Abstract
Non-typhoidal Salmonella (NTS) remains a global pathogen that affects a wide range of animal species. We analyzed a large number of NTS isolates of different host origins, including Salmonella Heidelberg (n = 80, avian), S. Dublin (50, bovine), S. Typhimurium var 5- (n = 40, porcine), S. 4,5,12,:i:- (n = 40, porcine), S. Cerro (n = 16, bovine), and S. Montevideo (n = 14, bovine), using virulence profiling of the bcfC, mgtC, ssaC, invE, pefA, stn, sopB, and siiE virulence-associated genes, a biofilm production assay, pulsed field gel electrophoresis, and the full-length sequencing of the fimA (adhesin) and iroN (receptor) genes. We determined a key amino acid substitution, A169 (i.e., threonine changed to alanine at position 169), in the FimA protein that changed ligand affinity of FimA toward N-acetyl-D-glucosamine. This finding clearly indicates the important role of non-synonymous single nucleotide polymorphism (nsSNPs) in adhesin functionality that may impact the host tropism of NTS. This nsSNP was found in S. Heidelberg and S. Cerro isolates. Although this was not the case for the IroN receptor, the phylogeny of this receptor and different host origins of NTS isolates were positively correlated, suggesting existence of specific host immune selective pressures on this unique receptor in S. enterica. We found that pefA, a gene encoding major fimbrial subunit, was the most-segregative virulence factor. It was associated with S. Heidelberg, S. Typhimurium var 5- and S. 4,5,12,:i:- but not with the rest of NTS strains. Further, we observed a significantly higher frequency of non-biofilm producers among NTS strains that do not carry pefA (42.5%) compared to S. Heidelberg (2.5%) and S. Typhimurium var 5- (7.5%) and S. 4,5,12,:i:- (0%). This study provides new insights into the host adaptation of avian and mammalian NTS isolates that are based on the bacterial antigens FimA and IroN as well as the interrelationships between host adaptation, overall genetic relatedness, and virulence potential in these NTS isolates.
Highlights
Non-typhoidal Salmonella (NTS) remains a serious zoonotic pathogen worldwide (Bangtrakulnonth et al, 2004)
Yue et al (2015), examining patho-adaptation of S. enterica serovar Typhimurium in diverse hosts, reported that non-synonymous single-nucleotide polymorphisms in certain antigen genes play an important role in host adaptation of NTS
The occurrence of the eight virulence-associated genes, plasmid-encoded major fimbrial subunit (pefA), siiE, stn, sopB, bcfC, mgtC, ssaC, and invE, among 240 NTS isolates is shown in Table 3, Figure 1
Summary
Non-typhoidal Salmonella (NTS) remains a serious zoonotic pathogen worldwide (Bangtrakulnonth et al, 2004). In contrast to host-range diversity of NTS lineages, typhoidal serovars (TS) of S. enterica have a predilection for specific hosts. Yue et al (2015), examining patho-adaptation of S. enterica serovar Typhimurium in diverse hosts, reported that non-synonymous single-nucleotide polymorphisms (nsSNPs) in certain antigen genes play an important role in host adaptation of NTS. They found distinct host-specific nsSNP signatures within the fimH gene (i.e., gene encoding the type 1 fimbrial adhesion) that may determine NTS host tropism. The genome degradation occurs via the formation of pseudogenes and the shedding of genes involved in the gut colonization and anaerobic catabolism of inflammationderived nutrients (Feasey et al, 2016)
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