Salmonella

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Salmonella
Scientific classification
Superkingdom: Bacteria
Kingdom: Bacteria
Phylum: Proteobacteria
Class: Gammaproteobacteria
Order: Enterobacteriales
Family: Enterobacteriaceae
Genus: Salmonella
Lignieres 1900
Species

S. bongori
S. enterica

Salmonella /ˌsælməˈnɛlə/ is a genus of rod-shaped, Gram-negative bacteria. There are only two species of Salmonella, Salmonella bongori and Salmonella enterica, of which there are around six subspecies and innumerable serovars. The genus belongs to the same family as Escherichia, which includes the species E.coli.

Salmonellae are found worldwide in both cold-blooded and warm-blooded animals, and in the environment. They cause illnesses such as typhoid fever, paratyphoid fever, and food poisoning.[1]

Features[edit]

Salmonella are non-spore-forming, predominantly motile enterobacteria with diameters around 0.7 to 1.5 µm, lengths from 2 to 5 µm, and peritrichous flagella (flagella that are all around the cell body).[2] They are chemoorganotrophs, obtaining their energy from oxidation and reduction reactions using organic sources, and are facultative anaerobes.

History[edit]

The story of the term Salmonella starts in 1885 with the discovery of the bacterium Salmonella enterica (var. Choleraesuis) by medical research scientist Theobald Smith. At the time Theobald was working as a research lab assistant in the Veterinary Division of the US Department of Agriculture. The USDA was under the administration of Daniel Elmer Salmon, a veterinary pathologist, and that is for whom the Salmonella was named.[3]

During the search for the cause of hog cholera it was proposed that the causal agent be name Salmonella. While it happened eventually that Salmonella did not cause that cholera (its enteric pathogen was actually a virus)[4], all species of the bacterial genus Salmonella, it turned out, cause infectious diseases. In 1900 J. Lignières re-adopted the name for the many subspecies ofSalmonella, after Smith's first type-strain Salmonella cholera.

Detection, culture and growth conditions[edit]

Most subspecies of Salmonella produce hydrogen sulfide,[5] which can readily be detected by growing them on media containing ferrous sulfate, such as is used in the triple sugar iron test (TSI). Most isolates exist in two phases: a motile phase I and a nonmotile phase II. Cultures that are nonmotile upon primary culture may be switched to the motile phase using a Cragie tube.[citation needed]

Mathematical models of salmonella growth kinetics have been developed for chicken, pork, tomatoes, and melons.[6][7][8][9][10] Salmonella reproduce asexually with a cell division rate of 20 to 40 minutes under optimal conditions.[citation needed]

Salmonella bacteria can survive for weeks outside a living body, and they are not destroyed by freezing.[11][12] Ultraviolet radiation and heat accelerate their demise - they perish after being heated to 55 °C (131 °F) for 90 min, or to 60 °C (140 °F) for 12 min.[13] To protect against Salmonella infection, heating food for at least ten minutes at 75 °C (167 °F) is recommended, so the centre of the food reaches this temperature.[14][15]

Salmonella nomenclature[edit]

Initially, each Salmonella "species" was named according to clinical considerations,[16] e.g., Salmonella typhi-murium (mouse typhoid fever), S. cholerae-suis. After it was recognized that host specificity did not exist for many species, new strains (or serovars, short for serological variants) received species names according to the location at which the new strain was isolated. Later, molecular findings led to the hypothesis that Salmonella consisted of only one species,[17] S. enterica, and the serovars were classified into six groups,[18] two of which are medically relevant. But as this now formalized nomenclature[19][20] is not in harmony with the traditional usage familiar to specialists in microbiology and infectologists, the traditional nomenclature is common. Currently, there are two recognized species: S. enterica, and S. bongori. In 2005 a third species, Salmonella subterranean, was thought to be added but this has since been ruled out and is seen as another serovar.[21] There are six main subspecies recognised: enterica (I), salamae (II), arizonae (IIIa), diarizonae (IIIb), houtenae (IV), and indica (VI).[22] Historically, serotype (V) was bongori, which is now considered its own species.

The serovar (i.e. serotype) is a classification of Salmonella into subspecies based on antigens that the organism presents. It is based on the Kauffman-White classification scheme that differentiates serological varieties from each other. Serotypes are usually put into subspecies groups after the genus and species, with the serovars/serotypes capitalized but not italicized: an example is Salmonella enterica serovar Typhimurium. More modern approaches for typing and subtyping Salmonella include DNA-based methods such as pulsed field gel electrophoresis (PFGE), Multiple Loci VNTR Analysis (MLVA), Multilocus sequence typing (MLST) and multiplex-PCR-based methods.[23][24]

Salmonella as pathogens[edit]

Salmonella species are facultative intracellular pathogens.[25] Many infections are due to ingestion of contaminated food. They can be divided into two groups - typhoidal and nontyphoidal Salmonella serovars. Nontyphoidal serovars are more common, and usually cause self-limiting gastrointestinal disease. They can infect a range of animals, and are zoonotic, meaning they can be transferred between humans and other animals. Typhoidal serovars include Salmonella Typhi and Salmonella Paratyphi A, which are adapted to humans and do not occur in other animals.

Nontyphoidal Salmonella[edit]

Infection with nontyphoidal serovars of Salmonella will generally result in food poisoning. Infection usually occurs when a person ingests foods that contain a high concentration of the bacteria. Infants and young children are much more susceptible to infection, easily achieved by ingesting a small number of bacteria. In infants, infection through inhalation of bacteria-laden dust is possible.

After a short incubation period of a few hours to one day, the bacteria multiply in the intestinal lumen, causing an intestinal inflammation. Most people with salmonellosis develop diarrhea, fever, vomiting, and abdominal cramps 12 to 72 hours after infection.[26] Diarrhea is often mucopurulent (containing mucus or pus) and bloody. In most cases, the illness lasts four to seven days, and most people recover without treatment. In some cases, though, the diarrhea may be so severe that the patient becomes dangerously dehydrated and must be taken to a hospital. At the hospital, the patient may receive intravenous fluids to treat the dehydration, and may be given medications to provide symptomatic relief, such as fever reduction. In severe cases, the Salmonella infection may spread from the intestines to the blood stream, and then to other body sites, and can cause death, unless the person is treated promptly with antibiotics.

In otherwise healthy adults, the symptoms can be mild. Normally, no sepsis occurs, but it can occur exceptionally as a complication in the immunocompromised. However, in people at risk such as infants, small children, the elderly, Salmonella infections can become very serious, leading to complications. In infants, dehydration can cause a state of severe toxicity. Extraintestinal localizations are possible, especially Salmonella meningitis in children, osteitis, etc. Children with sickle cell anaemia who are infected with Salmonella may develop osteomyelitis. Treatment of osteomyelitis, in this case, will be to use fluoroquinolones (Ciproflaxacin, Levofloxacin, etc. and Nalidixic acid).

The organism enters through the digestive tract and must be ingested in large numbers to cause disease in healthy adults. An infectious process can only begin after living salmonellae (not only their toxins) reach the gastrointestinal tract. Some of the microorganisms are killed in the stomach, while the surviving salmonellae enter the small intestine and multiply in tissues (localized form). Gastric acidity is responsible for the destruction of the majority of ingested bacteria, however Salmonella has evolved a degree of tolerance to acidic environments that allows a subset of ingested bacteria to survive.[27] Bacterial colonies may also become trapped in mucus produced in the oesophagus. By the end of the incubation period, the nearby cells are poisoned by endotoxins released from the dead salmonellae. The local response to the endotoxins is enteritis and gastrointestinal disorder.

Those whose only symptom is diarrhea usually completley recover, but it can be several months until their bowel habits are normal.[28] A small number of people afflicted with salmonellosis experience reactive arthritis, which can last months or years and can lead to chronic arthritis.[29]

Invasive non-typhoidal salmonella disease[edit]

While in developed countries, nontyphoidal serovars present mostly as gastrointestinal disease, in sub-Saharan Africa these serovars 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 a case fatality rate of 20-25%. Most cases of invasive nontyphoidal salmonella infection (iNTS) are caused by S Typhimurium or S Enteritidis. A new form of Salmonella Typhimurium (ST313) emerged in the southeast of the continent 75 years ago, followed by a second wave, which came out of central Africa 18 years later. The second wave of iNTS possibly originated in the Congo Basin, and early in the event picked up a gene making it resistant to the antibiotic chloramphenicol. This created the need to use expensive antimicrobial drugs in areas of Africa that were very poor, thus making treatment difficult. The variant is the cause of an enigmatic disease in sub-Saharan Africa called invasive non-typhoidal salmonella (iNTS), which affects Africa far more than other continents. This is thought to be due to the large proportion of the population with some degree of immune suppression or impairment due to the burden of HIV, malaria and malnutrition, especially in children. Its genetic makeup is evolving into a more typhoid-like bacteria, 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.[30]

Typhoidal Salmonella[edit]

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 thermal regulation, vomiting and diarrhea. 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 cause hypovolemic shock. Septic shock may also develop. Shock of mixed character (with signs of both hypovolemic and septic shock) are more common in severe salmonellosis. Oliguria and azotemia develop in severe cases as a result of renal involvement due to hypoxia and toxemia.

Global monitoring[edit]

In Germany, food poisoning infections must be reported.[31] Between 1990 and 2005, the number of officially recorded cases decreased from approximately 200,000 to approximately 50,000 cases. In the USA, about 40,000 cases of Salmonella infection are reported each year.[32] According to the World Health Organization, over 16 million people worldwide are infected with typhoid fever each year, with 500,000 to 600,000 fatal cases.[citation needed]

Molecular mechanisms of infection[edit]

Mechanisms of infection differ between typhoidal and nontyphoidal serovars, 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. Therefore, study of host-pathogen interface has found interest among Salmonella researchers.[33]

Nontyphoidal serovars preferentially enter M cells on the intestinal wall by bacterial-mediated endocytosis, a process associated with intestinal inflammation and diarrhoea. They are also able to disrupt tight junctions between the cells of the intestinal wall, impairing their ability to stop the flow of ions, 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.[34]

Salmonellae are also able to breach the intestinal barrier via phagocytosis and trafficking by CD18-positive immune cells, which may be a mechanism key to typhoidal Salmonella 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 typhoidal Salmonella are required for infection than nontyphoidal Salmonella.[34] Salmonella are able to enter macrophages via macropinocytosis.[35] Typhoidal serovars can use this to achieve dissemination throughout the body via the mononuclear phagocyte system, a network of connective tissue that contains immune cells, and surrounds tissue associated with the immune system throughout the body.[34]

Much of the success of Salmonella in causing infection is attributed to two type three secretion systems which function at different times during infection. One is required for the invasion of non-phagocytic cells, colonization of the intestine and induction of intestinal inflammatory responses and diarrhoea. The other is important for survival in macrophages and establishment of systemic disease.[34] These systems contain many genes which must work co-operatively to achieve infection.

The AvrA toxin injected by the SPI1 type three secretion system of Salmonella Typhimurium works to inhibit the innate immune system by virtue of its serine/threonine acetyltransferase activity, and requires binding to eukaryotic target cell phytic acid (IP6).[36] This leaves the host more susceptible to infection. In a 2011 paper,[37] Yale University School of Medicine researchers described in detail how Salmonella is able to make these proteins line up in just the right sequence to invade host cells. "These mechanisms present us with novel targets that might form the basis for the development of an entirely new class of antimicrobials," said Professor Dr. Jorge Galan, senior author of the paper and the Lucille P. Markey Professor of Microbial Pathogenesis and chair of the Section of Microbial Pathogenesis at Yale. In the new National Institutes of Health-funded study, Galan and colleagues identify what they call a bacterial sorting platform, which attracts needed proteins and lines them up in a specific order. If the proteins do not line up properly, Salmonella, as well as many other bacterial pathogens, cannot "inject" them into host cells to commandeer host cell functions, the lab has found. Understanding how this machine works raises the possibility of new therapies that disable this protein delivery machine, thwarting the ability of the bacterium to become pathogenic. The process would not kill the bacteria as most antibiotics do, but would cripple its ability to do harm. In theory, this means bacteria such as Salmonella might not develop resistance to new therapies as quickly as they usually do to conventional antibiotics.

Sources of infection[edit]

An infographic illustrating how Salmonella spreads from the farm
  • Contaminated food, often having no unusual look or smell;
  • Poor kitchen hygiene, especially problematic in institutional kitchens and restaurants because this can lead to a significant outbreak;
  • Excretions from either sick or infected but apparently clinically healthy people and animals (especially dangerous are caregivers and animals);
  • Polluted surface water and standing water (such as in shower hoses or unused water dispensers);
  • Unhygienically thawed fowl (the meltwater contains many bacteria);
  • An association with reptiles (pet tortoises, snakes, iguanas,[38][39] aquatic turtles, and also amphibians such as frogs) is well described.[40]

Salmonella bacteria can survive for some time without a host; thus, they are frequently found in polluted water, with contamination from the excrement of carrier animals being particularly important.

The European Food Safety Authority (EFSA) highly recommends that when handling raw turkey meat, consumers and people involved in the food supply chain should pay attention to personal and food hygiene.[41]

An estimated 142,000 Americans are infected each year with Salmonella Enteritidis from chicken eggs,[42] and about 30 die.[citation needed] The shell of the egg may be contaminated with Salmonella by feces or environment, or its interior (yolk) may be contaminated by penetration of the bacteria through the porous shell or from a hen whose infected ovaries contaminate the egg during egg formation.[43][44]

Nevertheless, such interior egg yolk contamination is theoretically unlikely.[45][46][47][48] Even under natural conditions, the rate of infection was very small (0.6% in a study of naturally contaminated eggs[49] and 3.0% among artificially and heavily infected hens[50]). However, the natural infection rate would result in roughly one in fourteen cartons (one dozen eggs) to contain at least one egg with interior egg yolk contamination.

Vaccine status[edit]

There is an urgency to develop an effective salmonella vaccine because of the recent outbreaks in Africa of antibiotic-resistant strains of the food-borne bacteria that are killing hundreds of thousands of people there, as well as the heavy annual worldwide death toll each year. Researchers say they have paved the way toward an effective Salmonella vaccine by identifying eight antigenic molecules from human and mouse infections. These antigens provide the research community with a foundation for developing a protective salmonella vaccine. [51] A recent study has tested a vaccine on chickens which offered efficient protection against salmonellosis.[52]

Deaths[edit]

In 2010, an analysis of death certificates in the United States identified a total of 1,316 Salmonella-related deaths from 1990 to 2006. These were predominantly among older adults and those who were immunocompromised.[53]

See also[edit]

References[edit]

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  32. ^ Centers for Disease Control and Prevention
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  41. ^ Multi-Country Outbreak Of Salmonella In Europe SGS SafeGuards Bulletin, Retrieved 04/18/2013
  42. ^ "Playing It Safe With Eggs". FDA Food Facts. 2013-02-28. Retrieved 2013-03-02. "The U.S. Food and Drug Administration (FDA) estimates that 142,000 illnesses each year are caused by consuming eggs contaminated with Salmonella." 
  43. ^ Gantois, Inne; Richard Ducatelle, Frank Pasmans, Freddy Haesebrouck, Richard Gast, Tom J. Humphrey, Filip Van Immerseel (July 2009). "Mechanisms of egg contamination by Salmonella Enteritidis". FEMS Microbiology Reviews 33 (4): 718–738. doi:10.1111/j.1574-6976.2008.00161.x. PMID 19207743. "Eggs can be contaminated on the outer shell surface and internally. Internal contamination can be the result of penetration through the eggshell or by direct contamination of egg contents before oviposition, originating from infection of the reproductive organs. Once inside the egg, the bacteria need to cope with antimicrobial factors in the albumen and vitelline membrane before migration to the yolk can occur" 
  44. ^ Humphrey, T. J. (January 1994). "Contamination of egg shell and contents with Salmonella enteritidis: a review". International Journal of Food Microbiology 21 (1–2): 31–40. doi:10.1016/0168-1605(94)90197-X. PMID 8155476. Retrieved 2010-08-19. "Salmonella enteritidis can contaminate the contents of clean, intact shell eggs as a result of infections of the reproductive tissue of laying hens. The principal site of infection appears to be the upper oviduct. In egg contents, the most important contamination sites are the outside of the vitelline membrane or the albumen surrounding it. In fresh eggs, only a few salmonellae are present. As albumen is an iron-restricted environment, growth only occurs with storage-related changes to vitelline membrane permeability, which allows salmonellas to invade yolk contents." 
  45. ^ Stokes, J.L.; W.W. Osborne, H.G. Bayne (September 1956). "Penetration and Growth of Salmonella in Shell Eggs". Journal of Food Science 21 (5): 510–518. doi:10.1111/j.1365-2621.1956.tb16950.x. "Normally, the oviduct of the hen is sterile and therefore the shell and internal contents of the egg are also free of microorganisms (10,16). In some instances, however, the ovaries and oviduct may be infected with Salmonella and these may be deposited inside the egg (12). More frequently, however, the egg becomes contaminated after it is laid." 
  46. ^ Okamura, Masashi; Yuka Kamijima, Tadashi Miyamoto, Hiroyuki Tani, Kazumi Sasai, Eiichiroh Baba (2001). "Differences Among Six Salmonella Serovars in Abilities to Colonize Reproductive Organs and to Contaminate Egges in Laying Hens". Avian Diseases 45 (1): 61–69. doi:10.2307/1593012. JSTOR 1593012. PMID 11332500. "when hens were artificially infected to test for transmission rate to yolks: "Mature laying hens were inoculated intravenously with 106 colony-forming units of Salmonella Enteritidis, Salmonella Typhimurium, Salmonella Infantis, Salmonella Hadar, Salmonella Heidelberg, or Salmonella Montevideo to cause the systemic infection. Salmonella Enteritidis was recovered from three yolks of the laid eggs (7.0%), suggesting egg contamination from the transovarian transmission of S. enteritidis."" 
  47. ^ Gast, RK; D.R. Jones, K.E. Anderson, R. Guraya, J. Guard, P.S. Holt (August 2010). "In vitro penetration of Salmonella Enteritidis through yolk membranes of eggs from 6 genetically distinct commercial lines of laying hens". Poultry Science 89 (8): 1732–1736. doi:10.3382/ps.2009-00440. PMID 20634530. Retrieved 2010-08-20. "In this study, egg yolks were infected at the surface of the yolk (vitelline membrane) to determine the percentage of yolk contamination (a measure used to determine egg contamination resistance, with numbers lower than 95% indicating increasing resistance): --Overall, the frequency of penetration of Salmonella Enteritidis into the yolk contents of eggs from individual lines of hens ranged from 30 to 58% and the mean concentration of Salmonella Enteritidis in yolk contents after incubation ranged from 0.8 to 2.0 log10 cfu/mL.--" 
  48. ^ Jaeger, Gerald (Jul-Aug 2009). "Contamination of eggs of laying hens with S. Enteritidis". Veterinary Survey (Tierärztliche Umschau) 64 (7–8): 344–348. Retrieved 2010-08-20. "The migration of the bacterium into the nutritionally rich yolk is constrained by the lysozyme loaded vitelline membrane, and would need warm enough storage conditions within days and weeks. The high concentration on of antibodies of the yolk does not inhibit the Salmonella multiplication. Only seldom does transovarian contamination of the developing eggs with S. Enteritidis make this bacterium occur in laid eggs, because of the bactericidal efficacy of the antimicrobial peptides" 
  49. ^ Humphrey, T.J.; A. Whitehead, A. H. L. Gawler, A. Henley and B. Rowe (1991). "Numbers of Salmonella enteritidis in the contents of naturally contaminated hens' eggs". Epidemiology and Infection 106 (3): 489–496. doi:10.1017/S0950268800067546. PMC 2271858. PMID 2050203. Retrieved 2010-08-19. "Over 5700 hens eggs from 15 flocks naturally infected with Salmonella enteritidis were examined individually for the presence of the organism in either egg contents or on shells. Thirty-two eggs (0·6%) were positive in the contents. In the majority, levels of contamination were low." 
  50. ^ Gast, Richard; Rupa Guraya, Jean Guard, Peter Holt, Randle Moore (March 2007). "Colonization of specific regions of the reproductive tract and deposition at different locations inside eggs laid by hens infected with Salmonella Enteritidis or Salmonella Heidelberg". Journal of Avian Diseases 51 (1): 40–44. PMID 17461265. Retrieved 2010-08-20. "when hens are artificially infected with unrealistically large doses (according to the author): --In the present study, groups of laying hens were experimentally infected with large oral doses of Salmonella Heidelberg, Salmonella Enteritidis phage type 13a, or Salmonella Enteritidis phage type 14b. For all of these isolates, the overall frequency of ovarian colonization (34.0%) was significantly higher than the frequency of recovery from either the upper (22.9%) or lower (18.1%) regions of the oviduct. No significant differences were observed between the frequencies of Salmonella isolation from egg yolk and albumen (4.0% and 3.3%, respectively)--." 
  51. ^ "Discovery paves way for salmonella vaccine". UC Davis. 
  52. ^ Nandre, Rahul M.; Lee, John Hwa (Jan 2014). "Construction of a recombinant-attenuated Salmonella Enteritidis strain secreting Escherichia coli heat-labile enterotoxin B subunit protein and its immunogenicity and protection efficacy against salmonellosis in chickens.". Vaccine 32 (2): 425–431. PMID 24176491. 
  53. ^ Cummings, PL; Sorvillo F, Kuo T (November 2010). "Salmonellosis-related mortality in the United States, 1990-2006". Foodborne pathogens and disease 7 (11): 1393–9. doi:10.1089/fpd.2010.0588. PMID 20617938. 

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