Listeria monocytogenes is the species of pathogenic bacteria that
causes the infection listeriosis. It is a facultative anaerobic
bacterium, capable of surviving in the presence or absence of oxygen.
It can grow and reproduce inside the host's cells and is one of the
most virulent foodborne pathogens, with 20 to 30% of food borne
listeriosis infections in high-risk individuals may be fatal.
Responsible for an estimated 1,600 illnesses and 260 deaths in the
United States (U.S.) annually, listeriosis ranks third in total number
of deaths among food borne bacterial pathogens, with fatality rates
Clostridium botulinum. In the European
Union listeriosis follows an upward trend that began in 2008, causing
2,161 confirmed cases and 210 reported deaths in 2014, 16% more than
Listeriosis mortality rates in the US are also higher in the
EU than for other food-borne pathogens.
Listeria monocytogenes is a
Gram-positive bacterium, in the division
Firmicutes, named after Joseph Lister. Its ability to grow at
temperatures as low as 0 °C permits multiplication at typical
refrigeration temperatures, greatly increasing its ability to evade
control in human foodstuffs. Motile via flagella at 30 °C and
below, but usually not at 37 °C, L. monocytogenes can instead
move within eukaryotic cells by explosive polymerization of actin
filaments (known as comet tails or actin rockets).
Studies suggest up to 10% of human gastrointestinal tracts may be
Nevertheless, clinical diseases due to
Listeria monocytogenes are more
frequently recognized by veterinarians, especially as
meningoencephalitis in ruminants. See: listeriosis in animals.
Due to its frequent pathogenicity, causing meningitis in newborns
(acquired transvaginally), pregnant mothers are often advised not to
eat soft cheeses such as Brie, Camembert, feta, and queso blanco
fresco, which may be contaminated with and permit growth of Listeria
monocytogenes. It is the third-most-common cause of meningitis in
Listeria monocytogenes can infect the brain, spinal cord
membranes and/or the bloodstream of the host through the ingestion
of contaminated food such as unpasteurized dairy or raw foods.
3.1 Regulation of pathogenesis
Pathogenicity of lineages
6 Use as a transfection vector
6.1 Cancer treatment
8 Routes of infection
9 Infectious cycle
11 External links
Listeria monocytogenes is a Gram-positive, non spore-forming, motile,
facultatively anaerobic, rod-shaped bacterium. It is catalase-positive
and oxidase-negative, and expresses a beta hemolysin, which causes
destruction of red blood cells. This bacterium exhibits characteristic
tumbling motility when viewed with light microscopy. Although L.
monocytogenes is actively motile by means of peritrichous flagella at
room temperature (20−25 °C), the organism does not synthesize
flagella at body temperatures (37 °C).
Listeria belongs to the class
Bacilli and the order
Bacillales, which also includes
Bacillus and Staphylococcus. The genus
Listeria currently contains 10 species: L. fleischmannii, L. grayi, L.
innocua, L. ivanovii, L. marthii, L. monocytogenes, L. rocourtiae, L.
seeligeri, L. weihenstephanensis and L. welshimeri. L. denitrificans,
previously thought to be part of the
Listeria genus, was reclassified
into the new genus Jonesia. Both L. ivanovii and L. monocytogenes
are pathogenic in mice, but only L. monocytogenes is consistently
associated with human illness. The 13 serotypes of L.
monocytogenes can cause disease, but more than 90% of human isolates
belong to only three serotypes: 1/2a, 1/2b, and 4b. L. monocytogenes
serotype 4b strains are responsible for 33 to 5% of sporadic human
cases worldwide and for all major foodborne outbreaks in Europe and
North America since the 1980s.
Listeria monocytogenes was first described by E.G.D. Murray in 1924
based on six cases of sudden death in young rabbits, and published a
description with his colleagues in 1926 . Murray referred to the
Bacterium monocytogenes before
Harvey Pirie changed the
genus name to
Listeria in 1940. Although clinical descriptions of
L. monocytogenes infection in both animals and humans were published
in the 1920s, it was not recognized as a significant cause of neonatal
infection, sepsis and meningitis until 1952 in East Germany.
Listeriosis in adults would later be associated with patients living
with compromised immune systems, such as individuals taking
immunosuppressant drugs and corticosteroids for malignancies or organ
transplants, and those with HIV infection.
L. monocytogenes was not identified as a cause of foodborne illness
until 1981, however. An outbreak of listeriosis in Halifax, Nova
Scotia, involving 41 cases and 18 deaths, mostly in pregnant women and
neonates, was epidemiologically linked to the consumption of coleslaw
containing cabbage that had been contaminated with L.
monocytogenes-contaminated sheep manure. Since then, a number of
cases of foodborne listeriosis have been reported, and L.
monocytogenes is now widely recognized as an important hazard in the
Stages in the intracellular lifecycle of L. monocytogenes. (Center)
Cartoon depicting entry, escape from a vacuole, actin nucleation,
actin-based motility, and cell-to-cell spread. (Outside)
Representative electron micrographs from which the cartoon was
derived. LLO, PLCs, and ActA are all described in the text. The
cartoon and micrographs were adapted from Tilney and Portnoy (1989).
Main article: Listeriosis
Invasive infection by L. monocytogenes causes the disease listeriosis.
When the infection is not invasive, any illness as a consequence of
infection is termed febrile gastroenteritis. The manifestations of
listeriosis include septicemia, meningitis (or
meningoencephalitis), encephalitis, corneal ulcer,
pneumonia, and intrauterine or cervical infections in pregnant
women, which may result in spontaneous abortion (second to third
trimester) or stillbirth. Surviving neonates of fetomaternal
listeriosis may suffer granulomatosis infantiseptica — pyogenic
granulomas distributed over the whole body — and may suffer
from physical retardation. Influenza-like symptoms, including
persistent fever, usually precede the onset of the aforementioned
disorders. Gastrointestinal symptoms, such as nausea, vomiting, and
diarrhea, may precede more serious forms of listeriosis or may be the
only symptoms expressed. Gastrointestinal symptoms were
epidemiologically associated with use of antacids or cimetidine. The
onset time to serious forms of listeriosis is unknown, but may range
from a few days to three weeks. The onset time to gastrointestinal
symptoms is unknown but probably exceeds 12 hours. An early study
suggested that L. monocytogenes is unique among
in that it might possess lipopolysaccharide, which serves as an
endotoxin. Later, it was found to not be a true endotoxin. Listeria
cell walls consistently contain lipoteichoic acids, in which a
glycolipid moiety, such as a galactosyl-glucosyl-diglyceride, is
covalently linked to the terminal phosphomonoester of the teichoic
acid. This lipid region anchors the polymer chain to the cytoplasmic
membrane. These lipoteichoic acids resemble the lipopolysaccharides of
Gram-negative bacteria in both structure and function, being the only
amphipathic polymers at the cell surface.
L. monocytogenes has D-galactose residues on its surface that can
attach to D-galactose receptors on the host cell walls. These host
cells are generally M cells and
Peyer's patches of the intestinal
mucosa. Once attached to this cells, L. monocytogenes can translocate
past the intestinal membrane and into the body.
The infective dose of L. monocytogenes varies with the strain and with
the susceptibility of the victim. From cases contracted through raw or
supposedly pasteurized milk, one may safely assume that, in
susceptible persons, fewer than 1,000 total organisms may cause
disease. L. monocytogenes may invade the gastrointestinal epithelium.
Once the bacterium enters the host's monocytes, macrophages, or
polymorphonuclear leukocytes, it becomes bloodborne (septicemic) and
can grow. Its presence intracellularly in phagocytic cells also
permits access to the brain and probably transplacental migration to
the fetus in pregnant women. The pathogenesis of L. monocytogenes
centers on its ability to survive and multiply in phagocytic host
cells. It seems that
Listeria originally evolved to invade membranes
of the intestines, as an intracellular infection, and developed a
chemical mechanism to do so. This involves a bacterial protein
"internalin"(InlA/InlB) which attaches to a protein on the intestinal
cell membrane "cadherin" and allows the bacteria to invade the cells
through a zipper mechanism. These adhesion molecules are also to be
found in two other unusually tough barriers in humans — the
blood-brain barrier and the fetal–placental barrier, and this may
explain the apparent affinity that
Listeria has for causing meningitis
and affecting babies in utero. Once inside the cell,
acidifies the lumen of the vacuole formed around it during cell entry
to activate listeriolysin O, a cholesterol-dependent cytolysin capable
of disrupting the vacuolar membrane. This frees the pathogen and gives
it access to the cytosol of the cell, where it continues its
Motility in the intracellular space is provided by
actin assembly-inducing protein (ActA) which allows the bacteria to
use the host cell's actin polymerization machinery to polymerize the
cytoskeleton to give a "boost" to the bacterial cell so it can move in
the cell. The same ActA mechanism also allows the bacteria to travel
from cell to cell.
Regulation of pathogenesis
L. monocytogenes can act as a saprophyte or a pathogen, depending on
its environment. When this bacterium is present within a host
organism, quorum sensing causes the up-regulation of several virulence
genes. Depending on the location of the bacterium within the host
organism, different activators up-regulate the virulence genes. SigB,
an alternative sigma factor, up-regulates Vir genes in the intestines,
whereas PrfA up-regulates gene expression when the bacterium is
present in blood. Little is known about how this
bacterium switches between acting as a saprophyte and a pathogen;
however, several noncoding RNAs are thought to be required to induce
Pathogenicity of lineages
L. monocytogenes has three distinct lineages, with differing
evolutionary histories and pathogenic potentials. Lineage I
strains contain the majority of human clinical isolates and all human
epidemic clones, but are underrepresented in animal clinical
isolates. Lineage II strains are overrepresented in animal cases
and underrepresented in human clinical cases, and are more prevalent
in environmental and food samples. Lineage III isolates are very
rare, but significantly more common in animal than human isolates.
Colonies of typical L. monocytogenes as they appear when grown on
The Anton test is used in the identification of L. monocytogenes;
instillation of a culture into the conjunctival sac of a rabbit or
guinea pig causes severe keratoconjunctivitis within 24 hours.
Listeria species grow on media such as Mueller-Hinton agar.
Identification is enhanced if the primary cultures are done on agar
containing sheep blood, because the characteristic small zone of
hemolysis can be observed around and under colonies. Isolation can be
enhanced if the tissue is kept at 4 °C for some days before
inoculation into bacteriologic media. The organism is a facultative
anaerobe and is catalase-positive and motile.
Listeria produces acid,
but not gas, in a variety of carbohydrates. The motility at room
temperature and hemolysin production are primary findings that help
differentiate listeria from coryneform bacteria.
The methods for analysis of food are complex and time-consuming. The
present U.S. FDA method, revised in September 1990, requires 24 and 48
hours of enrichment, followed by a variety of other tests. Total time
to identification takes five to seven days, but the announcement of
DNA probes should soon allow a simpler and
faster confirmation of suspect isolates.
Recombinant DNA technology may even permit two- to three-day positive
analysis in the future. Currently, the FDA is collaborating in
adapting its methodology to quantitate very low numbers of the
organisms in foods.
When listeric meningitis occurs, the overall mortality may reach 70%,
from septicemia 50%, and from perinatal/neonatal infections greater
than 80%. In infections during pregnancy, the mother usually survives.
Reports of successful treatment with parenteral penicillin or
Trimethoprim-sulfamethoxazole has been shown
effective in patients allergic to penicillin.
Listeria phage P100, has been proposed as food
additive to control L. monocytogenes.
have been developed by several companies. EBI Food Safety and
Intralytix both have products suitable for treatment of the bacterium.
The U.S. Food and Drug Administration (FDA) approved a cocktail of six
bacteriophages from Intralytix, and a one-type phage product from EBI
Food Safety designed to kill L. monocytogenes. Uses would potentially
include spraying it on fruits and ready-to-eat meat such as sliced ham
Use as a transfection vector
Because L. monocytogenes is an intracellular bacterium, some studies
have used this bacterium as a vector to deliver genes in vitro.
Current transfection efficiency remains poor. One example of the
successful use of L. monocytogenes in in vitro transfer technologies
is in the delivery of gene therapies for cystic fibrosis cases.
Listeria monocytogenes is being investigated as a cancer immunotherapy
for several types of cancer.
A live attenuated
Listeria monocytogenes cancer vaccine, ADXS11-001,
is under development as a possible treatment for cervical
Researchers have found
Listeria monocytogenes in at least 37 mammalian
species, both domesticated and feral, as well as in at least 17
species of birds and possibly in some species of fish and shellfish.
Laboratories can isolate
Listeria monocytogenes from soil, silage, and
other environmental sources.
Listeria monocytogenes is quite hardy and
resists the deleterious effects of freezing, drying, and heat
remarkably well for a bacterium that does not form spores. Most
Listeria monocytogenes strains are pathogenic to some degree.[citation
Routes of infection
Listeria monocytogenes has been associated with such foods as raw
milk, pasteurized fluid milk, cheeses (particularly soft-ripened
varieties), ice cream, raw vegetables, fermented raw-meat sausages,
raw and cooked poultry, raw meats (of all types), and raw and smoked
fish. Most bacteria can survive near freezing temperatures, but cannot
absorb nutrients, grow or replicate. L. monocytogenes ability to grow
at temperatures as low as 0 °C permits exponential
multiplication in refrigerated foods. At refrigeration temperature,
such as 4 °C, the amount of ferric iron can affect the growth of
The primary site of infection is the intestinal epithelium, where the
bacteria invade nonphagocytic cells via the "zipper" mechanism. Uptake
is stimulated by the binding of listerial internalins (Inl) to
E-cadherin, a host cell adhesion factor, or Met (c-Met), hepatocyte
growth factor. This binding activates certain Rho-GTPases, which
subsequently bind and stabilize Wiskott Aldrich syndrome protein
(WAsp). WAsp can then bind the
Arp2/3 complex and serve as an actin
nucleation point. Subsequent actin polymerization creates a
"phagocytic cup", an actin-based structure normally formed around
foreign materials by phagocytes prior to endocytosis. The net effect
of internalin binding is to exploit the junction-forming apparatus of
the host into internalizing the bacterium. L. monocytogenes can also
invade phagocytic cells (e.g., macrophages), but requires only
internalins for invasion of nonphagocytic cells.
Following internalization, the bacterium must escape from the
vacuole/phagosome before fusion with a lysosome can occur. Three main
virulence factors that allow the bacterium to escape are listeriolysin
O (LLO-encoded by hly) phospholipase A (encoded by plcA) and
phospholipase B (plcB). Secretion of LLO and PlcA disrupts the
vacuolar membrane and allows the bacterium to escape into the
cytoplasm, where it may proliferate.
Once in the cytoplasm, L. monocytogenes exploits host actin for the
second time. ActA proteins associated with the old bacterial cell pole
(being a bacillus, L. monocytogenes septates in the middle of the
cell, thus has one new pole and one old pole) are capable of binding
the Arp2/3 complex, thereby inducing actin nucleation at a specific
area of the bacterial cell surface.
Actin polymerization then propels
the bacterium unidirectionally into the host cell membrane. The
protrusion formed may then be internalized by a neighboring cell,
forming a double-membrane vacuole from which the bacterium must escape
using LLO and PlcB. This mode of direct cell-to-cell spread involves a
cellular mechanism known as paracytophagy.
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Type strain of
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Firmicutes (low-G+C) Infectious diseases
Bacterial diseases: G+
primarily A00–A79, 001–041, 080–109
Viridans streptococci: S. mitis
bacitracin susceptible: S. pyogenes
Group A streptococcal infection
bacitracin resistant, CAMP test+: S. agalactiae
Group B streptococcal infection
Streptococcus iniae infection
Urinary tract infection
Staphylococcal scalded skin syndrome
Toxic shock syndrome
Clostridial necrotizing enteritis
Peptostreptococcus (non-spore forming)