Last Update: March 2000
Author: F. A. Leighton
Reviewer: H. Artsob
(Revised October 2007)
Type E Botulism is a form of food poisoning that occurs when animals ingest toxin produced by the putrefactive bacterium Clostridium botulinum. There are 8 different strains of C. botulinum, each associated with different ecological circumstances and each commonly affecting a different range of species. Type E is a strain closely associated with freshwater and marine environments, and has been a cause of death primarily in fish-eating birds.
Since 1998, Type E botulism has been confirmed, by mouse protection test, in the 22 avian species from the lower Great Lakes (Lakes Ontario, Erie and Huron):
|Species of Birds Known to have died of Type E Avian Botulism on the Lower Great Lakes|
|English Name||Latin Name||English Name||Latin Name|
|Common Loon||Gavia immer||Bald Eagle||Haliaeetus leucocephalus|
|Red-throated Loon||Gavia stellata||Great Blue heron||Ardea herodias|
|Horned Grebe||Podiceps auritus||American Coot||Fulica americana|
|Red-necked Grebe||Podiceps grisegena||Great Black-backed Gull||Larus marinus|
|Eared Grebe||Podiceps nigricollis||Bonaparte's Gull||Larus philadelphia|
|Double-crested Cormorant||Phalacrocorax auritus||Ring-billed Gull||Larus delawarensis|
|Greater Scaup||Athya marila||Herring Gull||Larus argentatus|
|Common Goldeneye||Bucephala clangula||American Golden Plover||Pluvialis dominica|
|White-winged Scoter||Melanitta deglandi||Sanderling||Calidris alba|
|Long-tailed Duck||Clangula hyemalis||Semipalmated Sandpiper||Calidris pusilla|
|Red-breasted Merganser||Mergus serrator||American Crow||Corvus americanus|
Occurrence of type E Botulism in Canada There are very few records of incidents of Type E Botulism in wildlife, all of them originating in the Great Lakes. The bacterium is known to occur in other locations, such as the arctic and in the northern Europe. Although Type E botulism has been described in people in these locations, it has not been recognized as causing disease in wildlife. Botulism was first seen in Common Loons in Lake Michigan in the 1960ís. It was a common occurrence on Lake Michigan, and later in upper Lake Huron, during that decade. No cases were reported during the 1970ís, but a large-scale event occurred in Lake Michigan in the early 1980ís. Since 1998, annual outbreaks of Type E botulism have occurred in Lake Huron and in Lakes Erie and Ontario, involving many thousands of shorebirds, gulls, terns, diving ducks, mergansers, grebes and loons.
The harbinger of this series of annual outbreaks occurred on the southeastern shore of Lake Huron in autumn 1998, when Type E botulism killed hundreds of Common Loons. In 1999 and 2002, outbreaks in this area involved not only loons but gulls (Larus spp.) and grebes (Podiceps spp.). Type E botulism on Lake Erie was first confirmed in gulls dying during summer 1999 on the southern shore, at Presque Isle, Pennsylvania. In autumn 1999, Type E botulism killed about 6,000 Red-breasted Mergansers, loons and grebes along the north shore of the west basin of Lake Erie.
Over the next four years, Type E botulism on Lake Erie adopted a general annual pattern. In summer, local, usually relatively small-scale outbreaks involved scores to hundreds, rarely thousands, of resident gulls, terns (Sterna spp), Double-crested Cormorants (Phalacrocorax auritus) and shorebirds (Scolopacidae). In autumn larger outbreaks killed many hundreds to many thousands of southbound migrant fish-eating birds (mainly Red-breasted Mergansers, Common Loons, grebes) and diving ducks (mainly Long-tailed Ducks). Fish-eating birds and diving ducks generally died off-shore; where the carcasses drifted in was determined by the prevailing winds.
The location of major outbreaks on Lake Erie shifted from the west basin (1999) to involve both the central basin and east basin (2000-2004), latterly concentrating in the east basin (2002-2004). Major mortalities occurred in 1999 (referred to above), 2000, when about 6,000 fish eating birds washed onto the New York shore at the east end of the lake, 2001, when 3,000 gulls, fish-eating birds and Long-tailed Ducks died along the New York shore, 2002, when over 3,000 Ring-billed Gulls (Larus delawarensis) died near Buffalo NY, and 12,600 long-tailed ducks and over 3,000 fish-eating birds came ashore on the New York coast, 2003 when 2,000 loons and hundreds of gulls and Long-tailed Ducks died on both sides of the east basin, 2004, when about 2,800 loons, 2,700 Long-tailed Ducks, and hundreds of birds of other species were found on the New York shore.
Type E botulism was first confirmed on Lake Ontario in 2002, when it occurred in gulls and affected about 675 Long-tailed Ducks along the New York shore. About 1,500 deaths attributed to botulism occurred in gulls, diving ducks, cormorants and loons on the New York side of Lake Ontario in 2003, and botulism occurred in Great Black-backed Gulls at the east end of the lake on the Canadian side. In 2004, over 1,750 carcasses were counted on breeding colonies and beaches at the east and west ends of Lake Ontario in late summer/fall: mainly Double-crested Cormorants, Great Black-backed Gulls, Long-tailed Ducks and White-winged Scoters. On the New York shore, about 1700 birds died, including Long-tailed Ducks, Ring-billed Gulls, cormorants, and Common Loons. Since 2004, botulism has occurred annually on Lake Ontario, following this same general pattern of incidents involving gulls, terns and cormorants during the summer months, with diving ducks, loons and grebes being the principal species involved in the autumn.
Clostridium botulinum exists in 2 forms: a resting, or dormant spore that is resistant to changes in physical conditions and which allows persistence in the environment, and a growing or vegetative form. It is during growth and replication that the bacterium produces its toxin. In order to grow, it requires a rich nutrient substrate, a complete lack of oxygen, and an optimum temperature.
Very little is known about the ecology of Type E Botulism The spores are likely widespread in the waters and sediments of the Great Lakes. These spores, themselves, are harmless. It is not until the bacterium begins to grow and produce toxin that disease can occur. There likely are a number of circumstances under which the growth requirements of the bacterium are met and toxin is produced. The death, for any reason, of fish, mudpuppies or birds that have spores in their bodies will allow the production of toxin during decomposition of the carcasses. Anecdotally, it has been observed that mortalities in fish or mudpuppies often precede botulism events during the summer.
The typical pattern of mortality that has been observed since 1999 includes the sporadic deaths of a variety of species during the mid-to-late summer (late July to the end of August). The affected species include terns, gulls and cormorants. As migrating shorebirds, such as sandpipers and sanderlings arrive in August, they often are caught up in a botulism event. As later migrants arrive on the lower Great Lakes, the pattern changes. Fish-eating birds such as loons, mergansers and grebes are commonly involved, as are mussel-eating ducks such as Long-tailed Ducks, scoters and scaup.
It is probable that each of these groups of birds is intoxicated by slightly different, but overlapping, routes. Gulls acquire toxin from a wide variety of sources as they scavenge on the carcasses of dead fish, mudpuppies and birds. Shorebirds may pick up toxin from adult insects or larvae that have been feeding on the carcasses of botulism-affected animals and which have picked up and concentrated the toxin. The fish-eating and mussel-eating birds are likely ingesting the toxin directly with their prey.
An unresolved question with the latter group is whether their prey are alive (and carrying toxin) or dead (with toxin formed during putrefaction) when consumed. Loons, grebes, cormorants and mergansers are all predators of live fish, and it seems most likely that they become intoxicated through the consumption of live, sick fish that contain toxin. Experimental infection of a variety of fish species has demonstrated that fish affected by Type E botulism change their behaviour, often in ways that render them more susceptible to predation. (Yule et al, 2006a, 2006b)
Identification of the stomach contents of birds dying during botulism events indicates that a substantial proportion of them have been eating Round Gobies (Neogobius melanostomas). This fish is an invasive species, having arrived within the last 15 years from the Black Sea area, likely in the ballast water of ocean going ships. This goby is a predator of the Zebra and Quagga Mussels (Dreissena polymorpha and Dreissena rostriformis bugensis), which also are newly-introduced non-native species originating from the Black Sea area (Zebra mussel) and Dnieper River in the Ukraine (Quagga mussel). These mussels have been found in the stomachs of many of the diving ducks found dead during botulism episodes. Thus, there appears to be a likely link between mussels, gobies and botulism in the birds. It is possible that the mussels are dying in large numbers due to an unknown cause. Their tissue, in an anoxic environment within their closed shells, could provide the substrate for growth of C. botulinum and toxin production. Consumption of these dead mussels by either ducks or fish would move toxin, respectively, directly to mussel-eating ducks or .via gobies, upwards in the food chain to fish-eating birds
The highest mortality of birds occurs during the autumn months. It may be that there is more toxin produced at this time of year, as the bacterium favours slightly cool conditions. However, it may also be that this is merely the time of year when the greatest numbers of fish- and mussel-eating birds are present.
Botulinum toxin exerts its effect at nerve endings to cause a flaccid paralysis of muscle. Birds affected by botulism often appear bright and alert, but are weak and unable to move. As the extent of paralysis progresses, the birds are unable to fly or walk and eventually are unable to hold up their heads. Often, if they do not die from respiratory failure due to the paralysis of respiratory muscles, they drown, once they are unable to hold their heads above water.
There are no characteristic changes of any kind in the organs or tissues of birds that die of botulism. It is necessary to rule out the occurrence of other disease in these birds, and a large number of birds have been tested for the presence of other bacterial diseases, viruses such as Newcastle Disease virus and West Nile virus, and toxins such as heavy metals and organophosphate and carbamate insecticides. Rarely have other diseases been identified in any of these birds. The birds examined during botulism events on the Great Lakes have typically been in good to excellent body condition, as would be expected in birds preparing for a long migratory flight
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.
Currently, the most sensitive test for Type E Botulism is the mouse protection test, which 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.
Type E botulism is a well-recognized condition in people. Most instances of poisoning involve the consumption of marine or freshwater animals (fish, seals, whales, walrus) that have been prepared without cooking. This would include the consumption of fermented seal or walrus, smoked fish, air-dried fish and raw marine mammal meat. (Chiou et al, 2002). The toxin is destroyed by cooking.
In a contaminated environment, such as the lower Great Lakes, spores are likely to be widespread in the environment and in the tissues or digestive tracts of animals present there. Thus, when an animal is harvested, if the meat is kept under conditions which allow for the growth of the bacterium and the production of toxin, the possibility of intoxication occurs. This risk emphasizes the importance of cooking all food of animal origin derived from an environment in which Clostridium botulinum spores are likely to be present.
A lesser risk is presented by the consumption of fish or birds that are clinically affected by botulism at the time of death. Birds affected by botulism are unlikely to be able to fly and would likely be recognized as abnormal. Intoxication in fish would be more difficult to detect (Yule et al, 2006c) In either instance, as long as the meat is cooked prior to eating, the toxin will be destroyed.
There is no particular risk to people from handling birds or fish that have died of botulism. As with all dead animals, common sense precautions, such as the wearing of gloves and the practice of good personal hygiene, should be effective in protecting an individual against other infectious agents which might be present.
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 - the Caspian Tern, for example.
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 due to Type C botulism). On the other hand, certain species or regional populations may be critically affected.
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. 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.
Control of Type E Botulism is not possible at this time, as most of the causal factors are outside of human control. However, its occurrence in epidemic proportions on the lower Great Lakes is likely due to the effects of unplanned human actions, in this case the introduction of several species, including Zebra and Quagga Mussels and Round Gobies.
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.
Chiou, L.A., Hennessy T.W., Horn A., Carter G., Butler J.C. 2002. Botulism among Alaska natives in the Bristol Bay area of Southwestern Alaska: A survey of knowledge, attitudes and practices related to fermented foods known to cause botulism. International Journal of Circumpolar Health. 61: 50-60.
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.
Yule AM, LePage V, Austin JW, Barker IK, Moccia RD. 2006a. Repeated low-level exposure of the round goby (Neogobius melanostomas) to
Clostridium botulinum type E neurotoxin.
Journal of Wildlife Diseases. 42(3):494-500.
Yule AM, Barker IK, Austin JW, Moccia RD. 2006b. Toxicity of Clostridium botulinum type E neurotoxin to Great Lakes fish:
implications for avian botulism. Journal of Wildlife Diseases. 42(3):479-93.
Yule AM, Austin JW, Barker IK, Cadieux B, Moccia RD. 2006c. Persistence of Clostridium botulinum neurotoxin type E in tissues from selected
freshwater fish species: implications to public health.
Journal of Food Protection. 69(5):1164-7.
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