Beta lactamase-producing Neisseria gonorrhoeae alleviates Amoxicillin-induced chlamydial persistence in a novel in vitro co-infection model.

Chlamydia trachomatis (CT) and Neisseria gonorrhoeae (NG) cause most bacterial sexually transmitted infections (STIs) worldwide. Epidemiological studies have shown high percentages of co-infections with CT/NG and indicate that NG co-infection can reactivate CT shedding during persistent chlamydial infection. These data also suggest that biological interaction between the two bacteria may increase susceptibility or transmissibility. CT is an obligate intracellular bacterium with a developmental cycle that alternates between two forms: infectious elementary bodies (EBs) which invade the epithelium and non-infectious reticulate bodies (RBs) which divide and replicate inside the inclusion. Adverse environmental conditions can interrupt chlamydial development, with a consequent temporary halt in RB division, reduction in infectious EB production and formation of enlarged chlamydiae (aberrant bodies, ABs) - characterizing chlamydial persistence. When the stressor is removed, the chlamydial developmental cycle is restored, together with production of infectious EBs. The beta-lactam amoxicillin (AMX) induces chlamydial persistence, both in vitro and in mice. We investigated the impact of penicillinase-producing NG strain (PPNG) on AMX-persistent chlamydial infection utilizing our recently developed, contact-independent in vitro model of co-infection. We hypothesized that co-infection with PPNG could prevent and/or reverse AMX-induced chlamydial persistence. Our results showed that PPNG can ameliorate AMX-persistence in two chlamydial species, CT and C. muridarum (CM), providing novel evidence for a range of Chlamydia/NG interactions.