Chikungunya
Section snippets
Overview
Chikungunya virus is a zoonotic, vector-borne pathogen that has been responsible for numerous outbreaks of febrile arthralgia since its discovery in the early 1950s. In the past decade, the virus has re-emerged more frequently, causing massive epidemics that have moved from Africa throughout the Indian Ocean to India and Southeast Asia. A discussion of the virus, its epidemiology, diagnostic criteria, and immunity are presented in this article.
Microbiology
Chikungunya virus (CHIKV) is one of 29 recognized species within the genus Alphavirus in the family Togaviridae (Table 1).1 Like all alphaviruses, the virus contains a positive-sense, single-stranded, nonsegmented RNA genome of approximately 11.8 kilobase in length. The genome encodes 4 nonstructural proteins that are responsible for the cytoplasmic replication of the viral genome and 5 structural proteins that are encoded in the 3' one-third of the genome and translated from a subgenomic
Epidemiology
The first documented outbreak of Chikungunya fever occurred in 1952 to 53 on the Makonde plateau of Tanganyika. During this period, a high proportion of residents of all ages were affected by a distinctive disease with “very sharp onset of crippling joint pains, severe fever, and eventually, the conspicuous rash.” The elders of the Makonde tribes could not recall any previous, similar epidemics, suggesting that this was indeed a new illness.3, 4, 5 After that, only minor outbreaks occurred
Clinical presentation
The classical presentation of chikungunya fever includes the rapid onset of high fever (>102°F), severe and incapacitating joint pain, and rash.23 These 3 symptoms have been documented from the earliest outbreaks and remain the most prevalent disease pattern to this day. Furthermore, the vast majority of infected individuals show clinical illness, with as few as 3% of cases remaining asymptomatic.24, 25 Symptoms can appear within 2 days postinfection with the acute phase typically lasting from
Pathogenesis
Because CHIKV has historically been understudied, little is known regarding the specific mechanisms of viral pathogenesis. However, a closely related alphavirus manifesting with similar clinical presentation, Ross River virus (RRV), has been more fully evaluated for disease development. During RRV infection, the T-cell–mediated immune response is postulated to play a role in persistence of symptoms. Patients who quickly recover from RRV have a predominance of CD8+ T cells in contrast to
Diagnosis
Depending on the availability, timing of collection, and sample volume, CHIKV infection can be diagnosed and confirmed by direct virus detection, viral RNA detection, or presence of CHIKV-specific antibodies. An acute serum sample collected within 7 days of illness onset is likely to have high levels of viremia (up to 106·8 pfu/mL)12, 42 making the best options for diagnosis either nucleic acid detection or virus isolation. Both approaches are extremely sensitive and specific and can be
Differential diagnosis
Laboratory confirmation of CHIKV infection using CHIKV-specific tests is critical for accurate diagnosis, because the clinical presentation can be similar to numerous other sympatric pathogens. Malaria and dengue viruses cause a clinical syndrome mimicking that of CHIKV infection. In fact, the 2004 epidemic in Lamu, Kenya was originally thought to be malarial, and in 2005 in Comoros, the outbreak was first reported as a denguelike epidemic.14, 17 Other arboviruses that must also be considered
Treatment, prognosis, and long-term outcomes
Because there is no specific treatment available, supportive treatment of symptoms, including rest, fluids, antipyretics and analgesics, is the only option. Several antiviral drugs have been tested for their efficacy against chikungunya fever. These include ribavirin, sulfated polysaccharides, interferon, corticosteroids, and chloroquine.58, 59, 60 Although there has been some evidence that these options may provide some relief, side effects exist and the long-term benefits and
Immunity and reinfection
Infection with CHIKV, like all arboviruses, is presumed to result in lifelong immunity. CHIKV-specific neutralizing antibodies have been detected as early as 2 weeks postinfection, and IgG antibodies have been documented to persist for years suggesting that immunologic memory would provide protection on rechallenge.
Although no commercial vaccine is available for CHIKV, a live-attenuated strain has been developed and extensively characterized for its vaccine potential. This strain, designated
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