Clinical signs: Botulism causes LMN tetraparesis that starts in the pelvic limbs as mild weakness but progresses to tetraplegia in severe cases. Cranial nerves are often involved, producing facial paresis, dysphonia, megaoesophagus and regurgitation. Au-tonomic signs such as mydriasis and dry eye are variably present. Onset of signs usually occurs over 2-4 days and is often preceded by a history of dietary indiscretion (usually consuming spoiled meat) and vomiting or diarrhoea. Botulism has not been reported in cats.
Pathogenesis: Botulism is caused by absorption of the botulinum toxin following ingestion of spoiled carrion or raw meat. The botulinum toxin, produced by Clostridium botulinum, is taken up at the neuromuscular junction and prevents synaptic release of acetylcholine at the neuromuscular junction. There are several forms of the botulinum toxin, but botulinum C is the only form associated with canine disease ().
Diagnosis: History and clinical signs are indicative of the disease. Electrophysiological studies may be supportive of the diagnosis (decreased amplitudes of compound muscle action potential, CMAP). Reduced motor nerve conduction velocity has been reported suggesting that there is a concurrent neuropathy (). Definitive diagnosis is difficult to establish: presence of the botulinum toxin in the serum, faeces or vomitus may be detected using a specific antitoxin to perform a neutralization test in mice, and use of an ELISA has been reported. Often the toxin is no longer detectable by the time neurological signs are evident.
Treatment and prognosis: Treatment is supportive and recovery occurs over a period of approximately 3 weeks. Affected dogs should be turned regularly, kept clean and dry, and their bladder expressed if necessary. Megaoesophagus and regurgitation should be managed by intermittent suction of the oesophagus by means of a nasooesophageal tube, antacids (e.g. famotidine) to decrease acidity of stomach contents (decreases oesphagitis and effects of aspiration), and antibiotics for aspiration pneumonia if necessary. Ampicillin, aminoglycosides, erythromycin, ciprofloxacin and imipenem interfere with neuromuscular conduction and should be avoided. If megaoesophagus is present, the dog should be fed while held or propped with the head up and that position maintained for approximately 30 minutes after feeding. Arterial blood gas analysis should be performed to check for hypoventilation in tetraplegic animals and in animals that may have aspirated. Passive range-of-motion exercises and massage should be performed every 6 hours while the animal is recumbent.
If pulmonary function is not adversely affected, dogs have a good prognosis with adequate nursing. If aspiration pneumonia or hypoventilation develop, prognosis is grave, but recovery can occur if appropriate ventilatory support can be provided.
Drug-induced toxic neuropathy
These disorders are rarely encountered in clinical practice but certain drugs and substances have the potential to cause peripheral neuropathies. Examples include the chemotherapeutic drugs vincristine and cis-platinum. One case of vincristine-induced neuropathy has been reported: the dog was given 16 weekly doses of vincristine at a dose rate of 0.5 mg / m2 (). Signs improved following discontinuation of the drug. As radiation becomes more routine for the treatment of neoplasia, radiation-induced neuropathies will become more common. This can be a late effect and in an experimental study on intraoperative radiation in dogs paraparesis developed between 1 and 19 months after radiation if the dose exceeded 15 gray. There are rare reports of organophosphate-induced delayed neuropathy in cats occurring with chronic exposure. Thallium toxicity, from ingestion of insecticides and rodenticides that contain this substance, has been reported in dogs and cats but the banning of this substance has made this an extremely unlikely occurrence. In Europe there was an outbreak of a generalized peripheral neuropathy in cats that was determined to be the result of contamination of their food with the ionophore salinomycin (). The cats developed tetraplegia and many died or were euthanased. Similar signs have been reported in dogs that ingested food contaminated with lasalocid (). Contamination of food in both these instances occurred at the processing plant, as ionophores are frequently added to ruminant or porcine feed as a growth promoter.
Certain species of female ticks contain a toxin within their saliva that causes presynaptic blockade of acetylcholine release and a flaccid tetraplegia (). Signs appear after the tick has been attached for 3-5 days and progress over 1-3 days. They usually resolve within an equal period following removal of the tick, except in the case of the Australian tick, in which signs can progress following tick removal. This disease is not a problem in the UK as the tick species involved are not present in this country. It is encountered commonly in the USA and more severe forms occur in Australia and Africa.