| Salmonella enterica | |
|---|---|
 | |
| S. enterica Typhimurium colonies on aHektoen enteric agar plate | |
Scientific classification | |
| Domain: | Bacteria |
| Kingdom: | Pseudomonadati |
| Phylum: | Pseudomonadota |
| Class: | Gammaproteobacteria |
| Order: | Enterobacterales |
| Family: | Enterobacteriaceae |
| Genus: | Salmonella |
| Species: | S. enterica |
| Binomial name | |
| Salmonella enterica (ex Kauffmann & Edwards 1952) Le Minor & Popoff 1987 | |
| Subspecies | |
Salmonella enterica (formerlySalmonella choleraesuis) is arod-shaped,flagellate,facultative anaerobic,Gram-negativebacterium and aspecies of thegenusSalmonella.[1] It is divided into six subspecies, arizonae (IIIa), diarizonae (IIIb), houtenae (IV), salamae (II), indica (VI), and enterica (I).[2] A number of itsserovars are serious humanpathogens; many of them are (more specifically) serovars ofSalmonella enterica subsp.enterica.
Most cases of salmonellosis are caused by food infected withS. enterica, which often infects cattle and poultry, though other animals such as domestic cats[3][4] andhamsters[5] have also been shown to be sources of infection in humans. It primarily resides in the intestinal tract of animals and humans and can be found in feedstuff, soil, bedding, litter, and fecal matter.[6]
The primary reservoir for the pathogen is poultry and 70% of human cases are attributed to the consumption of contaminated eggs, chicken, or turkey.[7] Rawchicken eggs andgoose eggs can harborS. enterica, initially in theegg whites, although most eggs are not infected. As the egg ages at room temperature, the yolk membrane begins to break down andS. enterica can spread into theyolk. Refrigeration and freezing do not kill all the bacteria, but substantially slow or halt their growth.Pasteurizing andfood irradiation are used to killSalmonella for commercially produced foodstuffs containing raw eggs such as ice cream. Foods prepared in the home from raw eggs, such asmayonnaise, cakes, and cookies, can spread salmonellae if not properly cooked before consumption. Salmonella is the leading foodborne pathogen in the United States, causing the most deaths and having the highest cost burden.[8] It is a resilient microorganism capable of surviving long periods of time in hot and dry environments, increasing its effectiveness as a pathogen and making it able to survive the harsh environments of the gastrointestinal tract and farms.
S. enterica genomes have been reconstructed from up to 6,500 year old human remains across Western Eurasia, which provides evidence for geographic widespread infections with systemicS. enterica during prehistory, and a possible role of theNeolithization process in the evolution of host adaptation.[9] Additional reconstructed genomes from colonial Mexico suggestS. enterica as the cause ofcocoliztli, an epidemic in 16th-centuryNew Spain.[10] In 1545, this outbreak ofS. enterica spread explosively across what is now Mexico. Over the next century, the disease killed up to 90% of the Indigenous population.[11]
Children under the age of five years, the elderly, andimmunosuppressed adults are at an increased risk of systemic dissemination of the disease and need specialized treatment to combat the disease. Drinking extra fluids andantibiotics such asfluoroquinolones are typical treatments.[12] Complications of the disease often appear as anemia or septicaemia, and the mortality rate is 15% once these symptoms arise.[13]
The serogroupS. Typhi is the cause oftyphoid fever.
S. enterica has six subspecies, and each subspecies has associatedserovars that differ by antigenic specificity.[14]S. enterica has over 2500 serovars.[15]Salmonella bongori was previously considered a subspecies ofS. enterica, but it is now the other species in the genusSalmonella. Most of the humanpathogenicSalmonella serovars belong to theenterica subspecies. These serogroups includeS. Typhi,S. Enteritidis,S. Paratyphi,S. Typhimurium, andS. Choleraesuis. The serovars can be designated as written in the previous sentence (capitalized and nonitalicized following the genus), or as follows: "S. enterica subsp.enterica, serovar Typhi".[16]
SubspeciesS. e.arizonae, named after the state ofArizona, is most commonly found in cold-blooded animals (especially snakes), but can also infect turkey, sheep, and humans. It is endemic in southwestern United States.[17] The similarS. e. subsp.diarizonae also infects snakes and occasionally humans.[18]
Secreted proteins are of major importance for thepathogenesis of infectious diseases caused byS. enterica. A remarkably large number offimbrial and nonfimbrialadhesins are present inSalmonella, and mediatebiofilm formation and contact to host cells. Secreted proteins are also involved in host-cell invasion and intracellular proliferation, two hallmarks ofSalmonella pathogenesis.[19] Regulatory proteins such asIgaA are also involved in maintaining envelope integrity and modulating stress responses during pathogenesis.
Exposure ofS. enterica tobile salts, such as sodiumdeoxycholate, induces theSOS DNA damage response indicating that in this organism bile salts causeDNA damage.[20] Bile salt exposure is found to increaseGC to AT transition mutations and also to induce genes of theOxyR and SoxRS regulons suggesting further that bile salts specifically cause oxidative DNA damage.[20] Mutants ofS. enterica that are defective in enzymes required for the process ofbase excision repair are sensitive to bile salts. This indicates that wild-typeS. enterica uses base excision repair to remove DNA damages caused by the bile salts.[20] TheRecBCD enzyme which functions inrecombinational repair of DNA is also required for bile salt resistance.[citation needed]
Small nonprotein-coding RNAs (sRNA) are able to perform specific functions without being translated into proteins; 97 bacterial sRNAs fromSalmonella Typhi were discovered.[21]
AsdA (antisense RNA of dnaA) is acis-encodedantisense RNA ofdnaA described inS. enterica serovar Typhi. It was discovered by deep sequencing and its transcription was confirmed by Northern blot and RACE analysis. AsdA is estimated to be about 540nucleotides long, and represents the complementary strand to that encoding DnaA, a protein that plays a central role in the initiation of DNA replication and hence cellular division. In rich media, it is highly expressed only after reaching the stationary growth phase, but under limiting iron or osmotic stress, it is already expressed during exponential growth. Overexpression of AsdA stabilizes dnaA mRNA, increasing its levels and thereby enhancing its rate of translation. This suggests that AsdA is a regulator of DNA replication.[22]
