Neonatal invasive Streptococcus gallolyticus subsp. pasteurianus infection with delayed central nervous system complications.

Group D streptococci are known to cause newborn septicemia and meningitis, but the Streptococcus bovis group strains rarely cause serious neonatal infections in Korea. Central nervous system (CNS) complications of neonatal S. bovis group infection have rarely been reported. In adults, S. bovis group strains cause bacteremia and endocarditis, and are associated with gastrointestinal malignancy. However, only a few studies have reported meningitis and septicemia in infants. Here, we describe a case of bacteremia and meningitis due to Streptococcus gallolyticus subsp. pasteurianus with a delayed CNS complication in an infant. A 28-day-old male infant was admitted to the hospital with a 1-day history of fever. Cultures of blood, cerebrospinal fluid, and urine showed the presence of S. bovis group strain-S. gallolyticus subsp. pasteurianus. He was discharged after 21 days of intravenous ampicillin and cefotaxime administration. Two weeks later, he was readmitted with a fever and short episodes of tonic-clonic movements. Brain magnetic resonance imaging showed marked bilateral frontal subdural effusion. He was discharged after 31 days of antibiotic therapy, and no neurological sequelae were observed at the 9-month follow-up. In conclusion, we present a rare case of neonatal S. gallolyticus subsp. pasteurianus infection causing urinary tract infection, septicemia, meningitis, and delayed CNS complications. This case emphasizes the need for physicians to be aware of S. bovis infection in infants.

Ten years of experience in the prevention of mother-to-child human immunodeficiency virus transmission in a university teaching hospital.

PURPOSE: Administration of antiretroviral drugs to mothers and infants significantly decreases mother-to-child human immunodeficiency virus (HIV) transmission; cesarean sections and discouraging breastfeeding further decreases this risk. The present study confirmed the HIV status of babies born to mothers infected with HIV and describes the characteristics of babies and mothers who received preventive treatment. METHODS: This study retrospectively analyzed medical records of nine infants and their mothers positive for HIV who gave birth at Korea University Ansan Hospital, between June 1, 2003, and May 31, 2013. Maternal parameters, including HIV diagnosis date, CD4+ count, and HIV ribonucleic acid (RNA) copy number, were analyzed. Infant growth and development, HIV RNA copy number, and HIV antigen/antibody test results were analyzed. RESULTS: Eight HIV-positive mothers delivered nine babies; all the infants received antiretroviral therapy. Three (37.5%) and five mothers (62.5%) were administered single- and multidrug therapy, respectively. Intravenous zidovudine was administered to four infants (50%) at birth. Breastfeeding was discouraged for all the infants. All the infants were negative for HIV, although two were lost to follow-up. Third trimester maternal viral copy numbers were less than 1,000 copies/mL with a median CD4+ count of 325/µL (92-729/µL). Among the nine infants, two were preterm (22.2%) and three had low birth weights (33.3%). CONCLUSION: This study concludes that prophylactic antiretroviral therapy, scheduled cesarean section, and prohibition of breastfeeding considerably decrease mother-to-child HIV transmission. Because the number of infants infected via mother-to-child transmission may be increasing, studies in additional regions using more variables are necessary.

Estrogen therapy for experimental intracerebral hemorrhage in rats.

OBJECT: The aims of this study were to determine the following: whether there are sex differences in intracerebral hemorrhage (ICH) induced brain injury in rats, whether delayed administration of 17beta-estradiol can reduce ICH-induced brain damage, and whether these effects are estrogen receptor (ER)-dependent. METHODS: Male and female Sprague-Dawley rats received an infusion of 100 microl autologous whole blood into the right basal ganglia. Twenty-four hours later the rats were killed. The effects of 17beta-estradiol on ICH-induced brain injury were examined by measuring brain edema and neurological deficits. Both ER-alpha and hemeoxygenase (HO)-1 were investigated through Western blot and immunohistochemical analysis. Brain edema was significantly less severe in female compared with that in male rats. The ER antagonist ICI 182,780 exacerbated ICH-induced brain edema in female but not in male rats, indicating that ER-alpha activation during ICH is protective in female rats. Administration of exogenous 17beta-estradiol in male, but not in female, rats significantly attenuated brain edema, neurological deficits, and ICH-induced changes in HO-1 when given 2 hours after hemorrhage. The effects of exogenous 17beta-estradiol occurred through an ER-independent mechanism. CONCLUSIONS: Results in this study indicate that 17beta-estradiol could be a potential therapeutic agent for ICH.

Holo-transferrin and thrombin can interact to cause brain damage.

BACKGROUND AND PURPOSE: Previous studies have suggested that delayed release of hemoglobin degradation products, particularly iron, is involved in intracerebral hemorrhage (ICH)-induced brain injury. However, a recent study found evidence of iron-induced brain injury soon after ICH. This study, therefore, examined whether another iron-containing component of blood, holo-transferrin (holo-Tf), might also induce brain injury either alone or in combination with thrombin, another factor involved in early ICH-induced brain injury. METHODS: Male Sprague-Dawley rats received an intracerebral infusion of holo-Tf, apo (noniron-loaded)-Tf, thrombin, or a combination of Tf with thrombin into the right basal ganglia. The rats were euthanized 24 hours later for measurement of brain edema and assessment of DNA damage (single- and double-strand breaks and 8-hydroxyl-2'-deoxyguanosine immunohistochemistry). Iron distribution was examined histochemically. RESULTS: Holo-Tf, apo-Tf, and the dose of thrombin used (1 U) all failed to induce brain edema when administered alone. However, the combination of holo-Tf with thrombin (but not apo-Tf with thrombin) caused brain edema, DNA damage, and intracellular iron accumulation in the ipsilateral basal ganglia. CONCLUSIONS: These results suggest that in addition to hemoglobin-bound iron, Tf-bound iron may contribute to ICH-induced brain injury and that thrombin may contribute to the latter by facilitating cellular iron uptake.