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Experimentally induced pulmonary aspergillosis in one-day-old chicks resulted in some with no clinical signs or little damage while others developed marked interstitial pneumonia. Chicks with severe lung damage died from respiratory failure (60%) or developed pulmonary hypertension followed by right ventricular hypertrophy and dilation, right ventricular failure from valvular insufficiency, portal hypertension and ascites (10.7%). Chicks that developed ascites before day 16 (13/31) had shown mouth-breathing and other signs of hypoxia and developed pulmonary hypertension, probably from hypoxia-induced polycythaemia. Most chicks that developed ascites after day 16 (18/31) had not shown an increased depth or rate of respiration indicating that they had not been significantly hypoxic. Microscopic examination of lung tissue indicated that in these chicks the pulmonary hypertension was caused by lung consolidation and fibrosis restricting blood capillary space and resulting in cor pulmonale.

SUMMARYCryptosporidial infection was found in 25 layer and four broiler chickens, aged 40 to 80 days, from 11 flocks on six poultry farms. The infection appeared in 1975 in broiler chickens and in 1976 in layers. On one of the poultry farms the infection occurred over a period of 2.5 years. Tissues most frequently affected with cryptosporidia were the bursa of Fabricius (85%), followed by the respiratory tract (nasal cavity, infraorbital sinus, larynx and trachea) (41%) and caeca (11%). Cryptosporidia in various stages of its life cycle were demonstrated histologically and electron microscopically attached to the host cells, and they were identical to those previously reported in other animals and humans. Hypertrophy and hyperplasia of the lining epithelial cells were noted in both the bursa of Fabricius and the respiratory tract. The histological alterations in the respiratory tract, especially the trachea, were sufficient to consider cryptosporidia as a primary cause of respiratory disease.

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ABSTRACT. A female Shetland sheep dog died suddenly with hemorrhagic diarrhea and vomitting, and was examined pathologically and microbiologically. Gross pathological change was restricted to the intestinal tract. The intestine contained watery, blood-stained fluid. Histopathologically, the principal intestinal lesion was superficial mucosal hemorrhagic necrosis at the jejunoileum. Many Gram-positive bacilli were found adhering to the necrotic mucosal surface in parts of the intestinal tract. Clostridium perfringens in pure culture were isolated from jejunal contents by anaerobic culture. These results suggested that the typical lesion of this case coincided with canine hemorrhagic enteritis and enterotoxemia due to C. perfringens infection could be the cause of sudden death.-KEY WORDS: Clostridium perfringens, enterotoxemia, hemorrhagic enteritis.