Species: Pig Strain/breeder: German cross bred Sex: Female Age: 9 months Study type: Nutritional intoxication Treatment: - Animal status: Euthanasia Clinical findings: Hind limb incoordination, posterior paralysis Organ: Spinal cord Macroscopic finding(s): muscle degeneration adjacent to the ischiadic tuber Staining: H&E Literature: Summers BA, Cumming JF, deLahunta A (1995) Veterinary neuropathology. Mosby, St. Louis, Baltimore, pp 208-350 Shaw IC, Parker RM, Porter S, Quick MP, Lamont MH, Patel RKP, Norman IM, Johnson MK (1995) Delayed neuropathy in pigs induced by isofenphos. Vet Rec 136: 95-97 Done SH (1992) Organophosphorus poisoning in sows. Pig Vet J 28: 110-115

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Abstract

Aim of the study
Organophosphorus poisoning in pigs can occur as an acute intoxication with clinical signs of parasympathetic overstimulation or as transplacental intoxication inducing cerebellar hypoplasia in piglets. A delayed neuropathy caused by organophosphorus compounds is characterized by a paralytic syndrome.

Materials & methods
In a breeding herd of 270 sows a sudden onset of atactic gait and hind limb paralysis was observed. The affected animals had received a commercially produced feed mix. Three sows were referred to the veterinary school of Hannover for clinical and pathomorphological investigations.

Results
Clinically, the animals were afebrile, reluctant to stand with the hind limbs and remained in a dog sitting position. The cutaneous sensitivity was normal. Pathomorphological findings consisted of degenerative or necrotizing skin and muscle alterations due to the hind limb paralysis. Histologically, bilaterally symmetric demyelinisation of the dorsal spinocerebellar tracts of the cervical, thoracic and lumbar spinal cord were found characterized by dilated myelin sheaths, swollen axons and occasional infiltration of myelinophages. No signs of inflammation were present. Toxicologic analysis of a feed sample revealed an organophosphorus contamination with a concentration of 2.01 mg/kg isofenphos. As source of the toxic compound a seed dressing was identified in the feed. The case history revealed that the contamination of the feed was caused by mixing incriminated rape seeds into the feed. The calculated dose of isofenphos was about 1.7 mg/kg body weight.

Conclusions
Selected compounds of organophosphorus have a neurotoxic effect by inhibition of a "neuropathy target esterase". The function of this enzyme is not well characterized. Following phosphorylation and "aging" of this protein, an interference with protein synthesis occurs leading to progessive axonal degeneration with clinically preferential hind limb paresis.