Mechanisms of resistance to imipenem and extended-spectrum cephalosporins in Acinetobacter baumannii clinical isolates
Abstract number: P788
Objectives: Nosocomial infections caused by multidrug-resistant (MDR) Acinetobacter baumannii have been increasing in recent years. In order to elucidate the current resistance mechanisms, 27 A. baumannii clinical isolates from a regional hospital in Taiwan in 2009 were examined in this study.
Methods: E-test analysis was employed to test the minimum inhibitory concentrations (MIC) to these isolates of 8 antibiotics. Primers specific for resistance genes (blaOXA-23, blaOXA-24, blaOXA-40, blaOXA-54, blaOXA-58, blaOXA-51, blaADC, blaIMP-1, blaVIM-1) were designed for PCR amplification and sequence identification. The upstream regions of the resistance genes were tested for ISAba1 as well.
Results:A. baumannii isolates showed the highest rate of susceptibility (100%) to colistin, followed by tigecycline (63.0%), ampicillin/sulbactam (55.6%), imipenem (51.9%), amikacin (30.0%), ceftazidime (22.2%), gentamicin (18.5%), and ceftriaxone (0%). PCR amplification and sequence analysis identified blaOXA-23 in 9 isolates, blaOXA-51-like in 22 isolates, blaOXA-58 in 2 isolates and blaADC-25 in all isolates. Most blaOXA-51-like resistance genes were similar to blaOXA-138. The upstream ISAba1 was found in 6 isolates with blaOXA-23 and 5 isolates with blaOXA-51-like and offered these 11 isolates with full resistance to imipenem (all MIC >32) (Table 1). The upstream ISAba1 was also found in 21 isolates with blaADC-25 and offered these isolates with full resistance to both ceftriaxone and ceftazidime. In the opposite, all other 6 isolates carried blaADC-25 without upstream ISAba1 showed intermediately resistant to ceftriaxone but susceptible to ceftazidime. Isolates with combination of upstream ISAba1 and OXA-type b-lactamases or Acinetobacter-derived cephalosporinases had significant full resistant ability to imipenem or extended-spectrum cephalosporins than those without such combination (both p < 0.001). None of isolates carried blaIMP-1. Therefore, the resistant mechanisms were quite different from previous study in which the major resistant gene contributing to imipenem resistance in A. baumannii clinical isolates in 2006 was metallo-b-lactamase blaIMP-1.
Conclusion: Resistant mechanisms of A. baumannii changed rapidly. Current results showed the upstream ISAba1 combined with OXA-type b-lactamases or Acinetobacter-derived cephalosporinases offered A. baumannii isolates in 2009 with full resistance to imipenem or extended-spectrum cephalosporins, individually.
Table 1. Imipenem minimum inhibitory concentrations (MICs) of A. baumannii with different carbapenemase genes and insertion sequences
|Session name:||Abstracts 20th European Congress of Clinical Microbiology and Infectious Diseases|
|Location:||Vienna, Austria, 10 - 13 April 2010|
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