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Biomedical subjects

J K Davis

Publications and source records attributed to J K Davis.

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

Polyclonal activation of rat splenic lymphocytes after in vivo administration of Mycoplasma pulmonis and its relation to in vitro response.

The plaque-forming cell (PFC) assay with sheep erythrocytes (SRBC) sensitized with different antigens and a 4-h tritiated thymidine pulse assay were used to determine whether polyclonal activation occurs in rats following in vivo administration of Mycoplasma pulmonis. Injection of M. pulmonis into F344 rats resulted in an increase in the number of splenic immunoglobulin M-secreting PFC that produced antibodies reactive with the trinitrophenyl hapten and with SRBC. This polyclonal response reached a peak by 72 h after injection and returned to normal levels by 96 h, at which time the specific response to M. pulmonis reached its peak. Heat treatment and preopsonization of M. pulmonis with antiserum before injection resulted in reduced numbers of PFC against M. pulmonis-sensitized SRBC, trinitrophenyl hapten-sensitized SRBC, and SRBC. The number of PFC against the three types of target cells also increased in LEW rats after immunization with M. pulmonis. The number of PFC against SRBC and staphylococcal protein A-sensitized SRBC was higher in immunized LEW rats than in immunized F344 rats. Examination of unimmunized animals also revealed that LEW rats had higher initial numbers of PFC than did F344 rats. These results showed that polyclonal activation occurs in rats following in vivo administration of M. pulmonis and that LEW rats have an inherent propensity to develop higher nonspecific responses in vivo than F344 rats.

Animals↗
PubMed1986

Development of an aerosol model of murine respiratory mycoplasmosis in mice.

Animal models of murine respiratory mycoplasmosis due to Mycoplasma pulmonis provide excellent opportunities to study respiratory disease due to an infectious agent. The purpose of the present study was to develop and characterize an aerosol model for the production of murine respiratory mycoplasmosis in mice. The exposure of mice for 30 min to aerosols generated with a DeVilbiss 45 nebulizer in a nose-only inhalation chamber consistently reproduced typical lesions. The chamber was operated with a nebulizer air flow of 5.3 liters/min at 5.0 lb/in and a diluting air flow of 20 liters/min, with the nebulizer containing 5 ml of a suspension of viable M. pulmonis organisms (a concentration between 6 X 10(5) to 6 X 10(10) CFU/ml). Infective aerosol particles of less than a 4.0-micron median aerodynamic diameter with a geometric standard deviation of approximately 2.0 reached the lungs and were evenly distributed among the different lung lobes. A minimum 1.5-log loss of viability in the M. pulmonis suspension was demonstrated. With the exception of the 50% lethal dose, all of the parameters previously established by intranasal inoculation could be examined with the aerosol model. The major advantages of the aerosol model were excellent reproducibility of exposure (both between different experiments and between animals in a given experiment), the avoidance of anesthetization, and the ability to immediately deposit the majority of the organisms in the lung. The only disadvantage was the requirement for large volumes of mycoplasmal cultures.

Aerosols↗
PubMed1986

Evaluation by scoring and computerized morphometry of lesions of early Mycoplasma pulmonis infection and ammonia exposure in F344/N rats.

To evaluate lesions of ammonia exposure and Mycoplasma pulmonis infection in gnotobiotic F344/N rats, groups of rats were inoculated with M. pulmonis, exposed to 76 micrograms/liter (100 parts per million) ammonia, or both, or served as controls. Six rats from each group were killed 3, 5, 7, and 9 days after inoculation and their respiratory organs prepared for histologic examination. Lesions were assessed by subjective scoring and computerized morphometry, and results obtained by the two methods were compared to assess agreement of results. Lesions were limited to the nasal passages. Ammonia exposure resulted in hyperplastic and degenerative changes in the anterior nasal epithelium. Lesions of mycoplasmosis were more severe in ammonia-exposed than unexposed rats, but qualitative differences in lesions were not apparent. Results of the two methods agreed in assessment of submucosal inflammatory cell accumulation. Epithelial lesions were difficult to evaluate by both methods in infected, ammonia-exposed rats. In evaluation of lesions of ammonia exposure alone, agreement was adequate. Both methods indicated that exudates were significantly greater in ammonia-exposed infected rats than in non-exposed infected rats. Thus, scoring and morphometry provided similar assessments of differences in lesion severity among the treatment groups.

Ammonia↗
PubMed1986

Distribution of Ia antigens and T lymphocyte subpopulations in rat lungs.

In order to examine the mechanism of specific immunity in the lung, the distribution of Ia antigens and T lymphocyte populations was determined using immunoperoxidase-staining of cryostat sections of lungs from specific pathogen-free rats. BALT was found to be divided into three regions of lymphoid tissue. The central region was primarily composed of B cells, and was surrounded by a peripheral region of T cells (MRC OX-19+) which included both T helper (W3/25+) and T suppressor/cytotoxic (MRC OX-8+) cells. The subepithelial region contained a dense network of W3/25+, non-T cells. A majority of BALT cells, including the lymphoepithelial cells, were Ia+. The alveolar walls were found to contain numerous Ia+ dendritic-shaped cells. Alveolar macrophages found in sections, as well as those collected using bronchoalveolar lavage, were Ia- and W3/25-. Mechanisms for the induction of immunity within both BALT and the alveolar region are proposed.

Animals↗
PubMed1985

Assessment of knowledge and clinical judgment in the pediatric residency.

Multiple-choice examinations were given three times each year in a pediatric residency training program. The test scores correlated highly with subsequent scores on the intraining examination of the American Board of Pediatrics. The results were replicated and cross-validated in another study the following year. Use of the local tests and the board examination to evaluate the residents makes it possible to provide continual feedback to the residents regarding the adequacy of their performance and feedback to faculty members regarding the effectiveness of the program. Local test scores can be used to predict the residents' standing on the national examination, and they provide a sound basis for counseling individual residents and for improving specific components of the training program.

Clinical Competence↗
PubMed1985

Nonspecific lymphocyte responses in F344 and LEW rats: susceptibility to murine respiratory mycoplasmosis and examination of cellular basis for strain differences.

Mycoplasma pulmonis produces a mitogen which may play a role in the pathogenesis of murine respiratory mycoplasmosis in rats. Since LEW rats are more susceptible to this disease than F344 rats are, these two strains were used to examine a possible association between disease severity and the level of nonspecific lymphocyte stimulation by mitogens, including M. pulmonis membrane preparations. F344 and LEW spleen, lung, blood, and lymph node lymphocytes were exposed to various mitogens. LEW lymphocytes gave a significantly higher response to mitogenic stimulation, regardless of their anatomical source. These differences in lymphocyte responsiveness were primarily due to differences within the nonadherent cell population. Significantly higher numbers of W3/25+ (T helper) cells were found in LEW lymphoid populations, whereas no difference was found in MRC OX-8+ (T suppressor/cytotoxic) cells. These data suggest an association between disease severity and host responsiveness to nonspecific stimuli.

Animals↗
PubMed1985

Strain differences in susceptibility to murine respiratory mycoplasmosis in C57BL/6 and C3H/HeN mice.

Not only is murine respiratory mycoplasmosis, due to Mycoplasma pulmonis, a complication of biomedical research, it provides excellent animal models to study the development of a naturally occurring respiratory disease induced by an infectious agent. The understanding of pathogenic mechanisms of disease can be greatly facilitated by studying genetic differences in susceptibility. Five strains of mice with various H-2K haplotypes were examined for their susceptibility to murine respiratory mycoplasmosis; of these, C57BL/6 and C3H/HeN mice were chosen for additional study. There were no significant differences in the incidence of infection in either the upper or lower respiratory tract or in the severity of upper respiratory tract lesions in the two strains as determined at 14 days postinfection. In striking contrast, the C57BL/6 mice were significantly more resistant to the development of gross and microscopic lung lesions and to death due to pneumonia as shown by an almost 100-fold difference in the 50% lethal dose, 50% gross pneumonia dose, and 50% microscopic lesion dose. The most apparent differences in lung lesions between the two strains were in the severity of acute lesions of the bronchial epithelium, the amount of mixed inflammatory response in the alveoli, and the amount of lymphoid infiltrates. All were significantly more severe in C3H/HeN mice. In addition, more C3H/HeN mice developed antibody responses to M. pulmonis. The amount of antibody correlated with lesion severity in both strains.

Animals↗
PubMed1984

Mycoplasma pulmonis detection in rodents: lessons for diagnosis in other species.

Evaluation is made of cultural and serological tests used in the diagnosis of mycoplasma infections in normal and barrier-maintained colonies of rats and mice. Special emphasis is put on the significance of positive ELISA tests for immunoglobulin M and G (IgM and IgG) and on the difficulty resulting from the presence of cross-reactive antigens in Mycoplasma pulmonis and M. arthritidis. Recommendations are made as to the diagnostic tests most adequate for monitoring laboratory animal colonies for mycoplasma infections.

Animals↗
PubMed1983

Structural teratogenicity evaluation of methyl chloride in rats and mice after inhalation exposure.

One hundred bred Fischer-344 female rats were exposed daily for 6 hours to atmospheres containing 0, 100, 500, or 1,500 ppm methyl chloride, 25 females per exposure concentration, from gestation day (gd) 7 through gd 19. On gd 20, the females were sacrificed for evaluation of maternal reproductive and fetal parameters. Maternal and fetal toxicity was apparent at the highest exposure concentration. There were no methyl chloride-induced external, skeletal, or visceral abnormalities seen in the fetuses. One hundred thirty-two C57BL/6 female mice bred to C3H males to produce B6C3F1 offspring were exposed daily for 6 hours to atmospheres containing 0, 100, 500, or 1,500 ppm methyl chloride, 33 females per exposure concentration, from gd 6 through gd 17. Exposure to the entire 1,500-ppm group was terminated on gd 10-14, with the animals killed in extremis. Selective necrosis of neurons in the internal granular layer of the cerebellum, ranging from individual cell involvement to focal areas comprising large numbers of neurons, was found in all females. On gd 18, the females from the other treatment groups, all of which survived, were killed for evaluation of maternal reproductive and fetal parameters. No evidence was seen of maternal or fetal toxicity in these exposure groups. There were no significant alterations in external appearance in fetuses from any of the exposure groups. Visceral examination of mouse fetuses revealed a small, but statistically significant, incidence of heart defects in litters of the 500-ppm group. The anomaly, a reduction or absence of the atrioventricular valve, chordae tendineae, and papillary muscle, was observed on the left side (bicuspid valve) in three fetuses and the right side (tricuspid valve) in six fetuses: three males and six females. It is concluded that methyl chloride inhalation exposure in pregnant rats, during critical periods of embryo and fetal development, is not teratogenic at concentrations which elicit maternal and fetal toxicity. In pregnant mice, methyl chloride was severely toxic to dams following 4 days or more of exposure to 1,500 ppm in air. Methyl chloride, at 500, but not 100 ppm, was teratogenic in mice, leading to a malformation in the heart. No embryo-fetal toxicity or teratogenicity was associated with exposure of mice, during critical periods of embryo and fetal development, to 100 ppm of ethyl chloride.

Air↗
PubMed1983

The properties of lenses used for the correction of aphakia.

There is a wide variety of aphakic lenses available but remarkably little quantitative data to assist the optometrist in his choice of product. This paper presents the results of a survey of nearly all the available lens types. Quantitative data is given for the products of those manufacturers who cooperated. Data covers off axis acuity, magnification, distortion, thickness, weight and ultraviolet protection.

Aphakia, Postcataract↗
PubMed1982

Murine respiratory mycoplasmosis in F344 and LEW rats: evolution of lesions and lung lymphoid cell populations.

By comparison of two strains, LEW and F344, which are known to differ in susceptibility to Mycoplasma pulmonis respiratory disease, it was shown that differences in lesion severity and progression were associated with changes in lung lymphocyte populations. Lung lesions in LEW rats developed earlier after infection, became more severe, and were characterized by continued proliferation of all classes of lymphoid cells, T lymphocytes, B lymphocytes, and plasma cells, throughout the 120-day observation period. In contrast, lymphoid proliferation in F344 rats reached a plateau at 28 days and was restricted to an increase in T lymphocytes, immunoglobulin A (IgA)-bearing B lymphocytes, and IgA and IgG plasma cells. Although approximately 10 times as many IgG B cells and 4 times as many IgG plasma cells were found in infected LEW rats as compared with F344 rats, the specific anti-M. pulmonis IgG response in the two strains was roughly parallel. The same relationships held true, although to a lesser extent, for specific IgA antibody responses and cellular responses. Whereas lung lesions showed a tendency to resolve in F344 rats by 120 days, severe lesions persisted in LEW rats. The disparity between the cellular response and specific antibody response, the seemingly uncontrolled lymphocyte proliferation in LEW rats, and the mitogenic potential of M. pulmonis suggest that differences between LEW and F344 rats in lung lesion severity and progression are related to differences in the degree of nonspecific lymphocyte activation in the two strains, an imbalance in regulation of lymphocyte proliferation in LEW rats, or both.

Animals↗
PubMed1982

Murine respiratory mycoplasmosis in LEW and F344 rats: strain differences in lesion severity.

Pathogen-free weaning rats of the LEW and F344 strains were caged together for two months to eliminate microbial and environmental differences, and then infected intranasally with 10-fold dilutions of viable Mycoplasma pulmonis. At necropsy 28 days post-inoculation, F344 rats had no gross lung lesions, even those given the maximum dose of 1.4 X 10(9) colony-forming units of M. pulmonis. LEW rats often had extensive gross lesions with a gross-pneumonia-dose50 of 1.1 X 10(7) colony-forming units/rat. Histological examination of the respiratory tract (nasal passages, larynges, tracheae, and lungs) and tympanic cavities showed both qualitative and quantitative differences in lesions between the two strains, particularly in the lungs. Hyperplasia of bronchus-associated lymphoid tissue occurred in both strains, but was more extensive in LEW rats. Atelectasis, alveolar consolidation (due primarily to mononuclear inflammatory cells), and suppurative bronchitis and bronchiolitis were seen only in LEW rats. Infiltrates of lymphoid cells into the lungs distal to bronchi and around blood vessels also were seen primarily in LEW rats. These differences between the two rat strains provide excellent model systems with which to dissect the role of cell responses in the pathogenesis of a naturally occurring chronic lung disease.

Animals↗
PubMed1981

Mycoplasma host-cell interactions resulting in chronic inflammation: acquisition of host antigens and other mechanisms.

Many pathogenic mycoplasmas induce chronic inflammation as a consequence of their ability of circumvent or block immunological attack. This may be due to the organisms's intrinsic properties or to factors that arise from mycoplasma host-cell interactions. Based upon present evidence, the most likely mechanisms are antibody and/or phagocyte inefficiency, alteration of lymphocyte responsiveness due to the nonspecific mitogenicity of mycoplasmas, and antigenic disguise via acquisition of host antigens. The latter is not only an important mechanism by which the organisms could evade or alter the host immunological response, but one which may serve as a stimulus for autoimmune reactions.

Animals↗
PubMed1981

Detection of natural Mycoplasma pulmonis infection in rats and mice by an enzyme linked immunosorbent assay (ELISA).

A total of 2,194 rats and mice representing 10 rat and nine mouse strains from eight commercial breeding facilities and 19 research institutions were tested for Mycoplasma pulmonis antibodies of the IgG and IgM classes by an enzyme-linked immunosorbent assay (ELISA). Cultural data also were obtained from 1,139 of these animals and histopathological data from 410. Reliability of the IgG ELISA for detection of infection in rats and mice was found to be excellent. Virtually no rat or mouse colony was culturally negative and IgG ELISA positive, or vice versa. However, discrepancies between ELISA and cultural results were observed in individual animals. Discrepancies occurred significantly more often with the IgM than IgG ELISA and more so in mice than in rats, particularly in barrier-maintained animals. Agreement of the IgG and IgM ELISA with culture in barrier-maintained rats was 100% and 94%, respectively and in barrier-maintained mice 87% and 69%, respectively. Available evidence suggested that some of the discrepancies in mice could be due to either active or previous low level infection or failure to culture multiple sites. However, the greatly reduce correlation of the IgM ELISA and culture in mice was incompletely understood, and in the absence of other evidence of infection must be interpreted with caution. Even though the present study was not designed to determine comprehensive incidence figures, the results indicated widespread Mycoplasma pulmonis infection both in conventional and "barrier-maintained" colonies as demonstrated by ELISA a well as cultural isolation.

Animals↗
PubMed1981

Respiratory and genital mycoplasmosis of laboratory rodents: implications for biomedical research.

Murine respiratory mycoplasmosis (formerly murine chronic respiratory disease) has been conclusively shown to be due to Mycoplasma pulmonis. Based upon experimental studies, it is clear that the disease is an insidious, protracted process involving a variety of interrelated factors. Intracage NH3 (25 to 250 ppm) greatly increases disease incidence, severity and progression. In mice, the presence of other infectious agents, like Sendai virus, also potentiates disease. However, comparisons of animals matched for age, sex, microbial, and environmental factors indicate that heredity is one of the most critical determinants of disease. M. pulmonis is generally thought to be transmitted via aerosol, but recent evidence indicates that in utero transmission is also possible. M. pulmonis can colonize and produce disease in all parts of the female genital tract. While the natural occurrence of both respiratory and genital mycoplasmoses seriously restricts the usefulness of rats and mice for other research purposes, the experimental diseases represent useful models for the study of human disease, particularly mechanisms involved in chronic pulmonary inflammation and reproductive failure.

Animals↗
PubMed1981

Arthritis of rats and mice: implications for man.

Numerous attempts to implicate mycoplasmas in rheumatoid arthritis of man have resulted in complete failures or inconsistent results. The striking similarity of rheumatoid arthritis to a number of chronic mycoplasmal arthritides in animals, and new information on the pathophysiology of mycoplasmas and their complex interplay with the immunological apparatus of the host, suggest that the search for mycoplasmas in human disease should not be abandoned. Furthermore, increasing knowledge of mycoplasmal arthritis in animals emphasizes possible serious deficiencies of past studies in man.

Animals↗