The word “chikungunya” is a derivation of the Kimakonde (a Mozambique dialect) word “kungunyala” meaning “to become desiccated or contorted”. In the Democratic Republic of the Congo it is called “buka-buka”, translated as “broken-broken”, reflecting the incapacitating arthralgias that are common manifestations of Chikungunya fever.
Chikungunya, first diagnosed in Tanganyika in 1952, is found in a large percentage of countries in Africa, Asia, Southeast Asia and is prevalent in India. Outbreaks occur periodically and in 2013 it was identified in the Caribbean.
Chikungunya has been diagnosed in nearly all of the states of the United States. Until the summer of 2014, all of the cases of Chikungunya detected in the U.S. were imported, occurring in individuals returning from endemic countries. During the summer of 2014, several locally transmitted cases were diagnosed in Florida non- travelers, indicating that the disease was now borne by the Aedes mosquitoes of mainland U.S. Local transmission has now been identified in 45 countries or territories in North, Central and South American, totaling at least 1.7 million cases.
Some believe the Chikungunya virus originated in Africa and migrated to Asia 200 years ago. Evidence derived from molecular genetics suggests it evolved around 1700; the first recorded outbreak of this disease was probably in 1779.
Interestingly, some medical historians believe that a pandemic of Chikungunya occurred in the western hemisphere in the 1800’s but was diagnosed as dengue fever. The 21st century researchers who have examined the accounts of this pandemic now speculate that it was caused by Chikungunya because the cases exhibited severe joint arthritis which is more indicative of Chikungunya than dengue. The virus then disappeared from the Americas until it re-emerged during the last decade.
Chikungunya epidemics appear suddenly and unpredictably and proceed explosively.
Individuals at the highest risk of contracting Chikungunya and enduring more severe symptoms are those who have chronic arthritis, underlying chronic medical conditions, those over the age of 65, and pregnant women. Travelers who spend extended periods of time in endemic areas are at greater risk. These include missionaries, humanitarian aid workers and those who frequently work outdoors.
Chikungunya is an arthropod transmitted disease caused by a single- stranded RNA arbovirus. As with dengue fever and yellow fever, Chikungunya cycles from mosquito to human to mosquito. The mosquito Aedes aegypti is the usual vector for transmission of Chikungunya. Aedes albopictus, the Asian tiger mosquito, is also a vector. Both species are found in the southeastern United States and limited parts of the southwest. The Aedes albopictus species survives further north into the Mid-Atlantic states and into the lower Midwest. The risk of person to mosquito transmission is highest during the viremic first week of illness. Birds, cattle, monkeys and other vertebrates may serve as reservoirs. The incubation period is 3 – 7 days (range 1–12 days). Between 72% and 97% of those infected will develop symptoms. Chikungunya can be transmitted during childbirth but there are no reported cases of transmission during breastfeeding. Theoretically, Chikungunya can be transferred via blood transfusion but there have been no reported cases. Previous infection is believed to convey long lasting immunity.
There is no current vaccine. The best preventive measures are wearing permethrin treated, bite-proof long sleeves and trousers, and using a mosquito repellant such as 30% DEET, 20% Oil of Lemon Eucolyptus or 30% picaridin. Screening windows and doors has only a limited effect, since most contacts between the Aedes mosquitoes and humans occur outside.
Standing water, a breeding ground for mosquitoes, should be drained. Aedes aegypti breeding sites are associated with human habitation and are seemingly innocuous (i.e. flower vases, water storage vessels and birdbaths).
Standard blood handling procedures are recommended.
If a Chikungunya epidemic were to occur in the U.S., the standard public health measures of avoidance and mosquito control would be major lines of defense.
Most people who contract Chikungunya are symptomatic. Clinical onset is abrupt. The hallmark of chikungunya is erratic, relapsing, and incapacitating arthralgia. High fever, headache, back pain, myalgia, and bilateral symmetric arthralgias predominate. Arthralgias can be intense, affecting mainly the extremities (ankles, wrists, phalanges) but also the large joints. Typically, the fever lasts for two days and then ends abruptly. Headache and an extreme degree of prostration may persist for a variable period, usually about five to seven days.
Rare symptoms include uveitis, retinitis, myocarditis, hepatitis, nephritis, hemorrhage, and neurologic problems such as myelitis, meningoencephalitis, Guillain-Barré syndrome and cranial nerve palsies.
In 40–50% of cases skin involvement is present consisting of a pruritic maculopapular rash predominating on the thorax, facial edema and localized petechia. Though rarely affected, children may exhibit a bullous rash with pronounced sloughing.
The case fatality ratio is approximates 1 per 1000, with most deaths occurring in newborns, the elderly, and the infirm.
The instructions for serum diagnostic testing are found on the CDC website. (http://www.cdc.gov/chikungunya/hc/diagnostic.html).
Blood should be collected in a tiger/speckled-top serum separator tube or a red-top tube. Serum may be sent to the CDC; some state and commercial laboratories have testing capabilities. Green-top heparin and purple top EDTA tubes are not appropriate tubes for testing. The virus may be cultured within the first 3 days of illness. Virus isolation provides the most definitive diagnosis, but requires one to two weeks for completion and must be carried out in biosafety level 3 laboratories. Chikungunya viral RNA may be identifiable in the serum during the first 8 days of illness as Chikungunya virus antibodies usually develop by the end of the first week of illness. IgM antibody levels peak three to five weeks after the onset of illness and persist for approximately two months. In some cases, paired acute- phase and convalescent-phase antibody sampling may be required for accurate diagnosis. False positive results may occur due to infection from closely related viruses.
A complete blood count (CBC) may show lymphopenia and thrombocytopenia. Liver enzymes may elevate and the serum creatinine might also increase. Radiological findings are normal and biological markers of inflammation are normal or modestly elevated.
In many parts of the world, Chikungunya is a clinical diagnosis of exclusion, particularly when laboratory testing is not readily available. The probability of accurate clinical diagnosis depends on the epidemiology of endemic diseases and the patient’s clinical symptoms.
The differential diagnosis for Chikungunya includes influenza, a multitude of viruses (particularly dengue fever), malaria and rickettsia. Dengue and Chikungunya viruses are transmitted by the same mosquitoes and have similar features. The two viruses can occasionally co-infect the same individual. Clinically differentiating Chikungunya from dengue fever may be difficult but in Chikungunya the onset of fever is typically more abrupt, shorter lived and rash and arthralgia more prevalent.
Seasonally, Chikungunya is more likely to be seen in the summer months when Aedes mosquitos proliferate.
Medical treatment is primarily supportive. The use of antiviral agents is unproven. Though it is generally recommended that acetaminophen, NSAIDs and corticosteroids be used for treatment of joint pain, some experts suggest that typical anti-inflammatory agents may paradoxically make symptoms worse because the arthritis of Chikungunya arises from the virus itself, not an inflammatory response. Typical anti-inflammatory agents may actually inhibit the immune response required to suppress the Chikungunya virus.
Suspected chikungunya cases should be reported immediately to state or local health departments to facilitate diagnosis and mitigate the risk of local transmission.
Twenty percent of infected patients have severe recurrent joint pains for a year or more after acute illness. During the La Reunion outbreak in 2006, more than 50% of subjects over the age of 45 reporting prolonged painful joints for up to three years following initial infection.
Some patients may have relapses of underlying rheumatologic disorders in the months following acute infection. Others may suffer long-term asthenia.
Chikungunya is one of the agents researched as a potential biological weapon.
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