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Genetic characteristics: Parkhill et al. sequenced the complete genome (4,809,037 bp) of Salmonella Typhi (CT18) and found this isolate exhibited substantial genetic decay with over 200 pseudogenes, including homologs of key Salmonella Typhimurium virulence genes (e.g., sopE2 and fliB), potentially explaining its human-restricted host specificity. This isolate carries two plasmids: a 218,150 bp multidrug-resistant IncHI1 plasmid (pHCM1) and a 106,516 bp cryptic plasmid (pHCM2) phylogenetically linked to a virulence plasmid of Yersinia pestis. Additionally, it harbors up to 15 Salmonella pathogenicity islands (SPIs 1–7, 9, 11–13, and 15–18). Comparative genomics and phylogenetic analyses have shown that serovar Typhi (i) had a monophyletic origin (ii) emerged approx. 30,000 to 50,000 years ago (iii) belonged to clade A, according to den Bakker et al. (2011) classification, and (iv) had 349 gene families unique to this serovar.

REPJP01, an emerging multidrug-resistant strain of Salmonella Typhi, was first identified in Pakistan (2016) and subsequently reported in US cases (2018). Notably, 90% of clinical isolates demonstrate resistance to five first-line antimicrobials: ampicillin, ceftriaxone, chloramphenicol, ciprofloxacin, and trimethoprim-sulfamethoxazole. Marchello et al. collectively analyzed 55,459 isolates (from 198 studies) and revealed that in Asia (2015–2018), 32.6% of isolates were multidrug-resistant (MDR; resistant to chloramphenicol, ampicillin, and trimethoprim-sulfamethoxazole in their study), with 5.7% resistant to third-generation cephalosporins and 8.3% to azithromycin. Interestingly, Pakistan reported extensively drug-resistant (XDR) strains (2.6% of isolates; MDR plus fluoroquinolone and cephalosporin resistance). In Africa, MDR prevalence rose steadily each decade (1990–2018), though XDR emergence remains unreported. 

Animal reservoir: Salmonella Typhi is a human-restricted serovar.

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