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The emergence of mobile mcr genes mediating resistance to colistin is a critical public health issue that has hindered the treatment of serious infections caused by multidrug‐resistant pathogens in humans and other animals. We report the emergence of the mcr‐9.1 gene in a polymyxin‐resistant extended‐spectrum β‐lactamase (ESBL)‐producing Enterobacter kobei infecting a free‐living franciscana dolphin (Pontoporia blainvillei), threatened with extinction in South America. Genomic analysis confirmed the presence of genes conferring resistance to clinically relevant β‐lactam [blaCTX‐M‐15, blaACT‐9, blaOXA‐1 and blaTEM‐1B], aminoglycoside [aac(3)‐IIa, aadA1, aph(3'')‐Ib and aph(6)‐Id], trimethoprim [dfrA14], tetracycline [tetA], quinolone [aac(6')‐Ib‐cr and qnrB1], fosfomycin [fosA], sulphonamide [sul2] and phenicol [catA1 and catB3] antibiotics. The identification of mcr‐9.1 in a CTX‐M‐15‐producing pathogen infecting a critically endangered animal is of serious concern, which should be interpreted as a sign of further spread of critical priority pathogens and their resistance genes in threatened ecosystems. [ABSTRACT FROM AUTHOR]

Critical priority pathogens have globally disseminated beyond clinical settings, thereby threatening wildlife. Andean Condors (Vultur gryphus) are essential for ecosystem health and functioning, but their populations are globally near threatened and declining due to anthropogenic activities. During a microbiological and genomic surveillance study of critical priority antibiotic‐resistant pathogens, we identified pandemic lineages of multidrug‐resistant extended‐spectrum β‐lactamase (ESBL)‐producing Escherichia coli colonizing Andean Condors admitted at two wildlife rehabilitation centres in South America. Genomic analysis revealed the presence of genes encoding resistance to hospital and healthcare agents among international E. coli clones belonging to sequence types (STs) ST162, ST602, ST1196 and ST1485. In this regard, the resistome included genes conferring resistance to clinically important cephalosporins (i.e., CTX‐M‐14, CTX‐M‐55 and CTX‐M‐65 ESBL genes), heavy metals (arsenic, mercury, lead, cadmium, copper, silver), pesticides (glyphosate) and domestic/hospital disinfectants, suggesting a link with anthropogenic environmental pollution. On the other hand, the presence of virulence factors, including the astA gene associated with outbreak of childhood diarrhoea and extra‐intestinal disease in animals, was identified, whereas virulent behaviour was confirmed using the Galleria mellonella infection model. E. coli ST162, ST602, ST1196 and ST1485 have been previously identified in humans and food‐producing animals worldwide, indicating that a wide resistome could contribute to rapid adaptation and dissemination of these clones at the human–animal–environment interface. Therefore, these results highlight that Andean Condors have been colonized by critical priority pathogens, becoming potential environmental reservoirs and/or vectors for dissemination of virulent and antimicrobial‐resistant bacteria and/or their genes, in associated ecosystems and wildlife. [ABSTRACT FROM AUTHOR]

Serratia fonticola is a human pathogen widely found in the environment, with birds being reported as possible natural hosts. During an epidemiological and genomic surveillance study conducted to monitor the occurrence of extended-spectrum β-lactamase (ESBL)-producing Enterobacterales in South American wild birds, we identified an ESBL-positive S. fonticola in a fecal sample collected from a Hudsonian Whimbrel, during its non-breeding range on the Pacific Coast of Chile. Whole genome sequencing analysis and "in silico" modeling revealed a novel variant of the class A ESBLs FONA family, designated FONA-7, which shows 96.28% amino acid identity with FONA-6; with amino acid substitutions occurring in the signal peptide sequence (Thr22→Ser), and in the mature protein (Ser39→Asn and Thr227→Ile). This finding denotes that migratory birds can be potential vectors for the transboundary spread of ESBL-producing bacteria, creating a further theoretical risk for the origin of novel plasmid-encoded β-lactamases. [ABSTRACT FROM AUTHOR]