This fact sheet was updated on 2/10/21.
This fact sheet was updated on 2/10/21.
Botulism is caused by a toxin produced by the soil bacterium, Clostridium botulinum. It causes paralysis and death in birds and is one of the deadliest know toxins. There are 7 different types of botulism toxin, A through F. Types C and E are most important in wild birds. Botulism in humans is mostly caused by Types A, B and E, but it is not a zoonotic disease.
Avian botulism is one of the most significant diseases of migratory birds; estimates suggest 10,000-50,000 birds are lost in most years. While losses from botulism not thought to affect wildlife populations, there is concern that endangered species may be at risk of dangerous impacts because of the disease. Botulism in wild birds has not been known to cause botulism in humans.
Botulism has been detected in at least 117 species of wild birds, but it is likely that all bird species are susceptible with a few exceptions. Vultures and other scavengers appear to be resistant to the toxin. Waterfowl and shorebirds are most susceptible. Filter feeding and dabbling waterfowl such as mallards, teal, and shovelers seem to be at greater risk because of their feeding habits. Fish eating birds such as common loons and gulls are also at high risk, while mergansers, mute swans, and grebes are at lower risk. Botulism likely occurs in any bird or mammal that scavenges dead fish, and it has been observed in bald eagles, wood ducks, and muskrats.
Many species of mammals and some fish can be affected by botulinum toxin. More commonly affected mammals include mink, foxes, cattle, horses, and sheep. Cats, dogs, and swine appear to be somewhat resistant, although this toxicity is occasionally diagnosed in dogs and swine.
Humans can contract botulism from food poisoning. Botulism is usually associated with aquatic habitats, so some cases of human botulism result from consumption of uncooked fish or marine products containing the toxins. Human cases are also often associated with home canned food items that have not been heated sufficiently.
Botulism has been reported in wild birds on every continent except Antarctica, but outbreaks occur more often in the United States and Canada than in other countries. The western United States in particular experiences large mortality events in waterfowl with relative frequency, especially dabbling ducks, due to Type C botulism. Type E botulism is relatively common in wild birds of the Great Lakes region, particularly fish-eating birds. In Michigan, birds inhabiting Lakes Huron and Michigan are often affected, while Ontario, Ohio, Pennsylvania, and New York observe botulism toxicities in birds near Lakes Ontario and Erie. Outbreaks usually occur in late summer or early fall when water temperatures are highest and water levels are low. Avian botulism was first detected around Lake Erie in 1964. Outbreaks of botulism in wild birds have occurred on the Pennsylvania border of Lake Erie from 1999 through 2004 and as recently as 2008. In 2008 roughly 10,000 birds from the Lake Erie region died of avian botulism, while in 2002 as many as 19,000 birds died in the area.
Transmission occurs when C. botulinum or the toxin in the environment or in a prey item is ingested. The bacteria are common in the soil of both terrestrial and aquatic environments and will only produce toxin under certain environmental conditions that favor growth, including high temperatures, no oxygen, abundant invertebrate populations and decomposing vertebrate carcasses.
Aquatic invertebrates ingest C. botulinum when feeding on sediment, and many die during the summer because of high water temperatures and low water levels. The bacteria within the invertebrates produce the toxin as the invertebrates decay, and waterfowl become intoxicated when they consume the dead invertebrates. The affected birds then die and maggots feeding on the carcasses pick up the toxin. These maggots are then eaten by other birds, which become sick, and the cycle continues. Large-scale bird die-offs occur as a result of this toxin amplification.
This mode of transmission is common with type C botulism in the western United States, but the maggot-carcass cycle also occurs with type E botulism outbreaks in the Great Lakes. Fish can also ingest the bacteria by directly feeding on sediment or by consuming invertebrates carrying the bacteria. After the fish die, the toxin is produced in the decaying carcasses and can affect any bird or mammal that may scavenge the dead fish. The zebra mussel and round gobie, a small fish, and both invasive species now common to the Great Lakes, appear to play a role in the transmission of botulism in the Eastern US. Zebra mussels seem to create an environment that is favorable for the growth of C. botulinum type E. The type E toxin becomes concentrated within the zebra mussels as they filter the water. Round gobies feed on these intoxicated zebra mussels. It is theorized that the botulinum toxin causes the round gobies to become easy prey for fish-eating and scavenging birds, which in turn become intoxicated and suffer from botulism.
The severity of clinical signs is influenced by multiple factors including the amount of toxin consumed, the type of toxin, and the animal species. Clinical signs appear more quickly and are more severe when animals consume larger amounts of toxin. The toxin prevents nerves from transmitting signals to muscles, which leads to flaccid paralysis. Intoxicated birds will exhibit progressive weakness. At first they may have difficulty flying due to weakening muscles. This will progress to a complete inability to fly, followed by inability to stand. Some birds drown because they are unable to hold their head above the water, while others die from an inability to breath due to paralysis of the respiratory muscles. Many affected animals will remain conscious and alert even though they cannot move. During outbreaks many birds are simply found dead. Birds found dead from botulism have no obvious post-mortem lesions and are usually in good body condition.
Laboratory tests must be performed to isolate the toxin from blood or tissue.
Birds with mild clinical signs can often be successfully treated by removing them from the contaminated environment and providing shelter, fresh water, and food. More severely affected birds require more intensive supportive care and may not survive. Antitoxins may be helpful, but they are rarely used for wildlife because of high cost and the need for large quantities during major outbreaks.
C. botulinum occurs naturally in soil and aquatic sediments, so it is unrealistic to attempt to completely eliminate botulism from wildlife populations. Most outbreaks occur in aquatic habitats in late summer when water temperatures are higher and water levels are lower, so attempts to stabilize water level and temperature may help prevent outbreaks. Fly control may reduce the risk of toxic maggots in the environment. Most importantly, prompt removal of dead fish, bird, and other animal carcasses is critical in preventing and limiting outbreaks. Several thousand toxic maggots can be produced from a single waterfowl carcass and consumption of just two or four of these toxic maggots can kill a duck, perpetuating the botulism cycle.
It is recommended to cook fish and waterfowl to at least 180F to destroy the botulinum toxin. Fish or waterfowl that appear sick or are dying in areas where avian botulism is known to be present should not be harvested for human consumption.