Further observations on the murine model of Mycoplasma hominis infection

Abstract

Mycoplasma hominis, the first mycoplasma of human origin to be isolated, has been associated with several diseases, notably bacterial vaginosis, pelvic inflammatory disease, prematurity and puerperal fever. The mouse model does not mimic closely these features of human disease, but has some notable features. Given intravaginally to mice, M. hominis does not colonize unless the mice have been pre-treated with oestradiol. As shown here, endogenous hormone has no part to play because removal of the ovaries does not interfere with vaginal colonization. Persistent colonization occurs in hysterectomized mice so that organisms in the upper tract, which are sometimes found, are not responsible, by retrograde leakage, for those in the lower tract. Organisms in the lower tract can be eliminated by treating mice with a tetracycline, or progesterone or by natural resolution. Elimination by whatever means results in a rather weak immunity to recolonization. In contrast, intravenous inoculation of viable, and particularly killed, M. hominis organisms results in strong resistance to recolonization. This is, in part, genetically influenced, being seen in mice of strain BALB/c but not of strain CBA. Resistance is inversely proportional to the presence and titre of M. hominis specific serum antibody. The possible role of cell-mediated immunity is discussed.