Abstract
A “fast” egg-killing human strain ofChlamydia trachomatis was inoculated into normal CBA and congenic CBA/nu mice, which have an impairment of T-cell function and do not produce anti-chlamydial antibodies. The mice were inoculated by the intra-uterine, intra-articular, or intravenous routes. Some of the mice were first treated with progesterone, which allows successful chlamydial infection of the mouse genital tract when the organisms are introduced genitally. Mice were sacrificed up to 27 days after inoculation. Homogenates of joints, genital tract, spleen, liver, kidneys, eyes and lungs were prepared and tested for chlamydiae in cycloheximide-treated McCoy cell cultures.
Chlamydiae were detected in the genital tracts and spleens, but not in the joints, of mice inoculated via the intra-uterine route. They were found in the joints and spleens of mice inoculated intra-articularly, and were detected also in spleens and, from the 4th to 6th day after inoculation, in joints of mice given the organisms intravenously. These results were obtained irrespective of whether or not the mice had received progesterone. The numbers of chlamydiae in the spleens and joints of the nude mice were larger and they persisted longer than in the corresponding immunocompetent animals, although this was not true for chlamydiae in the genital tract of mice inoculated via the intra-uterine route.
Compartmentalisation of chlamydiae was evident although the spleen was infected consistently irrespective of the route of inoculation and, as mentioned, chlamydiae were found transiently in the joints following intravenous inoculation. This suggests that chlamydiae might also enter the human joint. However, the observations in mice have not, so far, been helpful in establishing the mechanism of human arthritis thought to be chlamydial because none of the mice given chlamydiae extra-articularly developed arthritis either in the presence or the absence of antibody.
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References
Keat A, Thomas BJ, Taylor-Robinson D (1983) Chlamydial infection in the aetiology of arthritis. Br Med Bull 39:168–174
Keystone E, Taylor-Robinson D, Pope C, Taylor G, Furr P (1978) Effect of inherited deficiency of the fifth component of complement on arthritis induced in mice byMycoplasma pulmonis. Arthritis Rheum 21:792–797
Thomas BJ, Reeve P, Oriel JD (1976) Simple serological test for antibodies toChlamydia trachomatis. J Clin Microbiol 4:6–10
Thomas BJ, Evans RT, Hutchinson GR, Taylor-Robinson D (21977) Early detection of chlamydial inclusions combining the use of cycloheximide-treated McCoy cells and immunofluorescence staining. J Clin Microbiol 6:285–292
Tuffrey M, Taylor-Robinson D (1981) Progesterone as a key factor in the development of a mouse model for genital-tract infection withChlamydia trachomatis. FEMS Microbiol Lett 12:111–115
Tuffrey M, Falder P, Taylor-Robinson D (1982) Genital-tract infection and disease in nude and immunologically competent mice after inoculation of a human strain ofChlamydia trachomatis. Br J Exp Pathol 63:539–546
Wang S-P, Grayston JT (1971) Studies on the identity of the ‘fast’ egg-killing Chlamydia strains. In: Nichols R (ed) Trachoma and related disorders caused by chlamydial agents. Excerpta Medica, Amsterdam, pp 322–336
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Tuffrey, M., Falder, P., Thomas, B. et al. The distribution and effect ofChlamydia trachomatis in CBA mice inoculated genitally, intra-articularly or intravenously. Med Microbiol Immunol 173, 29–35 (1984). https://doi.org/10.1007/BF02123566
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DOI: https://doi.org/10.1007/BF02123566