False coccidioidomycosis in a cow.
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Biomedical subjects
Publications and source records attributed to C Itakura.
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Simultaneous administration of monensin and tiamulin to pigs resulted in enhanced myotoxicity. Skeletal muscles of tongue, diaphragm and legs were preferentially affected, whereas the masseter, longissimus thoracis and cardiac muscles, including the left auricle, were spared. Histochemical examination revealed an involvement of both type I and II fibers of skeletal muscles.
Pneumonia with aspiration of foreign bodies and adenovirus infection was identified in a wild Japanese macaque which died 1 month after capture. The adenovirus infection was considered to be secondary in importance to the pneumonia.
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Ultrastructural studies were conducted on the parathyroid glands (PTG) of 2- to 7-week-old nontreated control growing broiler chickens (group A, 6 chickens); the same aged chickens with experimentally induced vitamin D deficiency rickets (18 morbid chickens each from groups B, C, and D); and in 4- to 9-week-old chickens naturally affected with rickets (group E, 8 chickens). Four types of principal cells were classified in the PTG of clinically normal birds and in PTG of birds with secondary hyperparathyroidism as follows: Type I cell (small cell in the resting phase); type II cell (medium-sized cell with well-developed rough-surfaced endoplasmic reticulum in the synthesizing phase); type III cell (large cell with well-developed Golgi apparatus and cytoplasmic organelles in the packaging and secretory phase); and type IV cell (medium-sized cell with poor cytoplasmic organelles in the involuting phase). Many coated vesicles were observed in type II and type III cells. In young control chickens, principal cells of the PTG were considered in the resting phase; in older control chickens, there were increased numbers of cells in the synthesizing phase. In the vitamin D deficiency groups, principal cells were in the synthesizing and packaging and secretory phases. In birds with naturally occurring rickets, principal cells were in packaging and secretory phases, with a small number of cells in the involuting phase. The ultrastructural changes of the PTG from the initial to final phases in growing chickens with secondary hyperparathyroidism were demonstrated.
Histopathological findings of pulmonary alveolar proteinosis occurring spontaneously in aged KK mice (72 weeks of age) were described. The lung tissues examined were obtained from the mice used for a one-year toxicity study of some oral hypoglycemic drugs, but there was no relationship between the incidence of the disease and the drug treatment. The disease occurred in 67 of 319 males (21.0%) and 124 of 284 females (43.7%). The gross lesions of the lungs were solitary or multiple nodules. Microscopically, the lesions developed in the peribronchial areas and were well-circumscribed. The initial lesions consisted of the aggregation of foamy cells in the alveoli. In the advanced lesions, amorphous substance resulting from destructed foamy cells and proteinous material accumulated in the alveoli. In the more advanced lesions, neutrophils and nuclear fragments were contained in the proteinous material and some of the alveolar walls were thickened with cell infiltration, fibrosis and so-called epithelialization. The etiology of the present condition was unknown.
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Pathological findings were described on nephroblastomas occurrred spontaneously in 3 young Sprague-Dawley rats. One side of kidneys was affected in each animal. Microscopically, the tumors consisted of epithelial elements showing undifferentiated to well-differentiated tubular arrangements, sometimes with glomeruloid and glomerular structures. A metastatic tumor nodule was found in the lung of one rat.
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The skin of 15 hairless newborn pigs with parenchymatous goiter was studied histopathologically. Most of the lesions were in the hair follicles; follicles were scarce and reduced in size, contained slender hairs, and revealed a shortage of penetration into the hypodermis. Hair follicles in the immature stages, hair pegs, and germs also were recognized, with the thin epidermis lacking in keratinization. It was felt that these changes resulted from a retardation of cellular differentiation of the germinal layer. In view of these findings, skin lesions were regarded as hypoplasia of hair.