Biomedical subjects
Publications and source records attributed to S W Barthold.
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.
Cultured cells from bovine papilloma virus (BPV)-induced fibroblastic tumors and normal dermis of cattle, horses, and hamsters were examined for cell membrane or internal neoantigens, using the indirect immunofluorescence technique. Sera from cattle and horses bearing BPV-induced fibromas cross reacted with cell membranes of tumor, but not with normal dermal cells of both species. The reaction could be blocked with homologous, but not heterologous, serum of these 2 species. Immunofluorescence was not detected with sera from hamsters bearing BPV-induced sarcomas if incubated with bovine, equine, or hamster cells. Internal neoantigens were not found in any of the acetone-fixed tumor cells, using sera from the 3 species. Both tumor and normal cells were all found free of BPV antigen, using direct immunofluorescence.
Cecal mucosal hyperplasia associated with diarrhea, runting, and high mortality in suckling and weanling hamsters occurred as a natural disease outbreak in a production colony. Young hamsters were runted, and their perineal hair was stained and matted with liquid feces. Their ceca were thickened, contracted, congested, and had scant luminal content. There were severe hyperplasia of cecal crypts, accompanied by increased mitotic activity, inflammation, and focal mucosal erosion. A variety of bacteria was isolated, but none was considered pathogenic. No relationship of cecal hyperplasia to transmissible ileal hyperplasia of hamsters was found. Hyperimmune serum from hamsters with transmissible ileal hyperplasia did not react by immunofluorescence against hyperplastic cecal mucosa. Electron microscopy did not reveal a caustive agent. Transmission attempts have been unsuccessful. Cecal mucosal hyperplasia is apparently a newly discovered disease entity in hamsters with the clinical sign of diarrhea.
Transmissible murine colonic hyperplasia, cuased by a variant of Citrobacter freundii (4280). was shown to be modified by diet and by host strain and species. Four different diets fed to mice inoculated with C frundii 4280 were found to have a significant but varying influence on the severity of hyperplasia. Diet also influenced the colonic crypt height of uninoculated, control mice. F344 rats, Syrian hamsters, and NIH Swiss [N:(S)], C57BL/6J, C3H/HeJ, and DBA/2J mice were inoculated with C freundii 4280. Marked strain differences were noted in the mice in mortality and severity of the colonic hyperplasia. The NIH Swiss mice had the greatest and the C57BL/6J mice had the least mucosal hyperplasia. The rats and hamsters did not develop disease or maintain infection after inoculation with the organism. Twenty isolates of Citrobacter from a range of biologic sources were inoculated into susceptible mice, but only mice inoculated with C freundii 4280 developed the disease.
The morphogenesis of 1, 2-dimethylhydrazine (DMH)-induced lesions in the colon of outbred NIH Swiss mice was determined for up to 5 months of treatment. The effect of hyperplasia on DMH carcinogenesis was also evaluated by introducing a transient hyperplastic stimulus to the colon during the chronic weekly treatment regimen of DMH. The hyperplastic stimulus was a naturally occurring disease of mice, transmissible murine colonic hyperplasia, which is caused by a variant of Citrobacter freundii. In control mice, those not receiving the bacterium, weekly injections of the carcinogen induced neoplastic changes first detectable at two months of treatment in all segments of the colon and in both sexes. The changes increased in frequency and severity with time. Diffuse mucosal hyperpladia and chronic inflammatory and degenerative changes were also associated with DMH after prolonged treatment. The hyperplastic stimulus of C. freundii reduced the latent period for appearance of early DMH tumors, but it had no influence on already established DMH tumors.
Sprague-Dawley rats were given ip injections of bovine culture and sheep cultures of bovine leukemia virus (BLV) and Gross passage-A leukemia virus [MuLV(G)]. Sera were tested to BLV antigens. BLV did not induce tumors in Sprague-Dawley rats, but the rats were susceptible to MuLV(G) at low doses.
The etiology of a transmissable colonic mucosal hyperplasia of mice was investigated. Hyperplasia was produced in mice inoculated with unfiltered colonic suspension from affected mice, but infectivity was lost after passage through a 0.45 mum filter. The etiologic agent was subsequently identified as a variant of Citrobacter freundii. The organism induced colonic mucosal hyperplasia when inoculated into germfree mice, and it was recovered in pure culture from the affected animals.
Fifty young bulls were given commercial wart vaccine upon their arrival at a bull stud establishment. The bulls were given 2 additional vaccinations 2 and 24 weeks later. The precipitin antibody response of these bulls to bovine papilloma virus was monitored. Antibody levels increased significantly, particularly after the 3rd vaccination was given at 24 weeks, but decreased markedly within 20 weeks after the last vaccination was given. These results demonstrated that formalin-inactivated bovine papilloma virus was capable of inducing precipitin antibody similar to infective bovine papilloma virus. Multiple, repeated vaccination provided the best serologic response.
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Sendai virus (SV) infection in aged BALB/c mice was evaluated as a natural model for age-associated susceptibility to viral pneumonia. Young (2 month-old) and aged (22-24 month-old) BALB/c mice were inoculated intranasally with 100 median pneumonia doses (PD50) of SV and examined at 6, 10, and 20 days by virus titration, immunohistochemistry, histopathology, and serology. The aged mice had significantly higher virus titers in lung, prolonged infection, delayed development, and resolution of pneumonia and significantly lower serum antibody titers. In a second experiment, the responses of young mice were compared to intermediate-aged mice (11-13 and 17-18 months old). The intermediate-aged mice had some characteristics of young mice and others of aged mice. The results indicate that SV infection can be used to study aging-associated susceptibility to a pneumotropic virus in a natural host, and that susceptibility of mice to viral pneumonia increases gradually during aging.
A Borrelia burgdorferi chromosomal gene encodes a 30-kDa antigen (P30) that has considerable homology with periplasmic substrate-binding proteins of Gram-negative bacteria, and is recognized by antibodies in sera from a subset of patients with Lyme disease and from B. burgdorferi-infected mice. The p30 gene is 801 nucleotides in length and P30 contains 267 amino acids, with a predicted molecular mass of 30 kDa. The P30 amino acid region 36-258 has homology to conserved domains of the oligopeptide permease A of Gram-negative bacteria. Immunofluorescence studies using murine anti-P30 serum suggest that P30 is on the outer surface of B. burgdorferi. P30 expression could be detected in representatives of all 3 subspecies of B. burgdorferi sensu lato, but not in all of the tested strains. Antibodies to P30 were detected in sera of 18 out of 82 patients (22%) with Lyme disease, including individuals with early- or late-stage infection. Although antibodies to P30 are present in the sera of C3H/HeN mice infected with B. burgdorferi for at least 90 days, immunization with recombinant P30 does not protect mice from infection. We conclude that P30 is a putative substrate-binding protein of B. burgdorferi and is immunologically recognized in human and murine Lyme borreliosis.
The influence of viruses and bacteria on Pneumocystis carinii pneumonia (PCP) is suspected but not known for certain. A number of adventitious viruses and bacteria are common among commercially available and institutionally raised rodents, which may impact upon, or interfere with, the induction of PCP in rodents in several ways. Based upon the biological behavior and prevalence of certain rodent agents, the potential for such impact is great. Infectious agents can directly interfere with research by inducing severe disease in the immunocompromised host. They may also influence the course of P. carinii infection or disease via direct effects upon the respiratory tract or via indirect effects on lymphoreticular cells or other organ systems. Examples of likely agents and their potential effects are discussed.