Trio‐o‐cresyl phosphate (TOCP), leptophos [O‐methyl O‐(4‐bromo‐2,5,‐dichlorophenyl) phenylphosphonothioate] and cyanofenphos [O‐ethyl O‐(4‐cyanophenylj 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· d for 30 d, respectively. Another group of ducks received cyanofenphos at 4 mg/kg·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 for 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.