Veterinary pathology. Supplement最新文献

Acute gastric dilatation occurs sporadically in laboratory-housed nonhuman primates. Clinical histories often include chronic drug administration, food restriction, accidental overfeeding, and prior anesthesia. Monkeys may be found dead or may have clinical signs of colic, abdominal distention, and dyspnea. Death in untreated cases is due to impaired venous return and cardiopulmonary failure. Gastric distention with fermented gaseous ingesta and congestion of the abdominal viscera are the predominant lesions. The cause of acute gastric dilatation is unknown, but it probably is multifactorial. Two principal factors seem to be intragastric fermentation associated with Clostridium perfringens, and abnormal gastric function.

Features and pathogenesis of adenoviral pancreatitis in rhesus monkeys were studied with an immunofluorescence staining procedure on tissues from two previously documented cases. Fluorescing adenovirus antigen in epithelial cells of the pancreatic ducts, duodenum, and jejunum suggests that under as yet undefined conditions, a primary adenovirus infection of the gastrointestinal tract ascends to the pancreatic parenchyma via pancreatic ducts. In a retrospective survey, over 3,000 microslides of pancreas taken at necropsy from several species of nonhuman primates (1,002 animals) were studied to determine the incidence of and species susceptibility to adenoviral pancreatitis. Other than the two documented cases from our files, we found comparable lesions in only one rhesus monkey. Adenoviral pancreatitis seems to be a distinct entity in rhesus monkeys, and it should be considered when pancreatitis is found in this species. Our findings also suggest a possible viral cause for some cases of pancreatitis in man.

Approximately 3,000 microslides of hematoxylin and eosin (HE)-stained sections of pancreas from 1,000 nonhuman primates were reviewed. Sections were from 557 females and 443 males; 658 were adults of unknown age and 342 were laboratory-born animals of known age. The latter included 94 animals less than one year old, 92 from one to five years old, and 156 from five to more than 20 years old. There were 326 squirrel monkeys, 319 rhesus monkeys, 100 great apes, 123 other macaques, 61 other Old World monkeys, 39 other New World monkeys, and 32 prosimians. Pancreatic lesions of varied severity found in 187 (18.7%) of these nonhuman primates included focal parenchymal or periductal accumulations of mononuclear inflammatory cells with varied degrees of periductal fibrosis in 77; hyalinized islets (amyloidosis) in 29; acute or chronic diffuse pancreatitis in 18; chronic focal pancreatitis with or without ductal hyperplasia in ten; neoplasms in 11; hemorrhage of the parenchyma or islets in eight; parasites in seven; lymphoid or ectopic splenic nodules of the parenchyma in six; acinar ectasia in six; focal parenchymal fat in six; ectopic pancreas in four; parenchymal cysts without fibrosis in three; acinar cell atrophy in one; and cystic fibrosis-like changes in one.

In a colony of rhesus monkeys (Macaca mulatta), 42 cases of nontuberculous mycobacterial-related disease were identified from 1970 to 1978. The disease affected young and old colony-born and wild-caught monkeys of both sexes. Serotypes 1, 2, 4, 8, and 18 of the Mycobacterium avium-intracellulare group were isolated from different monkeys. The lesions were primarily intestinal in 36 monkeys. Lesions of the large intestine, small intestine, and mesenteric lymph nodes were characterized by diffuse accumulations of large macrophages containing many acid-fast bacteria. Acid-fast bacteria could not be identified histologically in four monkeys with typical histories of diarrhea and weight loss, positive skin reactions to the tuberculin test with M. avium tuberculin, and isolation of the organism from tissues on one or more occasions. Two monkeys had histologically positive lesions limited to the lungs, although chronic colitis of undetermined cause was present.

Retrospective pathology data from necropsies of 162 marmosets, Saguinus oedipus, were studied to determine the nature of chronic wasting syndrome, a poorly defined entity associated with a high mortality rate in many marmoset colonies. Paraffin sections of the gastroenteric organs of 116 of these marmosets were re-examined in detail; lesions were identified, quantitated, and analyzed with a method of multiple chi-square testing for possible associations between findings. Five distinct disease entities were identified: prosthenorchosis, amebiasis, paramyxovirus disease, sepsis, and chronic colitis. Lesions of several of these often occurred in the same monkey, and all but the first were associated with cachexia. Lesions of chronic colitis were crypt abscesses, mononuclear and polymorphonuclear infiltration of the lamina propria, epithelial cell atypia, karyorrhexis, and lymphoid hyperplasia. The cause of chronic colitis was not identified, nor was any explanation found for weight loss and increased susceptibility to disease.

A review of the literature concerning the gross and histologic lesions associated with protozoal and metazoal parasitism in the alimentary tract and pancreas of nonhuman primates is presented. In addition, the natural history, morphology, life cycle, methods for diagnosis, and potential for zoonotic disease are reviewed briefly for each parasite discussed. The parasite species reviewed in detail are those most common or most likely to produce lesions in the alimentary tract and pancreas of the nonhuman primate host. All parasites, both pathogenic and nonpathogenic, in each major group (protozoa: flagellates, sarcodines, sporozoans, neosporans, and ciliates; and metazoa: trematodes, cestodes, nematodes, acanthocephalans, and pentastomids) that have been reported in the nonhuman primate alimentary tract and pancreas are presented in tables.

Rhesus monkeys (Macaca mulatta), given 3 X 10(8) to 5 X 10(10) Shigella flexneri 2a orally, developed signs of acute shigellosis within 24 hours. A diffuse acute colitis was well established at 48 hours. The inflammatory reaction was confined to the mucosa. The submucosa showed only edema. The shigellae were found predominantly in the columnar cells of the surface epithelium, less frequently in those of the crypt, and least frequently in the lamina propria. Shigella bacilli invaded the columnar cells from the intestinal lumen. The bacilli multiplied within epithelial cells and spread laterally to adjacent epithelial cells and penetrated the lamina propria. The bacterial invasion affected epithelial cells unevenly and resulted in the disappearance of goblet cells and pyknotic shrinkage of the surface epithelial cells. Epithelial cells had abnormal and accelerated exfoliation which resulted in multifocal epithelial defects. There was a distinct correlation between the quantity of bacilli present in tissues and the intensity of the inflammatory response. The small intestines were spared.

Retrospective pathology data from necropsies of 162 marmosets, Saguinus oedipus, were studied to determine the nature of chronic wasting syndrome, a poorly defined entity associated with a high mortality rate in many marmoset colonies. Paraffin sections of the gastroenteric organs of 116 of these marmosets were re-examined in detail; lesions were identified, quantitated, and analyzed with a method of multiple chi-square testing for possible associations between findings. Five distinct disease entities were identified: prosthenorchosis, amebiasis, paramyxovirus disease, sepsis, and chronic colitis. Lesions of several of these often occurred in the same monkey, and all but the first were associated with cachexia. Lesions of chronic colitis were crypt abscesses, mononuclear and polymorphonuclear infiltration of the lamina propria, epithelial cell atypia, karyorrhexis, and lymphoid hyperplasia. The cause of chronic colitis was not identified, nor was any explanation found for weight loss and increased susceptibility to disease.

Rhesus monkeys (Macaca mulatta), given 3 x 10(8) to 5 x 10(10) Shigella flexneri 2a orally, developed signs of acute shigellosis within 24 hours. A diffuse acute colitis was well established at 48 hours. The inflammatory reaction was confined to the mucosa. The submucosa showed only edema. The shigellae were found predominantly in the columnar cells of the surface epithelium, less frequently in those of the crypt, and least frequently in the lamina propria. Shigella bacilli invaded the columnar cells from the intestinal lumen. The bacilli multiplied within epithelial cells and spread laterally to adjacent epithelial cells and penetrated the lamina propria. The bacterial invasion affected epithelial cells unevenly and resulted in the disappearance of goblet cells and pyknotic shrinkage of the surface epithelial cells. Epithelial cells had abnormal and accelerated exfoliation which resulted in multifocal epithelial defects. There was a distinct correlation between the quantity of bacilli present in tissues and the intensity of the inflammatory response. The small intestines were spared.

Evaluation of mortality during a two-year period at a primate colony indicated that 34% of nonexperimental deaths in macaques one year of age and older were due to gastrointestinal disease. Of deaths related to gastrointestinal disease, 12% had acute gastric dilatation, 18% had shigellosis, 12% had nontuberculous mycobacterial disease, and 58% were of undetermined cause. Histologic evaluation of the alimentary tract indicated that the large intestine was the most common site of anatomical change in monkeys that had diarrhea at the time of death. Monkeys that had a single terminal episode of diarrhea had less gastric inflammatory lesions than those that had multiple episodes of diarrhea in the last year of life.