Chikungunya pathophysiology: Difference between revisions
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{{Chikungunya}} | {{Chikungunya}} | ||
==Overview== | |||
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| [[File:Ae aegypti ae albopictus.jpg|center|thumb|350px|Aedes mosquitoes transmit chikungunya virus to people.]] | |||
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* Chikungunya virus is primarily transmitted to humans through the bites of infected mosquitoes, predominantly Aedes aegypti and Aedes albopictus. | * Chikungunya virus is primarily transmitted to humans through the bites of infected mosquitoes, predominantly Aedes aegypti and Aedes albopictus. | ||
* Humans are the primary host of chikungunya virus during epidemic periods. | * Humans are the primary host of chikungunya virus during epidemic periods. | ||
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* The risk of a person transmitting the virus to a biting mosquito or through blood is highest when the patient is viremic during the first week of illness. | * The risk of a person transmitting the virus to a biting mosquito or through blood is highest when the patient is viremic during the first week of illness. | ||
==Pathophysiology== | |||
Following transmission through bites by infected mosquito (''Aedes aegypti'' or ''Aedes albopictus''), Chikungunya virus replicates in the skin and fibroblasts, enters the bloodstream, and disseminates to the liver, muscle, joints, lymphoid tissues, and brain . After an incubation period of two to four days, affected individuals typically experience an abrupt onset of symptoms including high fever, rigors, headache, photophobia, incapacitating arthralgia, and rash characterized by petechiae and/or maculopapular lesions. Unlike other members of arthritogenic Alphavirus, Chikungunya virus may also cause symptoms of meningoencephalitis and hemorrhagic disease. In parallel with the development of acute symptoms, the upsurge of viral load triggers the activation of the innate immune response hallmarked by the robust production of type I interferons and other proinflammatory cytokines and chemokines. Cell-mediated immunity and antibody-mediated viral clearance occur approximately a week after infection. Chronic symptoms of recurrent joint pain have been reported and may be related to the induction of autoantibodies. | |||
==References== | ==References== | ||
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[[Category:Disease]] | [[Category:Disease]] | ||
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[[Category:Togaviruses]] | [[Category:Togaviruses]] | ||
[[Category:Tropical disease]] | [[Category:Tropical disease]] | ||
Revision as of 11:30, 6 June 2014
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Chikungunya Microchapters |
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Diagnosis |
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Chikungunya pathophysiology On the Web |
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American Roentgen Ray Society Images of Chikungunya pathophysiology |
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Risk calculators and risk factors for Chikungunya pathophysiology |
Overview
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- Chikungunya virus is primarily transmitted to humans through the bites of infected mosquitoes, predominantly Aedes aegypti and Aedes albopictus.
- Humans are the primary host of chikungunya virus during epidemic periods.
- Blood-borne transmission is possible; cases have been documented among laboratory personnel handling infected blood and a health care worker drawing blood from an infected patient.
- Rare in utero transmission has been documented mostly during the second trimester.
- Intrapartum transmission has also been documented when the mother was viremic around the time of delivery.
- Studies have not found chikungunya virus in breast milk.
- The risk of a person transmitting the virus to a biting mosquito or through blood is highest when the patient is viremic during the first week of illness.
Pathophysiology
Following transmission through bites by infected mosquito (Aedes aegypti or Aedes albopictus), Chikungunya virus replicates in the skin and fibroblasts, enters the bloodstream, and disseminates to the liver, muscle, joints, lymphoid tissues, and brain . After an incubation period of two to four days, affected individuals typically experience an abrupt onset of symptoms including high fever, rigors, headache, photophobia, incapacitating arthralgia, and rash characterized by petechiae and/or maculopapular lesions. Unlike other members of arthritogenic Alphavirus, Chikungunya virus may also cause symptoms of meningoencephalitis and hemorrhagic disease. In parallel with the development of acute symptoms, the upsurge of viral load triggers the activation of the innate immune response hallmarked by the robust production of type I interferons and other proinflammatory cytokines and chemokines. Cell-mediated immunity and antibody-mediated viral clearance occur approximately a week after infection. Chronic symptoms of recurrent joint pain have been reported and may be related to the induction of autoantibodies.