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Genetic characteristics:

This Salmonella Typhimurium has been found to be polyphyletic with four lineages identified. According to den Bakker et al. (2011) classification, Salmonella Typhimurium belongs to clade A of Salmonella enterica. This serovar is classified according to the susceptibility to typing phages, in definite phage types (DT); one common DT DT (DT104) has been found to have resistance to ampicillin, chloramphenicol, streptomycin, sulphonamide and tetracycline (ACSSuT resistance type). In England, two outbreaks caused by a multidrug resistant (MDR) strain (ASSuTTm resistant type) of S. Typhimurium DT120 occurred in 2011. A review paper concluded that lineages of S. Typhimurium was associated with different sequence types (STs). While ST19 exhibits a broad host range and commonly causes gastroenteritis in humans, the host-restricted ST313 is predominantly associated with invasive bloodstream infections in sub-Saharan Africa. According to EnteroBase, ST19 accounts for 86% of available S. Typhimurium genomes, whereas ST313 represents only 7%. Epidemic ST19 strains encompass multiple phage types, including DT104 (mainly cattle), DT193/DT120 and U288 (primarily swine), DT8 (ducks/geese), and DT160 (wild birds). Recent advances in genomic classification have introduced a hierarchical clustering (HC) system for Salmonella based on single nucleotide variations (SNVs). At the serotype-defining level (HC900), most S. Typhimurium isolates cluster within HC900_2, with a minority assigned to HC900_6511 and HC900_6910.

Most of the strains of S. Typhimurium contain a plasmid of approx. 90 kb that carry virulence genes (Salmonella virulence plasmid (SVP)). Large resistant plasmids of approx. 200 kb that represented different incompatibility types (e.g., IncHI1), have also been identified in S. Typhimurium. Prophages and genomic islands are important genomic components of serovar Typhimurium; for example, S. Typhimurium str. LT2 has four prophages (Fels-1, Fels-2, Gifsy-1, and Gifsy-2). Pathogenicity islands (SPIs) are found in all S. Typhimurium sequenced to date, this include SPIs-1 to 6, 9, 11 to 14, and 16; being SPI-14 specific to S. Typhimurium. In addition, some genomic islands are strain-specific; for example, S. Typhimurium MDR strain ST1660/06 has three strain-specific genomic islands that encode putative virulence and resistance genes. Genomic islands that encode antibiotic resistance appear to be a common feature of a number of S. Typhimurium MDR strains, these genomic islands include, e.g., Salmonella genomic island 1 (SGI1) described in S. Typhimurium DT104 and genomic island GI-DT12 in S. Typhimurium T000240. The latest genomic island (GI-DT12) contains antibiotic resistance genes (i.e., bla(oxa-30), aadA1, qacEΔ1, and sul1, cat, and tetA) and virulence genes (i.e., the aerobactin iron-acquisition siderophore system (lutA and lucABC), and an iron transporter (sitABCD)). Similarly, another study found that all S. Typhimurium ST313 isolates collected from Nigeria and the Democratic Republic of Congo carried resistance genes, including blaTEM1b, catA1, strA/B, sul1, and dfrA1, along with the aac(6')1aa gene. Phylogenetic analysis showed that Congolese and Nigerian isolates—from both blood and stool—were closely related. Furthermore, comparative genomic analysis uncovered a unique virulence-associated fragment (ST313-TD) shared exclusively by S. Typhimurium ST313 and S. Dublin.

In Sub-Sahara regions of Africa, invasive strains of S. Typhimurium emerged, single nucleotide polymorphism (SNP)-based phylogeny of these invasive strains and strains from other regions, showed two lineages of invasive strains that clustered together. According to den Bakker et al. (2011) classification, Salmonella Typhimurium belongs to clade A.Okoro et al. estimated that these lineages emerged independently around 52 and 35 years ago, closely coinciding with the onset of the current HIV pandemic. The shift from lineage I to lineage II isolates may have been driven by clonal replacement, possibly influenced by chloramphenicol use in treating invasive NTS disease.

Schultz et al. revealed that infection with S. Typhimurium enhances susceptibility to intestinal inflammation in both DSS-treated and IL-10^−/− mice. This heightened vulnerability is linked to the bacterium's ability to persist in the liver and spleen, a process mediated by virulence factors secreted through the type III secretion system encoded by Salmonella Pathogenicity Island 2 (SPI-2/T3SS-2). While vaccination with a live attenuated vaccine moderately reduced the susceptibility of IL-10^−/− mice to S. Typhimurium-induced intestinal inflammation, it failed to eliminate bacterial persistence in these tissues. During 4 to 6 weeks of chronic infections of S. Typhimurium, one mouse harbored phenotypically distinct adapted clones in the spleen versus liver, demonstrating tissue-specific bacterial evolution. Meanwhile, three co-housed mice became intestinally colonized by an identical clone containing a conserved non-synonymous mutation in kdgR (a metabolic transcriptional regulator), strongly suggesting cross-mouse transmission. Phylogenetic tracking revealed this mutation emerged in an index mouse within 14 days post-infection before spreading to two cage-mates. Subsequent challenge experiments confirmed this kdgR-variant possesses superior intestinal colonization capacity compared to wild-type, providing direct evidence of adaptive evolution enhancing enteric fitness.

Animal reservoir: Serovar Typhimurium is host-generalists that can colonize and cause diseases in multiple animal species, including but not limited to cattle, poultry, swine, wild animals, and insects.

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