Molecular epidemiology of carbapenem-resistant Acinetobacter baumanniiin Istria county, Croatia (CROSBI ID 634114)
Prilog sa skupa u zborniku | sažetak izlaganja sa skupa | međunarodna recenzija
Podaci o odgovornosti
Vranić-Ladavac, Mirna ; Barišić, Nada ; Ladavac, Ranko ; Karčić, Natali ; Stojanović, Aleksandar ; Ferenčić, Antun ; Vraneš ; Jasmina ; Krilanović, Marija ; Frančula-Zaninović, Sonja ; Bedenić, Branka
engleski
Molecular epidemiology of carbapenem-resistant Acinetobacter baumanniiin Istria county, Croatia
Background: Carbapenem resistance in Acinetobacter baumannii can be mediated by production of carbapenemases of class A (KPC), class B (IMP, VIM, SIM, NDM) and class D. Carbapenem-resistant A. baumannii was rare in Istria until 2013. Since 2013 emergence of isolates with high level resistance carbapenems A.baumannii was observed in General Hospital (GH) in Pula. This prompted us to analyze the mechanisms of carbapenem-resistance and molecular epidemiology of isolates resistant to imipenem and meropenem. Material/methods: In total 27 carbapenem- resistant strains were analyzed. The isolates were collected from June 2013 till June 2014 from different clinical specimens and hospital wards. Antimicrobial susceptibility testing was performed by broth microdilution method. PCR was used to detect genes encoding carbapenemases of class A, B (MBL-metallo-β- lactamases) and D (CHDL) and extended-spectrum β-lactamases (ESBL). Epidemiologic typing was performed by determination of sequence groups (SG). Plasmid incompatibility group was determined by PCR-based replicon typing (PBRT). Results: Urinary tract was the most important source of the isolates (37%), followed by respiratory tract (29%), wounds (15%), tissue samples (11%), blood cultures (4%) and pus (4%). Most strains originated from intensive care units (48%), surgery (41%) and internal ward (11%). The strains were uniformly resistant to ESC (extended-spectrum cephalosporins), piperacillin/tazobactam, ciprofloxacin and gentamicin, but uniformly susceptible to ampicillin/sulbactam, tigecycline and colistin. All strains were phenotypically for MBLs but negative for ESBLs. They all harboured acquired CHDL and two were additionaly positive for VIM-MBL. Out of 27 strains, 20 harboured blaOXA-24-like, 4 blaOXA- 58-like and 3 blaOXA-23-like genes. BlaOXA-23 and blaOXA-51 genes were preeceded by ISAba1 while blaOXA-58 were associated with ISAba3. Strains were allocated to SG 1 (ICL II). The plasmids encoding OXA-23 belonged to Inc group 2. OXA-24/40 positive strains harboured plasmids belonging to group 6 (aci6) Conclusions: The previous study conducted in 2009-2010 showed that reduced susceptibility to carbapenems in GH Pula was only associated with upregulation of intrinsic OXA-51 β-lactamase by ISAba1 located upstream of blaOXA-51 gene. From 2013 the strains with high level of resistance to carbapenems were observed and molecular analysis revealed the resistance to be due to the production of acquired oxacillinases (class D) or MBLs. Such isolates pose serious therapeutic problem because of their extensive drug resistant phenotype.
Acinetobacter baumannii; carbapenems; resistance; oxacillinases
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Podaci o prilogu
P0248-x.
2016.
objavljeno
Podaci o matičnoj publikaciji
Podaci o skupu
26th European congress of Clinical Microbiology and Infectious Diseases
poster
09.04.2016-12.04.2016
Amsterdam, Nizozemska