Pathology of Taenia taeniaeformis infection in the rat: gastrointestinal changes.
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Biomedical subjects
Publications and source records attributed to R W Cook.
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Development of the cestode parasite Taenia taeniaeformis in the liver of rats results in gross hyperplastic changes in the stomach and small intestine. In this study we investigated the mechanism by which these lesions are induced. Acutely infected rats were joined surgically to syngeneic noninfected partners in parabiosis. When hyperplastic gastropathy developed in those rats with heavy hepatic infections with cestodes, it also occurred in the uninfected partners of the parabiotic pairs. Gastric changes were usually more severe in the uninfected partner. Duodenal mastocytosis developed in both partners, even when parasite burdens were light in the infected rats. intact chronically infected rats with hyperplastic gastropathy developed markedly elevated serum levels of the hormone, gastrin (approximately 30-fold greater than normal). When rats were antrectomized 24-48 h after infection, gastric hyperplasia still developed, but hypergastrinemia was prevented or was of only moderate degree. There was no correlation between serum gastrin levels and the degree of gastrointestinal change in the intact rats, but hypergastrinemia never developed in infected animals which did not show hyperplasia in the stomach or intestine. When infected rats were bled serially over the first 100 days of infection, hypergastrinemia developed abruptly between 50 and 60 days after infection. These results suggest that the alterations in serum gastrin levels were secondary to the development of hyperplastic changes in the gastrointestinal tract of infected rats. The primary stimuli for both the hyperplasia and the hypergastrinemia remain unknown.
A method was devised for surgical removal of the pyloric antrum in 3-week-old rats. Contrary to published experiences with older rats, it was found that ligation of right and left gastroepiploic arteries was not necessary in young animals. Erythrocytes and fluids were routinely administered postoperatively, and recovered animals were denied access to water and food for 2 and 3 days, respectively. When the rats were fasted overnight prior to surgery, the recovery rate was 87% (27 of 31 attempted). Surgical sites were intact and showed minimal adhesions 2 months later. When overnight fasting was omitted, only 57% survived (8 of 14 attempted), because extensive manipulations were necessary to remove gastric contents, and this often produced shock.
A 10-month-old female, Wire-haired Pointing Griffon dog had a hamartoma of the hypothalamus. Episodes of sudden flaccid collapse had increased in frequency and duration for 7 months. Cerebrospinal fluid pressure was normal. A flat, pedunculated mass, 2.5 X 3.0 X 0.9 cm, covered the brain stem between the pituitary gland and pons. Its 1.2-cm-diameter connection to the hypothalamus obliterated the mammillary bodies and extended to the tuber cinereum, distorting the hypothalamus and displacing the third ventricle which also divided the rostral part of the mass. The tissue of the hamartoma resembled gray matter with bullous cytoplasmic vacuolation of many neurons, spongiform change, gemistocytosis and microscopic foci of calcification.
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Dermatophilosis was diagnosed in 2 of 13 captive polar bears (Thalarctos maritimus), causing generalized dermatitis of 3 years' and 6 months' duration, respectively. Progressive clinical signs included yellowing and darkening of the hair, pruritus, encrustation of skin, and reluctance to bathe. Dramatic resolution of lesions occurred during 8 weeks of twice-weekly intramuscular treatment with long-acting penicillin.
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