Arsenic Poisoning
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), degeneration of the spinal cord, optic nerve, and peripheral nerves occurs.
Clinical signs consist of tremors and paraparesis.
Mildly affected animals can recover after withdrawal of the feed additive.
Delayed Organophosphate Intoxication
Delayed organophosphate intoxication can occur after oral or topical administration of organophosphate-containing insecticides or anthelmintics, including haloxon.
Suffolk sheep have an inherited predisposition to this neurotoxicosis because they have low plasma arylesterase activity.
In addition to acute clinical signs, delayed paralysis can develop 1–4 weeks after exposure. Affected animals have progressive, symmetric paraparesis and occasionally become tetraplegic.
Diagnosis is based on clinical signs and history of exposure. On histological examination, Wallerian degeneration is most prominent in the spinal cord and brainstem.
The prognosis for severely affected animals is poor.
Sorghum Poisoning
Ingestion of cyanogenic (as well as nitrate-accumulating) plants such as Sorghum spp (eg, sorghum, Sudan grass, and Johnson grass) can cause degeneration of the spinal cord in horses and occasionally in cattle and sheep. Ingestion of these plants can also cause nitrate and nitrite poisoning.
The pathogenesis of spinal cord degeneration might be related to the high content of hydrocyanide in these grasses. Affected animals show 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 might improve with removal of the feed causing the problem; however, persistent deficits are possible.
Tetanus
Tetanus is a toxin-mediated neurological disease caused by the tetanus toxin (tetanospasmin) produced by the vegetative form of the bacterium Clostridium tetani. Manifestations of tetanus occur subsequent to the toxin entering peripheral nerve endings, traveling retrograde along the axons and synapses, and ultimately entering the CNS. Tetanus can also affect the autonomic nervous system, such as when the brainstem is involved.
Susceptibility to tetanus varies markedly among species; dogs and cats are fairly resistant compared with horses. Humans are also susceptible to tetanus.
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 is recumbent with opisthotonos and reflex muscle spasms.
Diagnosis of tetanus is based on characteristic clinical signs.
Treatment consists of wound care, administration of antimicrobials to kill any remaining organisms, and tetanus antitoxin. In mild cases, the prognosis is good with early treatment. In severe cases, death can occur because of respiratory paralysis.
