The first known autochthonous transmission of chikungunya virus (CHIKV) fever in the Western Hemisphere occurred in October 2013 in the French sector of the island of Saint Martin, approximately 150 miles east from Puerto Rico [1]. Chikungunya virus is a mosquito-borne arbovirus widely distributed in Africa, Southeast Asia, and India, but until the last decade it was responsible mainly for sporadic, limited outbreaks of illness [2–5]. Its recent epidemic spread through the Caribbean now poses a threat to the continental countries of South, Central, and North America [6–10]. Chikungunya virus is a member of the Togaviridae family, belonging to the genus Alphavirus, and has 3 genogroup lineages that have evolved in different geographic regions [2–6]. The virus was first isolated from a febrile patient during an outbreak in 1952–1953 on the Makonde Plateau in the southern province of Tanzania (formerly Tanganyika) and the north of Mozambique [11]. The name chikungunya is derived from the Kimakonde language, meaning “to become contorted” or “that which bends up” [2–4]. Chikungunya virus has the same urban epidemic transmission ecology as does dengue virus and yellow fever virus, with Aedes aegypti and Aedes albopictus mosquitoes serving as vectors for all three viruses. Similar to dengue and yellow fever, epidemic CHIKV fever is an anthroponosis that does not require a nonhuman vertebrate amplifier host (ie, epidemics are maintained by person-to-person spread from mosquito bites without the need for mosquitoes feeding on birds, rodents, horses, etc) [2–4]. The Ae aegypti and Ae albopictus mosquitoes are common in the Western Hemisphere, and they are considered to be aggressive day-time biters of humans. Because CHIKV is new to the Americas, most people in the region are not immune. This means that the estimated 3.6 billion persons in 124 countries at risk for dengue are also at risk for CHIKV fever [8]. The evolutionarily older Asian CHIKV lineage seems to be present in the Caribbean; it is better adapted to the Ae aegypti mosquito rather than the mutated East, Central, and South African-Indian Ocean lineage highly adapted to the Ae albopictus mosquito, which was responsible for the recent explosive outbreaks in the Indian Ocean and Europe. During the first 4 months of 2014, more than 31 000 confirmed and probable autochthonous cases were reported from numerous Caribbean islands [8]. Infected travelers originating from the island countries now have carried the virus around the region. By the end of 2014, 5 countries in South America, 7 in Central America, and 3 in North America had experienced 1 million suspected and 20 000 confirmed cases of autochthonous transmission of CHIKV (including 11 in the United States, all in Florida) (Table 1). Confirmed autochthonous transmission of CHIKV has been reported in all countries in the Western Hemisphere except Canada, Cuba, Bolivia, Peru, Chile, and Argentina. Total Number of Reported Cases of Chikungunya Fever in the Americas [12] Total Number of Reported Cases of Chikungunya Fever in the Americas [12] Chikungunya virus fever is characterized by fever and joint pain, the latter usually symmetric in the hands and feet [3, 4, 9, 10]. Headache and backache, myalgia, and rash may be noted, along with frank arthritis. Although most symptoms resolve in a few days to weeks, some patients (estimated 20% to 40%) have joint pain that can persist for months to years, and the pain can be so severe that patients adopt a bent or stooping posture. The incubation period is 3 to 7 days after the mosquito bite, and the acute illness lasts 3 to 10 days. Most infections (estimated 75% to 95%) are symptomatic, with fever and arthralgia. Approximately half of patients develop a rash 2 to 5 days after the fever occurs. Other less typical symptoms include photophobia, conjunctivitis, several forms of dermatitis, aphthous ulcers, and meningoencephalitis. During outbreaks, the large percentage of symptomatic infections places a considerable strain on resources of local healthcare providers and hospitals. Fortunately, death from CHIKV fever is rare. The mortality rate is 4%. Serious CHIKV fever and death may be more common among newborns and older people. Vertical transmission to the newborn is uncommon but possible if the mother is viremic just before delivery. The diagnosis of CHIKV fever is made by a combination of clinical, epidemiological, and laboratory criteria (Figure 1) [3, 4, 10]. However, it is not necessary to have a laboratory diagnostic result for CHIKV fever to initiate clinical management for suspected cases. Currently, no specific treatment is available, but symptomatic relief may be given with acetaminophen (paracetamol), along with fluid resuscitation. Neither aspirin nor nonsteroidal anti-inflammatory drugs such as naproxen are generally recommended until the possibility of dengue fever is excluded, because of the risk of bleeding. Persons infected with CHIKV fever should be protected from mosquito exposure during the first week of illness to prevent further spread of the virus to others, because patients are initially highly viremic. Diagnostic criteria for chikungunya virus (CHIKV) fever (modified from Reference 3). BSL3, biosafety level 3; CRP, C-reactive protein; ESR, erythrocyte sedimentation rate; Ig, immunoglobulin; RT-PCR, reverse transcription-polymerase chain reaction. There are currently no CHIKV vaccines, although several approaches are under investigation, including live, attenuated vaccine constructs and viral-like particles. The only public health interventions available are reduction of mosquito-to-human contact through personal protection measures and vector control efforts to reduce mosquito abundance. The differential diagnosis of CHIKV fever includes dengue fever, leptospirosis, malaria, enterovirus infection, and, depending upon travel exposures, possibly infection by other arboviruses. Dengue fever tends to present with more neutropenia and thrombocytopenia, and less arthralgia, than CHIKV fever, but it may be difficult to differentiate on purely clinical grounds. Uncommonly, a patient may be simultaneously coinfected by both CHIKV and dengue. The clinician must remain alert for signs of impending severe dengue fever in all patients presenting with suspected CHIKV fever; these include severe abdominal pain, mucosal bleeding, or increased hematocrit with decreasing platelet count [4]. All health agencies and healthcare providers in areas of the Americas where dengue is endemic, as well as in parts of temperate North and South America where Ae aegypti and Ae albopictus are present, should be aware of the potential for CHIKV introduction and establishment in their region. Existing diagnostic and surveillance networks must be enhanced, and effective vector control activities must be intensified to address the spread of this Old World pathogen into the New World. In preparation for the possible spread of CHIKV fever in the region (as imported cases in travelers had occurred), the Pan American Health Organization, World Health Organization, and the Centers for Disease Control and Prevention published a useful collaborative guideline in 2011, to help countries throughout the Americas to improve their ability to detect CHIKV and be prepared to monitor and control the disease, should it appear [13]. These guidelines remain one of the best comprehensive sources of information on CHIKV; several concise fact sheets are also available [14, 15, 16]. Potential conflicts of interest. All authors: No reported conflicts. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest.
No takes yet. Share an insight, caveat, or question.
Gutierrez-Saravia et al. (2015) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: