Late-onset and Recurrent Neonatal Group B Streptococcal Disease Associated with Breast-milk Transmission

The purpose of the study was to determine the epidemiological relationships in three unrelated cases of neonatal late-onset Group B streptococcal (GBS) disease and maternal breast-milk infection with GBS. All deliveries were by cesarean section; case 1 was at term, and cases 2 and 3 were at 32- and 33-wk gestation, respectively. Case 1 relates to a mother with clinical mastitis and recurrent GBS infection in a 20-day-old male infant. Following antibiotic therapy and cessation of breast-feeding, the infant recovered without sequelae. Case 2 refers to a mother with clinical mastitis and the occurrence of late-onset GBS disease in 5-wk-old male twins. Despite intervention, one infant died and the second became ill. Following antibiotic therapy and cessation of breast-feeding, the surviving infant recovered without sequelae. Case 3 refers to a mother with sub-clinical mastitis and late-onset GBS infection occurring in a 6-day-old female twin. Following intervention, the infant recovered but suffered a bilateral thalamic infarction resulting in developmental delay and a severe seizure disorder. Following recovery of GBS from an inapparent mastitis and cessation of breast-feeding, the second infant remained well. Blood cultures from all affected infants and maternal breast milk were positive for GBS. Epidemiological relationships between neonatal- and maternal-derived GBS isolates were confirmed by a random amplified polymorphic DNA polymerase chain reaction assay (RAPD-PCR). This study is significant in that it has demonstrated that maternal milk (in cases of either clinical or sub-clinical mastitis) can be a potential source of infection resulting in either late-onset or recurrent neonatal GBS disease.     

Men’s pathways to risky sexual behavior: Role of co-occurring childhood sexual abuse,posttraumatic stress disorder,and depression histories

Recent reports of sexually transmitted infection-rate increases among men indicate the need for renewed study of male sexual risk behavior to aid development of updated and novel risk reduction interventions. Men who have childhood sexual abuse (CSA) histories consistently report frequent sexual risk behavior. The objective of this sturdy is to explore whether posttraumatic stress disorder (PTSD) and depression are moderators and/or mediators of the association between CSA and sexual risk in adult men. A cross-sectional survey study employing random digit dial recruitment was administered to men aged 18–49 years from Philadelphia County. Two bundred ninety eight men were recruited and screened for CSA history, administered items from the Posttraumatic Stress Diagnostic Scale (PDS) and Center for Epidemiologic Studies—Depression (CES-D), and asked to estimate their number of lifetime sexual partners (LSPs). Effects of sociodemographic characteristics, CSA, PTSD, and depression on the number of LSPs were modeled using Poisson regression. Results show that 197 (66%) men participated; 43 (22%) had CSA histories. CSA was significantly associated with PTSD/depression (P=.03). Four sociodemographic variables (age, race, sexual identity, and education), CSA (incidence rate ratio, IRR=1.47, P<.001), PTSD (IRR=1.19, P=.04), depression (IRR=1.29, P=.001), all 2-way interactions, and the 3-way CSA/PTSD/depression interaction (IRR=11.00, P<.001) were associated with the number of LSPs (R²=0.27). In conclusion, sexual partnership patterns unique to men with CSA histories and comorbid PTSD/depression appear to lead to substantially higher numbers of LSPs. Estimates of this relationship may have been biased toward the null by underreporting that can occur with phone surveys. Cross-sectional studies do not support causal inferences; however, the identification of a moderating and mediating influence of PTSD/depression on the relationship between CSA and sexual risk behavior is important and suggests the need for future studies with larger samples that examine trajectories for CSA, psychiatric illness, and sexual partnerships.     

Association of the GNAS1 gene variant with hypertension is dependent on alcohol consumption.

The beta-adrenoceptor (beta-AR)-stimulatory guanine nucleotide-binding (Gs) protein system has been shown to play important roles in the cardiovascular system. The gene encoding the alpha-subunit of Gs proteins (GNAS1) is a candidate genetic determinant for hypertension. Because alcohol consumption is known to affect blood pressure partly through the beta-AR-Gs protein system, we examined the possible interaction between GNAS1 T393C polymorphism and drinking status in the association with hypertension in the present study. As a result, a non-significant but reasonable trend supporting the presence of an interaction was shown (p = 0.076). In line with this trend, the T393C polymorphism significantly interacted with drinking status in the association with systolic blood pressure (p = 0.028). Moreover, supporting the presence of an interaction, T allele carriers consistently had a higher probability of hypertension, higher systolic blood pressure, and higher diastolic blood pressure than CC homozygotes in non-drinkers and light drinkers. In contrast, CC homozygotes consistently had a higher probability of hypertension, higher systolic blood pressure, and higher diastolic blood pressure than T allele carriers in moderate to heavy drinkers. The present study also showed a significant interaction between the T393C polymorphism and drinking status in the association with pulse pressure (p = 0.026), reflected by a significant association between the T393C polymorphism and pulse pressure in moderate to heavy drinkers (p = 0.026). These findings may be helpful in conducting further molecular and biological studies on the relationship among the effects of alcohol, the beta-AR-Gs protein system, and hypertension.