Infertility in mice infected genitally with a human strain of Chlamydia trachomatis.
Progesterone-treated C3H and TO mice were inoculated genitally with a human C. trachomatis strain, serovar E, designated N.I. 1 or with 2SP control medium. Of the C3H mice serving as controls 93% had litters by the end of a 6-month period compared to 31% of mice infected with chlamydiae. This infertility could not be explained by tubal occlusion, since the oviducts appeared normal at autopsy. Some of the mice were induced to superovulate. Eggs were never recovered from the oviducts on the inoculated sides of infertile mice although they were sometimes found in the lumen of the uninoculated oviducts. In contrast, eggs were recovered routinely from both oviducts of control mice. In addition, eggs and/or their accompanying cumulus cells could be seen in the periovarial space of mice inoculated with chlamydiae, indicating a failure of the transportation of eggs to the oviduct. This could explain the high incidence of ectopic pregnancies in women after chlamydial infection. No adverse effect on fertility was seen in TO mice inoculated genitally with strain N.I.1. Of the mice given 2SP medium, 73% had litters, but 87% of the mice inoculated with chlamydiae were also fertile. There was, however, a significantly greater variation in the birth weights of mice born to infected TO mothers than those born to control mice. This difference in the susceptibility of mouse strains suggests that a genetic predisposition should also be considered for man.
D000818:Animals; D002690:Chlamydia Infections / Q000150:complications* / Q000503:physiopathology; D004195:Disease Models, Animal; D004198:Disease Susceptibility; D005260:Female; D007247:Infertility, Female / Q000209:etiology* / Q000503:physiopathology; D051379:Mice; D008809:Mice, Inbred C3H; D008815:Mice, Inbred Strains; D010066:Ovum Transport; D012488:Salpingitis / Q000150:complications* / Q000503:physiopathology; D013480:Superovulation