[Nasopharyngeal carriage, antibiotic susceptibility and serotyping of Streptococcus pneumoniae and Haemophilus influenzae in children attending day care centers]. / Portage nasopharyngé, sensibilités et sérotypes de Streptococcus pneumoniae et Haemophilus influenzae chez les enfants de crèches.

UNLABELLED: The aim of this study was to investigate the nasal carriage of Streptococcus pneumoniae (SP) and Haemophilus influenzae (HI) in children. METHODS: Nasal samples were swabbed from children 3 months to 3 years of age, between December 2006 and April 2007, in 10 day-care centers in Dijon. RESULTS: Three hundred and eighty-five children, 22.7 ± 8.4 months, were included. All were vaccinated against H1 and 92% had received at least one dose of PCV7 vaccine. HI colonization (55%) was associated with young age and concomitant pneumococcal carriage (52.4% vs. 39%). Amoxicillin/clavulanate and cefotaxime resistance rates were 17% and 0.5%. Pneumococcal carriage (48%) was increased in case of prior hospitalization. The rate of PDSP, 50%, was increased in case of recent infection (91% vs. 81%), previous antibiotherapy (64% vs. 41%), and decreased if PCV7 was completed (40.2% vs. 61,8%). There was no resistance to amoxicillin. The erythromycin resistance rate was 50.5%. 15% of the strains were vaccinal serotypes. Thirty-six and 41% of the strains were related and non-related to vaccine serotypes. Twenty-four and 11.6% of the strains were serotypes 19A and 6A respectively. CONCLUSION: Over the last 10 years the global antibiotic resistance in children decreased for SP (22.9%) but nasal colonization remained stable due to the increase of some serotypes, such as 19A, most often resistant to antibiotics. The vaccine effectiveness against HI is optimal since no HIb serotypes were detected; resistance to betalactam is currently due equally to enzymatic mechanism and alteration of protein binding penicillin.

[Malignancy risk and Wiedemann-Beckwith syndrome: what follow-up to provide?]. / Risque tumoral et syndrome de Wiedemann-Beckwith: quelle surveillance proposer?

Wiedemann-Beckwith syndrome (WBS) is a syndrome of excessive growing with a high predisposition to developing embryologic tumours within the first years of life. This risk is evaluated between 7.5 and 10%; it varies with the mechanisms of mutations involved. These take place in two distinct domains of 11p15, which are under parental printing. Emerging techniques of cytogenetic and molecular biology now have shown correlations between genotypes and phenotypes, and can identify the 30% of WBS who are especially at risk of developing tumours. A specific follow-up, integrating the specificity of developing tumours of each 11p15 mutations involved, is now proposed to patients with WBS.