Maternal Effects of Respiratory Syncytial Virus Infection during Pregnancy.

Given the illness and deaths caused by respiratory syncytial virus (RSV) infection during the first year of life, preventing infant RSV infections through maternal vaccination is intriguing. However, little is known about the extent and maternal effects of RSV infection during pregnancy. We describe 3 cases of maternal RSV infection diagnosed at a US center during winter 2014. Case-patient 1 (26 years old, week 33 of gestation) received a diagnosis of RSV infection and required mechanical ventilation. Case-patient 2 (27 years old, week 34 of gestation) received a diagnosis of infection with influenza A(H1N1) virus and RSV and required mechanical ventilation. Case-patient 3 (21 years old, week 32 of gestation) received a diagnosis of group A streptococcus pharyngitis and RSV infection and was monitored as an outpatient. Clarifying the effects of maternal RSV infection could yield valuable insights into potential maternal and fetal benefits of an effective RSV vaccination program.

Plasma concentrations of defensins and lactoferrin in children with severe sepsis.

BACKGROUND: We hypothesized that systemic release of endogenous leukocyte-derived polypeptide antimicrobial defensins (polymorphonuclear leukocyte-specific) and lactoferrin (polymorphonuclear leukocyte and epithelial cell derived) occurs in nonneutropenic children with severe sepsis. METHODS: We performed a prospective cross-sectional and longitudinal study in a university children's hospital pediatric intensive care unit. Ninety-two consecutive children meeting criteria for sepsis and 14 critically ill children without sepsis (controls) were enrolled, and plasma defensins and lactoferrin concentrations were measured on Days 1 and 3 of sepsis. RESULTS: Nonneutropenic sepsis patients (n = 71) had increased defensins and lactoferrin plasma concentrations compared with critically ill control patients [defensins, 450 ng/ml vs. 150 ng/ml; lactoferrin, 332 ng/ml vs. 176 ng/ml (median values); P < 0.05] and neutropenic sepsis patients [n = 21; defensins, 450 ng/ml vs. 50 ng/ml; lactoferrin, 332 ng/ml vs. 20 ng/ml (median values); P < 0.05]. Neutropenic sepsis patients had similar plasma defensin concentrations and a decrease in plasma lactoferrin concentrations compared with control patients (P < 0.05). Defensins and lactoferrin plasma concentrations correlated to total white blood cell and absolute neutrophil count (P < 0.05). There was no association between plasma defensin concentration and organ failure or outcome; however, increased plasma lactoferrin concentrations were observed with the development of organ failure (P < 0.05). CONCLUSION: These data suggest that increased circulating defensins and lactoferrin release are dependent in part on neutrophil count and might play a role in host defense in children with severe sepsis.

Seroprevalence of antibodies to Chlamydia pneumoniae in women with preeclampsia.

OBJECTIVE: Preeclampsia shares many risk factors and pathophysiologic features with coronary heart disease. We studied whether, like atherosclerosis, preeclampsia is related to seroprevalence of immunoglobulin (Ig) G antibodies to Chlamydia pneumoniae. METHODS: Cross-sectional comparisons were made for 37 women with preeclampsia and 37 women with normal pregnancies at term. In these two groups, antibody titers for IgG, IgM, and IgA seroprevalence to C pneumoniae and IgG to Chlamydia trachomatis and Chlamydia psittaci were compared. RESULTS: Immunoglobulin G antibodies to C pneumoniae at a titer of at least 1:16 were more common in women with preeclampsia (25 of 37) than in women without (15 of 37) (odds ratio 3.1; 95% confidence interval 1.2, 7.9). There were no significant differences in the seroprevalence of IgA or IgM antibodies to C pneumoniae. Women with preeclampsia were also no more likely to have IgG antibodies to C trachomatis or C psittaci. CONCLUSION: Women with preeclampsia had an increased IgG seroprevalence to C pneumoniae but not to C trachomatis or C psittaci. These preliminary data suggest a specific association between infection with C pneumoniae and preeclampsia.

Obstetric rectal injury: risk factors and the role of physician experience.

OBJECTIVE: To identify the risk factors for rectal injury following vaginal delivery and to determine the impact of accoucheur experience (resident vs. attending) on those risk factors. METHODS: A database at our institution was used to identify women with a singleton gestation, vertex presentation, and no prior cesarean delivery who underwent a vaginal delivery over a three year period. The outcome of interest was rectal injury. We performed logistic regression evaluating the association of parity, birthweight, forceps, vacuum, midline episiotomy, epidural anesthesia, and operator status with rectal injury. We calculated population attributable risk to estimate the relative contribution of each risk factor. RESULTS: A total of 17,722 women met the inclusion criteria. The frequency of rectal injury was 8.9% (n = 1572). Our data demonstrate a significant increase in risk of rectal injury with birthweight > 4000 g, midline episiotomy, or operative vaginal delivery. Multiparity is significantly protective from rectal injury. Neither epidural anesthesia nor operator status altered the risk of rectal injury. The population attributable risk of each risk factor for rectal injury was similar regardless of operator group. CONCLUSION: The risk factors for rectal injury were present regardless of operator status, and the factors contributed to a similar extent for each group.

Predictive value of the clinical diagnosis of lower genital tract infection in women.

OBJECTIVE: We hypothesized that diagnostic approaches to lower genital tract infections are inaccurate and proposed this study to evaluate typical approaches. STUDY DESIGN: Clinical diagnoses were made with symptoms, direct observation, wet mount, vaginal pH, and amines in 598 women with genital complaints. Laboratory testing for N gonorrhoeae, yeast, T vaginalis, C trachomatis, and bacterial vaginosis by Gram stain. RESULTS: The most frequent symptoms were vaginal discharge (64%), change in discharge (53%), malodor (48%), and pruritus (32%). The infection rates were 46% bacterial vaginosis, 29% yeast, 12% trichomoniasis, 11% chlamydia or gonorrhea; 21% of the patients had no infection. The symptoms did not predict laboratory diagnosis. Clinical signs and symptoms with office-based tests and microscopy improved the accuracy of diagnoses. Amsel's clinical diagnosis of bacterial vaginosis was the most sensitive at 92%. The sensitivity of wet mount diagnosis of trichomoniasis was 62%, of yeast by microscopy was 22%, and of mucopus for the prediction of gonorrhea and/or chlamydia was 30%. CONCLUSION: Symptoms alone should not be used to direct treatment in instances in which resources permit more complete evaluation with office-based testing that includes microscopy. Treatment failures or diagnostic uncertainty should prompt specific laboratory testing.

Association between elevated neutrophil defensin levels and endometritis.

The role of host defenses in the pathogenesis of pelvic inflammatory disease (PID) remains largely uncharacterized. The antimicrobial peptides defensins are important components of innate host defense. To explore the relationship between neutrophil defensins and upper genital tract infection, 377 women who were at risk for PID were enrolled in a study. Women infected with Neisseria gonorrhoeae, Trichomonas vaginalis, or Chlamydia trachomatis had higher median levels of neutrophil defensins (human neutrophil peptides 1-3) in the vagina than did uninfected women. Neutrophil defensins were strongly associated with the presence of endometritis after the analysis was controlled for the presence of sexually transmitted diseases. Vaginal neutrophils were associated with endometritis only in the presence of elevated defensin levels, which highlights the importance of neutrophil activation, rather than the presence of neutrophils alone, in this inflammatory process. Neutrophil defensins appear to participate in the host defense in ascending pelvic infection and the pathogenesis of PID.

Sexual intercourse association with asymptomatic bacterial vaginosis and Trichomonas vaginalis treatment in relationship to preterm birth.

OBJECTIVE: The purpose of this study was to determine whether sexual intercourse was associated with the treatment efficacy or the incidence of preterm birth in two large randomized trials in which metronidazole treatment of bacterial vaginosis or Trichomonas vaginalis did not reduce preterm birth. STUDY DESIGN: Secondary analysis of two multicenter, double-blind, placebo-controlled trials in which women with asymptomatic bacterial vaginosis on Gram stain or asymptomatic T vaginalis on culture were randomized at 16 to 23 weeks of gestation to metronidazole or placebo. In both studies, women took 2 g of metronidazole or placebo in the presence of a nurse (first dose) and were given a second dose to take 48 hours later. This regimen was repeated (third and fourth doses) at 24 to 29 weeks. At the time of the third dose, bacterial vaginosis and T vaginalis specimens were collected again. Patients who were randomly selected to receive metronidazole were analyzed for bacterial vaginosis and T vaginalis at 24 to 29 weeks and for preterm birth of <37 weeks of gestation, according to intercourse between first and second doses and between the second and third doses. Continuous variables were compared with the use of the Wilcoxon rank-sum test; categoric variables were compared with the use of the chi(2 ) test, Fisher exact test, or the Mantel-Haenzel test of trend. RESULTS: Sexual intercourse between the first and second doses or between the second and third doses did not influence the incidence of bacterial vaginosis (18% vs 24%; relative risk, 0.7; 95% CI, 0.5-1.1; and 23% vs 20%; relative risk, 1.2; 95% CI, 0.9-1.6, respectively) or T vaginalis (4% vs 8%; relative risk, 0.5; 95% CI, 0.1-3.6; and 5% vs 10%; relative risk, 0.5; 95% CI, 0.2-1.1; respectively) at 24 to 29 weeks of gestation compared with no intercourse. In the T vaginalis trial, sexual intercourse between the first and second doses or between the second and third doses did not influence the incidence of preterm birth (13% vs 17%; relative risk, 0.8; 95% CI, 0.3-2.1; and 16% vs 17%; relative risk, 1.0; 95% CI, 0.6-1.6; respectively) compared with no intercourse. In the bacterial vaginosis trial, although sexual intercourse between the first and second doses did not influence the incidence of preterm birth (11% vs 12%; relative risk, 0.9; 95 % CI, 0.6-1.5), sexual intercourse between the second and third doses was associated with a reduction in the incidence of preterm birth (10% vs 16%; relative risk, 0.6; 95% CI, 0.4-0.9) compared with no intercourse. CONCLUSION: Sexual intercourse was associated with neither the efficacy of metronidazole treatment of bacterial vaginosis or T vaginalis nor with the incidence of preterm birth. In the bacterial vaginosis study, intercourse between the second and third doses had a negative association with preterm birth.