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Listeria is a facultatively anaerobic, and non spore-forming.[3] The major human pathogen in the Listeria genus is L. monocytogenes. It is usually the causative agent of the relatively rare bacterial disease listeriosis, a serious infection caused by eating food contaminated with the bacteria. The disease affects pregnant women, newborns, adults with weakened immune systems, and the elderly.

Listeriosis is a serious disease for humans; the overt form of the disease has a case-fatality rate of about 20%. The two main clinical manifestations are sepsis and meningitis. Meningitis is often complicated by encephalitis, when it is known as meningoencephalitis, a pathology that is unusual for bacterial infections. L. ivanovii is a pathogen of mammals, specifically ruminants, and has rarely caused listeriosis in humans.[4]


  • Background 1
  • Pathogenesis 2
  • Epidemiology 3
  • Prevention 4
  • Treatment 5
  • Research 6
  • See also 7
  • Notes 8
  • References 9
  • External links 10


The first documented case of Listeria was in 1924. In the late 1920s, two researchers independently identified L. monocytogenes from animal outbreaks. They proposed the genus Listerella in honor of surgeon and early antiseptic advocate Joseph Lister , but that name was already in use for a slime mold and a protozoan. Eventually, the genus Listeria was proposed and accepted. All species within the Listeria genus are gram-positive, not spore-forming, catalase-positive rods. The genus Listeria was classified in the family Corynebacteriaceae through the seventh edition of Bergey's Manual of Systematic Bacteriology. The 16S rRNA cataloging studies of Stackebrandt, et al. demonstrated that L. monocytogenes is a distinct taxon within the Lactobacillus-Bacillus branch of the bacterial phylogeny constructed by Wöse. In 2004, the genus was placed in the newly created family Listeriaceae. The only other genus in the family is Brochothrix.[5]

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. Listeria dinitrificans, previously thought to be part of the Listeria genus, was reclassified into the new genus Jonesia.[6] Under the microscope, Listeria species appear as small, gram-positive rods, which are sometimes arranged in short chains. In direct smears, they may be coccoid, so they can be mistaken for streptococci. Longer cells may resemble corynebacteria. Flagella are produced at room temperature, but not at 37°C. Hemolytic activity on blood agar has been used as a marker to distinguish L. monocytogenes from other Listeria species, but it is not an absolutely definitive criterion. Further biochemical characterization may be necessary to distinguish between the different species of Listeria.

Listeria can be found in soil, which can lead to vegetable contamination. Animals can also be carriers. Listeria has been found in uncooked meats, uncooked vegetables, fruit such as cantaloupes[7] and apples,[8] pasteurized or unpasteurized milk, foods made from milk, and processed foods. Pasteurization and sufficient cooking kill Listeria; however, contamination may occur after cooking and before packaging. For example, meat-processing plants producing ready-to-eat foods, such as hot dogs and deli meats, must follow extensive sanitation policies and procedures to prevent Listeria contamination.[9] Listeria monocytogenes is commonly found in soil, stream water, sewage, plants, and food.[10] Listeria is responsible for listeriosis, a rare but potentially lethal foodborne illness. The case fatality rate for those with a severe form of infection may approach 25%.[11] (Salmonellosis, in comparison, has a mortality rate estimated at less than 1%.[12]) Although Listeria monocytogenes has low infectivity, it is hardy and can grow in temperatures from 4°C (39.2°F) (the temperature of a refrigerator), to 37°C (98.6°F), (the body's internal temperature).[10] Listeriosis is a serious illness, and the disease may manifest as meningitis, or affect newborns due to its ability to penetrate the endothelial layer of the placenta.[11]


Listeria uses the cellular machinery to move around inside the host cell: It induces directed polymerization of actin by the ActA transmembrane protein, thus pushing the bacterial cell around.[13]

L. monocytogenes, for example, encodes virulence genes that are thermoregulated. The expression of virulence factor is optimal at 39°C, and is controlled by a transcriptional activator, PrfA, whose expression is thermoregulated by the PrfA thermoregulator UTR element. At low temperatures, the PrfA transcript is not translated due to structural elements near the ribosome binding site. As the bacteria infect the host, the temperature of the host melts the structure and allows translation initiation for the virulent genes.

The majority of Listeria bacteria are targeted by the immune system before they are able to cause infection. Those that escape the immune system's initial response, however, spread through intracellular mechanisms and are, therefore, guarded against circulating immune factors (AMI).[11]

To invade, Listeria induces macrophage

External links

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See also

Some Listeria species are opportunistic pathogens: L. monocytogenes is most prevalent in the elderly, pregnant mothers, and patients infected with HIV. With improved healthcare leading to a growing elderly population and extended life expectancies for HIV infected patients, physicians are more likely to encounter this otherwise-rare infection (only seven per 1,000,000 healthy people are infected with virulent Listeria each year).[10] Better understanding the cell biology of Listeria infections, including relevant virulence factors, may lead to better treatments for listeriosis and other intracytoplasmic parasite infections. Researchers are now investigating the use of Listeria as a cancer vaccine, taking advantage of its "ability to induce potent innate and adaptive immunity."[15][29]


Asymptomatic patients who have been exposed to Listeria are not recommended for treatment. These patients should be informed of the signs and symptoms of the disease and to return for medical care if symptoms present.[25]

Prompt treatment of listerial infections in pregnancy is critical to prevent the bacteria from infecting the fetus, and antibiotics may be given to pregnant women even in non-invasive listeriosis.[27] These oral therapies in less severe cases can include amoxicillin or erythromycin.[26] In addition to antibiotics, infected pregnant women may be recommended to receive ultrasounds to monitor the health of the fetus. Higher doses of antibiotics are sometimes given to pregnant women to ensure penetration of the umbilical cord and placenta.[28]

In invasive listeriosis, the bacteria have spread to the bloodstream and central nervous system. Treatment includes intravenous delivery of high-dose antibiotics and in-patient hospital care.[25] Duration of hospital care varies depending on how widespread the infection is, but is usually no less than 2 weeks.[25] Ampicillin, penicillin, or amoxicillin are often given for invasive listeriosis, and gentamicin is often added in patients with compromised immune systems.[26] Trimethoprim-sulfamethoxazole, vancomycin, and fluoroquinolones can be used in cases of allergy to penicillin.[26] For treatment to be effective, the antibiotic must penetrate the host cell and bind to penicillin-binding protein 3 (PBP3). Cephalosporins are not effective for treatment of listeriosis.[26]

In non-invasive listeriosis, the bacteria often remain within the digestive tract, causing mild symptoms lasting only a few days and requiring only supportive care. Muscle pain and fever in mild cases can be treated with over-the-counter pain relievers, and diarrhea and gastroenteritis can be treated with over-the-counter medications if needed.[25]


Preventing listeriosis as a foodborne illness requires effective sanitation of food contact surfaces.[24] Ethanol is an effective topical sanitizer against Listeria. Quaternary ammonium can be used in conjunction with alcohol as a food contact safe sanitizer with increased duration of the sanitizing action. Refrigerated foods in the home should be kept below 4°C (39.2°F) to discourage bacterial growth.


The Center for Science in the Public Interest has published a list of foods that have sometimes caused outbreaks of Listeria: hot dogs, deli meats, pasteurized or unpasteurized milk, cheeses (particularly soft-ripened cheeses such as feta, Brie, Camembert, blue-veined, or Mexican-style queso blanco), raw and cooked poultry, raw meats, ice cream, raw fruit,[18] vegetables, and smoked fish.[19] Improperly handled cantaloupe was implicated in the outbreak of listeriosis from Jensen Farms in Colorado,[20] and the Australian company GMI Food Wholesalers was fined A$236,000 for providing L. monocytogenes-contaminated chicken wraps to the airline Virgin Blue.[21] Caramel apples have also been cited as a source of listerial infections which hospitalized 26 people, including five who died.[22][23]


Listeria must then navigate to the cell's periphery to spread the infection to other cells. Outside the body, Listeria has flagellar-driven motility, sometimes described as a "tumbling motility". However, at 37°C, flagella cease to develop and the bacterium instead usurps the host cell's cytoskeleton to move.[11] Listeria, inventively, polymerizes an actin tail or "comet",[14] from actin monomers in the host's cytoplasm [15] with the promotion of virulence factor ActA.[11] The comet forms in a polar manner [16] and aids the bacteria's migration to the host cell's outer membrane. Gelsolin, an actin filament severing protein, localizes at the tail of Listeria and accelerates the bacterium's motility.[16] Once at the cell surface, the actin-propelled Listeria pushes against the cell's membrane to form protrusions called filopods[10] or "rockets". The protrusions are guided by the cell's leading edge [17] to contact adjacent cells, which then engulf the listeria rocket and the process is repeated, perpetuating the infection.[11] Once phagocytosed, the bacterium is never again extracellular: it is an intracytoplasmic parasite [14] like Shigella flexneri and Rickettsia.[11]

[11] The bacteria then replicate inside the host cell's cytoplasm.[10].listeriolysin O now characterized as the exotoxin [14],hemolysin, however, escapes the phagolysosome by lysing the vacuole's entire membrane with secreted Listeria [10]

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