Vibrio cholerae is a genetically diverse species, and pathogenic strains can encode different virulence factors that mediate colonization and secretory diarrhea. Although the toxin-coregulated pilus (TCP) is the primary colonization factor in epidemic-causing V. cholerae strains, other strains do not encode the TCP and instead promote colonization via the activity of a type 3 secretion system (T3SS). Using the infant mouse model and T3SS-positive O39 serogroup strain AM-19226, we sought to determine which of 12 previously identified, T3SS-translocated proteins (Vops) are important for host colonization. We constructed inframe deletions in each of the 12 loci in strain AM-19226 and identified five Vop deletion strains, including ⌬VopM, which were severely attenuated for colonization. Interestingly, a subset of deletion strains was also incompetent for effector protein transport. Our collective data therefore suggest that several translocated proteins may also function as components of the structural apparatus or translocation machinery and indicate that while VopM is critical for establishing an infection, the combined activities of other effectors may also contribute to the ability of T3SS-positive strains to colonize host epithelial cell surfaces. The toxin-coregulated pilus (TCP) is the major colonization factor encoded by all pathogenic O1 and O139 serogroup Vibrio cholerae strains, which cause epidemic cholera. In contrast, most clinically isolated non-O1/non-O139 serogroup strains do not encode TCP and thus must employ other mechanisms to effectively colonize the human intestinal epithelium and cause sporadic, cholera-like disease (1-3). Genome sequence analysis of a clinically isolated O39 serogroup strain, named AM-19226, identified a pathogenicity island on the large chromosome that encodes the structural proteins for a type 3 secretion system (T3SS) (4). T3SSs function as principal virulence mechanisms in many Gram-negative bacterial pathogens (e.g., Escherichia, Salmonella, Pseudomonas, Shigella, and Yersinia spp.), and in vivo studies using different animal models confirmed that the V. cholerae T3SS is essential for causing disease (5-7). In addition, numerous groups have identified T3SS-positive V. cholerae strains in laboratory collections, from patients, and from endemic environments, suggesting that a subset of non-O1/non-O139 serogroup strains depends on T3SS activity for virulence (1,3,4,(8)(9)(10).The V. cholerae T3SS is most closely related to the Vibrio parahaemolyticus T3SS2. T3SS2 is associated with pandemic V. parahaemolyticus strains, whereas T3SS1 is present in all strains (11). Comparison of the T3SS genomic islands in V. cholerae strain AM-19226 and V. parahaemolyticus strain RIMD2210633 reveals synteny within a conserved, central "core" region, flanked by 5= and 3= regions of greater coding diversity between clades and species (4, 10, 12-14). The core region encodes proteins that form the T3SS structural apparatus and is transcriptionally organized into four main operons in V. cholera...

The rising prevalence of extended-spectrum β-lactamase (ESBL)-producing Enterobacterales is a significant threat to animal and human health. This study aims to describe the clinical features, antimicrobial susceptibility patterns, and genotypic features of infections associated with ESBL-producing Enterobacterales in dogs and cats seen at a tertiary referral veterinary teaching hospital. Enterobacterales isolated from dogs and cats that underwent ESBL testing during the study period were identified using a search of the hospital antimicrobial susceptibility test software database. Medical records of confirmed ESBL isolates were reviewed, and the source of infection, clinical findings, and antimicrobial susceptibility were recorded. Genomic DNA from bacterial isolates was evaluated for antimicrobial resistance genes with whole genome sequencing. Thirty ESBL-producing isolates were identified based on phenotypic testing (twenty-nine from dogs, one from a cat); twenty-six were Escherichia coli and the remainder were Klebsiella spp. Bacterial cystitis was the most commonly identified (8/30, 27%) clinical problem associated with infection. Resistance to three or more antimicrobial classes was identified in 90% (27/30) of isolates, and all isolates were susceptible to imipenem. Over 70% of isolates were susceptible to piperacillin-tazobactam, amikacin, and cefoxitin. BlaCTX-M-15 was the most common ESBL gene identified, present in 13/22 (59%) isolate genomes. A wide range of clinical infections were identified. Piperacillin-tazobactam and amikacin may be alternatives to carbapenem therapy. Further, larger-scale studies are needed.

Rodents and bats are the most diverse mammal group that host Bartonella species. In the Americas, they were described as harboring Bartonella species; however, they were mostly characterized to the genotypic level. We describe here Bartonella isolates obtained from blood samples of one rodent (Peromyscus yucatanicus from San José Pibtuch, Yucatan) and two bat species (Desmodus rotundus from Progreso, and Pteronotus parnellii from Chamela-Cuitzmala) from Mexico. We sequenced and described the genomic features of three Bartonella strains and performed phylogenomic and pangenome analyses to decipher their phylogenetic relationships. The mouse-associated genome was closely related to Bartonella vinsonii. The two bat-associated genomes clustered into a single distinct clade in between lineages 3 and 4, suggesting to be an ancestor of the rodent-associated Bartonella clade (lineage 4). These three genomes showed <95% OrthoANI values compared to any other Bartonella genome, and therefore should be considered as novel species. In addition, our analyses suggest that the B. vinsonii complex should be revised, and all B. vinsonii subspecies need to be renamed and considered as full species. The phylogenomic clustering of the bat-associated Bartonella strains and their virulence factor profile (lack of the Vbh/TraG conjugation system remains of the T4SS) suggest that it should be considered as a new lineage clade (L5) within the Bartonella genus.

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