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Biomedical subjects

R O Jacoby

Publications and source records attributed to R O Jacoby.

At least 73 records · Page 4Linked to original sources
PubMed1986

Contamination of transplantable murine tumors with lymphocytic choriomeningitis virus.

Lymphocytic choriomeningitis virus (LCMV) was isolated from a transplantable tumor after mice bearing the tumor began to die prematurely. Tumor lines, mice and laboratory personnel that had an association with the index laboratory were tested for LCMV infection. Testing of tumor lines from the index laboratory and four other laboratories revealed that 16 of 55 tumor samples used in vivo and one of eight tumor samples maintained in vitro were contaminated with LCMV. Laboratory personnel and uninoculated mice that were exposed to infected tumors had no LCMV antibody. The use of carefully monitored seed stocks is recommended to protect transplantable tumors that may be inadvertently contaminated by viruses.

Animals↗
PubMed1985

Epizootiological observations of natural and experimental infection with sialodacryoadenitis virus in rats.

The epizootiology of sialodacryoadenitis (SDA) was studied in experimentally and naturally infected rats. The infectivity of SDA virus (SDAV) in intranasally infected rats was lost by seven days after infection as determined by contact transmission. After experimental infection, SN antibody appeared earlier and titers were detectable longer than CF antibody. The prevalence of SN antibody-positive rats in naturally infected colonies remained high, whereas an increase in the prevalence of CF antibody-positive rats appeared to coincide with the introduction or resurgence of SDAV. A SDAV-free colony was established by allowing recovered dams to litter in a separate room. A spontaneous cessation of SDAV infection also was observed in an enzootically-infected colony. Clinical observations indicated that SDA can occur as a mild or asymptomatic disease, and that its clinical expression may vary from one inbred strain to another.

Animals↗
PubMed1983

Naturally occurring lethal parvovirus infection of juvenile and young-adult rats.

A lethal disease characterized by hemorrhage and necrosis of the brain, testes, and epididymides developed in young adult rats housed in specific pathogen free quarters. Morphological, virological, and serological investigations of the outbreak indicated that the probable causative agent was rat virus (Kilham), a common parvovirus of rats that usually induces persistent, asymptomatic infection in adult rats.

Animals↗
PubMed1983

Pathogenesis of vaccinia (IHD-T) virus infection in BALB/cAnN mice.

The pathogenesis of lesions produced by the IHD-T strain of vaccinia virus during vaccination of BALB/cAnN mice was characterized by virological, morphological, and serological methods. Infectious vaccinia virus was detected at the vaccination site for up to 16 days and was also found, to a variable extent, in lung, thymus, spleen, and liver between days 3 and 5. Viral antigen was detected at the vaccination site by avidin-biotin-linked immunoperoxidase cytochemistry, but only when viral concentrations were at least 10(5.0) log10 TCID per mg of tissue. The primary vaccination lesions were typical pocks characterized by sequential development of epidermal necrosis, vesicle formation, and ulceration and by dermal inflammation dominated by mononuclear cells. Type B inclusions were found in epidermis, but Type A inclusions were not seen. Seroconversion to vaccinia viral antigen was detected by day 8 with complement-fixation and immunofluorescence assays and by day 10 with an enzyme-linked immunosorbent assay.

Animals↗
PubMed1982

Epizootic coronaviral typhlocolitis in suckling mice.

Multiple epizootics of typhlocolitis associated with high morbidity and mortality occurred among suckling mice in an arbovirology research laboratory. Affected mice had necrosis and hyperplasia of cecal, colonic, and less often, small intestinal mucosa. Epithelial syncytia were present throughout the affected areas. Other organs generally were not involved. The etiologic agent was a coronavirus antigenically related to mouse hepatitis virus strains 1 and S. Sera from dams of affected litters and recovered animals did not contain detectable complement fixing antibody to coronavirus antigen. The lesions and the causative agent differed from previously reported coronaviral syndromes in mice. The source of the infection was not definitely found.

Animals↗
PubMed1981

Genetic resistance to lethal flaviviral encephalitis. III. Replication of Banzi virus in vitro and in vivo in tissues of congeneic susceptible and resistant mice.

The replication of Banzi virus, flavivirus, was compared in vitro and in vivo in tissues of congenic mice genetically resistant (C3H/RV) or genetically susceptible (C3H/He) to lethal infection. Ultrastructural changes in brains of resistant and susceptible adult mice following intracerebral or intraperitoneal inoculation of virus also were compared. Banzi virus replicated equally well in monolayer cultures of infant and adult brain, stimulated and non-stimulated macrophages and embryonic cells from both strains of mice. Similarly, no significant differences were found between strains in virus growth in brain, spleen or thymus of peripherally-inoculated infant mice. In intracerebrally-inoculated adult mice, virus titers in brains of resistant mice were consistently lower than in susceptible mice. Visualization of virus particles was dependent on virus concentration in tissues. The changes in brain tissues of both strains of mice were similar, differing only in the time of onset which was noted two days later in C3H/RV mice than in C3H/He mice. These results indicate that, in the case of Banzi virus, the phenotypic expression of genetically-determined resistance of lethal flavivirus infection cannot be attributed primarily to the ability of host cells to support virus replication.

Animals↗
PubMed1980

Protection of mice from lethal flaviviral encephalitis by adoptive transfer of splenic cells from donors infected with live virus.

C3H/RV mice, which are genetically resistant to lethal flaviviral infection were susceptible to lethal challenge with Banzi virus after they were given rabbit antiserum to mouse thymocytes. Congenic C3H/He mice, which are genetically susceptible to lethal flaviviral infection, were protected from lethal challenge with Banzi virus by adoptive immunization with splenic cells from syngeneric or congenic donor mice infected with live virus, as measured by amelioration of clinical disease, death rates, and viral replication. Protection was dependent on thymus cells; mice given immune splenic cells treated with rabbit antiserum to mouse brain and complement had high death rates. Transfer of protection was dependent on time and the dosage of splenic cells. Immune splenic cells from c3h/rv donors were, on a cell-for-cell basis, more effective than immune splenic cells from C3H/He donors in preventing viral replication, encephalitis, and death in C3H/He recipients.

Animals↗
PubMed1979

T cell-mediated cytotoxicity for L 929 fibroblasts infected with Banzi virus (flavivirus).

During infection with Banzi virus, splenic thymus-derived cells of C3H/RV mice developed immunologically specific cytotoxicity for Banzi virus-infected, C3H-derived L 929 fibroblasts. Cytotoxic activity was detected by six days after viral inoculation, was maximal by eight days, and decreased to background levels by 16 days. There was no consistently significant difference in Banzi virus-specific cytotoxicity of spleen cells from C3H/RV and C3H/He mice, which are genetically resistant and susceptible, respectively, to the lethal flaviviral encephalitis. Therefore, the ability of the host to develop killer cells did not, in itself, lead to protection from lethal infection. These experiments are, to our knowledge, the first demonstration of cell-mediated cytotoxicity to a flavivirus.

Animals↗
PubMed1978

Transmissible murine colonic hyperplasia.

After exposure to a variant of Citrobacter freundii, suckling and adult mice developed transmissible murine colonic hyperplasia of the same degree of severity. Mucosal hyperplasia was most severe 2 to 3 weeks after inoculation and then regressed. Suckling mice had a high mortality because of secondary inflammatory and erosive changes. Severe hyperplasia was characterized by mitotic activity along the entire crypt column and surface mucosa.

Animals↗
PubMed1978

Transmissible ileal hyperplasia of hamsters. I. Histogenesis and immunocytochemistry.

Transmissible ileal hyperplasia (TIH) was experimentally induced in weanling hamsters, and the development of lesions was characterized. Ileal lesions developed in two phases: a hyperplastic phase which was detected by Day 10 and an inflammatory phase which began by Day 20. Hyperplasia began as focal lengthening of villi with expansion of crypt-type epithelium onto villus walls. Diffuse hyperplasia of distal ileum developed; dilated, tortuous crypts penetrated subjacent supporting tissues; but metastases were not seen. Inflammation began in association with focal or segmental necrosis of crypt epithelium, and crypt abscesses developed. Severe pyogranulomatous inflammation of the ileal wall, focal peritonitis, mesenteric lymphadenitis, and portal hepatitis were common in advanced lesions. Development of ileal lesions was closely correlated with accumulation of particulate antigen, detectable by immunofluorescence, in the cytoplasm of mucosal epithelial cells. Antigen was also detected in ileal granulomas, mesenteric lymph nodes, and liver. There was simultaneous development of serum antibody specific for intracytoplasmic antigen. These studies comfirm that mucosal hyperplasia is the primary lesion in TIH.

Animals↗
PubMed1978

Transmissible ileal hyperplasia of hamsters. II. Ultrastructure.

The ultrastructure of developing ileal lesions was characterized in weanling hamsters with experimentally induced transmissible ileal hyperplasia (TIH). The primary lesion was mucosal hyperplasia with progressive replacement of mature villus columnar absorptive cells by undifferentiated crypt-type cells. The undifferentiated, mitotically active cells expanded onto villus walls from their normal location in crypts by Day 10 and reached villus tips by Day 14. Aggregates of slightly curved, 0.3 X 1.5 mu, rod-shaped bacteria were detected in the apical cytoplasm of crypt epithelium by Day ;. They replicated intracellularly and accumulated in progressively greater numbers in hyperplastic cells. Active penetration of cells by intralumenal bacteria was not seen. The appearance and distribution of TIH-associated antigen, demonstrated by indirect immunofluorescence, was identical to that observed for intracellular bacteria. Hyperplastic, bacteria-laden crypt epithelium penetrated adjacent supporting tissues. Dilated crypts with flattened epithelium ruptured and released organisms into surrounding tissues. Pyogranulomatous inflammation began at 17 to 25 days and preceded or accompanied penetration of the muscle layers by expanding crypts. Macrophages and neutrophils in inflammatory lesions contained many phagocytized bacteria. In some advanced lesions mature, bacteria-free absorptive cells and goblet cells reappeared. These observations support the hypothesis that intestinal bacteria cause TIH.

Animals↗
PubMed1978

Age-related and light-associated retinal changes in Fischer rats.

Morphological changes in retinas of aging Fischer 344 rats were characterized. The numbers of photoreceptor cells gradually decreased as rats aged. The outer nuclear layer was 12 cells thick at 3 months, but was reduced to less than 8 cells by 18 months. The decrease of photoreceptor cells was more pronounced in rats housed under a light intensity of 32-ft-c than in rats housed under a light intensity of 1 ft-c. Inner and outer segments of surviving photoreceptor cells were morphologically normal. A new form of retinal degeneration was discovered in aged Fischer rats characterized by selective degeneration of peripheral retina. Degeneration was characterized by severe loss of photoreceptor cells in the far peripheral retina. Microcystoids were found in about 25% ofthe affected retinas, and the loss of photoreceptor cells was followed by proliferation and vascularization of the retinal pigment epithelium and disorganization of retinal structures. The incidence and severity of peripheral retinal degeneration increased with aged and prolonged exposure to comparatively high-intensity light. All Fischer rats ((5/5) housed under light intensity of 32 ft-c developed severe peripheral retinal degeneration by 24 months. Peripheral retinal degeneration was an age-related change but appeared to be exaggerated by ambient light.

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