Not Found

Find information on animal health topics, written for the veterinary professional.

Toxic Disorders of the Peripheral Nerve and Neuromuscular Junction

By William B. Thomas, DVM, MS, DACVIM (Neurology), Neurology and Neurosurgery, Department of Small Animal Clinical Sciences, University of Tennessee


Botulism is intoxication with a neurotoxin produced by Clostridium botulinum. It is seen in horses, cattle, sheep, and birds worldwide. It is uncommon in dogs and pigs. (For a complete discussion, see Botulism and Botulism.)

Ionophore Toxicity:

(Also see Ionophores.) Ionophore toxicity has been seen in cattle, sheep, pigs, dogs, cats, and poultry; horses are particularly susceptible. Lasalocid-contaminated food has caused flaccid tetraparesis with hyporeflexia in dogs. In 1995, cat food contaminated with sialinomycin caused an outbreak of polyneuropathy in ~850 cats in the Netherlands and Switzerland. Affected cats had acute onset of tetraparesis, hyporeflexia, dysphagia, respiratory weakness, and eventual muscle atrophy. Histopathologic findings consisted of degeneration of distal sensory and motor axons. Affected animals usually recover with supportive care and removal of the offending food.

Organophosphate Poisoning:

Poisoning involving organophosphates (see Organophosphates (Toxicity)) can cause three syndromes. The acute form is due to irreversible inhibition of acetylcholinesterase, resulting in increased acetylcholine activation of the nicotinic and muscarinic receptors in the parasympathetic nervous system, nicotinic receptors at the neuromuscular junction, nicotinic receptors of the sympathetic nervous system, and cholinergic pathways within the CNS. Clinical signs of acute toxicity include muscarinic signs (eg, vomiting, diarrhea, salivation, bronchoconstriction, increased bronchial secretions), nicotinic signs (eg, muscle tremor and twitching), and CNS signs (eg, behavioral change, seizures).

The intermediate form is primarily manifest as generalized muscle weakness due to accumulation of acetylcholine at the nicotinic neuromuscular junction, causing a depolarizing block. Cats are especially prone to this form of toxicity, most commonly due to chlorpyrifos. Affected cats often do not have obvious signs of acute toxicity, instead developing tetraparesis and ventroflexion of the neck several days after exposure. Mydriasis is common. Diagnosis is based on a history of exposure and the presence of typical clinical signs. Decreased cholinesterase activity in whole blood is supportive. Treatment of acute or subacute toxicity should include administration of atropine (0.2 mg/kg, IM) if dyspnea due to bronchial secretions and bronchoconstriction is present. Atropine will not relieve the nicotinic signs of tremors and weakness, which should be treated with pralidoxime chloride (20 mg/kg, IM or SC, bid). Diphenhydramine (4 mg/kg, IM or PO, bid) may help alleviate muscle weakness. Treatment for several weeks may be necessary.

The delayed form of toxicity is associated with degeneration of distal axons in the peripheral and central nervous systems. It is unrelated to inhibition of acetylcholinesterase and is seen only with certain organophosphates. Signs develop several weeks after exposure and are characterized by weakness and ataxia of the pelvic limbs. In horses, laryngeal paralysis has also been reported. There is no specific treatment.

Tick Paralysis:

Rapidly progressive paralysis may be caused by several species of ticks (see Tick Paralysis). Some female ticks produce a salivary toxin that interferes with acetylcholine release at the neuromuscular junction. In North America, Dermacentor variabilis and D andersoni may affect dogs, sheep, and cattle. In Australia, Ixodes holocyclus causes an especially severe form of tick paralysis in dogs, cats, cattle, sheep, pigs, llamas, horses, and occasionally people. In Africa, the major tick associated with paralysis is I rubicundus, with cattle, sheep, goats, and rarely dogs affected. A wide variety of ticks affect animals in Europe and Asia.

Clinical signs consist of paraparesis that progresses within 24–72 hr to flaccid tetraplegia, with weak to absent spinal cord reflexes. Sensory perception and consciousness remain normal. Dysphagia, facial paralysis, masticatory muscle weakness, and respiratory paralysis may develop in severe cases. Treatment consists of removal of the tick and application of a topical acaricide to kill any hidden ticks. For all except I holocyclus paralysis, prognosis is good, and recovery occurs within 1–2 days. Tick antiserum is available for treatment of I holocyclus paralysis, but prognosis is guarded because death from respiratory paralysis may occur despite treatment.