Veterinary pathology. Supplement最新文献

Lesions of candidiasis, mucormycosis (phycomycosis), entomophthoramycosis, geotrichosis, cryptococcosis, paracoccidioidomycosis and coccidioidomycosis have been reported in the alimentary tract of nonhuman primates. Candidiasis and mucormycosis were reported most often. Both Old and New World monkeys and great apes are susceptible; infection is rare in prosimians. Ulcers and necrosis of the mucosa of the alimentary tract are the principal gross lesions. A granulomatous inflammatory process occurs in which the fungi are visible histologically on hematoxylin and eosin (HE)-stained sections, but they are seen and characterized better when stained with periodic acid-Schiff (PAS) or Gomori methenamine silver (GMS) techniques. Cultural or immunofluorescence studies, or both, are necessary for specific identification of the fungi. Immunosuppression is suggested as a predisposing factor in certain mycotic diseases.

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.

Lesions of candidiasis, mucormycosis (phycomycosis), entomophthoramycosis, geotrichosis, cryptococcosis, paracoccidioidomycosis and coccidioidomycosis have been reported in the alimentary tract of nonhuman primates. Candidiasis and mucormycosis were reported most often. Both Old and New World monkeys and great apes are susceptible; infection is rare in prosimians. Ulcers and necrosis of the mucosa of the alimentary tract are the principal gross lesions. A granulomatous inflammatory process occurs in which the fungi are visible histologically on hematoxylin and eosin (HE)-stained sections, but they are seen and characterized better when stained with periodic acid-Schiff (PAS) or Gomori methenamine silver (GMS) techniques. Cultural or immunofluorescence studies, or both, are necessary for specific identification of the fungi. Immunosuppression is suggested as a predisposing factor in certain mycotic diseases.

Reported gastrointestinal neoplasms in nonhuman primates are reviewed, and the clinical and pathologic features of 11 new cases are described. The 11 monkeys had a total of 12 malignant gastrointestinal neoplasms; one had two primary carcinomas, one in the colon and one in the duodenum. Ten of the 12 tumors were adenocarcinomas: two in the duodenum, one in the jejunum, four in the distal ileum or region of the ileocecal valve and three in the large intestine. The remaining two lesions were a histiocytic lymphosarcoma of the stomach and a poorly differentiated sarcoma of the cecum. The 11 animals included nine Macaca mulatta, one Saguinus oedipus oedipus and one Galago crassicaudatus. All were adults and most were aged. There were six females and five males. Clinical signs included progressive weight loss, a palpable abdominal mass and intermittent diarrhea. Grossly, five of the adenocarcinomas were annular, and constricted the intestinal lumen. Microscopically, the carcinomas generally were well differentiated, and two produced mucin in quantities warranting the modifier "mucinous" adenocarcinoma. All tumors were locally invasive and six of nine monkeys with carcinomas had metastases, with the regional lymph nodes the principal site of involvement.

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.

Microhernias of colonic mucosal glands through the muscularis mucosae are common in human and nonhuman primate colons, and are related to submucosal lymphoid nodules. In nonhuman primates they have been shown to play an important role in the spread of inflammatory diseases from the lamina propria to the submucosa by allowing the infective agents to pass through the muscularis mucosae. The lymphoid tissue of the alimentary tract is composed predominantly of B lymphocytes and produces humoral antibodies. This property of the lymphoid component of these microhernias may thus play a significant role in determining which infective colonic diseases penetrate into the submucosa and which remain largely confined to the lamina propria.

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.

The phylogenetic relationship of nonhuman primates to man implies that many of these animals could serve as surrogates for studies of diseases of man. Many nonhuman primate species are susceptible not only to viruses of human origin but also to nonhuman primate viruses that are counterparts of viruses of man. All monkeys and great apes do not respond similarly to an antigenic stimulus. Some agents are highly pathogenic for one species and completely innocuous for another. For example, poliovirus causes disease and fatalities in great apes, but picornaviruses given orally cause few lesions in most nonhuman primates. Other enteroviruses (coxsackie-, echoviruses) have caused disease in nonhuman primates. It is difficult to separate viruses into distinct categories according to their anatomic affinities. Many viruses not considered to be enteric may be recovered from the intestinal tract. Adenoviruses, both human and nonhuman strains, which are not considered enteric viruses, nonetheless are recovered frequently from the intestinal tract. Adult animals show little evidence of disease, with the possible exception of diarrhea, after adenovirus infection. Newborns, however, may respond with a fatal pneumoenteritis. Adenovirus may be associated with diseases in organs other than the intestines. The reoviruses, which may be recovered from the intestinal tract, also are generally innocuous. Rotaviruses as pathogens in nonhuman primates are presently under study, and it is suspected that rotaviruses of man may produce experimental disease in nonhuman primates. Production of diabetes by several of the enteric viruses has been suggested but not demonstrated conclusively.

Sections of pancreas from 21 nonhuman primates with diabetes mellitus were examined by light and electron microscopy. All monkeys showed amyloid accumulation in the islets of Langerhans. Amyloid was identified by its dichroism with three different stains: Congo red, changing from red to yellowish-green; standardized toluidine blue, changing from blue to red; and sulfated alcian blue, changing from blue-green to pink. Sulfated alcian blue was a rapid and effective means of detecting amyloid. The characteristic fibrillar structure of amyloid was seen with transmission electron microscopy. Deposition of islet amyloid was independent of the presence or absence of amyloid in other organs. Results indicate that nonhuman primates offer a model for studying the sequential development of insular amyloidotic diabetes mellitus.

Microhernias of colonic mucosal glands through the muscularis mucosae are common in human and nonhuman primate colons, and are related to submucosal lymphoid nodules. In nonhuman primates they have been shown to play an important role in the spread of inflammatory diseases from the lamina propria to the submucosa by allowing the infective agents to pass through the muscularis mucosae. The lymphoid tissue of the alimentary tract is composed predominantly of B lymphocytes and produces humoral antibodies. This property of the lymphoid component of these microhernias may thus play a significant role in determining which infective colonic diseases penetrate into the submucosa and which remain largely confined to the lamina propria.