Chlamydiae have little if any intrinsic toxicity and thus disease is primarily a factor of the host response to infection. The immunologic interactions between chlamydial organisms and their host are extremely complex and not fully understood. The humoral and cellular immune responses elicited by these organisms may aid in control and elimination or actually be responsible for exaggerated inflammatory reactions and tissue damage. Primary focus on immunopathologic targets has been directed toward the chlamydial heat shock protein 60, which is thought to interact with certain inflammatory cell receptors resulting in cell activation.37
Following infection, the host's initial response is the formation of an acute local inflammatory reaction, which may resolve spontaneously with the eradication of the causative organism. However, the most frequent outcome is a chronic inflammatory process that may be protective but may also contribute to the pathogenesis of the disease process. Following infection, serovar-specific neutralizing antibodies to C. trachomatis can be detected in the patient's serum. However, serum antibody does not appear to play any significant role in recovery from superficial epithelial infections of the eye and genital tract. In contrast, secretory IgA and IgG in ocular secretions do appear to play a role in recovery from chlamydial ocular infection. Cell-mediated immune responses appear to be more important in recovery from genital tract infections, although they could be a key factor in the pathogenesis of both ocular and genital tract disease.
In both ocular and genital infections caused by C. trachomatis, the initial polymorphonuclear leukocytic (PMN) response is followed by a mixed infiltrate comprising lymphocytes, PMNs, plasma cells, macrophages, and eosinophils.38 In the conjunctiva, urethra, and endocervix, the lymphocytes and other mononuclear cells aggregate to form lymphoid follicles with B cells and macrophages in the center, surrounded by a peripheral region comprised of T cells. An enhanced inflammatory response occurs following repeated reinfections both in naturally occurring infections and in animal models of both ocular and genital tract disease. These enhanced responses result in rapid clearance of C. trachomatis and thus increased difficulty in recovering the organisms from infected sites. Unfortunately, the severe inflammation also results in enhanced tissue damage and the formation of scars. These scars are a direct cause of the sight-threatening sequelae of trachoma, namely entropion and trichiasis,39 and may also be responsible, in part, for the loss of patency of the fallopian tubes, which could result in ectopic pregnancy or tubal infertility following several episodes of salpingitis.40
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