Togaviridae: Alphaviruses

Chikungunya Virus

Chikungunya virus is transmitted from one human to another primarily by infected Aedes aegypti and Aedes albopictus mosquitoes. Enzootic transmission cycles between forest-dwelling mosquitoes and wild mammals are documented in Africa. ^, Before 2013, chikungunya outbreaks were documented in countries in Africa, Asia, Europe, and the Indian and Pacific Oceans. In 2013, the first locally acquired cases in the Americas were identified on islands in the Caribbean. The virus quickly spread throughout the region, with local transmission eventually reported from 45 countries and territories in the Americas. As of July 2020, >3 million suspected and confirmed locally-acquired chikungunya virus cases have been reported in the Americas and sporadic outbreaks continue to be reported in countries throughout the world, including in Africa, Asia, Europe, and Central and South America. ^,

After an incubation period of 3–7 days (range, 2−12 days), chikungunya virus infection causes acute fever and polyarthralgia in most (72%–98%) infected persons. Joint pains are usually bilateral and symmetric, typically affecting the small joints, and they can be severe and debilitating. ^, Other symptoms may include headache, myalgia, arthritis, conjunctivitis, vomiting, and maculopapular rash. During large outbreaks of disease that occurred in and around the Indian Ocean from 2004 to 2007, a number of atypical disease manifestations were noted, including neurologic disease (e.g., meningoencephalitis, Guillain-Barré syndrome), eye and other organ involvement (e.g., uveitis, retinitis, hepatitis, nephritis, or myocarditis), and unusual dermatologic manifestations (e.g., bullous lesions). ^,

The acute symptoms of chikungunya typically resolve in 7–10 days. Mortality is rare and mostly occurs in older adults and those with underlying comorbidities. ^, Some patients have a relapse of rheumatologic symptoms, such as polyarthralgia, polyarthritis, tenosynovitis, or Raynaud’s syndrome, in the months following acute illness. Studies have reported variable proportions (5%−60%) of patients with persistent joint pains lasting from months to years after their illness. ^{, , ,}

Modes of transmission other than mosquitoes have been reported. Intrapartum transmission occurs in almost 50% of neonates when the mother was viremic around the time of delivery. ^, Infected neonates most commonly have had fever, pain, rash, and edema, but intracerebral and gastrointestinal hemorrhage, myocarditis, dermatosis bullosa, meningoencephalitis, and severe encephalopathy with seizures also have been reported. ^{, ,} Second trimester in utero transmission has been reported to be associated with three miscarriages, in which chikungunya viral RNA was detected in fetal tissue. ^{, ,} Chikungunya viral RNA has been detected in the breast milk from at least one symptomatic woman, but her 3-month-old infant showed no evidence of being infected (no viral RNA or antibodies in serum) despite breastfeeding during the mother’s illness. In addition, two small studies did not identify chikungunya virus or viral RNA in breast milk from viremic women, making transmission through breast milk unlikely. ^, In the laboratory, the virus has been transmitted through percutaneous needlestick and airborne routes of exposure from infected blood or virus culture. ^, Given that humans develop a high level of viremia, it is expected but not yet documented that transmission can occur through blood transfusions and organ or tissue transplantation.

O’nyong-Nyong Virus

O’nyong-nyong virus and its variant virus, Igbo-Ora virus, are unusual among arboviruses in that they are transmitted between humans in Africa by infected anopheline mosquitoes, primarily Anopheles funestus and Anopheles gambiae, which also are vectors of malaria. After an incubation period of about 8 days, the virus causes epidemic febrile polyarthralgia often accompanied by headache, pruritic rash, cervical lymphadenopathy, and conjunctivitis. There is no specific treatment; virtually all patients recover completely, but many are incapacitated for up to 2 weeks during the illness. Mild or asymptomatic cases also may occur as indicated by the presence of o’nyong-nyong virus−specific antibodies in areas without epidemic disease transmission.

Ross River Virus

Ross River virus is transmitted to humans in Australia and the Western Pacific by a broad range of mosquito vectors but primarily Aedes vigilax, Aedes camptorhynchus, Aedes polynesiensis, and Culex annulirostris. The virus is transmitted enzootically between mosquitoes and kangaroos and other marsupials, horses, and other vertebrates; human-to-mosquito-to-human transmission also occurs. ^, One case of transfusion-associated transmission has been documented. After an average incubation period of 7–9 days (range, 3−21 days), Ross River virus causes sudden onset of arthralgia, arthritis, rash, myalgias, fatigue, and fever to a variable degree. ^{, ,} Glomerulonephritis and suspected encephalitis have been reported rarely. ^, Disease affects primarily those between 20 and 60 years of age, whereas symptomatic illness is rare in children. ^{, ,} Infection generally is not life-threatening, and symptoms usually resolve within 6 months.

Venezuelan Equine Encephalitis Virus

Venezuelan equine encephalitis virus is transmitted in tropical areas of the western hemisphere by a variety of mosquitoes, including Psorophora confinnis, Psorophora columbiae, Aedes sollicitans, Aedes taeniorhynchus, and Culex (Melanoconion) species. ^, Enzootic Venezuelan equine encephalitis virus strains are transmitted in sylvatic cycles between mosquitoes, primarily Culex (Melanoconion) species, and rodents; equines are the primary amplifying hosts for epizootic strains. ^, Direct human-to-human transmission appears to be rare, but the virus has been isolated from the oropharynx of ill humans, aerosol transmission has occurred in laboratories, and the virus has been considered a possible bioterrorism threat. ^, After a typical incubation period of 2–5 days, Venezuelan equine encephalitis virus causes the abrupt onset of fever, headache, malaise, myalgia, and nausea. A high proportion of fatal cases in one epidemic had pneumonia. During an outbreak in Colombia, <5% of all symptomatic infections were estimated to result in neurologic disease. Two more recent studies of hospitalized patients infected with enzootic strains in Panama found that neurologic disease was seen most frequently in children. ^, Overall, the case-fatality rate for symptomatic disease is <1% but can be as high as 5% among patients who are hospitalized. ^{, ,}