Sepsis is a leading cause of mortality and morbidity in neonates. Presenting clinical symptoms are unspecific. Sensitivity and positive predictive value of biomarkers at onset of symptoms are suboptimal. Clinical suspicion therefore frequently leads to empirical antibiotic therapy in uninfected infants. The incidence of culture confirmed early-onset sepsis is rather low, around 0.4–0.8/1000 term infants in high-income countries. Six to 16 times more infants receive therapy for culture-negative sepsis in the absence of a positive blood culture. Thus, culture-negative sepsis contributes to high antibiotic consumption in neonatal units. Antibiotics may be life-saving for the few infants who are truly infected. However, overuse of broad-spectrum antibiotics increases colonization with antibiotic resistant bacteria. Antibiotic therapy also induces perturbations of the non-resilient early life microbiota with potentially long lasting negative impact on the individual‘s own health. Currently there is no uniform consensus definition for neonatal sepsis. This leads to variations in management. Two factors may reduce the number of culture-negative sepsis cases. First, obtaining adequate blood cultures (0.5–1 mL) at symptom onset is mandatory. Unless there is a strong clinical or biochemical indication to prolong antibiotics physician need to trust the culture results and to stop antibiotics for suspected sepsis within 36–48 h. Secondly, an international robust and pragmatic neonatal sepsis definition is urgently needed. Neonatal sepsis is a dynamic condition. Rigorous evaluation of clinical symptoms (“organ dysfunction”) over 36–48 h in combination with appropriately selected biomarkers (“dysregulated host response”) may be used to support or refute a sepsis diagnosis.

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We studied the outcome of pneumococcal meningitis in 83 children who were admitted to a referral hospital and whose meningitis was diagnosed between 1970 and 1994. The median age of the children was 8 months. The most frequently isolated capsular serotypes and/or serogroups of Streptococcus pneumoniae were 6, 14, 18, 19, and 23. Twenty-nine children (35%) were referred by other hospitals. A mortality rate of 17% (primary referrals, 7%; secondary referrals, 35%) was observed. At discharge, 25 survivors (36%) had sequelae: hearing loss (> or = 30 dB) in 19% and neurological sequelae in 25%. During admission, the presence of coma, respiratory distress, shock, a cerebrospinal fluid (CSF) protein level of > or = 2.5 g/L, a peripheral white blood cell count of < 5 x 10(9)/L, and a serum sodium level of < 135 mmol/L were associated with mortality. Sequelae were associated with the presence of coma and a CSF glucose level of < 0.6 mmol/L. We conclude that the mortality rate of pneumococcal meningitis is lower among children than among adults. Children often die of neurological sequelae, while adults frequently die of cardiorespiratory failure due to underlying diseases. For children, coma, respiratory distress, and shock during admission were the clinical findings with the strongest predictive value for sequelae or death.

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Small for gestational age and prolonged hospitalization were associated with CoNS sepsis. The icaA gene is a predictor for biofilm formation in S. epidermidis, but not in other species. Multiresistance is not associated with clonality.