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It’s not Ebola, but it’s also out of control
With all the headline news and hype about the Ebola outbreak, other outbreaks have been pushed to the last page, if they even make the news. One of these outbreaks is chikungunya virus infection in the Western Hemisphere. Since late November 2013 when the first autochthonous cases of chikungunya virus infection were reported on the island of Saint Martin in the Caribbean, spread has been dramatic and far. After involving virtually every Caribbean island and first gaining a foothold on the mainland in French Guiana, it has spread to multiple countries in Central and South America. Locally acquired cases have been reported from Costa Rica, El Salvador, Guatemala, Honduras and Panama in Central America; and Brazil, Colombia, Venezuela, Suriname and Guyana in South America. There also have been 11 locally acquired cases reported from Florida as of early October. There have been 503 cases imported to the United States, and it has been reported from 47 states as of Oct. 6. This number increases each week. The total number of cases in the Western Hemisphere is probably close to 1 million as of mid-October.
The vector for chikungunya virus is the Aedes mosquito, both A. aegypti and A. albopictus. A. aegypti is found throughout the Caribbean, including Puerto Rico, in Central and South America and in some warmer parts of the mainland US. While A. aegypti mosquitoes are present year-round in the southeastern part of the US, they generally are only active in the warmer months. A. albopictus is present in parts of Central and South America and in many states in the eastern and central US. With the onset of colder weather, the mosquito vectors will decrease in most of the US but will be maintained in the more tropical countries. Therefore, chikungunya virus infection will probably eventually become an endemic infection in many countries in Central and South America and islands in the Caribbean where the dengue viruses are also transmitted. This may happen also in some parts of the South in the US.
Thomas Yuill
Donald Kaye
The obvious comparison is to West Nile virus infection, which started in the New York City area and spread and became endemic throughout the US and southern Canada. However, West Nile virus has a very different life cycle. West Nile virus is generally not acquired by mosquitoes that bite humans, as the level of viremia is low, but depends upon transmission and amplification between mosquitoes and birds. Humans are dead-end hosts. The mosquito-bird relationship guarantees maintenance of West Nile virus in nature. The better comparison is to dengue fever. Both chikungunya and dengue viruses have no intermediate host and depend on Aedes mosquitoes acquiring the virus by feeding on viremic humans.
Mosquitoes can survive during winter in protected sites such as sewers, and it is possible that this could occur with mosquitoes carrying chikungunya virus. However, the likelihood is that chikungunya virus infection will behave more like dengue has in the past in the US. That is, despite imported cases, it will remain primarily an imported disease in most of the US with periodic local transmission during the seasons when mosquitoes are present and active.
While chikungunya virus infection is an unpleasant disease with potentially disabling joint pain, mortality is rare and usually occurs in the elderly, who also tend to have more severe disease and comorbidities. The major problem with the infection is distinguishing it from dengue, which can be a life-threatening infection. Both dengue and chikungunya infections are caused by the bite of an Aedes mosquito that has fed on people with viremia. Both infections start with acute onset of fever with headache, myalgias and arthralgias with or without rash. Joint manifestations (ie, joint pain and stiffness) are more common with chikungunya than with dengue. Furthermore, chikungunya virus infection may cause ongoing arthralgias or even arthritis, which can recur for weeks or even months. Dengue, on the other hand, can cause the life-threatening syndrome of dengue hemorrhagic fever and shock syndrome.
Diagnosis of both acute dengue and chikungunya virus infection is made by positive reverse transcription-polymerase chain reaction for the viral genome using serum or plasma or by finding an elevated serological IgM titer. There is no specific therapy for either. Promising vaccines for dengue are currently in clinical trials, and one from Sanofi Pasteur has recently completed phase 3 trials. There is at least one experimental vaccine for chikungunya virus, but even if it is developed, it is questionable how much it would be used in the US based on a cost/benefit basis. At present, vector control measures and mosquito avoidance are the primary approaches to prevention of both diseases.
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Thomas Yuill, PhD, is a ProMED-mail viral diseases moderator and professor emeritus, department of pathobiology and department of forest and wildlife ecology, University of Wisconsin-Madison, Madison, Wis.
Donald Kaye, MD, is a professor of medicine at Drexel University College of Medicine, associate editor of ProMED-mail, section editor of news for Clinical Infectious Diseases and an Infectious Disease News Editorial Board member.
Disclosure: Kaye and Yuill report no relevant financial disclosures.