Listeriosis pathophysiology: Difference between revisions

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{{Listeriosis}}
{{Listeriosis}}
{{Seealso|Listeria monocytogenes|Listeria ivanovii}}
{{CMG}}; {{AE}} {{JS}}; {{YD}}
 
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==Overview==
==Overview==
''[[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.


Most human infections follow consumption of contaminated food. Rare cases of nosocomial transmission have been reported.
==Transmission==
 
*In adults, ''[[Listeria monocytogenes|Listeria]]'' is usually found in soil, water, vegetation and fecal material. It is commonly transmitted via contaminated food.
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.
:* Uncooked meats and vegetables (including refrigerated foods)
 
:* Unpasteurized (raw) milk and cheeses, as well as other foods made from unpasteurized milk
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.
:* Cooked or processed foods, including certain soft cheeses, processed (or ready-to-eat) meats, and smoked seafood
 
*In [[neonates]], ''[[Listeria monocytogenes|Listeria]]'' is usually transmitted by [[vertical transmission]] from mother to [[fetus]].
==Pathophysiology==
 
===Microbiology: ''Listeria monocytogenes''===
 
* ''[[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 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 ''[[Listeria ivanovii|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.
==Genetics==
*''[[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.
*At low temperatures, the PrfA transcript is not translated due to [[Cis-regulatory element|structural elements]] near the [[ribosome]] binding site.
*As ''[[Listeria monocytogenes|Listeria]]'' infects the human host, the translation of the virulent genes is initiated.


* ''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.
==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 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
:* Host's susceptibility
:* [[Virulence]] of the [[organism]]
*''[[Listeria monocytogenes|Listeria]]'' may also cross the [[blood-brain barrier]], and fetoplacental barrier, and cause [[meningoencephalitis]], and mother-to-fetus [[infections]].


* ''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.
===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 monocytogenes|Listeria]]'' expresses [[D-galactose]] [[receptors]] on its surface. D-galactose binds to the [[macrophage]]'s [[polysaccharide]] receptors and induces [[phagocytosis]].
:*Once [[phagocytosed]], ''[[Listeria monocytogenes|Listeria]]'' is encapsulated by the host [[cell]]'s [[acidic]] [[phagolysosome]].
:*''[[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 monocytogenes|Listeria]]'' then replicates [[Intracellular|intracellularly]] within the host [[cytoplasm]].


===Mechanism of Infection===
===Motility and Cell-to-Cell Invasion===
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).
*[[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><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>
To invade, ''Listeria'' induces macrophage [[phagocytosis|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, <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> now characterized as the exotoxin [[listeriolysin O]].  The bacteria then replicate inside the host cell's cytoplasm.
* 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 monocytogenes|Listeria]]''. [[Gelsolin]] accelerates the [[bacterium]]'s [[motility]].  
''Listeria'' must then navigate to the cell's periphery to spread the infection to other cells.  Outside of the body, ''Listeria'' has [[flagella]]r-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 <ref name="rts4">{{cite web
* 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".   
  | last =
* 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>
  | 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> with the promotion of virulence factor ActA. The comet forms in a polar manner <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> 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 [[filopod]]s or "rockets".  The protrusions are guided by the cell's leading edge <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>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]]''.


==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]].
*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]].<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.
==References==
==References==
{{reflist|2}}


{{reflist|2}}
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Latest revision as of 22:31, 29 July 2020

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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

Genetics

Pathogenesis

Invasion of the Intestinal Epithelium

  • 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.

Intracellular Activity Within Phagocytes

Motility and Cell-to-Cell Invasion

Microscopic Pathology

References

  1. ↑ "Risk assessment of Listeria monocytogenes in ready-to-eat foods" (PDF).
  2. ↑ 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)
  3. ↑ "Listeria". MicrobeWiki.Kenyon.edu. 16 August 2006. doi:. Check |doi= value (help). Retrieved 2007-03-07.
  4. ↑ Southwick FS, Purich DL (1996). "Intracellular pathogenesis of listeriosis". N. Engl. J. Med. 334 (12): 770–6. doi:10.1056/NEJM199603213341206. PMID 8592552.
  5. ↑ 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)
  6. ↑ 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)
  7. ↑ Kumar, Vinay (2014). Robbins and Cotran pathologic basis of disease. Philadelphia, PA: Elsevier/Saunders. ISBN 1455726133.
  8. ↑ Kumar, Vinay (2014). Robbins and Cotran pathologic basis of disease. Philadelphia, PA: Elsevier/Saunders. ISBN 1455726133.

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