Trio-o-cresyl
phosphate (
TOCP),
leptophos [O-methyl O-(4-bromo-2,5,-dichlorophenyl) phenylphosphonothioate] and
cyanofenphos [O-ethyl O-(4-cyanophenyl) phenyl-phosphonothioate] were used to determine whether adult peking ducks would exhibit neurotoxicity after exposure to such chemicals. Clinical, histopathological, and specific biochemical tests were used to detect the
neurologic dysfunctions that were induced by these neurotoxic agents. Ducks were orally treated with
TOCP or
leptophos at 100 or 10 mg/kg X d for 30 d, respectively. Another group of ducks received
cyanofenphos at 4 mg/kg X d for 10 d. All the
TOCP- and
leptophos-treated ducks developed clinical signs of delayed neuropathy, as manifested by
ataxia and
paralysis. Two of the
cyanofenphos-treated ducks died from
cholinergic effect during the course of dosing. Surviving ducks of this group completely recovered from the
cholinergic effect 2 or 3 d after finishing the dosing regimen. However, they developed signs of delayed neurotoxicity 10-17 d later. Surviving ducks of all groups were sacrificed for biochemical and/or histopathologic tests 1 d after the last treatment or when they became paralyzed. Histopathologic examinations indicated that degenerative lesions of axons consistent with the type occurring in delayed neurotoxicity were seen in all
TOCP-,
leptophos-, or
cyanofenphos-treated ducks and were specially evident in sections of spinal cord. Biochemically, it was found that duck brain
neurotoxic esterase (NTE) activity was inhibited in vivo to less than 15% of control levels as measured 24 h after the last treatment with
TOCP,
leptophos, or
cyanofenphos. These results indicate that adult peking ducks could be used to screen
organophosphorus compounds for delayed toxic neuropathy.