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C. trachomatis is an obligate intracellular bacterium that causesdiseases of many systems in humans.
The ability to multiply intracellularly in the infected cell is the key mechanism of virulence of C. trachomatis. The bacteria pre-vent fusion of phagolysosome with cellular liposomes, thereby preventing intracellular killing of the bacteria by the host cell. Repeated infections caused by C. trachomatis contribute to pathology seen in the infected eye in trachoma.
C. trachomatis causes disease mainly by (a) direct destructionof infected host cells during multiplication and (b) inducing inflammatory responses in the host. C. trachomatis enters the host through minute abrasions or injuries in the skin. The bacteria react specifically with the receptors that are found on the non-ciliated columnar, cuboidal, or transitional epithelial cells. These epithelial cells are typically found on the mucous membranes of the conjunctiva and genitourinary system, such as urethra, endocervix, endometrium, fallopian tube, and respiratory tract.
The LGV biovar multiplies in mononuclear phagocytes found in the lymphatic system. The pathological lesions are typically found in the lymph nodes draining the site of pri-mary infection. Granuloma is characteristic pathological lesion. Subsequently inflammatory process spreads to other surrounding tissues and finally rupture of the lymph nodes leads to the formation of abscess or sinus tracts.
Infections with trachoma serovars are associated with severe inflammatory reaction consisting of neutrophils, lymphocytes, and plasma cells as seen in case of trachoma.
Infections with C. trachomatis do not induce any long-lasting immunity. Instead reinfection by C.trachomatis typically produces a strong inflammatory response with severe tissue damage. Such responses are responsible for causing loss of vision in patients with chronic ocular infections and sterility and sexual dysfunction in patients with genital infections.
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