JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. American Association of Avian Pathologists is collaborating with JSTOR to digitize, preserve and extend access to Avian Diseases. SUMMARY Clostridium perfringens type A, Eimeria acervulina, andEimeria necatrix were used to produce necrotic enteritis in chickens. The disease was produced in all groups of birds that received feed contaminated with C. perfringens. Mortality due to necrotic enteritis was highest (53%) in birds infected with E. acervulina before infection with clostridia. There was a significant difference in mortality rates between birds infected with E. acervulina and birds infected with E. necatrix before infection with C. perfringens. Mortality rates also differed significantly between the group infected with E. necatrix and the group that received only feed contaminated with C. perfringens.It was concluded that under field conditions, coccidia can play a significant role in the occurrence of necrotic enteritis when a sufficient number of toxigenic strain of C. perfringens type A is present.The pathologic changes induced by clostridia and coccidia are described.

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Necrotic enteritis was consistently reproduced when enough active broth culture of Clostridium perfringens type A was infused intraduodenally. Typical lesions of necrotic enteritis were seen as early as 5 hr after infusion was begun. The histologic lesions observed at 1 hr were characterized by edema in the lamina propria and desquamation of epithelial cells. Large numbers of clostridia were seen among these sloughed cells. Coagulation necrosis of the tips of villi became evident at 3 hr and was marked at 5 hr. Many clumps of clostridia were obvious among the necrotic tissue. At 8 and 12 hr the necrotic lesions extended to involve most of the villus structures. Morphologically abnormal erythrocytes were evident in the visceral organs at 12 hr.

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Twenty-four 4-week-old poults, free from Mycoplasma meleagridis and M. gallisepticum, were inoculated with a velogenic viscerotropic strain of Newcastle disease virus. Clinical signs (gasping, coughing, and dyspnea) developed 4-5 days postinoculation, continued until nervous derangement appeared, and then (usually 3 days after initial clinical signs appeared) declined in severity. Prominent nervous signs were paresis and paralysis of the extremities, with pronounced head-shaking. The most constant gross lesions detected involved the airsacs. The abdominal sacs of a few poults contained a large accumulation of yellowish, cheesy exudate and there was cloudiness of the thoracic airsacs of all inoculated poults. A few turkeys had tracheitis with some catarrhal exudates and casts in the lower part of the tracheal lumen. Congestion of lepto-meningeal vessels usually correlated with the severity of the nervous signs. The histologic lesions were characterized by both degenerative and proliferative changes with predominantly mononuclear cell and heterophil infiltrations throughout the body. The obvious lesion seen in the recovery stage of the disease was proliferation of lymphofollicular nodules in the parenchymatous organs.