Correlation of infertility with altered tubal morphology and function in mice with salpingitis induced by a human genital-tract isolate of Chlamydia trachomatis.

Progesterone-treated C3H mice were inoculated into the uterus or ovarian bursa with a human genital tract isolate of C. trachomatis (serovar E), or with control medium alone. The mice were then observed at various times up to 260 days after inoculation. Before being killed the mice were given pituitary gonadotrophins to induce ovulation. Eggs were sought in the oviducts and ciliary activity in the fimbrial and ampullary sections of the oviducts was determined by light microscopy, before detailed examination by scanning electron microscopy. Eggs were visible in all control oviducts and both mucosal ultrastructure and ciliary activity appeared normal. By contrast, eggs were not recovered from the inoculated oviducts of mice infected intrabursally, nor was ciliary activity observed up to 28 days after inoculation. After this, ciliary activity reappeared but eggs were still not transported to the oviduct. Ultrastructural studies suggested that severe mucus congestion accompanied by tubal oedema and loss of ciliated epithelia play a major role in the aetiology of chlamydial-induced tubal damage. Infertility following chlamydial salpingitis could be associated with failure of egg transportation to the oviduct. Egg transport was still impaired even when luminal ciliary activity, ultrastructural integrity and patency had recovered. Our results suggest that chlamydial salpingitis in this mouse model closely resembles the human disease in its pathology and consequences for fertility, making the model particularly relevant for research on chlamydial vaccine development.