Chikungunya Fever Diagnosed Among International Travelers --- United States, 2005--2006

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Chikungunya virus (CHIKV) is an alphavirus indigenous to tropical Africa and Asia, where it is transmitted to humans by the bite of infected mosquitoes, usually of the genus Aedes (1). Chikungunya (CHIK) fever, the disease caused by CHIKV, was first recognized in epidemic form in East Africa during 1952--1953. The word "chikungunya" is thought to derive from description in local dialect of the contorted posture of patients afflicted with the severe joint pain associated with this disease. Because CHIK fever epidemics are sustained by human-mosquito-human transmission, the epidemic cycle is similar to those of dengue and urban yellow fever. Large outbreaks of CHIK fever have been reported recently on several islands in the Indian Ocean and in India (2--6). In 2006, CHIK fever cases also have been reported in travelers returning from known outbreak areas to Europe, Canada, the Caribbean (Martinique), and South America (French Guyana) (2,3,5--7). During 2005--2006, 12 cases of CHIK fever were diagnosed serologically and virologically at CDC in travelers who arrived in the United States from areas known to be epidemic or endemic for CHIK fever. This report describes four of these cases and provides guidance to health-care providers. Clinicians should be alert for additional cases among travelers, and public health officials should be alert to evidence of local transmission of chikungunya virus (CHIKV), introduced through infection of local mosquitoes by a person with viremia.

Case Reports

Minnesota. On May 12, 2005, an adult male resident of Minnesota returned from a 3-month trip to Somalia and Kenya. He had onset of illness hours after arrival in the United States, including fever, headache, malaise, and joint pain mainly in a shoulder and a knee. Serum obtained on May 13 was tested at CDC and determined to be equivocal for CHIKV RNA by reverse-transcription polymerase chain reaction (PCR), consistent with low-level viremia. A recent CHIKV infection was confirmed by demonstration of IgM antibody in this acute-phase serum specimen and neutralizing antibody in convalescent-phase serum (collected 214 days after illness onset). Arthralgias resolved after several weeks.

Louisiana. On January 15, 2006, an adult female resident of India had onset of an illness characterized by fever, joint pain (in the knees, wrists, hands, and feet), and muscle pain (in the thighs and neck). In March 2006, she traveled to Louisiana, where she sought medical attention for persistent joint pain. At CDC, tests of a single serum sample collected on March 30 (74 days after illness onset) were positive for IgM and neutralizing antibodies to CHIKV. The patient was subsequently lost to follow-up.

Maryland. An adult female resident of Maryland visited the island of Réunion in the Indian Ocean from October 2005 through mid-March 2006. On February 18, 2006, during an ongoing CHIK fever outbreak on the island, she had onset of fever, joint pain (in the hands and feet), and rash. A local physician clinically diagnosed CHIK fever, but no laboratory tests were conducted. After returning to the United States, the patient sought medical attention for persistent joint pain. At CDC, tests of a single serum sample collected on March 22 (32 days after illness onset) were equivocal for IgM and positive for neutralizing antibody to CHIKV, consistent with a recent CHIKV infection in which IgM antibody was waning. At 5 months after onset, the patient had persistent joint pain (in the hands and feet).

Colorado. An adult male resident of Colorado visited Zimbabwe during April 17--May 29, 2006. On April 29, he had onset of illness with fever, chills, joint pain (in the wrists and ankles), and neck stiffness; a rash appeared a few days later. All symptoms resolved within 2 weeks, except for joint pain, which persisted for approximately 1 month. At CDC, tests of a single serum sample collected on June 12 (44 days after illness onset) were positive for IgM and neutralizing antibody to CHIKV.

Reported by: E Warner, Denver, Colorado. J Garcia-Diaz, MD, Ochsner Clinic Foundation, New Orleans; G Balsamo, DVM, Louisiana Dept of Health and Hospitals. S Shranatan, DO, Johns Hopkins Community Physicians at Hager Park, Hagerstown; A Bergmann, MS, Maryland Dept of Health and Mental Hygiene. L Blauwet, MD, M Sohail, MD, L Baddour, MD, Mayo Clinic College of Medicine, Rochester, Minnesota. C Reed, MD, H Baggett, MD, Div of Global Migration and Quarantine, National Center for Preparedness, Detection, and Control of Infectious Diseases (proposed); G Campbell, MD, T Smith, MD, A Powers, PhD, N Hayes, MD, A Noga, J Lehman, Div of Vector-Borne Infectious Diseases, National Center for Zoonotic, Vector-Borne, and Enteric Diseases (proposed), CDC.

Editorial Note:

Most CHIKV infections are symptomatic (8). In clinical infections, the incubation period typically is 2--4 days. Illness is characterized by sudden onset of fever, headache, malaise, arthralgias or arthritis, myalgias, and low back pain. Skin rash occurs in approximately half of cases (9). Joint symptoms can be severe and involve small and large joints. Although CHIK fever typically lasts 3--7 days and full recovery is the usual outcome, certain patients experience persistent joint symptoms for weeks or months and occasionally years after illness onset (1). Serious complications (e.g., neuroinvasive disease) are rare, and fatal cases have not been documented conclusively. Transplacental CHIKV transmission and severe congenital CHIKV disease have been described (10). CHIKV infection is believed to confer life-long immunity (1). Because no specific drug therapy is available, treatment of CHIK fever is supportive. No licensed CHIKV vaccine exists. Therefore, prevention recommendations for travelers to tropical Asia and Africa should emphasize mosquito repellent and avoidance measures. Additional information is available at http://www.cdc.gov/ncidod/dvbid/chikungunya/chickvfact.htm.

During May 2004--May 2006, approximately 300,000 suspected CHIK fever cases were reported on islands in the Indian Ocean, including approximately 264,000 suspected cases on Réunion, a French overseas department (2,3). Other affected areas included Mombasa, Kenya, and the islands of Comoros, Lamu, Madagascar, Mauritius, Mayotte, and the Seychelles. In addition, since early 2006, an estimated 180,000 suspected CHIK fever cases have occurred in the Indian states of Andhra Pradesh, Karnataka, and Maharashtra (4). In recent years, extensive CHIKV activity also has been documented in Southeast Asia (9). In 2006, as of May 11, approximately 340 imported CHIK fever cases were reported in Europe, mainly in France, reflecting the high frequency of travel between Europe and islands in the Indian Ocean (2). To date, no known local mosquito-borne CHIKV transmission has occurred in Europe or other nonindigenous areas.

Aedes aegypti is the primary CHIKV vector in Asia, but Ae. albopictus (the Asian tiger mosquito) likely was the primary vector in Réunion (2,3). In Asia, CHIKV epidemics involve a human-mosquito cycle, with humans serving as the sole vertebrate amplifying hosts (1). In Africa, sylvatic cycles involving nonhuman primates and forest-dwelling Aedes species (e.g., Ae. furcifer) also occur. Most CHIKV epidemics occur during the tropical rainy season and abate during the dry season (1,9). Human CHIKV infections include a transient, high-titered viremia (typically detectable during the first 2 days of illness, ranging up to 6 days after illness onset) that is adequate to infect feeding mosquitoes (1). Ae. aegypti and Ae. albopictus are abundant peridomestic species and aggressive daytime blood-feeders in all tropical and most subtropical areas of the world, and Ae. albopictus now lives in many temperate areas of the eastern and western hemispheres, including Europe and the United States. Therefore, some risk exists that CHIKV might be introduced into previously nonendemic areas by travelers with viremia, leading to local transmission of the virus, especially in tropical or subtropical areas of the United States (e.g., the Gulf Coast and Hawaii) or its territories (e.g., Guam, Puerto Rico, and the U.S. Virgin Islands). Early recognition of local transmission followed by prompt, aggressive vector control and other public health measures might prevent long-term establishment of the virus in new areas. Of the four patients described in this report, three posed no substantial public health risk because they probably no longer had viremia upon arrival in the United States; although the fourth patient was likely viremic upon arrival in Minnesota in mid-May, transmission to competent local mosquito vectors in that climate was unlikely.

In early illness, the clinical features of CHIK fever can be similar to those of dengue and malaria, especially in patients without joint symptoms. In both dengue and CHIK fever, rash usually is generalized and maculopapular, but petechial rashes occur in certain dengue cases. During 1991--2004, nine confirmed or probable cases of CHIK fever were diagnosed serologically at CDC among travelers to the United States (CDC, unpublished data, 2006). Additional imported but unrecognized cases likely occurred. Clinicians should be aware of possible CHIKV infection in travelers returning from CHIK-fever--endemic or outbreak areas, particularly if an acute febrile illness with arthralgias or arthritis occurs. Suspected cases should be reported promptly to local and state public health officials and to CDC. Mosquito exposure should be strictly avoided (e.g., by staying within a screened environment and using barrier clothing and repellents) during the first week of illness to prevent infection of local mosquitoes.

In the United States, diagnostic tests for CHIKV infection are not available commercially but are available at CDC by special arrangement through state health departments. Laboratory diagnosis depends on antibody-capture IgM ELISA and plaque-reduction neutralization tests of serum. Comparative serologic tests for closely related alphaviruses (e.g., o'nyong-nyong and Sindbis viruses) should be conducted as geographically appropriate, and tests for dengue usually are indicated. Virus isolation attempts and PCR assays are performed selectively. Serologic tests should be performed on both acute- and convalescent-phase serum specimens collected at least 2 weeks apart, but clinicians should not delay submission of acute-phase samples pending collection of convalescent-phase samples. To arrange submission of specimens to CDC for diagnostic testing, clinicians should consult their state public health laboratory and CDC's Arboviral Diseases Branch (telephone, 970-221-6400). Specimen shipping and handling instructions are available at http://www.cdc.gov/ncidod/dvbid/misc/specimen-submission.htm.

References

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