| Salmonella entericasubsp. enterica | |
|---|---|
 | |
| Salmonella Typhimurium colonies on aHektoen enteric agar plate | |
Scientific classification | |
| Domain: | Bacteria |
| Kingdom: | Pseudomonadati |
| Phylum: | Pseudomonadota |
| Class: | Gammaproteobacteria |
| Order: | Enterobacterales |
| Family: | Enterobacteriaceae |
| Genus: | Salmonella |
| Species: | |
| Subspecies: | S. e.subsp. enterica |
| Trinomial name | |
| Salmonella entericasubsp. enterica | |
| Synonyms | |
Bacillus typhosus | |
Salmonella enterica subsp.enterica is asubspecies ofSalmonella enterica, the rod-shaped,flagellated, aerobic,Gram-negativebacterium. Many of the pathogenicserovars of theS. enterica species are in this subspecies, including that responsible fortyphoid.[1]
Salmonella enterica subsp.enterica serovars are defined based on theirsomatic (O) andflagellar (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, likeSalmonella, spread between the environment and people.[3]
A number of techniques are currently used to differentiate betweenserotypes. These include looking for the presence or absence ofantigens,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]
In the United States, the 10Salmonella serovars that caused the most human infections in 2016 are:[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 ofSalmonella enterica subsp.enterica serovars possess serotype-specific virulenceplasmids. 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] In 2012, CDC'sPulseNet became aware of an emergent multi-drug resistant Serovar InfantisSNP cluster, named REPJFX01. This SNP cluster has a large megaplasmid (pESI) that contains multiple drug-resistance genes.[8] The USDA NARMS stated that because of this pESI-plasmid, serovar Infantis is the leading serovar in poultry.[9]NCBI has over 12,500 isolates in the REPJFX01 SNP cluster, with over 3,700 being clinical isolates.[10] Serovar Enteritidis, which is the most common serovar isolated in human clinical cases, has also been found to produceendotoxins, coded by thestn andslyA genes, that attribute to the pathogenicity of Enteritidis.[11]S. enterica serovar Typhimurium can be used to deliver various cancer therapies. Tumors with their immune-suppressive microenvironments allow 1000-fold greater localization of engineeredSalmonella Typhimurium than healthy tissues which are then able to enter tumor cells, lyse and deliver therapies.[12]
In November 2016, a new strain of extensively drug resistant (XDR)Salmonella enterica serovar Typhi emerged in Pakistan, primarily from the cities ofHyderabad andKarachi.[13]Multidrug resistant strains have been present since the late 1970s in Africa and Asia.[14] These XDR strains are resistant to all antibiotic treatment options:chloramphenicol,ampicillin,trimethoprim-sulfamethoxazole,fluoroquinolones, andthird-generation cephalosporins. The outbreak has been ongoing since 2016.[15]
The nomenclature ofSalmonella enterica has long been a topic of debate in the microbiology community.[16] 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.[17] It was not until 2005, that Le Minor and Popoff reproposed and established that "Salmonella enterica" would be the approved species name – excludingSalmonella bongori – and thatSalmonella enterica contains six subspecies, of whichSalmonella enterica subsp.enterica contains the most serovars.[18] Technological advancements allow researchers to use whole genome sequencing data to identify and group serovars using two methods: sequence typing and antigen recognition.[19]
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 designationSalmonella enterica subsp.enterica serovar Typhi is written as such, but in short designation it is written asSalmonella Typhi.[20] Each serovar can have many strains, as well, which allows for a rapid increase in the total number ofantigenically variable bacteria.[21]
The World Health Organization characterizessalmonellosis as a foodborne disease whose symptoms include diarrhea, fever, nausea, vomiting, and in severe cases death.[22]Salmonellosis has been assessed to primarily occur in human hosts due to bacterial colonization of the intestinal tract after the consumption of contaminated food or water, but it is also known to spread from person-to-person via the fecal-oral route.[23] To reduce the risk associated with contracting this disease, proper food safety measures should be applied to high-risk food products including poultry, beef, pork, lamb, eggs, and fresh produce.[24] Food manufacturers, ingredient suppliers, restaurants, and home cooks should practice sanitary processing procedures, store foods below 5 °C, and thoroughly cook all foods to their designated safe-to-eat temperatures.[24] It has become increasingly difficult to mitigate the presence of salmonellosis infections across the human population due to the unique nature of multidrug-resistant serovars as a result of the counterproductive effects to use antibiotics as a broad spectrum treatment.[25] Key hostimmune deficiencies associated withHIV,malaria and malnutrition have contributed to a wide spread of this disease and the need to use expensiveantimicrobial drugs in the poorest health services in the world.[26] But also bacterial factors, such as upregulated activity of the virulence genepgtE, due to asingle nucleotide polymorphism (SNP) in itspromoter region, have been shown to have a great impact upon the pathogenesis of this particularSalmonella sequence type.[27]
There are factors that can increase the infection risk. These include a higher pH in the stomach, gastric resection, and treatment with anti acid buffering.[28] If the stomach has a lower pH, then this helps as adefensive technique to potentially avoid infection.[29]
This strain ismesophilic and some can survive extremely low or high temperatures which can range from 2 °C – 54 °C.[30]Sigma factors inside the cell control thegene expression and they can sense the changes in the environment from theouter membrane by activation of genes that then respond to heat stress and adapt accordingly.[31]S. enterica also can quickly respond to cold temperatures by cold shock proteins (CSP) by synthesizing themselves so that the cell can later resume growth.[32] Chlorine can be a chemical stressor toS. enterica because once chlorine is present,S. enterica can produce abiofilm that provides itself with an exopolysaccharide matrix that has the ability of a chemical attack against chlorine.[33] From this, chlorine has preventative measures for biofilm formation in poultry drinking systems and this reduces the risk ofS. enterica.[34] Successful adaptation allowsS. enterica to withstand more acidic conditions, counteracting stomach antibacterial effects.[35]