High concentrations of calcitonin-like immunoreactivity have been found in the blood of patients with various extrathyroid diseases. By means of a monoclonal immunoradiometric assay for calcitonin precursors, we have measured serum concentrations of procalcitonin in patients with various bacterial and viral infections. 79 children (newborn to age 12 years) in hospital with suspected infections were investigated prospectively. 19 patients with severe bacterial infections had very high serum concentrations of procalcitonin at diagnosis (range 6-53 ng/mL) in comparison with 21 children found to have no signs of infection (baseline concentrations < 0.1 ng/mL). Serum procalcitonin values decreased rapidly during antibiotic therapy. 11 patients with peripheral bacterial colonisation or local infections without invasive sepsis and 18 (86%) of 21 patients with viral infections had concentrations within or slightly above the normal range (0.1-1.5 ng/mL). Among 9 severely burned patients studied in an intensive care unit, the post-traumatic course of procalcitonin concentrations (range 0.1-120 ng/mL) was closely related to infectious complications and acute septic episodes. Concentrations of mature calcitonin were normal in all subjects, whatever procalcitonin concentrations were found. Concentrations of a substance immunologically identical to procalcitonin are raised during septic conditions. Serum concentrations seem to be correlated with the severity of microbial invasion.

We found large differences in NI frequency and microbial epidemiology in this European study. Viruses were the main pathogens in general pediatrics units. Catheter-related sepsis and CNS were frequent in newborns. A high frequency of multiresistant bacteria was observed in some units. Clinical monitoring of NIs and bacterial resistance profiles are required in all pediatric units.

We developed a simple, specific, and sensitive two-multiplex-PCR assay that enabled the detection of all known group B streptococcal (GBS) capsular polysaccharides. This test is well adapted for GBS capsular polysaccharide typing in large-scale epidemiological studies.

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The aim of this prospective study of a population of children (age, 2-15 years) hospitalized for severe asthma was to test them for acute infection due to Mycoplasma pneumoniae and acute infection due to Chlamydia pneumoniae. Of 119 patients with previously diagnosed asthma, acute M. pneumoniae infection was found in 24 (20%) and C. pneumoniae infection was found in 4 (3.4%) of the patients during the current exacerbation. Of 51 patients experiencing their first asthma attack, acute M. pneumoniae infection was proven in 26 (50%) of the patients (P<.01) and C. pneumoniae in 4 (8.3%). In the control group of 152 children with stable asthma or rhinitis, 8 (5.2%) had M. pneumoniae infection (P<.005). Of the 29 patients experiencing their first asthma attack and infected with M. pneumoniae or C. pneumoniae, 18 (62%) had asthma recurrences but only 6 (27%) of the 22 patients who did not have such infections had asthma recurrences (P<.05). M. pneumoniae may play a role in the onset of asthma in predisposed children and could be a trigger for recurrent wheezing.

We measured the plasma procalcitonin levels in 59 children who were admitted to the hospital because of bacterial or viral meningitis. Eighteen children with acute bacterial meningitis had elevated procalcitonin levels (mean level, 54.5 micrograms/L; range, 4.8-110 micrograms/L). The procalcitonin levels in 41 children with viral meningitis were low (mean level, 0.32 micrograms/L; range, 0-1.7 micrograms/L; P < .0001). Assay of cerebrospinal fluid (CSF) cells and proteins and serum C-reactive protein showed a zone of overlapping values between the two groups. Procalcitonin was not produced in CSF. Plasma procalcitonin levels decreased rapidly during antibiotic therapy. These data suggest that the measurement of plasma procalcitonin might be of value in the differential diagnosis of meningitis due to either bacteria or viruses.

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Clinical features and molecular characterization of 109 group B streptococci causing neonatal invasive infections were determined over an 18-month period in France. Sixtyfour percent of the strains were from late-onset infections, and 75% were capsular type III. The hypervirulent clone ST-17 was recovered in 80% of meningitis cases. G roup B Streptococcus (GBS)is the leading cause of infectious illness among newborns. Invasive infections in neonates can result in pneumonia, sepsis, or meningitis. Early-onset disease (EOD) occurs within the fi rst week. Lateonset disease (LOD) occurs after the fi rst week and accounts for most meningitis cases and deaths (1). Because recommendations for intrapartum antibioprophylaxis (IAP) for mothers in labor at risk for GBS infection have been widely implemented in many countries, the incidence of EOD has declined to <1/1,000 births, but the incidence of LOD has remained unchanged (2). To date, 10 capsular serotypes have been described (Ia, Ib, and II-IX). Among these, serotype III is of particular importance because it is responsible for a substantial proportion of EOD and most cases of . Different studies have suggested that most neonatal invasive diseases and almost all cases of meningitis are caused by a limited number of strains belonging to a homogeneous serotype III clone. This clone is defi ned by multilocus sequence typing (MLST) analyses as ST-17, the so-called highly virulent clone (4-8). However, data available in Europe are limited regarding the distribution of GBS genotypes among invasive isolates recovered from neonates.We describe clinical characteristics, capsular type, and MLST allelic and antimicrobial drug-susceptibility profi les of 109 nonredundant GBS isolates that caused neonatal invasive infections. These isolates were collected during an active surveillance performed in France from May 2006 through December 2007. The StudyClinical data on 109 infants up to 4 months of age were analyzed. Sepsis was defi ned as GBS bacteremia in the presence of consistent clinical signs and symptoms. Meningitis was diagnosed if GBS was recovered from cerebrospinal fl uid. GBS isolates were identifi ed by using a commercial Lancefi eld group-specifi c latex agglutination test. Capsular typing was performed by a multiplex PCR as described (9), and the hypervirulent ST-17 clone was detected by real-time PCR, as reported (6). Susceptibility testing, antibiograms, and MICs were performed according to Clinical and Laboratory Standards Institute recommendations (www.clsi.org). Antimicrobial drug-resistance genes were detected by using the multiplex PCR as described (10). Statistical analysis was performed according to the Fisher exact and χ 2 tests. A p value of <0.05 was used as the threshold for statistical signifi cance.We studied 109 GBS strains responsible for neonatal invasive infections; 36% (n = 39) and 64% (n = 70) were responsible for EOD and LOD, respectively (Table). Eighty percent of EOD cases occurred during the fi rst 24 hours after birth, with a male:female rati...