Plasmid-Mediated AmpC β-Lactamase and Underestimation of Extended-Spectrum β-Lactamase in Cefepime-Susceptible Elevated-Ceftazidime-MIC Enterobacteriaceae Isolates.

Abstract

Phenotypic detection of extended-spectrum β-lactamase (ESBL) is important for public health and infection control; however, plasmid-mediated AmpC β-lactamases (pAmpCs) can interfere with the ESBL phenotyping. We focused on Enterobacteriaceae strains that were susceptible to cefepime but had a mildly elevated minimum inhibitory concentration (MIC) of ceftazidime and studied the effect of pAmpC on the ESBL phenotyping in this population. Genotyping of ESBL and pAmpC was performed on 528 clinical isolates of Escherichia coli, Klebsiella spp., and Proteus spp. with a ceftazidime MIC of ≥2 μg/mL and cefepime MIC≤8 μg/mL; these isolates were collected at Nagasaki University Hospital from January 2005 to March 2011. In this sample, 145 isolates (27.5%) tested positive for pAmpC (pAmpC group). The concordance rates of phenotypic and genotypic detection of ESBLs were 69.2% in the pAmpC group and 88.8% in the non-pAmpC group (P=0.04). pAmpC was more commonly detected in isolates with non-CTX-M genes (5/53, 9.4%) than in isolates with CTX-M genes (8/121, 6.6%). Our data suggest that the presence of pAmpC increases the false negative detection of ESBL. When ESBL phenotyping is used, the underestimation of the prevalence of ESBL producers should be taken into account.