Chlamydia trachomatis is an obligate intracellular bacterium whose only natural host is humans. Although presenting as asymptomatic in most women, genital tract chlamydial infections are a leading cause of pelvic inflammatory disease, tubal factor infertility, and ectopic pregnancy. C. trachomatis has evolved successful mechanisms to avoid destruction by autophagy and the host immune system and persist within host epithelial cells. The intracellular form of this organism, the reticulate body, can enter into a persistent nonreplicative but viable state under unfavorable conditions. The infectious form of the organism, the elementary body, is again generated when the immune attack subsides. In its persistent form, C. trachomatis ceases to produce its major structural and membrane components, but synthesis of its 60-kDa heat shock protein (hsp60) is greatly upregulated and released from the cell. The immune response to hsp60, perhaps exacerbated by repeated cycles of productive infection and persistence, may promote damage to fallopian tube epithelial cells, scar formation, and tubal occlusion. The chlamydial and human hsp60 proteins are very similar, and hsp60 is one of the first proteins produced by newly formed embryos. Thus, the development of immunity to epitopes in the chlamydial hsp60 that are also present in the corresponding human hsp60 may increase susceptibility to pregnancy failure in infected women. Delineation of host factors that increase the likelihood that C. trachomatis will avoid immune destruction and survive within host epithelial cells and utilization of this knowledge to design individualized preventative and treatment protocols are needed to more effectively combat infections by this persistent pathogen.

Epithelial cells exhibit a higher level of autophagy, lower induction of stress-related hsp70, and release lower level of mediators when L crispatus is most abundant as compared to when L iners dominates the vaginal microbiota.

Objective Screening tools, including the Systemic Inflammatory Response Syndrome (SIRS) criteria and Sequential Organ Failure Assessment (SOFA) criteria, have not been validated in the pregnant population. We aimed to determine if pregnancy-specific modifications to the quick SOFA (qSOFA) can improve prediction of severe maternal morbidity in pregnant women with serious infections. Methods We performed a retrospective cohort study of pregnant patients with severe infections admitted to a single institution from January 1, 2011, through December 31, 2017. The primary outcome was severe maternal morbidity, defined as a composite of adverse maternal outcomes: intensive care unit (ICU) admission for >48 hours, need for invasive monitoring (central line or arterial line), intubation, pharmacologic hemodynamic support (intravenous vasopressors or inotropes), and/or maternal death. A logistic regression was then applied and the resulting predictors were analyzed individually and in combination with receiver operating characteristic (ROC) curves to modify qSOFA for pregnancy, that is, qSOFA-P. Results Analysis of 104 pregnant patients with severe infections found that the standard qSOFA did not accurately predict severe maternal morbidity (ROC area under the curve [AUC] = 0.54, p = 0.49, sensitivity = 0.38, and specificity = 0.70). Pregnancy-specific modifications or “qSOFA-P” (respiratory rate [RR] ≥ 35 breaths/minute and systolic blood pressure [SBP] ≤ 85 mm Hg) significantly improved prediction of severe maternal morbidity (AUC = 0.77, p < 0.001, sensitivity = 0.79, and specificity = 0.74). Conclusion The standard qSOFA is a poor screening tool in the prediction of severe maternal morbidity in pregnant patients with infections. A pregnancy-specific screening system, qSOFA-P, improved prediction of severe maternal morbidity in pregnant women with severe infections. Further prospective and large multicenter studies are needed to validate this scoring system in pregnant women. Key Points

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