Chlamydia trachomatis

Chlamydia are gram-negative bacteria which have a unique developmental cycle. C. trachomatis is the only reproductive tract pathogen. The C. trachomatis serovars D-K and L,_, are involved in urogenital infections and cause in excess of 50 million cases of genital infection worldwide, including urethritis, mucopurulent cervicitis, and salpingitis (serovars D-K), as well as lymphogranulovenerium (l.GV) (serovars L,_3).

The chlamydia infect primarily columnar epithelial cells where the organisms undergo a unique rep-licative cycle. Multiplication occurs in intercytoplas-mic vacuoles where they are energy parasites and use ATP producedby the host cell. The cell wall contains the major outer membrane protein (MOMP) which is responsible for the rigidity of the cell wall since chlamydia lack peptidoglycan. These molecules are responsible for the species-specificity of the organisms. The cell wall also contains a lipopolysaccharide (LPS) (Figure 2).

Although nonspecific host responses to C trachomatis and its antigens exist, specific immune responses (both humoral and cellular) appear to be involved in modifying infection or conferring immunity to reinfections. The presence of serovar-specific antibody has been documented in women with upper genital tract infection but correlation between the humoral immune response and resistance to infection has been difficult to make. The role of the cell-mediated response is even less well understood in humans than in many animal models. In experimental infection both responses are involved in the resolution of infection. Most of the immune response involves local mucosal immunity as the infection is restricted to the epithelial layer of the cervix, endometrium and fallopian tubes. However, it is generally accepted that mucosal immunity to chlamydial genital infection does not exist and recurrent infections are common. T Cells are recruited to the area of infection and through the release of inflammatory cytokines there is host cell-mediated damage to the mucosa.

Although no vaccine is available for clinical use, a number of laboratories are evaluating vaccine components of C. trachomatis for their efficacy in inducing a protective immune response.

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