Chikungunya Virus

Updated: Feb 17, 2022
Author: Suganthini Krishnan Natesan, MD, FIDSA; Chief Editor: Michael Stuart Bronze, MD 



Chikungunya fever is a self-remitting febrile viral illness that has been associated with frequent outbreaks in tropical countries of Africa and Southeast Asia. The illness has only recently become a concern in Western countries and temperate zones around the world. The recent re-emergence and travel-related spread of Chikungunya infection to Europe and the United States has drawn global attention. In fact, international travel stands out as one of the major risk factors for the rapid global spread of the disease.[1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13]

The term “Chikungunya” often refers to both the virus (CHIKV) and the illness or fever (CHIKF) caused by this virus. It was derived from the African dialect Swahili or Makonde and translates as “to be bent over.” In Congo, it is referred to as “buka-buka,” which means “broken-broken.” These terms refer to the “stooped-over posture” exhibited by individuals with the disease as a consequence of severe chronic incapacitating arthralgias.

The roots of this viral illness date back to 1953, when it was first described during an outbreak in a Swahili village in the Newala district of Tanzania, Africa.[14, 15] Chikungunya virus is transmitted to humans through day-biting mosquitoes that belong to the Aedes genus\.

Aedes aegypti. Image courtesy of the CDC. Aedes aegypti. Image courtesy of the CDC.

See 11 Travel Diseases to Consider Before and After the Trip, a Critical Images slideshow, to help identify and manage infectious travel diseases.



The exact pathophysiology of Chikungunya virus remains to be investigated. To date, most of the research in this field has been from the Indian subcontinent and other Asian countries.

Chikungunya virus infection has a clinical presentation that overlaps with that of Ross River virus infection (fever, rash, polyarthritis) and dengue fever virus transmitted by the same mosquitoes. Evaluation of the T-cell– and B-cell–mediated immunity has shed light on some possible mechanisms.

Using a murine model, Lum et al showed that anti–Chikungunya virus antibodies were elicited early in the course of the illness and were directed against the C-terminus of the viral E2 glycoprotein. They found that both natural and Chikungunya virus infection–induced specific antibodies were essential for controlling Chikungunya virus infections.[16]

Waquier et al conducted a large ex vivo multiplex study of T-cell immunity and 50 cytokine, chemokine, and growth factor plasma profiles in 69 acutely infected patients from the Gabonese outbreak in 2007. They concluded that Chikungunya virus infection elicited strong innate immunity with an abundant production of proinflammatory markers and cytokines, including high levels of alpha interferon, interleukin (IL)–4, IL10, and gamma interferon. By flow cytometric analysis, the authors also demonstrated that humans show a CD8+ lymphocytic response in the early stages and a CD4+ predominant response in the later stages. Most importantly, the authors described a CD95-based apoptosis of CD4+ lymphocytes that could partially explain the lymphopenia in these patients. Hence, severe or chronic infections could be attributed to an absence or deregulation of one of these pathways.[17]

A 2017 study reported that Chikungunya infection activates toll-like receptors (TLR), triggering the innate immune system. This results in release of inflammatory cytokines and type 1 interferons. Three different single-nucleotide polymorphisms (SNPs) in human TLR-7 (rs179010, rs5741880, rs3853839) and one SNP in TLR-8 (rs3764879) were associated with increased susceptibility to infection and related clinical manifestations.[18]

The exact mechanism of entry of the virus into mammalian cells is under investigation.[19, 20] Bernard et al evaluated this mechanism and found that Chikungunya virus enters mammalian epithelial cells via a clathrin-independent, Esp-15–dependent, dynamin 2–dependent route and requires an endocytic pathway in combination with other unknown pathways. The authors speculate that Chikungunya virus is capable of undergoing genetic drifts and could acquire alternate entry mechanisms.[21]

Several murine models with Chikungunya virus–related joint and neurological diseases are being investigated. Other state-of-the-art in vivo imaging techniques using bioluminescence imaging with luciferase-tagged pathogens and intravital 2-photon imaging systems are being evaluated for study of Chikungunya infection’s chronic phase.[22, 23, 24, 25]  It has now been shown that type 1 interferon sensing by nonmyeloid cells plays a significant role in fighting Chikungunya infection.[26]

Aedes aegypti was the primary vector for Chikungunya infection in India and other countries during the 2006-2010 epidemics. Analysis of a 2016 outbreak in Brazil revealed two novel mutations in the virus (K211T in E1 and V156A in E2). These mutations enhanced viral fitness, as they could infect host cells independent of cholesterol, causing the outbreak to become an epidemic.[27]

Research on antiviral agents to treat Chikungunya infection is ongoing. Molecules that inhibit chikungunya viral replication by direct inhibition of the virus or that act via host defense mechanisms have been identified.[28] Das et al have designed and validated a set of 12 compounds that inhibit the functional moiety of the nsP2 viral protease. All these compounds suppressed Chikungunya viral replication in cell culture assays and appear promising.[29]

Further research in this field would undoubtedly provide a better understanding of the in vivo interactions between Chikungunya virus and immune cells, and shed light on the immunopathogenesis.


Chikungunya virus is an alpha virus that belongs to the Togaviridae family. It is a single-stranded RNA virus and is approximately 11.8 kb long with a capsid and a phospholipid envelope. Phylogenetic analysis has revealed three distinct groups based on partial sequences of NS4 and E1 genes: (1) the West African, (2) the East-Central-South African (ECSA), and (3) the Asian.[7, 8]

Chikungunya virus is transmitted to humans through day-biting mosquitoes that belong to the Aedes genus. Being an arbovirus, the virus is maintained in the environment between humans or other animals and mosquitoes. Humans serve as major reservoirs during epidemics.

During inter-epidemic quiescence in Africa, the virus is thought to be maintained in an epizootic cycle that involves vertebrates such as monkeys, rodents, and birds. In Africa, the virus is maintained in a sylvatic cycle among wild primates, monkeys, and wild Aedes mosquitoes (Aedes furcifer, Aedes taylori, Aedes luteocephalus, Aedes africanus, Aedes neoafricanus). A sylvatic cycle has not been identified outside the African continent.

In Asia, the virus is maintained in an urban cycle involving A aegypti mosquitoes and humans. The method of viral maintenance in the environment during the quiescent inter-epidemic periods in Asia remains unknown. Unlike its counterpart, the dengue virus, a transovarian transmission has not yet been reported, supporting the historical theory that the virus first originated in Africa and later spread to other countries in Asia. Historically, Chikungunya outbreaks are known to demonstrate a secular, cyclical, and seasonal trend.[30, 31, 32]

Aedes aegypti. Image courtesy of the CDC. Aedes aegypti. Image courtesy of the CDC.

Epidemics are characterized by explosive outbreaks between years-long periods of quiescence. The exact reason for this is unknown. Several socioeconomic factors, susceptibility of humans and mosquitoes to the virus, and ability of transmission all seem to play a role.

Evolution of Chikungunya virus

Phylogenetic analysis has revealed that the Chikungunya virus genome has remained stable over the years since its first discovery in 1952.[32] Comparison of two Asian Chikungunya virus strains that were isolated 10 years apart showed 99.4% identity. Most of the early strains isolated from the Reunion Island Chikungunya virus outbreak were similar to the ECSA cluster.[5, 33, 34] However, the strains isolated from the 2006-2007 outbreak revealed an alanine to valine amino acid mutation at position 226 in the E1 glycoprotein. The presence of alanine (A226) denotes cholesterol-dependent growth and replication of Chikungunya virus in certain Aedes species.

This particular mutation raised considerable interest in the research field, as it resulted in cholesterol-independent growth and replication of Chikungunya virus and was exclusively seen in Chikungunya virus isolated from Aedes albopictus mosquitoes. This mutation was also associated with enhanced fitness in Chikungunya virus, enabling it to infect A albopictus mosquitoes and other species that normally lack cholesterol. This ability of the Chikungunya virus to adapt to a new species has significant implications with respect to the range of transmission and spread across the globe.[35, 36, 37, 38, 39]

The above findings led experts to speculate that Chikungunya virus would no longer be restricted to the tropical countries but could spread to temperate regions, as A albopictus predominates in temperate zones where A aegypti is scarce (the Americas, Europe, China, Japan).[40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50]


Numerous Chikungunya epidemics have been reported in several countries in Southern and South East Asia. Distinct strains of Chikungunya virus within varying transmission cycles have been reported from different locations. The African variant has managed to persist over the years with frequent outbreaks due to a sylvatic cycle maintained between monkeys and wild mosquitoes. Conversely, the Asian variant causes epidemics that are maintained by an urban cycle, characterized by long inter-epidemic quiescence for more than 10 years or so.

The first Asian epidemic was reported in Bangkok, Thailand, in 1958; continued until 1964; reappeared after a hiatus in the mid-1970s; and declined again in 1976. Major outbreaks were also reported from northwestern and southern parts of India, Sri Lanka, Myanmar, and Thailand in the early 1960s. The cases then declined before sporadic outbreaks were later reported in the Philippines and Indonesia in the 1980s and Malaysia in the 1990s.[7, 9, 11]

The next major outbreak occurred in 2001 on islands in the Indian Ocean (Mauritius, Mayotte, Madagascar, Reunion Island). The most severe Chikungunya fever outbreak was reported in 2006 on Reunion Island, where one third of the population was infected, resulting in 237 deaths. Around the same time, an historic outbreak on the Indian subcontinent involved 1.42 million people, with high morbidity rates.[5]

By 2007, the disease was no longer considered a tropical illness, as it had spread to several nontropical and temperate areas, including Singapore.

According to figures from 2013-2014 from the Centers for Disease Control and Prevention (CDC), European Center for Disease Prevention and Control (ECDC), and the Pan American Health Organization (PAHO), several imported cases of travel-related Chikungunya fever have been reported in the United States, Caribbean islands, Britain, France, Germany, Sweden, Portugal, Canary Islands, and the archipelagos off the coast of Western Africa.[41, 42, 43, 44, 45, 46] Chikungunya virus emerged in the Americas in late 2013 and has continued to spread to neighboring countries. As of 2017, about 1.8 million cases had been reported from 44 countries.[51]

In 2018, a literature review group published one of the largest seroprevalence studies (mostly based on IgG ELISA and/or multiplex assay) that included data from 2000-2018. Continents included in these studies included Africa (46%) and Asia (24%). Most reports were from Kenya, Madagascar, India, and French Polynesia. Among these regions, the highest seroprevalence was noted among the general population in Lamu Island, Kenya (72%); pregnant women in Thailand (71.2%); the general population in French Polynesia (76%); and children in Haiti (75.6%).[52]

CDC update

Chikungunya virus disease became a nationally notifiable condition in 2015. Cases are reported to the CDC by state and local health departments using standard case definitions.

Many travel-related cases of Chikungunya infection have been imported into the United States since 2006. As of December 2014, a total of 1,938 travel-associated cases from 47 states and two US territories (Puerto Rico, Virgin Islands) have been reported.

The first case of local transmission to a person who had not traveled outside the United States was reported in July 2014, which was the first documented case of mosquitoes in the United States spreading the illness to a nontraveler.[41] As of December 2014, a total of 11 locally transmitted cases have been reported in the United States, all in Florida.[53]

In addition, 3402 locally mosquito-transmitted cases in Puerto Rico and 86 cases in the Virgin Islands have been reported.[42, 43, 53] However, a recent study by the Puerto Rico Department of Health (PRDH) and the CDC shows that cases are underreported in Puerto Rico. From June 20 to August 19, 2014, The PRDH and CDC collected passive surveillance data in 250 participants, 70 (28%) of whom tested positive for past or current chikungunya virus infection. Only two of 25 participants (8%) with chikungunya infection who sought care had been reported to health authorities.[54]

A total of 124 cases of Chikungunya virus disease (116 from US states and 8 from US territories) were reported to ArboNET in 2018.[55] Cases in US states occurred in travelers returning from affected areas, whereas cases in US territories were all locally acquired in Puerto Rico. As of August 1, 2019, a total of 42 Chikungunya virus disease cases had been reported in the United States and its territories in 2019.[56]

These cases illustrate the magnitude of the global spread of Chikungunya infection. They also emphasize the need to maintain efficient surveillance networks and implementation of adequate prevention measures, both at the personal and community level, to contain the infection and to prevent outbreaks.


Although Chikungunya fever is a self-remitting illness, rare cases of complications have been reported in India during major outbreaks among patients with comorbidities (cardiovascular, respiratory, neurological), neonates, elderly patients, and immunocompromised patients. In a report from the Reunion Island outbreak in 2005, 610 patients with comorbidities had atypical presentations, 65 of whom died. Some of the complications included hepatitis, meningoencephalitis, bullous dermatosis, and pneumonia.[57]

The overall mortality in this report was 10.6% and was higher among elderly individuals. The most common risk factors associated with a high mortality and severe infection were cardiovascular (226 patients), respiratory (150 patients), and neurological (147 patients) conditions.[57, 58, 59]

Chikungunya virus is not known to be neurovirulent or neuroinvasive, unlike other alpha viruses. However, rare cases of encephalitis (predominantly demyelinating), myelitis, entrapment neuropathy, seizures, abnormal cerebrospinal fluid (CSF) chemistries, flaccid paralysis, neurological sequelae, and severe peripheral neuropathy and Guillain Barré–type presentations have been reported from several centers in India.[60, 61, 62] During the epidemic in the Reunion Islands, four newborns had severe attacks of meningoencephalitis, three with disseminated intravascular coagulation (DIC) and one with intracerebral hemorrhage from severe thrombocytopenia.[57]

Coinfection of Chikungunya fever with dengue has been reported from Yemen.[47, 63] Unlike dengue fever (see Table 1), hemorrhagic manifestations are uncommon with Chikungunya fever and generally are mild (epistaxis, gingival bleeding, subconjunctival hemorrhage, petechial or purpuric rash) if present. Other rare complications include sudden sensorineural hearing loss, granulomatous and nongranulomatous anterior uveitis, optic neuritis, retrobulbar neuritis, dendritic lesions, hypokalemic periodic paralysis, and multiorgan failure. The prognosis of eye disease was good, with most patients recovering their vision. In general, the neurologic outcome was good, with most patients recovering from the initial episode.

Complications were more commonly seen in infants, adults with comorbidities, and elderly patients.[64, 65, 66] Intrauterine infection in pregnant individuals with vertical transmission has also been reported.[67, 68]

Das et al have described the capacity of Chikungunya virus to infect the neurons and glial cells, indicating the neuroinvasive and neurovirulent potential of this virus.[66] However, the neurotropism of Chikungunya virus remains controversial and merits further investigation.

Persistent severe arthralgias could lead to long-term disability and loss of work days.[69, 70, 71, 72] Thus, the burden on the economy in terms of loss of productivity and income is estimated to be significant.

Patient Education

See Prevention.




Chikungunya fever is an acute febrile illness with an incubation period of 3 to  days. It affects all age groups and both sexes equally, with an attack rate (percentage of individuals who develop illness after infection) of 40% to 85%.

Patients present with abrupt onset of high-grade fever often reaching 102° to 105°F, with shaking chills that last 2 to 3 days. The fever may return for 1 to 2 days after an afebrile period of 4 to 10 days, hence called a “saddle-back fever.”

Prodromal symptoms are uncommon. However, sore throat, headache, abdominal pain, constipation, and retro-orbital pain have been reported during the acute phase of the illness.

Physical Examination

Clinical examination reveals high-grade fevers (up to 105°F), pharyngitis, conjunctival suffusion, conjunctivitis, and photophobia. Cervical or generalized lymphadenopathy has also been reported in rare cases. Other frequent manifestations include severe arthralgias, myalgias, and rash.[4, 7, 8]


The arthralgias are usually polyarticular and migratory, and frequently involve the small joints of the hands, wrist, and ankle, with lesser involvement of the large joints such as the knee or shoulder with associated arthritis. More than 10 joint groups may be involved simultaneously, incapacitating the patient. Swollen tender joints with tenosynovitis and crippling arthritis are often evident at the time of presentation. Joint pain is worse in the morning, gradually improving with slow exercise and movement but exacerbated by strenuous exercise.

Patients characteristically lie still in a flexed posture owing to the pain upon any movement. Rarely, sternoclavicular and temporomandibular joints are involved. Axial involvement is common, but hips are relatively spared. Inflammatory markers may be mildly elevated, but radiological findings are usually normal. Joint edema is seen, but effusion is uncommon.

Although joint manifestations resolve completely within 1 to 2 weeks in most patients, about 10% to 12% develop chronic joint symptoms that may last for months.[70, 71, 73, 74] In 2017, Chang et al reported that, although about 25% of individuals with Chikungunya infection eventually develop persistent arthritis, follow-up testing revealed no detectable Chikungunya virus on synovial fluid analysis among 38 study participants.[75]

Cutaneous manifestations

Individuals with Chikungunya fever frequently present with a flushed appearance involving the face and trunk, followed by a diffuse erythematous maculopapular rash of the trunk and extremities, sometimes involving the palms and soles. The rash gradually fades; evolves into petechiae, urticaria, xerosis, or hypermelanosis; or resolves with desquamation.[76, 77]

A tourniquet test is positive in some patients, similar to dengue fever. In fact, some of the symptoms and signs of Chikungunya fever are almost indistinguishable from those of dengue fever. As both illnesses are transmitted by the same vector, coinfection has been reported in the literature. The differences between these diseases are discussed below (see Diagnostic Considerations).

Neurological manifestations

In the acute phase of the illness (reported during the outbreak in the Indian Ocean in 2005-2006), 23 patients presented with neurological symptoms associated with abnormal CSF tests and positive CSF immunoglobulin M (IgM) or reverse-transcriptase polymerase chain reaction (RT-PCR) for Chikungunya virus. Clinical manifestations in this outbreak included altered mental status or behavior in 95%, headache in 30.4%, seizures in 26%, motor dysfunction in 4.3%, and sensorineural abnormalities in 8.7%.[78, 79, 80, 81, 82]


Rare presentations include severe rheumatoid arthritis, neuroretinitis, uveitis, hearing loss, myocarditis, and cardiomyopathy.[83, 84, 85, 86, 87, 88, 89, 90, 91, 92]

Diagnostic Criteria for Chikungunya Fever

The case definition of Chikungunya fever as proposed by the World Health Organization (WHO) Regional Office for Southeast Asia is discussed below.[93]

Suspected case

A suspected case involves a patient presenting with acute onset of fever, usually with chills/rigors, that lasts for 3 to 5 days, with pain in multiple joints/swelling of extremities that may continue for weeks to months.

Probable case

A probable case is characterized by conditions that support a suspected case (see above) along with one of the following conditions:

  • History of travel or residence in areas reporting outbreaks

  • Ability to exclude malaria, dengue, and any other known cause of fever with joint pains

Confirmed case

Chikungunya fever is confirmed if the patient meets one or more of the following findings irrespective of the clinical presentation (see also Workup):

  • Virus isolation in cell culture or animal inoculations from acute-phase sera 

  • Presence of viral ribonucleic acid (RNA) in acute-phase sera as determined with RT-PCR 

  • Presence of virus-specific IgM antibodies in single serum sample in acute phase or 4-fold increase in virus-specific IgG antibody titer in samples collected at least 3 weeks apart 


Chikungunya infection outbreaks result in large epidemics that can cause significant morbidity. Postinfection rheumatism with joint pain lasting months to years has been reported in the literature. Symptoms can range from transient arthritis with joint pains to severe joint destruction requiring antirheumatic therapy. It also has been shown to exacerbate pre-existing rheumatological conditions, resulting in impaired quality of life. Chronic pain and rheumatism have been shown to affect the mental health of patients.

Although neurologic complications have been controversial, a range of neurologic manifestations were reported from La Reunion Island, with 24 patients diagnosed with Chikungunya-related encephalitis. In addition, severe acute hepatitis, heart failure, respiratory insufficiency, cutaneous effects, and renal failure were also identified during this outbreak.

So far, Chikungunya infection in pregnant people has not been directly linked to congenital malformations. However, vertical transmission at the time of birth has been described in neonates, resulting in neurologic complications and cognitive developmental delays.[94, 95, 96]



Diagnostic Considerations

Other diseases to be considered in the differential diagnoses depend on the country of residence, local epidemiology, travel history, and exposure (see Differentials). 

Table 1. Clinical and Laboratory Features of Chikungunya virus Infections Compared with Dengue Virus Infections (Open Table in a new window)


Chikungunya Virus Infection

Dengue Virus Infection

Fever (>39°C)




































Table adapted from Centers for Disease Control and Prevention 


Viral infections

  • Dengue fever

  • West Nile fever

  • Adenovirus infection

  • O'nyong-nyong fever

  • Ross River fever

  • Sindbis fever

  • Crimean-Congo fever

  • Bussuquara fever

  • Mayaro fever

  • Ebola fever

  • Hantavirus infection

  • Kyasanur Forest disease

  • Lassa fever

  • Rubella

  • Parvovirus B19 infection

  • Hepatitis B

  • Mumps

  • Infection with herpes viruses

Parasitic infections

  • Falciparum malaria infection

Bacterial infections

  • Leptospirosis

  • Rickettsial infections

  • Gonococcemia

  • Postinfectious reactive arthritis

  • Group A streptococcal infection



Approach Considerations

Chikungunya infection is confirmed via serological tests, which take about 5 to 7 days into the illness to turn positive. Therefore, early diagnosis is based on a high index of clinical suspicion based on epidemiology and clinical presentation that includes the triad of high fever, rash, and associated rheumatologic manifestations.[97, 98, 99, 100]

Serologic Testing

Chikungunya virus–specific IgM antibodies usually appear upon cessation of viremia, usually by day 5 to 7 into the illness, and stay positive for 3 to 6 months. Immunoglobulin G (IgG)–neutralizing antibodies appear after 7 to 10 days and may persist for several months. These antibodies are detected with an enzyme-linked immunoassay (ELISA) test that is available through the CDC and several state health departments.

Viral Culture

Chikungunya virus may be isolated in culture within the first 3 days of illness during the period of active viremia by inoculation of blood into mice or mosquitoes. Culture-based detection is also available through the CDC.

Molecular Diagnostics

RT-PCR has been standardized using both structural and nonstructural domains of the Chikungunya virus genome and is available through the CDC. A genotyping assay has also been developed that would help in outbreak settings. The molecular assay detects viral RNA during the first 7 to 8 days of the illness.[101]



Approach Considerations

No specific antiviral treatment is available for Chikungunya fever.

It is important to exclude other serious infections similar to Chikungunya fever such as dengue, malaria, or bacterial infections.

Once other infections are excluded, management includes hydration, monitoring of hemodynamic status, collection of blood specimens for diagnosis, and antipyretic therapy. Severe arthralgia may be managed with nonsteroidal anti-inflammatory drugs (NSAIDS) (once dengue is excluded) and physiotherapy. Poor glycemic control in patients with diabetes who have Chikungunya infection has been reported. It is important to monitor the blood glucose closely in these patients.

Published evidence does not recommend the use of corticosteroids or antiviral agents.

Although a vaccine for Chikungunya virus appears promising, the process has been hampered by heterogeneity of serotypes, genetic alterations, lack of animal models, and scarcity of studies on immune responses to the virus.

Conservative treatment includes management of electrolyte imbalance, prerenal azotemia, and hemodynamic monitoring based on severity of illness. Indiscriminate use of corticosteroids, NSAIDS (especially aspirin), and other antibiotics could result in thrombocytopenia, gastritis, gastrointestinal bleeding, and renal failure, and indirectly contribute to overall mortality.


Vector control plays a key role in preventing the spread of Chikungunya virus. Humans traveling to endemic/epidemic areas are recommended to use mosquito repellents, to wear long-sleeve shirts and long pants, and to use air-conditioned rooms or rooms with window and door screens.

People with suspected Chikungunya fever should avoid mosquito exposure during the first week of viremia to prevent local transmission of the illness.

Appropriate education of the community and public health officials on eliminating mosquito breeding sites (stagnant water, weeds and tall grass) and spraying insecticides is essential for optimal vector control and for interrupting transmission of the disease.

Humans at risk for severe disease must avoid travel to areas with ongoing outbreaks.

Future Perspectives

Research into development of a live-virus and attenuated-virus vaccine against Chikungunya virus is ongoing. However, no vaccines are available at this time.[102, 103, 104]

Chikungunya fever is an emerging global disease with several intriguing and unanswered questions such as the reason for sudden major rapid outbreaks with disease-free intervals, mode of survival or maintenance of the virus in nature between epidemics, factors that trigger the outbreaks, and strain replacements during outbreaks.[95]

More research is needed to understand the epidemiology and natural history of this disease. Until then, prevention and vector control at personal and community level should be implemented.


Consultations may include the following:

  • Infectious disease specialist

  • Rheumatologist

  • Intensive care specialist

  • Neurologist

Long-Term Monitoring

Arthralgias resolve spontaneously within 3 weeks in about 70% of patients. However, they can persist for 3 months to 6 months in 30% of patients, for 20 months in 15%, and for 3 years to 5 years in 12%. Elderly patients and patients with prior rheumatologic conditions are at higher risk for chronic polyarthritis, tenosynovitis, and bursitis. Bouquillard et al have reported the possible unmasking or occurrence of rheumatoid arthritis in patients infected with Chikungunya virus. Patients with chronic arthritis may need long-term follow-up with both infectious disease and rheumatology experts.[85]

In 2017, Chang et al reported that, although about 25% of individuals with Chikungunya infection eventually develop persistent arthritis, follow-up testing revealed no detectable Chikungunya virus on synovial fluid analysis among 38 study participants. This finding suggests that immunomodulators may have a role in the treatment of such cases.[75]


Questions & Answers


What is Chikungunya virus infection?

What is the pathophysiology of Chikungunya virus infection?

How is Chikungunya virus transmitted?

How has the Chikungunya virus evolved?

What is the global prevalence of Chikungunya virus infection?

What is the incidence of Chikungunya virus infection in the US?

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What are the signs and symptoms of Chikungunya virus infection?

Which physical findings are characteristic of Chikungunya virus infection?

How is arthralgia characterized in Chikungunya virus infection?

Which cutaneous findings are characteristic of Chikungunya virus infection?

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Which viral infections should be included in the differential diagnoses of Chikungunya virus infection?

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Which parasitic infections should be included in the differential diagnoses of Chikungunya virus infection?

Which bacterial infections should be considered in the differential diagnoses of Chikungunya virus infection?


How is a diagnosis of Chikungunya virus infection confirmed?

What is the role of viral cultures in the workup of Chikungunya virus infection?

What is the role of molecular testing in the workup of Chikungunya virus infection?

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How is Chikungunya virus infection treated?

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