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Background Nearly 14% of US women report any lifetime infertility which is associated with healthcare costs and psychosocial consequences. Tubal factor infertility (TFI) often occurs as a result of sexually transmitted diseases and subsequent pelvic inflammatory disease. We sought to evaluate for and describe potential racial disparities in TFI and in vitro fertilization (IVF) prevalence. Methods Records of women aged 19-42 years in our retrospective cohort from two US infertility clinics were reviewed. We calculated TFI prevalence, IVF initiation prevalence, and prevalence ratios (PR), with 95% confidence intervals for each estimate, overall and by race. Results Among 660 infertile women, 110 (16.7%; 95% confidence interval [CI] 13.8-19.5%) had TFI which was higher in black compared to white women (30.3% [33/109] vs. 13.9% [68/489]; PR 2.2 [95% CI 1.5-3.1]). For women with TFI, IVF was offered to similar proportions of women by race (51.5% [17/33] versus 52.9% [36/68] for black versus white women); however, fewer black than white women with TFI started IVF (6.7% [1/15] versus 31.0% [9/29]; PR 0.2 [95% CI 0-1.0]), although the difference was not statistically different. Conclusions TFI prevalence was two-fold higher among black than white women seeking care for infertility. Among women with TFI, data suggested a lower likelihood of black women starting IVF than white women. Improved sexually transmitted disease prevention and treatment might ameliorate disparities in TFI.

BackgroundChlamydial infection is associated with tubal factor infertility (TFI); however, assessment of prior chlamydial infection and TFI is imperfect. We previously evaluated a combination of serological assays for association with TFI. We now describe the chlamydial contribution to TFI using a newer Chlamydia trachomatis Pgp3 enhanced serological (Pgp3) assay.MethodsIn our case-control study of women 19–42 years old with hysterosalpingogram-diagnosed TFI (cases) and non-TFI (controls) in two U.S. infertility clinics, we assessed possible associations and effect modifiers between Pgp3 seropositivity and TFI using adjusted odds ratios (aOR) with 95% confidence intervals (CI) stratified by race. We then estimated the adjusted chlamydia population attributable fraction (aPAF) with 95% CI of TFI.ResultsAll black (n=107) and 618 of 620 non-black women had Pgp3 results. Pgp3 seropositivity was 25.9% (19.3–33.8%) for non-black cases, 15.2% (12.3–18.7%) for non-black controls, 66.0% (95% CI 51.7–77.8%) for black cases, and 71.7% (59.2–81.5%) for black controls. Among 476 non-black women without endometriosis (n=476), Pgp3 was associated with TFI (aOR 2.6 [1.5– 4.4]), adjusting for clinic, age, and income; chlamydia TFI aPAF was 19.8% (95% CI 7.7–32.2%) in these women. Pgp3 positivity was not associated with TFI among non-black women with endometriosis nor among black women (regardless of endometriosis).ConclusionsAmong non-black infertile women without endometriosis in these clinics, 20% of TFI was attributed to chlamydia. Better biomarkers are needed to estimate chlamydia TFI PAF, especially in black women.

In a vaginal 16S ribosomal RNA gene quantitative PCR study of 17 pelvic inflammatory disease (PID) cases and 17 controls who tested positive for Chlamydia trachomatis, women who additionally tested positive for Atopobium vaginae, Sneathia spp., BVAB-TM7, Megasphaera spp., Eggerthella-like bacterium or Mobiluncus spp. were more likely to develop PID.

BACKGROUND Ideal management of sexually transmitted infections (STI) may require risk markers for pathology or vaccine development. Previously, we identified common genetic variants associated with chlamydial pelvic inflammatory disease (PID) and reduced fecundity. As this explains only a proportion of the long-term morbidity risk, we used whole-exome sequencing to identify biological pathways that may be associated with STI-related infertility. METHODS We obtained stored DNA from 43 non-Hispanic black women with PID from the PID Evaluation and Clinical Health Study. Infertility was assessed at a mean of 84 months. Principal component analysis revealed no population stratification. Potential covariates did not significantly differ between groups. Sequencing kernel association test was used to examine associations between aggregates of variants on a single gene and infertility. The results from the sequencing kernel association test were used to choose "focus genes" (P < 0.01; n = 150) for subsequent Ingenuity Pathway Analysis to identify "gene sets" that are enriched in biologically relevant pathways. RESULTS Pathway analysis revealed that focus genes were enriched in canonical pathways including, IL-1 signaling, P2Y purinergic receptor signaling, and bone morphogenic protein signaling. CONCLUSIONS Focus genes were enriched in pathways that impact innate and adaptive immunity, protein kinase A activity, cellular growth, and DNA repair. These may alter host resistance or immunopathology after infection. Targeted sequencing of biological pathways identified in this study may provide insight into STI-related infertility.

PEACH trial data were used to evaluate the relationship between subsequent sexually transmitted infection and recurrent pelvic inflammatory disease on infertility and chronic pelvic pain (CPP). Recurrent pelvic inflammatory disease was associated with an almost 2-fold increase in infertility and more than 4-fold increase in CPP. Subsequent sexually transmitted infection was associated with CPP, but not infertility.

Among urban, primarily African American pregnant women, 74% were identified with Nugent score bacterial vaginosis (BV). All BV-associated bacteria were more prevalent among women with Nugent score BV. Bacterial vaginosis-associated bacteria 3 (BVAB3) had the highest positive predictive value, whereas Gardnerella vaginalis and Atopobium spp. had the highest sensitivity. Atopobium spp. levels had the most significant area under the curve.

Pelvic inflammatory disease (PID), the infection and inflammation of the female genital tract, results in serious reproductive morbidity including infertility and ectopic pregnancy. Bacterial vaginosis (BV) is a complex alteration of the vaginal flora that has been implicated in PID. The role of BV in the etiology and pathogenesis of PID has not been studied extensively. Our objective was to extensively review data related to the relationship between BV and PID (n = 19 studies). Several studies found a link between BV and cervicitis, endometritis, and salpingitis. Furthermore, it seems that some BV-associated organisms are associated with PID, whereas others are not. However, studies demonstrating an independent association between BV-associated organisms and PID are sparse. In addition, a causal association between BV and PID has not been established. Prospective studies are needed to further delineate the role of BV in PID, with particular focus on individual BV-associated organisms.

We studied the microbial correlates of time to care and long-term outcomes among pelvic inflammatory disease (PID) patients, as delayed care may increase the risk for reproductive sequelae.Mean days of pain before care were compared by microbial pathogen (Chlamydia trachomatis only, Neisseria gonorrhoeae only, Mycoplasma genitalium only, coinfection with 2 or more pathogens, or no pathogens) among 298 women with histologically confirmed endometritis from the PID Evaluation and Clinical Health study. Times to pregnancy and recurrent PID were assessed over a mean of 84 months and compared between women who delayed care (≥14 days) and women who sought early care, in the entire cohort and in subsets defined by microbial infection. Analyses were adjusted for age and race, additionally time to pregnancy was adjusted for self-reported baseline infertility.Patients waited a mean of 7 days before seeking care for symptoms. Time to care was longest among women infected by C. trachomatis only (12.3 ± 9.4 days) and M. genitalium only (10.9 ± 8.9 days) and the shortest among women infected by N. gonorrhoeae only (4.6 ± 5 days) or coinfection (5.6 ± 5.1 days, P0.001). Rates of infertility, recurrent PID, and chronic pelvic pain were frequent overall (17%, 20%, and 36%) and tended to be higher, albeit nonsignificantly, after delayed care.Among women with clinically suspected PID, time to care was generally high. C. trachomatis and M. genitalium positive women had the longest times to care. Although reproductive morbidity was high in this cohort, associations with delayed care were nonsignificant.

The objective of this study was to assess the risk profile for chronic pelvic pain (CPP) after pelvic inflammatory disease (PID).Multivariate logistic regression was used to assess risk factors for CPP in a longitudinal study of 780 predominately black, urban women with clinically suspected PID: complaints of acute pain (30 days); a clinical finding of pelvic tenderness; and leukorrhea, mucopurulent cervicitis, or untreated gonococcal or chlamydial cervicitis. CPP was defined as pain reported ator=2 consecutive interviews conducted every 3 to 4 months for 2 to 5 years.Nonblack race (odds ratio [OR], 2.17; 95% confidence interval [CI], 1.31-3.58), being married (OR, 2.06; 95% CI, 1.02-4.18), a low SF-36 mental health composite score (OR, 2.71; 95% CI, 1.69-4.34),or=2 prior PID episodes (OR, 2.84; 95% CI, 1.07-7.54), and smoking (OR, 1.65; 95% CI, 1.01-2.71) independently predicted CPP. Histologic endometritis or evidence of endometrial Neisseria gonorrhoeae or Chlamydia trachomatis infection was negatively associated with CPP (OR, 0.69; 95% CI, 0.44-1.10).A range of demographic, clinical, historical, and behavioral factors predict CPP after PID.