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.     

Telmisartan and irbesartan therapy in type 2 diabetic patients treated with rosiglitazone: effects on insulin-resistance, leptin and tumor necrosis factor-alpha.

The aim of our study was to investigate the metabolic effect of telmisartan and irbesartan in subjects treated with rosiglitazone, a well-known insulin-sensitizing drug, in order to clarify the direct metabolic effects of the two former drugs. Patients were enrolled, evaluated, and followed at 3 Italian centers. We evaluated 188 type 2 diabetic patients with metabolic syndrome (94 males and 94 females in total; 49 males and 46 females, aged 56+/-5, treated with telmisartan; and 45 males and 48 females, aged 55+/-4, treated with irbesartan). All had been diabetic for at least 6 months, and glycemic control by the maximum tolerated dietary changes and maximum tolerated dose of oral hypoglycemic agents had been attempted and failed in all cases. All patients took a fixed dose of rosiglitazone, 4 mg/day. We administered telmisartan (40 mg/day) or irbesartan (150 mg/day) in a randomized, controlled, double-blind clinical manner. We evaluated body mass index (BMI), glycemic control (HbA1c fasting plasma glucose and insulin levels [FPG, and FPI, respectively], and homeostasis model assessment [HOMA] index), lipid profile (total cholesterol [TC], low density lipoprotein-cholesterol [LDL-C], high density lipoprotein-cholesterol [HDL-C], and triglycerides [TG]), systolic and diastolic blood pressure (SBP and DBP), tumor necrosis factor-alpha (TNF-alpha), and leptin during the 12 months of this treatment. No BMI change was observed after 6 or 12 months in either group. Significant decreases in HbAlc and FPG were observed after 6 months in the telmisartan group, and after 12 months in both groups. The decrease in HbA1c and FPG at 12 months was statistically significant only in the telmisartan group. A significant decrease in FPI was observed at 12 months in both groups, and this decrease was significantly greater in the telmisartan group. Significant decreases in the HOMA index were observed at 6 and 12 months in both groups, and the decrease in the HOMA index after 12 months was significantly greater in the telmisartan group than in the irbesartan group. Significant changes in SBP, DBP, TC, and LDL-C were observed after 6 and 12 months in both groups. Significant decreases in TNF-alpha and leptin levels were observed after 6 months in the telmisartan group, and after 12 months in both groups. In conclusion, in this study of patients with type 2 diabetes mellitus and metabolic syndrome, telmisartan seemed to result in a greater improvement in glycemic and lipid control and metabolic parameters related to metabolic syndrome compared to irbesartan. These observed metabolic effects of different angiotensin type 1 receptor blockers could be relevant when choosing a therapy to correct metabolic derangement of patients affected by metabolic syndrome and diabetes.