One-month-old boy with group B streptococcal meningitis, subdural effusion, and high levels of interleukin-6.

Meningitis is associated with elevated levels of inflammatory cytokines in the blood, cerebrospinal fluid (CSF), and subdural fluid. Subdural effusion prolongs fever in patients with meningitis. However, the reason for this remains unclear. A healthy one-month-old boy was admitted after presenting with bacterial meningitis. He was administered meropenem, cefotaxime, and dexamethasone intravenously. On the 3rd day, blood and CSF cultures revealed the presence of Group B Streptococcus from samples collected on day 1. Subsequently, ampicillin and gentamicin replaced the previous combination of antimicrobials used. On the 4th day, brain magnetic resonance imaging with contrast showed bilateral cerebral ventriculitis and left subdural effusion. On the 11th day, since the subdural effusion had worsened, we performed a subdural puncture from the anterior fontanelle. Owing to the prolonged fever, he was intravenously injected immunoglobulin on day 13. He was afebrile on day 23. Antimicrobials were administered for 28 days. Levels of interleukin-6 (IL-6) in the serum and CSF were the highest on the 1st day at 20,600 pg/mL and 170,000 pg/mL, respectively, and decreased upon treatment. IL-6 concentration in the subdural fluid (30,000 pg/mL) was much higher than that in the serum (9 pg/mL) and CSF (2600 pg/mL). To the best of our knowledge, this is the first report on the cytokines in subdural fluid in patients with group B Streptococcal meningitis. Subdural effusion maintained high levels of IL-6 even after the levels in the blood and CSF decreased dramatically. This could explain why subdural effusion prolongs fever in patients with meningitis.

Clinical Features of Febrile Urinary Tract Infection Caused by Extended-spectrum Beta-lactamase-producing Escherichia Coli in Children.

The global prevalence of infections caused by extended-spectrum beta-lactamase (ESBL)-producing Escherichia coli has been increasing. In children, ESBL-producing E. coli manifest mostly as febrile urinary tract infections (fUTIs). This study aimed to elucidate the clinical features of fUTI resulting from ESBL-producing E. coli in Japanese patients. The clinical features of children with E. coli-related fUTI were retrospectively examined. These children underwent treatment at the National Hospital Organization Saitama Hospital, Japan, between May 2010 and April 2018. Urine specimens were obtained by either bladder catheterization or the clean-catch method. All children having positive urine cultures (≥104 colony-forming unit/mL for catheter specimens and ≥105 colony forming unit/mL for clean-catch specimens) and a fever of ≥38°C were considered to have fUTI. During the study period, 171 patients were diagnosed with E. coli-related fUTI. Among these, 17 (9.9%) fUTI cases were caused by ESBL-producing E. coli. A significant difference was noted in the median age of the populations having ESBL-producing E. coli and non-ESBL-producing E. coli infections (2 and 5 months, respectively); other characteristics were not significantly different between the two patient groups. ESBL-producing E. coli infections markedly increased in our hospital between 2013 and 2018. In the present study, young age was the only risk factor for fUTI caused by ESBL-producing E. coli identified in Japanese children.

Predicting outcomes of neonates born to GBS-positive women who received inadequate intrapartum antimicrobial prophylaxis.

We determined the predicting factors of early-onset group B streptococcal (EOGBS) infection in neonates who were born to GBS carrier mothers with inadequate intrapartum antibiotic prophylaxis (IAP). Medical records of all neonates born from January 1, 2008 to April 1, 2010 were reviewed. Inadequate IAP was defined as delivery less than 4 hours (h) after the first administration of antimicrobial. Of 1910 neonates, 273 were born from mothers colonized with GBS, including 69 who received inadequate IAP. Of 69 neonates, nine showed symptoms, including respiratory distress, fever, tachycardia, vomiting, and irritability. Abnormalities in complete blood count (CBC) and C-reactive protein (CRP) were noted in three and four neonates, respectively. Three infants were diagnosed with EOGBS infection confirmed by positive rectal and throat cultures, and all three presented with respiratory distress and CRP abnormalities. Respiratory distress (p=0.0004) and CRP (p=0.0001) offered reliable indicators for detecting EOGBS infections.

Monochorionic twin fetuses showing a reversal of donor-recipient phenotypes in severe twin-twin transfusion syndrome without oligo-polyhydramnios sequence.

Antenatal sonographic diagnosis of twin-twin transfusion syndrome (TTTS) is based on findings of a twin oligo-polyhydramnios sequence (TOPS) observed in monochorionic twin fetuses. However, TTTS can develop without a significant characteristic intertwin discordance in the amniotic fluid volumes. We report an uncommon form of TTTS without TOPS showing severe anemia in one twin and polycythemia in the other. Based on sonographic findings, it is considered that the recipient twin became the donor later in gestation, and vice versa. It is concluded therefore that even in the absence of TOPS, the possibility of severe TTTS with a suspected reversal of donor-recipient phenotypes during pregnancy should not be excluded, and serial Doppler studies including the measurement of the middle cerebral artery peak systolic velocity should be routinely performed even in seemingly uncomplicated monochorionic twin fetuses without TOPS.

Intratracheal instillation of perfluorocarbon rescued mice with primary pulmonary hypoplasia.

The aim of this study was to investigate the effect of perfluorocarbon on the respiratory status of newborn mice with pulmonary hypoplasia without diaphragmatic defects, following intrauterine exposure to nitrofen. Three groups of newborn mice were compared: pups exposed to nitrofen antenatally without (group A) or with (group B) perfluorocarbon treatment and pups not exposed to nitrofen as a control (group C). Respiratory evaluation was performed by scoring, pressure-volume analysis, and histological examination. At 40 minutes after birth, the survival rates in groups A, B, and C were 51%, 94%, and 95%, respectively. The clinical scores of group B mice at 40 minutes were significantly better than those of group A mice in which pulmonary hypoplasia was induced. In group B, the hysteresis ratio was significantly higher than that in group A, and lung histology showed a significant increase in airspace. An immunohistochemical examination showed that perfluorocarbon did not alter the expression of mature surfactant protein B and surfactant proprotein C. This study demonstrated that treatment with perfluorocarbon was useful in stabilizing critically ill mice with primary pulmonary hypoplasia during the early phase of therapy.

The intrauterine expression of surfactant protein D in the terminal airways of human fetuses compared with surfactant protein A.

UNLABELLED: We investigated the expression of surfactant protein (SP)-D in pulmonary epithelial cells, compared with the expression of SP-A. A total of 15 fetuses aborted at 8, 15, 19, 20, 21 and 23 weeks gestation and four premature babies who were stillborn or died after birth between May 1997 and October 2001 were included in this study. Fetuses showing any findings associated with preterm premature rupture of membranes or infection were excluded. We performed immunohistochemical examinations for SP-D and SP-A. SP-D was not detected by immunostaining at 8, 15 and 19 weeks gestation. At 21 weeks gestation, SP-D was weakly localized, in some cases (5/9), in the epithelial lining of both bronchioles and terminal airways. In contrast at 21 weeks gestation, SP-A was more markedly detected in the epithelial lining of both bronchioles and terminal airways in all cases but not detected in bronchioles and terminal airways at 8, 15 and 19 weeks gestation. CONCLUSION: the findings in this investigation suggests that the production of SP-D in fetal human lungs begins in the bronchiolar and terminal epithelium from about 21 weeks of gestation.