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Also see the article about Carcass Collection For Botulism Testing
Botulism is a paralytic condition brought on by the consumption of a naturally occurring toxin produced by the bacterium Clostridium botulinum. It is an intoxication rather than an infectious disease. The bacterium is widespread in soils in North America and elsewhere in the world. The toxin produced during growth of the bacterium is one of the most poisonous substances known. We recognize two forms of botulism, type C and type E, affecting wildlife in Michigan.
Type C botulism - Type C botulism is associated with exposed bottom sediments and occurs principally in waterfowl and other birds living in an aquatic environment. It causes tremendous losses, most notably in waterfowl in the western United States. In addition to North America, it has been reported in birds in Europe, South Africa, Uruguay, and Australia. In the Great Lakes region, it was first identified in 1936 in ducks on Green Bay of Lake Michigan and, in 1941, in Monroe County marshes along Lake Erie. In Michigan, outbreaks occur in ducks and shorebirds whenever conditions are favorable for botulism. There have been reports of botulism along both coasts of the lower peninsula and on many inland lakes. Devastating outbreaks have occurred in game farm pheasant flocks in the U.S. and Canada.
Type E botulism - Type E botulism is associated with consumption of fish and occurs in common loons, double-crested cormorants, herring gulls, ring-billed gulls, horned grebes, red-necked grebes, long-tailed ducks, white-winged scoters, and red-breasted mergansers. It now appears that any birds or mammals susceptible to botulinal toxin run a risk of becoming poisoned if they scavenge dead fish. Evidence for this lies in the fact that type E toxin has been identified in a bald eagle, wood ducks, and muskrats having fish remains in their digestive tracts in Michigan.
Geographically, the disease has been recognized in wildlife only in the Great Lakes Region, specifically on Lakes Michigan and Huron, and more rarely on inland waters of Michigan. Die-offs in Lake Michigan normally occur in the fall in the northern portion of the lake as the bird's stage for the fall migration. It has been diagnosed in Ontario, Ohio, Pennsylvania, and New York on Lakes Ontario and Erie.
Botulism is a food poisoning. The toxin-producing bacterium, C. botulinum, is common in surface soils of both the terrestrial and the aquatic environment. Toxins are produced only when conditions favor growth and multiplication of the bacterium.
Type C toxin occurs in carcasses of dead invertebrates, in the flesh of birds dying of botulism, and in maggots feeding on toxic carcasses. In a type C botulism outbreak the sequence of events are: aquatic invertebrates ingest the bacterium when feeding and a lowering of water levels or an increase in water temperature causes large numbers of the invertebrates to die. The carcasses of the invertebrates provide a good medium for growth of the bacterium with subsequent production of toxin. Ducks feeding on the toxic dead invertebrates found in the bottom sediments become poisoned and die. Maggots infesting the duck carcasses become toxic and are eaten by ducks and other species of birds, thus increasing bird mortality in an explosive manner. Outbreaks among captive pheasants appear to stem from a few maggot-infected pheasant or other animal carcasses and expand to explosive proportions as toxic maggots become available to the general flock.
Type E toxin is found primarily in sick and in decaying fish but can also be present in mollusks. The bacterium, C. botulinum type E, is found in bottom mud, in aquatic invertebrates, and in the gut of fish taken from Lakes Michigan and Huron. The Clostridium bacterium thrives in anaerobic conditions and areas with mats of algae are prime for its growth. The bacterium can be ingested by feeding invertebrates; fish ingest the bacterium either directly from bottom mud, or from eating invertebrates arising from it, or fish that are sickly having ingested the bacterium. Carcasses of dead fish provide a good medium for growth of the bacterium and production of toxin. Birds and mammals become poisoned from feeding on toxic dead fish. In this manner, bird and mammal die-offs coinciding with fish die-offs are easily explained. Botulism mortality of loons and other birds in late fall in the absence of a coincidental fish die-off are probably the result of lake turn-over with invertebrates being ingested by the birds.
Though outbreaks are characterized by the presence of dead birds in varying numbers, the investigator can usually find a few sick individuals by careful searching. The only meaningful sign of botulism is the loss of strength due to muscular paralysis. The degree of paralysis is related to the dose and time of exposure and the amount of toxic material consumed. Gulls show wing-droop and difficulty in getting air-borne in mild intoxications. In more advanced cases, gulls are unable to stand, ducks are unable to hold up their heads. Consciousness is retained, and it is common to find gulls completely immobile but showing apprehension when approached (see illustration). Loons and other waterfowl are rarely discovered sick and appear to die on the water and drift ashore after death.
Botulism leaves no characteristic tissue lesions. The toxin chemically blocks nerve transmission at the site where the nerve endings meet the muscle fibers and causes no detectable cellular changes. Death is attributed to paralysis of respiratory muscles, or in the case of birds on the water, to drowning from being unable to hold their heads up. Birds with sublethal levels of toxin may make a full recovery.
Diagnosis is based on field evidence, flaccid muscular paralysis in sick birds, and detection through laboratory methods of detecting botulinal toxin in the blood of sick and dead animals. The laboratory test (mouse protection test) involves injecting mice intraperitoneally with blood/serum collected from carcasses of animals under investigation. One mouse is given serum plus a protective dose of antiserum to the type C toxin, one is given serum plus a protective dose of antiserum to the type E toxin, and one mouse is unprotected, given only serum. Death of the mice will normally occur within 8 hours with the mouse that was injected with the appropriate antiserum surviving, thus identifying the toxin involved.
Birds with sublethal doses of toxin will recover if removed from the source of toxin and given shelter, fresh water, and food. Use of antiserums is not feasible. They are not readily available in quantities needed, and their value when administered after signs of botulism become apparent is questionable, though some workers have claimed increased recoveries in ducks injected with type C antiserum.
Control procedures remain more theoretical than practicable to wildlife managers at this time. It would seem that type E botulism might be effectively controlled if accumulations of dead fish and birds can be avoided. Large-scale die-offs on the Great Lakes have been associated with low lake levels, high water temperatures, storms, invasive species (zebra and quagga muscles and round gobies), and algae. Large-scale outbreaks of type C botulism often are associated with periods of hot weather, high water temperatures, low water levels, or changing water levels. Outbreaks of botulism are initiated by die-offs of aquatic invertebrates; therefore, stabilization of water levels and temperatures in late summer would reduce the potential for an outbreak. For pheasants maintained in high populations under game farm conditions, strict policing to keep carcasses of dead pheasants and other animals picked up, as well as observing other sanitation practices, is essential since carrion of any sort is always a potential source of botulinal toxins.
Botulinal toxins are highly fatal to many animals, including man. Variations in incidence of poisonings among different species are generally attributable to differences in feeding habits, rather than to variations in susceptibility. In wildlife, botulism primarily impacts bird populations. The bacterium persists in lakes and marshes where botulism is endemic and poses a serious threat to waterfowl populations using these areas. Poisonings in humans from type E botulinal toxins usually are associated with eating uncooked, imperfectly canned, and improperly preserved fish and marine animal products. Since fish-eating birds normally are not eaten by people, and thorough cooking destroys the toxin, this wildlife source of type E toxin is not a serious public health problem.
Public health workers do not implicate type C toxin in human poisonings, though this is not to say it could not be fatal if C. botulinum is ingested. Since the toxin is destroyed by heat, it appears that no problem with botulism will result from eating cooked waterfowl.
