In recent years, besides the widespread occurrence of extended-spectrum β-lactamase (ESBL)- and/or plasmid-mediated AmpC (pAmpC)-producing Enterobacteriaceae in both healthcare and community settings of humans, the third-generation cephalosporin (3GC)-resistant microbes have also been reported from companion animals worldwide. Here, we characterized ESBL- and/or pAmpC-producing Enterobacteriaceae clinical isolates from companion animals. Among the 487 clinical isolates mainly from urine of dogs and cats between May and September 2016, 104 non-repetitive isolates were resistant to the 3GC, and they consisted of 81 of 381 (21.3%) Escherichia coli, 21 of 50 (42.0%) Klebsiella pneumoniae, and 2 of 56 (3.6%) Proteus mirabilis isolates. In the 81 E. coli, the predominant bla genes were bla and bla (n = 15 each), followed by bla (n = 14), bla (n = 10), and bla (n = 5). In 21 K. pneumoniae, 10 bla gene types including bla (n = 4), bla (n = 4), and bla (n = 3) were found. The bla was identified in 2 P. mirabilis. Twenty-four of the 42 E. coli belonging to phylogroup B2 were O25b-ST131 clone, mostly associated with uropathogenic E. coli pathotype, and 22 isolates of this clone were identified as specific H30R subclone. High prevalence of the bla-harboring isolates were noted among the H30R/non-Rx lineage (13/19, 68.4%) (p < 0.05). The genetic environment of bla of most isolates of this lineage was identical to that of human isolates, but unique flanking genetic structures were also identified. Newly emerging virulent lineage B2-non-O25b-ST1193 was also confirmed in 5 isolates. The fosA3 and/or armA genes were detected in E. coli and K. pneumoniae isolates. These data suggest that companion animals serve as a potential reservoir of antimicrobial resistant E. coli and K. pneumoniae. This also has considerable veterinary importance, since urinary tract infections are an important disease causing therapeutic challenges worldwide.

Over a 35-month period, group B Streptococcus isolates with reduced penicillin susceptibility (PRGBS) were detected from elderly patients at a regional hospital, accompanying population-level transition of PRGBS serotypes. Seventy-seven non-duplicate PRGBS recovered from 73 patients were analyzed to infer their genetic relatedness. Serotype III PRGBS predominated (16 serotype III/1 serotype Ib) in the first nine months (period I), then 3 serotype Ib isolates appeared transiently for the next three months (period II), which was replaced predominantly by serotype Ia (20 serotype Ia/1 serotype III/1 nontypeable) for nine months (period III). In the last 14 months (period IV), besides 25 serotype Ia, 10 serotype III isolates were also identified. Serotypes III and Ia isolates, belonging to ST1 shared G329V, G398A, V405A, and G429D in penicillin-binding protein2X. Of three strains subjected to whole-genome sequencing, serotype III strain SU12 (period I) had the higher degrees of genomic similarity with serotype Ia strain SU97 (period III) rather than serotype Ib strain SU67 (period II) based on average nucleotide identity and single nucleotide polymorphisms analyses. Analysis of the cps gene clusters and the upstream and downstream flanking sequences revealed that disruption of hyaluronidase gene located upstream of cpsY by insertion of an IS1548 was found in strain SU12, whereas ∆ISSag8 was inserted between tRNA-Arg and rpsA genes located downstream of cpsL for strain SU97. Interestingly, most of serotype III PRGBS re-emerged in phase IV had this tRNA-Arg-∆ISSag8-rpsA region. Capsular switching and nosocomial transmission may possibly contribute to population-level serotype replacement among ST1 PRGBS isolates.

No abstract

No abstract