BMC infectious diseases · 2014
An outbreak of extremely drug-resistant Pseudomonas aeruginosa in a tertiary care pediatric hospital in Italy.
СтатьяНазвание и аннотация: Перевод в очереди
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Ciofi Degli Atti Marta, Bernaschi Paola, Carletti Michaela, Luzzi Ida, García-Fernández Aurora, Bertaina Alice, Sisto Annamaria, Locatelli Franco, Raponi Massimiliano
Аннотация
BACKGROUND: Extensively drug-resistant Pseudomonas aeruginosa (XDR-PA) isolates are susceptible to only one or two classes of antibiotics. In 2011-2012, we investigated an outbreak of XDR-PA affecting children with onco-hematological diseases.
METHODS: Outbreak investigation included ascertainment of cases, tracing of intestinal carriers and environmental surveillance. Contact precautions were adopted for patients with infection or colonization. Isolates were tested for antimicrobial susceptibility; phenotypic confirmation of carbapenemase production was performed, and carbapenemase genes were tested by multiplex polymerase-chain-reaction (PCR). Genotypes were determined by pulsed-field gel electrophoresis (PFGE).
RESULTS: XDR-PA was isolated from 27 patients; 12 had bacteremia, 6 other infections and 9 were colonized. Severe neutropenia was significantly associated with bacteremia. Bloodstream-infection mortality rate was 67%. All isolates were resistant to carbapenems, cephalosporins and penicillins + β-lactamase inhibitors. Isolates were susceptible only to colistin in 22 patients, to colistin and amikacin in 4, and to ciprofloxacin and colistin in 1. PFGE results identified 6 subtypes of a single genotype, associated with clusters of cases, and 4 sporadic genotypes. Two sporadic isolates were metallo-β-lactamase producers, negative to PCR. All other isolates were metallo-β-lactamase producers due to the presence of a VIM carbapenemase. Incidence of XDR-PA infections decreased from 0.72 cases/1,000 inpatient-days in March 2011-March 2012, to 0.34/1,000 in April-December 2012, after implementation of active finding of intestinal carriers on all onco-hematological inpatients.
CONCLUSIONS: Control measures targeting intestinal carriers are crucial in limiting in-hospital transmission of XDR-PA polyclonal strains, protecting more vulnerable patients, such as severely neutropenic children, from developing clinical infections.
METHODS: Outbreak investigation included ascertainment of cases, tracing of intestinal carriers and environmental surveillance. Contact precautions were adopted for patients with infection or colonization. Isolates were tested for antimicrobial susceptibility; phenotypic confirmation of carbapenemase production was performed, and carbapenemase genes were tested by multiplex polymerase-chain-reaction (PCR). Genotypes were determined by pulsed-field gel electrophoresis (PFGE).
RESULTS: XDR-PA was isolated from 27 patients; 12 had bacteremia, 6 other infections and 9 were colonized. Severe neutropenia was significantly associated with bacteremia. Bloodstream-infection mortality rate was 67%. All isolates were resistant to carbapenems, cephalosporins and penicillins + β-lactamase inhibitors. Isolates were susceptible only to colistin in 22 patients, to colistin and amikacin in 4, and to ciprofloxacin and colistin in 1. PFGE results identified 6 subtypes of a single genotype, associated with clusters of cases, and 4 sporadic genotypes. Two sporadic isolates were metallo-β-lactamase producers, negative to PCR. All other isolates were metallo-β-lactamase producers due to the presence of a VIM carbapenemase. Incidence of XDR-PA infections decreased from 0.72 cases/1,000 inpatient-days in March 2011-March 2012, to 0.34/1,000 in April-December 2012, after implementation of active finding of intestinal carriers on all onco-hematological inpatients.
CONCLUSIONS: Control measures targeting intestinal carriers are crucial in limiting in-hospital transmission of XDR-PA polyclonal strains, protecting more vulnerable patients, such as severely neutropenic children, from developing clinical infections.