Toxicoses of the Spinal Column and Cord in Animals

Arsenic poisoning (toxicosis) can occur in swine because of an overdose of organoarsenicals, which are often used as feed additives to promote growth and to control swine dysentery. With 3-nitro-4-hydroxyphenylarsonic acid poisoning (“3-nitro poisoning”), there is degeneration of the spinal cord, optic nerve, and peripheral nerves. Clinical signs consist of tremors and paraparesis. Mildly affected animals can recover after withdrawal of the offending feed.

Delayed organophosphate intoxication can occur after oral or topical administration of organophosphate-containing insecticides or anthelmintics, including haloxon. In addition to the acute clinical signs, delayed paralysis can develop 1–4 weeks after exposure. Suffolk sheep have an inherited predisposition to this neurotoxicosis because they have low levels of plasma arylesterase activity. Affected animals have progressive, symmetric paraparesis and occasionally become tetraplegic. Diagnosis is based on clinical signs and history of exposure. On histologic examination, there is Wallerian degeneration, most prominent in the spinal cord and brainstem. The prognosis for severely affected animals is poor.

Ingestion of cyanogenic (as well as nitrate-accumulating) plants such as Sorghum spp (eg, Sorghum, Sudan, and Johnson grass) can cause degeneration of the spinal cord in horses and occasionally in cattle and sheep (or nitrate and nitrite poisoning). The pathogenesis may be related to the high content of hydrocyanide in these grasses. There is ataxia and weakness of the pelvic limbs and incontinence. Urine retention often leads to cystitis and hematuria. Diagnosis is based on clinical features and a history of exposure. Clinical signs of sorghum poisoning may improve with removal of the offending feed, although persistent deficits are possible. (Also see Sorghum Poisoning.)

Tetanus is caused by toxins produced by the vegetative form of Clostridium tetani. Susceptibility varies markedly among species; dogs and cats are fairly resistant compared with horses. Clinical signs of tetanus usually develop within 5–10 days after infection. These include localized or generalized muscle stiffness and extensor rigidity, dysphagia, protrusion of the third eyelid, and contracted masticatory (lockjaw) and facial (risus sardonicus) muscles. In severe cases, the animal may be recumbent with opisthotonos and reflex muscle spasms. Diagnosis of tetanus is based on characteristic clinical features. Treatment consists of wound care, administration of antimicrobials to kill any remaining organisms, and tetanus antitoxin. In mild cases, prognosis is good with early treatment. In severe cases, death may occur because of respiratory paralysis.