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. 2026 Aug 1;23:101536. doi: 10.1016/j.onehlt.2026.101536

Cross-species genomic analysis of Salmonella enterica subspecies enterica serovar Dublin isolated from dairy cattle, dogs, and humans in Florida from 2019 to 2024.

Asanka R DeZoysa a, Lekshmi K Edison b, Thomas Denagamage a, Abraham J Pellissery b,c, Yugendar R Bommineni c, Dilan Satharasinghe c, Destini Coiner c, David Simon c, Kelly Tomson d, Subhashinie Kariyawasam b,⁎
PMCID: PMC13475705  PMID: 42603017

Abstract

Salmonella enterica serovar Dublin (S. Dublin) is a cattle-adapted pathogen that can cause severe systemic infections in humans and animals. Understanding genomic relatedness across host species is essential for assessing the zoonotic potential and dissemination of antimicrobial resistance (AMR). In this study, 78 clinical S. Dublin strains, isolated in Florida between 2019 and 2024, were subjected to comparative genomic analysis. These included 19 animal-derived isolates (17 from dairy cattle and two from dogs) and 59 human-derived isolates. AMR gene profiling revealed widespread multidrug resistance, with genes conferring resistance to aminoglycoside (aac(6′)-Iaa, aph(6)-Id), tetracycline (tetA), and sulfonamide (sul2) detected in all isolates. Beta-lactamase genes, particularly blaTEM variants, were detected more frequently in human- and dog-derived isolates than in cattle-derived isolates. In contrast, rare blaCMY variants (blaCMY-61, blaCMY-130, blaCMY-153, and blaCMY-2b) were detected in only one cattle isolate. Plasmid analysis revealed that IncX1, IncFII(S), and IncC replicons were common among the isolates, highlighting their potential role in facilitating AMR dissemination via horizontal gene transfer. Virulence gene profiling revealed conserved Salmonella pathogenicity islands, type III and type VI secretion systems, and the spv operon across S. Dublin isolates from all host species. Multilocus sequence typing (MLST) confirmed that all isolates belonged to sequence type (ST) 10, and most harbored the Gifsy-2 prophage. The SNP-based phylogeny revealed distinct host-associated clades as well as mixed-host clusters, demonstrating close genomic relatedness among isolates from different host species and suggesting possible cross-species transmission, exposure to shared sources, or circulation of closely related lineages. These findings illustrate the interconnectedness of animal and human S. Dublin infections, emphasize the importance of responsible antimicrobial use, and highlight the value of genomic surveillance for detecting and controlling S. Dublin infections. Collectively, this study provides a genomic framework for assessing cross-species relatedness, virulence characteristics, and AMR patterns of S. Dublin.

Keywords: AMR, One-health, Salmonella Dublin, Virulence, Zoonotic potential, Comparative genomics

1. Introduction

Salmonella species encompasses over 2600 recognized serovars, the majority of which are classified as Salmonella enterica [1]. Among these, Salmonella enterica serovar Dublin (S. Dublin) is a host-adapted serovar predominantly associated with cattle [2], [3]. According to the October 2018 update from the National Veterinary Services Laboratories (NVSL), S. Dublin is the most frequently reported serotype among clinical bovine submissions in the United States. In neonatal calves, infection often causes septicemia and pneumonia, sometimes accompanied by diarrhea, resulting in high morbidity and mortality [4]. Respiratory signs, including labored breathing and nasal discharge, are also commonly observed in affected animals [2]. Transmission occurs transplacentally, but more commonly, via fecal-oral exposure to bacteria shed in feces, colostrum, or milk. In adult cattle, infection can lead to late-term abortion, reproductive disorders, and sudden decreases in milk production [4], [5], [6]. Persistence in herd-level is further exacerbated by asymptomatic carriers, which intermittently shed the organism due to prolonged colonization of lymphoid tissues [7], [8].

Although primarily adapted to cattle, S. Dublin occasionally infects other species. In small ruminants, the clinical presentation includes enteritis, septicemia, abortion, and systemic lesions such as suppurative peritonitis and multiorgan thrombosis [9]. Companion animals, particularly young dogs, may develop severe diseases, including hemorrhagic diarrhea, septicemia, and meningoencephalitis [10]. Sporadic isolation from wildlife, such as chamois and red foxes, further suggest possible environmental persistence and inter-species transmission potential [11]. S. Dublin also represents a significant public health concern. Human infections are typically severe and invasive, manifesting as septicemia, osteomyelitis or meningitis, and may result in death, especially in immunocompromised individuals and older adults [12], [13], [14]. Between 1973 and 2013, nine outbreaks were reported to the Foodborne Disease Outbreak Surveillance System (FDOSS), with implicated sources including raw milk, Mexican-style cheese, and undercooked beef [12]. Occupational exposure among farm workers, veterinarians, and others in close contact with livestock further increases the risk of zoonotic transmission [15].

A major challenge in treating S. Dublin infections is the high prevalence of multidrug resistance (MDR) among clinical isolates. In an analysis of 140 clinical S. Dublin isolates from animals submitted to National Veterinary Services Laboratories (NVSL) between 2014 and 2017, 98% were resistant to more than four antimicrobial classes, whereas only a single isolate remained pan-susceptible [16]. Virulence factors further amplify the pathogenic potential of S. Dublin. The virulence plasmid pSDV carries the spvRABCD operon, which promotes the intracellular survival and replication of Salmonella in macrophages [17]. Additional virulence determinants include type III and type VI secretion systems, fimbrial adhesins, motility-associated genes, and several chromosomal and plasmid-encoded effectors, such as mig-14 and mig-5, which may contribute to systemic dissemination and immune evasion [18], [19]. The Gifsy-2 prophage carries additional virulence associated genes including, sodCI, gtgE, and sseI, which contribute bacterial survival and persistence within host cells [20]. Although the clinical impact, antimicrobial resistance, and virulence factors of S. Dublin are well documented, the information on the genomic relatedness and diversity of isolates from different host species. In particular, conserved and host-specific genomic features that may influence host-adaptation, cross-host transmission, and pathogenicity remain poorly understood.

This study aimed to characterize the genomic relatedness and diversity of S. Dublin isolates obtained from dairy cattle, dogs, and humans, and to identify conserved and divergent genomic features across isolates from different host species.

2. Materials and methods

2.1. Collection of S. Dublin isolates

A total of 19 S. Dublin isolates of animal origin, isolated between 2019 and 2024, were obtained from two diagnostic laboratories in Florida. Eleven S. Dublin isolates from cattle, and two from dogs, were retrieved from the Bronson Animal Disease Diagnostic Laboratory (BADDL), Kissimmee, Florida. Six additional S. Dublin isolates from cattle were obtained from the Clinical Microbiology, Parasitology, and Serology Laboratory at the College of Veterinary Medicine, University of Florida, Gainesville, Florida. The raw whole genome sequencing (WGS) data for 59 human S. Dublin isolates, collected between 2019 and 2024, were also obtained from the Bureau of Public Health Laboratories, Florida Department of Health, Jacksonville, Florida. These isolates represented all available S. Dublin submissions from the participating laboratories during this period that met the inclusion criteria. Given the limited number of viable bacterial isolates or available WGS data, all qualifying isolates and sequence data were included, and randomization was not required.

2.2. Genomic DNA extraction and whole genome sequencing

Genomic DNA was extracted from pure overnight cultures using the Quick-DNA/RNA MagBead kit (Zymo Research, Irvine, California, USA) according to the manufacturer's instructions. DNA quality and quantity were evaluated using a Nanodrop spectrophotometer (Thermo Fisher Scientific, Wilmington, DE, USA). Samples were considered suitable for whole-genome sequencing if they met the following criteria: DNA concentration ≥ 20 ng/μL, a 260/280 absorbance ratio ≥ 1.8, and a 260/230 absorbance ratio ≥ 2.0. A 50 μL aliquot of each DNA sample was submitted to SeqCenter (Pittsburgh, PA, USA) for Illumina short-read and Oxford Nanopore Technologies (ONT) long-read sequencing.

2.3. Whole genome assembly and annotation

De novo genome assembly of raw WGS data was performed using Flye v2.9.2, with ONT long reads used for primary assembly and Illumina short reads used for sequence refinement and error correction. The reference S. Dublin chromosome sequence (accession no. CP001144) was retrieved from the National Center for Biotechnology Information (NCBI). For each isolate, the resulting contigs were imported into CLC Genomics Workbench v25.0.1 (QIAGEN, Aarhus, Denmark), and subsequently refined and, where appropriate, merged using the Join Contigs module. The longest joined contig was identified and provisionally designated as the candidate chromosomal sequence based on its size and was evaluated by comparison with the reference S. Dublin chromosome CP001144. The remaining contigs were extracted and subjected to Basic Local Alignment Search Tool (BLAST) analysis against the NCBI nucleotide database to access their similarities to known plasmid sequences. Contigs showing similarity to the plasmid references were further evaluated and joined by sequence overlap. These contigs were subsequently classified as putative plasmid-associated sequences for downstream analysis. Finally, all 78 assembled genomes were annotated using the Bakta Web server (https://bakta.computational.bio/), Proksee (https://proksee.ca/) and RAST (Rapid Annotations using Subsystems Technology) (https://rast.nmpdr.org/).

2.4. Multilocus sequence typing of isolates

Multilocus sequence typing (MLST) was performed for all S. Dublin isolates using MLST 2.0 (https://cge.food.dtu.dk/services/MLST/) with the Salmonella enterica MLST scheme, along with a minimum allele depth threshold of 10×. Raw sequencing reads in FASTQ format were used as input.

2.5. Single nucleotide polymorphism analysis and tree construction

Raw Illumina sequencing reads from all S. Dublin isolates were imported into CLC Genomics Workbench v.25.0 (QIAGEN). Reads were mapped to the reference chromosome CP001144, and single nucleotide polymorphisms (SNPs) were identified using a fixed-ploidy variant detection approach. The identified SNPs were subsequently used to construct and visualize a rooted SNP-based phylogenetic tree in CLC Genomics Workbench v25.0 (QIAGEN) to assess genomic relatedness among the isolates.

2.6. Plasmid typing

Plasmid replicon typing was performed using PlasmidFinder 2.1 (https://cge.food.dtu.dk/services/PlasmidFinder/). Assembled contigs in FASTA format from all isolates were analyzed using minimum thresholds of 95% sequence identity and 60% coverage. PlasmidFinder results were interpreted together with BLAST results showing similarities to known plasmid sequences to identify putative plasmid-associated contigs and characterize their replicon types. The analysis was conducted at the plasmid replicon level and was not intended to reconstruct or completely resolve individual plasmid structures.

2.7. Distribution analysis of Gifsy-2 prophage in S. Dublin isolates

The presence of the Gifsy-2 prophage in the isolates was assessed using PHAge Search Tool Enhanced Release (PHASTER; https://phaster.ca/). Chromosomal sequence from each isolate in FASTA format were submitted to the platform for prophage detection and annotation.

2.8. Detection of virulence genes

Virulence genes (VGs) present in both chromosomal and plasmid sequences were identified using the Virulence Factor Database (VFDB) within CLC Genomics Workbench v.25.0 (QIAGEN).

2.9. Salmonella pathogenicity island analysis

Salmonella pathogenicity islands (SPIs) were identified using SPIFinder 2.0 (https://cge.food.dtu.dk/services/SPIFinder/).

2.10. Identification of antimicrobial resistance genes

AMR genes (ARGs) were initially identified using the ResFinder databases in CLC Genomics Workbench v.25.0 (Qiagen). The results were further validated using NCBI AMRFinderPlus v4.2.7 (https://github.com/ncbi/amr).

3. Results

3.1. Sequencing results

Whole-genome sequencing of 78 S. Dublin isolates revealed a relatively conserved genome organization across hosts and years, with genome sizes ranging from approximately 4.55 to 6.17 Mb. Human isolates showed greater variability, with the largest genome being 6,170,857 bp (H14) and the smallest being 4,549,258 bp (H41). Coding DNA sequences (CDS) generally ranged from 3628 (H12) to 4986 (A9) genes per genome. All genomes carried one tmRNA gene except for one human S. Dublin isolate (H12), and most encoded between 55 (H18) and 88 (A9) tRNAs. rRNA counts varied from 7 (H12) to 23 (H45). Replication-associated elements were widely distributed: oriC was present in nearly all genomes (typically 1–2 copies), oriV was frequently detected in 3–4 copies, and oriT ranged from one to three copies. The details of the genome assembly data for all isolates are provided in Supplementary File 1.

3.2. MLST of 78 S. Dublin isolates

MLST analysis revealed no diversity among the S. Dublin isolates between human and animal, as all were assigned to the sequence type ST10 and shared identical allelic profiles for aroC, dnaN, hemD, hisD, purE, sucA, and thrA (Supplementary File 2).

3.3. SNP-based phylogenetic tree of S. Dublin isolates

The rooted SNP-based phylogenetic tree of the 78 S. Dublin isolates revealed a well-structured phylogeny with several distinct clades. Multiple well-supported clusters consisting exclusively of human isolates formed separate monophyletic groups within the tree. Several additional clades were composed solely of cattle isolates, indicating clear cattle-associated clustering patterns. In addition to these host-specific clusters, mixed host clades were identified. The two canine isolates (A8 and A14) clustered together with two human isolates (H43 and H44). This cluster was characterized by short branch lengths, indicating a high degree of SNP similarity among the four isolates tested. Outside this mixed-host clade, human isolates were interspersed with cattle isolates in several smaller clusters. The SNP tree of the 78 S. Dublin isolates generated using CLC Genomics Workbench v.25.0 (QIAGEN) is shown in Fig. 1.

Fig. 1.

Fig. 1

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A rooted single-nucleotide polymorphism (SNP)-based phylogenetic tree of 78 S. Dublin isolates based on core genome SNP differences. The tree illustrates both host-associated and mixed-host clustering patterns among isolates. Isolate labels are annotated by host origin, where A denotes animal isolates and H denotes human isolates. Numbers displayed along the branches represent branch-length values and indicate the estimated SNP distance along each branch. Branch lengths were proportional to the number of SNP differences.

3.4. Plasmid replicon types among S. Dublin isolates

The most prevalent plasmid type among the S. Dublin isolates was IncX1, detected in 75 (96.15%) isolates. The second most common plasmid type was IncFII(S), present in 72 isolates (92.31%), followed by IncC, identified in 70 isolates (89.74%). The least common plasmid type was IncI1-I(Alpha), which was detected in only one human-origin S. Dublin isolate. The distribution of plasmid types among the 78 S. Dublin isolates is shown in Fig. 2a.

Fig. 2.

Fig. 2

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Distribution of (a) plasmid replicons, (b) Gifsy 2 prophage, and (c) antimicrobial resistance genes among S. Dublin isolates. Heatmap showing the presence and absence of genetic determinants across S. Dublin isolates from human (H) and animal (A) sources. Each row represents an individual isolate, and each column represents a specific gene or replicon. Yellow indicates the presence, and gray indicates the absence of the corresponding gene. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

3.5. Occurrence of Gifsy-2 prophage in S. Dublin genomes

The presence of the Gifsy-2 prophage was assessed in 78 S. Dublin genomes. Gifsy-2 was detected in 75 of the 78 isolates and was absent in three human-derived isolates. The distribution of Gifsy-2 among the isolates is shown in Fig. 2b.

3.6. Distribution of antimicrobial-resistant genes

The aac(6′)-Iaa gene, which confers resistance to aminoglycosides, was detected in all 78 S. Dublin isolates (100%). The second most common AMR gene was tet(A), mediating tetracycline resistance, which was present in all animal isolates but absent in six human isolates thereby with a total presence in 72 isolates (92.31%). The sul2 gene, conferring sulfonamide resistance, and aph(3″)-Ib, conferring aminoglycoside resistance, were identified in 70 isolates (89.74%), including all 19 animal-derived isolates. The aph(6)-Id gene, also associated with aminoglycoside resistance, was detected in 69 isolates (88.46%) and was consistently present in all animal isolates. Other aminoglycoside resistance genes were detected at lower frequencies, such as aac(3)-IIa in one human isolate (1.28%), ant(2″)-Ia in three human isolates (3.85%), and aph(3′)-Ia in two canine and five human isolates and in a total of seven S. Dublin isolates (8.97%).

The distribution of β-lactam resistance genes among isolates revealed nine distinct bla gene variants belonging to TEM and CMY gene families. The most common was blaCMY-2, detected in 59 isolates (75.64%), but absent in 11 human and 8 cattle isolates. The genes blaTEM-125, blaTEM-206, and blaTEM-214 were identified in 27 isolates (34.62%), including both canine and single cattle isolates. blaTEM-1B was present in 30 isolates (38.46%), with its distribution among animal isolates similar to that of the other blaTEM variants above, and it was detected in three human isolates that did not harbor the other blaTEM genes. In contrast, the genes blaCMY-2b, blaCMY-61, blaCMY-130, and blaCMY-153 were identified in only one cattle isolate (1.28%).

Two genes responsible for phenicol resistance were identified: floR was detected in 56 isolates (71.79%), whereas cmlA1 was identified in only three human isolates (3.85%). Of the 19 AMR genes identified, aac(6′)-Iaa and blaCMY-130 were chromosomally encoded, whereas the remaining 17 genes were located on plasmids. A heatmap showing the distribution of AMR genes is shown in Fig. 2c.

3.7. Virulence gene profiling

The csgBAC and csgDEFG curli operons were detected in all 78 S. Dublin isolates. Genes of the type 1 fimbrial operon, including fimW, fimY, fimZ, fimF, fimH, fimD, fimC, fimI, and fimA, were also detected in all isolates. Two human-derived isolates lacked all five genes of the lpfABCDE operon, whereas the complete operon was present in the remaining 76 isolates. The misL gene was absent in three human-derived isolates but was present in the remaining 75 isolates. Similarly, ratB and sinH were absent in two human-derived isolates but were detected in the remaining 76 isolates. All cattle- and canine-derived isolates carried the evaluated curli, fimbrial, and adhesin-associated genes.

Most isolates retained the major SPI-1-associated type III secretion system genes. One human-derived isolate lacked multiple SPI-1 genes, including the inv/spa, prg/org, hil, iag/iac, sic/sip, and spt/avr operons and sprB, but retained the effector genes sopA, sopB/sigD, sopE2, and steB. Two additional human-derived isolates lacked the SPI-1 region encompassing STM0266, STM0267, STM0269–STM0274, STM0280–STM0282, STM0284, STM0285, STM0287, STM0289, and STM0290. Several other human-derived isolates exhibited partial loss of genes within the SPI-1 locus. Among the SPI-2-associated effector genes, gogB was detected in one canine-derived and two cattle-derived isolates, whereas sspH2 was detected in three human-derived isolates.

The tlde1 gene was absent in four human-derived isolates but was detected in the remaining 74 isolates. The SPI-3-associated genes mgtB and mgtC were absent in two human-derived isolates and present in the remaining 76 isolates. The mig-14 gene was absent in five human-derived isolates, whereas mig-5 was absent in four human-derived isolates; these genes were detected in 73 and 74 isolates, respectively. The sodCI gene was absent in seven human-derived isolates but was present in the remaining 71 isolates. The rpoS gene was absent in one human-derived isolate, and fur was absent in two human-derived isolates. In contrast, phoP and phoQ were detected in all 78 isolates. All cattle- and canine-derived isolates carried tlde1, mgtB, mgtC, mig-14, mig-5, sodCI, rpoS, fur, phoP, and phoQ.

3.8. Genomic distribution of the spv operon among isolates

Among the human-derived S. Dublin isolates, two lacked the entire spvB, spvC, and spvD genes, while four additional isolates lacked only spvD. All remaining isolates carried complete spvB, spvC, and spvD gene sets. Three representative S. Dublin virulence plasmid (pSDVs) regions carrying complete spv operons from cattle-, dog-, and human-derived S. Dublin isolates are illustrated in Fig. 3.

Fig. 3.

Fig. 3

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Representative S. Dublin virulence plasmid (pSDV) regions derived from (a) a cattle isolate (A4), (b) a dog isolate (A8), and (c) a human isolate (H42). Annotated open reading frames (ORFs) are shown as arrows, with gene names indicated above each feature. The spv operon genes are highlighted in red boxes. The scale bars indicate nucleotide length (kbp). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

3.9. Specific pathogenicity island profiles of 78 S. Dublin isolates

Among the 78 S. Dublin isolates studied, SPI-2 was the most prevalent, being detected in all isolates (100%). The next most common SPIs were SPI-1, SPI-3, SPI-9, and SPI-13, each present in 77 isolates (98.7%). The C63PI and CS54 pathogenicity islands were absent in two isolates each from S. Dublin originating from human clinical samples, resulting in their presence in 76 isolates (97.4%). SPI-14 was absent in three human isolates but was detected in the remaining 75 isolates (96.2%). SPI-5 and SPI-10 were identified in 70 (89.7%) and 68 (87.2%) isolates, respectively. The least prevalent SPIs were SPI-4 and SPI-12, each present in 52 isolates (66.7%) and absent in 26 Human S. Dublin isolates. Notably, all SPIs were consistently detected in the 19 animal-derived isolates, whereas human-derived isolates exhibited greater variability in SPI presence. The frequency distribution of SPIs among the 78 S. Dublin isolates is shown in Fig. 4.

Fig. 4.

Fig. 4

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The distribution of specific pathogenicity islands (SPIs) in 78 S. Dublin isolates revealed a highly conserved genomic architecture, with most isolates harboring SPI-1, SPI-2, SPI-3, SPI-5, SPI-9, SPI-10, SPI-13, SPI-14, C63PI, and CS54. In contrast, SPI-4 and SPI-12 showed the highest variability across populations.

4. Discussion

Comparative genomic analyses of S. Dublin from cattle, dogs, and humans are valuable for assessing cross-species genomic relatedness, host adaptation, and AMR determinants [21]. Such analyses provide insight into the genetic diversity of circulating strains, reveal host-associated genomic variation, and help inform assessment of possible cross-species transmission, which is of particular concern for a host-adapted serovar that infects multiple hosts species [22]. This study provides a One Health–focused comparative genomic analysis of S. Dublin derived from dairy cattle, dogs, and humans in Florida. By examining isolates from multiple host species, this study also offers a high-resolution assessment of the host-associated and shared genomic features of S. Dublin circulating in this region, allowing the evaluation of genomic relatedness and potential cross-species associations. The conserved genomic backbone of S. Dublin, together with observed host-associated variation in resistance and virulence features, may influence infection dynamics, therapeutic options, and overall public health risks.

The AMR profiles revealed widespread genomic multidrug-resistant S. Dublin isolates, with near-universal carriage of resistance determinants associated with aminoglycosides, tetracyclines, sulfonamides, and β-lactam, reflecting sustained antimicrobial selection pressure across veterinary and human clinical settings. The concordant results obtained using ResFinder, CARD, and AMRFinderPlus strengthen confidence in the genotypic AMR profiles identified in this study. This observation is consistent with reports that S. Dublin has become one of the most multidrug-resistant nontyphoidal Salmonella serovars affecting cattle and humans in North America and Europe [23]. The frequent detection of blaCMY-2 and blaTEM variants further emphasizes the serious clinical challenges posed by S. Dublin infections, particularly given the critical role of third-generation cephalosporins in both veterinary and human medicine. In particular, the enrichment of several blaTEM variants in human and dog isolates suggests stronger or more recent selective pressures in clinical and companion-animal settings, where β-lactams are widely used for empirical treatment [24]. Among aminoglycoside resistance genes, aph(3′)-Ia [25] was detected exclusively in both dog isolates and a subset of human isolates but was absent from all cattle isolates. This host-restricted distribution underscores the importance of monitoring antimicrobial use and the emergence of resistance not only in livestock but also in companion animals and human healthcare settings, which may serve as distinct reservoirs for specific resistance determinants. Similarly, cmlA1, which confers resistance to chloramphenicol and other phenicols [21], was detected only in three human isolates, indicating the sporadic emergence of phenicol resistance genes in human-associated S. Dublin and suggesting that rare determinants can arise and be maintained in niches where these drugs or co-selecting agents are used for treatment.

A particularly notable finding was the identification of a single cattle isolate carrying multiple blaCMY variants (blaCMY-61, blaCMY-130, blaCMY-153, and blaCMY-2b) [26], in contrast to the broader population in which blaCMY-2 or other extended-spectrum β-lactamases [27] typically dominate but usually as a single variant per strain. This observation underscores that even within apparently clonal and stable livestock-associated S. Dublin populations, rare but clinically important resistance configurations can emerge, potentially serving as reservoirs for wider dissemination if antimicrobial use or biosecurity practices are suboptimal [16]. The ongoing evolution of AMR, even within a largely clonal background, suggests that livestock populations may serve as long-term reservoirs for newly emerging β-lactamase variants, posing risks to human and animal health. The widespread presence of plasmids, particularly IncX1, IncFII(S), and IncC (IncA/C2) replicon types, across all host species aligns with previous studies demonstrating that these plasmids are central vehicles for AMR gene dissemination in S. Dublin and other Salmonella serovars [28]. Plasmid-mediated transmission of β-lactamase, aminoglycoside, sulfonamide, tetracycline, and phenicol resistance genes has been repeatedly linked to multidrug resistance and treatment failures in both veterinary and human medicine, emphasizing the importance of plasmid surveillance and stewardship strategies aimed at limiting horizontal gene transfer (HGT) within and between host populations [29].

Despite clear variation in AMR gene content, most virulence determinants, including the majority of SPIs, were highly conserved across host species in this study [21]. Prior genomic surveys have shown that S. Dublin typically harbors a broad repertoire of SPIs (e.g., SPI-1, −2, −3, −4, −5, −6, −12, −14, and others) together with the spvRABCD virulence operon, enabling efficient intestinal invasion, intracellular survival, and systemic dissemination in both cattle and humans [17]. In the present dataset, SPI deletions were predominantly observed in human isolates, particularly affecting SPI-1, SPI-3, SPI-4, SPI-12, and SPI-14. This may reflect host-specific adaptation or microevolution during chronic or recurrent human infections, as described for S. Dublin pathoadaptation in long-term human infections [20]. Nonetheless, the preservation of key virulence determinants, including the spv operon, type III and type VI secretion systems, and multiple fimbrial and adhesin loci across cattle, human, and dog isolates indicates that the capacity for systemic, invasive disease is broadly maintained, reinforcing the zoonotic potential of S. Dublin across mammalian hosts [30].  .

The VG profiles showed that most S. Dublin isolates retained a broad repertoire of determinants associated with biofilm formation, adhesion, intestinal colonization, and persistence within host tissues. The csgBAC structural operon and the csgDEFG assembly and regulatory operon were detected in all 78 isolates, indicating strong conservation of curli-associated functions involved in biofilm formation, surface attachment, and interactions with host epithelial cells [31]. Genes of the type 1 fimbrial operon, including fimW, fimY, fimZ, fimF, fimH, fimD, fimC, fimI, and fimA, were also present in all human-, cattle-, and canine-derived isolates, further supporting the conservation of fimbria-mediated adherence across host sources [32].

Limited variation was observed among other adhesin-associated loci, predominantly in human-derived isolates. Two human isolates lacked the complete lpfABCDE operon, which encodes long polar fimbriae involved in intestinal adhesion and colonization, whereas the operon was intact in all remaining human, cattle, and canine isolates [33]. Similarly, misL, which encodes an autotransporter adhesin involved in fibronectin binding, intestinal colonization, and tissue persistence, was absent from three human-derived isolates but present in all other isolates [34]. The autotransporter-associated genes ratB and sinH, which contribute to intestinal colonization and epithelial adhesion, were absent from two human isolates but were retained in the remaining 76 isolates [30]. The overall conservation of these loci suggests that most isolates retained substantial adhesive and colonization potential, whereas the restricted gene losses observed among a small subset of human isolates may be consistent with genomic diversification or host-associated microevolution.

A similar pattern was observed for type III secretion system-associated genes. Most isolates retained major components and effector genes associated with SPI-1-mediated host-cell invasion and SPI-2-mediated intracellular survival [35], [36]. However, complete or partial loss of SPI-1-associated genes was detected in a subset of human-derived isolates. The absence of structural, regulatory, chaperone, and effector genes within this region could potentially alter the assembly or function of the SPI-1 secretion machinery and thereby influence host-cell invasion. Variability was also observed among SPI-2-associated effector genes. The anti-inflammatory effector gogB, which contributes to limiting infection-associated tissue damage, was detected in only one canine-derived and two cattle-derived isolates [37]. In contrast, sspH2, which is involved in modulating host immune responses, was restricted to three human-derived isolates [38]. The restricted distribution of these effectors may reflect genomic diversification among the isolates, although its biological significance remains unclear.

Beyond adhesin- and secretion-system-associated loci, additional variation was identified in genes involved in bacterial competition, environmental adaptation, stress responses, and intracellular survival. The type VI secretion system effector gene tlde1, which contributes to interbacterial competition and host interactions, was absent from four human-derived isolates [39]. The SPI-3-associated genes mgtB and mgtC, which support adaptation to magnesium limitation and survival within macrophages, were absent from two human-derived isolates [40]. Likewise, mig-14, which contributes to resistance against host antimicrobial peptides, and mig-5, a putative carbonic anhydrase associated with antimicrobial peptide resistance and intracellular survival, were absent from several human-derived isolates [41], [42]. The absence of sodCI in seven human-derived isolates may also affect influence protection against reactive oxygen species during macrophage infection [43]. In contrast, the broad conservation of rpoS, fur, and the phoP/phoQ regulatory system indicates that most isolates retained major mechanisms involved in general stress adaptation, iron homeostasis, resistance to host-induced stress, and intracellular survival [44], [45], [46]. Collectively, these findings indicate that the principal adhesion, invasion, stress-response, and intracellular-survival systems were broadly conserved across host sources, while variation in selected loci occurred mainly among human-derived isolates.

Consistent with the well-documented clonal nature of this serovar, MLST showed that all 78 isolates in this study belonged to sequence type ST10, the dominant global lineage of S. Dublin and the most frequently reported sequence type in large international datasets [47]. In addition, most isolates in the current collection carried the Gifsy-2 prophage, a lambdoid prophage known to encode several virulence-associated genes, such as sodCI, sseI, and gtgE, which enhance oxidative stress resistance, immune evasion, and intracellular survival in macrophages, and have been implicated in the systemic invasive phenotype of S. Dublin [48]. The combination of a conserved ST10 chromosomal backbone, stable carriage of major SPIs, virulence plasmids, and Gifsy-2 prophage [22] provides a mechanistic basis for the consistently high invasiveness and clinical severity of S. Dublin infection in various host species [49].

The SNP-based phylogenetic analysis in this study revealed host-associated clades, with most human and cattle-derived isolates forming distinct clusters. Several mixed-host clusters, were also observed, including a cluster containing canine- and human-derived isolates, indicating close genetic relatedness among isolates from different host species [50]. Similar patterns have been observed in earlier studies using whole-genome data, which showed that human isolates often group together with cattle isolates or with strains from cattle products, providing clear evidence that S. Dublin can be transmitted from cattle to humans [22]. Conversely, the presence of mixed human–companion animal clusters raises the possibility of reverse-zoonotic or bidirectional transmission involving humans and dogs, consistent with emerging data on Salmonella transmission in companion animals and their owners [51]. However, genomic clustering alone does not establish direct zoonotic or reverse-zoonotic transmission. In the absence of temporospatial, exposure, contact-tracing, or additional epidemiological data, these mixed-host clusters cannot distinguish direct cross-species transmission from exposure to a shared source or circulation of closely related lineages. These findings reinforce the need for integrated, One Health genomic and epidemiological surveillance to clarify potential transmission pathways and detect emerging lineages with enhanced virulence or resistance profiles.  .

From a public health and disease control perspective, understanding these genomic relationships is particularly valuable for outbreak preparedness and targeted intervention [52]. Early detection of animal-origin strains closely related to human clinical isolates can guide interventions at the herd level, such as enhanced biosecurity, movement restrictions, and tailored antimicrobial stewardship, to interrupt transmission and prevent spillover events [53]. Likewise, identifying resistance determinants and plasmid profiles that are enriched in human or companion-animal isolates but are absent or rare in cattle populations can help prioritize surveillance targets before these elements become established in livestock reservoirs [27]. Taken together, the findings from this comparative genomic analysis underscore that S. Dublin in Florida constitutes a largely clonal, highly virulent, and multidrug-resistant ST10 population with extensive plasmid-encoded AMR and virulence factors shared by cattle, humans, and dogs. These findings highlight that effective control of S. Dublin will require coordinated action across livestock production, companion animal care, and human healthcare to prevent the emergence and dissemination of MDR and highly virulent strains [54].

Despite the insights provided by this study, several limitations should be considered. First, only two canine isolates were included, limiting the strength and generalizability of host-specific comparisons involving dogs. Therefore, the close genomic relatedness observed between canine and human isolates should not be interpreted as evidence of direct transmission. Second, AMR characterization was based on in silico detection of resistance determinants, and phenotypic antimicrobial susceptibility testing could not be performed consistently because the human isolates were available only as archived WGS data with no corresponding bacterial isolates. Therefore, the presence of AMR genes should be interpreted as indication of genotypic resistance potential rather than a confirmation of phenotypic resistance. Future studies should incorporate standardized antimicrobial susceptibility testing to validate the functional significance of the identified resistance determinants. Finally, the isolates were collected exclusively in Florida, which may limit the generalizability of the findings to other geographic regions. Therefore, future studies should include multiple host populations and integrate genomic data with epidemiological investigations and standardized antimicrobial susceptibility testing to better characterize S. Dublin genomic diversity on broader scale.

5. Conclusion

In conclusion, this study demonstrates that S. Dublin circulating in Florida represents a highly clonal, ST10-dominated population with widespread MDR, stable plasmid-mediated AMR dissemination, and conserved invasive virulence determinants in cattle, dogs, and humans. The coexistence of host-associated and mixed-host phylogenetic clusters demonstrates close genomic relatedness among some cattle-, canine-, and human-derived isolates and is consistent with the possible cross-species transmission or exposure to shared sources. However, as these findings are inferred solely from SNP-based genomic similarity and lack epidemiological linkage data, further studies integrating high-resolution genomic analyses with detailed epidemiological investigations are required to validate these associations and clarify potential transmission pathways between host species. The combined presence of MDR plasmids, virulence plasmids, and prophage-associated fitness factors may contribute to the clinical severity and outbreak potential of S. Dublin infections. These findings carry significant implications for animal health, food safety, and public health. The observed genomic relatedness among livestock, companion animals, and human derived isolates highlights the need for integrated One Health surveillance systems that link veterinary diagnostics, public health laboratories, and food production environments. Targeted antimicrobial stewardship in both livestock and companion animal medicine, along with enhanced biosecurity and molecular surveillance of resistance plasmids, will be essential to curtail further spread of multidrug-resistant S. Dublin. Ultimately, coordinated cross-sector control strategies are required to reduce zoonotic risk, protect therapeutic efficacy, and safeguard both animal and human health.

Declaration of generative AI and AI assisted technologies in writing process

During the preparation of this manuscript, the first author utilized AI-based tools to review grammar and spelling. All content was subsequently carefully reviewed and edited by the corresponding author, who assumes full responsibility for the accuracy and integrity of the published work.

CRediT authorship contribution statement

Asanka R. DeZoysa: Writing – review & editing, Writing – original draft, Methodology, Investigation, Formal analysis, Data curation, Conceptualization. Lekshmi K. Edison: Writing – review & editing, Supervision, Software, Methodology, Formal analysis, Data curation. Thomas Denagamage: Writing – review & editing, Validation, Supervision, Resources, Project administration, Methodology, Funding acquisition, Conceptualization. Abraham J. Pellissery: Writing – review & editing, Resources. Yugendar R. Bommineni: Writing – review & editing, Resources. Dilan Satharasinghe: Writing – review & editing. Destini Coiner: Writing – review & editing, Resources. David Simon: Writing – review & editing, Resources. Kelly Tomson: Writing – review & editing, Resources, Data curation. Subhashinie Kariyawasam: Writing – review & editing, Validation, Supervision, Resources, Project administration, Methodology, Funding acquisition, Conceptualization.

Funding

This work was supported by funding from the American Rescue Plan (ARP) for One Health Research through the Florida Department of Agriculture and Consumer Services (FDACS), Award No. 16262.

Declaration of competing interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Acknowledgements

The authors gratefully acknowledge the Bronson Animal Disease Diagnostic Laboratory, Kissimmee, Florida, and the Clinical Microbiology, Parasitology, and Serology Laboratory, College of Veterinary Medicine, University of Florida, for providing S. Dublin isolates for this study. We also thank the Bureau of Public Health Laboratories, Jacksonville, Florida, for sharing raw sequence data of human-derived S. Dublin collected between 2019 and 2024.

Footnotes

Appendix A

Supplementary data to this article can be found online at https://doi.org/10.1016/j.onehlt.2026.101536.

Appendix A. Supplementary data

Supplementary material 1

Genome assembly data of S. Dublin isolates.

mmc1.xlsx (16.7KB, xlsx)
Supplementary material 2

MLST profiles of S. Dublin isolates.

mmc2.xlsx (12KB, xlsx)

Data availability

Genome sequences of animal-derived Salmonella Dublin isolates are available in the NCBI database under the BioProject accession number PRJNA1213829. Genome data for human-derived isolates are not publicly available due to privacy and regulatory restrictions but may be available from the corresponding author upon reasonable request and with appropriate approvals.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

Supplementary material 1

Genome assembly data of S. Dublin isolates.

mmc1.xlsx (16.7KB, xlsx)
Supplementary material 2

MLST profiles of S. Dublin isolates.

mmc2.xlsx (12KB, xlsx)

Data Availability Statement

Genome sequences of animal-derived Salmonella Dublin isolates are available in the NCBI database under the BioProject accession number PRJNA1213829. Genome data for human-derived isolates are not publicly available due to privacy and regulatory restrictions but may be available from the corresponding author upon reasonable request and with appropriate approvals.

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