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S W Barthold

Publications and source records attributed to S W Barthold.

At least 145 records · Page 8Linked to original sources
PubMed1989

Duration of challenge immunity to coronavirus JHM in mice.

The duration of challenge resistance in mice immunized with mouse hepatitis virus (MHV) strain JHM was examined as a model of immunity to corona-virus infection. Genetically susceptible BALB/cByJ mice were immunized by intranasal (i.n.) or per os (p.o.) inoculation with MHV-JHM or sterile tissue culture fluid (sham) then challenged i.n. with MHV-JHM or sterile tissue culture fluid 1, 6, or 12 months later. Four days after challenge, virus in nasal turbinates and liver was quantified, and prevalence of microscopic lesions in liver and gut-associated lymphoid tissue was tabulated as indices of challenge resistance. MHV-immunized and challenged groups were compared to sham-immunized and challenged groups. Mice immunized by i.n. inoculation were strongly resistant to challenge at 1, 6, and 12 months. Mice immunized by p.o. inoculation were resistant at 1 month, but became partially susceptible to reinfection at 6 and 12 months, based upon all indices. These data indicate that, depending upon route of immunization, mice can become susceptible to reinfection with the same coronavirus strain over time.

Animals↗
PubMed1988

Olfactory neural pathway in mouse hepatitis virus nasoencephalitis.

The mechanism of brain infection with mouse hepatitis virus-JHM was studied in BALB/cByJ mice following intranasal inoculation, and found to be a consequence of direct viral spread along olfactory nerves into olfactory bulbs of the brain. Infection was followed sequentially from nose to brain, using microscopy, immunohistochemistry and virus quantification. Lesions, antigen and virus were observed in the olfactory bulb and anterior brain as early as 2 days and posterior brain by 4 days after inoculation. Viral antigen extended through nasal mucosa into submucosa, then coursed along the olfactory nerve perineurium and fibers, through the cribriform plate into the olfactory bulbs. On days 4 and 7, viral antigen was found in the antero-ventral brain, along ventral meninges, olfactory tracts and anterior ramifications of the lateral ventricles. Virus was cleared from nose by 10 days and anterior brain by 20 days, but persisted in posterior brain for 20 days after inoculation. Mice also developed disseminated infection, with viremia and hepatitis. Infection of brain did not correlate with presence of viremia. In contrast to intranasally inoculated mice, orally-inoculated mice did not develop encephalitis, despite evidence of disseminated infection.

Animals↗
PubMed1988

Mouse hepatitis virus and host determinants of vertical transmission and maternally-derived passive immunity in mice.

Transmission of mouse hepatitis virus (MHV) in utero following oronasal inoculation of pregnant mice was found to depend upon MHV strain and host genotype. Virulent, polytropic MHV-JHM was recovered from multiple maternal tissues, including liver and uterus, as well as placenta and fetus in susceptible BALB/cByJ mice. Fetuses were infected during all 3 trimesters of pregnancy. Low virulence, polytropic MHV-S infected fetuses in a low percentage of susceptible BALB/cByJ dams. Infection of resistant CD-1 mice with MHV-JHM was limited, with no fetal infection. Enterotropic MHV-Y was largely restricted to intestine of BALB/cByJ and CD-1 dams, with minimal dissemination and no fetal infection. Maternally-derived MHV IgG antibody was detectable in pup sera through 4 weeks of age. Antibody titers were generally lower in second litters of the same dam. Cross-fostering experiments showed that antibody was transferred via colostrum and not in utero, and that pups were capable of absorption through 2 weeks of age. Pups nursing immune dams were protected against MHV challenge at 1 and 2 weeks of age, compared to pups nursing naive dams. Immunity to MHV challenge was cross-protective against both antigenically homotypic and heterotypic strains of MHV.

Animals↗
PubMed1988

Graft-versus-host disease and sialodacryoadenitis viral infection in bone marrow transplanted rats.

The effect of a localized viral infection on the occurrence of graft-vs.-host disease (GVHD) was examined in allogeneic rat bone marrow chimeras (ACI/LEW). Animals without clinical evidence of GVHD, 62 days after bone marrow transplant, were infected in salivary and lacrimal glands with sialodacryoadenitis virus (SDAV), and sacrificed 8-25 days postinfection. Using established histologic criteria, GVHD was found more frequently in salivary and lacrimal glands of SDAV-infected chimeras than uninfected chimeras. Skin and oral mucosa, tissues not infected by the virus, showed no differences in occurrence of GVHD, suggesting that the viral infection induced only local and not systemic GVHD. GVHD and SDAV infection, which are histologically similar, were differentiated by examining tissues for SDAV antigen using immunoperoxidase technique. Histologic changes were present for at least 1 week longer than viral antigen, suggesting they represented GVHD rather than viral infection. GVHD and SDAV infection were also differentiated by looking for a histologic feature characteristic of GVHD and not found in SDAV infection (periductal lymphocytic infiltrate). This was found in SDAV-infected chimeras more frequently than uninfected chimeras, suggesting that the viral infection somehow induced GVHD. Results showed a localized increase in the occurrence of GVHD subsequent to localized viral infection.

Animals↗
PubMed1988

An animal model for Lyme arthritis.

A model of Lyme arthritis has been developed in laboratory rats. Intraperitoneal inoculation of a low-passage tick isolate of B. burgdorferi into neonatal and weanling LEW/N rats resulted in multisystemic infection and arthritis. Spirochetes were isolated from blood, liver, kidney, spleen, brain, and joints of inoculated rats. Arthritis, associated with the presence of spirochetes, developed in multiple joints by day 14 and persisted through day 90 after inoculation. Arthritic lesions resembled those found in human Lyme disease lesions. Lesions were not found in other organs, although spirochetes were present. Neonatal F344 and SD rats were also susceptible to infection and induction of arthritis. Three different isolates of B. burgdorferi were shown to be pathogenic. Pathogenicity of one isolate was retained after at least 11 in vitro passages. Formalin-killed spirochetes were not pathogenic. Other features of the Lyme disease complex have yet to be seen in the rat, but long-term studies are required to completely define the rat model. This highly reproducible model should allow in-depth studies on the pathogenetic mechanisms of this important human disease.

Animals↗
PubMed1988

The effect of selected viruses on Corynebacterium kutscheri infection in rats.

The influence of selected viral pathogens on rats that were previously infected with Corynebacterium kutscheri was investigated. A series of three separate experiments were performed to test the effect of sialodacryoadenitis virus, Sendai virus and rat virus. In each experiment, weanling rats were divided into three groups (C. kutscheri-inoculated, virus-inoculated and C. kutscheri plus virus-inoculated). Two groups were inoculated oronasally with C. kutscheri to establish subclinical infections. Two weeks later, two groups were inoculated intranasally with virus. At 5 weeks, the prevalence of C. kutscheri recovery from oral cavity and submaxillary lymph node and the prevalence of overt pseudotuberculosis was compared between treatment groups. Seroconversion of rats to C. kutscheri was measured by microagglutination and viruses by indirect immunofluorescence assays. Infection of rats with sialodacryoadenitis virus, Sendai virus or rat virus had no discernable effect on C. kutscheri-infected rats.

Animals↗
PubMed1987

Response of genetically susceptible and resistant mice to intranasal inoculation with mouse hepatitis virus JHM.

Mouse hepatitis virus (MHV)-JHM infection was studied in genetically susceptible (BALB/cByJ) and resistant (SJL/J) mice following intranasal inoculation at 1, 3, 6 or 12 wk of age. Markers of infection included histology, immunohistochemistry, virus quantification and virus serology. All BALB mice developed severe disseminated disease with high mortality due to encephalitis and hepatitis. Peak MHV titers appeared in brain, liver, spleen and intestine on days 3 or 5. Age at inoculation did not influence virus titers in brain, spleen or intestine, but virus titers in liver were inversely proportional to age at inoculation. In 6-wk-old BALB mice, virus was cleared from spleen, intestine and liver by day 30 and from brain by day 60. In intestine, MHV was localized to lymphoid tissue, without fecal excretion. SJL mice of all ages developed remarkably milder disease with low mortality occurring only among mice inoculated at 1 wk of age. SJL mice inoculated at 1 wk had disseminated infection at day 3, but lesions and antigen were cleared from most organs by day 5. Mice inoculated at 3 and 6 wk of age had minimal or no involvement of peripheral organs, and mice inoculated at 12 wk of age had infections restricted to the nose. At day 5, MHV titers in brain, liver, spleen and intestine were significantly lower or undetectable in SJL mice of all ages compared to age-matched BALB mice. In 6-wk-old mice, MHV was cleared from all organs by day 10. Serum antibody titers to MHV were many-fold higher in BALB mice, compared to SJL mice, which mounted only a modest response.

Age Factors↗
PubMed1987

Intranasally administered alpha/beta interferon prevents extension of mouse hepatitis virus, strain JHM, into the brains of BALB/cByJ mice.

Intranasally administered alpha/beta interferon blocked extension of the coronavirus, mouse hepatitis virus, strain JHM (MHV-JHM), from the nose to the brain of BALB/cByJ mice following intranasal inoculation with the virus. Two hundred units of alpha/beta interferon were administered intranasally to BALB/cByJ mice daily over a five day period. The mice were exposed intranasally to 10(3) median tissue culture infectious doses of MHV-JHM on the third day of interferon treatment. Two days after virus exposure, the proportion of mice with MHV in nasal turbinates was reduced from 10 of 10 in the untreated group to 7 of 10 in the interferon-treated group, and mean titers in virus-containing noses were lower in the interferon-treated group. Five days after virus exposure, the proportion of mice with infectious virus in the brain was significantly lower in the interferon-treated group (1 of 10 mice) than in the untreated group (10 of 10 mice). Systemic infection, as measured by presence and concentration of virus in the spleen, was not affected by intranasal interferon treatment. These results suggest that intranasally administered interferon protects against local extension of MHV-JHM from nose to brain, but not against dissemination of virus to other organs, such as the spleen.

Administration, Intranasal↗
PubMed1987

Elimination of mouse hepatitis virus from a breeding colony by temporary cessation of breeding.

During quarantine in a Trexler-type isolator, high mortality was noted among offspring in a breeding colony of C.B.-17 scid/+ mice. Histology and immunohistochemistry on tissues of surviving weanlings confirmed mouse hepatitis virus infection (MHV). Since MHV infection is reported to be acute and self limiting, elimination of infection was attempted by cessation of breeding for a 15-week period. F1 mice born thereafter were seropositive for MHV at 3 to 4 weeks old and seronegative 4 weeks later, attributed to decay of maternally-derived antibodies. F2 mice were seronegative for MHV at 3 to 9 weeks old. No deaths occurred in any litters. These results suggest that MHV can be eliminated from a colony by temporary cessation of breeding, as evidenced by seronegative progeny through the F2 generation.

Animals↗
PubMed1987

Host age and genotypic effects on enterotropic mouse hepatitis virus infection.

Intestinal lesions due to infection with an enterotropic strain of mouse hepatitis virus (MHV-Y) were found to be more severe and wide-spread in BALB/cByJ and Cr1:CD-1(ICR) mice than in SJL mice inoculated at 1 week of age, using nonparametric ranking analysis. Lesions and viral antigen were limited largely to the bowel, but also occurred in the liver and brain of some mice. BALB/cByJ mice developed a particularly high prevalence of brain infection, resulting in mortality after the enteric phase of infection had ceased. MHV-Y antigen was present in neurons, glia and vascular endothelium in a vascular distribution. Cr1:CD-1(ICR) pups inoculated with MHV-Y at 4 or 7 days of age developed severe typhlocolitis, enteritis and encephalitis with moderate mortality. Pups infected at 2 or 3 weeks of age had mild intestinal lesions with minimal alteration of mucosal architecture, no encephalitis and no mortality. These results demonstrate that host age and genotype influence the course of enterotropic mouse hepatitis virus, as has been shown previously with non-enterotropic, respiratory-type strains of mouse hepatitis virus.

Age Factors↗
PubMed1987

Further evidence for papovavirus as the probable etiology of transmissible lymphoma of Syrian hamsters.

The role of hamster papovavirus as the etiology of transmissible lymphoma was investigated under strict conditions that prevented natural exposure to the lymphoma agent. In an initial experiment, 19 hamsters that were exposed naturally to transmissible lymphoma were placed in direct and indirect contact with weanling hamsters from an uninfected source. Lymphoma developed in the original infected hamsters as well as hamsters maintained in direct and indirect contact. In addition, one of the contact hamsters developed cutaneous epitheliomas, containing hamster papovavirus. Epithelioma homogenate was inoculated into primary hamster embryo cultures, in which hamster papovavirus replicated. Second and third passage tissue culture fluid containing hamster papovavirus induced lymphomas in suckling and weanling hamsters. Cell culture fluid from uninoculated embryo cultures was not oncogenic.

Animals↗
PubMed1986

Primary hyperparathyroidism in a dog: biochemical, bone histomorphometric, and pathologic findings.

An adult Keeshond had clinical signs associated with hypercalcemia, including inappetence, polyuria, polydipsia, and vomiting. Blood biochemical findings and urinary clearance studies were consistent with a diagnosis of primary hyperparathyroidism. Histomorphometric analysis of trabecular bone in an iliac crest biopsy indicated increased bone remodeling activity. Surgical exploration of the neck revealed an oval mass, which was removed by blunt dissection. Histologic diagnosis was parathyroid gland adenoma. The dog died because of renal failure on the eighth postoperative day. This report defines primary hyperparathyroidism in the dog, thus facilitating diagnosis for the veterinary clinician.

Animals↗
PubMed1986

Mouse hepatitis virus nasoencephalopathy is dependent upon virus strain and host genotype.

Mouse hepatitis virus (MHV) S induced typical MHV spongiform lesions in brainstem 28 days following intranasal inoculation of adult A/J, BALB/cByJ, CBA/J, C 3 H/HeJ and C 3 H/RV, but not SJL mice. In all but SJL mice, brain lesions occurred at or near the infectious dose level, based on seroconversion by the indirect immunofluorescence assay. During the acute phase of infection (day 5), lesions were limited to the nose and brain in most genotypes. Exceptions were BALB mice, which had mild hepatitis and SJL mice, which had lesions restricted to the nose. No mortality occurred in any genotype. Following intranasal inoculation of adult mice, MHV-1, -3, -A 59, -JHM and -S all caused brain lesions at 28 days after inoculation. MHV-1 and -3 caused lesions that were usually restricted to the anterior olfactory tracts, while MHV-A 59, -S and -JHM also caused more generalized and pronounced lesions involving the midbrain and pons. These studies suggest that avirulent MHV-S given intranasally to most mouse genotypes is a good model for induction of brain infection in the absence of mortality. They also confirm observations made by others in which MHV-JHM, -S and -A 59 are relatively more neurotropic than other MHV strains, such as MHV-1 and -3.

Animals↗