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Biomedical subjects

S W Barthold

Publications and source records attributed to S W Barthold.

At least 163 records · Page 9Linked to original sources
PubMed1986

Spontaneous wasting disease in nude mice associated with Pneumocystis carinii infection.

Several cases of wasting disease and dyspnea occurred in outbred Crl: CDI(ICR) nu/nu mice obtained recently from a commercial supplier. Gross necropsy revealed pulmonary consolidation, and histologically there was alveolar-wall thickening and filling of alveoli with macrophages and honey-combed eosinophilic material. Electron microscopic examination of lung tissue confirmed infection with Pneumocystis carinii.

Animals↗
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

Enterotropic mouse hepatitis virus infection in nude mice.

The cause of emaciation and diarrhea in athymic nude mice was found to be hyperplastic typhlocolitis resulting from infection with enterotropic mouse hepatitis virus (MHV). The disease was reproduced in experimentally-inoculated nude mice using intestinal homogenates from affected mice and cell culture-derived virus. Material derived from an experimental mouse was passed into neonatal Swiss mice and caused acute typhlocolitis. Virus failed to grow in NCTC-1469 cells and 17Cl-1 cells, which are normally permissive for MHV, but grew to low titer in a mouse rectal carcinoma cell line, CMT 93. These results show that an enterotropic strain of MHV can cause chronic enteric disease in athymic nude mice. The pattern of infection differs markedly from the more common MHV wasting syndrome in nude mice caused by non-enteric strains of MHV.

Animals↗
PubMed1985

Experimental Corynebacterium kutscheri infection in rats: bacteriology and serology.

In a preliminary study, hydrocortisone-treated rats developed pseudotuberculosis when challenged with 6.2 X 10(5) to 3.1 X 10(7) colony forming units of Corynebacterium kutscheri by intranasal, intragastric, or subcutaneous inoculation. Oronasal exposure was selected as a likely natural route to further study inapparent infection. In Study 1, 50 rats received 1.2 X 10(5) colony forming units and various tissues were cultured at intervals to 12 weeks post-inoculation. At each interval, C. kutscheri was regularly isolated from submaxillary lymph nodes, but isolation was sporadic from other sites. In Study 2, 17 out of 21 rats given 1.2 X 10(5) colony forming units and killed weekly for 6 weeks had 2.0 X 10(2) to 1.8 X 10(5) colony forming units of C. kutscheri in oral washes, and 16 rats had 2.0 X 10(2) to 1.0 X 10(5) colony forming units in submaxillary lymph nodes, Serum antibody to C. kutscheri using both microagglutination and indirect immunofluorescence was first detected in some rats by 2 weeks, and in all rats at subsequent intervals. There was a significant (P less than 0.001) positive correlation (r = 0.93) between serum antibody titers and the duration of infection.

Animals↗
PubMed1984

Mouse hepatitis virus strain--related patterns of tissue tropism in suckling mice.

The pattern of tissue tropism for several prototype and uncharacterized strains of mouse hepatitis virus (MHV) was studied by intranasal inoculation of each virus strain into groups of neonatal Swiss mice under otherwise identical conditions. Mice were killed at intervals up to 18 days after inoculation, and their tissues were examined for the presence of MHV antigen by indirect immunofluorescence. Two patterns of infection were apparent. Prototype MHV strains 1, 3, A59, JHM, S and uncharacterized MHV strains Tettnang and wt-1 produced a respiratory pattern, in which nose and lung were consistently involved with dissemination to other organs in a vascular distribution. Pulmonary vascular endothelium and alveolar septal cells, but not airway epithelium, were infected. An enteric pattern was observed with MHV-Y and wt-2 in which MHV antigen was largely restricted to the nose and bowel, with limited dissemination to other abdominal organs but not lung. Intestinal lesions in these mice were severe compared to those manifesting the respiratory pattern of infection. These results indicate that, like coronaviruses of other species, different strains of MHV possess different primary and secondary organotropisms following a natural route of inoculation in a susceptible host.

Animals↗
PubMed1984

Alteration of viral respiratory infections of mice by prior infection with mouse hepatitis virus.

Pre-infection with mouse hepatitis virus (MHV) strains S, 3, or JHM reduced the ability of mice to seroconvert to PVM. Geometric mean antibody titers to PVM among MHV pre-infected mice were lower than those for control mice given only PVM, and dually infected mice seroconverted to PVM later than mice given PVM alone. PVM was not recovered from normally permissive respiratory tract tissues of MHV-S pre-infected mice. Pre-infection of DBA/2 mice with MHV-S compromised the susceptibility of these mice to lethal Sendai virus infection but did not substantially reduce the titers of infectious Sendai virus recovered from the lungs. Serologic responses to Sendai virus and lung Sendai virus titers were similar in Sendai virus-resistant C57BL/6 mice pre-infected or not with MHV-S.

Animals↗
PubMed1983

Mouse hepatitis virus S in weanling Swiss mice following intranasal inoculation.

Three-week-old outbred mice were inoculated intranasally with a mildly pathogenic strain of mouse hepatitis virus (MHV-S). Tissues were analyzed for distribution of infectious virus, lesions, and viral antigen at intervals up to 49 days after inoculation. Sera were tested for neutralizing antibody to MHV-S. Within the first week of infection, virus was isolated from lung and brain of most mice and liver of one mouse, but not from blood, spleen, or intestine. Microscopic lesions consisted of mild olfactory mucosal necrosis, neuronal necrosis of olfactory bulbs and tracts, lymphoplasmacytic infiltrates and vacuolation in the brain, mild nonsuppurative pulmonary perivascular lymphocyte infiltration, focal interstitial pneumonia, and focal necrotizing hepatitis. The presence and distribution of MHV antigen, as determined by indirect immunofluorescence, correlated with virus recovery and acute lesions. No virus or antigen was demonstrable beyond day 7. Serum antibody was first detected on day 10, and titers peaked on day 28 after infection.

Animals↗
PubMed1982

Mouse hepatitis virus immunofluorescence in formalin- or Bouin's-fixed tissues using trypsin digestion.

Mouse hepatitis viral antigens were demonstrated by immunofluorescence in formalin- and Bouin's-fixed tissues processed routinely for histopathology followed by partial digestion with trypsin. Staining was superior in tissues fixed in formalin and was not diminished in tissue sections from paraffin blocks stored at room temperature as long as 2 years. The relative ease of this procedure and the commercial availability of reagents makes this a useful technique for the definitive diagnosis of mouse hepatitis virus infection.

Acetates↗
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

Relationship of colonic mucosal background to neoplastic proliferative activity in dimethylhydrazine-treated mice.

Proliferative activity of background and neoplastic colonic mucosa was examined following five months of weekly injections of 1,2-dimethylhydrazine (20 mg/kg) and one or four months of rest to determine whether previously reported changes may result from an acute or chronic effect of dimethylhydrazine and whether differences exist between stages of neoplasia. To determine whether neoplasia is responsive to a proliferative stimulus, 1,2-dimethylhydrazine dihydrochloride-treated mice were inoculated with Citrobacter freundii. The labeling index and the proliferative zone increased in background mucosa after one month; whereas after four months labeling index, proliferative zone and crypt heights increased, but the mitotic index decreased. There was a positive linear correlation between advancing tumor grade and increasing tumor labeling index and mitotic index. Background labeling index, even when elevated by C. freundii inoculation, had no effect upon tumor labeling index. Mitotic index diminished in background and neoplastic mucosa following prolonged rest and increased in both following C. freundii inoculation. These studies show that 1,2-dimethylhydrazine dihydrochloride causes long-term changes in background mucosa that are apart from a reparative response to cytotoxicity. As tumors progress, labeling index and mitotic index increase, suggesting a multistage process of evolution.

1,2-Dimethylhydrazine↗
PubMed1980

Agglutinins to bacteria in Crohn's disease.

Sera from patients with Crohn's disease were tested for antibodies against organisms which are thought to cause inflammatory bowel disease in animals, or have been implicated in human Crohn's disease. Control sera were collected from healthy individuals and patients with ulcerative colitis. Sera from Crohn's disease and controls failed to agglutinate Clostridium colinum or Campylobacter sputorum subsp. mucosalis and two strains of Mycobacterium paratuberculosis (M26 and M27). Most of the sera agglutinated a Citrobacter freundii variant, Mycobacterium paratuberculosis (M28) and Mycobacterium avium (M41) but Crohn's disease sera did not differ from controls. A complement fixation test against Chlamydia gave more positive reactions in patients with Crohn's disease and colitis than in healthy controls. There was a clear difference between the sera from patients with Crohn's disease and other sera, including ulcerative colitis, in agglutination tests with the commensal coccoid rods of the genera Eubacterium and Peptostreptococcus; in these tests 54% of sera from Crohn's disease were positive compared with 11% in ulcerative colitis and none of the sera from healthy controls. All the results were essentially negative with the exception of those from Eubacterium and Peptostreptococcus and these bacteria merit investigation.

Agglutination Tests↗
PubMed1980

Reversible dermal atrophy in a cat treated with phenytoin.

Phenytoin, given to a cat in proportions therapeutic for man (5 to 8 mg/kg), induced severe dermal atrophy with excessive fragility of the skin following daily oral administration for 3 weeks. Dermal collagen was depleted, but remaining collagen seemed structurally normal. Upon cessation of phenytoin treatment, the cat recovered. In an effort to establish an association between phenytoin treatment and a dermal collagen disorder, phenytoin treatment was repeated and the dermal lesion confirmed.

Administration, Oral↗
PubMed1980

The microbiology of transmissible murine colonic hyperplasia.

The relationship of Citrobacter freundii (4280) to the development of colonic hyperplasia in mice was investigated. The number of Citrobacter freundii (4280) in the descending colon were quantitated at intervals following experimental inoculation, and findings were correlated with previously reported histological and ultrastructural findings. Citrobacter freundii (4280) was a transient infection, lasting 2-3 weeks, after which time mice no longer harbored the organism. Neomycin sulfate and tetracycline hydrochloride, when administered in the drinking water, were useful in the prevention of infection as well as ablation of established infection. The presence of Citrobacter freundii (4280) for as little as 2 days was sufficient stimulus to result in detectable mucosal hyperplasia. The longer the bacterium was present, through 10 days, the greater the hyperplasia.

Animals↗
PubMed1980

Modification of early dimethylhydrazine carcinogenesis by colonic mucosal hyperplasia.

The interaction of colonic mucosal hyperplasia with early 1,2-dimethylhydrazine (DMH) carcinogenesis was studied in random-bred NIH Swiss mice utilizing hyperplasia-inducing Citrobacter freundii. Mice inoculated with this bacterium developed significantly more DMH focal atypia than did mice without hyperplasia following a single dose of DMH (20 mg/kg). Mice with hyperplasia also developed DMH focal atypia with diminished doses of DMH (10 and 5 mg/kg), while normal mice did not. The effect of C. freundii on early DMH carcinogenesis was shown to be due to the hyperplasia rather than to a direct interaction of the bacterium with DMH. Focal atypia arose in high incidence 1 month after a single dose of DMH (20 mg/kg) but did not appear to progress to later stages of neoplasia, since significantly fewer atypia were present at 2 to 4 months among a randomized population. Colonic focal atypia may represent a reversible preneoplastic or precursor lesion as seen in other tissues, with features more aligned to neoplasia than to hyperplasia.

Animals↗
PubMed1979

The ultrastructure of transmissible murine colonic hyperplasia.

Transmissible murine colonic hyperplasia was examined ultrastructurally by sequential sampling after inoculation with the etiologic agent, Citobacter freundii. Light-microscopic changes in the descending colon of inoculated mice were correlated with scanning and transmission electron-microsopic findings. Bacteria were attached to the surface of the mucosa between 4 and 10 days after inoculation. Hyperplasia was most severe at 16 days and thereafter underwent regression. Regression was preceded by extrusion of infected cells from the surface mucosa and replacement by immature hyperplasia epithelium. Hyperplastic epithelium throughtout the crypt resembled undifferentiated crypt cells of controls. By 45 days, the mucosa had reverted to near normal structure. The results suggest that severe mucosal proliferation with minimal inflammatory change resulted from attachment of bacteria to the surface mucosal epithelium. The hyperplastic response appeared to be a defense mechanism of replacing infected cells with newly migrated, uninfected epithelium.

Animals↗
PubMed1979

Autoradiographic cytokinetics of colonic mucosal hyperplasia in mice.

The cytokinetics of a naturally occurring hyperplastic disease of the colon in mice were determined by autoradiography and compared to kinetic changes seen by others in nonneoplastic and neoplastic colonic disease. Cell cycle parameters were determined using the fraction-labeled mitosis method. Labeling index, labeling pattern, and migration rates were also evaluated. During colonic hyperplasia, there was an increase in variation of DNA synthesis times, resulting in prolongation of the S phase. There also was prolongation of the total cell cycle time and G1 phase. In addition, labeling index was increased 2-fold, the proliferative zone was extended to include the entire crypt column and surface mucosa, and the migration rate was accelerated. These findings parallel the "atypical" cytokinetics found in human and murine neoplastic and preneoplastic disorders of the colon and may be a typical proliferative response of mucosa to a variety of stimuli.

Animals↗