C. trachomatis spreads by direct contact with eye, nose, and throat secretions or through contact with towels or other objects that have had direct contact with these secretions. Flies can also transfer the bacterium. There is also the possibility that infection can be spread by aerosol from nasal infection [9]. Andreasen et al. [23] demonstrated differences in genotypes in the same individuals in their nasal and ocular forms of C. trachomatis, suggesting that one tissue is not the source of infection for the other tissue, perhaps due to a critical environmental difference between the 2 locations that prevents cross-infection. The same may be true for genital and ocular C. trachomatis infections in which different strains or serovars are found at the 2 sites. Serovars A-C cause ocular C. trachomatis, serovars D-K cause the genital forms. Serovar typing is based on differences in the major outer membrane protein of the bacterium. Caldwell et al. [24] suggested that the presence or absence of other bacteria is the critical environmental difference.C. trachomatis infection has an incubation period of 5 to 12 days and usually presents as a mild conjunctivitis with a scant watery purulent discharge, but it may be symptomless during some stages. Conjunctival inflammation is ��active trachoma,�� whether or not the bacterium is present. Active infection and active disease are difficult to distinguish due to (1) the short incubation period, during which infection is detectable, but there are no clinical signs; (2) a stage consisting of detectable infection and clinical signs; and (3) a recovery stage in which the infection is not detectable, but there are clinical signs that can last for many months [15, 25]. Active disease is not a good predictor of infection. The simplified WHO grading system is another issue, in which the threshold for active disease is the presence of a minimum of 5 follicles, while an assessment early in infection or a rapid clearance of the bacterium can result in less than 5 follicles. This can lead to infection rates lower than trachoma rates [26]. The WHO guidelines for diagnosing and staging trachoma infections also result in some confusion in the literature, because it is not always clear as to what constituted active infection in a specific report. A study [27] that compared the clinical signs of trachoma infection and the infection rate in Aboriginal communities in Australia found that infection, as detected by PCR, was a poor predictor of the presence of clinical disease. Clinical disease was also poorly correlated with infection. They did find, however, that organismal load was strongly correlated with the severity and prevalence of active trachoma by a grading system that allowed finer distinctions than that provided by the simplified system.
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