Page 795 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

754 SECTION | XI Bacterial and Cyanobacterial Toxins

VetBooks.ir reports of canine botulism in hunting breeds (Barsanti the exposed cats died, those that survived recovered sig-
nificantly by 6 days postintoxication.
et al., 1978; Richmond et al., 1978; Jensen and Price,
Lower motor neuron dysfunction and, to a lesser
1987). Farrow et al. (1983) reported the occurrence of
botulism in three dogs after the consumption of a rotten extent, cranial nerve and autonomic nervous system defi-
duck carcass. Outbreaks of botulism (typically toxins C cits are observed in canine botulism. Paresis begins in the
and D) in cattle and sheep have been associated with the hind limbs and progresses cranially, ultimately resulting
feeding of contaminated poultry litter in silage (Egyed, in flaccid muscle paralysis and quadriplegia. Interestingly,
1987; McLoughin et al., 1988). No cases of human botu- dogs with botulism maintain the ability to wag their tail.
lism resulting from the consumption or handling of con- Tremors of the masseter and temporal muscles may be
taminated birds have been reported, although both noticed. Muscle atrophy is variable throughout the course
scenarios have likely occurred. The risk for the human of the disease. Mydriasis, decreased pupillary light
acquisition of botulism from avian species appears to be response, decreased palpebral reflexes, and decreased or
limited. Although Smart et al. (1980) reported an outbreak weak vocalizations may occur. Hyperemic conjunctiva
of serotype C in nonhuman primates, humans do not and decreased Schirmer tear tests may be noted. Heart
appear to be susceptible to serotypes C or D following rates and respiratory patterns are variable; however, as
oral exposure (Jensen and Price, 1987). Furthermore, abdominal muscle tone diminishes, diaphragmatic breath-
proper cooking of poultry should denature any toxin pro- ing may be noted. Regurgitation, megaesophagus, urinary
tein and eliminate the possibility of transmission through retention, and constipation are also observed. Secondary
consumption. complications include aspiration pneumonia, bilateral
keratoconjunctivitis sicca, and urinary tract infections. If
paralysis progresses to the respiratory muscles, death may
Canine and Feline Botulism occur from respiratory failure; however, death may also
result from progressive secondary pneumonia or urinary
Although carnivores are thought to be more resistant to
the development of botulism, cases of canine botulism tract infections. If secondary complications do not arise,
have been occasionally documented in the United States, the prognosis for canine botulism is good. Recovery
Great Britain, continental Europe, and Australia. Most occurs in the reverse order from that of the onset of paral-
reported cases of botulism in dogs result from the inges- ysis; cranial nerve function and motor function of the
tion of botulinum toxin C1-contaminated carrion; how- neck and limbs return. In the one case study of natural
ever, a few cases of serotype D have been documented in botulism in cats, clinical signs were similar to those of
Senegal (Barsanti, 1990, 2006). Barsanti et al. (1978) dogs. Motor deficits and paresis were noted; however,
described an outbreak of type C1 botulism in a hunting cranial nerve reflexes were normal. Depression, anorexia,
mild dehydration, tachycardia, and urinary retention were
colony of American Foxhounds; however, the source of
also noted.
the toxin was not identified. Farrow et al. (1983)
As with EGS in the horse, there has also been specula-
described type C1 botulism in three young Australian
tion of an association between feline dysautonomia
Cattle Dogs following the ingestion of rotting duck car-
(Key Gaskell disease) and botulinum toxin serotype C.
casses found in a local Sydney park. Canine botulism has
Clinical signs for feline dysautonomia include depression,
also been associated with the ingestion of contaminated
anorexia, vomiting, regurgitation, mydriasis, constipation,
raw meat (Darke et al., 1976).
and urinary retention; however, the somatic lower motor
Until recently, the only documented cases of feline
neuron paralysis characteristic of classical botulism is not
botulism were experimentally induced; however, Elad
observed. Histological evidence of neuronal degeneration
et al. (2004) described a natural outbreak of botulism in
in autonomic ganglia confirms the diagnosis of dysauto-
eight cats that ingested parts of a pelican carcass contami-
nomia. Interestingly, botulinum toxin serotype C was
nated with botulinum toxin serotype C1. Serotype C1 bot-
detected in feces, ileal contents, and foodstuffs of cats dis-
ulism has also been reported in lions (Critchley, 1991).
playing symptoms of dysautonomia (Nunn et al., 2004).
Furthermore, affected cats had higher levels of antibotuli-
Clinical Signs, Diagnosis, and Treatment num toxin serotype C and C. botulinum surface antigen
The onset of canine botulism can occur within hours or as IgA in their feces compared to control cats.
late as 6 days postexposure. Severe cases are associated With the exception of dehydration or secondary infec-
with an earlier onset of clinical signs. The course of the tion, the CBC count, blood chemistry, urinalysis, and CSF
disease usually ranges from 12 to 24 days. In the clinical analysis are usually within normal limits in canine and
report of an outbreak of feline botulism, clinical symp- feline botulism. Thoracic radiographs may reveal a mega-
toms were first noted 3 days postingestion of contami- esophagus and aspiration pneumonia. Electromyographic
nated pelican muscle (Elad et al., 2004). Although 50% of findings may indicate lower motor neuron disease in