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==Overview== | ==Overview== | ||
''Listeria'' is commonly transmitted via contaminated food or via vertical transmission from mother to fetus. Following transmission, ''Listeria'' encodes thermoregulated [[virulence factor]] in the human host, invades the intestinal epithelium, and multiplies intracellularly within [[phagocytic]] | ''[[Listeria monocytogenes|Listeria]]'' is commonly transmitted via contaminated food or via [[vertical transmission]] from mother to [[fetus]]. Following transmission, ''[[Listeria monocytogenes|Listeria]]'' encodes thermoregulated [[virulence factor]] in the human host, invades the [[intestinal epithelium]], and multiplies [[Intracellular|intracellularly]] within [[phagocytic]] [[Phagolysosome|phagolysosomes]]. It is able to escape [[lysosomal]] destruction by secreting [[phospholipases]] and [[listeriolysin O]], a [[hemolysin]] that is responsible for [[lysis]] the [[vacuole]]'s [[membrane]]. ''[[Listeria monocytogenes|Listeria]]'' then migrates between [[cells]] by forming protrusions called filopods or "rockets" using [[polymerized]] [[actin]] and [[Gelsolin]], an [[actin-binding protein]]. Microscopically, [[tissue]] [[infected]] with ''[[Listeria monocytogenes]]'' often demonstrates [[microscopic]] features of [[inflammation]], [[exudate]] formation, and [[neutrophilia]]. In prolonged [[infections]], [[macrophages]] may be abundantly present in tissue specimens, and [[granuloma]] formation may occur. | ||
==Transmission== | ==Transmission== | ||
*In adults, ''Listeria'' is usually found in soil, water, vegetation and fecal material. It is commonly transmitted via contaminated food. | *In adults, ''[[Listeria monocytogenes|Listeria]]'' is usually found in soil, water, vegetation and fecal material. It is commonly transmitted via contaminated food. | ||
:* Uncooked meats and vegetables (including refrigerated foods) | :* Uncooked meats and vegetables (including refrigerated foods) | ||
:* Unpasteurized (raw) milk and cheeses, as well as other foods made from unpasteurized milk | :* 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 | :* 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 monocytogenes|Listeria]]'' is usually transmitted by [[vertical transmission]] from mother to [[fetus]]. | ||
==Genetics== | ==Genetics== | ||
*''Listeria'' ''monocytogenes'' genes encodes thermoregulated [[virulence factor]]. | *''[[Listeria monocytogenes|Listeria]]'' [[Listeria monocytogenes|''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, PrfA, whose expression is thermoregulated by the [[PrfA thermoregulator UTR]] element. | *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, | *As ''[[Listeria monocytogenes|Listeria]]'' infects the human host, the translation of the virulent genes is initiated. | ||
==Pathogenesis== | ==Pathogenesis== | ||
| Line 27: | Line 27: | ||
:* Subsequent [[actin]] polymerization extends the [[cell membrane]] around the [[bacterium]], eventually engulfing it. | :* Subsequent [[actin]] polymerization extends the [[cell membrane]] around the [[bacterium]], eventually engulfing it. | ||
:* The net effect of internalin binding is to exploit the junction forming-apparatus of the host into internalizing the [[bacterium]]. | :* The net effect of internalin binding is to exploit the junction forming-apparatus of the host into internalizing the [[bacterium]]. | ||
*''Listeria's'' ability to penetrate the [[gastrointestinal]] lining depends on the following factors:<ref name=WHO>{{cite web | title = Risk assessment of Listeria monocytogenes in ready-to-eat foods | url = http://whqlibdoc.who.int/publications/2004/9241562625_part1.pdf }}</ref> | *''[[Listeria monocytogenes|Listeria's]]'' ability to penetrate the [[gastrointestinal]] lining depends on the following factors:<ref name=WHO>{{cite web | title = Risk assessment of Listeria monocytogenes in ready-to-eat foods | url = http://whqlibdoc.who.int/publications/2004/9241562625_part1.pdf }}</ref> | ||
:* Number of ingested organisms | :* Number of ingested organisms | ||
:* Host's susceptibility | :* Host's susceptibility | ||
:* [[Virulence]] of the organism | :* [[Virulence]] of the [[organism]] | ||
*''Listeria'' may also cross the [[blood-brain barrier]], and fetoplacental barrier, and cause [[meningoencephalitis]], and mother-to-fetus [[infections]]. | *''[[Listeria monocytogenes|Listeria]]'' may also cross the [[blood-brain barrier]], and fetoplacental barrier, and cause [[meningoencephalitis]], and mother-to-fetus [[infections]]. | ||
===Intracellular Activity Within Phagocytes=== | ===Intracellular Activity Within Phagocytes=== | ||
*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 | *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 [[immune 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]]. | :*''[[Listeria monocytogenes|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]]. | :*Once [[phagocytosed]], ''[[Listeria monocytogenes|Listeria]]'' is encapsulated by the host [[cell]]'s [[acidic]] [[phagolysosome]]. | ||
:*''Listeria'' escapes | :*''[[Listeria monocytogenes|Listeria]]'' escapes [[lysosomal]] destruction by secreting [[phospholipases]] (encoded by ''PLCB'' gene) and [[listeriolysin O]] (encoded by ''HLY'' gene), a [[hemolysin]] that is responsible for [[lysis]] the [[vacuole]]'s membrane.<ref name="rtsjournal1">{{cite journal | quotes=no |author= Tinley, L.G. et al |year=1989|url=http://www.jcb.org/cgi/reprint/109/4/1597|title= Actin Filaments and the Growth, Movement, and Spread of the Intracellular Bacterial Parasite, ''Listeria monocytogenes'' |journal=The Journal of Cell Biology |volume=109 |pages=1597-1608}}</ref> | ||
:*''Listeria'' then replicates intracellularly within the host [[cytoplasm]]. | :*''[[Listeria monocytogenes|Listeria]]'' then replicates [[Intracellular|intracellularly]] within the host [[cytoplasm]]. | ||
===Motility and Cell-to-Cell Invasion=== | ===Motility and Cell-to-Cell Invasion=== | ||
*Extracellularly, ''Listeria'' has [[flagella]]r-driven [[motility]]. However, at 37°C, [[flagella]] cease to develop, and the [[bacteria]] has uses the host [[cell]]'s [[cytoskeleton]] to migrate. | *[[Extracellular|Extracellularly]], ''[[Listeria monocytogenes|Listeria]]'' has [[flagella]]r-driven [[motility]]. However, at 37°C, [[flagella]] cease to develop, and the [[bacteria]] has uses the host [[cell]]'s [[cytoskeleton]] to migrate. | ||
* ''[[Listeria]]'' polymerizes an [[actin]] tail or "comet" using [[virulence factor]] ActA.<ref name="rts4">{{cite web | last = | first = | authorlink = | coauthors = | title =Listeria | work = | publisher =MicrobeWiki.Kenyon.edu | date = 16 August 2006 | url =http://microbewiki.kenyon.edu/index.php?title=Listeria&oldid=5472 | format = | doi =.| accessdate = 2007-03-07 }}</ref> | * ''[[Listeria]]'' polymerizes an [[actin]] tail or "comet" using [[virulence factor]] ActA.<ref name="rts4">{{cite web | last = | first = | authorlink = | coauthors = | title =Listeria | work = | publisher =MicrobeWiki.Kenyon.edu | date = 16 August 2006 | url =http://microbewiki.kenyon.edu/index.php?title=Listeria&oldid=5472 | format = | doi =.| accessdate = 2007-03-07 }}</ref><ref name="pmid8592552">{{cite journal |vauthors=Southwick FS, Purich DL |title=Intracellular pathogenesis of listeriosis |journal=N. Engl. J. Med. |volume=334 |issue=12 |pages=770–6 |year=1996 |pmid=8592552 |doi=10.1056/NEJM199603213341206 |url=}}</ref> | ||
* The tail is formed in a polar manner. Its function is to aid the [[bacteria]] in migrating towards the host cell's outer membrane.<ref name="rtsjournal2">{{cite journal | quotes=no |author= Laine, R.O. et al |year=1998|url=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=108414|title= Gelsolin, a Protein That Caps the Barbed Ends and Severs Actin Filaments, Enhances the Actin-Based Motility of Listeria monocytogenes in Host Cells |journal=Infection and Immunity |volume=66(8) |pages=3775-3782}}</ref> | * The tail is formed in a polar manner. Its function is to aid the [[bacteria]] in migrating towards the host cell's outer membrane.<ref name="rtsjournal2">{{cite journal | quotes=no |author= Laine, R.O. et al |year=1998|url=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=108414|title= Gelsolin, a Protein That Caps the Barbed Ends and Severs Actin Filaments, Enhances the Actin-Based Motility of Listeria monocytogenes in Host Cells |journal=Infection and Immunity |volume=66(8) |pages=3775-3782}}</ref> | ||
* Gelsolin is an actin-binding protein that is located at the tail of ''Listeria''. Gelsolin accelerates the [[bacterium]]'s [[motility]]. | * [[Gelsolin]] is an [[actin-binding protein]] that is located at the tail of ''[[Listeria monocytogenes|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". | * Once at the [[cell]]'s inner surface, the actin-propelled ''[[Listeria monocytogenes|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".<ref name="rtsjournal3">{{cite journal | quotes=no |author= Galbraith, C.G. et al |year=2007|url= |title= Polymerizing Actin Fibers Position Integrins Primed to Probe for Adhesion Sites |journal=Science |volume=315 |pages=992-995}}</ref> | * The protrusions are guided by the [[cell]]'s leading edge to contact with adjacent [[cells]], which subsequently engulf the "''Listeria'' rocket".<ref name="rtsjournal3">{{cite journal | quotes=no |author= Galbraith, C.G. et al |year=2007|url= |title= Polymerizing Actin Fibers Position Integrins Primed to Probe for Adhesion Sites |journal=Science |volume=315 |pages=992-995}}</ref> | ||
==Microscopic Pathology== | ==Microscopic Pathology== | ||
*Tissue infected with ''Listeria monocytogenes'' often demonstrates microscopic features of [[inflammation]], exudate formation, and neutrophilia.<ref>{{cite book | last = Kumar | first = Vinay | title = Robbins and Cotran pathologic basis of disease | publisher = Elsevier/Saunders | location = Philadelphia, PA | year = 2014 | isbn = 1455726133 }}</ref> Occasionally, focal [[abscesses]] and yellow [[nodule|nodular]] formation may be present, suggestive of tissue [[necrosis]]. | *[[Tissue]] infected with ''[[Listeria monocytogenes]]'' often demonstrates microscopic features of [[inflammation]], exudate formation, and [[neutrophilia]].<ref>{{cite book | last = Kumar | first = Vinay | title = Robbins and Cotran pathologic basis of disease | publisher = Elsevier/Saunders | location = Philadelphia, PA | year = 2014 | isbn = 1455726133 }}</ref> Occasionally, focal [[abscesses]] and yellow [[nodule|nodular]] formation may be present, suggestive of [[tissue]] [[necrosis]]. | ||
*Commonly infected tissues include: | *Commonly [[infected]] tissues include: | ||
:* [[Lungs]] | :* [[Lungs]] | ||
:* [[Spleen]] | :* [[Spleen]] | ||
| Line 56: | Line 56: | ||
:* [[Lymph nodes]] | :* [[Lymph nodes]] | ||
:* Maternal [[placenta]] | :* Maternal [[placenta]] | ||
*Meningeal listeriosis cannot be | *[[Meningeal]] listeriosis cannot be distinguished from other causes of [[meningitis]] by microscopy alone. However, identification of [[intracellular]] [[gram-positive]] [[bacilli]] in the [[CSF]] is highly suggestive of the [[diagnosis]].<ref>{{cite book | last = Kumar | first = Vinay | title = Robbins and Cotran pathologic basis of disease | publisher = Elsevier/Saunders | location = Philadelphia, PA | year = 2014 | isbn = 1455726133 }}</ref> | ||
*In prolonged [[infections]], macrophages may be abundantly present in tissue specimens, and granuloma formation may occur. | *In prolonged [[infections]], [[macrophages]] may be abundantly present in [[tissue]] specimens, and [[granuloma]] formation may occur. | ||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
| Line 63: | Line 63: | ||
{{WH}} | {{WH}} | ||
{{WS}} | {{WS}} | ||
[[Category:Emergency mdicine]] | |||
[[Category:Disease]] | |||
[[Category:Up-To-Date]] | |||
[[Category:Infectious disease]] | |||
[[Category:Neurology]] | |||
[[Category:Gastroenterology]] | |||
Latest revision as of 22:31, 29 July 2020
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Listeriosis Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Listeriosis pathophysiology On the Web |
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American Roentgen Ray Society Images of Listeriosis pathophysiology |
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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]; Yazan Daaboul, M.D.
Overview
Listeria is commonly transmitted via contaminated food or via vertical transmission from mother to fetus. Following transmission, Listeria encodes thermoregulated virulence factor in the human host, invades the intestinal epithelium, and multiplies intracellularly within phagocytic phagolysosomes. It is able to escape lysosomal destruction by secreting phospholipases and listeriolysin O, a hemolysin that is responsible for lysis the vacuole's membrane. Listeria then migrates between cells by forming protrusions called filopods or "rockets" using polymerized actin and Gelsolin, an actin-binding protein. Microscopically, tissue infected with Listeria monocytogenes often demonstrates microscopic features of inflammation, exudate formation, and neutrophilia. In prolonged infections, macrophages may be abundantly present in tissue specimens, and granuloma formation may occur.
Transmission
- In adults, Listeria is usually found in soil, water, vegetation and fecal material. It 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.
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.
Pathogenesis
Invasion of the Intestinal Epithelium
- The primary site of infection is the intestinal epithelium, where the bacteria invade non-phagocytic cells via the "zipper" mechanism:
- Uptake is stimulated by the binding of listerial internalins (Inl) to host cell adhesion factors such as E-cadherin or Met.
- This binding activates certain Rho-GTPases which subsequently bind and stabilize the Wiskott-Aldrich syndrome protein (WASp).
- WASp can then bind the Arp2/3 complex and serve as an actin nucleation point.
- Subsequent actin polymerization extends the cell membrane around the bacterium, eventually engulfing it.
- The net effect of internalin binding is to exploit the junction forming-apparatus of the host into internalizing the bacterium.
- Listeria's ability to penetrate the gastrointestinal lining depends on the following factors:[1]
- Listeria may also cross the blood-brain barrier, and fetoplacental barrier, and cause meningoencephalitis, and mother-to-fetus infections.
Intracellular Activity Within Phagocytes
- 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 immune 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 escapes lysosomal destruction by secreting phospholipases (encoded by PLCB gene) and listeriolysin O (encoded by HLY gene), a hemolysin that is responsible for lysis the vacuole's membrane.[2]
- Listeria then replicates intracellularly within the host cytoplasm.
Motility and Cell-to-Cell Invasion
- Extracellularly, Listeria has flagellar-driven motility. However, at 37°C, flagella cease to develop, and the bacteria has uses the host cell's cytoskeleton to migrate.
- Listeria polymerizes an actin tail or "comet" using virulence factor ActA.[3][4]
- The tail is formed in a polar manner. Its function is to aid the bacteria in migrating towards the host cell's outer membrane.[5]
- 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".[6]
Microscopic Pathology
- Tissue infected with Listeria monocytogenes often demonstrates microscopic features of inflammation, exudate formation, and neutrophilia.[7] 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 distinguished from other causes of meningitis by microscopy alone. However, identification of intracellular gram-positive bacilli in the CSF is highly suggestive of the diagnosis.[8]
- In prolonged infections, macrophages may be abundantly present in tissue specimens, and granuloma formation may occur.
References
- ↑ "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. - ↑ Southwick FS, Purich DL (1996). "Intracellular pathogenesis of listeriosis". N. Engl. J. Med. 334 (12): 770–6. doi:10.1056/NEJM199603213341206. PMID 8592552.
- ↑ 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.