______________________________________________________________________________

Animal Health Hazards of

Concern During Natural

Disasters

_________________________________________________________

February 2002
Contributors

USDA: Animal and Plant Health Inspection Service (APHIS), Veterinary Services (VS), Centers

for Epidemiology and Animal Health (CEAH), Center for Emerging Issues (CEI)

Reginald Johnson, 970-490-7896, reginald.a.johnson@aphis.usda.gov

Miloslav Muller, 505-761-3160, miloslav.muller@aphis.usda.gov

Acknowledgements

The following reviewers are acknowledged for their editorial input into this publication:

Colleen S. Bruning-Fann, Area Epidemiology Officer, USDA/APHIS Veterinary Services,

Lansing, MI

David M.Ewey, Veterinary Medical Officer, USDA/APHIS Veterinary Services, Sacramento, CA

Dana Nelson, Area Epidemiology Officer, USDA/APHIS Veterinary Services, Sacramento, CA

Whitney A. Ross-Mauer, Epidemiologist, Kent County Health Department, Grand Rapids, MI

Gary E. Stevens, Area Epidemiology Officer, USDA/APHIS Veterinary Services, Lincoln, NE

Carol A. Tuszynski, Agricultural Economist, USDA/APHIS Veterinary Services, Fort Collins,

CO

Copies

For copies of this publication, please contact the Centers for Epidemiology and Animal Health:

Telephone (970) 490-8000

FAX (970) 490-8099

Internet www.aphis.usda.gov/vs/ceah/cei

The USDA is an equal opportunity employer.
Animal Health Hazards of Concern During Natural Disasters

Table of Contents

Summary......................................................................................................................................i

Introduction.................................................................................................................................1

Objective.....................................................................................................................................3

Target Audiences.........................................................................................................................3

Expected Outcome......................................................................................................................3

Summary of Federally-declared Natural Disasters in the U.S., Years 1998-2000..........................4

Infectious Hazards of Concern During Natural Disasters..............................................................7

Non-infectious Hazards of Concern During Natural Disasters....................................................26

Conclusions...............................................................................................................................31

Bibliography..............................................................................................................................32

Appendix...................................................................................................................................37
Animal Health Hazards of Concern During Natural Disasters

List of Abbreviations

EEE, eastern equine encephalomyelitis

FEMA, Federal Emergency Management Agency

SLE, St. Louis encephalitis

VEE,Venezuelean equine encephalomyelitis

WEE, western equine encephalomyelitis

List of Figures

Figure 1. Animal health hazards of concern and their consequences in natural disasters.

Figure 2. Annual number of Federally-declared, natural disasters in the U.S. during years

1998-2000.

Figure 3. Types of Federally-declared, natural disasters in the U.S. during years 1998-2000.

Figure 4. Types of Federally-declared, natural disasters in the U.S. by year during years

1998-2000.

List of Tables

Table 1. Types of natural and technological disasters, according to the United States Federal

Emergency Management Agency.

Table 2. Serogroup, taxonomy, virus, primary vector, geographic distribution, and diseases of

zoonotic and non-zoonotic arboviruses that are indigenous to Canada, the United States, Central

America, or South America.

Table 3. Ecological and climatic observations during: (1) enzootic and epizootic transmission of

selected arbovirus diseases that are prevalent in the U.S., Canada, Mexico, and Central America,

(2) epizootic transmission of anthrax in livestock and wildlife in the U.S., Canada, and Africa, and

(3) epizootic transmission of leptospirosis and cryptosporidiosis.

Table 4. Veterinary and human cases of vector-borne diseases during 12 natural disasters that

lead to excessive accumulations of water in the continental United States from 1975 through

1997.

Table 5. Estimated value of livestock and aquaculture species that died during Hurricane Floyd

in North Carolina in 1999.
Table 6. Anatomical location of injuries on horses that were admitted to an emergency health

care facility after Hurricane Andrew in Florida in 1992.

Table 7. Supplemental readings about the ecology and epidemiology of various infectious

diseases of concern during natural disasters.
Executive Summary

Damage from seemingly more frequent and more severe weather calamities and other

natural phenomena during the decade from 1990 to 1999 lead to 460 Presidential disaster

declarations. The number of disaster declarations that were issued for 1990 to 1999 was

approximately double the number that was issued for 1980 to 1989 and for all preceding decades

on record. An important concern during natural disasters is the potential for outbreaks of diseases

in animals and humans. The animal diseases for which there is concern may be classified broadly

into two categories, infectious hazards and non-infectious hazards. Examples of infectious

hazards commonly discussed in the aftermath of hurricanes or other disasters resulting in flooding

include the mosquito-borne diseases (e.g., eastern equine encephalomyelitis), leptospirosis,

anthrax, botulism, cryptosporidiosis, giardiasis and hoof rot. Frequently discussed non-infectious

hazards of animals during natural disasters include traumatic injuries, aspiration pneumonia, and

toxic and sewage-related gastroenteritis. There is little rigorous scientific documentation that the

incidence of animal diseases increases substantially, either during or shortly after natural disasters.

The absence of such scientific documentation suggests that there could be a significant disparity

between the perceptions and the realities of the incidence of animal diseases during natural

disasters. Thus, a valuable service that health professionals can provide during natural disasters is

communication to emergency management agencies, the news media and the public of accurate

scientific information about the potential risk of infectious and non-infectious hazards to animal

and human health.

The objective of this paper is to describe some of the major natural disasters that have

occurred in the U.S. during recent years and to review some infectious and non-infectious hazards

that, at the very least, are perceived to be related directly to natural disasters. The number and

types of natural disasters, the basic ecology and epidemiology of several infectious hazards that

are thought to be affected by the climatic and environmental changes during natural disasters, and

the impact of natural disasters on some non-infectious hazards of animals are presented.

The U.S. experienced 186 Federally-declared, natural disasters during years 1998-2000.

Thunderstorms and floods comprised slightly more than 50 percent of the total number of these

natural disasters. Regarding infectious hazards, during the past 25 years there was only one

natural disaster involving flooding (i.e., the Red River flood of 1975) to which significant animal

morbidity and mortality due to arbovirus disease was attributed. There is minimal to no scientific

evidence that links natural disasters in the U.S. to significantly consistent increases in the

incidence of other infectious diseases of animals such as anthrax, leptospirosis, and

cryptosporidiosis. While not documented, the destruction caused by some natural disasters might

in fact destroy ecosystems that normally harbor pathogens and their vectors and consequently

decrease, not increase, the risk of outbreaks of infectious disease. Regarding non-infectious

hazards, sporadic incidents of morbidity and mortality due to drowning, heat waves, and traumatic

injuries have been documented more clearly. Thus, the potential economic impact of

non-infectious hazards arising from natural disasters may be greater than the economic impact of

infectious hazards. While vigilant surveillance for outbreaks of infectious hazards during natural

disasters should not be discouraged, there should be appropriate resources allocated towards the

resolution of issues related to the prevention, control and treatment of non-infectious hazards.

i
Introduction

Damage from seemingly more frequent and more severe weather calamities and other

natural phenomena during the decade from 1990 to 1999 lead to 460 Presidential disaster

declarations (Federal Emergency Management Agency[FEMA], 2000a). The number of disaster

declarations that were issued for 1990 to 1999 was approximately double the number that was

issued for 1980 to 1989 and all preceding decades on record. For the 1990-1999 period, the

FEMA spent more than $25.4 billion for declared disasters and emergencies, compared to $3.9

billion (current dollars) in disaster aid for the 1980-1989 period. Hurricanes and typhoons were

the most costly of the weather-related events during the 1990s. A total of 88 declarations were

issued for these storms, including a single-year record of 19 declarations in 1999. The flooding

that resulted from severe storms and other causes of flooding was the most frequently declared

type of disaster. Approximately $7.3 billion in funding was committed by FEMA to response and

recovery from flooding during 1990 to 1999.

Natural disasters can impact livestock and companion animals. Pigs, chickens and turkeys

were killed in the wake of Hurricane Floyd in North Carolina in 1999. A disaster relief

management team was established by the North Carolina State University College of Veterianry

Medicine for companion animals including dogs, cats and horses during Hurricane Floyd. A

similar team provided care for horses during Hurricane Andrew in Florida in 1992. These events

have highlighted the need to include livestock and companion animals in disaster management

plans. The importance of caring for animals during disasters has bearing on two significant issues,

public health and animal well-being (Heath, 1999). The close relationship between companion

animals and their owners as well as livestock and their owners (Monti, 2000) suggests that

providing care for animals in disasters should be an integral component of providing care for

humans.

An important concern during natural disasters is the potential for outbreaks of diseases in

animals and humans. The animal diseases for which there is concern may be classified broadly

into two categories, infectious diseases and non-infectious diseases (Figure 1). Examples of

infectious diseases commonly discussed in the aftermath of hurricanes or other disasters resulting

in flooding include the mosquito-borne diseases (e.g., eastern equine encephalomyelitis),

leptospirosis, anthrax, botulism, cryptosporidiosis, giardiasis and hoof rot (Nasci and Moore,

1998; Heath, 1999; University of North Carolina, 1999). Frequently discussed non-infectious

diseases of animals during natural disasters include traumatic injuries, aspiration pneumonia, and

toxic and sewage-related gastroenteritis.

The potential for animal-related disease outbreaks during natural disasters is discussed in

media reports frequently (Heath, 1999). However, there is little confirmed documentation

(“scientific” or otherwise) that the incidence of diseases increases substantially, either during or

shortly after natural disasters. The absence of such scientific documentation suggests that there

could be a significant disparity between the perceptions and the realities of the incidence of animal

diseases during natural disasters. Thus, a valuable service that health professionals can provide

during natural disasters is communication to the news media and the public of accurate scientific

information about the potential risk of infectious and non-infectious hazards to animal and human 

1
Figure 1. Animal-health hazards of concern and their consequences during natural disasters.

2

Hazards

Infectious

Hazards

Viral

EEE

WEE

VEE

SLE

Bacterial

Anthrax

Leptospirosis

Parasitic

Cryptosporidium

Giardiasis

Non-infectious

Hazards

Water

Drown

Heat

Hyperthermia

Fire

Burns

Trauma

Cold

Hypothermia

Frostbite

Wind

Trauma
health. Being equipped with accurate information about the potential risk of disease will permit

emergency management agencies to direct their energy and resources towards issues that truly are

of utmost importance during disasters.

Objective

The objective of this paper is to describe some of the major natural disasters that have

occurred in the U.S. during recent years and to review some infectious and non-infectious hazards

that are perceived to be related directly to these natural disasters. Specifically, the number and

types of natural disasters, the basic ecology and epidemiology of several infectious hazards that

are thought to be affected by the climatic and environmental changes during natural disasters, and

the impact of natural disasters on some non-infectious hazards of animals will be presented.

Target Audiences

The project was undertaken with two audiences in mind. In the interest of generality,

brevity and handiness, the contents of this paper were written for veterinary health professionals

as well as other professionals who are involved, or who expect to be involved, in addressing

animal health issues that may arise during natural disasters. The section “Infectious Hazards of

Concern During Natural Disasters” is comprised of excerpts from a series of seven supplemental

readings (readings in preparation) in which the ecology and epidemiology of each infectious

hazard is discussed in greater detail. Beyond the scope of this paper, the supplemental readings

may be beneficial to those readers who, for purposes other than natural disasters, have an interest

in the basic ecology and epidemiology of the infectious diseases that are discussed herein.

Although humans are susceptible to each and every disease that has been included in this paper,

the primary focus of the paper is disease in domestic species, and to a lesser extent, wildlife

species. For comparative purposes, there will be an occasional reference to similar investigations

in human populations. Extensive bodies of literature about these diseases in humans are available

elsewhere.

Expected Outcome

The expected outcome for the reader is a greater awareness of : (1) the complexity of

transmission of infectious hazards that typically are of concern during natural disasters, (2) the

multitude of environmental and biologic factors that may be involved in the transition of these

infectious hazards from a sporadic to an enzootic state, and from an enzootic to an epizootic

state, and (3) the relative potential impact of infectious hazards versus non-infectious hazards

during natural disasters.

3
Summary of Federally-declared Natural Disasters In The U.S., 1998-2000

According to the United States Federal Emergency Management Agency, there are 17

forms of disasters, 13 of which are broadly categorized as natural disasters and 4 of which are

categorized as technological disasters (Table 1). The U.S. experienced 186 Federally-declared,

natural disasters during years 1998-2000. There were 58 Federally-declared natural disasters

during year 1998, 61 during year 1999, and 67 during year 2000 (Figure 2). The most prevalent

Federally-declared natural disaster was the thunderstorm. Thunderstorms and floods comprised

slightly more than 50 percent of the total number of these natural disasters (Figure 3). Wildfires,

mudslides, and earthquakes were among the least prevalent of these natural disasters during the

three-year period. After being stratified by year, the distribution of these natural disasters was

similar to the non-stratified distribution (i.e., from one year to the next, thunderstorms and floods

remained as the most prevalent types of natural disasters) (Figure 4).

Numerous states may be affected by a Federally-declared natural disaster such as a

hurricane. Because the geographic unit of concern that is used by FEMA is the state (or its

equivalent), a single natural disaster such as a hurricane may be recorded several times, but by a

different state each time. Thus, Hurricane Floyd was recorded as at least eight different natural

disaster declarations during year 1999.

Source. http://www.fema.gov/ptc/prep.htm. . 2001

Terrorism

Nuclear power plant emergency

House fires; building fires

Hazardous materials

Technological

Thunderstorms and lightning

Winter storms

Winter driving

Wildland fires

Volcanoes

Tsunamis

Tornadoes

Landslides and mudflows

Hurricanes

Floods and flash floods

Fire safety (during or after a disaster)

Extreme heat

Earthquakes

Natural 

Type of Disaster Form

Table 1. Types of natural and technological disasters, according to the United States

Federal Emergency Management Agency (FEMA).

4
Figure 2. Annual number of Federally-declared, natural disasters in the U.S. during years

1998-2000 ( Source http://www.gismaps.fema.gov/ ).

Figure 3. Types of Federally-declared, natural disasters in the U.S. during years 1998-2000 

( Source http://www.gismaps.fema.gov/ ).

5

67

61

58

Year

0

10

20

30

40

50

60

70

80

Number of Disasters

1998 1999 2000

29%

22%

15%

12%

10%

8%

2%

2%

1%

Thunder Storm

Flood

Tornado

Winter Storm

Hurricane

Tropical Storm

Wildfire

Mudslide

Earthquake

0% 5% 10% 15% 20% 25% 30% 35%

Percent of Total
Figure 4. Types of Federally-declared, natural disasters in the U.S. by year during years

1998-2000 ( Source: http://www.gismaps.fema.gov ).

6

Thunder Storm

Flood

Tornado

Hurricane

Tropical Storm

Winter Storm

Wildfire

Mudslide

Earthquake

0% 10% 20% 30% 40%

Percent of Total

1998

1999

2000
Infectious Hazards of Concern During Natural Disasters

One possible outcome of natural disasters is alteration of ecosystems that harbor

pathogens for infectious diseases of animals, as well as vectors of these pathogens. One of the

most common forms of natural disasters is the flooding that results from excessive rainfall.

Examples of infectious diseases of animals that become of concern due to proliferation of

mosquitoes during and after flooding are the arbovirus diseases such as eastern equine

encephalomyelitis and western equine encephalomyelitis, (Nasci and Moore, 1998; Heath, 1999)

(Figure 1). Bacterial and parasitic diseases of animals that are commonly discussed in the

aftermath of floods, hurricanes, droughts and similar natural disasters are leptospirosis, anthrax,

botulism, cryptosporidiosis, giardiasis and hoof rot (Nasci and Moore, 1998; Heath, 1999;

University of North Carolina, 1999). Various ecological, geographical, and climatic factors, some

of which have been studied more intensely than others, have been observed during outbreaks of

these diseases. Each of these groups of factors may be influenced to varying degrees by natural

disasters.

During natural disasters, animal health professionals are expected to provide a range of

veterinary services to protect animal and human health. One of these services includes prevention

and control of epizootic, zoonotic and food-borne diseases of animals and humans (Bartels and

Thornton, 1987; Shomer, 1987; Huxsoll et al., 1987; Heath 1999). To achieve their goals, at

least a fundamental understanding of the ecology and epidemiology of potentially infectious

hazards is indispensable. This information can be used to assess the potential influence of natural

disasters on these infectious hazards and is provided below.

Arbovirus Diseases

The word “arbovirus” is used to describe a diverse array of viruses that share a common

characteristic, namely transmission by arthropod vectors (Monath, 1988). The arbovirus group

includes at least 500 viruses, most of which have been assigned to five families, Togaviridae,

Flaviviridae, Bunyaviridae, Reoviridae, and Rhabdoviridae. More than 100 arboviruses have been

associated with naturally-acquired diseases in domestic animals and humans. Some viruses of

importance to animal and human health in the western hemisphere are listed in Table 2.

Ecology of Eastern Equine Encephalomyelitis

Eastern equine encephalitis (EEE) is caused by viruses that can be transmitted to equines

and humans by the bite of an infected mosquito. EEE viruses are alphaviruses that were first

identified in the 1930's. In addition to horses and humans, EEE viruses can produce severe

disease in some birds such as pheasant, quail, the ostrich and the emu (Centers for Disease

Control and Prevention, 1999).

7
Source: From Calisher, Clinical Microbiology Reviews, 1994. Revised, with permission.

CTF Reoviridae Coltivirus Colordo Tick Fever (CTF) Ticks Canada, U.S. Fever, myalgia

Encephalitis,

fever

Snowshoe hare Mosquitoes Canada, U.S.

Encephalitis,

fever

LaCrosse (LAC) Mosquitoes U.S.

Encephalitis,

fever

Jamestown Canyon Mosquitoes Canada, U.S.

Encephalitis,

fever

Group CAL Bunyaviridae Bunyavirus California encephalitis Mosquitoes Canada, U.S.

Encephalitis,

fever

St. Louis encephalitis Mosquitoes Canada, U.S.

(SLE)

Group B Flaviviridae Flavivirus Powassan (POW) Ticks Canada, U.S. Encephalitis

Encephalitis,

fever

Western Equine Mosquitoes Canada, U.S.

Encephalitis (WEE)

Encephalitis,

fever

South America,

Central America

Venzuelean Equine Mosquitoes

Encephalitis (VEE)

Encephalitis,

fever

Everglades (VEE II) Mosquitoes Florida

Encephalitis,

fever

Eastern Equine Mosquitoes Canada, U.S.

Encephalitis (EEE)

Group A Togaviridae Alphavirus

Geographic Disease

Distribution

Serogroup Family Genus Virus Vector

Table 2. Serogroup, taxonomy, virus, primary vector, geographic distribution, and diseases of zoonotic and non-zoonotic

arboviruses that are indigenous to Canada, the United States, Central America, or South America.

8
Regarding insect and arthropod vectors, EEE viruses have been isolated from mosquitoes,

gnats, horse flies, blackflies, mites, and lice. However, the majority of EEE viruses that have been

isolated were from 27 different species of mosquitoes, and 80 percent of the isolates were from a

single species, Culiseta melanura (Morris, 1994). The primary habitats for EEE viruses are

lowlands (Morris, 1994). Endemic EEE swamps located in Florida, Maryland, New Jersey, New

York, and Michigan are characterized by muck-peat soils that are dominated by hardwoods.

These hardwoods have a preference for wet, mucky habitats, and they provide a root system that

supports oviposition and larval development by C. melanura. C. melanura larvae require a

source of water that is darkly shaded and that contains a high concentration of organic matter.

However, C. melanura also breeds in un-shaded waters of cypress swamps in Florida during the

rainy season. The mosquito larvae that overwinter in these habitats develop into pupae. Adult

mosquitoes emerge from the pupae, first in February and March in Florida, and in April through

May in the northern U.S. Female adult mosquitoes may become dispersed as far as five miles

from the swamp from which they originated.

Specific weather conditions that precipitate disease outbreaks attributable to EEE viruses

have not been established clearly. However, outbreaks usually are observed during periods of

hot, rainy weather; these conditions are ideal for expansion of C. melanura and other mosquito

populations (Walton, 1992; Nasci et al., 1993). Outbreaks of EEE are expected to occur from

midsummer to late summer, with August being the peak month of incident cases. An

epidemiological investigation of EEE in Michigan showed that the incident equine cases were

most frequent during September (Ross and Kaneene, 1996). Although outbreaks occur during

the summer, the environmental temperature alone has not been shown to be a valuable predictor

for EEE outbreaks. The annual mean environmental temperatures in Michigan were

approximately normal during each of the years prior to and each of the years of an outbreak of

EEE (Ross and Kaneene, 1996).

An annual excess in precipitation of 20-plus centimeters of rainfall for two consecutive

years, (1) the year preceding the outbreak and (2) the year of the outbreak, has been reported as a

predictor of EEE outbreaks, but the source of this data was limited to a few states in the U.S.

(Grady et al 1978). Others have attempted to create a predictive model for EEE using rainfall

(Letson et al. 1993). The predictive value of the models by Letson et al. never exceeded 50

percent, suggesting that they would not have been very useful in making the predictions about

when outbreaks of these diseases would occur relative to the volume of rainfall. The annual

precipitation in Michigan was rarely 10 centimeters (approximately 8 percent) greater than

expected in each of the years prior to and each of the years of an outbreak of EEE. This eight

percent increase does represent above-average annual precipitation, but there is no indication that

it lead to flooding that was equivalent to that of a natural disaster. An analysis of precipitation

data from Michigan showed that precipitation in Michigan also was increased during late summer

and early fall of the year preceding the outbreak, and it was increased during the summer of the

outbreak (Ross and Kaneene, 1996). In Massachusetts and New Jersey, there were outbreaks of

EEE when there was unusually heavy rainfall during late summer and early fall of the year

preceding the outbreak, and during the summer of the year of the outbreak (Grady et al., 1978).

9
Although there have not been consistent observations of EEE outbreaks during specific

weather conditions, a specific type of land cover is one factor that has been observed consistently

in the habitats occupied by EEE virus vectors and wild-bird reservoir hosts for the virus (Morris

et al., 1980; Emord et al., 1984). The hydrographic (versus geographic) regions that are classified

as “incomplete drainage-lake type” regions are regions in which the glaciated surface does not

permit the streams to drain completely. The regions are characterized by numerous small lakes,

swamps, and bogs that are connected by streams and that usually have dry land between the lakes,

swamps, and bogs. Outbreaks of EEE have been observed in these hydrographic regions in New

York, Ohio and Michigan (Morris et al., 1980; Nasci et al., 1993; Ross and Kaneene, 1996).

For more information about the epidemiology and ecology of EEE, you are referred to the

supplemental readings listed in Appendix 1.

Ecology of Western Equine Encephalomyelitis

The alphavirus of western equine encephalitis (WEE) was first isolated in California in

1930 from the brain of a horse with encephalitis (Hardy, 1987). WEE remains an important cause

of encephalitis in horses and humans in North America, mainly in western parts of the USA and

Canada. WEE viruses also have been isolated from a variety of mammal species (Centers for

Disease Control and Prevention, 1999).

Epizootics of WEE have been reported mostly in the states west of the Mississippi River

in the U.S., and in the provinces of Alberta, Manitoba, and Saskatchewan in Canada. However,

both the ecology and epidemiology of WEE have been studied most intensively in the Central

Valley of California (Hardy, 1987). Two mosquito species are involved in the summer

transmission cycle of WEE viruses in California, Culex tarsalis and Aedes melanimon. These two

species of mosquitoes prefer to breed in sunlit grassy marshes and in open pools of stream beds,

especially in irrigated areas where seepage and improper flooding of agricultural lands create

favorable breeding sites (Walton, 1992).

Although flooding due to a natural disaster such as excessive rainfall may favor

transmission of WEE viruses, “human-made disasters” due to construction of irrigation systems

for cropland may be just as important, if not more important, in the transmission of WEE viruses.

The impact of these irrigation districts on WEE virus transmission has been demonstrated rather

clearly in the Central Valley of California (Reeves and Milby, 1989). Approximately 51 percent

of Culex tarsalis larval collections during a two-year plus period were from agricultural irrigation

water sources including waste water and residual water, pools of water due to leakage and

seepage from the irrigation canals, irrigation canals and ditches themselves, standpipes and valve

housings, and reservoirs. Incident cases of WEE and SLE in humans in California were greatest

during this two-year period. The remaining sources of water from which C. tarsalis larvae were

collected during this epidemic period were miscellaneous sources of agricultural water, domestic

water, industrial water, municipal water, natural streams, and recreational waters (e.g., duck

hunting clubs). More than 90 percent of mosquito breeding sites that were located in irrigated,

agriculturally developed, and partially urbanized areas were sites that were constructed by

humans. C. tarsalis populations will flourish even in deserts, if the deserts are reclaimed and

10
irrigated. The altered desert environment not only supports a vector population such as C.

tarsalis, but the environment also provides the vegetative cover and food supply to support birds

that are essential hosts for WEE viruses.

A qualitative model was developed by Gordon-Smith to explain the factors that influence

the enzootic (versus epidemic) transmission of WEE viruses between its vertebrate maintenance

hosts and from these maintenance hosts to humans (Gordon-Smith, 1987). The model was

derived from comprehensive studies of WEE virus transmission in numerous field and laboratory

studies in Kern County California during an approximate 45-year period between 1945 and 1985.

One example of the factors included in the model, factors that may be influenced by

environmental conditions, is the relationship between the ambient temperature and survival of

mosquitoes. The longevity of mosquitoes is influenced by both ambient temperature and relative

humidity, specifically the relative humidity of the vector’s resting environment and the

atmospheric relative humidity during its feeding periods. The favorable range of relative humidity

during the season of WEE virus transmission in Bakersfield, California is narrow, roughly 35 to

55 percent; therefore, it is logical that Culex tarsalis prefers to reside in humid refuges such as

culverts. The relative humidity of the vector’s resting environment can be correlated with the

atmospheric relative humidities of each season of the year. Thus, the survival of C. tarsalis will

be greater during August and September, versus June and July. Numerous other factors, perhaps

50 or more, may influence the ecology and epidemiology of WEE (Reeves, 1967).

For more information about the epidemiology and ecology of WEE, you are referred to

the supplemental readings listed in Appendix 1.

Ecology of Venezuelan Equine Encephalomyelitis

Like EEE and WEE viruses, Venezuelan equine encephalitis (VEE) virus is an alphavirus

that causes encephalitis in horses and humans. VEE is an important veterinary and public health

problem that is confined primarily to Central and South America. Occasionally, large regional

epizootics and epidemics can occur, resulting in thousands of equine and human infections. A

large epizootic that began in South America in 1969 spread to Texas in 1971. At least 200,000

horses died during that outbreak (Walton and Grayson, 1989; Centers for Disease Control and

Prevention, 1999).

Culex mosquitoes of the subgenus Melanoconion, the primary enzootic vector of VEE

viruses, reside in tropical and subtropical swamps and forests throughout North and South

America. These mosquitoes breed in pools of water or meandering streams that are closely

associated with aquatic plants such as water lettuce (Johnson and Martin, 1974). Some adult

mosquitoes remain within naturally shaded, moist locations while others may invade human

residences. Rodents are the mosquito’s primary vertebrate partner in maintaining VEE viruses in

the swamp and forest habitats.

 Mosquitoes of several different genera including Mansonia, Psorophora, and Aedes are

involved in epizootic transmission of VEE (Walton and Grayson, 1989). The favored ecological

zones for epizootics of VEE are tropical dry forest and tropical thorn forest, both of which also

11
support agricultural and cattle ranching enterprises. VEE epizootics occur typically during the

rainy season in these ecological zones. In addition to rainfall, a relative humidity of 90 percent

and an ambient temperature of 26.6o C are other environmental factors that may influence VEE

epizootics. Frequently, VEE epizootics are observed during periods of unusually intense rainfall

(Trapido, 1972; Johnson and Martin, 1974; Walton, 1981), but these levels of excessive rainfall

would not necessarily be the equivalent of the excessive rainfall that could be experienced during

a natural disaster.

For more information about the epidemiology and ecology of VEE, you are referred to the

supplemental readings listed in Appendix 1.

Ecology of St. Louis Encephalitis

St. Louis encephalitis (SLE) virus, a Group B arbovirus, is a member of the family

Flaviviridae and the genus Flavivirus. Unlike EEE, WEE, and VEE, SLE is a rarely diagnosed

disease of animals, but because chickens and wild birds are susceptible to SLE virus infection,

they are used as sentinels to predict transmission of SLE virus in humans. Serological evidence of

natural transmission of SLE virus was detected in an emu flock that was suspected of

experiencing morbidity due to an arbovirus (Day and Stark, 1996; Day and Stark, 1998) and in

small mammals (Day et al., 1996). In humans, SLE is the leading cause of epidemic flaviviral

encephalitis in the United States, and it is the most common mosquito-transmitted human

pathogen in the U.S. While periodic SLE epidemics have occurred in the U.S. in the Midwest and

southeast only, SLE virus is distributed throughout the lower 48 states (Centers for Disease

Control and Prevention, 1999). Some aspects of the ecology and epidemiology of SLE in humans

may be extremely beneficial in thoroughly understanding naturally-acquired SLE virus infections

of animals that may occur in the future, as well as arbovirus infections of animals such as WEE,

EEE and VEE.

Culex pipiens and Culex quinquefasciatus are the primary vectors of SLE virus in the

Ohio-Mississippi basin and eastern Texas. C. pipiens and C. quinquefasciatus breed in polluted

waters, especially where sanitary practices are poor. Thus, SLE in humans is typically a disease

of members of the lower socio-economic groups (Monath and Tsai, 1987). C. nigripalpus is the

epidemic vector of SLE virus in Florida. C. tarsalis, the primary vector for WEE viruses, is also

the epidemic vector for SLE virus in the western U.S. Thus, the transmission of SLE and WEE

viruses may occur concurrently in the western U.S. It is also for that reason that many of the

ecological and environmental conditions that favor transmission of SLE virus are similar to those

conditions that favor the transmission of WEE viruses (i.e., irrigated or flooded dryland areas).

The ambient temperature and rainfall profoundly influence the activity of SLE virus

(Monath and Tsai, 1987). The requirement of a high ambient temperature is consistent with the

epidemic curves of SLE outbreaks that occurred in central Florida in 1977 and in Houston, Texas

in 1980. These epidemic curves show that incident cases occurred during mid-summer through

late fall, specifically appearing first in July and continuing through August and September. High

ambient temperatures early in the year appear to favor transmission of SLE virus by decreasing

the amount of time required for the gonotrophic cycle, larval maturation, and the extrinsic

12
incubation period of SLE virus. In laboratory studies, SLE virus was transmitted more efficiently

by C. tarsalis and C. pipiens when the vectors were incubated at high ambient temperatures

(Hardy, 1986). C. quinquefasciatus is not an efficient transmitter of SLE virus normally;

however, high ambient temperatures in southern California may have increased the vector

potential of C. quinquefasciatus during an epidemic of SLE in Los Angeles in 1984.

For more information about the epidemiology and ecology of SLE, you are referred to the

supplemental readings listed in Appendix 1.

Bacterial Diseases

Ecology of Anthrax

Anthrax is an infectious disease caused by Bacillus anthracis. Historically, the geographic

distribution of anthrax has been global. Now, the incidence is lower in much of the western

hemisphere, but it is still a significant problem in parts of Africa and eastern Europe. Many

domestic and wild animals, as well as humans, are susceptible to anthrax (Hugh-Jones, 1999).

Ruminants and pigs are the most commonly affected food production animals, but horses located

in the same environment also may acquire the infection (Mosier and Chengappa, 1999).

“For the control of [anthrax] epidemics, it is important to understand not only the

pathogenesis and interactions of B. anthracis with host animals but also the ecology of the

spores.” (Dragon and Rennie, 1995). Generally speaking, anthrax epidemics occur during the

summer months in which there are dry periods that are punctuated by prolonged periods of

intense rain. The “incubator area” hypothesis, one attempt to explain why anthrax outbreaks

occur, is based on observations that alkaline soil pH, high soil moisture, high concentrations of

organic matter in the environment, and ambient temperature in excess of 15.5

oC provide a

microenvironment that promotes cycling of B. anthracis spores, the end result of which is an

increase in the exposure of susceptible hosts to infective doses of spores and more outbreaks of

anthrax (Van Ness, 1971). The validity of this hypothesis continues to be challenged.

Prolonged rainfall obviously promotes runoff and pooling of standing water. A proposed

role of water in anthrax epidemics is the collection (aggregation) and concentration of spores in

spore “storage areas”, a term that is intended to describe the stage of the life cycle of B. anthracis

more accurately than does the term “incubator areas” (Dragon and Rennie, 1995). The surface of

the B. anthracis spore is highly hydrophobic. Thus, the spores are resistant to dissolution by

water and may be tranported in clumps of organic matter by runoff to standing pools of water.

Subsequently, dry weather leads to evaporation of the standing pools of water and concentration

of floating anthrax spores as these pools of water gradually shrink. The high buoyant density of

B. anthracis spores provides an opportunity for the spores to adhere to vegetation as the

vegetation resurfaces during evaporation of the surrounding water. Dragon and Rennie (1995)

summarized the effects of water on anthrax spores essentially in three steps: (1) successive cycles

of run-off and evaporation concentrate anthrax spores in storage areas, (2) evaporation

13
redistributes the spores from the soil onto vegetation, and (3) susceptible herbivores consume the

contaminated vegetation, become exposed to B. anthracis , and some develop anthrax.

Several ecological observations have been made during outbreaks of anthrax (Fox et al.,

1973; Fox et al., 1977; Gainer and Saunders, 1989; Lindeque and Turnbull, 1994; Dragon and

Rennie, 1995; Turner et al., 1999). The consistency of these observations varies, not only in

reference to outbreaks that have occurred in livestock, but also in reference to outbreaks that have

occurred in wildlife species. Cycles of rainfall and drought, specific grazing conditions, and

specific soil types have been observed, but have not been observed consistently during outbreaks

of anthrax.

For more information about the epidemiology and ecology of anthrax, you are referred to

the supplemental readings listed in Appendix 1.

Ecology of Leptospirosis

Leptospirosis is a globally-distributed, bacterial disease of domestic and wildlife species as

well as humans. The parasitic strains of these spirochaetes are found in animal species, and the

saprophytic strains are found in water (Ellis, 1986; Ellis and McDowell, 1994). For taxonomic

and epidemiological purposes, the parasitic leptospires are further divided into 23 serogroups and

212 serovars. Leptospiral infections also are broadly categorized into host-adapted and non-host

adapted infections (Heath and Johnson, 1994). Host-adapted infections are endemic and are

characterized by high seroprevalance of subclinical infections, primarily in intensively managed

livestock production systems. Non-host-adapted infections are sporadic, of low seroprevalence,

and the economic impact of non-host-adapted infections is lower than that of host-adapted

infections (Ellis, 1994; Ellis and McDowell, 1994).

Environmental conditions are important in the survival of leptospires outside the host 

(Ellis and McDowell, 1994; Ellis, 1997). Prolonged viability of leptospires in the environment

increases the risk of contact between leptospires and susceptible hosts, assuming that the host

factors and pathogen factors involved in the transmission of leptospires remain equal. The

optimum environmental conditions for survival of leptospires outside the host are warmth,

moisture, and a nearly neutral pH (Michna, 1970; Ellis, 1986; Zaitsev et al., 1989; Ellis, 1994).

Leptospires can survive for 30 days in sterile tap water and for 14 days in moist environments

such as soils, mud, swamps and other watercourses that are relatively static. Water serves two

functions in the transmission of leptospirosis. Water aids in the survival and dissemination of 

leptospires, as well as the actual process of a susceptible host becoming infected. Moving waters

provide the force that promotes further physical spreading of leptospires within a contaminated

environment, as well as dispersal from a contaminated environment to a non-contaminated

environment (Ellis, 1997). Normally, intact skin provides an effective barrier against invasion by

leptospires, but after the skin has become softened due to prolonged immersion in water,

leptospires can penetrate the skin more easily and establish infection within the host.

A number of investigations of the survival of leptopires under various environmental

conditions have been done. pH values outside the range of 6.0 to 8.4 are clearly unfavorable to

14
survival of leptospires. On the other hand, the effect of soil pH values within the aforementioned

range on the duration of survival of leptospires has not been shown to be consistent. This

inconsistency is due possibly in part to differences in the methods that have been used to

investigate the relationship between pH and the duration of survival of leptospires.

Regarding temperature and other physical agents, the ambient temperature, the body

temperature within an infected host, and the temperature at which tissue specimens from an

infected host are held all affect the viability of leptospires. Most of the investigations of the affect

of temperature and other physical agents on survival of leptospires have been done in the

laboratory. While it is not evident that as many similar investigations in natural environments

have been undertaken, it is assumed that similar ambient temperatures (versus intra-uterine

temperatures, e.g.) would have the same affect on the survival of leptospires in the environment as

in the laboratory. In the laboratory, leptospires are susceptible to low and high temperature

extremes, specifically temperatures less than minus 8.0

oC and greater than 50.0oC. Leptospires

survive for several hours at temperatures that are less than minus 18oC and greater than 40oC. In

diagnostic specimens, leptospires die rapidly in tissues and body fluids, unless the tissues are

maintained at plus 4.0oC. Leptospires survive in tissues at 40oC, but they die in tissues that are

held at 30 to 39oC (Rocha, 1998). This latter temperature range is the same range to which dead

fetuses are exposed prior to being expelled by their dams; thus, the range may be one of the

difficulties in isolating leptospires from carcasses during laboratory diagnosis of leptospirosis

(Ellis, 1992). Leptospires are highly susceptible to dessication, UV light, and UV sunlight. They

survive for 3 to 10 hours in a dry environment, for less than 0.2 hour when exposed to UV light,

and less than 1.0 hours when exposed to UV sunlight (Michna, 1970; Faine, 1994).

Thus, the factors that determine the survival of some serovars of leptospires in the

environment are the pH, ambient temperature, moisture, constituents of the soil, and the presence

of other naturally-occuring, microbial competitors (Okazaki and Ringen, 1957). Regardless of the

duration of survival of leptospires under specific environmental conditions, a key issue is whether

they continue to remain infective to susceptible hosts under these conditions. Lastly,

environments that favor either the maintenance, or the proliferation, of rodent and rat populations

also favor the increased environmental contamination by leptospires. Examples of these

environments are sugar cane farms specifically, farms in general, grain stores, and sewage plants

(Ellis, 1997).

For more information about the epidemiology and ecology of leptospirosis, you are

referred to the supplemental readings listed in Appendix 1.

Parasitic Diseases

Ecology of Cryptosporidiosis

Transmission of Cryptosporidium parvum is a complex maze that involves several

reservoirs of infection. For purposes of this paper, transmission of C. parvum can be divided

roughly into two types, waterborne transmission and non-waterborne transmission.

15
Cryptosporidiosis has been recognized with increasing frequency as a waterborne infection during

the past 25 years (Rose et al., 1997).

Two sources of water involved in waterborne transmission of cryptosporidiosis are

drinking water and recreational water. C. parvum spores are present in 65 to 97 percent of

surface waters including rivers and lakes throughout the US (LeChevallier, 1991). Water that

was collected from rivers, lakes, springs and beneath the ground has been implicated as the source

of drinking water in at least five, well-documented outbreaks of water-borne cryptosporidiosis in

the US (Rose et al., 1997). Because of the small size and density of Cryptosporidium spp.

oocysts, approximately one year may pass before the suspended oocysts settle to the bottom of a

20 meter deep reservoir that contains standing water (versus flowing water). Thus, any

anticipated reduction in the number of oocysts in surface water through natural sedimentation is

not practical. However, properly operated, conventional water treatment methods can remove 99

percent of the oocysts, and microfiltration and ultrafiltration membrane processes may remove

100 percent of the oocysts.

Regarding the rivers, lakes, springs, and ground water that were implicated as the sources

of the drinking water in the five outbreaks of water-borne cryptosporidiosis in the US, all of these

sources were considered to be pristine sources prior to the outbreaks, indicating that only

chlorination of the water was necessary to satisfy the regulatory requirements. The contaminated

water was linked eventually to suboptimal treatment of water that was intended for human

consumption. It was determined later that the water that was treated did meet some of the

Environmental Protection Agency’s requirements that were in effect at the time of the outbreaks.

Wastewater was the suspected contaminant in two of these five outbreaks; however, the sources

of contamination in the remaining three outbreaks remain unknown.

The Milwaukee, Wisconsin outbreak of cryptosporidiosis in 1993 was the largest reported

cryptosporidiosis outbreak in US history (MacKenzie et al., 1994). Two rivers that discharge into

Lake Michigan, the source of drinking water in this outbreak, became swollen after heavy rain.

The rivers drain into the area of Lake Michigan where the water treatment facility collected its

untreated water that was intended to undergo purification subsequently. The watersheds of the

two rivers were sites for human sewage discharges, abattoirs, cattle grazing ranges, and

environments with numerous species of wild and domesticated animals. However, neither the

source nor time of entrance of oocysts into the water treatment facility was ever determined.

Seven possible water-treatment deficiencies were described for this Milwaukee outbreak, as well

as other outbreaks (Rose et al., 1997). Only one of the seven deficiencies in the Milwaukee

outbreak and two other outbreaks was related to a naturally occurring event (i.e., heavy rain;

melting snow). In regards to natural events, it was suggested that successful forecasting of events

that may favor outbreaks of cryptosporidiosis (e.g. floods) would be beneficial to personnel who

are involved in water treatment activities.

In addition to outbreaks of cryptosporidiosis in which the source was contaminated

drinking water, there are many reported outbreaks of cryptosporidiosis due to contaminated

recreational waters in the US and abroad. Recreational waterborne outbreaks have been linked to

public swimming pools. Children were identified as the primary victims in the majority of these

16
outbreaks. The source of cryptosporidium in recreational waterborne outbreaks were mostly

fecal accidents in combination with inoperable swimming pool filters and, in one case, overflow of

a human sewage system into the swimming pool. In general, these recreational water-borne

outbreaks were not associated with the source of the water itself. Thus, the outbreaks were

limited in their geographic distribution. As was the situation with outbreaks due to contaminated

drinking water, disinfection of the swimming pools failed to inactivate the oocysts. Instead, the

outbreaks were suppressed by closing and draining the contaminated pools, and the filters in the

pools either were cleaned or replaced (Rose et al., 1997).

For more information about the epidemiology and ecology of cryptosporidiosis, you are

referred to the supplemental readings listed in Appendix 1.

17
Discussion

Infectious diseases that are discussed frequently as potential animal health problems during

natural disasters are mosquito-borne diseases, anthrax, leptospirosis, cryptosporidiosis, giardiasis,

botulism, and hoof rot (Heath, 1999). A critical issue is whether the risk of these diseases during

natural disasters truly increases, or whether the risks are more perceived than they are real.

Plausible explanations of potential risks lie in part in the complex ecology and epidemiology of

these diseases. If the risk of these diseases is remote, an awareness of the remote risks will permit

those involved in the management of animals in natural disasters to direct their resources towards

issues that truly are of utmost importance.

There is no question that outbreaks, even major outbreaks, of these infectious diseases in

animal populations do occur occasionally, but there are few, rigorously controlled, scientific

investigations to evaluate the incidence of the diseases during natural disasters. Although such

studies are not readily available, a fundamental understanding of the ecology of these diseases will

provide assistance in placing the risk of occurrence of these diseases in proper perspective during

natural disasters. Many of the published investigations of outbreaks of these infectious diseases

reported a variety of ecological and climatic conditions that were observed during the outbreaks

(Table 3). For example, some of the weather conditions that have been observed during

outbreaks of arbovirus disease are increased precipitation, increased ambient temperature, and

high relative humidity. However, these same conditions also may be observed when there are no

outbreaks of disease. Regardless of the amount of precipitation, arbovirus diseases generally are

restricted to specific months of the year, depending on the specific disease and the geographic

region. The occurrence of anthrax outbreaks may be as much, if not more, a function of specific

characteristics of the soil rather than changes in specific climatic conditions. The pH appears to

have received the greatest amount of attention in the investigation of environmental factors that

influence leptospirosis. The influence of climatic conditions on waterborne outbreaks of

cryptosporidiosis appears to be even more vague than the influence of climatic conditions on the

arbovirus diseases, anthrax, and leptospirosis.

Floods and hurricanes are frequently followed by a proliferation of mosquitoes and by

concomitant requests from residents and government agencies to apply insecticides. However,

many of the species of mosquitoes that proliferate during these disasters are nuisance mosquitoes,

rather than mosquitoes that are competent vectors of infectious diseases (Centers for Disease

Control and Prevention, 1994; Nasci and Moore, 1998). Nuisance mosquito species are not a

significant threat to animal health or human health (Centers for Disease Control and Prevention,

1993a). Regardless, it has been suggested that a provision to monitor the following two

parameters should be included in disaster response policies for animals and humans: (1) monitor

increases in prevalence of mosquito species that can transmit infectious agents and (2) monitor the

risk of arboviral diseases in those geographic regions that are affected by natural disasters (Nasci

and Moore, 1998).

18
Disruption of soils during construction +

projects in which earth was moved 

Soils with poor drainage of surface water +

Calcareous soils +

Alluvial soils derived from loam and clay +

sediments (alkaline pH)

Optimum grazing conditions +

Poor grazing conditions + +

A wet spring that was followed by a summer +

drought

A “dry period” that was not followed by a +

“wet period”

A “dry period” that was followed +

immediately by a “wet period”

High ambient temperature immediately + +

preceding and during the outbreak

Late summer and fall season +

Mid-summer to late-summer season + + + + +

Permanent bodies of water; lowland +

swamps; coastlines

Sunlit grassy marshes, open pools of stream + +

beds, especially in irrigated areas

Wooded land on the affected premises +

Incomplete drainage-lake type hydrographic +

region

High relative humidity (90%) + + +

Increased annual ambient temperature + + +

Increased annual precipitation + +

Ecological Observation Livestock Wildlife

EEE WEE VEE SLE Anthrax Leptospirosis Cryptosporidiosis

Viral (i.e., Arbovirus) Bacterial Parasitic

Table 3. Ecological and climatic observations1 during: (1) enzootic and epizootic transmission of selected arbovirus diseases that are prevalent in the

U.S., Canada, Mexico, and Central America, (2) epizootic transmission of anthrax in livestock and wildlife in the U.S., Canada, and Africa, and (3)

epizootic transmission of leptospirosis and cryptosporidiosis.

19
1

 Use of the word “ observation(s) ” should not be equated with use of the words “risk factor(s)”. EEE, eastern equine encephalitis; WEE, western equine

encephalitis; VEE, Venzuelean equine encephalitis; SLE, St. Louis encephalitis. ?, inconclusive

Floods (e.g., excessive short-term rainfall) ?

Absence of UV light, UV sunlight +

Warm ambient temperature +

Moist environment containing static water +

Nearly neutral pH in the environment +

Poorly drained swamps that were located +

directly on, or immediately adjacent to,

affected premises

Ecological Observation Livestock Wildlife

EEE WEE VEE SLE Anthrax Leptospirosis Cryptosporidiosis

Viral (i.e., Arbovirus) Bacterial Parasitic

Table 3. Ecological and climatic observations1 during: (1) enzootic and epizootic transmission of selected arbovirus diseases that are prevalent in the

U.S., Canada, Mexico, and Central America, (2) epizootic transmission of anthrax in livestock and wildlife in the U.S., Canada, and Africa, and (3)

epizootic transmission of leptospirosis and cryptosporidiosis.

20
The three arbovirus diseases of primary concern to human health in the U.S. are WEE,

EEE, and SLE. Both WEE and EEE also are of concern to the health of horses, other livestock,

and some domesticated avian species. Each of these diseases has a distinct ecology that involves

different mosquito species, different amplifier hosts, and other factors that affect (by either

promoting or inhibiting) transmission of the infection. While concerns about the risk of disease

transmission by vector species may increase during natural disasters, natural disasters in the

continental United States have been accompanied only rarely by outbreaks of

mosquito-transmitted diseases of humans (Centers for Disease Control and Prevention, 1993a;

Centers for Disease Control and Prevention, 1994).

One investigation of the incidence of vector-borne diseases of animals and humans was

done during 12 natural disasters that occurred in the United States from 1975 to 1997 (Nasci and

Moore, 1998). The three types of natural disasters that were examined were floods, hurricanes,

and tropical storms. Surveillance for arboviruses was undertaken during 11 of the 12 natural

disasters (Table 4). Although most of the disasters, and therefore the surveillance programs,

were confined to three states or fewer, as many as seven states were involved in some of the 11

disasters. Arbovirus activity (i.e., for WEE, EEE, SLE) was detected in mosquitoes and sentinel

chickens during nine of the 11 disasters in which surveillance was undertaken. What is not clear is

whether a similar level of arbovirus activity also was detected in these same nine locations during

years in which there were no natural disasters. Regardless, human cases of arbovirus disease were

diagnosed during only two of the nine natural disasters during which arbovirus activity was

detected. There were 55 reported cases of WEE and 12 reported cases of SLE in humans in

North Dakota and Minnesota during the Red River flood of 1975, and there was only one case of 

EEE in humans during Hurricane Fran in North Carolina in 1996 (Table 4). Surveillance for SLE

and dengue fever in humans during Hurricane Andrew in 1992 failed to show an increased

incidence of either disease (Heath, 1999). During Hurricane Hugo in 1989, the most prevalent

problem related to insects was not infectious diseases, but insect bites and stings from nuisance

mosquitoes, hornets, wasps, and bees.

Regarding the veterinary cases that were examined by Nasci and Moore, arbovirus

diseases were diagnosed during four of the nine disasters in which arbovirus activity was detected

in mosquitoes and sentinel chickens. WEE was diagnosed in approximately 281 animals during

the Red River flood of 1975. The exact number of animals that were diagnosed with arbovirus

disease during the other three natural disasters was not reported (Table 4). While the number of

disease outbreaks in animals was greater than in humans (i.e., four versus one), there was only

one natural disaster involving flooding to which significant animal morbidity and mortality due to

arbovirus disease was attributed (i.e., WEE in North Dakota and Minnesota during the Red River

flood of 1975). Each of the other three natural disasters lead to excessive accumulations of

water, but in addition to excessive accumulations of water, outbreaks of arbovirus disease can be

influenced by other factors such as topography, the types of bodies of water, and the season of

year. In comparison to the Red River flood, the differences in these factors during the other three

natural disasters may account for the lower number of incident cases of vector-borne disease that

were identified.

21
1997 CO Summer floods Yes WEE in chickens None None

1996 NC Hurricane Fran Yes EEE in mosquitoes 1 EEE EEE in horses

1996 OR, WA Winter flood No No None None

WEE, SLE in None None

chickens; WEE in

mosquitoes

1996 CA Winter flood Yes

WEE, SLE in None WEE

sentinels

Winter and spring Yes

floods

1995 CA

EEE in horses

and emus

Tropical storm Yes EEE in AL and FL None

Alberto

1994 AL, FL, GA

WEE in SD; None None

SLE in IL

Mississippi, Yes (7 states)

Missouri River

flood

1993 Midwestern U.S.

SLE, WEE in None None

mosquitoes

1993 AZ Gila River flood Yes

1992 FL, LA Hurricane Andrew Yes None None None

EEEX in None No data

mosquitoes

1989 Southeastern U.S. Hurricane Hugo Yes

281 WEE

(estimated)

55 WEE;

12 SLEW

WEEU in

mosquitoes

1975 ND, MN Red River flood Yes

Veterinary

Cases

Pathogen or Human Cases

Disease

Year Region Event Surveillance?

Table 4. Veterinary and human cases of vector-borne diseases during 12 natural disasters that lead to excessive accumulations of water in the

continental United States from 1975 through 1997.*

22
Source: From Nasci and Moore, Emerging Infectious Diseases, 1998. Reproduced with permission. *Surveillance data collected by the Division of

Vector-Borne Infectious Diseases, Centers for Disease Control and Prevention (CDC). State and local health departments assisted during emergency

response. Federal Emergency Management Agency and Emergency Response Coordination Group, National Centers for Environmental Health, CDC,

provided field support. UWestern equine encephalitis. WSt. Louis encephalitis. XEastern equine encephalitis.

1997 ND, MN Red River flood Yes (sporadic) None reported None None

Veterinary

Cases

Pathogen or Human Cases

Disease

Year Region Event Surveillance?

Table 4. Veterinary and human cases of vector-borne diseases during 12 natural disasters that lead to excessive accumulations of water in the

continental United States from 1975 through 1997.*

23
Another investigation of the incidence of vector-borne diseases of horses and humans

during a natural disaster was done in Nebraska in 1994-1995, following the Midwest flood of

1993 (Janousek and Kramer, 1998). WEE virus was isolated from 1.29 percent of 2,788 pools of

Culex mosquitoes, and SLE virus was isolated from 0.14 percent of 1,359 pools. All arboviruses

that were isolated were from Culex tarsalis Coquillett, a major vector of WEE and SLE. No

incident cases of WEE were reported in horses in Nebraska in 1994-1995. Neither were there

reported cases of WEE or SLE in humans in Nebraska in 1994-1995. In yet another

investigation, there was no reported EEE and SLE virus activity during Hurricane Andrew in

1992. This surveillance program involved monitoring wild birds for exposure to virus (Centers

for Disease Control and Prevention, 1993a).

Hurricane Floyd in North Carolina in 1999 is one of the most recent natural disasters that

involved widespread flooding of animal and human populations. The median number of cases per

year of EEE, WEE, and SLE in humans in North Carolina from 1964-1997 was 1.5, 0, and 1.0,

respectively (Centers for Disease Control and Prevention, 1999). During the year of Hurricane

Floyd and the two years after Hurricane Floyd (i.e., 2000, 2001), there was no evidence that the

number of human cases of EEE in North Carolina increased (North Carolina Department of

Environment and Natural Resources, 2001). The incidence of WEE and SLE in North Carolina

was rare prior to Hurricane Floyd and remained so after the hurricane. Because these data for

years 1999, 2000 and 2001 do not indicate an apparent increase in the number of cases of 

arbovirus disease in humans in North Carolina, the incidence of these diseases could not be linked

to Hurricane Floyd in a temporal sense.

In general, arbovirus surveillance in animal populations in the U.S appears to be much less

refined than it is in the human population (Personal communication, Eileen Ostlund, USDA

National Veterinary Services Laboratory, 2001). Thus, a comparison of animal surveillance data

during the pre-natural disaster, natural disaster, and post-natural disaster periods would be

significantly less reliable than a comparison of human surveillance data from these same periods of

time. Nonetheless, it seems appropriate to conclude that during the past 25 years there was only

one natural disaster involving flooding to which significant human and animal morbidity and

mortality due to arbovirus disease was attributed. That disaster was the Red River flood of 1975.

The weather conditions that have been observed most frequently during anthrax outbreaks

differ depending on whether the affected animals are domestic species or wildlife. During anthrax

outbreaks in livestock, high ambient temperatures, calcareous soils, and a dry period which may

or may not have been followed by a wet period are some of the conditions that have been

observed most frequently (Table 3). During anthrax outbreaks in wildlife, a wet spring followed

by a summer drought, and either poor grazing conditions or optimum grazing conditions have

been observed frequently. Weather conditions that are common to anthrax outbreaks in both

livestock and wildlife are mid-summer to late summer season, high ambient temperature

immediately preceding and during the outbreak, and poor grazing conditions. The extent to

which any one or various combinations of these factors increases the risk of outbreaks of anthrax

is not clear. It seems appropriate to conclude that natural disasters, particularly floods and

droughts, would not favor outbreaks of anthrax since neither floods nor droughts produce the

wet/dry cycle which has been hypothesized to be essential for anthrax outbreaks to occur.

24
Cryptosporidiosis is endemic in animals in the U.S. Localized outbreaks are common, but

scientific reports of widespread outbreaks of cryptosporidiosis in animals are rare. The largest

outbreaks of cryptosporidiosis in humans in the U.S. in which water was the source of the

infection have not been linked to contamination of the water by waste products from domestic

animal populations, neither during natural disasters such as flooding, nor otherwise. The

“suspected cause” of each outbreak was categorized either as : (1) a water treatment deficiency

(ies), (2) contamination by human sewage, or (3) undetermined. Regardless of the source of each

outbreak, the solution to reducing waterborne outbreaks of cryptosporidiosis in humans lies in

adhering to firmly established, conventional water treatment practices (Rose et al., 1993; Rose et

al., 1997). There are other potential routes of transmission of cryptosporidiosis from animals to

humans, but these routes of transmission are influenced minimally to none by natural disasters

such as flooding.

There is little scientific evidence that links natural disasters in the U.S. to significant and

consistent increases in the incidence of infectious diseases of animals that are frequently discussed

during these disasters (e.g., vector-borne diseases, anthrax, leptospirosis, cryptosporidiosis, etc.).

The massive destruction of the crop ecosystems due to Hurricane Floyd in North Carolina in 1999

suggests that neither human-derived ecosystems nor natural ecosystems can be protected with

ease from the path of destruction of natural disasters such as floods, hurricanes, extreme heat,

extreme cold, and fires. Thus, the destruction caused by the natural disasters might in fact destroy

the human-derived and natural ecosystems which harbor infectious disease pathogens and their

vectors. Consequently, the risk of outbreaks of infectious disease in geographic regions that have

been overcome by natural disasters may not increase. Instead, the risk of outbreaks of infectious

disease in such regions may decrease, either temporarily and sometimes permanently.

25
Non-Infectious Hazards of Concern During Natural Disasters

Introduction

Two non-infectious diseases of animals that are commonly discussed during natural

disasters are aspiration pneumonia and injuries (Heath, 1999). Morbidity and mortality due to

non-infectious diseases can be attributed to excesses of water, excesses of wind, lightning,

deficiencies of water, heat extremes, fires and earthquakes. The animal health problems that may

arise due to these natural disasters include drowning, hyperthermia, burns, hypothermia, and

traumatic injuries (Figure 1).

Water Excesses (Floods)

Several thousand dairy cows perished during floods in Snohomish Valley, Washington in

1991 (Heath, 1999). Approximately 1,200 dairy cows perished during floods in Tilamook,

Oregon in 1996. During 1997, approximately 90,000 beef cows died during floods in Minnesota,

North Dakota, and South Dakota.

It is likely that some of the most recent and significant economic losses from livestock

deaths due to a natural disaster occurred during Hurricane Floyd in North Carolina in 1999.

Approximately 40 of the 100 counties in North Carolina experienced flooding during Hurricane

Floyd (Hudson et al., 2001). The total estimated value of livestock that died was $13 million

(Table 5). However, the total number of livestock deaths “. . . represented a small percentage . . .

“ when compared to North Carolina’s total livestock population (North Carolina Department of

Agriculture and Consumer Services, 1999).

Morbidity and mortality of pets during floods appears to be much more rare than livestock

deaths (Heath, 1999). Hypothermia is the most frequently reported illness of all animals that are

rescued from floodwaters. The actual number of reports of pets that have drowned during floods

is no more than ten (Heath, 1999). While this number would appear to be surprisingly small, it

does seem to be consistent with there being minimal reference to companion animal mortality that

may have been caused by Hurricane Floyd (Hudson et al., 2001). During Hurricane Floyd, a

disaster relief management program was established by the North Carolina State University

College of Veterinary Medicine for approximately 467 animals (375 dogs, 75 cats, and 17 animals

of other species) that were affected by the flood. The source of at least 130 of the animals that

were managed by the disaster relief management team was a crowded county animal shelter that

became flooded. That the source of these animals was a crowded shelter suggests that many of

the animals may have been separated involuntarily from their owners prior to the onset of

Hurricane Floyd. Still other animals may have become separated from their owners voluntarily

(i.e. abandoned) prior to the onset of Hurricane Floyd.

26
Source: http://www.agr.state/nc.us/state/c%26lloss.htm . NA = not available.

Total $13,012,172

Aquaculture NA $100,000

Cattle 1,180 $495,600

Turkeys 752,970 $7,153,215

Chickens 2,107,857 $3,583,357

Hogs 28,000 $1,680,000

Livestock Number of Deaths Cost ($)

Table 5. Estimated value of livestock and aquaculture species that died during Hurricane

Floyd in North Carolina in 1999.

Source: Heath, Animal Management in Disasters, 1999. Revised, with permission.

Total 122 100.0

Eyes 7 6.7

Upper fore limb 7 6.7

Head and neck 16 15.4

Upper hind limb 16 15.4

Torso 26 25.0

Lower hind limb 32 30.8

Anatomical Location Number of Injuries Percent of Total

Table 6. Anatomical location of injuries on horses admitted to an emergency health care

facility after Hurricane Andrew in Florida in 1992.

27
Approximately 300 of the 450-plus animals that were admitted to the field hospital were

adopted after Hurricane Floyd. Prior to adoption, 99 percent of the 300 animals had not

undergone spay/neuter, and more than 99 percent had not been vaccinated against rabies. A

logical question is whether the demand for the many types of fundamental health care services that

were provided to the animals by this veterinary medical assistance team could be attributed more

directly to animal abandonment and neglect that was present prior to Hurricane Floyd, rather than

to problems that were caused directly by Hurricane Floyd? Technically speaking, it appears that

many of the animals may have been “owned”, but they were permitted to roam freely and received

minimal veterinary medical care even prior to Hurricane Floyd (Personal communication, Lola C.

Hudson, North Carolina State University College of Veterinary Medicine, 2001).

Morbidity in humans was investigated during a severe thunderstorm in central Texas

during October, 1998 (Centers for Disease Control and Prevention, 2000). Of the 31 human

deaths, 29 were attributed directly to the thunderstorm, and two deaths were attributed indirectly

to the thunderstorm. Of the 29 deaths attributed directly to the thunderstorm, 83 percent (N =

24) were due to drowning, 10 percent (N = 3) were due to multiple traumatic injuries, 3 percent

(N = 1) were due to hypothermia, and 3 percent (N = 1) were due to cardiac arrhythmia.

Wind Excesses (Hurricanes, Tornadoes)

Damage from hurricanes may be due to: (1) direct damage from winds and rains that

generate flying debris and destroys structures, (2) direct damage from storm surge that leads to

flooding, and (3) secondary damage from electrocutions and hazardous materials during activities

that are aimed at restoration (Heath, 1999). Veterinary medical facilities are not immune to

hurricanes and tornadoes. An intact veterinary infrastructure is an essential prerequisite for

veterinary practices to provide services to injured animals and to coordinate relief efforts. Thus,

the single most important veterinary issue after a hurricane is to reestablish compromised

veterinary infrastructure.

The most prevalent health problem of animals that is caused by the wind forces generated

during hurricanes is trauma. Traumatic injuries were common after Hurricane Andrew in Florida

in 1992 and after Hurricane Fran in North Carolina in 1996. These injuries may be caused by

flying objects during hurricanes, or they may result from direct encounters with scattered debris

after the hurricane. Approximately 2000 pets received medical care for lacerations, fractures, and

urinary tract infections after Hurricane Andrew. Lower-limb injuries were the most prevalent type

of injury in horses (Table 6). However, the baseline incidence (i.e., pre-hurricane) and the

recovery-period incidence (i.e., post-hurricane) of these problems in the companion animals and

horses should be considered in evaluating the proportion of these problems that should be

attributed to hurricanes.

Both mortality and morbidity in humans were investigated during Hurricane Andrew in

Louisiana during August 1992 (Centers for Disease Control and Prevention, 1993b). Of 17

human deaths attributed to Hurricane Andrew, only nine occurred after landfall; 67 percent of

these were due to drowning, 11 percent were due to impact injury, 11 percent were due to crush

injury, and 11 percent were not categorized. The most prevalent, non-fatal, health problem was

28
categorized as cut/laceration/puncture wound, followed by strain/sprain. Sixty-percent of the

non-fatal health problems were confined to the extremities.

Lightning

Livestock and horses are the domestic animals that are most likely to be struck by

lightning because they reside outdoors (Heath, 1999). These animals are especially vulnerable if

they are confined near large, free-standing trees. If the animals have free access to the base of the

trees, they will congregate there during thunderstorms to protect themselves from rain and hail. If

lightning strikes the trees, the electricity can be conducted through the animals’ bodies enroute to

the earth. Lightning stroke in cattle is frequently fatal.

Water Deficiencies (Droughts)

A practical definition of drought is when precipitation and other water resources fall

below expectations, and this expectation is not met by a concomitant decrease in demand for

water (Heath, 1999). Droughts may be the most expensive natural disaster to the animal

industries in the U.S. because droughts tend to be more widespread in their geographical

distribution (Heath, 1999). Decreased availability of forage, decreased growth rates, and

decreased productivity are consequences of drought. During droughts, the greatest losses in

cattle production are from starvation. However, the scarcity of forage during droughts means

that livestock, horses, and wildlife may consume toxic plants. Drought-related poisonings of

cattle include salt poisoning, urea poisoning, nitrate poisoning, cyanide poisoning, selenium

poisoning, and rumen impaction (Heath, 1999; Howard and Smith, 1999).

Heat Extremes

Extreme heat is defined as an ambient temperature that is at least 5.5o C (i.e., 10o F) 

higher than the average high temperature for a specific geographical location (Heath, 1999).

There are differences in the average temperature in different geographical locations and at

different times of the year in the U.S; thus, the absolute temperature that should be used to define

extreme heat varies with the location. Although extreme heat occurs typically during the summer

months, high ambient temperatures even during the cool months may have the same adverse

biological affects on animals, if the animals have not had an opportunity to adapt to these

temperatures.

Hyperthermia, a body temperature of 42.0o C or 107.0o F, is a primary outcome of

extremely high ambient temperatures. Cattle mortality due to hyperthermia occurred in California

in 1977. The mortality increased significantly in a dairy herd during four consecutive days of

intense heat, and a total of 725 milking cows perished. Similarly, the mortality increased

significantly in feedlot cattle in Iowa and Nebraska during a period of intense heat in July 1995. A

total of 10,000 feedlot cattle perished, 3,750 within a single day (Bopp, 2001; Wren, 1997). The

estimated losses to livestock producers in central Iowa was $28 million, and the estimated losses

to poultry producers was $25 million. Another indicator of the impact of extreme heat is an

29
increase in rendering activity. The number of dairy cow carcasses that were rendered each week

during a heat wave in Wisconsin increased from 400 to 15,000 (Heath, 1999).

Ruminants do not sweat, so panting is the mechanism by which they avoid abnormal

increases in body temperature during environmental heat extremes. However, the increased air

exchange increases their susceptibility to the bovine respiratory disease complex. Experience has

shown that there are three critical factors that determine if feedlot fatalities will occur either

directly or indirectly from heat extremes (Bopp, 2001). These three factors are: (1) intensity of

heat, (2) duration of the heat extreme, and (3) opportunities at night for cattle to recover from

exposure to the heat extreme. Intensity is a function of the ambient temperature in combination

with humidity. Rainfall immediately prior to onset of a heat wave has been associated with high

percent mortality because the humidity will increase greatly. Approximately 72 consecutive hours

of extreme heat also has been associated with increased percent mortality. However, if the

ambient temperature decreases at night to 700 F or lower, feedlot cattle can recover from the

effects of exposure to the heat extremes that may have taken place during daylight hours. The

lower ambient temperature, although transient, will diminish the cumulative biological effects of

the heat.

Fires

Fires are classified as to whether they occur in buildings, wildlands, or elsewhere (Heath,

1999). The greatest impact of wildland fires (i.e., forest fires and wildfires) is on wildlife and the

environment, not domestic animals and humans. However, as urban dwellers, who will be

accompanied by their domestic animals, continue to encroach on natural environments, the impact

of forest fires and wild fires on the domestic animal population may increase.

The number of reported injuries to animals from fires is low, suggesting that injuries that

require medical therapy are rare. Burn injuries of horses and cats are reported more frequently

than of other species. Reports of burn injuries in horses are most frequently of extensive wounds

to the skin. The sequellae to burn injuries in horses include pulmonary edema, oliguria, polyuria,

infections, and anemia.

Earthquakes

The reports of animal injuries following earthquakes are mostly anecdotal (Heath, 1999).

Regardless, the impact of earthquakes on animal health in the U.S. appears to be small. Among

the medical problems associated with the Northridge earthquake in California were bruises and

fractures due to blunt-force trauma, wing-tip injuries to birds that had been housed in cages that

became dislodged, lacerations from broken glass, and prolonged hiding. While specific numbers

of injured animals have not been reported, the numbers do appear to be rather small. Infectious

diseases, especially tetanus, are a sequela to traumatic injuries (e.g., lacerations). Generally

speaking, horses are more susceptible to tetanus than are most other domestic species. Two

non-medical problems that were observed during the Northridge earthquake were animals that

strayed from damaged confinements and the excessive number of animals that became available

for adoption.

30
Conclusion

There is little scientific evidence that links natural disasters that have occurred in the U.S.

to significant and consistent increases in the incidence of infectious diseases of animals. The

transmission of infectious diseases at a level that is sufficient to alter the incidence from a sporadic

level to an enzootic level, and from an enzootic level to an epizootic level can be a complex

mixture of natural and human-made events. The complexity of these events may be even more

true for vector-borne infectious diseases which, again, are one group of diseases for which there

seems to be significant concern during natural disasters (Heath, 1999).

There are numerous ecological and climatic factors that have been observed during

epizootics of vector-borne and non-vector-borne infectious diseases. Some factors have been

observed rather consistently. Others have been observed far less consistently. Regardless, mere

observation of these climatic conditions during an outbreak does not necessarily imply that the

outbreak was caused by the climatic conditions. Nor have these observations, in and of

themselves, proven thus far to be very valuable in predicting whether an outbreak of infectious

disease will occur during a natural disaster. Attempts to rationalize the relationship between

weather, vector biology, and arboviral recrudescence have been summarized by a vector-borne

disease entomologist as “. . . the hope that weather forecasting and weather analysis might

eliminate the element of surprise in arboviral epidemics. The sobering truth is that arboviral

epidemiology is a complex, multifactorial process, and that coincidental events involving some or

all variables are the true precipitating factors for recrudescence . . . an aggressive approach is

clearly required to convert the wealth of random speculation on the weather/recrudescence

relationship into useful information.” (Reiter, 1988).

Based on data available from studies of natural disasters, the apparent morbidity and

mortality in animal populations that has been caused by non-infectious diseases, while involving

an almost insignificant percentage of the total population in affected geographical regions, is much

higher than the apparent morbidity and mortality that has been caused by infectious diseases. One

explanation is that, generally speaking, the sequence of events from a cause (e.g., excesses of

water) to an effect (e.g., drowning) for non-infectious diseases is more simple, direct, and

recognizable than the complex sequence of events that lead to major outbreaks of infectious

diseases (e.g., EEE). The epidemiological evidence suggests that the potential economic impact

of non-infectious diseases arising from natural disasters may be greater than the economic impact

of infectious diseases. While vigilant surveillance for outbreaks of infectious diseases during

natural diseasters should not be discouraged, there should be appropriate resources allocated

towards the resolution of issues related to the prevention, control and treatment of non-infectious

diseases during natural disasters.

31
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36
Appendix

WThese readings will be available at http//www.aphis.usda.gov/vs/ceah/cei by summer 2002.

Ecology and Epidemiology of Cryptosporidiosis

Ecology and Epidemiology of Leptospirosis

Ecology and Epidemiology of Anthrax

Ecology and Epidemiology of St. Louis Encephalitis

Ecology and Epidemiology of Venzuelan Equine Encephalomyelitis

Ecology and Epidemiology of Western Equine Encephalomyelitis

Ecology and Epidemiology of Eastern Equine Encephalomyelitis

Title

Table 7. Supplemental readings about the ecology and epidemiology of various infectious

diseases of animals that are of concern during natural disasters. W

37
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