Page 793 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

752 SECTION | XI Bacterial and Cyanobacterial Toxins

VetBooks.ir outbreaks are common, botulism is a more significant documented in birds as old as 14 weeks. Coprophagy has
also been implicated as a causative factor in poultry out-
problem for waterfowl, resulting in millions of deaths
breaks because both botulinum toxin C1 and C. botulinum
worldwide. Avian species are sensitive to serotypes A, B,
C1, and E, although serotype C1 is most commonly associ- are secreted in cecal droppings. Broiler outbreaks are also
ated with outbreaks. Outbreaks of serotype C1 intoxication more likely to occur in hot weather.
have been reported worldwide, whereas outbreaks of sero- As in other species, morbidity and mortality of avian
type A botulism have only been reported in western botulism increases with ingested dose. The onset of clini-
regions of North and South America; serotype B in the cal symptoms may be from a few hours to 2 days postex-
eastern United States, England, Europe, and China; and posure. The mortality rate in broilers has been reported to
serotype E in the Great Lakes and North Sea. Interestingly, be as high as 27%, whereas thousands to millions of birds
serotype A was found to be more toxic than serotype C1 may have been lost as a result of outbreaks in waterfowl.
when administered IV to chickens; however, when given Botulism may be a limiting factor for waterfowl popula-
orally, serotype C1 demonstrated greater toxicity. tion growth in predisposed areas of the United States
The etiology of botulism among wild avian species (Jensen and Price, 1987).
and waterfowl differs from that observed in other animals
and involves a complex cycle involving environmental
contamination, toxicoinfection, bird die-offs, bacterial Clinical Signs, Diagnosis, and Treatment
proliferation in bird carcasses, and invertebrate vectors. As in other species, avian botulism is characterized by
C. botulinum often colonizes the intestinal tract and lower motor neuron deficits resulting in flaccid muscle
cecum of clinically normal birds, increasing the potential paralysis. Paresis begins in the legs and progresses crani-
for toxicoinfection in avian species (Dohms, 2003). ally to involve the wings, neck, and eyelids. Mildly
Because these birds are already seeded with the bacteria, affected birds may appear ataxic, reluctant to move, have
upon death, avian carcasses provide an excellent substrate a ruffled coat, and have easily epilated feathers. The
for C. botulinum growth. The proliferating bacteria spread wings may droop and the neck may become flaccid,
from the GI tract to other tissues, the carcass becomes fly- hence the name “limberneck.” Diarrhea is often noted in
blown, and toxin accumulates in the fly larvae. broilers. As the disease progresses, birds become recum-
Invertebrates concentrate the bacterium or toxin after bent. Neck muscles become paralyzed, and birds eventu-
feeding on contaminated carcasses; however, due to their ally lie down with necks extended out, resting on the
neurophysiological differences, botulinum toxins do not ground. Birds may appear comatose due to eyelid paraly-
affect insects and aquatic invertebrates. Subsequently, sis. Dyspnea may develop as paralysis progresses. Birds
birds ingest these animals and accumulate lethal amounts usually die from respiratory failure and dehydration.
of the toxins. One gram of fly larvae may contain Broilers may succumb to hyperthermia as sick birds are
5
1.8 3 10 MU, and ingestion of as little as eight fly larvae smothered by others and the respiratory mucosal cooling
was sufficient to kill a pheasant. Bird and invertebrate mechanism is compromised.
die-offs perpetuate botulism outbreaks by increasing the The diagnosis of avian botulism is based on clinical
levels of C. botulinum in soils, lakes, rivers, and estuaries. signs, a lack of specific pathological changes, and the iso-
Environmental factors such as shallow alkaline waters, lation of toxin from serum/tissues of clinically ill birds.
warm seasons/summer months, and flooding of mudflats Although no pathognomonic changes have been
or dried-out lakes may promote invertebrate die-offs, fur- described, postmortem hepatic and renal congestion along
ther enhancing environmental levels of C. botulinum.As with signs of dehydration may be found. The most defini-
C. botulinum levels increase in the environment, the intes- tive diagnosis of botulism is the isolation of toxins from
tinal tracts of wild birds and waterfowl become seeded the sick bird. Ten mL of blood is the suggested minimum
with the bacteria, and any cause of bird deaths can trigger amount for the mouse bioassay; however, if necessary,
an outbreak of botulism. equal aliquots of blood from individual sick birds may be
Contaminated feed, water, litter, carcasses, and insects pooled to accommodate volume requirements of the assay
may be associated with botulism in broilers. Often, the (Dohms, 1987). Following a positive result from the
source of the toxins cannot be identified, and toxicoinfec- mouse bioassay, the serotype can be identified using the
tion has been hypothesized as the perpetuating factor. C. mouse neutralization test. Most outbreaks of avian botu-
botulinum has been isolated from the intestinal tract and lism are due to botulinum toxin/C1; therefore, antiserum
cecum of healthy birds; furthermore, the chicken body for serotype C1 is usually tested first. Isolation of toxins

temperature (41 C) and cecal pH (7.4) are optimum for or C. botulinum from the bird intestines, cecum, or other
C. botulinum growth (Miyazaki and Sakaguchi, 1978; tissues may aid in a diagnosis; however, these tests are
Trampel et al., 2005). Most broiler outbreaks have less valuable because the bacterium can be isolated from
occurred in chickens between 2 and 3 weeks of age; how- the intestinal tract of healthy birds. Furthermore, isolation
ever, an outbreak in postcaponized chickens was of toxins or the bacterium from carcass tissues is not