Salmonella is a genus of rod-shaped (bacillus) gram-negative bacteria
of the family Enterobacteriaceae. The two species of
Salmonella enterica and
Salmonella enterica is the
type species and is further divided into six subspecies that
include over 2,500 serotypes.
Salmonella species are non-spore-forming, predominantly motile
enterobacteria with cell diameters between about 0.7 and 1.5 µm,
lengths from 2 to 5 µm, and peritrichous flagella (all around
the cell body). They are chemotrophs, obtaining their energy from
oxidation and reduction reactions using organic sources. They are also
facultative anaerobes, capable of generating ATP with oxygen
("aerobically") when it is available; or when oxygen is not available,
using other electron acceptors or fermentation ("anaerobically").
S. enterica subspecies are found worldwide in all warm-blooded animals
and in the environment. S. bongori is restricted to cold-blooded
animals, particularly reptiles.
Salmonella species are intracellular pathogens: certain serotypes
cause illness. Nontyphoidal serotypes can be transferred from
animal-to-human and from human-to-human. They usually invade only the
gastrointestinal tract and cause
Salmonella food poisoning; symptoms
resolve without antibiotics. However, in sub-Saharan Africa they can
be invasive and cause paratyphoid fever, which requires immediate
treatment with antibiotics. Typhoidal serotypes can only be
transferred from human-to-human, and can cause
poisoning, typhoid fever and paratyphoid fever. Typhoid fever
Salmonella invades the bloodstream—the typhoidal form;
or in addition spreads throughout the body, invades organs, and
secretes endotoxins—the septic form. This can lead to
life-threatening hypovolemic shock and septic shock and requires
intensive care including antibiotics.
3 Detection, culture, and growth conditions
5 As pathogens
6 Nontyphoidal Salmonella
6.1 Invasive nontyphoidal salmonella disease
7 Typhoidal Salmonella
8 Global monitoring
9 Molecular mechanisms of infection
10 Resistance to oxidative burst
11 Host adaptation
13 See also
15 External links
Salmonella is part of the family of Enterobacteriaceae. Its
taxonomy has been revised and has the potential to confuse. The genus
comprises two species,
Salmonella bongori and
Salmonella 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, and S. e.
indica. The taxonomic group contains more than 2500 serotypes
(also serovars) defined on the basis of the somatic O
(lipopolysaccharide) and flagellar H antigens (the Kauffman–White
classification). The full name of a serotype is given as, for example,
Salmonella enterica subsp. enterica serotype Typhimurium, but can be
Salmonella Typhimurium. Further differentiation of
strains to assist clinical and epidemiological investigation may be
achieved by antibiotic sensitivity testing and by other molecular
biology techniques such as pulsed-field gel electrophoresis,
multilocus sequence typing, and, increasingly, whole genome
sequencing. Historically, salmonellae have been clinically categorized
as invasive (typhoidal) or noninvasive (nontyphoidal salmonellae)
based on host preference and disease manifestations in humans.
Salmonella was first visualized in 1880 by Karl Eberth in the Peyer's
patches and spleens of typhoid patients. Four years later in 1884
Georg Theodor Gaffky was able to successfully grow the pathogen in
pure culture. A year after that, medical research scientist
Theobald Smith discovered what would be later known as Salmonella
enterica (var. Choleraesuis). At the time, Smith was working as a
research laboratory assistant in the Veterinary Division of the United
States Department of Agriculture. The department was under the
administration of Daniel Elmer Salmon, a veterinary pathologist.
Salmonella Choleraesuis was thought to be the causative
agent of hog cholera, so Salmon and Smith named it
"Hog-cholerabacillus". The name
Salmonella was not used until 1900,
when Joseph Leon Lignières proposed that the pathogen discovered by
Salmon's group be called
Salmonella in his honor.:16
Detection, culture, and growth conditions
Most subspecies of
Salmonella produce hydrogen sulfide, which can
readily be detected by growing them on media containing ferrous
sulfate, such as is used in the triple sugar iron test. 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
Craigie tube or ditch plate. RVS broth
can be used to enrich for
Salmonella species for detection in a
Salmonella can also be detected and subtyped using multiplex or
real-time polymerase chain reactions (PCR) from extracted
Mathematical models of
Salmonella growth kinetics have been developed
for chicken, pork, tomatoes, and melons.
Salmonella reproduce asexually with a cell division interval of 40
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.
Salmonella is notorious for
its ability to survive desiccation and can persist for years in dry
environments and foods.
The bacteria are not destroyed by freezing, but UV 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. To protect against Salmonella
infection, heating food for at least 10 minutes to an internal
temperature of 75 °C (167 °F) is recommended.
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. Food
and water can also be contaminated with the bacteria if they come in
contact with the feces of infected people or animals.
Salmonella "species" was named according to clinical
considerations, for example
Salmonella typhi-murium (mouse typhoid
fever), S. cholerae-suis. After it was recognized that host
specificity did not exist for many species, new strains 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, S. enterica, and the
serotypes were classified into six groups, two of which are
medically relevant. As this now-formalized nomenclature is not
in harmony with the traditional usage familiar to specialists in
microbiology and infectologists, the traditional nomenclature is still
common. Currently, the two recognized species are S. enterica, and S.
bongori. In 2005, a third species,
Salmonella subterranean, was
proposed, but according to the World Health Organization, the
bacterium reported does not belong in the genus Salmonella. The
six main recognised subspecies are: enterica (serotype I), salamae
(serotype II), arizonae (IIIa), diarizonae (IIIb), houtenae (IV), and
indica (VI). The former serotype (V) was bongori, which is now
considered its own species.
The serotype or serovar, is a classification of
subspecies based on antigens that the organism presents. It is based
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
serotypes/serovars 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, multiple-loci VNTR analysis,
multilocus sequence typing, and multiplex-PCR-based methods.
Salmonella species are facultative intracellular pathogens. A
facultative organism uses oxygen to make ATP: when it is not available
it "exercises its option"—the literal meaning of the term—and
makes ATP via fermentation, or by substituting one or more of four
less efficient electron acceptors has oxygen at the end of the
electron transport chain: sulfate, nitrate, sulfur, or fumarate.
Most infections are due to ingestion of food contaminated by animal
feces; or by human feces, such as by a food service worker at a
Salmonella serotypes can be divided into two main
groups—typhoidal and nontyphoidal Salmonella. Nontyphoidal serotypes
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
Salmonella Typhi and
Salmonella Paratyphi A, which
are adapted to humans and do not occur in other animals.
See also: Salmonellosis
Infection with nontyphoidal serotypes of
Salmonella generally results
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.
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 merely Salmonella-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, but Salmonella
has evolved a degree of tolerance to acidic environments that allows a
subset of ingested bacteria to survive. 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 by
endotoxins released from the dead salmonellae. The local response to
the endotoxins is enteritis and gastrointestinal disorder.
About 2,000 serotypes of nontyphoidal
Salmonella 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
Invasive nontyphoidal salmonella disease
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 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 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
the Congo Basin, and early in the event picked up a gene that made it
resistant to the antibiotic chloramphenicol. 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 of HIV, 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.
Typhoid fever and Paratyphoid fever
Typhoid fever is caused by
Salmonella serotypes which are strictly
adapted to humans or higher primates—these include
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 cause hypovolemic shock.
Septic shock may also develop. Shock of mixed character (with signs of
both hypovolemic and septic shock) is more common in severe
Oliguria and azotemia may develop in severe cases as a
result of renal involvement due to hypoxia and toxemia.
In Germany, food poisoning infections must be reported. From 1990
to 2005, the number of officially recorded cases decreased from about
200,000 to about 50,000 cases. In the United States, about 50,000
Salmonella infection are reported each year. 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.
Molecular mechanisms of infection
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.
Nontyphoidal serotypes 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
the cells' 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
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 cells are able to enter macrophages via
macropinocytosis. Typhoidal serotypes 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
Much of the success of
Salmonella in causing infection is attributed
to two type III secretion systems which function at different times
during an infection. One is required for the invasion of nonphagocytic
cells, colonization of the intestine, and induction of intestinal
inflammatory responses and diarrhea. The other is important for
survival in macrophages and establishment of systemic disease.
These systems contain many genes which must work co-operatively to
The AvrA toxin injected by the SPI1 type III secretion system of S.
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). This leaves the host
more susceptible to infection.
Salmonellosis is known to be able to cause back pain or spondylosis.
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 localized
Salmonella infections are arthritis,
urinary tract infection, infection of the central nervous system, bone
infection, soft tissue infection, etc. Infection may remain as the
latent form for a long time, and when the function of reticular
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.
Resistance to oxidative burst
A hallmark of
Salmonella pathogenesis is the ability of the bacterium
to survive and proliferate within phagocytes. Phagocytes produce DNA
damaging agents such as nitric oxide and oxygen radicals as a defense
against pathogens. Thus,
Salmonella species must face attack by
molecules that challenge genome integrity. Buchmeier et al. showed
that mutants of
Salmonella 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 by S. enterica requires RecA and RecBC mediated
recombinational repair of DNA damage.
Salmonella enterica, through some of its serotypes such as Typhimurium
and Enteriditis, shows signs of the ability to infect several
different mammalian host species, while other serotypes such as Typhi
seem to be restricted to only a few hosts. Some of the ways that
Salmonella serotypes have adapted to their hosts include loss of
genetic material and mutation. In more complex mammalian species,
immune systems, which include pathogen specific immune responses,
target serovars of
Salmonella through binding of antibodies to
structures like flagella. Through the loss of the genetic material
that codes for a flagellum to form,
Salmonella can evade a host's
immune system. mgtC leader RNA from bacteria virulence gene
(mgtCBR operon) decreases flagellin production during infection by
directly base pairing with mRNAs of the fljB gene encoding flagellin
and promotes degradation. In the study by Kisela et al., more
pathogenic serovars of S. enterica were found to have certain adhesins
in common that have developed out of convergent evolution. This
means that, as these strains of
Salmonella have been exposed to
similar conditions such as immune systems, similar structures evolved
separately to negate these similar, more advanced defenses in hosts.
There are still many questions about the way that
evolved into so many different types but it has been suggested that
Salmonella evolved through several phases. As Baumler et al. have
Salmonella most likely evolved through horizontal gene
transfer, formation of new serovars due to additional pathogenicity
islands and through an approximation of its ancestry. So,
Salmonella could have evolved into its many different serotypes
through gaining genetic information from different pathogenic
bacteria. The presence of several pathogenicity islands in the genome
of different serotypes has lent credence to this theory.
In addition to its importance as a pathogen,
serovar 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, in Typhimurium that
allowed quick and easy genetic exchange that allowed fine structure
genetic analysis. The large number of mutants led to a revision of
genetic nomenclature for bacteria. Many of the uses of transposons
as genetic tools, including transposon delivery, mutagenesis,
construction of chromosome rearrangements, were also developed in
Typhimurium. These genetic tools also led to a simple test for
carcinogens, the Ames Test.
1984 Rajneeshee bioterror attack
2008 United States salmonellosis outbreak
2008–2009 peanut-borne salmonellosis
Bismuth sulfite agar
Food testing strips
List of foodborne illness outbreaks
Wright County Egg
Rappaport Vassiliadis soya peptone broth
American Public Health Association v. Butz
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Overview of Salmonellosis — The Merck Veterinary Manual
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