Editing Salmonella (section)

== Host adaptation ==
''S. enterica'', through some of its serotypes such as Typhimurium and Enteritidis, shows signs that it has the ability to infect several different mammalian host species, while other serotypes, such as Typhi, seem to be restricted to only a few hosts.<ref>{{cite journal | vauthors = Thomson NR, Clayton DJ, Windhorst D, Vernikos G, Davidson S, Churcher C, Quail MA, Stevens M, Jones MA, Watson M, Barron A, Layton A, Pickard D, Kingsley RA, Bignell A, Clark L, Harris B, Ormond D, Abdellah Z, Brooks K, Cherevach I, Chillingworth T, Woodward J, Norberczak H, Lord A, Arrowsmith C, Jagels K, Moule S, Mungall K, Sanders M, Whitehead S, Chabalgoity JA, Maskell D, Humphrey T, Roberts M, Barrow PA, Dougan G, Parkhill J | title = Comparative genome analysis of Salmonella Enteritidis PT4 and Salmonella Gallinarum 287/91 provides insights into evolutionary and host adaptation pathways | journal = Genome Research | volume = 18 | issue = 10 | pages = 1624–1637 | date = October 2008 | pmid = 18583645 | pmc = 2556274 | doi = 10.1101/gr.077404.108 }}</ref> Two ways that ''Salmonella'' serotypes have [[host adaptation|adapted]] to their hosts are by the loss of genetic material, and mutation. In more complex mammalian species, [[immune system]]s, which include pathogen specific immune responses, target serovars of ''Salmonella'' by binding antibodies to structures such as flagella. Thus  ''Salmonella'' that has lost the genetic material which codes for a flagellum to form can evade a host's [[immune system]].<ref>{{cite journal | vauthors = den Bakker HC, Moreno Switt AI, Govoni G, Cummings CA, Ranieri ML, Degoricija L, Hoelzer K, Rodriguez-Rivera LD, Brown S, Bolchacova E, Furtado MR, Wiedmann M | title = Genome sequencing reveals diversification of virulence factor content and possible host adaptation in distinct subpopulations of Salmonella enterica | journal = BMC Genomics | volume = 12 | page = 425 | date = August 2011 | pmid = 21859443 | pmc = 3176500 | doi = 10.1186/1471-2164-12-425 | doi-access = free }}</ref> ''mgtC'' [[Five prime untranslated region|leader RNA]] from bacteria virulence gene (mgtCBR operon) decreases flagellin production during infection by directly base pairing with mRNAs of the ''fljB'' gene encoding flagellin and promotes degradation.<ref>{{cite journal | vauthors = Choi E, Han Y, Cho YJ, Nam D, Lee EJ | title = A ''trans''-acting leader RNA from a ''Salmonella'' virulence gene | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 114 | issue = 38 | pages = 10232–10237 | date = September 2017 | pmid = 28874555 | pmc = 5617274 | doi = 10.1073/pnas.1705437114 | bibcode = 2017PNAS..11410232C | doi-access = free }}</ref> In the study by Kisela ''et al.'', more pathogenic serovars of ''S. enterica'' were found to have certain adhesins in common that have developed out of convergent evolution.<ref>{{cite journal | vauthors = Kisiela DI, Chattopadhyay S, Libby SJ, Karlinsey JE, Fang FC, Tchesnokova V, Kramer JJ, Beskhlebnaya V, Samadpour M, Grzymajlo K, Ugorski M, Lankau EW, Mackie RI, Clegg S, Sokurenko EV | title = Evolution of Salmonella enterica virulence via point mutations in the fimbrial adhesin | journal = PLOS Pathogens | volume = 8 | issue = 6 | pages = e1002733 | year = 2012 | pmid = 22685400 | pmc = 3369946 | doi = 10.1371/journal.ppat.1002733 | doi-access = free }}</ref> This means that, as these strains of ''Salmonella'' have been exposed to similar conditions such as immune systems, similar structures evolved separately to negate these similar, more advanced defenses in hosts. Although many questions remain about how ''Salmonella'' has evolved into so many different types, ''Salmonella'' may have evolved through several phases. For example, as Baumler ''et al.'' have suggested, ''Salmonella'' most likely evolved through [[horizontal gene transfer]], and through the formation of new serovars due to additional [[pathogenicity island]]s, and through an approximation of its ancestry.<ref name="ReferenceA">{{cite journal | vauthors = Bäumler AJ, Tsolis RM, Ficht TA, Adams LG | title = Evolution of host adaptation in Salmonella enterica | journal = Infection and Immunity | volume = 66 | issue = 10 | pages = 4579–4587 | date = October 1998 | pmid = 9746553 | pmc = 108564 | doi = 10.1128/IAI.66.10.4579-4587.1998 }}</ref> So, ''Salmonella'' could have evolved into its many different serotypes by gaining genetic information from different pathogenic bacteria. The presence of several [[pathogenicity island]]s in the genome of different serotypes has lent credence to this theory.<ref name="ReferenceA"/>

''Salmonella'' sv. Newport shows signs of adaptation to a plant-colonization lifestyle, which may play a role in its disproportionate association with food-borne illness linked to produce. A variety of functions selected for during sv. Newport persistence in tomatoes have been reported to be similar to those selected for in sv. Typhimurium from animal hosts.<ref name="Moraes MH 2018">{{cite journal | vauthors = de Moraes MH, Soto EB, Salas González I, Desai P, Chu W, Porwollik S, McClelland M, Teplitski M | title = Genome-Wide Comparative Functional Analyses Reveal Adaptations of ''Salmonella'' sv. Newport to a Plant Colonization Lifestyle | journal = Frontiers in Microbiology | volume = 9 | page = 877 | date = 2018 | pmid = 29867794 | pmc = 5968271 | doi = 10.3389/fmicb.2018.00877 | doi-access = free }}</ref> The ''papA'' gene, which is unique to sv. Newport, contributes to the strain's fitness in tomatoes, and has homologs in the genomes of other Enterobacteriaceae that are able to colonize plant and animal hosts.<ref name="Moraes MH 2018"/>