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After the Chlamydia is eliminated, the T cells remain in the mucosa with memory of the infection preserved.

In case of a new infection these cells will promptly respond, shortening the duration of subsequent infections.

Reports suggesting that genital Chlamydia infection may predispose to HIV-related AIDS and human Papilloma virus-associated cervical dysplasia have heightened these concerns.

Presence of Chlamydia trachomatis is independently associated with increased cervical cancer risk.

It is also suspected that Chlamydia can develop immune-pathogenic Chlamydia antigens.

The outer membrane protein (OMP2) of several Chlamydia trachomatis serovars, Chlamydia pneumoniae and Chlamydia psittaci capable of inducing autoimmune inflammation and are suspected to be responsible for the pathogenesis of Chlamydia-associated inflammatory and autoimmune-like diseases.

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While the lower compartment can harbor asymptomatic Chlamydia infection for years, the upper compartment will respond to Chlamydia infection with a wide-ranging alteration in reproductive performance, hormonal changes and immunological reactions.

The reproduction of the organism is obligate intracellular, relying on the host’s cell components for nourishment. Serovars allow organisms to be classified at the sub-species level.

They show Gram negative staining in histological specimens. Ocular infection is caused by the distinct serovar of Chlamydia trachomatis that causes Trachoma (the most common preventable blinding tropical disease).

Additional infections with different serovars, the role of stress, age of the individual at the time of infection and many other factors are postulated but the details are unclear.

Unfortunately, recently it became clear that Chlamydia could develop immune evasive mechanisms and produce immune-pathogenic Chlamydia antigens.

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