Listeriosis pathophysiology: Difference between revisions
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===Microbiology: ''Listeria monocytogenes''=== | ===Microbiology: ''Listeria monocytogenes''=== | ||
''Listeria'' | * ''[[Listeria monocytogenes]]'' is a facultatively [[anaerobic]], nonsporulating, [[Gram-positive]] bacillus with polar [[flagella]]e and exhibits tumbling motility at 25°C. ''L. monocytogenes'' is ubiquitous in the environment and can survive in a diverse array of environments such as soil, water, food products, and host cells. | ||
''Listeria'' ''monocytogenes'' for example, encodes virulence genes which are thermoregulated. The expression of virulence factor is optimal at 37 degrees Celsius 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 [[Cis-regulatory element|structural elements]] near the ribosome binding site. As the bacteria infects the host, the temperature of the host melts the structure and allows translation initiation for the virulent genes. | * Among ''Listeria'' species, only ''[[L. monocytogenes]]'' and ''[[L. ivanovii]]'' are known to be pathogenic to humans. Listeriosis typically manifests as [[gastroenteritis]], [[meningoencephalitis]], and mother-to-fetus infections, which reflect its ability to cross the intestinal barrier, blood-brain barrier, and fetoplacental barrier, respectively. | ||
* ''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. | |||
* ''Listeria'' ''monocytogenes'' for example, encodes virulence genes which are thermoregulated. The expression of virulence factor is optimal at 37 degrees Celsius 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 [[Cis-regulatory element|structural elements]] near the ribosome binding site. As the bacteria infects the host, the temperature of the host melts the structure and allows translation initiation for the virulent genes. | |||
===Mechanism of Infection=== | ===Mechanism of Infection=== | ||
Revision as of 03:30, 24 February 2014
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Most human infections follow consumption of contaminated food. Rare cases of nosocomial transmission have been reported.
When Listeria bacteria get into a food processing factory, they can live there for years, sometimes contaminating food products. The bacterium has been found in a variety of raw foods, such as uncooked meats and vegetables, as well as in foods that become contaminated after cooking or processing, such as soft cheeses, processed meats such as hot dogs and deli meat (both products in factory-sealed packages and products sold at deli counters), and smoked seafood. Unpasteurized (raw) milk and cheeses and other foods made from unpasteurized milk are particularly likely to contain the bacterium.
Listeria is killed by pasteurization and cooking; however, in some ready-to-eat foods, such as hot dogs and deli meats, contamination may occur after factory cooking but before packaging. Unlike most bacteria, Listeria can grow and multiply in some foods in the refrigerator.
Pathophysiology
Microbiology: Listeria monocytogenes
- Listeria monocytogenes is a facultatively anaerobic, nonsporulating, Gram-positive bacillus with polar flagellae and exhibits tumbling motility at 25°C. L. monocytogenes is ubiquitous in the environment and can survive in a diverse array of environments such as soil, water, food products, and host cells.
- Among Listeria species, only L. monocytogenes and L. ivanovii are known to be pathogenic to humans. Listeriosis typically manifests as gastroenteritis, meningoencephalitis, and mother-to-fetus infections, which reflect its ability to cross the intestinal barrier, blood-brain barrier, and fetoplacental barrier, respectively.
- 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.
- Listeria monocytogenes for example, encodes virulence genes which are thermoregulated. The expression of virulence factor is optimal at 37 degrees Celsius 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 infects the host, the temperature of the host melts the structure and allows translation initiation for the virulent genes.
Mechanism of Infection
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 though intracellular mechanisms and are therefore guarded against circulating immune factors (AMI).
To invade, Listeria induces macrophage phagocytic uptake by displaying D-galactose receptors that are then bound by the macrophage's polysaccharide receptors (Notably, in most bacterial infections it is the host cell, not the bacteria, that displays the polysaccharide). Once phagocytosed, the bacteria is encapsulated by the host cell's acidic phagolysosome organelle. Listeria, however, escapes the phagolysosome by lysing the vacuole's entire membrane with secreted hemolysin, [1] now characterized as the exotoxin listeriolysin O. The bacteria then replicate inside the host cell's cytoplasm.
Listeria must then navigate to the cell's periphery to spread the infection to other cells. Outside of the body, Listeria has flagellar-driven motility. However, at 37°C, flagella cease to develop and the bacteria instead usurps the host cell's cytoskeleton to move. Listeria, inventively, polymerizes an actin tail or "comet" , using host-produced actin filaments [2] with the promotion of virulence factor ActA. The comet forms in a polar manner [3] 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. Once at the cell surface, the actin-propelled Listeria pushes against the cell's membrane to form protrusions called filopods or "rockets". The protrusions are guided by the cell's leading edge [4]to contact adjacent cells which subsequently engulf the Listeria rocket and the process is repeated, perpetuating the infection. Once phagocytosed, the Listeria is never again extracellular: it is an intracytoplasmic parasite like Shigella flexneri and Rickettsia.
References
- ↑ Tinley, L.G.; et al. (1989). "Actin Filaments and the Growth, Movement, and Spread of the Intracellular Bacterial Parasite, Listeria monocytogenes". The Journal of Cell Biology. 109: 1597–1608. Unknown parameter
|quotes=ignored (help) - ↑ "Listeria". MicrobeWiki.Kenyon.edu. 16 August 2006. doi:. Check
|doi=value (help). Retrieved 2007-03-07. - ↑ Laine, R.O.; et al. (1998). "Gelsolin, a Protein That Caps the Barbed Ends and Severs Actin Filaments, Enhances the Actin-Based Motility of Listeria monocytogenes in Host Cells". Infection and Immunity. 66(8): 3775–3782. Unknown parameter
|quotes=ignored (help) - ↑ Galbraith, C.G.; et al. (2007). "Polymerizing Actin Fibers Position Integrins Primed to Probe for Adhesion Sites". Science. 315: 992–995. Unknown parameter
|quotes=ignored (help)