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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.
==Transmission==
*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)
:* 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 monocytogenes|Listeria]]'' is usually transmitted by [[vertical transmission]] from mother to [[fetus]].
==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.


==Pathogenesis==
==Pathogenesis==
''L monocytogenes'' is ubiquitous in the environment. The main route of acquisition of ''Listeria'' is through the ingestion of contaminated food products. ''Listeria'' has been isolated from raw meat, dairy products, vegetables, and seafood. Soft cheeses and unpasteurized milk are potential dangers, however post-[[pasteurization]] outbreaks of infection from dairy have been from pasteurized milk.<ref name=Sherris/>
===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]].
 
===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]].


There are four distinct clinical syndromes:
===Motility and Cell-to-Cell Invasion===
:*Infection in pregnancy: ''Listeria'' can proliferate asymptomatically in the vagina and uterus. If the mother becomes symptomatic, it is usually in the third trimester. Symptoms include [[fever]], [[myalgia]]s, [[arthralgias]] and [[headache]]. Abortion, stillbirth and preterm labor are complications of GU infection.
*[[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.
:*Neonatal infection (granulomatosis infantisepticum): There are two forms. One, an early-onset [[sepsis]], with ''Listeria'' acquired in utero, results in premature birth. ''Listeria'' can be isolated in the [[placenta]], [[blood]], [[meconium]], [[nose]], [[ear]]s, and [[throat]]. Another, late-onset meningitis is acquired through vaginal transmission, although it also has been reported with caesarean deliveries.
* ''[[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>
:*[[Central nervous system|CNS]] infection: ''Listeria'' has a predilection for the brain [[parenchyma]], especially the [[brain stem]], and the [[meninges]]. Mental status changes are common. Seizures occur in at least 25% of patients. Cranial nerve palsies, [[encephalitis]], [[meningitis]], [[meningoencephalitis]] and [[abscess]]es can all occur.
* 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>
:*[[Gastroenteritis]]: ''L monocytogenes'' can produce food-borne diarrheal disease, which typically is noninvasive. The median incubation period is 1-2 days, with diarrhea lasting anywhere from 1-3 days. Patients present with fever, muscle aches, gastrointestinal nausea or diarrhea, headache, stiff neck, confusion, loss of balance, or convulsions.
* [[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 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>


==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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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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