125 – 0.25 0.25 – 0.5 0.064 – 0.125 CTX-M-15+ CIT (n = 1) 120 min and 24 h *peaks m/z: 476.5, 498.5, 520.5 and 542.5 Da. A synthesis of the results showing the species, resistance mechanism and MIC range in the test panel and validation panel in relation to the results in the hydrolysis assay based on ertapenem. Pseudomonas aeruginosa (n = 25) Six out of elevenVIM producing P. aeruginosa, as well as the IMP-14-producing isolate tested, hydrolysed ertapenem after 120 minutes of incubation with the specific ertapenem hydrolysis peak pattern. The hydrolysis was fully inhibited in the presence of DPA in all cases. Ertapenem was not hydrolysed by the non-carbapenemase producing (no carbapenemase

confirmed genetically find more or phenotypically), carbapenem resistant, P. aeruginosa isolates (n = 10). Of the 4 P. aeruginosa isolates included in the validation panel (three VIM-1 and one

VIM-2) were correctly assigned as carbapenemase producers (both VIM-1). The carbapenemase production was inhibited Angiogenesis inhibitor by DPA both for VIM and IMP positive strains. Prolonged incubation (24 h) did not reveal any signs of hydrolysis in the strains tested negative after 120 min incubation (one VIM-1 and one VIM-2). There was no linkage between VIM-type and hydrolysis results. A summary of the results is presented in Table 1. Other species (Acinetobacter baumannii (n = 4), Escherichia coli (n = 3) None of the 4 Acinetobacter baumannii group isolates(OXA-23 like (n = 2), OXA-24-like (n = 1) and OXA-58 like (n = 1)) included in the validation panel hydrolysed ertapenem within 120 min incubation. All Teicoplanin isolates, however, displayed the specific pattern of ertapenem hydrolysis after a prolonged incubation (24 h). The two isolates of E. coli only producing a classical selleck compound ESBL-enzyme (two CTX-M-1 group and one CTX-M-1 group plus CIT-group plasmid mediated AmpC) did not hydrolyse ertapenem at any time point. The OXA-48 positive isolate of E. coli did not hydrolyse ertapenem

within 2 h, but prolonged incubation (24 h) revealed hydrolysis. A summary of the results is presented in Table 1. Discussion The drastic increase of isolates with the ability to produce carbapenemases in Enterobacteriacae, Acinetobacter spp. and P. aeruginosa rapidly challenges the treatment concept of severely ill patients [1]. Whether the carbapenem resistance is due to carbapenemase production or other mechanisms is considered important for infection control teams. Molecular methods are available for the verification of the genes responsible for carbapenemase production but have the limitation of not detecting new mechanisms [9–11]. The phenotypic assays so far on the market have problems with the time to result, isolates with low expression of the carbapenemase genes and that specific inhibitors are not available for several enzymes [2].