title: Chlamydial variants differ in ability to ascend the genital tract in the guinea pig model of chlamydial genital infection.
abstract: An important question in the study of chlamydial genital tract disease is why some women develop severe upper tract disease while others have mild or even "silent" infections with or without pathology. Animal studies suggest that the pathological outcome of an infection is dependent upon both the composition of the infecting chlamydial population and the genotype of the host, along with host physiological effects, such as the cyclical production of reproductive hormones and even the size of the infecting inoculum or the number of repeated infections. In this study, we compared two variants of Chlamydia caviae, contrasting in virulence, with respect to their abilities to ascend the guinea pig genital tract. We then determined the effect of combining the two variants on the course of infection and on the bacterial loads of the two variants in the genital tract. Although the variants individually had similar infection kinetics in the cervix, SP6, the virulent variant, could be isolated from the oviducts more often and in greater numbers than the attenuated variant, AZ2. SP6 also elicited higher levels of interleukin 8 (IL-8) in the lower genital tract and increased leukocyte infiltration in the cervix and uterus compared to AZ2. When the two variants were combined in a mixed infection, SP6 outcompeted AZ2 in the lower genital tract; however, AZ2 was able to ascend the genital tract as readily as SP6. These data suggest that the ability of SP6 to elicit an inflammatory response in the lower genital tract facilitates the spread of both variants to the oviducts.
authors.affiliation: Department of Pediatrics, University of Arkansas for Medical Sciences and Arkansas Children's Hospital Research Institute, Little Rock, Arkansas, USA.
authors.forename: Laxmi
authors.initials: L
authors.lastname: Yeruva
authors.affiliation: Department of Microbiology and Immunology, University of Arkansas for Medical Sciences and Arkansas Children's Hospital Research Institute, Little Rock, Arkansas, USA.
authors.forename: Anne K
authors.initials: AK
authors.lastname: Bowlin
authors.affiliation: Department of Pediatrics, University of Arkansas for Medical Sciences and Arkansas Children's Hospital Research Institute, Little Rock, Arkansas, USA.
authors.forename: Nicole
authors.initials: N
authors.lastname: Spencer
authors.affiliation: Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland, USA.
authors.forename: Anthony T
authors.initials: AT
authors.lastname: Maurelli
authors.affiliation: Department of Microbiology and Immunology, University of Arkansas for Medical Sciences and Arkansas Children's Hospital Research Institute, Little Rock, Arkansas, USA rankrogerg@uams.edu.
authors.forename: Roger G
authors.initials: RG
authors.lastname: Rank
mesh_terms: D000818:Animals; D002689:Chlamydia / Q000145:classification / Q000502:physiology*; D002690:Chlamydia Infections / Q000276:immunology / Q000382:microbiology*; D004195:Disease Models, Animal; D005260:Female; D006168:Guinea Pigs; D006801:Humans; D016209:Interleukin-8 / Q000276:immunology; D060737:Reproductive Tract Infections / Q000276:immunology / Q000382:microbiology*
chemical_list: D016209:Interleukin-8