First validation of D69C MASTDISCS ID AmpC detection discs

There is an increase in the prevalence of resistance to extended-spectrum cephalosporins among members of the Enterobacteriaceae in both the hospital and community setting. Such cephalosporin resistance is often mediated by the production of extended-spectrum beta-lactamases (ESBLs). It may also be due to AmpC cephalosporinase produced as a result of the acquisition of a plasmid-mediated ampC gene in Escherichia coli and Klebsiella pneumoniae, or alternatively the hyper-production of a chromosomally encoded AmpC enzyme in E. coli which is otherwise expressed at low levels.1

AmpC beta-lactamases are also present on the chromosome of many members of the Enterobacteriaceae, including Enterobacter cloacae and Citrobacter freundii, and can be induced or expressed at high levels due to a mutation that leads to depression of the chromosomal ampC gene (Fig 1). Enterobacteriaceae can also be co-producers of AmpC and ESBL enzymes, although this is rare.
 Many laboratories routinely test for ESBLs but do not test for AmpC resistance mechanisms2 because the tests available are time-consuming or difficult to perform and there is no approved standard method for their detection. However, there is a need for a simple diagnostic test for the detection
of these enzymes as chromosomal ampC genes are being disseminated on plasmids, mirroring the early dispersion and evolution of ESBLs.3

Such beta-lactamases can be distinguished from ESBLs by their ability to hydrolyse cephamycins and oxyiminocephalosporins, resulting in restricted therapeutic options and treatment failure.2 Kohner et al.3 described the proportion of ESBLs, AmpCs and concomitant ESBL and ampC genes typically found in clinical isolates (Fig 2).