The Epidemiology of Chlamydia trachomatis within a Sexually Transmitted Diseases Core Group

Female sex workers in Nairobi were prospectively evaluated for risk factors of incident Chlamydia trachomatis infection. Independent risk factors included cervical ectopy (P = .007), gonococcal infection (P = .002), human immunodeficiency virus (HIV) seropositivity (P = .003), HIV serocon­ version (P = .001), and duration of prostitution (P = .002). Eighteen different C. trachomatis outer membrane protein (ompl) genotypes were identified, with the allelic composition of the C. tracho­ matis population changing significantly over time (P = .005). Seventeen of 19 reinfections ~6 months apart were with different C. trachomatis ompi genotypes. Women with HIV infection had an increased proportion of visits with C. trachomatis infection (P = .001) and an increased risk of reinfection (P = .008). Overall, the data demonstrate significant fluctuations in the genotype composi­ tion of the C. trachomatis population and a reduced rate of same-genotype reinfection consistent with the occurrence of strain-specific immunity. Strains of Chlamydia trachomatis are antigenically variant and classifiable into stable serologic variants or serovars [1]. The major outer membrane protein (MOMP) of the organism is the predominant surface protein and determines the serologic properties for individual C. trachomatis serovars [2]. The sin­ gle-copy MOMP gene is termed omp], and the DNA sequence for the entire open-reading frame is known for at least 7 differ­ ent C. trachomatis serovars [3, 4]. The genetic basis for C. trachomatis serovar classification is due to allelic variation of the single-copy gene, with 15 different omp] alleles recognized for the 15 prototype serovars of C. trachomatis [5, 6]. The omp] gene is >80% identical in DNA sequence among differ­ ent serovars, with most DNA sequence polymorphism concen­ trated into four regularly spaced variable gene segments. Com­ parison of DNA sequences among closely related serovars shows that nucleotide variation within variable segments results in nonsynonymous codons, and thus amino acid differences among MOMPproteins are clustered into four variable domains (VDs) [5, 7]. In general, the four VDs are exposed on the chlamydial cell surface and recognizable by monoclonal anti­ bodies that are capable of neutralizing the organism in animal models of experimental infection [8]. Thus, MOMP displays