Salpingitis in mice induced by human strains of Chlamydia trachomatis.

Human strains of Chlamydia trachomatis were inoculated unilaterally into the genital tracts of female TO, CBA, CBA/nu and C3H mice via the intrauterine route or under the ovarian bursa. Inflammatory changes were not seen in the oviducts or uterus of mice given two laboratory-adapted LGV serovars (L1 and L2), although chlamydiae were recovered from the lower genital tract. However, salpingitis and endometritis occurred after each of three chlamydial strains (serovars D and E) had been inoculated. Oviduct inflammation was seen for up to 6 weeks after inoculation but reached maximum severity usually after about 2 weeks, the lumen sometimes being occluded by exudate and necrotic debris. Pathological changes were seen often in both oviducts indicating canalicular spread of the organisms through the uterus. Pre-treatment of the mice with progesterone had an enhancing effect in that the lesions developed more rapidly; such treatment, in halting the oestrous cycle, probably made a larger number of target cells available for more efficient infection. Involvement of the oviduct on the uninoculated side occurred more rapidly in T-cell impaired nude mice than in immunologically normal mice, although there was little or no effect on the severity of the oviductal changes. There was evidence that the susceptibility of different strains of mice to chlamydial salpingitis varied. Thus, inflammatory changes in C3H mice were more severe than in TO mice and the changes in C3H and CBA strains were longer lasting than those in TO mice. This suggests that a possible genetic predisposition in the human situation should not be ignored. Finally, one chlamydial strain of low passage produced more severe salpingitis in mice than another strain of similar passage. By analogy different chlamydial strains may not be of equal pathogenicity in the human situation.