Severe pelvic inflammatory disease and tuboovarian abscesses (TOAs) are common pelvic infections requiring inpatient admission. There are few large randomized trials guiding appropriate clinical management of TOA, including antibiotic selection and timing of surgical management and drainage. The pathogenesis, diagnosis, and management of severe pelvic inflammatory disease and TOA are summarized and reviewed from the most current literature.

Objectives Because of the opioid epidemic, hepatitis C virus (HCV) infection is increasing among pregnant women, resulting in an increased risk of perinatal transmission and HCV infection among children. Our primary objectives in this study were to determine the prevalence of HCV among pregnant women and the frequency of pediatric HCV screening. Methods A population-based, retrospective cohort of pregnant women who delivered between 2006 and 2014 was identified and classified as HCV infected or HCV uninfected by billing codes. Infant records linked to the HCV-infected pregnant women were identified and queried for HCV tests and the receipt of well-child services, which were defined as the presence of hemoglobin and/or lead testing at or after 9 months of age. Results Between 2006 and 2014, 1043 (1.2%) HCV-infected pregnant women delivered, and the HCV prevalence increased by 60%. HCV-infected women were more likely to be <30 years of age (67% vs 53%; P < .001), white (93% vs 72%; P < .001), insured by Medicaid (77% vs 29%; P < .001), and have opiate use disorder (68% vs 1%; P < .001) than HCV-uninfected women. Infants born to HCV-infected women were more likely to be preterm (<37 weeks’ gestation; 22% vs 10%; P < .001) and of low birth weight (<2500 g; 23% vs 8%; P < .001). Among 1025 HCV-exposed infants with available pediatric records, 323 (31%) received well-child services, and among these, only 96 (30%) were screened for HCV. Conclusions Despite the increased HCV prevalence among pregnant women and the risk of perinatal HCV transmission, HCV-exposed infants are not adequately screened, and many pediatric HCV infections remain undetected.

In this study, we characterized the glycome of cervical-vaginal fluid, collected with a Catamenial cup. We quantified: glycosidase levels; sialic acid and high mannose specific lectin binding; mucins, MUC1, MUC4, MUC5AC, MUC7; and albumin in the samples collected. These data were analyzed in the context of hormonal status (day of menstrual cycle, hormonal contraception use) and role, if any, of the type of the vaginal microflora present. When the Nugent score was used to stratify the subjects by microflora as normal, intermediate, or bacterial vaginosis, several important differences were observed. The activities of four of six glycosidases in the samples from women with bacterial vaginosis were significantly increased when compared to normal or intermediate women: sialidase, P = <0.001; α-galactosidase, P = 0.006; β-galactosidase, P = 0.005; α-glucosidase, P = 0.056. Sialic acid binding sites as measured by two lectins, Maackia amurensis and Sambucus nigra binding, were significantly lower in women with BV compared to women with normal and intermediate scores (P = <0.0001 and 0.008 respectively). High mannose binding sites, a measure of innate immunity were also significantly lower in women with BV (P = <0.001). Additionally, we observed significant increases in MUC1, MUC4, MUC5AC, and MUC7 concentrations in women with BV (P = <0.001, 0.001, <0.001, 0.02 respectively). Among normal women we found that the membrane bound mucin MUC4 and the secreted MUC5AC were decreased in postmenopausal women (P = 0.02 and 0.07 respectively), while MUC7 (secreted) was decreased in women using levonorgestrel-containing IUDs (P = 0.02). The number of sialic acid binding sites was lower in the postmenopausal group (P = 0.04), but the number of high mannose binding sites, measured with Griffithsin, was not significantly different among the 6 hormonal groups. The glycosidase levels in the cervical-vaginal mucus were rather low in the groups, with exception of α-glucosidase activity that was much lower in the postmenopausal group (P<0.001). These studies present compelling evidence that the vaginal ecosystem responds to the presence of different vaginal microorganisms. These effects were so influential that it required us to remove subjects with BV for data interpretation of the impact of hormones. We also suggest that certain changes occurring in vaginal/cervical proteins are due to bacteria or their products. Therefore, the quantitation of vaginal mucins and lectin binding offers a new method to monitor bacteria-host interactions in the female reproductive tract. The data suggest that some of the changes in these components are the result of host processing, such as the increases in mucin content, while the microflora is responsible for the increases in glycosidases and the decreases in lectin binding. The methods should be considered a valid marker for insult to the female genital tract.

Summary Background Hepatitis C virus (HCV) infection is increasing among pregnant women because of the opioid epidemic, yet there are no interventions to reduce perinatal HCV transmission or to treat HCV during pregnancy. Physiological changes in pregnancy alter the pharmacokinetics of some medications; thus, our aim was to compare the pharmacokinetic parameters of ledipasvir 90 mg plus sofosbuvir 400 mg during pregnancy with non-pregnant women. Methods This was an open-label, phase 1 study of pregnant women with genotype 1 HCV infection and their infants. A reference group of women who had participated in pharmacokinetic studies of ledipasvir–sofosbuvir during phase 2 and 3 trials was used. Participants were enrolled at Magee-Womens Hospital (Pittsburgh, PA, USA) between 23 and 24 weeks’ gestation and had a 12-week course of oral ledipasvir–sofosbuvir (daily 90 mg ledipasvir plus 400 mg sofosbuvir). Three 12-h intensive pharmacokinetic visits were done at 25–26, 29–30, and 33–34 weeks’ gestation and individual pharmacokinetics were summarised by geometric mean across the three visits. The primary outcome, analysed in all participants without suspected dosing errors, was the ledipasvir–sofosbuvir area under the concentration–time curve of the dosing interval (AUC tau ) during pregnancy compared with the reference group by geometric mean ratio. This study is registered with ClinicalTrials.gov , NCT02683005 . Findings From Oct 1, 2016, to Sept 30, 2018, 29 pregnant women were screened and nine (31%) were enrolled. Eight (89%) women were included in the primary analysis. Ledipasvir and sofosbuvir exposures were similar in the pregnant women versus the non-pregnant reference group (geometric mean ratio of AUC tau ledipasvir 89·3% [90% CI 68·7–116·1]; sofosbuvir 91·1% [78·0–106·3]). Interpretation Ledipasvir–sofosbuvir was safe and effective without clinically meaningful differences in drug exposure among pregnant versus non-pregnant women. Funding National Institutes of Health/Eunice Kennedy Shriver National Institute of Child Health and Human Development, the National Institutes of Health/Office of Research on Women’s Health, and Gilead Sciences.