Page 796 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Botulinum Neurotoxins Chapter | 55 755

VetBooks.ir clinically ill animals. Decreases in the amplitudes of com- serotypes A, B, and E is available in the United States;
this antitoxin is less useful for dogs and cats, which are
pound muscle action potentials and motor unit potentials
usually affected by serotype C (Barsanti, 2006). However,
are often detected. Furthermore, fibrillation potentials and
decreases in nerve conduction velocity may also be the heptavalent antitoxin is available in other countries
detected. In order to make a definitive diagnosis, toxin (Byrne and Smith, 2000; Arnon et al., 2001a,b). Because
must be identified in serum, vomitus or gastric contents, adverse reactions to antitoxin may occur, and patients
feces, or food samples from animals showing clinical with mild disease often recover with supportive care
signs. The gold standard MBA appears to have adequate alone, antitoxin administration is usually reserved for
sensitivity for the detection of toxin in canine and feline severe cases.
biological samples or in carrion. Note that the isolation of
C. botulinum bacteria through cultures of feces, GI con-
tents, or viscera is not a definitive diagnosis because this CONCLUDING REMARKS AND FUTURE
bacterium can be isolated from the GI tract and viscera of DIRECTIONS
healthy dogs.
Much of the recent research in to the modes of action of
Differential diagnoses for canine botulism should
botulinum toxins has been driven by the pharmaceutical
include tick paralysis, polyradiculoneuritis (coonhound
development of botulinum toxin serotype A as a pharma-
paralysis), myasthenia gravis, coral snake envenomiza-
ceutical product; however much less research effort has
tion, and the dumb form of rabies. Both the lower motor
been directed towards the control and treatment of the dis-
neuron deficits and EMG findings are similar to those of
ease. Control is still heavily based on reducing the risk of
tick paralysis and polyradiculoneuritis; however, due to
exposure via good husbandry techniques and vaccination
its action on cholinergic terminals, botulism also causes
(where available). Treatment is still heavily based on the
cranial nerve and autonomic deficits. The nature of botu-
use of antitoxins for the neutralization of toxin within the
lism outbreaks to affect multiple animals further differ-
circulation plus basic supportive care. Currently there are
entiates the disease from other causes of lower motor
no forms of treatment that directly block the effects of the
neuron dysfunction.
toxins in the presynaptic nerve terminals and/or reduce
Treatment of canine botulism consists mainly of sup-
the persistence of the toxins at these locations. This type
portive care (Critchley, 1991; Barsanti, 2006). If the
of treatment modality, as well as improvements in rapid
ingestion of toxin-contaminated food has been recent,
diagnosis and prevention are the likely areas of future
gastric lavage, cathartics, and enemas may be used to
research and development.
decrease toxin absorption from the GI tract. However, as
in other species, magnesium sulfate should be avoided.
Supplemental fluids should be administered as needed to REFERENCES
maintain hydration. Nutritional support via orogastric or
parenteral administration may also be needed. Animals Allison, M.J., Maloy, S.E., Matson, R.R., 1976. Inactivation of
should be monitored for aspiration pneumonia due to Clostridium botulinum toxin by ruminal microbes from cattle and
megaesophagus and decreased gag reflexes. If constipa- sheep. Appl. Environ. Microbiol. 32, 685 688.
Antonucci, F., Rossi, C., Gianfranceschi, L., et al., 2008. Long distance
tion develops, enemas and stool softeners may be admin-
retrograde effects of botulinum neurotoxin A. J. Neurosci. 28,
istered. Manual expression of the bladder may be required
3689 3696.
to decrease the occurrence of urinary tract infections.
Arnon, S.S., Schechter, R., Inglesby, T.V., et al., 2001a. Consensus state-
Topical ophthalmic ointments should be used to prevent
ment: botulinum toxin as a biological weapon: medical and public
corneal ulcers, which may result from diminished palpe- health management. J. Am. Med. Assoc. 25, 1059 1070.
bral tone and tear production. Adequate bedding and fre- Arnon, S.M., Schechter, R., Inglesby, T.V., et al., and Working Group
quent repositioning are necessary to prevent the on Civilian Biodefense, 2001b. Botulinum toxin as a biological
development of decubital ulcers. In cases in which respi- weapon: medical and public health management. JAMA 285:
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necessary. Antimicrobial therapy may be needed for sec- Barash, J.R., Arnon, S.S., 2014. A novel strain of Clostridium botulinum
ondary infections; however, as in other species, aminogly- that produces type B and type H botulinum toxins. J. Infect. Dis.
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cosides, tetracycline, procaine penicillin, metronidazole,
Barsanti, J.A., 1990. Botulism. In: Greene, C.E. (Ed.), Infectious Disease
aminopyridines, and guanidines should be avoided.
of the Dog and Cat. Saunders, Philadelphia, pp. 515 520.
Administration of the equine antitoxin in small ani-
Barsanti, J.A., 2006. Botulism. In: Greene, C.E. (Ed.), Infectious Disease
mals is controversial. By the time clinical signs are noted,
of the Dog and Cat, third ed. Saunders, Philadelphia, pp. 389 394.
antitoxin is likely to be ineffective because most of the Barsanti, J.A., Walser, M., Hatheway, C.L., et al., 1978. Type C botu-
toxin is already bound to the nerve cell or has translocated lism in American foxhounds. J. Am. Vet. Med. Assoc. 172,
into the neuron. Only the trivalent antitoxin vaccine for 809 813.