Salmonella enterica subsp. enterica

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Salmonella enterica subsp. enterica
Salmonella Typhimurium colonies on a Hektoen enteric agar plate
Scientific classification Edit this classification
Domain: Bacteria
Phylum: Pseudomonadota
Class: Gammaproteobacteria
Order: Enterobacterales
Family: Enterobacteriaceae
Genus: Salmonella
Species:
S. enterica
Subspecies:
S. e. subsp. enterica
Trinomial name
Salmonella enterica subsp. enterica

Salmonella enterica subsp. enterica is a subspecies of Salmonella enterica, the rod-shaped, flagellated, aerobic, Gram-negative bacterium. Many of the pathogenic serovars of the S. enterica species are in this subspecies, including that responsible for typhoid.[1]

Serovars

Salmonella enterica subsp. enterica serovars are defined based on their somatic (O) and flagellar (H) antigens, with over 2,600 serovars in total; only about 50 of these serovars are common causes of infections in humans.[2] Most of these serovars are found in the environment and survive in plants, water, and soil; many serovars have broad host ranges that allow them to colonize different species in mammals, birds, reptiles, amphibians, and insects. Zoonotic diseases, like Salmonella, spread between the environment and people.[3]

A number of techniques are currently used to differentiate between serotypes. These include looking for the presence or absence of antigens, phage typing, molecular fingerprinting and biotyping, where serovars are differentiated by which nutrients they are able to ferment. A possible factor in determining the host range of particular serovars is phage-mediated acquisition of a small number of genetic elements that enable infection of a particular host.[4] It is further postulated that serovars which infect a narrow range of species have diverged from ancestors with a broad host range, and have since specialised and lost the ability to infect some hosts.[5]

The CDC publishes a Salmonella Annual Report with a list of serovars most commonly associated with human illness, the top 10 serovars are listed below:[6]

Rank Serotype Percent
1 Enteritidis 16.8
2 Newport 10.1
3 Typhimurium 9.8
4 Javiana 5.8
5 I 4,[5],12:i:- 4.7
6 Infantis 2.7
7 Muenchen 2.6
8 Montevideo 2.2
9 Braenderup 2.1
10 Thompson 1.7
- Other 41.5

Studies have concluded most strains of Salmonella enterica subsp. enterica serovars possess serotype-specific virulence plasmids. These are plasmid-associated virulence characterized by low-copy-number plasmids and depending on the serovar, its size ranges from 50 to 100 kb.[7] Serovar Enteritidis, which is the most common serovar isolated in human clinical cases, has also been found to produce endotoxins, coded by the stn and slyA genes, that attribute to the pathogenicity of Enteritidis.[8]

In November 2016, a new strain of extensively drug resistant (XDR) Salmonella enterica serovar Typhi emerged in Pakistan, primarily from the cities of Hyderabad and Karachi.[9] Multidrug resistant strains have been present since the late 1970s in Africa and Asia.[10] These XDR strains are resistant to all antibiotic treatment options: chloramphenicol, ampicillin, trimethoprim-sulfamethoxazole, fluoroquinolones, and third-generation cephalosporins. The outbreak has been ongoing since 2016.[11]

Metabolism

Genetic evidence suggests that the serovars can be divided into two groups – one which causes enteric infection and has a broad repertoire of metabolic capabilities, and one which usually causes invasive infection, often in a narrow range of hosts, and shows degradation of anaerobic metabolic pathways. It is thought that these metabolic capabilities are important for obtaining nutrients in the challenging and nutrient-limited inflamed gut environment.[12]


Survival in the stomach

Under normal circumstances, Salmonella enterica infections range from 10^6 and 10^7 bacilli[13]. There are certain scenarios that can occur to decrease the infection risk[14]. These include, a higher pH in the stomach, gastric resection, and treatment with anti acid buffering[15]. It is important to note that if the stomach has a lower pH, then this helps as a defensive technique to potentially fight off this infection[16].

Salmonella Enterica subsp. enterica virulence potential can be linked to higher survival within work that is performed outside a living organism from a human gastrointestinal model. "Food Microbiology" evaluated whether Salmonella virulence could potentially be linked to a greater ability to survive consecutive digestive environments[17]. 13 different strains of S.enterica were selected based upon their high and low virulence phenotypes that were obtained from Dr. Daigle's Labratory[18]. Testing included using lettuce as a food source for the strains to examine the passage through the stomach[19]. After passage, both virulence phenotype strains survived but only the high virulence strain had a greater survival rate[20]. These survival rates could be linked to acid and bile resistant genes that are present. Certain capacities within S.enterica that survive in the human digestion tract have a low pH of the stomach and enzymatic secretions that overall affect the virulence[21].

Nomenclature

The nomenclature of Salmonella enterica has long been a topic of debate in the microbiology community.[22] Originally in the 1880s, Salmonella species were named after the disease, host, or geological location they were associated with; however, this taxonomic characterization was contested due to genus members being categorized incompatibly with their genetic similarities. In the 1980s, the emergence of nucleotide sequencing and DNA hybridization led many established bacteriologists such as Le Minor and Popoff (1987), Euzéby (1999), and Ezaki and Yabuuchi (2000) to put forth their proposals for nomenclature changes to the Judicial Commission.[23] It was not until 2005, that Le Minor and Popoff reproposed and established that "Salmonella enterica" would be the approved species name- excluding Salmonella bongori- and that Salmonella enterica contains six subspecies, of which, Salmonella enterica subsp. enterica contains the most serovars.[24] Today, technological advancements allow researchers to use whole genome sequencing data to identify and group serovars using two methods: sequence typing and antigen recognition[25].

In terms of written serovar nomenclature, it is widely accepted that serovar names are capitalized but not italicized or underlined. Serovars may be designated in full form or short form (includes just the genus and serovar names). For example, in full designation Salmonella enterica subsp. enterica serovar Typhi is written as such, but in short designation it is written as Salmonella Typhi.[26] Each serovar can have many strains, as well, which allows for a rapid increase in the total number of antigenically variable bacteria.[27]

Epidemiology

Main article: Salmonellosis

Invasive strains of non-typhoidal Salmonella, such as Salmonella Typhimurium ST313 have recently been labelled as causing emerging diseases in Africa. Key host immune deficiencies associated with HIV, malaria and malnutrition have contributed to a wide spread of this disease and the need to use expensive antimicrobial drugs in the poorest health services in the world.[28] But also bacterial factors, such as upregulated activity of the virulence gene pgtE, due to a single nucleotide polymorphism (SNP) in its promoter region, have been shown to have a great impact upon the pathogenesis of this particular Salmonella sequence type.[29]

References

  1. ^ Murray PR, Rosenthal KS, Pfaller MA (2009). Medical Microbiology (6th ed.). Philadelphia, PA: Mosby Elsevier. p. 307.
  2. ^ Grimont, Patrick A.D.; Weill, François-Xavier (2007). "Antigenic formulae of the Salmonella serovars". WHO Collaborating Centre for Reference and Research on Salmonella – via Academia.edu.
  3. ^ Silva, C.; Calva, E.; Maloy, S. (2014). "One Health and Food-Borne Disease: Salmonella Transmission between Humans, Animals, and Plants". Microbiology Spectrum. 2 (1).
  4. ^ Wolfgang R, Helene A, Robert K, Rita P, Helmut T, Garry A, Andreas B (May 2002). "Salmonella enterica Serotype Typhimurium and Its Host-Adapted Variants". Infection and Immunity. 70 (5): 2249–2253. doi:10.1128/IAI.70.5.2249-2255.2002. PMC 127920. PMID 11953356.
  5. ^ Langridge GC, Fookes M, Connor TR, Feltwell T, Feasey N, Parsons BN, Seth-Smith HM, Barquist L, Stedman A, Humphrey T, Wigley P, Peters SE, Maskell DJ, Corander J, Chabalgoity JA, Barrow P, Parkhill J, Dougan G, Thomson NR (January 2015). "Patterns of genome evolution that have accompanied host adaptation in Salmonella". Proceedings of the National Academy of Sciences of the United States of America. 112 (3): 863–8. Bibcode:2015PNAS..112..863L. doi:10.1073/pnas.1416707112. PMC 4311825. PMID 25535353.
  6. ^ "National Enteric Disease Surveillance: Salmonella Annual Report, 2016" (PDF). CDC.gov. 2016.
  7. ^ Rotger, R.; Casadesüs, J. (1999). "The virulence plasmids of Salmonella" (PDF). Int Microbiology: 177–184.
  8. ^ Ashkenazi, S.; Cleary, T.; Murray, B.; Wanger, A.; Pickering, L. (1988). "Quantitative analysis and partial characterization of cytotoxin production by Salmonella strains" (PDF). Infect. Immun.: 3089–3094.
  9. ^ "Typhoid Outbreak in Pakistan Linked to Extensively Drug-Resistant Bacteria". The Scientist Magazine®. Retrieved 2018-09-03.
  10. ^ Klemm, Elizabeth J.; Shakoor, Sadia; Page, Andrew J.; Qamar, Farah Naz; Judge, Kim; Saeed, Dania K.; Wong, Vanessa K.; Dallman, Timothy J.; Nair, Satheesh (2018-02-20). "Emergence of an Extensively Drug-Resistant Salmonella enterica Serovar Typhi Clone Harboring a Promiscuous Plasmid Encoding Resistance to Fluoroquinolones and Third-Generation Cephalosporins". mBio. 9 (1). doi:10.1128/mBio.00105-18. ISSN 2150-7511. PMC 5821095. PMID 29463654.
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  13. ^ Kingsley, Robert Anthony. Iron Uptake and Metabolism by Salmonella Enterica. Jan. 1997. EBSCOhost, search.ebscohost.com/login.aspx?direct=true&AuthType=ip,shib&db=edsble&AN=edsble.696232&site=eds-live.
  14. ^ Kingsley, Robert Anthony. Iron Uptake and Metabolism by Salmonella Enterica. Jan. 1997. EBSCOhost, search.ebscohost.com/login.aspx?direct=true&AuthType=ip,shib&db=edsble&AN=edsble.696232&site=eds-live.
  15. ^ Kingsley, Robert Anthony. Iron Uptake and Metabolism by Salmonella Enterica. Jan. 1997. EBSCOhost, search.ebscohost.com/login.aspx?direct=true&AuthType=ip,shib&db=edsble&AN=edsble.696232&site=eds-live.
  16. ^ Kingsley, Robert Anthony. Iron Uptake and Metabolism by Salmonella Enterica. Jan. 1997. EBSCOhost, search.ebscohost.com/login.aspx?direct=true&AuthType=ip,shib&db=edsble&AN=edsble.696232&site=eds-live.
  17. ^ Cavestri, C., Savard, P., Fliss, I., Emond-Rhéault, J. G., Hamel, J., Kukavica-Ibrulj, I., Boyle, B., Daigle, F., Malo, D., Bekal, S., Harris, L. J., Levesque, R. C., Goodridge, L., & Lapointe, G. (2021). Salmonella enterica subsp. enterica virulence potential can be linked to higher survival within a dynamic in vitro human gastrointestinal model. Food Microbiology, 101. https://doi.org/https://www.sciencedirect.com/science/article/pii/S0740002021001428
  18. ^ Crouse, A., Schramm, C., Emond, J.-G., Herod, A., Kerhoas, M., Rohde, J., Gruenheid, S., Greenwood, C., Goodridge, L.D., Garduno, R., Levesque, R.C., Malo, D., Daigle, F., 2020. Combining whole genome sequencing and multi-model phenotyping to identify genetic predictors of Salmonella virulence. mSphere 5. https://doi.org/ 10.1128/mSphere .00293-20 e00293-20.
  19. ^ Ribnicky, D.M., Roopchand, D.E., Oren, A., Grace, M., Poulev, A., Lila, M.A., Havenaar, R., Raskin, I., 2014. Effects of a high fat meal matrix and protein complexation on the bioaccessibility of blueberry anthocyanins using the TNO gastrointestinal model (TIM-1). Food Chem. 142, 349–357. https://doi.org/ 10.1016/j.foodchem.2013.07.073.
  20. ^ Cavestri, C., Savard, P., Fliss, I., Emond-Rhéault, J. G., Hamel, J., Kukavica-Ibrulj, I., Boyle, B., Daigle, F., Malo, D., Bekal, S., Harris, L. J., Levesque, R. C., Goodridge, L., & Lapointe, G. (2021). Salmonella enterica subsp. enterica virulence potential can be linked to higher survival within a dynamic in vitro human gastrointestinal model. Food Microbiology, 101. https://doi.org/https://www.sciencedirect.com/science/article/pii/S0740002021001428
  21. ^ Alvarez-Ord ´ o´nez, ˜ A., Begley, M., Prieto, M., Messens, W., Lopez, ´ M., Bernardo, A., Hill, C., 2011. Salmonella spp. survival strategies within the host gastrointestinal tract. Microbiology 157, 3268–3281. https://doi.org/10.1099/mic.0.050351-0
  22. ^ Su, Lin-Hui (2007). [chrome-extension://efaidnbmnnnibpcajpcglclefindmkaj/http://cgmj.cgu.edu.tw/3003/300302.pdf "Salmonella: Clinical Importance and Evolution of Nomenclature"] (PDF). Chang Gung Medical Journal. 30 (3): 210. {{cite journal}}: Check |url= value (help)
  23. ^ Agbaje, M.; Begum, R. H.; Oyekunle, M. A.; Ojo, O. E.; Adenubi, O. T. (November 2011). "Evolution of Salmonella nomenclature: a critical note". Folia Microbiologica. 56 (6): 497–503. doi:10.1007/s12223-011-0075-4. ISSN 0015-5632.
  24. ^ Brenner, F. W.; Villar, R. G.; Angulo, F. J.; Tauxe, R.; Swaminathan, B. (July 2000). "Salmonella Nomenclature". Journal of Clinical Microbiology. 38 (7): 2465–2467. doi:10.1128/JCM.38.7.2465-2467.2000. ISSN 0095-1137. PMC 86943. PMID 10878026.
  25. ^ Chattaway, Marie A.; Langridge, Gemma C.; Wain, John (2021-04-05). "Salmonella nomenclature in the genomic era: a time for change". Scientific Reports. 11 (1): 7494. doi:10.1038/s41598-021-86243-w. ISSN 2045-2322. PMC 8021552. PMID 33820940.
  26. ^ "Scientific Nomenclature". Emerging Infectious Dieases. Centers for Disease Control and Prevention. Retrieved 17 February 2020.
  27. ^ "Salmonella spp. comparative sequencing". Archived from the original on 2007-11-14.
  28. ^ Feasey NA, Dougan G, Kingsley RA, Heyderman RS, Gordon MA (June 2012). "Invasive non-typhoidal salmonella disease: an emerging and neglected tropical disease in Africa". Lancet. 379 (9835): 2489–99. doi:10.1016/s0140-6736(11)61752-2. PMC 3402672. PMID 22587967.
  29. ^ Hammarlöf DL, Kröger C, Owen SV, Canals R, Lacharme-Lora L, Wenner N, Schager AE, Wells TJ, Henderson IR, Wigley P, Hokamp K, Feasey NA, Gordon MA, Hinton JC (March 2018). "Salmonella". Proceedings of the National Academy of Sciences of the United States of America. 115 (11): E2614–E2623. doi:10.1073/pnas.1714718115. PMC 5856525. PMID 29487214.
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