République Tunisienne Ministère de l'Enseignement Supérieur et de la Recherche Scientifique

Dimanche 02 Juin 2024

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Article

First report of nosocomial infection caused by Klebsiella pneumoniae ST147 producing OXA-48 and VEB-8 b-lactamases in Tunisia 

OUERTANI Rym, LIMELETTE Anne, GUILLARD Thomas, BRASME Lucien, JRIDI Yahia, BARGUELLIL Farouk, EL SALABI Allaaeddin, DE CHAMPS Christophe, CHOUCHANI Chedly, 2016

Journal of Global Antimicrobial Resistance, 4, 53-56, Janvier 2016

Résumé

The aim of this study was to determine the origin of virulence and multiresistance of aKlebsiella pneumoniae isolate from an abdominal wound infection of a patient with a gunshot injury in the thoracoabdominal region. The isolate was identified using biochemical tests and PhoenixTM automated system and was confirmed by matrix-assisted laser desorption/ionisation time-of-flight mass spectrometry (MALDI-TOF/ MS). MICs of each antibiotic were determined by Etest. Screening for carbapenemase production was performed by themodified Hodge test and was confirmed by PCRamplification.Virulence factors were also studied. Plasmid replicon typing was used to classify Incompatibility (Inc) plasmids harbouring the resistance genes. The transferability of each plasmid was determined by conjugation using Escherichia coli J53. Finally, multilocus sequence typing (MLST) was performed to determine the ST of the strain. The bacterial isolate was identified as K. pneumoniae and was named KPM2, carrying entB, ybtS, mrkD and ycfM virulence genes, but it did not overexpress OqxAB. Isolate KPM2 belonged to ST147 and was classified as resistantto all ofthe testedantibioticswithMICs above the clinicalbreakpoints.These resistanceswere due to production of OXA-48, CMY-2, TEM-1, CTX-M-15 and VEB-8 b-lactamases. Genetic and molecular studies showedthat blaOXA-48was embedded intransposonTn1999.2 and was carried by a conjugative IncL/ M plasmid of ca. 60 kb; blaVEB-8 was harboured on a conjugative IncA/C plasmid of ca. 120 kb. This study confirmed that the resistance conferred by OXA-48 and VEB-8 contributed to the failure of antibiotic treatment and consequently death of the patient

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