Multidrug-resistant Acinetobacter baumannii in an intensive care unit: the never ending fight
Abstract number: P1306
Carretto E., Barbarini D., Carnevale L., Amatu A., Grosini A., Iotti G., Marone P.
Objective:Acinetobacter baumannii is an important cause of nosocomial infections in many hospitals, most often in critically ill patients admitted to intensive care units (ICUs). After the first isolation (April 2008) of a multi-drug resistant (MDR) A. baumannii strain (susceptible only to ampicillin-sulbactam and colistin) in an ICU of our Institution, we performed an active surveillance study up to July 2009. The results of the molecular typing of the strains collected and the molecular analysis of the mechanisms of carbapenems resistance are showed.
Methods: all the Acinetobacter strains showing a MDR phenotype were further characterized as belonging to the genomospecies 2/13 using the criteria of Gerner-Smidt et al. (JCM, 1991:277). We collected a single isolate for each patient, irrespective of the site of isolation. Susceptibility testing using the standardized disk-diffusion method (CLSI criteria) and E-test were performed. The molecular typing was performed using the rep-PCR Diversilab Microbial Typing System (bioMériéux, France). In the experiments the EU-AFLP type strains were included as control (Dijkshoorn et al., 1996:1519). The mechanisms of carbapenems resistance were investigated initially using a phenotypic screening to detect metallo-b-lactamases (MBL). The MBL-negative strains were subsequently investigated using a multiplex PCR to detect genes encoding the OXA carbapenemases prevalent in Acinetobacter species, using the PCR protocol described in Woodford et al.(Int. J. Antimicrob. Agents 2006:351).
Results: 41 different MDR Acinetobacter strains belonging to genomospecies 2/13 were collected. The microorganism was recognized to be endemic, with 23 patients per month colonized or infected. During the study period we documented two large outbreaks (June 2008, 6 patients and March 2009, 11 patients involved). The rep-PCR allowed us to demonstrate two major clones. The first one comprised different isolates collected in the first 6 months of the study; this clone was then replaced by another one, strictly related to the EU clone II (from July 2008 to July 2009). None of our isolates was MBL positive; the wide majority of our strains carried the OXA51/OXA58 carbapenemases.
Conclusions: our study confirms the wide circulation of the A. baumannii EU clone II, that replaced another lineage not linked to other EU clones. As expected, the OXA51/OXA58 profile was most commonly involved in the high-level resistance to carbapenems of our strains.
|Session name:||Abstracts 20th European Congress of Clinical Microbiology and Infectious Diseases|
|Location:||Vienna, Austria, 10 - 13 April 2010|
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