Shell L, Jortner B S, Ehrich M
Virginia-Maryland Regional College of Veterinary Medicine, Blacksburg 24061.
J Toxicol Environ Health. 1988;25(1):21-33. doi: 10.1080/15287398809531186.
The adult chicken provides the generally accepted animal model for organophosphorus-induced delayed neuropathy, exhibiting both clinical signs and histopathological damage after exposure. In this study, noninvasive electrodiagnostic methods were used for assessment of the development of neuropathy after administration of a single dose of protoxicant tri-ortho-tolyl phosphate (TOTP, 360 and 500 mg/kg po) and active congener phenyl saligen phosphate (PSP, 2.5 and 6 mg/kg im). Onset and severity of clinical signs were dose-related for both organophosphorus compounds. Extensive peripheral nerve lesions consistent with advanced stages of organophosphorus-induced delayed neuropathy were noted in selected chickens examined 19 d after TOTP administration. Needle electromyographic examinations of gastrocnemius, anterior tibialis, semitendinosus, and semimembranosus muscles were done before exposure and on d 8, 15, and 19 after exposure to TOTP and on d 8, 15 and 17 after exposure to PSP. Untreated chickens (negative controls) were also examined at each session. An untreated chicken with a transected sciatic nerve (positive control) was examined on d 13, 20, and 23 posttransection. Prolonged insertional activities were found in both treated and untreated chickens. Denervation potentials were found in only 2 of the 20 chickens administered organophosphates. Denervation potentials were, however, easily visible 13 d following transection of the sciatic nerve of a normal chicken. Needle electromyography could not evaluate organophosphorus-induced delayed neuropathy in chickens of this study.