Listeriosis pathophysiology: Difference between revisions
Jump to navigation
Jump to search
YazanDaaboul (talk | contribs) No edit summary |
YazanDaaboul (talk | contribs) No edit summary |
||
| Line 8: | Line 8: | ||
==Genetics== | ==Genetics== | ||
*''Listeria'' ''monocytogenes'' genes encodes thermoregulated [[virulence factor]] | *''Listeria'' ''monocytogenes'' genes encodes thermoregulated [[virulence factor]] | ||
*The expression of [[virulence factor]]s is optimal at 37 ºC and is controlled by a [[transcription|transcriptional]] activator, | *The expression of [[virulence factor]]s is optimal at 37 ºC and is controlled by a [[transcription|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. | *At low temperatures, the PrfA transcript is not translated due to [[Cis-regulatory element|structural elements]] near the [[ribosome]] binding site. | ||
*As ''Listeria'' infects the human host, the translation of the virulent genes is initiated. | *As ''Listeria'' infects the human host, the translation of the virulent genes is initiated. | ||
| Line 18: | Line 18: | ||
:* Cooked or processed foods, including certain soft cheeses, processed (or ready-to-eat) meats, and smoked seafood | :* Cooked or processed foods, including certain soft cheeses, processed (or ready-to-eat) meats, and smoked seafood | ||
*In neonates, ''Listeria'' is usually transmitted by vertical transmission from mother to fetus. | *In neonates, ''Listeria'' is usually transmitted by vertical transmission from mother to fetus. | ||
==Pathogenesis== | ==Pathogenesis== | ||
Revision as of 16:29, 25 January 2016
|
Listeriosis Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Listeriosis pathophysiology On the Web |
|
American Roentgen Ray Society Images of Listeriosis pathophysiology |
|
Risk calculators and risk factors for Listeriosis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]
Overview
Following ingestion, Listeria monocytogenes multiplies within phagocytic host cells and uses them to migrate within the body without mounting an immune response. Microscopically, the infected sites are characterized by the occurrence of inflammation, with exudate and presence of multiple neutrophils.
Genetics
- Listeria monocytogenes genes encodes thermoregulated virulence factor
- The expression of virulence factors is optimal at 37 ºC 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 Listeria infects the human host, the translation of the virulent genes is initiated.
Transmission
- In adults, Listeria is commonly transmitted via contaminated food.
- Uncooked meats and vegetables (including refrigerated foods)
- Unpasteurized (raw) milk and cheeses, as well as other foods made from unpasteurized milk
- Cooked or processed foods, including certain soft cheeses, processed (or ready-to-eat) meats, and smoked seafood
- In neonates, Listeria is usually transmitted by vertical transmission from mother to fetus.
Pathogenesis
- Listeria enters the body through the gastrointestinal lining.[1]
- Listeria may cross the intestinal barrier, blood-brain barrier, and fetoplacental barrier, and cause gastroenteritis, meningoencephalitis, and mother-to-fetus infections.
- Listeria's ability to penetrate the gastrointestinal lining depends on the following factors:[1]
- Number of ingested organisms
- Host's susceptibility
- Virulence of the organism
- The majority of bacteria are targeted by the immune system prior to proliferation and development of clinical manifestations. Organisms that escape the initial immune response avoid the immuune system by spreading though intracellular mechanisms within phagocytes.
- Listeria expresses D-galactose receptors on its surface. D-galactose binds to the macrophage's polysaccharide receptors and induces phagocytosis.
- Once phagocytosed, Listeria is encapsulated by the host cell's acidic phagolysosome.
- Listeria, however, escapes lyosomal destruction by secreting listeriolysin O, a hemolysin that is responsible for lysis the vacuole's membrane.[2]
- Listeria then replicates intracellularly within the host cytoplasm.
- Extracellularly, Listeria has flagellar-driven motility. However, at 37°C, flagella cease to develop, and the bacteria has usurps the host cell's cytoskeleton to migrate.
- Listeria polymerizes an actin tail or "comet" using virulence factor ActA.[3]
- The tail is formed in a polar manner. Its function is to aid the bacteria in migrating towards the host cell's outer membrane.[4]
- Gelsolin is an actin-binding protein that is located at the tail of Listeria. Gelsolin accelerates the bacterium's motility.
- Once at the cell's inner surface, the actin-propelled Listeria pushes against the cell membrane to form protrusions called filopods or "rockets".
- The protrusions are guided by the cell's leading edge to contact with adjacent cells, which subsequently engulf the "Listeria rocket".[5]
Microscopic Pathology
- Tissue infected with Listeria monocytogenes often demonstrates microscopic features of inflammation, exudate formation, and neutrophilia.[6] Occasionally, focal abscesses and yellow nodular formation may be present, suggestive of tissue necrosis.
- Commonly infected tissues include:
- Lungs
- Spleen
- Liver
- Lymph nodes
- Maternal placenta
- Meningeal listeriosis cannot be distinguishedd from other causes of meningitis by microscopy alone. However, identification of intracellular gram-positive bacilli in the CSF is highly suggestive of the diagnosis.[7]
- In prolonged infections, macrophages may be present in tissue specimens, and granuloma formation may occur. there may be multiple macrophages in these tissues, yet, granulomas occur rarely. Organs where these might be present include:[8]
References
- ↑ 1.0 1.1 "Risk assessment of Listeria monocytogenes in ready-to-eat foods" (PDF).
- ↑ 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) - ↑ Kumar, Vinay (2014). Robbins and Cotran pathologic basis of disease. Philadelphia, PA: Elsevier/Saunders. ISBN 1455726133.
- ↑ Kumar, Vinay (2014). Robbins and Cotran pathologic basis of disease. Philadelphia, PA: Elsevier/Saunders. ISBN 1455726133.
- ↑ Kumar, Vinay (2014). Robbins and Cotran pathologic basis of disease. Philadelphia, PA: Elsevier/Saunders. ISBN 1455726133.