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Hydrosalpinx induction in mice byChlamydia muridarum infection, a model that has been used to studyC. trachomatis pathogenesis in women, is known to depend on the cryptic plasmid that encodes eight genes designatedpgp1 topgp8 . To identify the plasmid-encoded pathogenic determinants, we evaluatedC. muridarum transformants deficient in the plasmid-borne genepgp3 , -4 , or -7 for induction of hydrosalpinx.C. muridarum transformants with an in-frame deletion of eitherpgp3 or -4 but not -7 failed to induce hydrosalpinx. The deletion mutant phenotype was reproduced by using transformants with premature termination codon insertions in the correspondingpgp genes (to minimize polar effects inherent in the deletion mutants). Pgp4 is known to regulatepgp3 expression, while lack of Pgp3 does not significantly affect Pgp4 function. Thus, we conclude that Pgp3 is an effector virulence factor and that lack of Pgp3 may be responsible for the attenuation inC. muridarum pathogenicity described above. This attenuated pathogenicity was further correlated with a rapid decrease in chlamydial survival in the lower genital tract and reduced ascension to the upper genital tract in mice infected withC. muridarum deficient in Pgp3 but not Pgp7. The Pgp3-deficientC. muridarum organisms were also less invasive when delivered directly to the oviduct on day 7 after inoculation. These observations demonstrate that plasmid-encoded Pgp3 is required forC. muridarum survival in the mouse genital tract and represents a major virulence factor inC. muridarum pathogenesis in mice.

Plasmid-Encoded Pgp3 Is a Major Virulence Factor for Chlamydia muridarum To Induce Hydrosalpinx in Mice