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Abstract Antimicrobials reserved for human medicines are permitted for companion animals and it is important to understand multidrug-resistant pathogens recovered from companion animals in terms of epidemiological correlation with human pathogens and possibility of transmission to human-beings. Seventeen of each CTX-M-type extended-spectrum beta-lactamase-producing Escherichia coli (ESBL-EC) and Klebsiella pneumoniae (ESBL-KP) canine isolates were assessed. Entire genomes of the 34 isolates were sequenced. Plasmid transfer and relative growth rates were assessed at differed temperature conditions indicating the body temperature of dogs, that of human-beings, and environment. ESBL-ECs were clonally diverse, while ESBL-KPs were not. The ESBL-ECs carried the bla CTX−M−15 gene in plasmids and the bla CTX−M−14-like gene either in chromosomes or in plasmids. The ESBL-KPs possessed the bla CTX−M−15 gene in plasmids (n = 15). One of the isolates carried another bla CTX−M−15 gene in a chromosome simultaneously and the other isolate had an additional bla CTX−M−9 gene-harbouring plasmid, together. Two ESBL-KP isolates carried the bla CTX−M−14 gene in plasmids. Plasmid transfer ESBL-EC to K. pneumoniae was efficient and the differed biological costs by temperature was much more in ESBL-EC than in ESBL-KP. Intersectoral dissemination of ESBL-ECs occurred mainly by horizontal gene transfer, while that of ESBL-KPs occurred by clonal dissemination.

Clostridioides difficile is a major causative pathogen for antibiotic-associated diarrhea and C. difficile infections (CDIs) may lead to life-threatening diseases in clinical settings. Most of the risk factors for the incidence of CDIs, i.e., antibiotic use, treatment by proton pump inhibitors, old age, and hospitalization, are associated with dysbiosis of gut microbiota and associated metabolites and, consequently, treatment options for CDIs include normalizing the composition of the intestinal microbiome. In this review, with an introduction to the CDI and its global epidemiology, CDI-associated traits of the gut microbiome and its metabolites were reviewed, and microbiome-targeting treatment options were introduced, which was approved recently as a new drug by the United States Food and Drug Administration (U.S. FDA), rather than a medical practice.

Acinetobacter baumannii is often highly resistant to multiple antimicrobials, posing a risk of treatment failure, and colistin is a “last resort” for treatment of the bacterial infection. However, colistin resistance is easily developed when the bacteria are exposed to the drug, and a comprehensive analysis of colistin-mediated changes in colistin-susceptible and -resistant A. baumannii is needed. In this study, using an isogenic pair of colistin-susceptible and -resistant A. baumannii isolates, alterations in morphologic and transcriptomic characteristics associated with colistin resistance were revealed. Whole-genome sequencing showed that the resistant isolate harbored a PmrBL208F mutation conferring colistin resistance, and all other single-nucleotide alterations were located in intergenic regions. Using scanning electron microscopy, it was determined that the colistin-resistant mutant had a shorter cell length than the parental isolate, and filamented cells were found when both isolates were exposed to the inhibitory concentration of colistin. When the isolates were treated with inhibitory concentrations of colistin, more than 80% of the genes were upregulated, including genes associated with antioxidative stress response pathways. The results elucidate the morphological difference between the colistin-susceptible and -resistant isolates and different colistin-mediated responses in A. baumannii isolates depending on their susceptibility to this drug.