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==Overview==
==Overview==
Typhus is a [[zoonotic]] disease, humans are [[infected]] by the bites from parasites such as fleas, lice, mites, and ticks or by the inoculation of infectious fluids or feces from the parasites into the skin. The incubation period of typhus fever varies from one to two weeks. Following transmission, rickettsia are ingested by macrophages and polymorphonuclear cells. The major pathology is caused by a vasculitis and its complications. This process may cause result in occlusion of blood vessels and initiates [[inflammatory response]] (aggregation of [[Leukocytes|leukocytes,]] [[macrophages]], and [[platelets]]) resulting in small nodules. This vasculitic process causes destruction of the [[endothelial cells]] and leakage of the blood leading to [[Hypovolemia|volume depletion]] with subsequent [[hypovolemia]] and decreased tissue perfusion and, possibly [[organ failure]].<ref name="pmid22449515">{{cite journal |vauthors=Rajapakse S, Rodrigo C, Fernando D |title=Scrub typhus: pathophysiology, clinical manifestations and prognosis |journal=Asian Pac J Trop Med |volume=5 |issue=4 |pages=261–4 |year=2012 |pmid=22449515 |doi=10.1016/S1995-7645(12)60036-4 |url=}}</ref><ref name="pmid12860594">{{cite journal |vauthors=Walker DH, Valbuena GA, Olano JP |title=Pathogenic mechanisms of diseases caused by Rickettsia |journal=Ann. N. Y. Acad. Sci. |volume=990 |issue= |pages=1–11 |year=2003 |pmid=12860594 |doi= |url=}}</ref><ref name="pmid18366341">{{cite journal |vauthors=Bechah Y, Capo C, Mege JL, Raoult D |title=Rickettsial diseases: from Rickettsia-arthropod relationships to pathophysiology and animal models |journal=Future Microbiol |volume=3 |issue=2 |pages=223–36 |year=2008 |pmid=18366341 |doi=10.2217/17460913.3.2.223 |url=}}</ref><ref name="pmid19327117">{{cite journal |vauthors=Sahni SK, Rydkina E |title=Host-cell interactions with pathogenic Rickettsia species |journal=Future Microbiol |volume=4 |issue=3 |pages=323–39 |year=2009 |pmid=19327117 |pmc=2775711 |doi=10.2217/fmb.09.6 |url=}}</ref><ref name="pmid24059918">{{cite journal |vauthors=Sahni SK, Narra HP, Sahni A, Walker DH |title=Recent molecular insights into rickettsial pathogenesis and immunity |journal=Future Microbiol |volume=8 |issue=10 |pages=1265–88 |year=2013 |pmid=24059918 |pmc=3923375 |doi=10.2217/fmb.13.102 |url=}}</ref><ref name="pmid18414502">{{cite journal |vauthors=Walker DH, Ismail N |title=Emerging and re-emerging rickettsioses: endothelial cell infection and early disease</ref>


==Pathophysiology==
==Pathophysiology==
 
The pathophysiology of typhus fever can be described in the following steps:<ref name="pmid22449515">{{cite journal |vauthors=Rajapakse S, Rodrigo C, Fernando D |title=Scrub typhus: pathophysiology, clinical manifestations and prognosis |journal=Asian Pac J Trop Med |volume=5 |issue=4 |pages=261–4 |year=2012 |pmid=22449515 |doi=10.1016/S1995-7645(12)60036-4 |url=}}</ref><ref name="pmid12860594">{{cite journal |vauthors=Walker DH, Valbuena GA, Olano JP |title=Pathogenic mechanisms of diseases caused by Rickettsia |journal=Ann. N. Y. Acad. Sci. |volume=990 |issue= |pages=1–11 |year=2003 |pmid=12860594 |doi= |url=}}</ref><ref name="pmid18366341">{{cite journal |vauthors=Bechah Y, Capo C, Mege JL, Raoult D |title=Rickettsial diseases: from Rickettsia-arthropod relationships to pathophysiology and animal models |journal=Future Microbiol |volume=3 |issue=2 |pages=223–36 |year=2008 |pmid=18366341 |doi=10.2217/17460913.3.2.223 |url=}}</ref><ref name="pmid19327117">{{cite journal |vauthors=Sahni SK, Rydkina E |title=Host-cell interactions with pathogenic Rickettsia species |journal=Future Microbiol |volume=4 |issue=3 |pages=323–39 |year=2009 |pmid=19327117 |pmc=2775711 |doi=10.2217/fmb.09.6 |url=}}</ref><ref name="pmid24059918">{{cite journal |vauthors=Sahni SK, Narra HP, Sahni A, Walker DH |title=Recent molecular insights into rickettsial pathogenesis and immunity |journal=Future Microbiol |volume=8 |issue=10 |pages=1265–88 |year=2013 |pmid=24059918 |pmc=3923375 |doi=10.2217/fmb.13.102 |url=}}</ref><ref name="pmid18414502">{{cite journal |vauthors=Walker DH, Ismail N |title=Emerging and re-emerging rickettsioses: endothelial cell infection and early disease events |journal=Nat. Rev. Microbiol. |volume=6 |issue=5 |pages=375–86 |year=2008 |pmid=18414502 |doi=10.1038/nrmicro1866 |url=}}</ref>
===Transmission===
===Transmission===
*Rickettsial agents are usually not transmissible directly from person to person except by blood transfusion or organ transplantation, although sexual and placental transmission has been proposed for Coxiella.  
*[[Rickettsial|Rickettsial pathogens]] are harbored by parasites such as fleas, lice, mites, and ticks.  
*Transmission generally occurs via an infected arthropod vector or through exposure to an infected animal reservoir host.
*Organisms are transmitted by the bites from these parasites or by the inoculation of infectious fluids or feces from the [[parasites]] into the skin.  
*Inhaling or inoculating conjunctiva with infectious material also causes infection.
*Inhaling or inoculating [[conjunctiva]] with infectious material also causes infection.
 
{| class="wikitable"
{|  
!Arthopod borne diseases
|-style="background:silver; color:black"
!Vector
| '''Type of Infection''' || '''Spread'''
|-
|-style="background:silver; color:black"
|[[Epidemic typhus]]
| [[Epidemic typhus]] || Body louse
|Body louse
|- style="background:silver; color:black"
|-
| [[Trench fever]] || Body louse
|[[Trench fever]]
|- style="background:silver; color:black"
|Body louse
| [[Murine typhus]] || Flea infested rats
|-
|- style="background:silver; color:black"
|[[Murine typhus]]
| Cat flea rickettsioses || Flea infested dogs and cats
|Flea infested rats
|- style="background:silver; color:black"
|-
| [[Scrub typhus]] || Mites
|[[Scrub typhus]]
|- style="background:silver; color:black"
|Mites
| [[Tick borne rickettsiosis]] || Ticks
|-
|- style="background:silver; color:black"
|[[Rickettsialpox]]
| [[Rickettsialpox]] || Mites
|Mites
|- style="background:silver; color:black"
|-
| [[Anaplasmosis]] || Ixodes tick
|[[Anaplasmosis]]
|- style="background:silver; color:black"
|Ixodes tick
| [[Ehrlichiosis]] || Lone star tick
|-
|- style="background:silver;cplor:black"
|[[Ehrlichiosis]]
| [[Q fever]] || Infected veterinary animals
|Lone star tick
|- style="background:silver;cplor:black"
|-
| [[Cat scratch disease]] || Infected cats
|[[Q fever]]
|- style="background:silver;cplor:black"
|Infected veterinary animals
| [[Oroya fever]] || Sandflies
|-
|[[Cat scratch disease]]
|Infected cats
|-
|[[Oroya fever]]
|Sandflies
|}
|}
===Incubation===
===Incubation===
*Incubation period of Typhus fever varies from one to two weeks.
*Incubation period of typhus fever varies from one to two weeks.


===Dissemination===
===Dissemination===
Line 47: Line 52:


===Pathogensis===
===Pathogensis===
*The major pathology is caused by a vasculitis and its complications.
*The major pathology is caused by a [[vasculitis]] and its complications.
*On transmission, Rickettsia is actively phagocytosed by the endothelial cells of the small venous, arterial, and capillary vessels.
*On transmission, [[Rickettsiae|Rickettsia]] is actively phagocytosed by the endothelial cells of the small venous, arterial, and capillary vessels.
*It is followed by systemic hematogenous spread resulting in multiple localizing vasculitis.
*It is followed by systemic hematogenous spread resulting in multiple localizing [[vasculitis]].
*This process may cause result in occlusion of blood vessels and initiates inflammatory response (aggregation of leukocytes, macrophages, and platelets) resulting in small nodules.
*This process may cause result in occlusion of blood vessels and initiates [[inflammatory response]] (aggregation of [[leukocytes]], [[macrophages]], and [[platelets]]) resulting in small nodules.
*Occlusion of supplying blood vessels may cause gangrene of the distal portions of the extremities, nose, ear lobes, and genitalia.
*Occlusion of supplying blood vessels may cause [[gangrene]] of the distal portions of the [[extremities]], [[nose]], ear lobes, and [[genitalia]].
*This vasculitic process causes destruction of the endothelial cells and leakage of the blood leading to volume depletion with subsequent hypovolemia and decreased tissue perfusion and, possibly, organ failure.
*This vasculitic process causes destruction of the endothelial cells and leakage of the blood leading to volume depletion with subsequent [[hypovolemia]] and decreased tissue perfusion and, possibly, [[organ failure]].
*Endotheleal damage also leads to activation of clotting system (DIC).
*Endothelial damage also leads to activation of clotting system ([[Disseminated intravascular coagulation|DIC]]).


===Immune response===
===Immune response===
*Higher-affinity leucocyte integrins (LFA-1 and Mac-1) binding to members of the immunoglobulin (Ig) mediate initial leucocyte contact with EC by capturing them from the bloodstream
*Cytokines like tumour necrosis factor-alpha, interleukin (IL)-1beta and IL-6 up-regulate cellular adhesion molecules (CAMs) on the surface of host leucocytes and endothelial cells (EC)
*CAMs help in leucocyte transmigration across the endothelium.<ref name="pmid7574477">{{cite journal |vauthors=Lasky LA |title=Selectin-carbohydrate interactions and the initiation of the inflammatory response |journal=Annu. Rev. Biochem. |volume=64 |issue= |pages=113–39 |year=1995 |pmid=7574477 |doi=10.1146/annurev.bi.64.070195.000553 |url=}}</ref>
*This is followed by characteristic rolling and firm tethering to the endothelium and enabling subsequent leucocyte diapedesis.
*Tumor necrosis factor α ([[TNF-α]]) produce on activation of [[cell mediated immunity]], stimulates [[T lymphocytes]] and [[macrophages]], which help in eliminating intracellular rickettsia. Virulent rickettsia tend to suppress the activity of tumor necrosis factor α (TNF-α) and  [[IFN|IFN-gamma]].
*Tumor necrosis factor α ([[TNF-α]]) produce on activation of [[cell mediated immunity]], stimulates [[T lymphocytes]] and [[macrophages]], which help in eliminating intracellular rickettsia. Virulent rickettsia tend to suppress the activity of tumor necrosis factor α (TNF-α) and  [[IFN|IFN-gamma]].
*Cytokines such as [[interleukin (IL)]] 12 promote production of Interferon γ ([[Interferon|IFN-γ]]) responses. IFN-γ, which drives [[TH1]]-type responses and stimulates [[macrophage]] activation. [[Cytokines]], which include , [[IL-6]], [[IL-4]]<nowiki/>and [[IL-10]], down-regulate the protective response.
*Cytokines such as [[interleukin (IL)]] 12 promote production of Interferon γ ([[Interferon|IFN-γ]]) responses. IFN-γ, which drives [[TH1]]-type responses and stimulates [[macrophage]] activation. [[Cytokines]], which include , [[IL-6]], [[IL-4]]<nowiki/>and [[IL-10]], down-regulate the protective response.
==Genetics==
==Genetics==
There is no known genetic association to Typhus fever.
There is no known genetic association to typhus fever.


==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
{{WH}}
{{WS}}


[[Category:Needs content]]
[[Category:Needs content]]
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[[Category:Biological weapons]]
[[Category:Biological weapons]]
[[Category:Rickettsiales]]
[[Category:Rickettsiales]]
[[Category:Needs overview]]
[[Category:Emergency mdicine]]
[[Category:Disease]]
[[Category:Up-To-Date]]
[[Category:Infectious disease]]
[[Category:Infectious disease]]
 
[[Category:Gastroenterology]]
[[Category:Needs overview]]
[[Category:Pulmonology]]
 
 
 
{{WH}}
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Latest revision as of 00:32, 30 July 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Overview

Typhus is a zoonotic disease, humans are infected by the bites from parasites such as fleas, lice, mites, and ticks or by the inoculation of infectious fluids or feces from the parasites into the skin. The incubation period of typhus fever varies from one to two weeks. Following transmission, rickettsia are ingested by macrophages and polymorphonuclear cells. The major pathology is caused by a vasculitis and its complications. This process may cause result in occlusion of blood vessels and initiates inflammatory response (aggregation of leukocytes, macrophages, and platelets) resulting in small nodules. This vasculitic process causes destruction of the endothelial cells and leakage of the blood leading to volume depletion with subsequent hypovolemia and decreased tissue perfusion and, possibly organ failure.[1][2][3][4][5][6]

Pathophysiology

The pathophysiology of typhus fever can be described in the following steps:[1][2][3][4][5][6]

Transmission

  • Rickettsial pathogens are harbored by parasites such as fleas, lice, mites, and ticks.
  • Organisms are transmitted by the bites from these parasites or by the inoculation of infectious fluids or feces from the parasites into the skin.
  • Inhaling or inoculating conjunctiva with infectious material also causes infection.
Arthopod borne diseases Vector
Epidemic typhus Body louse
Trench fever Body louse
Murine typhus Flea infested rats
Scrub typhus Mites
Rickettsialpox Mites
Anaplasmosis Ixodes tick
Ehrlichiosis Lone star tick
Q fever Infected veterinary animals
Cat scratch disease Infected cats
Oroya fever Sandflies

Incubation

  • Incubation period of typhus fever varies from one to two weeks.

Dissemination

  • Following transmission, rickettsia are ingested by macrophages and polymorphonuclear cells. On ingestion, they replicate intracellularly inside the lysed cells and disseminate systemically.

Pathogensis

  • The major pathology is caused by a vasculitis and its complications.
  • On transmission, Rickettsia is actively phagocytosed by the endothelial cells of the small venous, arterial, and capillary vessels.
  • It is followed by systemic hematogenous spread resulting in multiple localizing vasculitis.
  • This process may cause result in occlusion of blood vessels and initiates inflammatory response (aggregation of leukocytes, macrophages, and platelets) resulting in small nodules.
  • Occlusion of supplying blood vessels may cause gangrene of the distal portions of the extremities, nose, ear lobes, and genitalia.
  • This vasculitic process causes destruction of the endothelial cells and leakage of the blood leading to volume depletion with subsequent hypovolemia and decreased tissue perfusion and, possibly, organ failure.
  • Endothelial damage also leads to activation of clotting system (DIC).

Immune response

Genetics

There is no known genetic association to typhus fever.

References

  1. ↑ 1.0 1.1 Rajapakse S, Rodrigo C, Fernando D (2012). "Scrub typhus: pathophysiology, clinical manifestations and prognosis". Asian Pac J Trop Med. 5 (4): 261–4. doi:10.1016/S1995-7645(12)60036-4. PMID 22449515.
  2. ↑ 2.0 2.1 Walker DH, Valbuena GA, Olano JP (2003). "Pathogenic mechanisms of diseases caused by Rickettsia". Ann. N. Y. Acad. Sci. 990: 1–11. PMID 12860594.
  3. ↑ 3.0 3.1 Bechah Y, Capo C, Mege JL, Raoult D (2008). "Rickettsial diseases: from Rickettsia-arthropod relationships to pathophysiology and animal models". Future Microbiol. 3 (2): 223–36. doi:10.2217/17460913.3.2.223. PMID 18366341.
  4. ↑ 4.0 4.1 Sahni SK, Rydkina E (2009). "Host-cell interactions with pathogenic Rickettsia species". Future Microbiol. 4 (3): 323–39. doi:10.2217/fmb.09.6. PMC 2775711. PMID 19327117.
  5. ↑ 5.0 5.1 Sahni SK, Narra HP, Sahni A, Walker DH (2013). "Recent molecular insights into rickettsial pathogenesis and immunity". Future Microbiol. 8 (10): 1265–88. doi:10.2217/fmb.13.102. PMC 3923375. PMID 24059918.
  6. ↑ 6.0 6.1 {{cite journal |vauthors=Walker DH, Ismail N |title=Emerging and re-emerging rickettsioses: endothelial cell infection and early disease

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