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Purpose of Review: Antimicrobial resistance in sexually transmitted infections (STIs) has become an urgent global public health threat, raising the specter of untreatable infections. This review summarizes the determinants of resistance among the five most common curable STIs Neisseria gonorrhoeae, Chlamydia trachomatis, Mycoplasma genitalium, Treponema pallidum, and Trichomonas vaginalis, as well as strategies to mitigate the spread of resistance. Recent Findings: Genetic mutations are key drivers of resistance for N. gonorrhoeae and M. genitalium. Resistance in T. vaginalis can also occur because of genetic mutations, yet differential regulation of genes critical in antibiotic metabolism as well as co-infection with organisms that inactivate therapy play important roles. While resistance in C. trachomatis and T. pallidum has not been a substantial clinical concern, resistance selection via the continued widespread use of antimicrobials remains possible. Summary: While resistance determinants are diverse and differ by pathogen, the strategies required to mitigate the continued emergence of resistance are similar: prevention of infection and treatment diversification. Underpinning those strategies, surveillance remains essential for monitoring and responding to the threat of drug-resistant infections. [ABSTRACT FROM AUTHOR]

The in vitro phagocytosis of viable Treponema pallidum subsp. pallidum by isolated rat Kupffer cells, studied by immunofluorescence staining of Kupffer cells-associated bacteria, showed that ingestion of live, unopsonized treponemes was slow: in fact, Kupffer cells started to be positive 1 h after infection, when only 4% of the cells presented small round fluorescent inclusion-like bodies. Thereafter, the number of positive cells progressively increased with time: 7%, 17%, 36%, and 69% of Kupffer cells were positive, respectively, 2, 4, 6 and 8 h after infection. Opsonization of T. pallidum with human immune serum did not substantially modify the percentage (8%) of Kupffer cells ingesting T. pallidum 1 h after infection, whereas opsonization significantly (P<0.01) increased phagocytosis after 2, 4 and 6 h of incubation, when 44%, 58%, and 68% of Kupffer cells were positive, respectively. At 8 h after infection of Kupffer cells by opsonized T. pallidum, 75% of the cells were positive by immunofluorescence. Heat-inactivation of T. pallidum slightly enhanced phagocytosis. In contrast, opsonization of heat-inactivated spirochetes with specific antibodies significantly (P<0.01) increased the phagocytosis of bacteria by Kupffer cells, beginning as early as 30 min after infection, when 65% of the cells were positive by immunofluorescence. The reactive oxygen species (ROS) production by Kupffer cells following incubation with spirochetes was also determined by chemiluminescence. Treponemes induced an oxidative burst in Kupffer cells in a dose-dependent manner and the generation of ROS was already detectable 20 min after the exposure of the Kupffer cells to treponemes and peaked at 35 min of incubation. Live, as well as live and opsonized, and heat-inactivated treponemes, induced an O2– production lower than that induced by heat-inactivated and opsonized spirochetes. [ABSTRACT FROM AUTHOR]

We report a case of an asymptomatic 3-month-old girl presenting to the emergency department with concern for congenital syphilis. Radiographs of the lower limbs demonstrate mild diffuse periosteal reaction involving the femur, tibia, and fibula and bilaterally symmetric lucencies and erosions of the medial proximal tibial metaphysis (Wimberger's sign). [ABSTRACT FROM AUTHOR]