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BACKGROUND: A bacterial cause is not frequently identified in children with pneumonia complicated by parapneumonic effusion (ie, complicated pneumonia). OBJECTIVES: To determine the frequency of positive blood and pleural fluid cultures in children with complicated pneumonia and to determine whether broad‐range 16S rRNA polymerase chain reaction (PCR) improves identification of a microbiologic cause. METHODS: This prospective cohort study included children 1–18 years of age hospitalized with complicated pneumonia. RESULTS: Pleural fluid drainage was performed in 64 (51.6%) of 124 children with complicated pneumonia. A microbiologic cause was identified in 11 of 64 patients (17.2%; 95% confidence interval [CI]: 8.9%–28.7%). Bacteria were isolated from pleural fluid culture in 6 of 64 patients (9.4 %; 95% CI: 3.5%–19.3%) undergoing pleural drainage; the causative bacteria were Staphylococcus aureus (n = 5) and Streptococcus pneumoniae (n = 1). Blood culture identified a bacterial cause in 3 of 44 cases (6.8%; 95% CI: 1.4%–18.7%) undergoing pleural fluid drainage; S. pneumoniae (n = 1), Haemophilus influenzae (n = 1), and S. aureus (n = 1) were isolated. Only 3 of the 19 pleural fluid samples (15.8%; 95% CI: 3.4%–39.6%) analyzed with 16S rRNA PCR were positive. S. pneumoniae was the only organism detected in all three samples; two of these three had negative pleural fluid cultures and absence of bacteria on Gram stain. S. aureus was isolated from pleural fluid culture in one patient with a negative 16S rRNA PCR test. CONCLUSIONS: Causative bacteria were infrequently identified in children with complicated pneumonia. Broad‐range 16S rRNA PCR only modestly improved the microbiologic yield over conventional culture methods. Journal of Hospital Medicine 2011. © 2011 Society of Hospital Medicine

Biventricular hypertrophy was noted at 24 weeks' gestation in a fetus with isolated cytochrome-c oxidase (COX) deficiency. Shock, caused by hypertrophic cardiomyopathy and severe pulmonary hypertension, led to the patient's death on day 6. His phenotype defines a new lethal variant of COX deficiency characterized by prenatal-onset cardiopulmonary pathophysiology.

Necrotizing enterocolitis (NEC) is the most common gastrointestinal (GI) medical/surgical emergency of the newborn and a leading cause of preterm neonate morbidity and mortality. NEC is a challenge to diagnose since it often shares similar clinical features with neonatal sepsis. In the present study, plasma protein profiling was compared among NEC, sepsis and control cohorts using gel electrophoresis, immunoblot and mass spectrometry. We observed significant impairment in the formation of fibrinogen-γ dimers (FGG-dimer) in the plasma of newborns with NEC that could efficiently differentiate NEC and sepsis with a high level of sensitivity and specificity. Interestingly, the impaired FGG-dimer formation could be restored in NEC plasma by the addition of exogenous active factor XIII (FXIII). Enzymatic activity of FXIII was determined to be significantly lower in NEC subject plasma for crosslinking FGG when compared to sepsis. These findings demonstrate a potential novel biomarker and related biologic mechanism for diagnosing NEC, as well as suggest a possible therapeutic strategy.

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