Chlamydia trachomatis infections are prevalent worldwide, but current research, screening, and treatment are focused on women, with the burden of disease and infertility sequelae considered to be a predominantly female problem. The prevalence of chlamydial infection, however, is similar in males and females and the devastating consequences of male infection are largely ignored. Clinical testing confirms active infection in 9.7% of the young Australian male population and the current cost to the Australian health service is estimated at $140 million/annum. This is a recognized underestimate as 75% of all male chlamydial infections go undiagnosed, resulting in major female problems requiring expensive gynecological and assisted reproductive treatments. In addition, Chlamydia infections directly affect male fertility giving rise to poor quality semen and spermatozoa with elevated levels of DNA damage, impaired fertilizing ability, and increased embryonic loss. Furthermore, a role for this pathogen in the development of andrological problems, such as urethritis, epididymitis, orchitis and prostatitis is now widely accepted. Understanding the mechanisms of reproductive tract infection and concomitant development of a protective effective chlamydial vaccine for males remains a significant challenge to improving male, female and offspring health. Based on our pilot data in the mouse, we postulate that the reproductive potential of males is compromised following chlamydial exposure by persistent testicular infection. Our rationale is that Sertoli cells are particularly vulnerable to Chlamydia infection via testicular anti-inflammatory macrophages. Consequently, due to the immunosuppressive environment within the Sertoli cells, the infection is not cleared and Chlamydia persists in reproductive tract for an extended time. The resultant chronic testicular infection precipitates spermatogenic cell damage, aberrant sperm development and reduced fertility - subsequent to significant loss of Sertoli cell function. We also propose that exposure to Chlamydia infection results in poor health outcomes for offspring due to oxidative damage leading to DNA strand breaks and chromatin changes which compromise embryo development.

Supported by NHMRC Project grant # 553055