Institute for Global Health and Infectious Diseases, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA Chapel Hill, North Carolina, United States
Background: Chlamydia trachomatis is the most common bacterial sexually transmitted infection (STI) and causes a range of clinical manifestations, including lymphogranuloma venereum (LGV). LGV can cause genital ulcer disease (GUD) and lymphadenopathy and is classically associated with infection by C. trachomatis L1-L3 serovars; however, this is not well studied in Africa. C. trachomatis serovars reflect variation in ompA, which encodes the major outer membrane protein (MOMP). Characterizing C. trachomatis genetic variation across the globe is necessary for discovering vaccine targets and reducing its impact on reproductive health.
Methods: DNA was extracted from swabs taken from patients presenting with genital lesions at a large-volume STI clinic in Lilongwe, Malawi, as part of an ongoing syphilis vaccine development project. Samples were screened for Treponema pallidum, C. trachomatis, Haemophilus ducreyi and herpes simplex virus 1/2 using quantitative PCR. C. trachomatis-positive samples were further characterized by Sanger sequencing of nested ompA amplicons. A phylogenetic tree was generated using RAxML with 1000 rapid bootstraps for support. Associations between C. trachomatis serovar and patient demographics were assessed using Fishers Exact Test (α=0.05).
Results: Among the 674 DNA isolates extracted from genital lesion swabs from 603 participants, 46 (6.8%) were positive for C. trachomatis. Patients with a C. trachomatis-positive ulcer were mostly female (69.2%) with median age of 24 years (interquartile range 20.5-27.5). Only two (4.3%) were infected with C. trachomatis alone; the majority were co-infections including 39 (84.7%) with T. pallidum, 6 (13.0%) with HSV, and 2 (4.3%) with H. ducreyi. OmpA phylogenetic analysis confirmed a single (2.2%) L1 serovar, while most strains were assigned to serovar G (n=22, 47.8%), followed by E (10, 21.7%), D (3, 6.5%), and J (1, 2.2%), with nine (19.6%) remaining undetermined (Figure). No associations were found between serovar and sex, HIV status, or co-infection.
Conclusion: GUD caused by C. trachomatis L1-L3 serovars was rare in this population. We found that non-LGV C. trachomatis often co-infects genital lesions alongside other GUD-associated pathogens, most notably T. pallidum. Interactions between C. trachomatis and other GUD-causing pathogens, the implications of high G serovar prevalence in this population, and the possibility of recombination with L1-L3 strains warrants further study.
