Effect of experimental genital mycoplasmosis on gene expression in the fetal brain.

Neurodevelopmental disorders may have their origins during intrauterine development. We used a well-defined animal model to test whether hematogenous infection with genital mycoplasma would alter the expression of genes associated with autism spectrum disorders (ASD). In a preliminary experiment, rats were exposed at 14 days gestation (GD14) to Mycoplasma pulmonis or sterile broth and sacrificed at GD18. Infection and inflammation status of the pups was ascertained by culture and cytokine ELISA. Intra-cardiac injection of 10(6)CFU M. pulmonis resulted in amniotic infection of 100% of the pups and was accompanied by higher levels of IL-1ß in amniotic fluids. In a second experiment, animals were infected in a similar manner but dams and their litters were sacrificed at GD18, GD21 or postpartum day 3 (PPD3). Expression of proinflammatory cytokines and neurodevelopmental genes in the fetal brains was evaluated. M. pulmonis infection significantly increased the expression of IL-1ß, TNF-α and COX-2 in fetal and neonatal brains. Expression of GFAP and CD11b, markers for activation on astrocytes and microglial cells, respectively, was also increased for infected animals. M. pulmonis significantly increased SHANK-3 gene expression at GD21 and PPD3 and PCP-2 expression at GD21. No effect of M. pulmonis infection on Reelin, PTEN, BDNF or HGF was detected. These data suggest that M. pulmonis infection at GD14 increases the expression of proinflammatory genes in the perinatal brain. Further studies with earlier time-points of infection and ones that use behavioral outcomes are needed to better understand the potential role of genital mycoplasmosis on pychopathology.

Depression in pregnancy: time of screening and access to psychiatric care.

OBJECTIVE: To determine the timing of screening for postpartum depression that optimizes access to psychiatric care. METHODS: Cross-sectional evaluation of women receiving obstetric care in a community-based medical center clinic from March to July 2006, who were screened for depression at 36 weeks gestation, delivery, and 6 weeks postpartum using the Edinburgh Postnatal Depression Scale. Positive screens generated referrals for psychiatric evaluation. The rate of positive screens for depression and psychiatric follow-up at each time point was evaluated. RESULTS: Of the 293 patients evaluated, the distribution of the first screen which occurred during the study period was 21% at 36 weeks, 31% at delivery, and 48% at 6 weeks postpartum. The incidence of a positive screen was 5% at 36 weeks, 16% at delivery and 14% at 6 weeks postpartum. Access to psychiatric care occurred in 33% at 36 weeks, 15% at 6 weeks postpartum and 100% at delivery (p = 0.001). CONCLUSION: Screening for depression in the hospital after delivery improves access to psychiatric care.

The significance of a positive second trimester serum screen for trisomy 18.

OBJECTIVES: We designed this study to estimate the proportion of fetuses in pregnancies with positive second trimester serum screens for trisomy 18 who actually have trisomy 18, to estimate the proportion of women with trisomy 18 who have a negative serum screen, and to assess the role of ultrasound in the diagnosis of trisomy 18. METHODS: Retrospective study of two cohorts of pregnant women in 2004 and 2005: (1) those with a second trimester serum screen positive for trisomy 18 and (2) those with fetuses having trisomy 18. RESULTS: There were 93 women with positive serum screens for trisomy 18. Of these, only three had a fetus with trisomy 18. There were five other cases of trisomy 18, three of which had a negative second trimester serum screen for trisomy 18. All fetuses with trisomy 18 had multiple major structural abnormalities detected on targeted genetic sonography. CONCLUSIONS: A positive second trimester serum screen has a poor sensitivity and poor prediction for trisomy 18. Trisomy 18 is highly unlikely if a woman with a positive screen for trisomy 18 has no fetal abnormalities detected on targeted genetic sonography. Women with a positive second trimester serum screen for trisomy 18 should be offered genetic sonography, and the practice of routine amniocentesis for all women with a positive screen should be discouraged when targeted genetic sonography is available.

Contributions of ischaemic placental disease to preterm birth in twin gestations.

OBJECTIVE: To evaluate the extent to which ischaemic placental disease (IPD)--defined as women or newborns diagnosed with pre-eclampsia, small for gestational age (SGA), or abruption, is associated with preterm birth in twin gestations. METHODS: A population-based study of women who delivered twin live births and stillbirths at 20-44 weeks gestation from 1995-2004 in the US was performed (n=1,105,666). We compared the frequency of IPD in term and preterm (<37 weeks) twin births. SGA was defined as twins with birthweight<10th percentile for gestational age, and corrected for infant sex. The association between IPD and preterm birth was expressed as hazard ratio, derived from Cox proportional hazard regression models after adjusting for potential confounders. RESULTS: The overall rate of twin preterm birth was 57%. IPD was present in 20% of twin preterm births in comparison to a rate of 16% at term. Both pre-eclampsia and abruption, but not SGA, were associated with increased preterm birth rates. Women with two or more of the IPD conditions were more likely to deliver at preterm than at term gestations. CONCLUSION: In comparison to twin births delivered at term, IPD is more common in preterm births. Efforts to understand the role of IPD in twin gestations based on preterm birth subtypes may reveal important insights.