Abstract
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‐ortbo‐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.