Table of Contents
- Cause of Type C Botulism
- Bird Species Affected by Type C Botulism
- Occurrence of type C Botulism in Canada
- Importance of Type C Botulism to Human Health
- Ecology of Type C Botulism
- Spring Botulism
- Wildlife Management and Type C Avian Botulism
- Signs of Diesease in Affected Birds
- Pathology of Type C Botulisum
- Identification and Diagnosis of Botulism
- References
Cause of Type C Botulism
Type C Botulism is a form of food poisoning that occurs when animals ingest toxin from the strain of the putrefactive bacterium Clostridium botulinum that produces Type C botulinum toxin.
Redhead paralysed by Botulism. Photo T. Bollinger
Bird Species Affected by Type C Botulism
A very large number of different species of birds are susceptible to Type C botulinum toxin, as are some species of mammals such as mice, cattle and horses. Major outbreaks of Type C botulism have occurred on prairie wetlands, and the principle victims have been ducks, coots, grebes, gulls and shorebirds.
Cow with Type C Botulism Photo G. Wobeser
Farm animals also can be affected by Type C Botulism. Putrefying animal remains mistakenly included in cattle feed have caused large-scale mortality. At least once, Type C Botulism has occurred in cattle in association with an outbreak in wild waterfowl.
During a major outbreak of Type C Botulism on Old Wives Lake, Saskatchewan in 1997, nine cattle pastured on the lake shore developed Type C Botulism. The most likely source of toxin for the cattle was maggots ingested while drinking lake water. Seven cattle died or were destroyed for humanitarian reasons. Two animals recovered, one after 24 days and the other after 35 days.
Occurrence of type C Botulism in Canada
Type C botulism probably has always been a component of the ecology of prairie wetlands. Records of waterbird mortality in Canada confirmed or suspected to be from botulism date from the early 1900's. In the 1990's, annual losses of in the prairie provinces were conservatively estimated at hundred's of thousands to over a million waterbirds. High mortality was noted particularly on three large wetland-lake complexes: Whitewater Lake (Manitoba), Old Wives Lake (Saskatchewan) and Pakowki Lake (Alberta).
Incidents of Type C Avian Botulism in wild birds on the Canadian prairies in the summer of 1998. 1 - Old Wives Lake; 2 - Pakowki Lake; 3 - Whitewater Lake.
Botulism on the prairies during the 1990's is summarized in the CCWHC Newsletter: Vol 5, No 3 - Winter 1998; Vol 5, No 1 - Winter 1997; Vol 4, No 3 - Summer 1997; Vol 4, No 2 - Winter 1996; Vol 4, No 1 - Summer 1996; Vol 3 No 3 - Winter 1995; and Vol 2 No 3 - Autumn 1994.
Although Type C botulism has occurred most frequently and dramatically in the Prairie provinces, it can and does occur elsewhere in Canada and around the world. In the United States, it has occurred on east, west and Gulf coasts, and in the Mississippi valley, as well as in typical prairie habitats.
Map of all recorded outbreaks of Type C botulism in the CCWHC National Database
Importance of Type C Botulism to Human Health
There are no recorded occurrences of poisoning of people due to Type C botulinum toxin, although several other types of botulinum toxins are highly poisonous to humans. It is, thus, unlikely that Type C botulism in game birds poses a health hazard to hunters. In addition, birds affected by botulism are in various stages of paralysis and do not fly. It is, therefore, unlikely that a hunter would shoot and then consume such a bird.
Ecology of Type C Botulism
The bacterium, Clostridium botulinum (Type C), is a normal bacterium of marshland soils and sediments. It is more common in some marsh environments than in others, for reasons not yet fully understood. The bacterium persists in a dormant state as a spore. Animals that live and feed in the marsh will ingest spores of the bacterium along with water, soil and sediments. The bacterial spores do these animals no harm. However, when such an animal dies for any reason, the spores of the bacterium inside that animals's body find themselves in ideal conditions for growth. The bacterium grows only in the absence of oxygen, and requires both a rich nutrient substrate and moderately warm to very warm temperatures. Clostridium botulinum is just one of many putrefactive bacteria that function as decomposers in the ecosystem. However, when temperatures in the carcass are very warm (~25C or greater), Clostridium botulinum Type C produces Type C botulinum toxin as it grows. Thus, carcasses in which the bacterium is growing at warm temperatures come to contain Type C toxin.
Duck carcass with large number of blow-fly larvae (maggots). Just five such maggots may contain enough Type C botulinum toxin to kill another duck. Photo: T. Bollinger
Most waterbirds do not feed on putrefying animal carcasses. However, they feed on snails, insect larvae and other invertebrates and it is possible that Type C toxin develops in the carcasses of dead invertebrates and is consumed by water birds in this form. Probably of much greater importance in botulism outbreaks is the presence of blow-fly larvae (maggots) on the putrefying carcasses of dead animals.
The maggots absorb Type C toxin but are not harmed by it. Water birds of many, many species find maggots highly attractive and will feed on them readily. By feeding on maggots, the birds ingest Type C toxin and become poisoned. The birds that are feeding on these maggots also are likely to have spores of Clostridium botulinum (Type C) in their digestive tracts and they also may ingest spores of the bacterium along with the maggots. Thus, when these birds die because of poisoning with botulism, Clostridium botulinum will grow and produce toxin in their carcasses and the carcasses also will attract blow-flies. Thus, an amplifying cycle of poisoning, death, putrefaction with toxin production, and poisoning of new birds which ingest maggots can be established. Since each carcass has enough toxin and maggots to poison many, many new birds, it is possible for a small number of carcasses of dead animals in a marsh to result in the death of hundreds or thousands of birds through this cycle of amplification.
Northern Pintail ducklings dead of Type C Botulism in a natural outbreak. Each had fed heavily on maggots just prior to death. Each gram of the maggots pictured here contained enough Type C botulinum toxin to kill 10,000 laboratory mice. Photo G. Wobeser.
However, it is clear that an outbreak of botulism does not happen every time an animal dies in a wetland. Many environmental factors can affect whether or not an outbreak of botulism will occur on a marsh.
Some of these factors are the frequency with which animals die (for any reason) in the environment, the speed with which scavengers remove carcasses before they putrefy and produce toxin and maggots, the amount of Clostridium botulinum (Type C) in the environment, the number and density of birds in the environment (which will determine how likely it is that birds will encounter and feed on the maggots on a carcass) and ambient temperature (which influences rates of decomposition, toxin production and fly activity). Thus, botulism is a complex ecological phenomenon; the result of the interaction of a large number of different biological and physical components of the environment.
Although commonly cited in various publications, there are no data to support the view that Type C botulism in birds has resulted from ingestion of toxin that might be produced in decaying vegetation. Nor are there data to suggest that the toxin is produced in quantities sufficient to cause disease in birds in any substrate other than decaying animal remains. Even the contribution of decaying carcasses of dead invertebrates remains only a theoretical possibility which never has been documented to cause outbreaks of avian botulism.
Spring Botulism
In western Canada, Type C Botulism sometimes affects waterbirds in early spring when the ice has just melted from water bodies and the ambient temperature is too cold for blowfly activity. Spring migrant diving ducks such as Lesser Scaup are the species affected. The only plausible explanation for Type C Botulism in early spring is that the affected birds ingest toxin that was produced the previous summer or fall. Such toxin may be contained in maggots that sink to the bottom or perhaps in aquatic invertebrates that have fed on and absorbed toxin from carcasses in which Clostridium botulinum produced toxin the previous year. Outbreaks of spring botulism thus far detected have been small relative to the summer outbreaks. Some, but not all, have occurred in areas known to have been sites of summer botulism the previous year.
Wildlife Management and Type C Avian Botulism
The standard response to outbreaks of Type C Avian Botulism has been to attempt to remove the carcasses of dead and dying birds from the environment. This action is intended to remove the source of the toxin, and thus to prevent or reduce further poisoning. Until recently, the efficiency and effectiveness of this management response had not been evaluated. A multi-agency cooperative study of botulism outbreaks on large wetlands on the Canadian prairies (1998 and 1999) found that, in the face of large outbreaks on large wetlands, carcass pickup is not efficient. At best, no more than 30% of the carcasses present could be collected and removed, even with intensive effort and the best equipment. As many as 25 carcasses per hectare remained on the clean-up area after the pick-up effort. Evidence to date indicates that carcass pick-up during outbreaks of botulism on large wetlands also may not be effective in reducing further mortality. Only 5% of molting mallards marked with radio transmitters on one large wetland during a botulism outbreak in 1999 survived for as long as 30 days, despite intensive carcass pick-up effort.
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
Botulism causes a progressive, relaxing (flaccid) paralysis of muscles, beginning in the legs and the wings, then involving the neck and, finally, the muscles used for breathing.
Ducks are fairly resistant to Type C toxin, and will show various degrees of paralysis depending on how much toxin they have eaten and how long ago the toxin was consumed. It is common to see partially paralysed birds use their wings for locomotion on the water in compensation for paralysed legs. Many affected birds will be found on land close to the shoreline, alert and alive, but unable to move. Such birds may die of dehydration, rather than from respiratory paralysis.
This Green-winged Teal has come to a halt because of paralysis due to Type C botulism. Its final efforts at locomotion are imprinted in the shoreline mud. Birds such as this often will survive botulism poisoning and recover if they are provided with drinking water and protected from predators. Photo T. Bollinger
Neck paralysis is a striking feature of Type C botulism in birds.
Two Mallards showing relaxed paralysis of the neck muscles. Botulism has been called "Limber Neck" because of this feature of the disease. Such a bird on water could not hold its head above the water and would drown. Photo G. Wobeser
Large numbers of dead birds may be clearly evident in large-scale outbreaks of botulism. They will be found near the water's edge along shorelines. However, where emergent vegetation is dense, massive mortality from botulism may occur yet be completely hidden from view. Casual visual assessment can neither detect nor quantify wild bird mortality.
Birds dead of Type C botulism along the shore of Old Wives Lake, Saskatchewan, 1998. One million birds died of botulism on this lake in the outbreak pictured here. Photo T. Bollinger
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 diseases.
Identification and Diagnosis of Botulism
A definitive diagnosis of Type C botulism requires that Type C 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 that is 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 also show evidence of decomposition can not be interpreted in terms of cause of death.
The most sensitive test for Type C botulism requires inoculation of mice with serum from live, sick birds. Half the mice first are injected with antitoxin to Type C botulinum toxin. If the unprotected mice die or show clinical disease typical of botulism, and the protected mice are unaffected, the bird serum is shown to have contained Type C toxin. Tests that do not require use of experimental mice have been developed, based on ELISA technology. These tests will not detect the same low (yet toxic) levels of botulinum toxin that can be detected by mouse inoculation, but they are sufficiently sensitive to make a diagnosis of botulism in an outbreak from which a number of specimens can be tested. If 10 or so affected birds are tested individually with ELISA-based tests, some will have enough toxin in their blood to be detected, and this, together with clinical signs and autopsy that rules out other causes of disease, is sufficient for an outbreak diagnosis.
References
Wobeser, G. 1997. Diseases of Wild Waterfowl . 2nd Ed. Plenum Publishing Corp., New York 324 pp. ISBN 0-306-45590-0.
Wobeser, G., K. Baptiste, and E.G. Clark. 1997. Type C botulism in cattle in association with a botulism die-off in waterfowl in Saskatchewan. Canadian Veterinary Journal 38: 782.