The population dissemination of invasive genotypes of C. trachomatis and an increase of urogenital infections cases by non-invasive genotypes have been observed in many countries. In this epidemiological context, the descriptions of a high proportion of infections related to L-genotypes in asymptomatic patients, but also to infections caused by non-L genotypes in symptomatic patients have been unexpected finding. The plasmid copy number (PCN) has been proposed as a surrogate marker of virulence. We quantified the PCN in 233 samples and 179 samples carrying L-genotype and non-L genotypes respectively. A significant difference in the median of PCN was detected between symptomatic/asymptomatic patients (P < 0.001), independently of the genotype. Moreover, PCN could vary, in the same strain, among different anatomical sites suggesting that micro-environmental changes could affect virulence. These findings suggest that the quantification of PCN in clinical samples could improve the management of patients.
Keywords: Chlamydia trachomatis; Lymphogranuloma venereum; Plasmid copy number; Virulence factors.
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