Persistent “silent” Chlamydia trachomatis female genital tract infections

hronic chlamydial infections have been documented in numerous works 1,z as silently evolving diseases. Evidence of resistance to antibiotic therapy, as demonstrated by positive cultures long after treatment in infertile women, as well as positive chlamydial antigens or nucleic acids in culture-negative pelvic samples of infertile womens and the discovery of chlamydial RNA and inflammatory cytokines transcripts in tubes6 or joints, 7 have led investigators to consider persistence of the infectious material responsible for the acquisition of chronicity. So far, animal models in numerous works have proved the persistence of viable chlamydiae in altered cell cultures. Many authors have also associated serious sequelae of unsuspected silent infections with the genetically restricted host response to the heat shock proteins (Hsps) secreted by bacteria, especially Hsp60 and HspT0, which correspond to the chlamydial Gro-E1 and DNA-K genes, suggesting that repeated or prolonged exposure to the Hsp antigens is responsible for the strong host response against these bacterial Hsps and against self-Hsps homologous to the bacterial ones. The consequence of the alloimmunity to chlamydial antigens and Hsps, and of the autoimmunity to self-Hsps, is persistent inflammation, scarring, fibrosis, and necrosis. The clinical long-term female diseases documented are ectopic pregnancy with altered ciliary tubal function, tubal infertility with obstructed tubes, and early embryo rejection with immune interference 14,1s in women undergoing in vitro fertilization for tubal factor infertility. A normal chlamydial growth can give viable chlamydiae recovered from sick tissues of obstructed tubes without any previous notice of pelvic inflammatory disease (PID); conversely, persistent chlamydiae can produce overt infections. But, culture is almost impossible unless multiple serial passages 16 are performed in most chronic cases. It is not known whether chronic chlamydial disease is a consequence of an evolving silent (asymptomatic) infection, a natural infection, or a thoroughly treated and eradicated infection. The clinical assumption of persistent chlamydial infection in the genital tract has been reached by the observation of functional disease associated with a previous infection, documented by positive chlamydial antibodies. The infectious etiology of tubal obstruction has been assessed by several authors, most often by chlamydial antibody testing, a7 However, it has never been clear whether antichlamydial immunoglobulin (Ig) G is only a serologic scar in the absence of specific IgA or IgM, nor whether untreated cervical chlamydial infection would ascend to the upper genital tract or selfresolve, nor which infection would persist even after treatment with and evolve with the host tissue division. The implication of Chlamydia trachomatis with mucopurulent cervicitis and plasma cell endometritis was found of 64% of asymptomatic women in