Abstract
Antibiotic resistance (AR) phenotypes and acquired resistance determinants (ARDs) detected by in silico analysis of genome sequences were examined in 55 Shiga toxin-producing Escherichia coli (STEC) isolates representing diverse serotypes recovered from surfaces waters and sediments in a mixed use urban/agricultural landscape in British Columbia, Canada. The isolates displayed decreased susceptibility to florfenicol (65.5%), chloramphenicol (7.3%), tetracycline (52.7%), ampicillin (49.1%), streptomycin (34.5%), kanamycin (20.0%), gentamycin (10.9%), amikacin (1.8%), amoxicillin/clavulanic acid (21.8%), ceftiofur (18.2%), ceftriaxone (3.6%), trimethoprim-sulfamethoxazole (12.7%), and cefoxitin (3.6%). All surface water and sediment isolates were susceptible to ciprofloxacin, nalidixic acid, ertapenem, imipenem and meropenem. Eight isolates (14.6%) were multidrug resistant. ARDs conferring resistance to phenicols (floR), trimethoprim (dfrA), sulfonamides (sul1/2), tetracyclines (tetA/B), and aminoglycosides (aadA and aph) were detected. Additionally, narrow-spectrum β-lactamase blaTEM-1b and extended-spectrum AmpC β-lactamase (cephalosporinase) blaCMY-2 were detected in the genomes, as were replicons from plasmid incompatibility groups IncFII, IncB/O/K/Z, IncQ1, IncX1, IncY and Col156. A comparison with surveillance data revealed that AR phenotypes and ARDs were comparable to those reported in generic E. coli from food animals. Aquatic environments in the region are potential reservoirs for the maintenance and transmission of antibiotic resistant STEC, associated ARDs and their plasmids.
Highlights
The Shiga toxigenic Escherichia coli (STEC) pathotype is characterized by the production of one or more cytotoxic Shiga-like toxins, small proteins encoded by a temperate lambdoid phage on the main chromosome
We report on Antibiotic resistance (AR) phenotypes and associated acquired resistance determinants (ARDs) in Shiga toxin-producing Escherichia coli (STEC) recovered from surface waters in the Fraser
Four of the multidrug resistant (MDR) isolates were from serogroup O111 and the most complex phenotype was found in isolate 385-O111:NM, which was resistant to nine antibiotics
Summary
The Shiga toxigenic Escherichia coli (STEC) pathotype is characterized by the production of one or more cytotoxic Shiga-like toxins, small proteins encoded by a temperate lambdoid phage on the main chromosome. Infection with STEC causes diseases of variable severity, ranging from comparatively mild to acute hemorrhagic diarrhea, and potentially 4.0/). Foodborne outbreaks have been reported with increasing frequency since two epidemiologically significant disease clusters were definitively associated with the consumption of red meat in the US in 1983 [1], and STEC are recognized as significant water and foodborne threats to global public health [2,3,4]. A recent food-borne source attribution analysis performed using disease and surveillance data from several countries showed that foods from a broad range of categories are implicated in outbreaks [5]. The advisability of antibiotic therapies for the management of STEC infections is the subject of enduring debate due to reports of antibiotic-induced toxin release from dead cells or by the induction of Shiga toxin-converting prophage [6]. The fluoroquinolone antibiotic ciprofloxacin was shown to cause the induction of bacteriophage and
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