Open AccessInfectivity of urogenital C hlamydia trachomatis plasmid‐deficient, CT 135‐null, and double‐deficient strains in female mice
Author(s) -
Sturdevant Gail L.,
Zhou Bing,
Carlson John H.,
Whitmire William M.,
Song Lihua,
Caldwell Harlan D.
Publication year - 2014
Publication title -
pathogens and disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.983
H-Index - 105
ISSN - 2049-632X
DOI - 10.1111/2049-632x.12121
Subject(s) - infectivity , chlamydia trachomatis , biology , plasmid , virulence , microbiology and biotechnology , virology , phenotype , chlamydia , genitourinary system , gene , genetics , virus , anatomy
C hlamydia trachomatis is the most common cause of human bacterial sexually transmitted infections and is the world's leading cause of infectious preventable blindness. The chlamydial 7.5‐kb plasmid and chromosomal gene CT 135 have been shown to be important virulence factors in both nonhuman primate and mouse infection models. C hlamydia trachomatis plasmid‐deficient urogenital isolates and a predicted CT 135 null mutant have been evaluated independently in the female mouse genital tract model and both have been shown to reduce infectivity and virulence. However, these attenuating phenotypes have not been evaluated collectively in the murine model. Here, we test the infectivity of C . trachomatis serovar D strains in the mouse model that are plasmid‐deficient, CT 135 disrupted, or possess a combination of these attenuating genotypes. We find that the presence of the plasmid results in infections with higher infectious burdens, whereas CT 135 facilitates a more protracted or chronic infection. Not unexpectedly, a combination of these genetic deficiencies resulted in a strain with enhanced infection attenuation characteristics.