40 Chapter 3 The prevalence of AmpC rectal carriage over the four-year period is shown in Table 2. All AmpC-producing isolates were identified as E. coli. No AmpC producing Klebsiella spp were found. Eighteen of 19 (94.7%) of the pAmpC-producing isolates harboured blaCMY-2-like, one isolate blaDHA-like. The prevalence of 3rd generation cephalosporine resistant E. coli, based on growth on selective media in the evaluable cultures, and the amount of ESBL confirmed isolates are shown in Table 2 as well. Table 2. Prevalence of patients with AmpC-producing E. coli and distribution of pAmpC genes and cAmpC hyperproducers over the years. 2013 2014 2015 2016 Overall Total E.coli cultured on selective media (no. and %)1 43 (8.5%) 48 (8.6%) 41 (7.3%) 20 (3.9%) 152 (7.1%) Total AmpC isolates (no. and %)2 19(3.7%) 16(2.9%) 9(1.6%) 6(1.2%) 50(2.4%) Primary (no.) 18 14 9 6 47 Secondary (no.)2 1 2 0 0 3 AmpC genes (incl. secondary cases) blaCMY-2-like 7 6 2 3 18 blaDHA-like 0 0 0 1 1 cAmpC hyperproducers 11 10 7 2 31 Inconclusive4 1 Total ESBL isolates (no. and %)5 25 (4.9%) 29 (5.2%) 32 (5.7%) 13 (2.6%) 99 (4.7%) 1= Number of patients with E. coli rectal carriage based on selective media divided by the number of patients with evaluable cultures 2 = Number of patients with AmpC-producing E. coli rectal carriage divided by the number of patients with evaluable cultures 3 = Number of patients with isolates that were clonally related based on AFLP 4 = negative microarray results for pAmpC genes, but AmpC amplicon couldn’t be amplified 5 = Number of patients with ESBL-producing E. coli rectal carriage divided by the number of patients with evaluable cultures All but one (30 out of 31) of the isolates that were phenotypically AmpC producers and negative for pAmpC in the microarray, showed alterations in the promoter/attenuator
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