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Pathology of Chikungunya Virus Infection
Chikungunya virus is a togavirus belonging to the genus alphavirus, indigenous to tropical Africa and Asia, where it is transmitted to humans by the bite of infected mosquitoes, usually of the genus Aedes.
Chikungunya fever, the disease caused by Chikungunya virus, was first recognized in epidemic form in East Africa during 1952-1953.
Since the beginning of 2006, this crippling mosquito-borne disease (Chikungunya virus infection) has shown an explosive emergence in nations in the Indian Ocean area.
By March 7, 2006, 157,000 people had been infected in the French island La Reunion, and the disease had spread to the islands of Seychelles, Mauritius, and Mayotte (French). Subsequently, the disease appeared in India, China, and European countries.
Infection in Aedes aegypti salivary glands is asymptomatic and lifelong. It is transmitted by Aedes aegypti to human, there is no human to human transmission.
The disease is highly infectious.
Its main symptoms are sudden onset of chills, fever, headache , rash, and debilitating arthralgia.
The symptoms may persist for several weeks.
The word "chikungunya" is thought to derive from description in local dialect of the contorted posture of patients afflicted with the severe joint pain associated with this disease.
May rarely cause hemorrhagic fever, specially in children.
Incubation period is 1 to 12 days. Fever lasts for 3 - 7 days, arthralgia may persit for upto 3 weeks.
Because Chikungunya fever epidemics are sustained by human-mosquito-human transmission, the epidemic cycle is similar to those of dengue and urban yellow fever.
Large outbreaks of Chikungunya fever have been reported recently on several islands in the Indian Ocean and in India.
Though fetal contamination risks appear to be rare before 22 weeks of gestation, they are potentially dangerous.
After 22 weeks gestation, newborns infection occurs if the mother is viremia positive at delivery.
Transplacental transmission is suspected, but the pathogenic mechanism remains unknown.
Warm, humid climates and water reservoirs serve as an excellent breeding ground for the vector of the virus, Aedes mosquitoes. With an increase in temperature, susceptibility of mosquitoes to CHIKV increases.
Although the disease is self-limiting, the risk to non-immune travellers from other parts of the world to areas with a chikungunya epidemic, continues to exist and should be included in the differential diagnosis of travellers returning home with fever.
Due to similarities in clinical presentation with dengue, limited awareness, and a lack of laboratory diagnostic capability, CHIKV is probably often underdiagnosed or misdiagnosed as dengue .
Treatment is supportive. Analgesic and anticonvulsants are often used.
The prognosis is generally good, although some patients experience chronic arthritis. There are very few recorded fatalities.
With no vaccine or antiviral available, prevention and control depends on surveillance, early identification of outbreaks, and vector control.
CHIKV should be borne in mind in sporadic cases, and in patients epidemiologically linked to ongoing local or international outbreaks or endemic areas.
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