Botulism is a systemic toxemia in dogs caused by Clostridium botulinum.
Toxemia associated with this disease is often seen in dogs that have consumed C. botulinum type C exotoxin or spores present in carcases of birds. The ingested preformed toxin, absorbed into the blood, binds to nerve terminals and blocks release of acetylcholine. The result is flaccid muscle paralysis. Death is due to cardiac and respiratory arrest.
Clostridium botulinum produces 7 potent neurotoxins, but only 1 type (type C, BoNT/C) has been implicated in botulism in dogs.
Clinical signs in affected dogs are usually vague initially, followed rapidly by progressive tetraparesis/plegia due to peripheral nerve dysfunction. Other signs such as facial weakness, dysphonia and respiratory compromise are common.
Diagnosis requires demonstration of the toxin via ELISA in serum, feces, vomitus, or samples of the ingested food. It is often difficult to make a definitive diagnosis of botulism because circulating toxin levels are often low, source material may be absent, and available analytical methods lack sensitivity.
Electromyography and electroneurography are usually supportive of a diagnosis and affected dogs have characteristic prolonged insertional activity, low amplitude of the evoked muscle action potential, decreased amplitude of muscle action potential and slowing of motor and sensory velocities in the peripheral nerve.
Treatment is usually supportive. Placement of a urinary catheter is usually required due to retention overflow.
Broad-spectrum antimicrobials are often indicated, such as cephalosporin 15 mg/kg twice daily. Gastric feeding tube are recommended in dysphagic dogs.
Most dogs eventually recover in 1 - 2 weeks.
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