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==Overview==
==Overview==
''[[Listeria monocytogenes]]'' is able to enter de body through the [[gastrointestinal]] lining, causing [[infection]] in otherwise [[sterile]] sites. The [[pathogenesis]] of ''L. monocytogenes'' is centered on its ability to survive and multiply within [[phagocytic]] host [[cells]], which it uses to travel to difference sites in the body. ''[[Listeria monocytogenes]]'' is transmitted through contaminated food and causes [[infection]] particularly in [[immunosuppressed]] patients, elderly, and pregnant women. Microscopically, the [[infected]] sites are characterized by the occurrence of [[inflammation]], with [[exudate]] and presence of multiple [[neutrophils]].
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==
==Genetics==
''Listeria'' ''monocytogenes'' encodes [[virulence factor]] [[genes]], which are thermoregulated. 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.
*''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, '''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'' 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.


As the [[bacteria]] [[infect]] the host, the higher temperature "melts" this structure, and allows initiation of [[translation]] of the virulent [[genes]].


==Pathogenesis==
==Pathogenesis==
''[[Listeria]]'' is able to enter de body through the [[gastrointestinal]] lining, causing [[infection]] in otherwise sterile sites.<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> [[Listeriosis]] may cause [[gastroenteritis]], [[meningoencephalitis]], and mother-to-fetus [[infections]]. These reflect its ability to cross the [[intestinal]] barrier, [[blood-brain barrier]], and fetoplacental barrier, respectively.
*''Listeria'' enters the body through the [[gastrointestinal]] lining.<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'' may cross the [[intestinal]] barrier, [[blood-brain barrier]], and fetoplacental barrier, and cause [[gastroenteritis]], [[meningoencephalitis]], and mother-to-fetus [[infections]].
The [[bacteria]]'s ability to penetrate the [[gastrointestinal]] lining will depend on:<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'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
   
   
The majority of [[bacteria]] are targeted by the [[immune system]] before they are able to cause [[infection]]. Those that escape the initial attack of the [[immune system]], spread though [[intracellular]] mechanisms, therefore being protected from circulating [[immune]] factors.
*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]].
To invade host [[cells]], ''Listeria'' induces [[phagocytosis|phagocytic]] uptake by the [[macrophages]]. The [[bacteria]] display D-galactose receptors on its surface, that bind to the [[macrophage]]'s [[polysaccharide]] receptors, inducing [[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.<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>
Once [[phagocytosed]], the [[bacteria]] are encapsulated by the host [[cell]]'s acidic [[phagolysosome]]. ''Listeria'', however, escapes this organelle by secreting [[hemolysin]], that lysis the [[vacuole]]'s membrane, now described as the [[exotoxin]] [[listeriolysin O]].<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> The [[bacteria]] will then replicate inside the host cell's [[cytoplasm]].
:*''Listeria'' then replicates intracellularly within the host [[cytoplasm]].
 
*Extracellularly, ''Listeria'' has [[flagella]]r-driven [[motility]]. However, at 37°C, [[flagella]] cease to develop, and the [[bacteria]]  has usurps the host [[cell]]'s [[cytoskeleton]] to migrate.
''Listeria'' must relocate to the [[cell]]'s periphery to spread the [[infection]] to other [[cells]].
:* ''[[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>  
Outside of the [[cell]], ''Listeria'' has [[flagella]]r-driven [[motility]]. However, at 37°C, [[flagella]] cease to develop and the [[bacteria]]  has instead to usurp the host [[cell]]'s [[cytoskeleton]] to move:
:* 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>  
:* ''[[Listeria]]'' polymerizes an [[actin]] tail or "comet", using host-produced [[actin]] filaments, by 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>  
:* Gelsolin is an actin-binding protein that is located at the tail of ''Listeria''. Gelsolin accelerates the [[bacterium]]'s [[motility]].  
:* The comet is formed in a polar manner. Its function is to aid the [[bacteria]] to migrate 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, an [[actin filament]] severing [[protein]], is located at the tail of ''Listeria'' and 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'' 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". The process is repeated, perpetuating the [[infection]].<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>  
 
Once phagocytosed, ''[[Listeria]]'' is never again [[extracellular]]: it is an intracytoplasmic parasite.
 
Once the [[bacterium]] enters the host's [[monocyte]]s, [[macrophage]]s, or [[polymorphonuclear leukocyte]]s, it becomes blood-borne ([[septicemic]]). Its presence within the [[phagocytosis|phagocytic]] cells also allows access to the [[brain]] and probably [[transplacental]] migration to the [[fetus]] in pregnant women.
 
The [[pathogenesis]] of ''L. monocytogenes'' is centered on its ability to survive, and multiply within [[phagocytic]] host [[cells]], which it uses to travel to difference sites in the body.<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]]'' is known for causing disease in the following patients:
* [[Immunosuppressed]] patients
* [[Neonates]]
* Elderly
* [[Pregnant]] women
* Healthy individuals (rare cases, mostly in outbreaks)
 
==Transmission==
Most human cases of [[listeriosis]] are due to consumption of contaminated food, with rare cases of hospital-acquired [[transmission]] reported in newborns.
 
When ''[[Listeria]]'' gets into a food processing factory, it can remain there for years, often contaminating food products. [[Bacteria]] have been found in a variety of foods, such as:
* Uncooked meats and vegetables
* 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
 
[[Listeria]] is killed by [[pasteurization]] and cooking. However, in some ready-to-eat meats, such as hot dogs and deli meats, contamination may occur after factory cooking, but before packaging or even at the deli counter.
 
Unlike most [[bacteria]], ''[[Listeria]]'' can grow and multiply in some foods inside the refrigerator.


==Microscopic Pathology==
==Microscopic Pathology==
''[[Listeria monocytogenes]]'' is characterized by the occurrence of [[inflammation]], with [[exudate]] and presence of multiple [[neutrophils]] at the site of [[infection]].<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>
*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:
When there is [[meningeal]] involvement, [[meningitis]] cannot be microscopically nor macroscopically distinguished from that caused by other [[pathogens]]. However, the 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>
:* [[Lungs]]
 
:* [[Spleen]]
Other [[organs]] may show focal [[abscesses]] and yellow [[nodules]], indicating [[necrotic]] tissues. In prolonged [[infections]], there may be multiple [[macrophages]] in these tissues, yet, [[granulomas]] occur rarely. [[Organs]] where these might be present include:<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>
:* [[Liver]]
* [[Lungs]]
:* [[Lymph nodes]]
* [[Spleen]]
:* Maternal [[placenta]]
* [[Liver]]
*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]].<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>
* [[Lymph nodes]]
*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:<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>
* Maternal [[placenta]] (in [[infected]] newborns with ''[[Listeria monocytogenes]]'') - smear of [[meconium]] shows [[gram-positive]] [[bacilli]])


==References==
==References==
{{reflist|2}}
{{reflist|2}}
[[Category:Bacterial diseases]]
[[Category:Bacterial diseases]]
[[Category:Disease]]
[[Category:Disease]]
[[Category:Infectious disease]]
[[Category:Infectious disease]]
[[Category:Wikinfect]]

Revision as of 16:28, 25 January 2016

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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]

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

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

  • 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 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:
  • 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. ↑ 1.0 1.1 "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. ↑ 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)
  5. ↑ 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)
  6. ↑ Kumar, Vinay (2014). Robbins and Cotran pathologic basis of disease. Philadelphia, PA: Elsevier/Saunders. ISBN 1455726133.
  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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