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Chapter 7 - Avian Cholera

Authors: Milton Friend.

Information available:

Synonyms

Fowl cholera, avian pasteurellosis, avian hemorrhagic septicemia.

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Cause

Avian cholera is a contagious disease resulting from infection by the bacterium Pasteurella multocida. Several subspecies of bacteria have been proposed for P. multocida, and at least 16 different P. multocida serotypes or characteristics of antigens in bacterial cells that differentiate bacterial variants from each other have been recognized. The serotypes are further differentiated by other methods, including DNA fingerprinting. These evaluations are useful for studying the ecology of avian cholera (Fig. 7.1), because different serotypes are generally found in poultry and free-ranging migratory birds. These evaluations also show that different P. multocida serotypes are found in wild birds in the eastern United States than those that are found in the birds in the rest of the Nation (Fig. 7.2).

Acute P. multocida infections are common and they can result in bird deaths 6–12 hours after exposure, although 24–48 hours is more common. Susceptibility to infection and the course of disease — whether or not it is acute or chronic — is dependent upon many factors including sex, age, genetic variation, immune status from previous exposure, concurrent infection, nutritional status, and other aspects of the host; strain virulence and other aspects of the bacterium; and dose and route of exposure. Infection in poultry generally results when P. multocida enters the tissues of birds through the mucous membranes of the pharynx or upper air passages. The bacterium can also enter through the membranes of the eye or through cuts and abrasions in the skin. It is assumed that transmission is similar in wild birds.

Environmental contamination from diseased birds is a primary source for infection. High concentrations of P. multocida can be found for several weeks in waters where waterfowl and other birds die from this disease. Wetlands and other areas can be contaminated by the body discharges of diseased birds. As much as 15 milliliters of nasal discharge containing massive numbers of P. multocida have been collected from a single snow goose. Even greater amounts of bacteria enter the environment when scavengers open the carcasses of diseased birds. Avian cholera can be transmitted within this contaminated environment in several ways. Ingestion of bacteria in contaminated food and water, including scavenging of diseased carcasses, is an important source of infection for wild birds. The disease can be transmitted by direct bird-to-bird contact, either between infected and noninfected live birds, or between infected carcasses that serve as "decoys" and noninfected live birds. Aerosol transmission is also thought to take place. In wetlands where avian cholera breaks out, the highest concentrations of P. multocida are found near the water surface rather than deep in the water column. Birds landing, taking flight, bathing, and otherwise causing disturbance of the water surface cause bacteria-laden aerosols, which can serve to infect those birds. Other means for transmission of avian cholera have also been reported, each of which may occur for specific situations, but none of which are primary means for disease transmission in wild birds (Fig. 7.3).

The role of disease carriers as a means for initiating avian cholera outbreaks in wild birds has long been postulated because chronically infected birds are considered to be a major source for infection of poultry. It has been reported that the only limit to the duration of the chronic carrier state is the lifespan of the infected bird. Disease carriers have been conclusively established for poultry, and P. multocida can commonly be isolated from the mouth area or tonsils of most farm animals, dogs, cats, rats, and other mammals (Fig. 7.4). However, types of P. multocida that are found in most mammals do not generally cause disease in birds (see Species Affected, this chapter). The role of disease carriers among migratory species of wild birds has long been suggested by the patterns of avian cholera outbreaks in wild waterfowl, but it has not been clearly established by scientific investigations. Recent findings by investigators at the National Wildlife Health Center (NWHC) have provided evidence that disease carriers exist in snow goose breeding colonies. Shedding of P. multocida by disease carriers is likely to be through excretions from the mouth, which is the area where the bacteria are sequestered in carriers and is the means for dissemination of P. multocida by poultry. Poultry feces very seldom contain viable P. multocida, and there is no evidence that P. multocida is transmitted through the egg.

Figure 7.1 Distribution of Pasteurella multocida serotypes from 561 wild bird isolates from the United States
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Figure 7.2 Distribution of Pasteurella multocida serotypes from 561 wild birds isolated by waterfowl flyway
Click Illustration for full-page view

 

Figure 7.3 Potential means for transmission of avian cholera to free-ranging wild birds
Route of transmission and field situation Comments
Bird-to-bird contact Secretions from infected birds shedding P.multocida.

Requires close contact, such as when individuals struggles over aquatic plants that they are feeding on.

Ingestion Probably the most common route for transmission.

Consumption of diseased carcasses by scavengers and predators.
Ingestion of P. multocida in food and water from contaminated environments.

Aerosol May be important in heavily contaminated environments, such as during major die-offs.

Activities that result in splashing of surface waters result in bacteria-laden sprays when water becomes contaminated.

Insects Biting insects that feed on birds after having fed on contaminated carcasses or contaminated environments (ticks, mites, flies).

Insects fed upon by birds (maggots, flies) following ingestion of P. Multocida by the insect when feeding.

Animal bites Not thought to be an important route for infection of wild birds.

Nonfatal bites from small animals, such as raccoon, can result in P. Multocida infections that become systemic and possibly initiate disease outbreaks.

Thought to occur in some domestic turkey flocks, not yet demonstrated in wild birds.

Fomites
(inanimate objects)
Contaminated cages, equipment, clothing used in field operations can serve as mechanical transport mechanisms for introducing P. multocida

Environmental persistence of P. multocida is sufficient for this to be a consideration when personnel and equipment are used to combat and avian cholera outbreak and then are to be redirected for other activities

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Species Affected

It is likely that most species of birds and mammals can become infected with P. multocida; however, there are multiple strains of this bacterium and those different strains vary considerably in their ability to cause disease in different animals. These differences are most pronounced for cross-infections between birds and mammals. Strains isolated from birds will usually kill rabbits and mice but not other mammals. Strains isolated from cattle and sheep do not readily cause clinical disease in birds. However, some strains from pigs have been shown to be highly virulent (very few organisms cause serious disease) for poultry. Also, cultures from the mouths of raccoons were pathogenic or caused disease in domestic turkeys. Bite-wound infections by raccoons have been postulated as a source of avian cholera outbreaks in poultry. An interspecies chain of avian cholera transmission has been described in free-ranging California wildlife that involved waterbirds, mice, and avian scavengers and predators (Fig. 7.5).

More than 100 species of free-ranging wild birds are known to have been naturally infected with P. multocida (Fig. 7.6) in addition to poultry and other avian species being maintained in captivity. Infection in free-ranging vultures has not been reported, although a king vulture is reported to have died from avian cholera at the London Zoo. As a group, waterfowl and several other types of waterbirds are most often the species involved in major avian cholera mortalities of wild birds. Scavenger species, such as crows and gulls, are also commonly diagnosed with avian cholera, but deaths of raptors, such as falcons and eagles, are far less frequent (Fig. 7.7). However, there have been several reports of avian cholera in birds kept by falconers, both from birds consuming infected prey when being flown and from being fed birds that died from avian cholera. Waterfowl and coots experience the greatest magnitude of wild bird losses from this disease (Fig. 7.8). In general, species losses during most major outbreaks are closely related to the kinds of species present and to the numbers of each of those species present during the acute period of the die-off. During smaller events, although several species may be present, mortality may strike only one or several species and the rest of the species that are present may be unaffected. Major outbreaks among wild birds other than waterbirds are uncommon.

Impacts on population levels for various species are unknown because of the difficulty of obtaining adequate assessments in free-ranging migratory birds. However, the magnitude of losses from individual events and the frequency of outbreaks in some subpopulations have raised concerns about the biological costs from avian cholera. Disease that is easily spread through susceptible hosts can be devastating when bird density is high, such as for poultry operations and wild waterfowl aggregations (Fig. 7.9). Mortality from avian cholera in poultry flocks may exceed 50 percent of the population. An outbreak in domestic geese killed 80 percent of a flock of 4,000 birds. Similar explosive outbreaks strike in free-ranging migratory birds. Peak mortality in wild waterfowl has exceeded more than 1,000 birds per day.

Studies by researchers at the NWHC indicate that some flocks of snow geese wintering in California have significantly reduced survival rates because of this disease. Evaluation of band returns from midcontinent white-fronted geese and field assessments of other waterfowl populations also suggest decreased survival rates due to avian cholera during some years. Avian cholera has periodically caused heavy losses of breeding eiders and these outbreaks devastate those colonies.

Avian cholera is clearly an important disease of North American waterfowl and it requires more intensive studies to adequately assess impacts on population dynamics. Avian cholera now rivals avian botulism for the dubious honor of being the most important disease of North American waterfowl. Its threat to endangered avian species is continually increasing because of increasing numbers of avian cholera outbreaks and the expanding geographic distribution of this disease.

Figure 7.4 Partial list of domestic species and wild mammals from which Pasteurella multocida has been isolated.
Domestic animals Cattle, horses, swine, goats, sheep,
Dogs, cats,
Gerbils, rabbits.
Big game Elk and deer,
Caribou and reindeer,
Bighorn sheep,
Bison,
Pronghorn antelope.
Carnivores Bears,
Lynx, bobcat, puma,
Foxes,
Weasels, mink,
Raccoon.
Rodents Rats, mice, voles,
Muskrats, nutria,
Chipmunks.
Pinnipeds Sea lions, Fur seals.
Rabbits Cottontail rabbits.
Domestic poultry Chickens, turkeys,
Ducks, geese,
Pigeons.

 

Figure 7.5 Example of an interspecies chain for transmission of avian cholera that occurred in California wetland.
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Figure 7.6 Free-ranging wild birds that have been diagnosed with avian cholera.
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Figure 7.7 Relative occurrence of avian cholera in wild birds.
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Distribution

Avian cholera is believed to have first occurred in the United States during the middle to late 1880s, but it was unreported as a disease of free-ranging migratory birds prior to the winter of 1943–44 when many waterfowl died in the Texas Pan handle and near San Francisco, California. Avian cholera outbreaks involving free-ranging wild birds have now been reported coast-to-coast and border-to-border within the United States. Although avian cholera is found in many countries, there have been few reports in the scientific literature of die-offs from avian cholera affecting free-ranging wild birds in countries other than the United State and Canada. This disease undoubtedly causes more infections and deaths than are reported, and it is an emerging disease of North American free-ranging migratory birds.

Sporadic cases of avian cholera have been documented in the United States since the early 1940s, and perhaps before, in species such as crows, starlings, grackles, sparrows, and other birds that are closely associated with poultry operations. Most of these wild species are now seldom found to be infected, perhaps due to changes in poultry husbandry and waste disposal practices. Avian cholera also broke out in California in free-ranging quail during the early 1940s and in cedar waxwings in Ohio during 1968. However, waterfowl are the primary species that are affected by this disease.

The emergence of avian cholera as a significant disease for North American waterfowl began about 1970. The frequency and severity of avian cholera outbreaks vary greatly among years and geographic areas but the pattern of continual spread is of major concern (Fig. 7.10). The first outbreaks in eastern Canada involving wild waterfowl were reported during 1964 in eiders nesting on islands in the St. Lawrence Seaway. The first outbreaks in western Canada took place in snow geese during 1977; this disease has occurred annually in western Canada ever since. Several suspect diagnoses of avian cholera have been reported for waterfowl mortality events in Mexico during recent years, but these events lack laboratory confirmation. The absence of confirmed reports of this disease in wild waterfowl in Mexico is likely due to lack of surveillance and reporting rather than to the absence of avian cholera.

In the United States, there are four major focal points for avian cholera in waterfowl: the Central Valley of California; the Tule Lake and Klamath Basins of northern California and southern Oregon; the Texas Panhandle; and Nebraska’s Rainwater Basin below the Platte River in the south-central part of the State. The movement of avian cholera from these areas follows the well-defined pathways of waterfowl movement. The spread of this disease along the Missouri and Mississippi River drainages is also consistent with waterfowl movement. No consistent patterns of avian cholera outbreaks exist within the Atlantic Flyway. There are periodic outbreaks in eider ducks nesting off of the coast of Maine and occasional major die-offs of sea ducks, including eiders, within the Chesapeake Bay of Maryland and Virginia (Fig. 7.11).

Figure 7.8 Examples of major avian cholera outbreaks in wild birds
Click Illustration for full-page view

 

Figure 7.9
Click Photo for full-page view(A) Dense aggregations of waterfowl facilitate the rapid spread of avian cholera because of the highly infectious nature of the disease. Click Photo for full-page view(B) Large-scale mortality has occurred in such situations.

 

Figure 7.10
Click Illustration for full-page view(A) Reported frequency of avian cholera in free-ranging waterfowl in the United States.
Click Illustration for full-page view(B) Reported occurrence of avian cholera in free-ranging migratory birds in the United States.

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Seasonality

Losses can occur at any time of the year. For poultry, outbreaks of avian cholera are more prevalent in late summer, fall, and winter. Those time periods have no special biological associations, except, possibly, with production schedules in response to holiday market demands that influence poultry age-classes within production facilities. Chickens become more susceptible as they reach maturity. Turkeys are much more susceptible than chickens, and turkeys die at all ages, but the disease usually occurs in young mature turkeys. Losses in domestic ducks are usually in birds older than 4 weeks of age.

For wild waterfowl, a predictably seasonal pattern exists in areas where avian cholera has become well established. This pattern is closely associated with seasonal migration patterns and it has resulted in avian cholera becoming a "disease for all seasons," killing waterfowl during all stages of their life cycle (Fig. 7.12). Some areas experience prolonged periods of avian cholera mortality. Outbreaks in California normally start during fall and continue into spring. Other areas have seasonal avian cholera outbreaks in the same geographic location. For example, Nebraska, which has had outbreaks most springs since 1975, now frequently also has outbreaks in the fall.

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Field Signs

Few sick birds are seen during avian cholera outbreaks because of the acute nature of this disease. However, the number of sick birds increases when a die-off is prolonged over several weeks. Sick birds often appear lethargic or drowsy (Fig. 7.13), and they can be approached quite closely before they attempt to escape. When captured, these birds often die quickly, sometimes within a few seconds or minutes after being handled. Other birds have convulsions (Fig. 7.14), swim in circles, or throw their heads back between their wings and die (Fig. 7.15). These signs are similar to those seen in duck plague and in some types of pesticide poisoning. Other signs include erratic flight, such as flying upside down before plunging into the water or onto the ground, and attempting to land a foot or more above the surface of the water; mucous discharge from the mouth; soiling and matting of the feathers around the vent, eyes, and bill; pasty, fawn-colored, or yellow droppings; and blood-stained droppings or nasal discharges, which also are signs of duck plague (duck virus enteritis or DVE).

Always suspect avian cholera when large numbers of dead waterfowl are found in a short time, when few sick birds are seen, and when the dead birds appear to be in good flesh. Death can be so rapid that birds may literally fall out of the sky or die while feeding, with no signs of illness. When sick birds are captured and die within a few minutes, avian cholera should also be suspected. None of the signs described above are unique to this disease; these signs should be recorded as part of any history being submitted with specimens and are considered along with lesions seen at necropsy.

Figure 7.11
Click Illustration for full-page viewThe occurrence of avian cholera in waterfowl seems to be closely related to bird movements west of the Mississippi River. There is no apparent pattern for outbreaks along the Atlantic seaboard.

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Gross Lesions

Under most conditions, birds that have died of avian cholera will have substantial amounts of subcutaneous and visceral fat, except for seasonal losses of fat. The most prominent lesions seen at necropsy are in the heart and liver and, sometimes, the gizzard. Hemorrhages of various sizes are frequently found on the surface of the heart muscle or the coronary band or both (Fig. 7.16). Hemorrhages are also sometimes visible on the surface of the gizzard. Areas of tissue death that appear as small white-to-yellow spots are commonly seen within the liver. Where the area of tissue death is greater, the spots are larger and, in some instances, the area of tissue death is quite extensive (Fig. 7.17).

The occurrence of the abnormalities described for the heart, liver, and gizzard are dependent upon how long the bird lived after it became infected. The longer the survival time, the more abundant and dramatic the lesions. In addition, there may be changes in the color, size, and texture of the liver. There is darkening or a copper tone to the liver, and it may appear swollen and rupture upon handling. Because birds infected with avian cholera often die so quickly, the upper portions of the digestive tract may contain recently ingested food. All of these findings are similar to what might also be seen with duck plague; therefore, laboratory diagnosis is needed.

Freshly dead ducks and geese that have succumbed to avian cholera may have a thick, mucous-like, ropy nasal discharge. The lower portions of the digestive tract (below the gizzard) commonly contain thickened yellowish fluid (Fig.7.18). Both of these fluids are heavily laden with P. multocida and care must be taken to not contaminate the environment, field equipment, or one's self with these fluids.

Figure 7.12
Click Illustration for full-page viewRelative monthly probability for the occurrence of avian cholera in migratory waterfowl, expressed as a percentage of outbreaks throughout the year. Information from the National Wildlife Health Center database.

 

Figure 7.13
Click Photo for full-page viewLethargic appearance of drake northern pintail with avian cholera.

 

Figure 7.14
Click Photo for full-page viewAvian cholera-infected crow in convulsions.

 

Figure 7.15 Avian cholera-infected drake mallard.
Click Photo for full-page view(A) Note tossing of head toward back and circular swimming as evidenced by ripples in water. Click Photo for full-page view(B) Bird at death with head resting on back.

 

Figure 7.16 Hemorrhages of varying degrees of severity are often seen on the hearts of avian cholera-infected birds.
Click Photo for full-page view(A) Pinhead-sized hemorrhages along fatty areas of the heart are readily evident in this bird. Click Photo for full-page view(B) Broad areas of hemorrhage also occur.

 

Figure 7.17 Lesions in the livers of avian cholera-infected birds generally appear as small, discrete, yellowish spots, which are dead tissue. Note the variation in size and appearance of these lesions. (A) Note also the absence of any apparent heart lesions in one bird, (B) only a few minor hemorrhages on the coronary band of another bird, (C) and more extensive hemorrhages on the heart muscle of a third bird. Also note the abundance of fat covering the gizzard of all of these birds. This fat attests to the excellent condition these birds were in before exposure to the bacterium and to the rapidity with which each bird died.
Click Photo for full-page view(A) Click Photo for full-page view(B) Click Photo for full-page view(C)

 

Figure 7.18 The thickened, yellowish fluid present in the intestines of this avian cholera-infected bird contains millions of bacteria. These bacteria contaminate the environment when the carcass decomposes or is scavenged, serving as a source of infection for other wildlife.
Click Photo for full-page view

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Diagnosis

As with all diseases, isolation of the causative agent is required for a definitive diagnosis. A whole carcass provides the diagnostician with the opportunity to evaluate gross lesions seen at necropsy and also provides all appropriate tissues for isolation of P. multocida.

When it is not possible to send whole carcasses, send tissues that can be collected in as sterile a manner as possible in the field. The most suitable tissues for culturing are heart blood, liver, and bone marrow. Remove the entire heart and place it in a Whirl-Pak bag for shipment as identified in (Chapter 2: Specimen Collection and Preservation); do not attempt to remove the blood from the heart. The liver should also be removed and placed in a separate bag. A major portion of this organ (at least half) should be submitted if it cannot be removed intact. These samples must be refrigerated as soon as possible after collection and kept cool during shipment. When shipment is to be delayed for more than 1 day or when transit time is expected to exceed 24 hours, freeze these specimens.

P. multocida persists several weeks to several months in bone marrow. The wings of badly scavenged or decomposed carcasses should be submitted whenever avian cholera is suspected as the cause of death, and when more suitable tissue samples are not available.

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Control

Numerous factors must be considered in combating avian cholera (Fig. 7.19). Avian cholera is highly infectious and it spreads rapidly through waterfowl and other bird populations. This process is enhanced by the gregarious nature of most waterfowl species and by dense concentrations of migratory waterbirds resulting from habitat limitations. The prolonged environmental persistence of this bacterium further promotes new outbreaks (Table 7.1). Pond water remained infective for 3 weeks after dead birds were removed from one area in California; bacterial survival in soil for up to 4 months was reported in another study; and the organism can persist in decaying bird carcasses for at least 3 months.

Figure 7.19
Click Illustration for full-page viewSome of the many interrelated factors associated with avian cholera outbreaks in free-ranging wild birds.

Early detection of avian cholera outbreaks is a first line of defense for controlling this disease. Frequent surveillance of areas where migratory birds are concentrated and the timely submission of carcasses to disease diagnostic laboratories allows disease control activities to be initiated before the outbreaks reach advanced stages. The opportunity to prevent substantial losses is greatest during the early stages of outbreaks, and costs are minimal in comparison with handling a large-scale die-off. Control actions need to be focused on minimizing the exposure of migratory and scavenger bird species to P. multocida and minimizing environmental contamination by this organism.

The NWHC recommends carcass collection and incineration as standard procedures. Carcass collection contributes to avian cholera control in several ways. Several milliliters of fluids containing large concentrations of P. multocida are often discharged from the mouths of birds dying from this disease, resulting in heavy contamination of the surrounding area. Carcass decomposition results in additional contamination. These carcasses attract (decoy) other birds, thereby increasing the probability for infection. Scavenging of carcasses also transmits the disease through the direct consumption of diseased tissue (oral exposure).

Care must be exercised during carcass collection to minimize the amount of fluid discharged from the mouths of birds into the environment. Birds should be picked up head first, preferably by the bill, and immediately placed in plastic bags. Care must also be taken to avoid contaminating new areas while carcasses are transported to the disposal site. Double-bagging is recommended to prevent fluids leaking from punctures to the inner bag. Bags of carcasses should always be securely closed before they are removed from the area.

Prompt carcass removal also prevents scavenging by avian species that can mechanically transport infected material to other sites or by feeding or drinking at other locations following consumption of infected tissue. This situation is aggravated by apparently longer disease-incubation times in gulls, crows, and some other avian scavengers. Instead of dying within hours or 1–2 days after exposure to virulent strains of P. multocida, avian scavengers more typically die after several days to 1–2 weeks, and they may die far from the site of exposure. When these birds die, they may serve as new potential focal points for contamination.

In some instances, population reduction of gulls and crows has been used to limit the role of these species in spreading and transmitting avian cholera. This technique has limited application and it is not recommended as normal operating procedure. To be most effective, population reduction must be undertaken before there is a major influx of scavengers in response to carcass availability. Also, the techniques used must not result in dispersal of infected birds out of the area.

Population reduction of infected American coots, gulls, terns, and eiders has also been used to directly combat avian cholera. Destruction of migratory birds infected with this disease can be justified only under special circumstances and conditions:
  1. The outbreak must be discreet and localized rather than generalized and widespread.
  2. Techniques must be available that will allow complete eradication without causing widespread dispersal of potentially infected birds.
  3. The methods used must be specific for target species and pose no significant risk for nontarget species.
  4. Eradication must be justified on the basis of risk to other populations if the outbreak is allowed to continue.
  5. The outbreak represents a new geographic extension of avian cholera into an important migratory bird population.

Habitat management is another useful tool for combating avian cholera outbreaks. In some instances, it may be necessary to prevent further bird use of a specific wetland or impoundment because it is a focal point for infection of waterfowl migrating into the area. Drainage of the problem area in conjunction with creation or enhancement of other habitat within the area through water diversion from other sources or pumping operations denies waterfowl the use of the problem area and redistributes them into more desirable habitat. The addition of a large volume of water to a problem area can also help to dilute concentrations of P. multocida to less dangerous levels. These actions require careful evaluation of bird movement patterns and of the avian cholera disease cycle. Movement of birds infected with avian cholera from one geographic location to another site is seldom desirable.

Under extreme conditions, disinfection procedures to kill P. multocida may be warranted in wetlands where large numbers of birds have died during a short time period. The environmental impact of such measures must be evaluated and appropriate approvals must be obtained before these actions are undertaken. A more useful approach may be to enhance the quality of the wetland in a way that reduces the survival of P. multocida; the best means of accomplishing this is still being investigated.

Hazing with aircraft has been successfully used to move whooping cranes away from a major outbreak of avian cholera. This type of disease prevention action can also be accomplished by other methods for other species. Eagles can be attracted to other feeding sites using road-killed animals as a food source, and waterfowl can be held at sites during certain times of the year by providing them with refuge and food. During an avian cholera outbreak in South Dakota, a large refuge area was temporarily created to hold infected snow geese in an area by closing it to hunting. At the same time, a much larger population of snow geese about 10 miles away was moved out of the area to prevent transmission of the disease into that population. The area closed to hunting was reopened after the desired bird movement had occurred.

Vaccination and postexposure treatment of waterfowl have both been successfully used to combat avian cholera in Canada goose propagation flocks. The NWHC has developed and tested a bacterin or a killed vaccine that totally protected Canada geese from avian cholera for the entire 12 months of a laboratory study. This product has been used for several years with good results in a giant Canada goose propagation flock that has a great deal of contact with free-flying wild waterfowl and field outbreaks of avian cholera. Before use of the bacterin, this flock of Canada geese suffered an outbreak of avian cholera and was successfully treated with intramuscular infections of 50 milligrams of oxytetracycline followed by a 30-day regimen of 500 grams of tetracycline per ton of feed. A NWHC avian cholera bacterin has also been used to successfully vaccinate snow geese on Wrangle Island, Russia, and Banks Island, Canada. Vaccine use in these instances was in association with studies to evaluate avian cholera impacts on survival rates rather than to control disease in those subpopulations.

As yet, there is no practical method for immunizing large numbers of free-living migratory birds against avian cholera. However, captive propagation flocks can be protected by this method. Endangered species can be trapped and immunized if the degree of risk warrants this action. Live vaccines should not be used for migratory birds without adequate safety testing.

Table 7.1 Examples of reported environmental persistence for Pasteurella multocida.

Substrate Survival Time Comments
General Highly variable
  • Amount of moisture, temperature, and pH affect survival of P. multocida.
  • Survival in soils enhanced when moisture content is 50 percent or greater.
  • Survival in water is enhanced by high organic content and turbidity.
  • Survival in wetland waters enhanced by presence of magnesium and chloride ions.
Garden soil 3 months --
Unspecified soil 113 days at 3C;
15-100 days at 20C;
21 days at 26C
Soil chemistry information needed to properly evaluate data.
Poultry yard 2 weeks Infectious for birds after last death and removal of all birds
Water 3 weeks following removal of 100 dead snow geese; no other waterfowl use.
99 days Water contaminated with turkey litter.
30 days In marsh near carcass that had been opened.
Infected tissues 120 days but not 240 days American coot hearts buried in marsh after birds died from avian cholera.
Fomites (Inanimate objects) 8 days but not 30 days Dried turkey blood on glass at room temperature

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Human Health Considerations

Avian cholera is not considered a high risk disease for humans because of differences in species susceptibility to different strains of P. multocida. However, P. multocida infections in humans are not uncommon. Most of these infections result from an animal bite or scratch, primarily from dogs and cats. Regardless, the wisdom of wearing gloves and thoroughly washing skin surfaces is obvious when handling birds that have died from avian cholera.

Infections unrelated to wounds are also common, and in the majority of human cases, these involve respiratory tract exposure. This is most apt to happen in confined areas of air movement where a large amount of infected material is present. Processing of carcasses associated with avian cholera die-offs should be done outdoors or in other areas with adequate ventilation. When disposing of carcasses by open burning, personnel should avoid direct exposure to smoke from the fire.

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Supplementary Reading

  • Botzler, R.G., 1991, Epizootiology of avian cholera in wildfowl:
    Journal of Wildlife Diseases, 27 p. 367–395.
  • Brand, C.J., 1984, Avian cholera in the Central Mississippi Flyways during 1979–80: Journal of Wildlife
    Management, 48, p. 399–406.
  • Rimler, R.B., and Glisson, J.R. 1997, Fowl cholera, in Calnek, B.W., and others, eds., Diseases of poultry (10th
    ed.): Ames, Iowa, Iowa State University Press, p. 143–159.
  • Wobeser, G.A., 1997, Avian cholera, in Diseases of wild waterfowl (2nd ed): New York, N.Y., Plenum Press, p. 57–69.

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