When should clinicians suspect group A streptococcus empyema in children? A multicentre case-control study in French tertiary care centres.

BACKGROUND: The incidence of invasive group A streptococcus (GAS) infections is increasing worldwide, whereas there has been a dramatic decrease in pneumococcal invasive diseases. Few data describing GAS pleural empyema in children are available. OBJECTIVE: To describe the clinical and microbiological features, management and outcome of GAS pleural empyema in children and compare them with those of pneumococcal empyema. DESIGN, SETTING AND PATIENTS: Fifty children admitted for GAS pleural empyema between January 2006 and May 2013 to 8 hospitals participating in a national pneumonia survey were included in a descriptive study and matched by age and centre with 50 children with pneumococcal empyema. RESULTS: The median age of the children with GAS pleural empyema was 2 (range 0.1-7.6) years. Eighteen children (36%) had at least one risk factor for invasive GAS infection (corticosteroid use and/or current varicella). On admission, 37 patients (74%) had signs of circulatory failure, and 31 (62%) had a rash. GAS was isolated from 49/50 pleural fluid samples and from one blood culture. The commonest GAS genotype was emm1 (n=17/22). Two children died (4%). Children with GAS empyema presented more frequently with a rash (p<0.01), signs of circulatory failure (p=0.01) and respiratory disorders (p=0.02) and with low leucocyte levels (p=0.04) than children with pneumococcal empyema. Intensive care unit admissions (p<0.01), drainage procedures (p=0.04) and short-term complications (p=0.01) were also more frequent in patients with GAS empyema. CONCLUSIONS: Pleural empyema following varicella or presenting with rash, signs of circulatory failure and leucopenia may be due to GAS. These features should prompt the addition to treatment of an antitoxin drug, such as clindamycin.

Aucun n'est recommandé et ne remplace la désobstruction rhino-pharyngée.

Use of inhaled treatments in acute viral bronchiolitis in infants. Inhaled therapies are widely used by practitioners for treating acute viral bronchiolitis. Therefore, their efficacy has a low level of proof that does not sustain their use. Even if they need to be better studied in atopic infants, beta-2 agonists have no effect, excepted side effects. Anticholinergic drugs are not recommended. Adrenaline, despite some positive effects, is not recommended too. Corticosteroids are not useful, both for treating the acute problem and for preventing a possible post-viral asthma. Ribavirine, an antiviral agent, is reserved to very precise indications. At last, hypertonic saline, which has given some hopes, nowadays cumulates negative studies, and is no longer recommended. At all, in 2016, any inhaled treatment is recommended for treating acute viral bronchiolitis in infants..

Place des traitements inhalés dans la bronchiolite aiguë du nourrisson. Les traitements inhalés sont largement proposés en pratique clinique en cas de bronchiolite aiguë du nourrisson. Cependant, les niveaux de preuve d'efficacité sont en défaveur de ces traitements. Même s'ils méritent d'être mieux étudiés chez l'enfant atopique, les bêta-2-agonistes ne semblent pas avoir d'autres effets que latéraux. Les anticholinergiques ne sont pas recommandés. L'adrénaline, même si quelques effets positifs sont notés, non plus. Les corticoïdes ne sont utiles ni en aigu ni en prévention d'un potentiel asthme viral. La ribavirine, agent antiviral, est réservée à des indications très ciblées. Le sérum salé hypertonique, après avoir été un espoir, accumule les études négatives et n'est pas non plus indiqué. Au total, en 2016, aucun traitement inhalé n'est recommandé dans la bronchiolite aiguë du nourrisson.

ISPa46, a novel insertion sequence in the oprD porin gene of an imipenem-resistant Pseudomonas aeruginosa isolate from a cystic fibrosis patient in Marseille, France.

Clinical isolates of Pseudomonas aeruginosa exhibiting high-level resistance to carbapenems were recovered from a French patient with cystic fibrosis (CF) who had not received carbapenem therapy. This study was conducted to investigate the molecular mechanism conferring the carbapenem-resistant phenotype in clinical isolates of P. aeruginosa recovered from the same CF patient chronically colonised since 2005. Investigation of imipenem resistance of P. aeruginosa strain_02 isolated in May 2011 showed no carbapenemase activity. However, amplification and sequencing of the oprD porin gene revealed disruption of this gene by an insertion sequence (IS) element of 1337 bp that contained a novel transposase of 1227 bp (ISPa46) bordered by two terminal imperfect inverted repeats of 28 bp, which was associated with carbapenem resistance. Retrospective analysis of five additional strains of P. aeruginosa isolated before May 2011 from the same patient revealed that all isolates were likely to be the same clone by multilocus sequence typing analysis (ST540/551), but one of the five isolates was imipenem-susceptible. Although it was possible to demonstrate the presence of ISPa46 in all strains by PCR, this IS was transposed in the oprD gene only for imipenem-resistant isolates. Therefore, this study reports a novel IS element (ISPa46) in P. aeruginosa clinical isolates of a CF patient in Marseille, France, that was associated with carbapenem resistance and was selected in the absence of carbapenem treatment.