Type E Botulism in Birds

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Last Update: March 2000

Author: F. A. Leighton

Reviewer: H. Artsob

Cause of Type E Botulism

Type E Botulism is a form of food poisoning that occurs when animals ingest toxin produced by the strain of the putrefactive bacterium Clostridium botulinum that produces Type E botulinum toxin.

Common Loon

Common Loon - Photo: G. Bortolotti

Bird Species Affected by Type E Botulism

Major outbreaks of Type E Botulism have occurred in fish-eating birds on the Great Lakes and have involved loons, mergansers, grebes, scaup and gulls in particular. A very large number of different species of birds are susceptible to Type E botulinum toxin, as are some species of mammals, including humans and mice.

Occurrence of type E Botulism in Canada

There are very few records of incidents of Type E Botulism in wildlife worldwide. Small-scale occurrences may occur but may not be recognized an unreported. In the fall of 1999, there were major outbreaks on Lakes Huron and Erie in southern Ontario. At least 700 Common Loons died on Lake Huron and several thousand birds, mostly Red-Breasted Mergansers, died on Lake Erie. Numbers of Horned Grebes, various diving ducks, and three species of gull (Ring-billed, Herring and Bonapart's) also died in these incidents. This outbreak is described in the Winter 1999 issue of the CCWHC Newsletter en français. An outbreak in the United States on Lake Michigan, affecting Common Loons in particular, occurred in October and November 1983 (see Brand et al. 1988 reference list). There are other reports of Type E Botulism on the Great Lakes at least as early as the 1960's (cited in Brand et al. 1983 in reference list).

Birds dead of Type E Botulism

Type E Botulism, Lake Erie, 1999: Dead loons and mergansers litter the beach. Photo I.K. Barker

Birds dead of Type E Botulism

Type E Botulism, Lake Erie, 1999: Dead loons and mergansers litter the beach. Photo I.K. Barker

Birds dead of Type E Botulism

Type E Botulism, Lake Erie, 1999: Red-breasted Mergansers dead of Type E Botulism. Photo I.K. Barker

Type E Botulism 1983, 1999

Map showing location of the outbreaks of Type E Botulism in fish-eating birds in Canada in 1999 and in the United States in 1983.

Importance of Type E Botulism to Human Health

People are susceptible to poisoning with Type E botulinum toxin. It is unlikely that people would become poisoned from eating wild birds. Affected birds are partially paralysed and are unlikely to be hunted. Loons, grebes, and gulls are not legally hunted in Canada and mergansers are not widely hunted and consumed . Spores of Clostridium botulinum Type E are present in water and in the flesh of fish in many parts of Canada. One outbreak of Botulism in people occurred when fish from Canada was shipped frozen to Finland, where it was then smoked and sold to consumers elsewhere in Europe. The final smoked product contained Type E botulinum toxin and poisoned a number of people. The toxin probably developed because the bacteria grew and produced toxin during the smoking process. The bacterial spores themselves were present in the fish caught in Canada (See Korkeala et al. in the reference list). People in Canada also have suffered from Type E Botulism. In 1995, 1996 and 1997 there were 11, 10 and 18 human cases of Type E. Botulism recognized in Canada; one case in 1997 was fatal. Nearly all cases have been associated with consumption of foods derived from marine mammals or fish (reference list).

Ecology of Type E Botulism

Very little is known about the ecology of Type E Botulism. It is known that the spores of Clostridium botulinum Type E are abundant in the water of many Canadian lakes and that the spores also can readily be found in the gills and digestive tracts of fish from such lakes. These spores, themselves, are harmless. Type E Botulism occurs only under conditions when these spores grow and produce toxin. The ecological role of the bacterium appears to be that of a decomposer - a bacterium of putrefaction. The bacterium will grow only in a rich nutrient substrate that is free of oxygen. Fish that die for any reason and that contain the bacterial spores in their tissues are suitable substrate for growth and toxin production by the bacterium.

It seems clear that the fish-eating wild birds that have died of Type E Botulism have become poisoned from eating fish that contain the toxin. It is not clear exactly how this happens. Birds such as loons and mergansers normally capture and eat only live fish. Yet, Clostridium botulinum Type E should not grow and produce toxin in living fish. It may be that there are circumstances under which toxin is produced in the tissues of live, possibly dying, fish, possibly within their digestive tracts. Alternatively, it may be that the fish captured alive and eaten by the birds had themselves fed on some source of Type E toxin. Thus, it would be the toxin in the digestive tracts of the live fish that was the source of toxin for the birds in these outbreaks. It is even possible that the live fish captured by the birds were partially paralysed by the Type E toxin they had recently eaten and thus were particularly easy prey for the birds. This might account for preferential feeding on toxin-containing fish by the affected birds.

It seems likely that there are outbreaks of Type E Botulism only when a variety of particular ecological factors occur simultaneously. There must be toxin produced in food material eaten by fish, and those fish must then be eaten by birds. The two outbreaks in Canada and the United States occurred in the fall when fish-eating birds congregate in favourable feeding habitat during fall migration.

Wildlife Management and Type E Avian Botulism

Until more is known about the ecology and causal factors that lead to outbreaks of Type E Botulism, it will not be possible to consider interventions to mitigate or prevent outbreaks of Type E Botulism in wild birds. Some of the species that have died in large numbers in the few outbreaks recognized and reported are species whose populations are in decline and for which there is continent-wide concern - the Common Loon, for example. It is not known whether or not carcasses of birds poisoned by Type E Botulism are important sources of toxin for other birds, as is clearly the case in Type C Botulism. Thus, it is not known whether or not removal of carcasses from the environment would be useful as a control measure. It is very important to investigate, quantify and determine the cause of such outbreaks, especially when critical species such as loons are involved. Accurate data on the number of birds killed and the cause of mortality are needed for accurate population models which, in turn, are the basis for national and international wildlife conservation planning.

It is clear that more research is needed to determine the impact of botulism on wild bird populations and, from this, to identify realistic management goals and methods to achieve them. Continental waterfowl populations may be relatively unaffected by even the massive outbreaks that have been investigated (e.g. 1,000,000 birds dead on Old Wives Lake alone in 1998). On the other hand, certain species or regional populations may be critically affected.

Carcass pick-up may remain an important and useful response to botulism on small wetlands that are under intensive surveillance and management; early removal of a high proportion of carcasses may be feasible under these circumstances. Other management options include monitoring but otherwise letting outbreaks run their course and incorporating the mortality figures into continental population models used to set hunting limits and conservation strategies, and targeting specific subsets of the populations at risk (for example, mature hen Northern Pintails) for interventions such as clinical treatment and vaccination.

Signs of Diesease in Affected Birds

Birds suffering from Botulism show varying degrees of relaxed (flaccid) paralysis of muscles. Thus, they may appear weak or bright and alert but unable to move.

Pathology of Type C Botulisum

Botulism causes no lesions; there are no characteristic changes of any kind in the organs or tissues of birds that die of Botulism. However, autopsy of birds suspected to have died of Botulism is essential to rule out other possible diseases.

Identification and Diagnosis of Botulism

A definitive diagnosis of Type E Botulism requires that Type E botulinum toxin be found in the blood of a live, clinically-affected (sick) bird. Finding the toxin in the heart blood of a very freshly-dead bird is evidence that the bird may have died of Botulism, but it also is possible that the toxin detected was produced after death, during putrefaction and that it had nothing to do with the death of the bird. Finding toxin in bird carcasses that show any evidence of decomposition can not be interpreted in terms of cause of death.

The most sensitive test for Type E Botulism requires inoculation of mice with serum from live, sick birds. Half the mice first are injected with antitoxin to Type E botulinum toxin. If the un-protected mice die or show clinical disease typical of Botulism, and the protected mice are unaffected, the bird serum is shown to have contained Type E toxin.

References

Brand, C.J. et al. 1988. An outbreak of Type E Botulism among Common Loons (Gavia immer) in Michigan's upper peninsula. Journal of Wildlife Diseases 24(3): 471-476.

Campbell, D.G. and Barker, I.K. 1999. Botulism Type E in fish-eating birds, Lake Erie and Lake Huron. CCWHC Newsletter. 6(3)7-8. (version française)

Dodds, K.L. and J.W. Austin. 1997. Clostridium botulinum. In: Doyle, M.P., L.R. Beuchat, and T.J. Montvillw (eds.). Food Microbiology: Fundamentals and Frontiers. ASM Press, Washington, D.C. pp. 288-304.

Korkeala, H. et al. 1998. Type E Botulism associated with vacuum-packed hot-smoked whitefish. International Journal of Food Microbiology. 43: 1-5.

Health Canada's Web Sites on Botulism
Summary Reports from Health Canada 1995 1996 1997
Health Canada's Web Sites on Botulism English Français

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