Clinical Laboratory Detection of AmpC beta-Lactamase

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Abstract and Introduction

Abstract


Plasmid-mediated AmpC-producing Escherichia coli and Klebsiella pneumoniae have been associated with poor clinical outcomes, but they are not readily identified in hospital microbiology laboratories. We tested 753 gram-negative bloodstream isolates for AmpC by using the EDTA disk test and the modified Hodge test (n = 172) and the modified Hodge test alone (n = 581). The 30-day mortality for the AmpC group was 9% (2/23) and was 6% (3/51) for the control group. The clinical response was similar: afebrile on day 2 (AmpC group, 16/23 [70%]; control group, 32/45 [71%]) and on day 4 (AmpC group, 19/22 [86%]; control group, 37/44 [84%]). Patients with isolates in the AmpC group were more likely to be in an intensive care unit at the time of the positive blood culture (P = .01) and more likely to be intubated (P = .05) than patients with isolates in the control group. Effective antibiotic treatment within the first 48 hours was given to 47 (92%) of 51 patients with isolates in the control group but to only 14 (61%) of 23 patients with isolates in the AmpC group (P = .001). The modified Hodge test and the EDTA disk test did not identify patients at risk for a poor outcome from AmpC-producing bacterial infections.

Introduction


Escherichia coli and Klebsiella pneumoniae containing plasmid-mediated AmpC β-lactamases have been associated with treatment failure in a case-control study of bacteremia compared with organisms without plasmid-mediated AmpC β-lactamases. Pai et al reported a treatment failure rate of almost 52% for AmpC-containing K pneumoniae bloodstream isolates at 72 hours.

Unfortunately, plasmid-mediated AmpC β-lactamases are not reliably detected by standard susceptibility testing methods in the clinical microbiology laboratory. Black et al described the EDTA disk test, and Yong et al described the "modified" Hodge test for detecting the presence of AmpC β-lactamases that could be carried out routinely in a busy clinical laboratory. A similar test using boronic acid was described by Coudron. However, none of these tests can distinguish plasmid-mediated hyperproduction of AmpC from derepressed chromosomal or any other mechanism of overproduction of an AmpC β-lactamase. Intuitively, we believe the mechanism of AmpC overproduction should not matter for clinical outcome because, either way, such organisms should be resistant to all extended-spectrum cephalosporins, although perhaps not to the advanced-spectrum cephalosporins, cefepime and cefpirome. We compared the clinical outcome for 26 (23 evaluable) patients with bacteremic gram-negative isolates with overproduction of AmpC as measured by the modified Hodge test with 52 (51 evaluable) control patients whose isolates did not produce AmpC.

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