VIM-1 producing Enterobacter cloacae strains from Madrid, Spain: report from the SENTRY Antimicrobial Surveillance Program 2005
Abstract number: p1405
Deshpande L., Sader H., Tato M., Baquero F., Jones R., Canton R.
To characterize Enterobacteriaceae (ENT) strains with reduced susceptibility (S) to carbapenems (CARB) isolated in Madrid, Spain.
As part of the SENTRY Program bacterial isolates are S tested by reference CLSI methods against >25 antimicrobial agents. ENT isolates (except Proteus mirabilis and indole + Proteae) exhibiting MIC results at >=2 mg/L to imipenem (IMI) and meropenem (MER) were screened for metallo-beta-lactamases (MBL) and Bush-Jacoby-Medeiros group 2f carbapenemases by disk approximation (DA) and PCR. PCR amplicons were sequenced for epidemiological purposes as well as to reveal genetic context of resistance genes. Isolates were also typed by PFGE.
Two E. cloacae (ECL) strains (2700A and 726C) showed elevated CARB MIC values as well as resistance to all beta-lactams, except aztreonam (AZT) in strain 726C (Table 1). The strains were isolated in March 2005 (12 days apart) from bloodstream and respiratory tract infections of patients hospitalized in two distinct hospital units. The strains showed distinct antibiograms and PFGE patterns (Table 1). Both strains showed positive DA test results and PCR screens positive for blaVIM with a Class 1 integron of approximately 2.5 kb. Sequencing of integron from the index strain (726C) revealed blaVIM-1 along with aacA4 and aadA1 genes.
This is the first report of VIM-1-producing ECL from Spain. VIM-1 has been recently reported in ENT (K. pneumoniae and E. coli) from Barcelona, Spain. The finding of blaVIM-1 in two clonally unrelated strains emphasizes the mobility of these genes. Thus, MBL may be emerging as a significant, geographically diverse resistance mechanism among ENT in Spain. It is imperative to screen ENT isolates with modestly elevated (not resistant) MIC values of either IMI or MER for carbapapenamse production and to control the spread of this resistance mechanism in ENT isolates causing nosocomial infections
|Session name:||XXIst ISTH Congress|
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