Salmonella species areintracellular pathogens,[6] of which certain serotypes cause illness such assalmonellosis. Most infections are due to the ingestion offood contaminated by feces. TyphoidalSalmonella serotypes can only be transferred between humans and can causefoodborne illness as well astyphoid and paratyphoid fever. Typhoid fever is caused by typhoidalSalmonella invading the bloodstream, as well as spreading throughout the body, invading organs, and secretingendotoxins (the septic form). This can lead to life-threateninghypovolemic shock andseptic shock, and requiresintensive care, includingantibiotics.
NontyphoidalSalmonella serotypes arezoonotic and can be transferred from animals and between humans. They usually invade only thegastrointestinal tract and cause salmonellosis, the symptoms of which can be resolved without antibiotics. However, insub-Saharan Africa, nontyphoidalSalmonella can be invasive and causeparatyphoid fever, which requires immediate antibiotic treatment.[7]
The genusSalmonella is part of the family of Enterobacteriaceae. Its taxonomy has been revised and has the potential to confuse. The genus comprises two species,S. bongori andS. enterica, the latter of which is divided into six subspecies:S. e. enterica,S. e. salamae,S. e. arizonae,S. e. diarizonae,S. e. houtenae, andS. e. indica.[8][9] The taxonomic group contains more than 2500serotypes (also serovars) defined on the basis of the somatic O (lipopolysaccharide) and flagellar H antigens (theKauffman–White classification). The full name of a serotype is given as, for example,Salmonella enterica subsp.enterica serotype Typhimurium, but can be abbreviated toSalmonella Typhimurium. Further differentiation of strains to assistclinical andepidemiological investigation may be achieved byantibiotic sensitivity testing and by othermolecular biology techniques such aspulsed-field gel electrophoresis,multilocus sequence typing, and, increasingly,whole genome sequencing. Historically, salmonellae have been clinically categorized as invasive (typhoidal) or non-invasive (nontyphoidal salmonellae) based on host preference and disease manifestations in humans.[10]
Salmonella was first visualized in 1880 byKarl Eberth in thePeyer's patches andspleens of typhoid patients.[11] Four years later,Georg Theodor Gaffky was able to grow the pathogen in pure culture.[12] A year after that, medical research scientistTheobald Smith discovered what would be later known asSalmonella enterica (var. Choleraesuis). At the time, Smith was working as a research laboratory assistant in the Veterinary Division of theUnited States Department of Agriculture. The division was under the administration ofDaniel Elmer Salmon, a veterinary pathologist.[13] Initially,Salmonella Choleraesuis was thought to be the causative agent ofhog cholera, so Salmon and Smith named it "Hog-cholera bacillus". The nameSalmonella was not used until 1900, whenJoseph Leon Lignières proposed that the pathogen discovered by Salmon's group be calledSalmonella in his honor.[14]: 16
In the late 1930s, AustralianbacteriologistNancy Atkinson established a salmonella typing laboratory – one of only three in the world at the time – at theGovernment of South Australia'sLaboratory of Pathology and Bacteriology inAdelaide (later the Institute of Medical and Veterinary Science). It was here that Atkinson described multiple new strains of salmonella, including Salmonella Adelaide, which was isolated in 1943. Atkinson published her work on salmonellas in 1957.[15]
Serotyping is done by mixing cells with antibodies for a particular antigen. It can give some idea about risk. A 2014 study showed thatS. Reading is very common among youngturkey samples, but it is not a significant contributor to human salmonellosis.[16] Serotyping can assist in identifying the source of contamination by matching serotypes in people with serotypes in the suspected source of infection.[17] Appropriate prophylactic treatment can be identified from the known antibiotic resistance of the serotype.[18]
Newer methods of "serotyping" include xMAP andreal-time PCR, two methods based on DNA sequences instead of antibody reactions. These methods can be potentially faster, thanks to advances in sequencing technology. These "molecular serotyping" systems actually performgenotyping of the genes that determine surface antigens.[19][20]
Most subspecies ofSalmonella producehydrogen sulfide,[21] which can readily be detected by growing them onmedia containingferrous sulfate, such as is used in thetriple sugar iron test. Most isolates exist in two phases, a motile phase and a non-motile phase. Cultures that are nonmotile upon primary culture may be switched to the motile phase using aCraigie tube or ditch plate.[22]RVS broth can be used to enrich forSalmonella species for detection in a clinical sample.[23]
Mathematical models ofSalmonella growth kinetics have been developed for chicken, pork, tomatoes, and melons.[26][27][28][29][30]Salmonella reproduce asexually with a cell division interval of 40 minutes.[14][16][17][18]
Salmonella species lead predominantly host-associated lifestyles, but the bacteria were found to be able to persist in a bathroom setting for weeks following contamination, and are frequently isolated from water sources, which act as bacterial reservoirs and may help to facilitate transmission between hosts.[31]Salmonella is notorious for its ability to survive desiccation and can persist for years in dry environments and foods.[32]
The bacteria are not destroyed by freezing,[33][34] butUV light and heat accelerate their destruction. They perish after being heated to 55 °C (131 °F) for 90 min, or to 60 °C (140 °F) for 12 min,[35] although if inoculated in high fat, high liquid substances like peanut butter, they gain heat resistance and can survive up to 90 °C (194 °F) for 30 min.[36] To protect againstSalmonella infection, heating food to an internal temperature of 75 °C (167 °F) is recommended.[37][38]
Salmonella species can be found in the digestive tracts of humans and animals, especially reptiles.Salmonella on the skin of reptiles or amphibians can be passed to people who handle the animals.[39] Food and water can also be contaminated with the bacteria if they come in contact with the feces of infected people or animals.[40]
Initially, eachSalmonella "species" was named according to clinical consideration, for exampleSalmonella typhi-murium (mouse-typhoid),S. cholerae-suis (pig-cholera). After host specificity was recognized not to exist for many species, new strains received species names according to the location at which the new strain was isolated.[41]
In 1987, Le Minor and Popoff used molecular findings to argue thatSalmonella consisted of only one species,S. enterica, turning former "species" names intoserotypes.[42] In 1989, Reeveset al. proposed that the serotype V should remain its own species, resurrecting the nameS. bongori.[43] The current (by 2005) nomenclature has thus taken shape, with six recognised subspecies underS. enterica:enterica (serotype I),salamae (serotype II),arizonae (IIIa),diarizonae (IIIb),houtenae (IV), andindica (VI).[3][44][45][46] As specialists in infectious disease are not familiar with the new nomenclature, the traditional nomenclature remains common.[citation needed]
The serotype or serovar is a classification ofSalmonella based on antigens that the organism presents. TheKauffman–White classification scheme differentiates serological varieties from each other. Serotypes are usually put into subspecies groups after the genus and species, with the serotypes/serovars capitalized, but not italicized: An example isSalmonella enterica serovar Typhimurium. More modern approaches for typing and subtypingSalmonella include DNA-based methods such aspulsed field gel electrophoresis,multiple-loci VNTR analysis,multilocus sequence typing, and multiplex-PCR-based methods.[47][48]
In 2005, a third species,Salmonella subterranea, was proposed, but according to theWorld Health Organization, the bacterium reported does not belong in the genusSalmonella.[49] In 2016,S. subterranea was proposed to be assigned toAtlantibacter subterranea,[50] but LPSN rejects it as aninvalid publication, as it was made outside of IJSB and IJSEM.[51]GTDB and NCBI agree with the 2016 reassignment.[52][53]
GTDB RS202 reports thatS. arizonae,S. diarizonae, andS. houtenae should be species of their own.[54]
Most infections are due to ingestion of food contaminated by animal feces, or by human feces (for example, from the hands of a food-service worker at a commercial eatery).Salmonella serotypes can be divided into two main groups—typhoidal and nontyphoidal. Typhoidal serotypes includeSalmonella Typhi andSalmonella Paratyphi A, which are adapted to humans and do not occur in other animals. Nontyphoidal serotypes are more common, and usually cause self-limitinggastrointestinal disease. They can infect a range of animals, and arezoonotic, meaning they can be transferred between humans and other animals.[57][58]
Salmonella pathogenicity and host interaction has been studied extensively since the 2010s. Most of the important virulent genes ofSalmonella are encoded in five pathogenicity islands—the so-calledSalmonella pathogenicity islands (SPIs). These are chromosomal encoded and make a significant contribution to bacterial-host interaction. More traits, like plasmids, flagella orbiofilm-related proteins, can contribute in the infection. SPIs are regulated by complex and fine-tuned regulatory networks that allow the gene expression only in the presence of the right environmental stresses.[59]
Molecular modeling and active site analysis of SdiA homolog, a putative quorum sensor for Salmonella typhimurium pathogenicity, reveals the specific binding patterns of AHL transcriptional regulators.[60] It is also known that Salmonella plasmid virulence gene spvB enhances bacterial virulence by inhibiting autophagy.[61]
Typhoid fever is caused bySalmonella serotypes which are strictly adapted to humans or higher primates—these includeSalmonella Typhi, Paratyphi A, Paratyphi B, and Paratyphi C. In the systemic form of the disease, salmonellae pass through the lymphatic system of the intestine into the blood of the patients (typhoid form) and are carried to various organs (liver, spleen, kidneys) to form secondary foci (septic form). Endotoxins first act on the vascular and nervous apparatus, resulting in increased permeability and decreased tone of the vessels, upset of thermal regulation, and vomiting and diarrhoea. In severe forms of the disease, enough liquid and electrolytes are lost to upset the water-salt metabolism, decrease the circulating blood volume and arterial pressure, and causehypovolemic shock.Septic shock may also develop. Shock of mixed character (with signs of both hypovolemic and septic shock) is more common in severesalmonellosis.Oliguria andazotemia may develop in severe cases as a result of renal involvement due tohypoxia andtoxemia.[citation needed]
Infection with nontyphoidal serotypes ofSalmonella generally results infood poisoning. Infection usually occurs when a person ingests foods that contain a high concentration[clarification needed] of the bacteria. Infants and young children are much more susceptible to infection, easily achieved by ingesting a small number[clarification needed] of bacteria. In infants, infection through inhalation of bacteria-laden dust is possible.[62]
The organisms enter through the digestive tract and must be ingested in large numbers to cause disease in healthy adults. An infection can only begin after living salmonellae (not merelySalmonella-produced toxins) reach the gastrointestinal tract. Some of the microorganisms are killed in the stomach, while the surviving ones enter the small intestine and multiply in tissues. Gastric acidity is responsible for the destruction of the majority of ingested bacteria, butSalmonella has evolved a degree of tolerance to acidic environments that allows a subset of ingested bacteria to survive.[63] Bacterial colonies may also become trapped in mucus produced in the esophagus. By the end of the incubation period, the nearby host cells are poisoned byendotoxins released from the dead salmonellae. The local response to the endotoxins is enteritis and gastrointestinal disorder.[citation needed]
About 2,000 serotypes of nontyphoidalSalmonella are known, which may be responsible for as many as 1.4 million illnesses in the United States each year. People who are at risk for severe illness include infants, elderly, organ-transplant recipients, and the immunocompromised.[40]
While, in developed countries, nontyphoidal serotypes present mostly as gastrointestinal disease, in sub-Saharan Africa, these serotypes can create a major problem in bloodstream infections, and are the most commonly isolated bacteria from the blood of those presenting with fever. Bloodstream infections caused by nontyphoidal salmonellae in Africa were reported in 2012 to have acase fatality rate of 20–25%. Most cases of invasive nontyphoidalSalmonella infection (iNTS) are caused bySalmonella enterica Typhimurium orSalmonella enterica Enteritidis. A new form ofSalmonella Typhimurium (ST313) emerged in the southeast of the African continent 75 years ago, followed by a second wave which came out of central Africa 18 years later. This second wave of iNTS possibly originated in theCongo Basin, and early in the event picked up a gene that made it resistant to the antibioticchloramphenicol. This created the need to use expensive antimicrobial drugs in areas of Africa that were very poor, making treatment difficult. The increased prevalence of iNTS in sub-Saharan Africa compared to other regions is thought to be due to the large proportion of the African population with some degree of immune suppression or impairment due to the burden ofHIV,malaria, and malnutrition, especially in children. The genetic makeup of iNTS is evolving into a more typhoid-like bacterium, able to efficiently spread around the human body. Symptoms are reported to be diverse, including fever,hepatosplenomegaly, and respiratory symptoms, often with an absence of gastrointestinal symptoms.[64]
Due to being considered sporadic, between 60% and 80% of salmonella infections cases go undiagnosed.[65] In March 2010, data analysis was completed to estimate anincidence rate of 1140 per 100,000 person-years. In the same analysis, 93.8 million cases ofgastroenteritis were due to salmonella infections. At the 5th percentile the estimated amount was 61.8 million cases and at the 95th percentile the estimated amount was 131.6 million cases. The estimated number of deaths due to salmonella was approximately 155,000 deaths.[66] In 2014, in countries such as Bulgaria and Portugal, children under 4 were 32 and 82 times more likely, respectively, to have a salmonella infection.[67] Those who are most susceptible to infection are: children, pregnant women, elderly people, and those with deficient immune systems.[68]
Risk factors for Salmonella infections include a variety of foods. Meats such as chicken and pork have the possibility to be contaminated. A variety of vegetables and sprouts may also have salmonella. Lastly, a variety of processed foods such as chicken nuggets and pot pies may also contain this bacteria.[69]
Successful forms of prevention come from existing entities such as theFDA,United States Department of Agriculture, and theFood Safety and Inspection Service. All of these organizations create standards and inspections to ensure public safety in theU.S. For example, theFSIS agency working with the USDA has a Salmonella Action Plan in place. Recently, it received a two-year plan update in February 2016. Their accomplishments and strategies to reduce Salmonella infection are presented in the plans.[70] TheCenters for Disease Control and Prevention also provides valuable information on preventative care, such has how to safely handle raw foods, and the correct way to store these products. In theEuropean Union, theEuropean Food Safety Authority created preventative measures through risk management and risk assessment. From 2005 to 2009, the EFSA placed an approach to reduce exposure toSalmonella. Their approach included risk assessment and risk management of poultry, which resulted in a reduction of infection cases by one half.[71] InLatin America an orally administered vaccine for Salmonella in poultry developed by Dr. Sherry Layton has been introduced which prevents the bacteria from contaminating the birds.[72]
ASalmonella Typhimurium outbreak in 2022 was linked to chocolate produced in Belgium, leading to the country temporarily halting Kinder chocolate production.[73][74]
In Germany, food-borne infections must be reported.[75] From 1990 to 2016, the number of officially recorded cases decreased from about 200,000 to about 13,000 cases.[76] In the United States, about 1,200,000 cases ofSalmonella infection are estimated to occur each year.[77] A World Health Organization study estimated that 21,650,974 cases of typhoid fever occurred in 2000, 216,510 of which resulted in death, along with 5,412,744 cases of paratyphoid fever.[78]
The mechanisms of infection differ between typhoidal and nontyphoidal serotypes, owing to their different targets in the body and the different symptoms that they cause. Both groups must enter by crossing the barrier created by the intestinal cell wall, but once they have passed this barrier, they use different strategies to cause infection.[citation needed]
While travelling to their target tissue in the gastrointestinal tract,Salmonella is exposed to stomach acid, to the detergent-like activity of bile in the intestine, to decreasing oxygen supply, to the competing normal gut flora, and finally to antimicrobial peptides present on the surface of the cells lining the intestinal wall. All of these form stresses thatSalmonella can sense and reacts against, and they formvirulence factors and as such regulate the switch from their normal growth in the intestine intovirulence.[79]
The switch to virulence gives access to a replicationniche inside the host (such as humans), and can be summarised into several stages:[citation needed]
Approach, in which they travel towards a host cell via intestinalperistalsis and through active swimming via theflagella, penetrate the mucus barrier, and locate themselves close to theepithelium lining the intestine,
Invasion, in whichSalmonella enter the host cell (see variant mechanisms below),
Replication, in which the bacterium may reproduce inside the host cell,
Spread, in which the bacterium can spread to other organs via cells in the blood (if it succeeded in avoiding the immune defence). Alternatively, bacteria can go back towards the intestine, re-seeding the intestinal population.
Re-invasion (asecondary infection, if now at a systemic site) and further replication.
Nontyphoidal serotypes preferentially enterM cells on the intestinal wall by bacterial-mediatedendocytosis, a process associated with intestinal inflammation and diarrhoea. They are also able to disrupttight junctions between the cells of the intestinal wall, impairing the cells' ability to stop the flow ofions, water, and immune cells into and out of the intestine. The combination of the inflammation caused by bacterial-mediated endocytosis and the disruption of tight junctions is thought to contribute significantly to the induction of diarrhoea.[80]
Salmonellae are also able to breach the intestinal barrier viaphagocytosis and trafficking byCD18-positive immune cells, which may be a mechanism key to typhoidalSalmonella infection. This is thought to be a more stealthy way of passing the intestinal barrier, and may, therefore, contribute to the fact that lower numbers of typhoidalSalmonella are required for infection than nontyphoidalSalmonella.[80]Salmonella cells are able to entermacrophages viamacropinocytosis.[81] Typhoidal serotypes can use this to achieve dissemination throughout the body via themononuclear phagocyte system, a network of connective tissue that contains immune cells, and surrounds tissue associated with the immune system throughout the body.[80]
Much of the success ofSalmonella in causing infection is attributed to twotype III secretion systems (T3SS) which are expressed at different times during the infection. The T3SS-1 enables the injection of bacterial effectors within the host cytosol. These T3SS-1 effectors stimulate the formation of membrane ruffles allowing the uptake ofSalmonella bynonphagocytic cells.Salmonella further resides within a membrane-bound compartment called theSalmonella-Containing Vacuole (SCV). The acidification of the SCV leads to the expression of the T3SS-2. The secretion of T3SS-2 effectors bySalmonella is required for its efficient survival in the host cytosol and establishment of systemic disease.[80] In addition, both T3SS are involved in the colonization of the intestine, induction of intestinal inflammatory responses and diarrhea. These systems contain many genes which must work cooperatively to achieve infection.[citation needed]
Salmonellosis is known to be able to causeback pain orspondylosis. It can manifest as five clinical patterns: gastrointestinal tract infection, enteric fever, bacteremia, local infection, and the chronic reservoir state. The initial symptoms are nonspecific fever, weakness, and myalgia among others. In the bacteremia state, it can spread to any parts of the body and this induces localized infection or it forms abscesses. The forms of localizedSalmonella infections are arthritis, urinary tract infection, infection of the central nervous system, bone infection, soft tissue infection, etc.[83] Infection may remain as the latent form for a long time, and when the function ofreticular endothelial cells is deteriorated, it may become activated and consequently, it may secondarily induce spreading infection in the bone several months or several years after acute salmonellosis.[83]
A hallmark ofSalmonella pathogenesis is the ability of the bacterium to survive and proliferate withinphagocytes. Phagocytes produce DNA-damaging agents such asnitric oxide and oxygenradicals as a defense against pathogens. Thus,Salmonella species must face attack by molecules that challenge genome integrity. Buchmeier et al.[86] showed that mutants ofS. enterica lacking RecA or RecBC protein function are highly sensitive to oxidative compounds synthesized by macrophages, and furthermore these findings indicate that successful systemic infection byS. enterica requires RecA- and RecBC-mediated recombinational repair of DNA damage.[86][87]
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.[88] Two ways thatSalmonella serotypes haveadapted to their hosts are by the loss of genetic material, and mutation. In more complex mammalian species,immune systems, which include pathogen specific immune responses, target serovars ofSalmonella by binding antibodies to structures such as flagella. ThusSalmonella that has lost the genetic material which codes for a flagellum to form can evade a host'simmune system.[89]mgtCleader RNA from bacteria virulence gene (mgtCBR operon) decreases flagellin production during infection by directly base pairing with mRNAs of thefljB gene encoding flagellin and promotes degradation.[90] In the study by Kiselaet al., more pathogenic serovars ofS. enterica were found to have certain adhesins in common that have developed out of convergent evolution.[91] This means that, as these strains ofSalmonella 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 howSalmonella has evolved into so many different types,Salmonella may have evolved through several phases. For example, as Baumleret al. have suggested,Salmonella most likely evolved throughhorizontal gene transfer, and through the formation of new serovars due to additionalpathogenicity islands, and through an approximation of its ancestry.[92] So,Salmonella could have evolved into its many different serotypes by gaining genetic information from different pathogenic bacteria. The presence of severalpathogenicity islands in the genome of different serotypes has lent credence to this theory.[92]
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.[93] ThepapA 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.[93]
In addition to their importance as pathogens, nontyphoidal Salmonella species such asS. enterica serovar Typhimurium are commonly used ashomologues of typhoid species. Many findings are transferable and it attenuates the danger for the researcher in case of contamination, but is also limited. For example, it is not possible to study specific typhoidal toxins using this model.[94] However, strong research tools such as the commonly used mouse intestinegastroenteritis model build upon the use ofSalmonella Typhimurium.[95]
Forgenetics,S. Typhimurium has been instrumental in the development of genetic tools that led to an understanding of fundamental bacterial physiology. These developments were enabled by the discovery of the first generalized transducing phage P22[96] inS. Typhimurium, that allowed quick and easygenetic editing. In turn, this made fine structure genetic analysis possible. The large number of mutants led to a revision of genetic nomenclature for bacteria.[97] Many of the uses of transposons as genetic tools, including transposon delivery, mutagenesis, and construction of chromosome rearrangements, were also developed inS. Typhimurium. These genetic tools also led to a simple test for carcinogens, the Ames test.[98]
As a natural alternative to traditional antimicrobials, phages are being recognised as highly effective control agents for Salmonella and other foodborne bacteria.[99]
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 the Neolithization process in the evolution of host adaptation.[100][101] Additional reconstructed genomes from colonial Mexico suggestS. enterica as the cause ofcocoliztli, an epidemic in 16th-centuryNew Spain.[102]
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