Characterization of exogenous type D retrovirus from a fibroma of a macaque with simian AIDS and fibromatosis.

A novel type D retrovirus was isolated by cocultivation of explants of fibromatous tissue from a rhesus monkey (Macaca mulatta) with immunodeficiency and retroperitoneal fibromatosis. This type D virus, isolated from a macaque with simian acquired immunodeficiency syndrome (SAIDS-D/Washington), is exogenous and is partially related to the Mason-Pfizer and the langur monkey type D viruses. The SAiDS-D virus can be distinguished from all other primate retroviruses by antigenicity and molecular hybridization. Nucleic acid hybridization studies reveal that the origin of the SAIDS-D isolate may reside in Old World monkey (subfamily Colobinae) cellular DNA.

Nasal cavity neoplasia in F344/N rats and (C57BL/6 x C3H)F1 mice inhaling propylene oxide for up to two years.

Propylene oxide (CAS: 75-56-9) was studied for potential carcinogenicity and chronic toxicity by inhalation in F344/N rats and (C57BL/6 x C3H)F1 mice. Groups of 50 animals of each sex were exposed to 0, 200, or 400 ppm propylene oxide for 6 hours/day, 5 days/week, for up to 103 weeks. Survival decreased in mice exposed to propylene oxide; the decrease was significant (P less than .005) in mice exposed to 400 ppm. Survival of exposed rats was comparable to that of controls. Mean body weight of rats and mice exposed to 400 ppm propylene oxide decreased, when compared to that of controls, during the 2d year of exposure. Exposure to propylene oxide for up to 2 years induced inflammatory and proliferative responses in nasal cavity of both species. There was clear evidence of carcinogenicity in mice exposed to 400 ppm propylene oxide; 10 of 50 males and 5 of 50 females had hemangiomas or hemangiosarcomas of the nasal submucosa. Papillary adenomas involving the nasal respiratory epithelium and underlying submucosal glands were observed in 3 female rats and 2 male rats exposed to 400 ppm propylene oxide.

Toxicologic and marrow transplantation studies in rhesus monkeys given dimethyl myleran.

The hematologic and pathologic effects of single doses of dimethyl myleran (DMM) were evaluated in rhesus monkeys with and without the infusion of marrow. DMM 3 to 5 mg/kg produced severe but reversible myelotoxicity and no non-marrow toxicity. All animals given DMM 10 mg/kg died of marrow failure which was consistently reversed by the infusion of cryopreserved autologous marrow. At higher doses of DMM the protective effect of autologous marrow was less consistent due to increased gastrointestinal toxicity. Allogeneic engraftment was not achieved following administration of 10 mg/kg of DMM. In two animals receiving 15 mg/kg, proliferating allogeneic donor cells were present in recipient marrow seven days after marrow infusion.

Selective myocardial cell necrosis in nonhuman primates.

A retrospective study was performed to describe the histologic stages of selective myocardial cell necrosis (SMCN) in nonhuman primates, and to compare the incidence of SMCN in two groups of nonhuman primates. Myocardial tissues taken at the time of autopsy from 50 primates at an experimental center were compared with similar tissues from 50 primates housed in a breeding colony. SMCN was confirmed in 20% of the experimental primates and 30% of the breeding primates, proportions that were not significantly different. The incidence and histologic characteristics of SMCN in nonhuman primates were similar to those described in humans, and resembled the lesion produced in experimental primates by administration of catecholamines of by hypokalemia.

Retrospective analysis of an outbreak of B virus infection in a colony of DeBrazza's monkeys (Cercopithecus neglectus).

In 1981, an outbreak of herpetic disease developed in a colony of DeBrazza's monkeys (Cercopithecus neglectus). In seven of eight infected animals, clinical signs of infection included vesicular and ulcerative lesions on the lips, tongue, and/or palate. Histologic examination of lesions revealed intranuclear inclusion bodies, and electron microscopy revealed nucleocapsids and virions with typical herpesvirus morphology. Although a virus was isolated that appeared similar to monkey B virus, techniques available at the time did not allow precise identification of the virus. Analysis of serum from one surviving monkey collected 12 years after the outbreak revealed a pattern of reactivity characteristic of B virus-positive serum on the basis of results of ELISA and western immunoblot analysis. Polymerase chain reaction analysis of archived paraffin-embedded tissue specimens and molecular analysis of the one viral isolate obtained from a DeBrazza's monkey indicated that the virus responsible for the outbreak was a new genotype of B virus. Testing of sera from lion-tailed macaques (Macaca silenus) housed in an adjacent cage at the same zoo indicated that these animals harbored this virus and, thus, were the likely source of the virus that infected the DeBrazza's monkeys. This study documents usefulness of archiving samples from disease outbreaks for later analysis. In addition, this incident underscores the importance of considering herpes B virus infection when outbreaks of disease having characteristics of herpetic infections develop in nonhuman primates kept at institutions that also house macaques.

Atrophic rhinitis in New Zealand white rabbits infected with Pasteurella multocida.

Atrophic rhinitis was detected in New Zealand White rabbits when upper respiratory tract disease was evaluated during a vaccine field trial for the prevention of pasteurellosis. Of 52 adult rabbits euthanatized and necropsied, 26 (50%) had evidence of turbinate atrophy. Atrophy was detected in 77% of rabbits with Pasteurella multocida infection only, 71% of rabbits with concurrent P multocida and Bordetella bronchiseptica infections, and 6% of rabbits with B bronchiseptica infection only. Grossly, turbinate atrophy was characterized by a mild to severe loss or diminution in the maxilloturbinates. Histologically, turbinate bones were small and irregular in thickness and had numerous osteoclasts and osteoblasts. A neutrophilic exudate filled the nasal passages, and infiltrates of neutrophils and lymphocytes were detected in the mucosa and submucosa of the nasal turbinates. Rhinitis was significantly (P less than 0.001) associated with turbinate atrophy. Isolates of P multocida from rabbits with turbinate atrophy were serotype A:12.

Salmonellosis in laboratory-housed iguanid lizards (Sceloporus spp.).

Fifteen wild-caught iguanid lizards (14 Sceloporus variabilis and one S. malachiticus) were used in a 3 mo study on thermal acclimation. Over a 2 mo period, five of the lizards showed decreased activity, anorexia and enlarged joints, and were either found moribund or were euthanatized due to their poor condition. Specimens taken from lesions in four of the five lizards were cultured and were infected with Salmonella spp. Salmonella spp. was cultured from cloacal swabs in six of the 10 surviving lizards. Standard metabolic rates of those that were infected did not differ significantly from those that were not infected. We postulate that the lizards were inapparent carriers of Salmonella spp. at the time of capture and, as a result of stress, five developed active overwhelming systemic infections.

Clinical and pathologic features of parvoviral diarrhea in pound-source dogs.

From June 1980 through May 1982, 161 pound-source dogs that developed diarrhea while being used in research were evaluated to determine whether canine parvovirus (CPV) type 2 was the etiologic agent. Evaluation included notation of clinical signs, determination of serum CPV-specific immunoglobulin (Ig) M and IgG titers, virus isolation attempts, and histologic examination of tissues. Criteria for diagnosis of canine parvoviral enteritis were serum CPV-specific IgM antibodies, isolation of CPV from feces, and histologic evidence of intestinal crypt cell necrosis. Upon arrival, 67 clinically normal pound-source dogs were evaluated to determine the prevalence of fecal shedding of CPV and to determine their antibody titers to CPV. Parvovirus was not isolated from any of these dogs, although 76% had IgG antibodies and 3% had IgM antibodies. Of the 161 dogs with diarrhea, 40 (25%) had parvoviral enteritis. Of dogs with parvoviral enteritis, 71% had IgG antibodies and 68% had IgM antibodies. Canine parvovirus was isolated from 18 dogs. Serum IgG antibodies were found in 85% of dogs with diarrhea due to other causes. The geometric mean titer of IgG antibodies to CPV was not significantly different among the 3 groups. Clinical signs that appeared significantly (P less than 0.05) more often in dogs with parvoviral enteritis included bloody diarrhea, anorexia, fever (greater than or equal to 39.4 C), and leukopenia (WBC less than 6,000/mm3). Cases occurred throughout the year, without apparent seasonal variation. The duration between arrival and onset of diarrhea was significantly (P less than 0.05) shorter for dogs with parvoviral enteritis.(ABSTRACT TRUNCATED AT 250 WORDS)

Studies of cultured lymphocytes of the owl monkey (Aotus trivirgatus) infected with Herpesvirus saimiri.

The lymphocytes of five owl monkeys (Aotus trivirgatus) infected with Herpesvirus saimiri and three control monkeys were studied. Lymphocytes were separated on Ficoll-Hypaque gradients, incubated in suspension cultures, and prepared for electron microscopic and immunofluorescent study at 24, 48, and 72 hours after the beginning of culture. Buffy coats of whole blood obtained immediately after bleeding were also prepared for study. At the time of the study, four of the five infected monkeys had died with malignant lymphoma and lymphocytic leukemia. Herpesvirus saimiri virions were demonstrated by electron microscopy and H saimiri antigens by immunofluorescence in 1-20% of the lymphocytes from infected monkey in two of five cultures at 24 hours after culture, four of five at 48 hours after culture, and all of five at 72 hours after culture. There was good agreement between the electron microscopic and the immunofluorescent data. None of the control monkey cultures and none of the buffy coat preparations contained H saimiri virions or antigens. By electron microscopy, the great majority of the virus particles were nucleocapsids within the nuclei of lymphocytes. Enveloped virions were seldom observed. There was some evidence to suggest that the higher the percentage of lymphocyte containing H saimiri, the poorer the prognosis for the monkey. Herpesvirus saimiri was isolated from all five infected monkeys by co-cultivation of lymphocytes with Vero cells. Control lymphocyte co-cultivations were negative.

Ultrastructural and immunofluorescent studies of the replication of herpesvirus saimiri in cultured lymphocytes of infected owl monkeys.

The lymphocytes of five owl monkeys infected with herpesvirus saimiri (HVS) and of three control owl monkeys were studied by electron microscopic (EM) and immunofluorescent (IF) techniques. Buffy coats of whole blood immediately after bleeding were also prepared for study. At the time of the study, two of the five infected monkeys were leukaemic; within 50 days after the study, four of the five had died with malignant lymphoma and lymphocytic leukaemia. HVS virions were demonstrated by EM and HVS antigens by IF in 1-20% of the lymphocytes from infected monkeys in 2/5 cultures at 24 hours AC, 4/5 at 48 hours AC, and 5/5 at 72 hours AC. There was quite good agreement between the EM and IF data. None of the control monkey cultures and none of the buffy coat preparations contained HVS virions or antigens. By EM, the great majority of the virus particles were nucleocapsids within the nuclei of lymphocytes. Enveloped virions were rare. There was some evidence to suggest that the higher the percentage of lymphocytes containing HVS, the poorer the prognosis for the monkey. HVS was isolated from all five infected monkeys by co-cultivation of lymphocytes with Vero cells. Control lymphocyte co-cultivations were negative.

Replication of Herpesvirus saimiri in cultured lymphocytes of infected owl monkeys (Aotus trivirgatus). An electron microscopic and immunofluorescent study.

The lymphocytes of five owl monkeys infected with Herpesvirus saimiri (HVS) and three control monkeys were studied. Lymphocytes were separated on Ficoll-Hypaque gradients, incubated in suspension cultures, and prepared for electron microscopic and immunofluorescent study at 24, 48, and 72 hours after the beginning of culture (AC). Buffy coats of whole blood immediately after bleeding were also prepared for study. At the time of the study, four of the five infected monkeys had died of malignant lymphoma and lymphocytic leukemia. HVS virions were demonstrated by electron microscopy and HVS antigens by immunofluorescence in 1 to 20 per cent of the lmyphocytes from infected monkeys in two of five cultures at 24 hours AC, four of five at 48 hours AC, and all five at 72 hours AC. There was quite good agreement between the electron microscopic and the immunofluorescent data. None of the control monkey cultures and none of the buffy coat preparations contained HVS virions or antigens. By electron microscopy the great majority of the virus particles were nucleocapsids within the nuclei of lymphocytes. Very seldom were enveloped virions observed. There was some evidence to suggest that the higher the percentage of lymphocytes containing HVS the poorer the prognosis for the monkey. HVS was isolated from all five infected monkeys by cocultivation of lymphocytes with Vero cells. Control lymphocyte cocultivations were negative.