2009 60 

Reference Location Year of Outbreak Etiologic Agent Predominant Illness Number of Cases Water Source Water Quality Inform

Morgan et al. 2002 

Illinois, U.S. 1998 Leptospira 

spp. 

Leptospirosis 98 Lake One of the 27 lake water sam

detected a pathogenic Leptoshowever, no organism was issamples were culture positiveboth isolated organisms were Leptospira spp. 

Cransberg et al., 1996 

The Netherlands 

1993 E. coli

O157:H7 

Hemolytic uremic syndrome 

4 Lake O157:H7-DNA not detected, 

occurred ~2 weeks after date 

Joce et al., 1991 

Doncaster, U.K. 

1988 Cryptosporid

ium 

Gastroenteritis 79 Pool Cryptosporidium oocysts dete

learner pool; Cryptosporidium detected in main pool; rotavirin learner pool 

Porter et al., 1988 

New Jersey, U.S. 

1985 Giardia Gastroenteritis 9 Pool Coliform not detected; standa

plate counts of 1-2 per mL de

Sorvillo et al., 1988 

California, U.S. 

1985 Shigella 

sonnei 

Gastroenteritis 68 Humanmade lake High fecal coliform detected 

Khabbaz et al., 1983 

Georgia, U.S. 1981 P. 

aeruginosa 

Skin 75 Pool(s) P. aeruginosa serotype 0:9 d

Reid and Porter, 1981 

U.K. 1980 P. 

aeruginosa 

Otitis externa 18 Pool P. aeruginosa detected in sw

various places around pool abag used to clean pool 

Baron et al., 1982 

Michigan, U.S. 

1979 Norwalk 

agent 

AGI 121 Lake Fecal coliform detected but w

acceptable range (<200 colonmL of water) 

Kappus et al., 1982 

Ohio, U.S. 1977 Norwalk 

agent 

AGI 103 Pool Moderate numbers of fecal co

detected; total coliform (1/100 coliform (1/100 mL), and fecastreptococci (4/100 mL to 9/1detected in samples sent to Echlorinator was not functioninoutbreak 

Rosenberg et al., 1976 

Iowa, U.S. 1974 S. sonnei Gastroenteritis 31 River Fecal coliform detected (mea

organisms per 100 mL); Shig

detected 
U.S. Environmental Protection Agency

February 2009 61 

Minas Gerais, Brazil (snails) 

Seventeen cases of acute schistosomiasis occurred in Minas Gerais, Brazil in 2002 (Enk et al., 

2003). Affected individuals bathed in a swimming pool at a holiday resort. Water in the pool 

was provided from a nearby stream. Environmental sampling from the stream included a survey 

of site snails (mollusks), which tested positive for Schistosoma mansoni. 

Quebec City, Canada (snails) 

In August 1999, 53 cases of cercarial dermatitis were associated with a recreational tourist lake 

in Quebec City, Quebec Canada (Lévesque et al., 2002). Water samples showed low 

concentrations of fecal pollution. Pseudomonas aeruginosa was not detected, though 

Staphylococcus aureus was detected at levels corresponding to good quality surface water in 

Canada. Snails were analyzed for schistosomes, and two forms of furcocercaria type cercariae 

were identified. The snails were located in only in one location, which is where 42 of the 53 

cases occurred. 

Rochefort, France (rodent urine) 

Five cases of leptospirosis were diagnosed in Rochefort, France in 2001 among teenagers who 

had swum in the Genouillé canal (Perra et al., 2002). Water samples revealed moderate quality 

according to France’s swimming water criteria (E. coli between 100 to 2,000/100 mL). An 

environmental survey also included trapping rodents and conducting a serological status analysis. 

Results of this analysis showed that the prevalence of seropositive rodents was 30.8 percent, 23.1 

percent, 4.6 percent, and 3.8 percent for total antigens, L. icterohaemorrhagiae, L. saxkoebing, 

and L. australis, respectively. Consequently, rodent urine was believed to be the primary source 

of contamination. 

Washington, U.S. (duck feces) 

In 1999, an outbreak of E. coli O157:H7 occurred at a state lake in Vancouver, Washington 

(Samadpour et al., 2002). The number of cases was not reported; however, the CDC summary of 

recreational water outbreaks in 1999 and 2000 reported an E. coli O157:H7 outbreak that also 

occurred at a state lake in Vancouver and had 396 cases. Environmental sampling occurred a 

month after the outbreak and consisted of 108 samples, including water, soil, sand, sediment, and 

animal fecal matter (cow, coyote, deer, duck, and rabbit). E. coli O157:H7 was recovered from 

both the water and the duck fecal samples. Water samples tested positive for Stx, eaeA, and hly

genes by a PCR technique; duck fecal samples tested positive for Stx and eaeA genes. These 

virulence factors (Stx, eaeA, and hly genes) were also found in patient stool samples. 

Additionally, the study used a pulsed-field gel electrophoresis to compare duck feces and water; 

all isolates resulted in the same restriction fragment patterns. According to the authors, 

regardless of the evidence, duck feces could still not be confirmed as the primary fecal 

contamination source. Ducks and the lake could have been transiently infected by the 

contaminated water, so the initial source of contamination could be human feces or anther animal 

feces. Also, the delay between the outbreak and the sampling may support the notion that duck 

feces were not the original source. 
U.S. Environmental Protection Agency

February 2009 62 

IV.7.2 Environmental Sampling not Including Animal Sources 

California, U.S. (cattle or deer feces) 

An outbreak of seven cases of E. coli O157:nonmotile (NM) occurred at a lake in California 

during August 1999 (Feldman et al., 2002). Potential sources of contamination were fecal matter 

from cattle or deer based on the presence of a herd of cattle on the opposite bank of the river and 

the observation by a park manager of numerous deer in the area. Fecal matter from these 

animals, however, was not analyzed for E. coli O157:NM. 

Minnesota, U.S. (geese feces) 

According to the CDC summary of recreational water outbreaks in 2002 and 2001, there was an 

outbreak of E. coli O157:H7 at a lake beach in which 20 cases were identified (Yoder et al., 

2004). A brief case description indicated that an environmental investigation revealed a high 

level of fecal coliforms. According to local officials, the large number of geese that occupied the 

beach during the summer may have contributed to the elevated overall fecal coliform (and thus 

potentially E. coli O157:H7) levels. 

The Netherlands (cattle feces) 

In 1993, four cases of hemolytic uremic syndrome in children were reported in the Netherlands 

(Cransberg et al., 1996). All four affected individuals bathed in a shallow recreational lake 

within a 5-day period. E. coli O157:H7 was isolated in the stool of two of the patients. Water 

samples were taken 16 days after the latest date of patient contamination; however, no O157:H7 

DNA was detected in filter-concentrated lake water after using PCR enhancement. According to 

the study authors, the contamination source could have been human- or cattle-based. Cattle feces 

were identified as a plausible source because the water in the lake is derived from ditches, which 

drain their water from meadows with cattle. Cattle feces, however, were not analyzed for 

O157:H7. 
U.S. Environmental Protection Agency

February 2009 63 

V. COMPILATION OF DATA AND SUMMARY

Numerous epidemiological investigations have been conducted since the 1950s to evaluate the 

association between the density of suitable fecal indicators and the risk of illness to recreational 

water users. Reviews of these studies are provided in Prüss (1998); Sinton et al. (1998); Wade et 

al. (2003); and Zmirou et al. (2003). Taken as a whole, the weight of evidence from these 

studies indicates that fecal indicator bacteria (fecal streptococcus/Enterococcus, in particular) are 

able predict GI and respiratory illnesses from exposure to recreational waters (Prüss, 1998; Wade 

et al., 2003; Zmirou et al., 2003). This broad base of information stems from studies conducted 

in the following countries (NZME, 2003): 

• Australia (Corbett et al., 1993; Harrington et al. 1993) 

• Canada (EHD, 1980; Lightfoot, 1989; Seyfried et al., 1985a,b) 

• Egypt (Cabelli, 1983b; El-Sharkawi and Hassan, 1979) 

• France (Ferley et al., 1989; Foulon et al., 1983) 

• Hong Kong (Cheung et al., 1990; Kueh et al., 1995) 

• Israel (Fattal et al., 1986, 1987, 1991) 

• Netherlands (Medema et al., 1995, 1997) 

• New Zealand (McBride et al., 1998) 

• South Africa (von Schirnding et al., 1992, 1993) 

• Spain (Mariño et al., 1995; Mujeriego et al., 1982) 

• United Kingdom (Alexander et al., 1992; Balarajan et al,. 1991; Fewtrell et al., 1992, 

1994; Fleisher et al. 1996; Kay et al., 1994) 

• United States (Cabelli et al., 1983a; Dufour, 1984; Stevenson, 1953) 

However, as indicated above, most of these studies investigated waters that were impacted or 

influenced by wastewater effluent, and close inspection reveals that few studies addressed 

sources of contamination other than wastewater effluent in the investigated waters.In fact, prior 

to 1999, the only peer-reviewed publications that substantially addressed this topic were Cheung 

et al. (1990), Calderon et al. (1991), and McBride et al. (1998). In recent years, researchers have 

conducted several additional epidemiological studies focusing on waters not predominately 

impacted by wastewater effluent, including Haile et al. (1999); Dwight et al. (2004); 

Wiedenmann et al. (2006); and Colford et al. (2007). Additionally, the SCCWRP is also 

conducting a series of epidemiological studies that investigate recreational water with various 

contamination sources other than wastewater effluent. Section III.2 provided a brief overview of 

each of these studies. 

Review of the epidemiological studies that address recreational water predominantly impacted 

by fecal contamination sources other than wastewater effluent indicates that the results are 

equivocal. On one hand, Colford et al. (2007) found that the incidence of swimmer illness was 

not associated with any of the traditional fecal indicators at a marine beach with primarily avian 

contamination. Similarly, Calderon et al. (1991) found no statistically significant association 

between swimmers’ illness risk and animal fecal contamination in a freshwater pond. On the 

other hand, McBride (1993) suggested that if more swimmers had been included in the Calderon 
U.S. Environmental Protection Agency

February 2009 64 

et al. (1991) study, achieving statistically significant results would have been possible. 

Furthermore, the marine bathing study in New Zealand (McBride et al. 1998) indicated that 

illness risks posed by animal versus human fecal material were not substantially different; 

however, the study’s limited range of beach contamination precluded the development of a 

detailed statistical model of health risks versus indicator density. 

In the first study to be conducted in waters directly impacted by urban runoff, Haile et al. (1999) 

reported rates of illnesses in Southern California similar to those conducted in waters 

contaminated with domestic sewage. However, this nonpoint runoff source was known to have 

human sources of fecal contamination (Colford et al., 2007). Similarly, Dwight and colleagues 

(2004) found that surfers exposed to Southern California urban runoff had higher illness rates 

than surfers exposed to Northern California rural runoff. The results from the Hong Kong 

marine water study (Cheung et al., 1990) and the German freshwater study (Wiedenmann et al., 

2006) are more difficult to interpret regarding risks from human versus nonhuman sources 

because in both studies, the analyses combined the results from sites with different predominant 

contamination sources. 

In reviewing outbreak information for drinking water and recreational waters, several 

overarching points emerge. One is that the pathogen source in the majority of drinking waterrelated outbreaks remains unknown. The source of pathogens in drinking water outbreaks in 

many cases could have been humans or animals; however, most reports offered little detail, 

leaving a critical information gap for the purposes of this review. Keeping in mind the 

previously noted limitations of outbreak investigations, it is noteworthy that several outbreak 

investigation studies were able to link pathogens isolated from patients with water samples, 

animals, or both using laboratory analysis (e.g., CCDR 2000; Howe et al., 2002; Licence et al., 

2001). Other reports used circumstantial evidence to link animal waste to outbreaks, but 

although compelling, laboratory results were not available to confirm the contamination source. 

The animal sources linked to outbreaks included beavers, cats/cougars, deer, elk, pigs, cattle, and 

chickens/poultry, and the corresponding animal-related pathogens in these outbreaks were 

Giardia intestinalis, Cryptosporidium spp., E. coli O157:H7, Campylobacter spp., Toxoplasma 

gondii, and S. typhimurium. In general, 14 percent of the drinking water outbreaks reported by 

the CDC from 1999 to 2004 were possibly animal-related (Blackburn et al., 2004; Lee et al., 

2002; Liang et al., 2006). In addition, about 15 percent of Canadian outbreaks between 1974 and 

2001 were linked to animal sources (Schuster et al., 2005) and about half of the outbreaks linked 

to private water supplies in England and Wales listed animals as possible factors (Said et al., 

2003). 

Given that outbreaks are known to be a notoriously poor measure of the actual number of 

infections and illnesses caused by waterborne pathogens (Craun, 2004), those investigations that 

link pathogens isolated from patients, water samples, or both with animals provide unequivocal 

evidence that human illnesses can and do occur from animal-based contamination. 

Unfortunately, the drinking water outbreak literature does not substantially enhance the current 

ability to differentiate risks from animal- versus human-related pathogen sources for recreational 

water exposures in a quantitative manner. 
U.S. Environmental Protection Agency

February 2009 65 

The recreational water outbreak literature (Craun et al., 2005) indicates that of the 259 

recreational water outbreaks that occurred in the United States between 1970 and 2000, only 

approximately half included any information about possible sources of the contamination or 

contributing factors to it. Over two-thirds of the outbreaks that did list possible sources were 

associated with either bacteria or protozoa; over 15 percent had unidentified etiologies; and 7 

percent were viral. In untreated recreational water outbreaks (streams, lakes, etc.), feces or ill 

bathers in the water, bather overcrowding, and the presence of children in diapers accounted for 

the vast majority of the assumed sources; however, the report by Craun et al. (2005) did not 

indicate that laboratory analyses, other than microbial indicator measures, supported these 

attributions. Their analysis estimated that 18 percent of these outbreaks were associated with 

animals and that the likely etiologic agents included E. coli spp., Schistosomes spp., and 

Leptospira spp. E. coli was associated with cattle, deer, or duck feces; Schistosomes spp. were 

associated with snails; and Leptospira spp. were associated with rat urine. Similar to the 

drinking water outbreak compilation, the recreational water outbreak literature does not appear to 

enhance substantially the current state of knowledge on quantitatively characterizing risks from 

animal-related pathogen sources compared with human sources for recreational water exposures. 

Given that relatively few investigations worldwide have evaluated the risk to human health from 

recreational exposure to waters primarily impacted by sources of contamination other than 

wastewater effluent, and that the potential range of those sources is broad, the findings from this 

literature review are not surprising. In fact, the results of this literature review seem consistent 

with WHO’s (2004) report on zoonoses, which indicated the following: 

• Inadequate information exists on differentiating human versus animal strains of human 

pathogens, both in the field (e.g., pathogen typing and microbial source tracking) and 

analytically (e.g., relative infectivity and pathogenicity). Both of these areas are priorities 

for targeted research. 

• Currently available surveillance data on both sporadic (endemic) and outbreak diseases 

are of limited use in understanding the importance of zoonotic waterborne infection. 

Surveillance for waterborne disease in general and waterborne zoonoses in particular has 

failed to provide a meaningful indication of the associated burden of disease, even in 

countries with established surveillance systems. 

• The risk of exposure to animal-contaminated water is unknown. Studies to define the 

risk associated with swimming in animal-contaminated water have not clearly indicated 

that this type of exposure results in an excess illness rate. These results of these studies 

do not support the premise that all fecally contaminated waters should be treated the 

same. New research to define the risk of illness posed by animal fecal wastes is needed 

(Till et al., 2004). 

Furthermore, because pathogens can evolve rapidly depending on their previous host 

environments due to changing host factors and other mechanisms of phenotypic change, it is 

reasonable to suspect that zoonotic pathogens propagated in animals would be different from 

pathogens from human sources. However, data remain incomplete on how zoonotic pathogens 

are attenuated or increase infectivity or virulence when passaged through animal hosts. 
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February 2009 66 

Although conclusive information on differentiating human versus animal sources of pathogens is 

lacking, several research organizations and countries have suggested novel approaches for 

addressing risks from nonhuman sources (e.g., NZME, 2003; WSSA, 2003). For example, New 

Zealand, where about 80 percent of total notified illnesses are zoonotic and potentially 

waterborne, has recently updated its recreational water quality criteria to address the issue of 

animal-source waterborne contamination by basing its freshwater guidelines principally on the 

risks associated with campylobacteriosis using E. coli concentrations as an indicator (Till and 

McBride, 2004). 

In 1992, the New Zealand Department of Health issued provisional microbiological water quality 

guidelines for recreational waters, which advised that exposure to animal fecal microorganisms 

was much less of a risk than exposure to pathogens of human origin. In 1998, Sinton et al. 

concluded that there was no reliable epidemiological information on the relative risks to humans 

associated with human and animal fecal pollution in water, but that the high ratio of grazing 

animals to humans in the country made animal fecal sources a greater health risk to humans than 

previously assumed. Because Campylobacter-related illness is of great public health concern in 

New Zealand, research has been especially focused on the dairy industry and its impact on 

microbial water quality (Till and McBride, 2004). Thus, although New Zealand’s current marine 

water guidelines (NZME, 2003) derive directly from WHO’s 2003 recommendations, the 

country bases its freshwater guidelines principally on the risks associated with 

campylobacteriosis (using E. coli concentrations as an indicator). Notably, Till and McBride 

(2004) stated that current investigations in New Zealand have focused on determining the source 

of human Campylobacter infections in part because that information “...may help to shed light 

on the relative health risk of animal versus human wastes.” 

Based on the results of this detailed literature review, it appears that: (1) insufficient information 

is available to support a robust and quantitative characterization of the relative risks of human 

illness from the range of various sources of fecal contamination in recreational waters, and (2) 

epidemiological studies are more likely to provide salient insights than outbreak investigations. 

Continued epidemiological work in this arena is consistent with ongoing international efforts to 

understand and manage human health risks associated with exposure to waterborne zoonoses 

(Till and McBride, 2004). 

Tools that complement epidemiology may help address the characterization of the relative risks 

of human illness from various sources of fecal contamination in recreational waters; for example, 

quantitative microbial risk assessment (QMRA) is one alternative that could supplement 

traditional epidemiological investigations to identify potential excess human health risks for 

defined pathways of particular pathogens (Carr and Bartram, 2004). Because QMRA has the 

potential to provide much greater sensitivity in quantifying risk than epidemiological studies 

(Carr and Bartram, 2004), the potential synergy from using both methods could be helpful to 

manage risks of water-related infectious diseases (see Bartram et al., 2001). To date, data gaps 

have limited the degree to which QMRA has been used to inform public policy decisions and 

manage recreational waters. The greatest data deficiencies appear to be a lack of dose-response 

and environmental occurrence data for many waterborne zoonotic pathogens (Carr and Bartram, 

2004; Till and McBride, 2004). 
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February 2009 67 

In addition, more robust environmental testing in recreational and drinking water outbreak 

investigations using rapidly evolving molecular methods is another complementary tool that 

could supplement traditional epidemiological investigations in characterizing the relative risks of 

human illness from the range of various sources of fecal contamination in recreational waters. A 

notable drawback to this approach is that state and local health departments, who are responsible 

for investigating outbreaks, are unlikely to have the technical or financial resources to pursue this 

sort of testing, so extramural funding would likely be needed. 

Finally, even if or when sufficient information becomes available to support robust and 

quantitative characterization of the relative risks of human illness from the range of fecal 

contamination sources in recreational waters, a number of issues will likely remain regarding the 

use of indicator organisms to predict human illnesses from exposure to these waters. The 

essential intent of fecal indicators is that they represent the overall “pathogenicity” of the water 

(NZME, 2003). Within this context, it is not surprising that indicator organisms correlate well to 

some pathogens in some waters but correlate poorly in other cases (e.g., Ashbolt et al., 1993; 

Elliott and Colwell, 1985; Ferguson et al., 1996; Grabow et al., 1989; Jiang et al., 2001). If new 

or revised water quality criteria are to address quantitatively the various sources of fecal 

contamination of potential interest in recreational waters covering diverse geographic regions, 

the approach will likely require a set or toolbox of indicators (as measured by specific methods). 

Recent research documenting the extreme variability in densities of traditional indicators over 

very short time periods (Boehm, 2007) underscores the need for a variety of indicator/method 

combinations that address a range of contamination sources and geographic areas. 

In summary, both human and animal feces in recreational waters continue to pose threats to 

human health. Although the public health importance of waterborne zoonotic pathogens is being 

increasingly recognized, it is still not well characterized. Policy makers and researchers have 

often assumed that the human health risk from pathogens associated with domestic and 

agricultural animal and wildlife feces is less than the risk from human feces, in large part 

because viruses are predominately host-specific. This literature review illustrates a lack of 

detailed and unequivocal information concerning the relative risks of human illness from various 

sources of fecal contamination in recreational waters. In addition, the ability to measure how the 

infectivity and virulence of known waterborne zoonotic pathogens are affected when passaged 

through animal hosts remains in its infancy. Thus, the findings of this literature review support 

the perspectives set forth by WHO (2004) and indicate that addressing fecal contamination 

sources in recreational water quality criteria will require additional research to better define the 

risk posed by animal fecal matter. 
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February 2009 68 

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waters in relation to the concentration of Escherichia coli, intestinal Enterococci, Clostridium 

perfringens, and somatic coliphages. Environmental Health Perspectives 114(2): 228-236. 

Yoder, J.S., Blackburn, B.G., Craun, G.F., Hill, V., Levy, D.A., Chen, N., Lee, S.H., Calderon, 

R.L., Beach, M.J. 2004. Surveillance for waterborne-disease outbreaks associated with 

recreational water–United States, 2001-2002. Mortality and Morbidity Weekly Report CDC 

Surveillance Summaries 53(8): 1-22. 

Zmirou, D., Pena, L., Ledrans, M., Letertre, A. 2003. Risks associated with the microbiological 

quality of bodies of fresh and marine water used for recreational purposes: summary estimates 

based on published epidemiological studies. Archives of Environmental Health 58(11): 703-711 
U.S. Environmental Protection Agency

February 2009 A-1 

APPENDIX A 

LITERATURE SEARCH STRATEGY AND RESULTS

The literature search strategy consisted of a number of combined approaches. Search terms and 

a synopsis of information needed were given to a professional librarian to search the online 

DIALOG databases. To supplement the DIALOG searches, individual authors used free search 

engines on the internet to find articles pertaining to specific information needed. Experts that 

participated in EPA’s Experts Scientific Workshop on Critical Research Needs for the 

Development of New or Revised Recreational Water Quality Criteria1

 were contacted by email 

and requested to contribute literature they felt was important. The titles of literature cited in 

specific reports, books, review articles, and conference proceedings were evaluated for 

relevance. 

A.1 Initial Literature Search Strategy Conducted by Professional Librarian 

Selection of DIALOG data base files used for this search: 

 File 155:MEDLINE(R) 1950-2007/Nov 12 

 (c) format only 2007 Dialog 

 File 266:FEDRIP 2007/Sep 

 Comp & dist by NTIS, Intl Copyright All Rights Res 

 File 245:WATERNET(TM) 1971-2007Jul 

 (c) 2007 American Water Works Association 

 File 144:Pascal 1973-2007/Oct W4 

 (c) 2007 INIST/CNRS 

 File 117:Water Resources Abstracts 1966-2007/Aug 

 (c) 2007 CSA. 

 File 40:Enviroline(R) 1975-2007/Sep 

 (c) 2007 Congressional Information Service 

 File 110:WasteInfo 1974-2002/Jul 

 (c) 2002 AEA Techn Env. 

 File 143:Biol. & Agric. Index 1983-2007/Oct 

 (c) 2007 The HW Wilson Co 

 File 6:NTIS 1964-2007/Nov W3 

 (c) 2007 NTIS, Intl Cpyrght All Rights Res 

 File 5:Biosis Previews(R) 1926-2007/Nov W2 

 (c) 2007 The Thomson Corporation 

 File 73:EMBASE 1974-2007/Nov 12 

 (c) 2007 Elsevier B.V. 

Search strategies used for this search: 

#1: Waterborne terms NEAR fecal terms 

S1 3210 WATERBORNE()(DISEASE? ? OR OUTBREAK? ? OR ZOONOT? OR ZOONOS? 

 OR EPIDEMIC? ? OR EPIDEMIOLOG?) 

S2 43 WATERBORNE()(HEPATITIS OR ROTAVIRUS? OR NOROVIRUS?) 

S3 232098 FECAL OR FECES FAECAL OR (LIVESTOCK OR BOVINE OR CATTLE)(S) 

 1

 Report from this workshop: http://www.epa.gov/waterscience/criteria/recreation/. 
U.S. Environmental Protection Agency

February 2009 A-2 

 CONTAMINATION 

S4 1637 PATHOGEN()FECAL()SHEDDING OR PATHOGENS (S) SEWAGE OR RAW() 

 SEWAGE()CONTAMINATION 

S8 207 S1 (S) S3 

S9 250 S2 OR S8 

S10 140 RD S9 (unique items--deduped; no year/language limits) 

#2: Pathogen terms NEAR Sewage terms AND (Waterborne or Recreational Water Terms)

S4 1637 PATHOGEN()(FECAL OR FAECAL)()SHEDDING OR PATHOGENS (S) SEWAGE 

 OR RAW()SEWAGE()CONTAMINATION 

S29 1282 S4 NOT (S9 OR S13 OR S16 OR S21) 

S30 717 RD S29 (unique items) 

S31 110 S30 AND (S11 OR S12 OR S1) (WATERBORNE/RECREATIONAL WATER 

 SETS) 

#3: (Remaining Pathogen terms OR Indicator Terms) AND Selected Authors

S34 592 S30 NOT (S31 OR S33) [REMAINING PATHOGEN RESULTS] 

S35 2164 S7 NOT (S9 OR S13 OR S16 OR S33 OR S21 OR S31) [INDICATORS] 

S36 1078 RD S35 (unique items) 

S37 2011 AU=(ASHBOLT ? OR PAYMENT ? OR PRUSS ?) 

S38 33410 S37 OR AU=(BYAPPANAHALLI? OR COLFORD ? OR DUFOUR ? OR 

 MCBRIDE ? OR GANNON ? OR CICMANEC? OR COTRUVO?) 

S39 38 (S34 OR S36) AND (S37 OR S38) [AUTHORS ON THOSE 2 TOPICS] 

#4: (Remaining Pathogen terms OR Indicator Terms) AND Waterborne or Recreational 

Water Terms)

S5 462847 CLOSTRIDIUM OR BACTEROIDES OR TOTAL()(FECAL OR FAECAL)() 

 COLIFORM OR E()COLI OR ECOLI OR ENTEROCOCC? OR FECAL() 

 STREPTOCOCC? OR COLIPHAGE 

S6 540854 INDICATOR? ? 

S7 2551 S5 (5N) S6 

S42 1611 (S34 OR S36) NOT S39 

S43 243 S42 AND (S1 OR S11 OR S12) [combined w/waterborne/ 

 recreational terms] 

Dates: 1985-present [2002-present is more crucial] 

Language: no restrictions 

Descriptions of these files are available at http://library.dialog.com/bluesheets/. 
U.S. Environmental Protection Agency

February 2009 A-3 

Retrieve: titles and year 

Format: MS Word 

Additional information: Interested in international and domestic journals and government 

reports. 

Search terms: 

Fecal waterborne disease* (i.e., * allows for multiple endings) 

Waterborne zoono* (for zoonotic, zoonosis, zoonoses) 

Waterborne outbreak* 

Waterborne disease epidemiology 

Livestock contamination of water 

Fecal load 

Pathogen fecal shedding 

Pathogens AND sewage 

Microbial quality of effluent 

Waterborne Hepatitis 

Waterborne rotavirus* 

Waterborne Norovirus* 

Raw sewage contamination 

Clostridium AND indicator* 

Bacteroides AND indicator* 

total fecal coliform, AND indicator* 

E. coli and Indicator* 

Enterococcus AND indicator* 

fecal streptococcus AND indicator* 

coliphage AND indicator* 

Key authors: 

Ashbolt N 

Payment P 

Prüss A 

Byappanahalli M 

Colford J 

Dufour A 

McBride GB 

Gannon VPJ 

Cicmanec JL 

Cotruvo JA 

Specific literature: 

WHO. (2004) Waterborne Zoonoses. http://www.who.int/water_sanitation_health/

diseases/zoonoses.pdf

All MMWR supplements on waterborne illness (1983 to present) 

Airlie report (USEPA, 2007) references 
U.S. Environmental Protection Agency

February 2009 A-4 

Objectives of this literature search: 

• All epidemiological studies of waterborne illness due to ambient recreational exposures 

(any location) 

• Morbidity and Mortality Weekly Report surveillance summaries and papers that evaluate 

trends based on CDC data for waterborne illnesses due to recreational exposures (ambient 

and pools) 

• Papers on outbreaks due to ambient recreational exposures (not pools) 

• References to illness resulting from waterborne exposure to fecal materials from a variety 

of sources (emphasis on animal-derived waste, including point and nonpoint sources) 

• Prevalence of fecal indicators in humans and animals (livestock and wild animals): (total 

and fecal coliform, E. coli, Enterococcus, fecal streptococcus, Bacteroides, coliphage 

(somatic and F+), and Clostridium) variation of quantities in fecal material (temporal and 

within a population)

o References for a Fecal Shedding Table (average for a species): columns – 

indicator and pathogen shedding quantification, ratio of indicator to pathogens (if 

known or can be calculated without being misleading), primary literature 

citations; rows – species

• Variation and uncertainty in shedding data (how much and how frequently do 

infected animals shed pathogens in feces) 

• magnitude and duration of fecal excretion of specific pathogens during illness 

• Pathogen prevalence in herds or wild animals 

• number of infected per herd 

• geographic distribution of herds 

• seasonal, temporal, event driven (calving) variation 

• Pathogen prevalence in raw and treated sewage (mostly human source) – likely variation 

• human point and nonpoint source contaminant levels quantified in receiving waters 

A.2 Literature Search Strategy and Results Specific to Epidemiological Studies 

Conducted in Recreational Waters

The following terms were searched on the Web of Science: 

• Recreational water + epidemiology + fecal matter 

• Recreational water + epidemiology + nonpoint source 

• Recreational water + epidemiology + point source 

• Recreational water + epidemiology + animal fecal matter 

• Recreational water + epidemiology + animal waste 

• Recreational water + exposure to fecal matter 

• Recreational water + epidemiological studies + microbiological indicators of fecal matter 

• Recreational water + epidemiology + fecal matter + European Union 

• Recreational water + epidemiology + fecal matter + United Kingdom 

A summary of the results of this literature search is provided in Table A.2.1 
U.S. Environmental Protection Agency

February 2009 A-5 

Table A.2.1. Summary of Epidemiological Studies in Recreational Waters 

Search Topic # 

Citations 

Citations 

Reviewed 

(Web 

information

only) 

# 

Citations

of 

Interest 

Recreational water + epidemiology + fecal matter 50 Yes 1 

Recreational water + epidemiology + nonpoint source 30 Yes 3 

Recreational water + epidemiology + point source 30 Yes 3 

Recreational water + epidemiology + animal fecal matter 20 Yes 1 

Recreational water + epidemiology + animal waste 30 Yes 4 

Recreational water + exposure to fecal matter 30 Yes 1 

Recreational water + epidemiological studies + microbiological 

indicators of fecal matter 40 Yes 5 

Recreational water + epidemiology + fecal matter + European Union 40 Yes 2 

Recreational water + epidemiology + fecal matter + United Kingdom 40 Yes 4 

New + recreational waters + epidemiological studies + EU 60 Yes 10 

The results of this literature review were then combined into a library with the relevant citations 

from a reverse literature citation search on several of the key epidemiological studies (e.g., the 

Wade et al., 2003; Zimrou et al., 2003; Prüss 1998; and Sinton et al., 1998 review articles), and 

duplicates were discarded. Additionally, publications describing studies conducted in Europe 

were obtained for free from Dr. David Kay, one of the key investigators of epidemiological 

studies in Europe (http://www.aber.ac.uk/iges/staff/kaydavid.shtml). Furthermore, unpublished 

information on current and ongoing activities in the European Union was obtained through 

personal communications with Dr. Kay and a review of the relevant activity’s website. 

A.3 Literature Search Strategy and Results Specific to Outbreak Data

Drinking Water 

The purpose of the literature search was to capture published articles on waterborne disease 

outbreaks that identified an etiological pathogen and linked it to a drinking water source. Due to 

the broad nature of the topic, many more papers have been published in the peer-reviewed 

literature related to drinking water outbreaks, and this literature search by no means represents 

all of them. The searches were performed on December 5 to 6, 2007. 

A Google Scholar search of “waterborne AND outbreak” resulted in 9,940 hits, and a search of 

“drinking AND water AND outbreak” resulted in 42,900 hits, which were not reviewed. A 

search of Scirus scientific database of “waterborne AND outbreak” resulted in 13,694 hits which 

were not reviewed. 

The following terms were searched on the National Library of Medicine’s PubMed database: 

• water + outbreak 
U.S. Environmental Protection Agency

February 2009 A-6 

• waterborne + outbreak 

• drinking + water + outbreak 

• zoono* + water + outbreak (title only) 

A summary of the results of this literature search is provided in Table A.3.1. 

Table A.3.1. Summary of Outbreak Investigations in Drinking Water 

Search Topic # 

Citations 

Citations 

Reviewed 

# Citations 

of Interest 

Water AND outbreak 3,344 No 

Waterborne AND outbreak 448 Yes 118 

Drinking AND water AND outbreak 497 Yes 146 

Zoono* AND water AND outbreak 81 Yes 0 

The results of the two searches that produced citations of interest were combined, and duplicates 

and articles in languages other than English were discarded. The resulting list was narrowed to 

55 articles, which were chosen based on an indication in the abstract that the etiological pathogen 

in the outbreak was actually detected in the drinking water source. 

Recreational Water 

For the literature search regarding recreational water outbreaks, the following terms were 

searched on the U.S. National Library of Medicine’s PubMed system: 

• (beach OR lake OR stream OR pond OR swim OR recreation) AND water AND 

(outbreak OR epidemic) 

A summary of the results of this literature search is provided in Table A.3.2. 

Table A.3.2. Summary of Outbreak Investigations in Recreational Water 

Search Topic # 

Citations

Citations 

Reviewed 

# 

Citations

of 

Interest 

(Beach OR lake OR stream OR pond OR swim OR recreation) AND

water AND (outbreak OR epidemic) 52 Yes 40 

Abstracts from the literature identified were reviewed, and studies were included if the abstract 

showed evidence that the etiologic agent was detected in the source water. 

A.4 Summary of Literature Search Results

This process resulted in a total order of 365 citations of which a total of 273 (75 percent) were 

received during the expedited writing process, not all of which could be reviewed. There are 
U.S. Environmental Protection Agency

February 2009 A-7 

many more papers in the peer-reviewed literature and this by no means represents all of them. 

Of the articles reviewed, 182 citations were included in the white paper. 

A.5. Supplemental Literature Search Strategy 

In addition to the literature search conducted by the professional librarian several other resources 

were consulted. 

The flowing experts in the field were contacted directly by email and asked to suggest 

references: 

Nicholas Ashbolt, USEPA 

Thomas Atherholt, New Jersey Department of Environmental Protection 

Michael Beach, Centers for Disease Control and Prevention 

Bart Bibler, Florida Department of Health 

Alexandria Boehm, Stanford University, California 

Rebecca Calderon, USEPA 

Jennifer Clancy, Clancy Environmental Consultants 

Jack Colford, University of California, Berkeley 

Elizabeth Doyle, USEPA 

Alfred Dufour, USEPA 

Lee Dunbar, Connecticut Department of Environmental Protection 

Lora Fleming, University of Miami School of Medicine and Rosenstiel School of Marine and 

Atmospheric Sciences, Florida 

Charles Hagedorn, Virginia Tech 

Joel Hansel, USEPA 

Lawrence Honeybourne, Orange County Health Care Agency, Santa Ana, California 

Donna Francy, U.S. Geological Survey 

Roger Fujioka, University of Hawaii, Manoa 

Toni Glymph, Wisconsin Department of Natural Resources 

Mark Gold, Heal the Bay, California 

Paul Hunter, University of East Anglia, U.K. 

Dennis Juranek, Centers for Disease Control and Prevention (retired) 

David Kay, University of Wales, U.K. 

Sharon Kluender, Wisconsin State Laboratory of Hygiene 

Erin Lipp, University of Georgia 

Graham McBride, National Institute of Water and Atmospheric Research, New Zealand 

Charles McGee, Orange County Sanitation District, California 

Samuel Myoda, Delaware Department of Natural Resources 

Charles Noss, USEPA 

Robin Oshiro, USEPA 

James Pendergast, USEPA 

Mark Pfister, Lake County Health Department, Illinois 

John Ravenscroft, USEPA 

Stephen Schaub, USEPA 

Mark Sobsey, University of North Carolina, Chapel Hill 
U.S. Environmental Protection Agency

February 2009 A-8 

Jeffrey Soller, Soller Environmental, California 

Michael Tate, Kansas Department of Health and Environment 

Peter Teunis, RIVM (National Institute of Public Health and the Environment), Netherlands 

Gary Toranzos, University of Puerto Rico, Rio Piedras 

Timothy Wade, USEPA 

John Wathen, USEPA 

Stephen Weisberg, Southern California Coastal Water Research Project 

David Whiting, Florida Department of Environmental Protection 

Richard Zepp, USEPA 

In addition to contacting experts in the field, specific reports were obtained and the titles of the 

references cited in the reports were reviewed for relevance. 

• NRC. 2004. Indicators for waterborne pathogens. National Academies Press. 

Washington, DC. 315 pp. 

• USEPA. 2007. Report of the experts scientific workshop on critical research needs for 

the development of new or revised recreational water quality criteria. EPA 823-R-07-006. 

Available online at http://www.epa.gov/waterscience/criteria/recreation

• References cited by the Natural Resources Defense Council reviewers of the EPA Critical 

Path Science Plan 

• Prüss (1998) Review of Epidemiological Studies on Health Effects from Exposure to 

Recreational Water. International Journal of Epidemiology 27:1-9. 

• Wade, T.J., Pai, N., Eisenberg, J.N., and Colford, Jr., J.M. 2003. Do U.S. Environmental 

Protection Agency water quality guidelines for recreational waters prevent 

gastrointestinal illness? A systematic review and meta-analysis. Environmental Health 

Perspectives 111(8):1102-1109. 

• Zmirou, D., Pena, L., Ledrans, M., and Letertre, A. 2003. Risks associated with the 

microbiological quality of bodies of fresh and marine water used for recreational 

purposes: Summary estimates based on published epidemiological studies. Archives of 

Environmental Health 58(11): 703-711. 

• Sinton, L.W., Finlay, R.K., Hannah, D.J. 1998. Distinguishing human from animal fecal 

contamination in water: A review. New Zealand Journal of Marine and Freshwater 

Research 32: 323-348. 

• Boehm et al. 2008. A sea change ahead for recreational water quality criteria (peer review 

in progress) 

In addition, Clancy Environmental Consultants, ICF International, Soller Environmental, 

WaltJay Consulting, and EPA’s Health and Ecological Criteria Division all maintain extensive 

literature databases and reference lists from previously completed projects. All of those in house 

resources were also sources of literature.