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infections, moving from self-culture-based assays to culture-independent assays. Nevertheless, even the best molecular assays to date have only a 70 percent sensitivity in high-prevalence populations or symptomatic infections, and less than that in low-prevalence populations or asymptomatic infections. Once diagnosed, chlamydia can be treated with antibiotics and there are as yet no signs of antibiotic resistance, although the infection hasn’t really been challenged to date.

Behavior change might be one preventative strategy, but like other STDs, chlamydia is predominantly an infection of teenagers and young adults, with all the problems that entails in terms of recognizing and changing high-risk behavior. There are two biological strategies for preventing the disease: one is the development of a competitive analogue, the other is the development of a vaccine.

Pathobiology. The chlamydiae are nonmotile, obligate intracellular parasites with a distinctive life cycle. The extracellular forms can be detected by direct fluorescent antibody and enzyme immunoassay, but while they are infectious, they are metabolically inactive. The extracellular forms attach to a cell by a mechanism that is not yet understood and, once attached, enter the cell by endocytotic mechanisms. Inside the cell, it remains inside an inclusion—a membrane-bound vacuole that inhibits fusion with lysosomes—throughout its growth cycle.

Chlamydiae can propagate only inside a cell. Once inside, it undergoes changes in its membrane and DNA and begins to differentiate. Researchers believe that it follows one of two pathways: it can multiply and grow like other bacteria, or it can remain in a cryptic state. The latter, which is one of the mechanisms by which this organism persists in the host, is poorly understood. If it multiplies, it will divide by binary fusion some 24 to 72 hours after infection, after which it again differentiates from the vegetative to the elementary or infectious form and is released, by another unknown mechanism, to infect new cells. Importantly, chlamydia does not seem to be able to transmit by cell-to-cell interaction but must leave the cell and thus be exposed to antibodies and other host activity.

Chlamydia is a mucosal pathogen that does not so much kill host cells as cause persistent inflammation. The inflammation causes scarring in both the ocular and genital models, and the scarring accounts for the disease problem—for example, deformation of the eyelashes and blindness. Infection of epithelial cells leads to a potent gamma T-cell response and the excretion of inflammatory cytokines, especially IL-8, which in this case fits the requirements for a mediator for pathogenesis. Other pathogens elicit a similar response early upon uptake, which then fades away; whereas with chlamydia it occurs late in the cycle and endures throughout the infection process.

Adhesion Molecules and Analogues. Researchers believe that the parasite attaches and enters the host cell using a carbohydrate-like ligand that is synthesized on the surface of the chlamydia and somehow mediates entry. This ligand is similar to the heparin sulfate molecule and apparently can be cleaved

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