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Biomedical subjects

J L Stookey

Publications and source records attributed to J L Stookey.

15 recordsLinked to original sources

Pathology of Bolivian Hemorrhagic fever in the African green monkey.

Gross and microscopic pathological findings are presented for an African green monkey model of fatal Bolivian hemorrhagic fever. Six animals were inoculated with 1,000 plaque-forming units of Machupo virus, the etiological agent of Bolivian hemorrhagic fever. Five of the monkeys died within 13 days with signs of fever, anorexia, shock, and hemorrhage. The sixth monkey survived until the 24th day and died with signs of central nervous system disease. Gross lesions in the five monkeys that die in the acute stage included hepatic necrosis, necrotic enteritis, bronchopneumonia, and hemorrhages in the subcutis, lungs, intestine, liver, and lymph nodes. Microscopically, necrosis was consistently seen in liver, intestine, skin, oral cavity, and adrenal cortex. Acute thrombosis was observed in four monkeys, in blood vessels of the intestine, lung and choroid of the brain. Gram-negative bacteria were seen in many tissues, suggesting terminal bacteremia. The sixth monkey was emaciated and had bronchopneumonia, but did not have the necrotic hepatic and enteric lesions observed in the other five monkeys. The significant microscopic lesions in this monkey included encephalomyelitis, ganglionitis, and bronchopneumonia.

Animals

Lesions in guinea pigs infected with Coxiella burnetii strain M-44.

Guinea pigs inoculated with the live M-44 vaccine strain of Coxiella burnetii were examined grossly and microscopically for the presence of Q fever-related lesions. Mild myocarditis was observed in 38% of the infected animals but in none of the control animals. Livers showed significant incidence of hepatitis, necrosis, and granuloma formation, especially during the first eight days of the infection. A much lower incidence of splenitis was also found but was considered to be of borderline significance. Generally, lesions were mild in nature, and none seemed to endanger the life of the animal or to cause observable distress.

Adrenal Glands

Intestinal Tyzzer's disease and spirochetosis in a guinea pig.

Tyzzer's disease (bacillus pilirformis infection) was diagnosed in young guinea pig killed because of diarrhea and poor condition. There was necrosis and inflammation of the colon, cecum and ileum. Typical B. piliformis were in intestinal epithelial cells. Spirochetes were in large numbers in intestinal crypts and were often adjacent to the intracellular B. piliformis. Extracellular B. piliformis occasionally were surrounded by spirochetes.

Animals

Fibrosarcoma in a white-tailed deer.

A large, rapidly growing subcutaneous fibrosarcoma was observed on the head of an aged male white-tailed deer (Odocoileus virginianus) from Frederick County, Maryland. Although there was no evidence of distant metastasis, the large neoplastic mass had extensively invaded the osseous supraorbital process, and had several small satellite nodules nearby.

Animals

Pathology of experimental Rocky Mountain spotted fever in rhesus monkeys.

Rhesus monkeys were inoculated intravenously or intraperitoneally with various numbers of Rickettsia rickettsii. Monkeys that were given more than 10(4) organisms intravenously died on days 3-6 after inoculation, whereas those given less than 10(3) intravenously or more than 10(4) intraperitoneally died on day 7 or later. There was no significant difference in incidence of lesions between the early- and late-death groups. Vasculitis and thrombosis occurred most frequently in the nares, pinna of the ear, scrotal skin, and testicle. Adrenal cortical necrosis was caused by capillary thrombosis. Rickettsiae, estimated by plaque formation in culture, were most numerous in the lung and spleen.

Adrenal Cortex

Pathology of chronic Bolivian hemorrhagic fever in the rhesus monkey.

Gross and microscopic lesions of Bolivian hemorrhagic fever (BHF) are described in 10 rhesus monkeys that survived from 30 to 78 days after subcutaneous inoculation with a dose of 10(3) plaque-forming units (PFU) of Machupo virus, a dose which produces a severe and generally fatal disease. Six of the monkeys had been given low doses of homologous immune globulin when initial signs of infection appeared. Monkeys exhibited clinical signs in two phases. The initial signs of acute infection which began to appear about 1 week following inoculation included: diarrhea, depression, anorexia, dehydration, and skin rash. The survivors of this early phase of the illness usually showed improvement before relapsing into the second (or chronic) phase, which was characterized clinically by central nervous system disturbances including incoordination, tremors, convulsions, paresis, and muscle atrophy. Microscopic lesions were similar in both immune globulin-treated and untreated animals. These included widespread lymphoreticular infiltrates in the walls and adventitia of blood vessels of the brain, spinal cord, pancreas, intestine, liver kidney, adrenal, parathyroid, heart, and skeletal muscle. Diffuse lymphocytic infiltrates not confined to the vascular or perivascular tissues were present to a variable degree in many of these and other organs. Several monkeys exhibited lymphocytic inflammation of the choroid, meninges, peripheral nerves, and ganglia.

Adrenal Glands

Anatrichosoma cynamolgi (Nematoda: Trichinellida) in rhesus monkeys, Macaca mulatta.

Young adult rhesus monkeys were examined for Anatrichosoma spp. by means of nasal swab, by histological study, and by gross examination with the aid of a dissecting microscope. Of 394 monkeys examined by nasal swab, 25 (6.3%) were found to be positive. Of 166 monkeys that died while in the colony, 23 (13.9%) were found to be infected when examined by histological study. Of 18 unfixed samples of external nasal vestibule, five (27.2%) were found to be infected when they were examined grossly with the aid of a dissecting microscope. Inflammatory response to the nematodes was limited. The nematodes were compared to type specimens of Anatrichosoma from monkeys, and were identified as A. cynamolgi Smith and Chitwood 1954. A. rhina and A. nacepobi are considered to be synonyms of A. cynamolgi.

Animals

Functional and morphologic changes during experimental Rocky Mountain spotted fever in guinea pigs.

Experimental Rocky Mountain spotted fever was studied in guinea pigs following intraperitoneal inoculation of 10(7) Rickettsia rickettsii. After a 2-day incubation period, animals developed fever, progressive emaciation, and scrotal swelling with necrosis. Vasculitis, with increased small vessel permeability for colloidal carbon, was evident in cremaster muscles as early as 1 day after inoculation. Inflammatory changes in vessels became progressively more severe as numbers of circulating rickettsiae increased. Thrombosis and vascular occlusion were first evident on day 4. Mild thrombocytopenia developed, coinciding with the development of vasculitis, and preceding the appearance of either fibrin-split products in blood or thrombi in vessels. Rickettsiae were first detected in blood on day 2; peak rickettsemia occurred on days 5 to 8. Rickettsiae were demonstrated in inflamed vessels on day 5 and later, but not at earlier stages. Serum lysozyme concentration was moderately elevated and hemolytic complement was moderately depressed throughout the illness. Agglutinating antibody was present in low titers on days 3 to 10. Antibody titers increased on days 12 to 16 after the rickettsiae were cleared from blood. These studies indicate that vasculitis seen early in the course of Rocky Mountain spotted fever is the result of rickettsial infection, but is not dependent on the presence of rickettsiae in endothelial cells or other blood vessel components.

Agglutination Tests

Cerebral tuberculosis in a rhesus monkey.

Tuberculosis of the cerebrum was diagnosed in a young adult male rhesus monkey (Macaca mulatta). Tuberculous granulomas were also found in the lungs, bronchial lymph nodes, liver, and spleen. The affected monkey was the probable index case for 7 other Macaca mulatta with tuberculosis.

Animals

Pneumocystis carinii infection in splenectomized owl monkeys.

Interstitial pneumonia due to Pneumocystis carinii was diagnosed in 2 splenectomized owl monkeys. Pneumonia was considered an important lesion in 1 monkey, but only an incidental finding in the 2nd monkey. Nephritis was considered to be the primary lesion in both monkeys.

Animals

Myxosarcoma in a young rhesus monkey.

A myxosarcoma that arose spontaneously in the ilial region of a young male Rhesus monkey grew rapidly and invaded and lysed the pelvic bones. It consisted of large pleomorphic cells, with single or multiple nuclei and dilated rough endoplasmic reticulum, in abundant intercellular matrix.

Animals

Fibrous osteodystrophy in an opossum.

A free living opossum (Didelphis marsupialis) was found to have severe fibrous osteodystrophy of the maxilla and mandibles. No significant lesions were found in the kidneys, ruling out an etiology of renal secondary hyperparathyroidism. An etiology of primary phperthyroidism or nutritional secondary hyperparathyroidism is suggested.

Animals

Pathogenesis of tularemia in immune and nonimmune rats.

Pathogenesis of tularemia in nonimmune rats given (intraperitoneal inoculation) virulent strain (SCHU S4) or vaccinal strain (LVS) of Francisella tularensis and in immune rats given SCHU S4 is described. Both LVS and SCHU S4 caused pyogranulomas in liver and spleen of nonimmune rats. Nonimmune rats given 10(4) SCHU S4 organisms did not survive beyond 72 hours, but immune rats given challenge inoculum of 10(8) SCHU S4 organisms developed lesions and survived. Larger doses of LVS resulted in earlier onset of characteristic hepatitis and splenitis in nonimmune rats. Periportal lymphocytic infiltrates were present in the liver 48 hours after SCHU S4 challenge inoculation of immune rats and 96 hours after inoculation of LVS in nonimmune rats and were associated with intense macrophage aggregation. These changes indicate that the pathogenesis of tularemia is a result of the interdependency of the dose and virulence of the causative agent with the immune status of the host and that cellular immunity has a significant role in the response of the rat to tularemia.

Animals

A disease of freshwater fishes caused by Tetrahymena corlissi Thompson, 1955, and a key for identification of holotrich ciliates of freshwater fishes.

Tetrahymena corlissi, a free-living protozoan, apparently caused the death of large number of guppies (Poecilia reticulatus) and occasionally other fishes, in aquaria and hatcheries at several locations. Apparently the disease occurs when the fish and protozoan populations are both at a high level of density. The signs include white spots and epidermal damage. Histologically, T. corlissi could be seen in skin, muscle, and viscera; in some there was marked inflammation, in others there was little tissue reaction. A key is presented for the identification of invasive fish ciliates: Chilodonella, Hemiophrys, Ichthyophthirius, Ophryoglena, and Tetrahymena.

Animals