Association of Uterine and Salpingeal Fibrosis with Chlamydial Hsp60 and Hsp10 Antigen-Speciﬁc Antibodies in Chlamydia-Infected Koalas
Damien P. Higgins,* Susan Hemsley, and Paul J. Canﬁeld
Faculty of Veterinary Science, B01, University of Sydney, Sydney, NSW 2006, Australia
Infection by Chlamydia pneumoniae or Chlamydia pecorum commonly causes chronic, ﬁbrotic disease of the urogenital tracts of female koalas. Studies of humans have associated titers of serum immunoglobulin G (IgG) against chlamydial hsp60 and hsp10 antigens with chronic infection, salpingeal ﬁbrosis, and tubal infertility. To determine whether a similar relationship exists in Chlamydia-infected koalas, samples were collected opportunistically from 34 wild female koalas and examined by gross pathology and histopathology, PCR, and immunohistochemistry for Chlamydia spp. and enzyme-linked immunosorbent assay for serological responses to chlamydial hsp10 and hsp60 antigens. Greater anti-hsp titers occurred in Chlamydia-infected koalas with ﬁbrous occlusion of the uterus or uterine tube than in other Chlamydia-infected koalas (for hsp10 IgG, P 0.005; for hsp60 IgG, P 0.001; for hsp10 IgA, P 0.04; for hsp60 IgA, P 0.09). However, as in humans, some koalas with tubal occlusion had low titers. Among Chlamydia-infected koalas with tubal occlusion, those with low titers were more likely to have an active component to their ongoing uterine or salpingeal inﬂammation (P 0.007), such that the assay predicted, with 79% sensitivity and 92% speciﬁcity, tubal occlusion where an active component of inﬂammation was absent. Findings of this study permit advancement of clinical and epidemiological studies of host-pathogen-environment interactions and pose intriguing questions regarding the signiﬁcance of the Th1/Th2 paradigm and antigen-presenting and inﬂammation-regulating capabilities of uterine epithelial cells and the roles of latency and reactivation of chlamydial infections in pathogenesis of upper reproductive tract disease of koalas.