National Wildlife Health Center

...advancing wildlife and ecosystem health

NBS Status and Trends

Draft: March 27, 1996 by Michael D. Samuel, National Biological Service

Avian cholera is a highly infectious disease caused by the bacterium, Pasteurella multocida. Since the 1940's, when avian cholera was first diagnosed in wild migratory birds, the disease has been documented from coast to coast in the United States and has spread to Canada and likely Mexico. Most of this expansion has occurred during the past 20 years as outbreaks in new geographic areas continue to be documented. Frequently areas with prior outbreaks become the sites for recurring annual losses. Avian cholera epizootics have occurred at all times of the year, but major losses are most frequently observed when waterfowl are concentrated on wintering areas or during spring migration. In addition, avian cholera losses have occurred on the Canadian breeding grounds of snow and Ross' geese (Wobeser et al. 1983; Brand 1984; NWHC, unpublished) and in breeding colonies of eiders in Maine and Quebec (Reed and Cousineau 1967, Korschgen et al. 1978). Outbreaks also occur in diverse habitats including freshwater wetlands, brackish marshes, and saltwater environments.

More than 100 species of birds are commonly affected by the disease (Botzler 1991) with acute mortality occurring shortly (less than 24 hours) following infection. Because of the acute nature of this disease, few sick birds are typically observed, and dead birds appear to be in good flesh. Under the circumstances of crowded conditions found on many managed wetlands, transmission of the bacteria among birds may occur rapidly and "explosive" die-offs involving hundreds of waterfowl per day have been observed frequently. In addition, more chronic infections and low-level losses also occur, but these losses are less apparent.

Despite the fact that avian cholera is one of the most important diseases of waterbirds in North America (Friend 1985), little is known about ecological interactions involving the host (birds), the agent (P. multocida), and the environment. The disease is believed to be transmitted to susceptible birds through direct contact, by ingestion of contaminated water, or the inhalation of water droplets aerosolized when birds take flight. The probability of transmission is likely related to the density and distribution of bacteria and birds, interactions among birds, virulence of the bacteria, bird susceptibility, and ecological conditions that favor persistence of the bacteria in marsh environments. How this disease is maintained during the annual migratory life cycle of waterfowl is unknown. Many biologists believe that the reservoir for the P. multocida bacteria is either in the environment where recurrent outbreaks are found or in carrier birds that have survived previous infection (Botzler 1991, Wobeser 1992). Recent research has shown that lesser snow geese can be carriers of the disease (NWHC, unpublished). In addition, more than 50% of the larger avian cholera epizootics have involved snow geese; although many other species of waterbirds are also affected during these outbreaks. In spite of these recent findings, convincing evidence for either the carrier or environmental reservoir hypotheses is still lacking.

Conditions that initiate an avian cholera epizootic remain unknown. Epidemiological theory suggests that density of susceptible and infected birds may be an important factor in determining whether an outbreak occurs and the number of birds that become infected and die (Botzler 1991). Large concentrations of waterfowl may be increased when alternative habitat is lost, intensively managed wetland refuges are created, and agricultural practices provide concentrated food resources. Other stresses such as precipitation, cold temperatures, and lack of food (Windingstad et al. 1988, Botzler 1991, Wobeser 1992) have also been suggested as factors that initiate or prolong avian cholera mortality. The role of particular waterfowl species (especially snow and Ross' geese) or specific populations in spreading or maintaining the disease has also been suggested (Brand 1984, Botzler 1991, Wobeser 1992). Finally, even conditions that eventually lead to cessation of an outbreak, and thus potential control mechanisms, are also unknown.

Despite the considerable interest in disease problems of migratory birds, few firm facts are available to develop management strategies for prevention and control of avian cholera outbreaks. Most recommendations are designed to reduce exposure of susceptible birds. Regular monitoring, especially in enzootic areas, can help to identify early stages of an outbreak. Carcass removal is recommended to reduce contamination of the environment and hence transmission, but its effectiveness in reducing overall mortality has not been tested (Botzler 1991). Natural carcass removal by predators and scavengers may act to reduce transmission when the number of carcasses is low. However, these natural systems may become saturated as more birds die, and scavengers may also transmit P. multocida to other sites (Botzler 1991). Population and habitat management activities that alter bird distribution to reduce crowding or disperse birds away from outbreak areas have also been utilized (Friend 1987). Vaccination may be a useful strategy for captive or endangered flocks of water birds (Price 1985).

Currently, the National Biological Service is conducting scientific studies to determine the impact of avian cholera on waterfowl populations and to better understand the relationship between environmental conditions, waterfowl, and avian cholera outbreaks. Several waterfowl populations are being tested to understand the importance of carrier birds in spreading or transmitting the disease and experimental studies are also being conducted to determine the impact of avian cholera on annual survival rates. Other research investigations are concentrating on an improved understanding of the environmental conditions that affect survival of the bacteria in wetlands and transmission to birds. Knowledge gained from these studies may lead to the development of waterfowl and wetland management strategies to prevent or reduce avian cholera mortality in wild bird populations.


  • Botzler, R. G. 1991. Epizootiology of avian cholera in wildfowl. J.
    Wildl. Dis. 27:367-395.
  • Brand, C. J. 1984. Avian cholera in the central and Mississippi Flyways during 1979-80. J. Wildl. Manage. 48:399-406.
  • Friend, M. 1985. Interpretation of criteria commonly used to determine lead poisoning problem areas. U.S. Fish and Wildl. Serv., Fish and Wildl. Leaflet No. 2. Washington, D.C. 4 pp.
  • ----------. 1987. Avian cholera. Pages 69-82 in M. Friend, ed. Field guide to wildlife diseases. U.S. Fish and Wildl. Serv., Resour. Publ. 167. 225pp.
  • Korschgen, C. E., H. C. Gibbs, and H. L. Mendall. 1978. Avian cholera in eider ducks in Maine. J. Wildl. Dis. 14:254-258.
  • Price, J. I. 1985. Immunizing Canada geese against avian cholera. Wildl. Soc. Bull. 13:508-515.
  • Reed, A., and J. G. Cousineau. 1967. Epidemics involving the common eider (Somateria mollissima) at Ile Blanche, Quebec. Naturaliste Canadien 94:327-334.
  • Windingstad, R. M., S. M. Kerr, R. M. Duncan, and C. J. Brand. 1988. Characterization of an avian cholera epizootic in wild birds in western Nebraska. Avian Dis. 32:124-131.
  • Wobeser, G. 1992. Avian cholera and waterfowl biology. J. Wildl. Dis. 28:674-682.
  • ----------, R. Kerbes, and G. W. Beyersbergen. 1983. Avian cholera in Ross' and lesser snow geese in Canada. J. Wildl. Dis. 19:12.

Caption for photograph (to be submitted later): Biologists collect samples to determine relationships between environmental conditions and avian cholera mortality.

For further information: Michael D. Samuel, National Wildlife Health Center, at (608) 270-2441.


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