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Salmonella enterica serovar Kentucky is a frequent cause for clinical infections in human patients. They are isolated and reported with multidrug resistance from the foods of animal origin from various countries. However, studies inferring the colistin resistance are limited. Hence, the current study reports the genetic factors and genomic analysis of the colistin-resistant Salmonella enterica serovar Kentucky strain COL-R for better understanding of its pathogenic potential and phylogenetic relatedness. The S. Kentucky strain COL-R was successfully isolated from chicken meat during ongoing surveillance of food of animal origin. Antimicrobial susceptibility testing revealed resistance to cefoxitin, erythromycin, gentamicin, tetracycline, and most disturbingly to ciprofloxacin and colistin (broth microdilution method). Whole-genome sequence of the COL-R strain was subjected to various in silico analysis to identify the virulence factors, antimicrobial resistance genes, pathogenicity islands and sequence type. The S. Kentucky COL-R strain belonged to sequence type (ST) 198 with a high probability (0.943) of being a human pathogen. Besides presence of integrated phage in the S. Kentucky COL-R genome, 38 genes conferring resistance to various antimicrobials and disinfectants were also identified. Nucleotide Polymorphism analysis indicated triple mutations in gyrA and parC genes conferring fluoroquinolone resistance. Phylogenomic analysis with 31 other S. Kentucky genomes revealed discernible clusters with S. Kentucky COL-R strain latching onto a cluster of high diversity (geographic location and isolation sources). Taken together, our results document the first occurrence of colistin resistance in a fluoroquinolone resistant S. Kentucky COL-R strain isolated from retail chicken and provide crucial information on the genomic features of the strain. [ABSTRACT FROM AUTHOR]

Objective: Salmonella enterica serotype Kentucky ST198 (S. Kentucky) is frequently associated with human infections and has been identified in travellers to North Africa, South Asia, Europe, and North America. The antimicrobial resistance of this serotype to multiple drugs, including ciprofloxacin (CIP), is a growing concern. However, little information is available regarding the occurrence and characterization of S. Kentucky in Korea. Methods: To investigate the characteristics and possible origin of these infections, we characterized highly CIP-resistant S. Kentucky isolates collected through a national surveillance program. Single-nucleotide polymorphisms (SNPs) were identified by whole-genome sequencing (WGS), and genome sequencing was performed to investigate the genetic relationships and resistance mechanisms of the isolates. Results: Ten CIP-resistant S. Kentucky strains were isolated from diarrheal patients in Korea from 2008 to 2017. The travel histories of the patients indicated that seven had returned from Southeast Asia. WGS of all the isolates revealed the presence of Salmonella genomic island 1 (SGI1) and substitutions in the gyrA and parC genes, which are known to confer resistance to CIP. A multilocus sequence type (MLST) analysis revealed that the isolates belonged to ST198, which has been prevalent in Europe and Africa. Furthermore, a phylogenetic analysis showed that all 10 isolates shared close genetic relationships. Conclusions: We report the identification of S. Kentucky in Korea through long-term surveillance. International travel, especially to Southeast Asia, has been a major risk factor for human infections of CIP-resistant S. Kentucky in Korea.

Objectives: Human infection by ciprofloxacin-resistant Salmonella enterica serovar Kentucky sequence type 198 (ST198) has been reported in the USA, Europe and Korea. In this study, we report the complete genome sequence of the first Salmonella Kentucky ST198 strain isolated from a chicken carcass in South Korea. Methods: The recovered Salmonella Kentucky, designated as K13SK002, was isolated from a chicken carcass in 2013. Genomic DNA was sequenced using a combination of 20-kb PacBio SMRTbell library and PacBio RS II. Antimicrobial susceptibility testing was performed and minimum inhibitory concentration (MIC) values were determined. Antimicrobial resistance and virulence genes were investigated in silico using ResFinder and VirulenceFinder tools, respectively, available at the Center for Genomic Epidemiology server. Results: The genome of K13SK002 consists of contiguous sequences (contigs) with a total length of 4 847 849 bp and a GC content of 52.20%. We detected a total of 4352 protein-coding sequences, 85 tRNA genes and 22 rRNA genes. MICs for ampicillin, ciprofloxacin, gentamicin, streptomycin, sulfisoxazole and tetracycline were 64, 16, 16, 64, >256 and 128 μg/mL, respectively. We found six antimicrobial resistance genes, however no plasmids and genes associated with adherence, toxins and exoenzyme were found. Ciprofloxacin-resistant Salmonella Kentucky K13SK002 was found to have mutations in DNA gyrase A (S83F and D87Y). Conclusion: This is the first report of the complete genome sequence of a Salmonella Kentucky ST198 strain isolated from a chicken carcass in South Korea. This genome sequence provides useful information on the genomic features associated with virulence and antimicrobial resistance in Salmonella Kentucky ST198.

Salmonella enterica serovar Kentucky (S. Kentucky) with sequence type (ST) 198 and highly resistant to ciprofloxacin (ST198-CipR) has emerged as a global MDR clone, posing a threat to public health. In the present study, whole genome sequencing (WGS) was applied to characterize all CipRS. Kentucky detected in five Spanish hospitals during 2009–2018. All CipR isolates (n = 13) were ST198 and carried point mutations in the quinolone resistance-determining regions (QRDRs) of both gyrA (resulting in Ser83Phe and Asp87Gly, Asp87Asn, or Asp87Tyr substitutions in GyrA) and parC (with Thr57Ser and Ser80Ile substitutions in ParC). Resistances to other antibiotics (ampicillin, chloramphenicol, gentamicin, streptomycin, sulfonamides, and tetracycline), mediated by the blaTEM–1B, catA1, aacA5, aadA7, strA, strB, sul1, and tet(A) genes, and arranged in different combinations, were also observed. Analysis of the genetic environment of the latter resistance genes revealed the presence of multiple variants of SGI1 (Salmonella genomic island 1)-K and SGI1-P, where all these resistance genes except catA1 were placed. IS26 elements, found at multiple locations within the SGI1 variants, have probably played a crucial role in their generation. Despite the wide diversity of SGI1-K- and SGI1-P-like structures, phylogenetic analysis revealed a close relationship between isolates from different hospitals, which were separated by a minimum of two and a maximum of 160 single nucleotide polymorphisms. Considering that S. enterica isolates resistant to fluoroquinolones belong to the high priority list of antibiotic-resistant bacteria compiled by the World Health Organization, continuous surveillance of the S. Kentucky ST198-CIPR clone is required.

Salmonella enterica serovar Kentucky (S. Kentucky) with sequence type (ST) 198 and highly resistant to ciprofloxacin (ST198-Cip R ) has emerged as a global MDR clone, posing a threat to public health. In the present study, whole genome sequencing (WGS) was applied to characterize all Cip R S. Kentucky detected in five Spanish hospitals during 2009–2018. All Cip R isolates (n = 13) were ST198 and carried point mutations in the quinolone resistance-determining regions (QRDRs) of both gyrA (resulting in Ser83Phe and Asp87Gly, Asp87Asn, or Asp87Tyr substitutions in GyrA) and parC (with Thr57Ser and Ser80Ile substitutions in ParC). Resistances to other antibiotics (ampicillin, chloramphenicol, gentamicin, streptomycin, sulfonamides, and tetracycline), mediated by the bla TEM– 1 B , catA1, aacA5 , aadA7, strA , strB , sul1 , and tet (A) genes, and arranged in different combinations, were also observed. Analysis of the genetic environment of the latter resistance genes revealed the presence of multiple variants of SGI1 (Salmonella genomic island 1)-K and SGI1-P, where all these resistance genes except catA1 were placed. IS 26 elements, found at multiple locations within the SGI1 variants, have probably played a crucial role in their generation. Despite the wide diversity of SGI1-K- and SGI1-P-like structures, phylogenetic analysis revealed a close relationship between isolates from different hospitals, which were separated by a minimum of two and a maximum of 160 single nucleotide polymorphisms. Considering that S. enterica isolates resistant to fluoroquinolones belong to the high priority list of antibiotic-resistant bacteria compiled by the World Health Organization, continuous surveillance of the S. Kentucky ST198-CIP R clone is required. [ABSTRACT FROM AUTHOR]

Introduction: Highly fluoroquinolone-resistant Salmonella enterica serovar Kentucky ( S. Kentucky) of sequence type (ST) 198 has emerged as a global multidrug-resistant (MDR) clone, posing a threat to public health., Methods: Whole genome sequencing and antibiotic susceptibility testing was used to characterize the population structure and evolutionary history of 54 S. Kentucky isolates recovered from food and human clinical cases in Beijing from 2016 to 2023., Results: All 54 S. Kentucky ST198 isolates exhibited resistance to quinolones, carrying point mutations in the quinolone resistance-determining regions ( gyrA _S83F and parC _S80I). Resistance to other antibiotics (folate pathway inhibitors, cephems, aminoglycosides, phenicols, rifamycin, fosfomycin, macrolides, and tetracyclines), mediated by the sul1 , sul2 , dfrA14 , bla CTX-M , bla TEM-1B , aac(3)-Id , aadA2 , aadA7 , aph(3')-I , aph(3'')-Ib , rmtB , floR , arr-2 , fosA , mph(A) , and tet(A) genes, was also observed in different combinations. The Beijing S. Kentucky ST198 evolutionary tree was divided into clades 198.2-1 and 198.2-2, which were further differentiated into three subclades: 198.2-2A, 198.2-2B, and 198.2-2C. Compared with the extended-spectrum β-lactamase-encoding gene bla CTX-M-14b in 198.2-1, the co-existence of bla CTX-M-55 and bla TEM-1B , as well as chromosomally located qnrS1 , was detected in most 198.2-2 isolates, which showed more complex MDR phenotypes. S. Kentucky ST198 outbreak isolates derived from two predominant clonal sources: 198.2-1 with cgST236434 and 198.2-2A with cgST296405., Conclusions: The S. Kentucky population in Beijing is genetically diverse, consisting of multiple co-circulating lineages that have persisted since 2016. Strengthening surveillance of food and humans will aid in implementing measures to prevent and control the spread of AMR., (Copyright and License information: Editorial Office of CCDCW, Chinese Center for Disease Control and Prevention 2024.)

We report emergence of ciprofloxacin-resistant Salmonella enterica serovar Kentucky in Canada during 2003–2009. All isolates had similar macrorestriction patterns and were multilocus sequence type ST198, which has been observed in Europe and Africa. Ciprofloxacin-resistant S. enterica serovar Kentucky represents 66% of all ciprofloxacin-resistant nontyphoidal Salmonella sp. isolates observed in Canada since 2003.

Abstract: Food-borne diseases caused by Salmonella enterica are a significant public health concern around the world. Since 2002, S. enterica serovar Kentucky has shown an increase in several countries with the concurrent emergence of multidrug-resistant isolates. The spread of such strains in the environment poses a major public health problem. A total of 57 Salmonella Kentucky strains isolated from different sources during the period 2005 to 2008 in Tunisia, were characterized by their antimicrobial and mercury resistance profiles; ability to form a biofilm; virulence invA/spvC genes and quorum sensing sdiA gene. A total of 10.6% of the isolates demonstrated multidrug-resistance against 3 to 13 antibiotics with ciprofloxacin resistance occurring in 33% of human isolates. In addition, 37% of the isolates exhibited minimum inhibitory concentrations value to mercuric chloride, ranging from 8 to 32μgml−1 and were considered as resistant strains. The majority of strains tested were able to form a biofilm, especially for environmental and animal derived isolates. Therefore, the biofilm seems to comprise a normal and favorable capability in the life of Salmonella Kentucky in the environment. Interestingly, all the isolates possessed the sdiA gene, 87.7% of isolates possessed the invA gene, and no isolate harbored the spvC gene. The emergence of resistance to ciprofloxacin in human Salmonella Kentucky isolates, added to the presence of invA and sdiA genes, and the production of biofilm could be the decisive factors in the dissemination of S. Kentucky strains on a large scale. [Copyright &y& Elsevier]

We report emergence of ciprofloxacin-resistant Salmonella enterica serovar Kentucky in Canada during 2003-2009. All isolates had similar macrorestriction patterns and were multilocus sequence type ST198, which has been observed in Europe and Africa. Ciprofloxacin-resistant S. enterica serovar Kentucky represents 66% of all ciprofloxacin-resistant nontyphoidal Salmonella sp. isolates observed in Canada since 2003. [ABSTRACT FROM AUTHOR]

An outbreak of salmonellosis occurred in a group of 7 long-nosed fur seals Arctocephalus forsteri undergoing rehabilitation after being found injured and malnourished on beaches along the northern New South Wales and southern Queensland coasts of Australia. Three of the 7 individuals developed clinical disease and died within 3 d. Clinical signs included profuse diarrhea, vomiting, depression, and lethargy. Salmonella enterica subsp. enterica serovar Kentucky (S. Kentucky) was cultured from 2 of the 3 deceased animals. The other 4 animals showed similar signs and recovered following treatment. S. Kentucky (antigenic formula 8,20:i:z6) was isolated from the survivors and tissues recovered from post-mortem samples of deceased animals. The bacterium was susceptible to cephalothin and sulfamethoxazole/trimethoprim and resistant to amoxicillin-clavulanate, ampicillin/amoxicillin, tetracycline, and enrofloxacin. This organism has the potential to cause disease in aquatic wildlife, as well as posing a zoonotic threat to people who utilise the aquatic environment.