High Prevalence and Mechanism Associated With Extended Spectrum Beta-Lactamase-Positive Phenotype in .

In this study, we reported the prevalence and mechanism associated with the extended-spectrum beta-lactamase (ESBL)-positive phenotype in isolated from patients and fish. Using the inhibition zone enhancement test, 20 (95.2%) of the 21 patient strains and 8 (57.1%) of the 14 fish strains were tested ESBL-positive. However, ESBL genes, including SHV, TEM, CTX-M, GES, and PER, were not detected in all of these 28 isolates. No ESBL gene could be detected in either the complete genome of HLHK9 or the draft genome of PW3643. PCR and DNA sequencing revealed that all the 35 isolates (showing both ESBL-positive and ESBL-negative phenotypes) were positive for the gene. When the AmpC deletion mutant, HLHK9, was subject to the zone enhancement test, the difference of zone size between ceftazidime/clavulanate and ceftazidime was less than 5 mm. When boronic acid was added to the antibiotic disks, none of the 28 "ESBL-positive" isolates showed a ≥ 5 mm enhancement of inhibition zone size diameter between ceftazidime/clavulanate and ceftazidime and between cefotaxime/clavulanate and cefotaxime. A high prevalence (80%) of ESBL-positive phenotype is present in . Overall, our results suggested that the ESBL-positive phenotype in results from the expression of the intrinsic AmpC beta-lactamase. Confirmatory tests should be performed before issuing laboratory reports for isolates that are tested ESBL-positive by disk diffusion clavulanate inhibition test.