Diffuse lower motor neuron dysfunction developed in a group of American Foxhounds while they were hunting. Of 19 dogs, 10 became weak and 9 became quadriplegic. Three of the quadriplegic dogs died before treatment could be instituted. The remaining quadriplegic dogs recovered after being given supportive treatment, with (4 dogs) or without (2 dogs) trivalent (types A, B, E) botulinal antitoxin. The 10 dogs that were weak recovered without treatment. A markedly decreased amplitude of evoked potentials and increased chronaxy were found by electromyographic examination of 2 of the quadriplegic dogs. A toxic substance that was neutralized by type C botulinal antitoxin in mouse inoculation tests was in the serum and feces of the most severly affected dog presented alive and in a fecal extract of another affected dog. In the one dog necropsied, neither gross nor histologic lesions were found in the central or peripheral nervous systems or in the skeletal musculature. The history, clinical signs, electromyographic findings, toxin neutralization tests in mice, and absence of histologic abnormalities in the neuromuscular system provided evidence for the diagnosis of C botulism.