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Genetic characteristics: This serovar is further classified according to the susceptibility to typing phages (phage typing (PT)), the most common PTs are PT8 and PT4. Molecular subtyping with Pulse field gel electrophoresis (PFGE) shows that approx. 40% of the isolates fall in the same PFGE type. Invasive strains of serovar Enteritidis emerged in sub-Sahara regions of Africa and have caused systemic salmonellosis in travelers returning from Africa. Serovar Nitra and Enteritidis have antigenic formulas that differ only in their O antigens. Although serovar Nitra is very rare, it is genetically indistinguishable from serovar Enteritidis. Chen et al. found that Salmonella Enteritidis is a polyphyletic serovar comprised of six phylogenetic groups and two stand-alone singletons that do not cluster with any other Salmonella Enteritidis isolates. Within Enteritidis-A-7 (chicken-associated; estimated emergence in 1633), they identified four clonal sub-clades. Cao et al. analyzed Enteritidis isolates collected worldwide from humans and concluded that in clades I and IV, most isolates were pan-susceptible, while 81.8% (9/11) of isolates in clade III and 22.4% (13/58) in clade II were multidrug-resistant (MDR). Notably, 77% (10/13) of the MDR isolates in clade II originated from China. The most common antimicrobial resistance genes (ARGs) found in the Chinese isolates were aph(3′)-IIa, blaCTX-M-55, and blaTEM-1B, whereas the most prevalent ARGs in the African isolates (clade III) were blaTEM-1B, sul1, sul2, drfA7, aph(3")-Ib/strA, and aph(6)-Id/strB. Of the 14 plasmid types identified, IncX1 and IncFII(pHN7A8) were exclusive to the Chinese MDR isolates, while IncQ1 was strongly linked to the African MDR isolates. A Chinese study revealed that serovar Enteritidis triggers an inflammatory response through SPI-1 and SPI-2, which enhances intracellular proliferation and bacterial virulence. A protein–protein interaction prediction revealed a connection between virulence proteins and T3SS proteins, with PagN interacting with T3SS-related proteins to collectively mediate the invasion of the Enteritidis 27A strain into the human body.
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