Skip Navigation LinksSkip Navigation Links
Centers for Disease Control and Prevention
Safer Healthier People
Blue White
Blue White
bottom curve
CDC Home Search Health Topics A-Z spacer spacer
Blue curve MMWR spacer

Dengue Type 2 Virus in East Africa

In the past year, the Virus Research Centre, Nairobi, Kenya, has received convalescent-phase serum samples from travelers or workers who became ill with dengue-like disease while working or visiting several areas in Somalia. More recently, acute- or convalescent-phase serum samples have been received from patients who lived near or visited the Kenya coast. Some of the sera reacted against the antigen of dengue type 2 by indirect fluorescence, but because of the serological overlapping within the flavivirus family, diagnosis could not be certain. Since the end of March 1982, 15 acute-phase serum samples have been obtained from people who developed febrile illnesses during or after visiting Somalia (2 samples) or coastal Kenya (13 samples). Serum was inoculated into 1-day-old mice, LLC MK((2)), and vero cell cultures. Mice developed signs of illness, and both cell lines developed slight cytopathic changes; after passaging, three virus strains were recovered: one from a tourist who visited Malindi, Kenya, in March and became ill upon returning to Nairobi, one from a Malindi resident who was hospitalized in late May, and one from a European who became ill while working in Mogadisho, Somalia, and returned to Nairobi on May 24.

Indirect immunofluorescence on acetone fixed infected LLC MK((2)) cells using NIH arbovirus grouping fluids were positive for NIH Group B (flaviviruses) and dengue 1, 2, 3, and 4 immune mouse ascitic fluids. Using dengue type-specific hybridoma-derived monoclonal antibodies, fluorescence was seen only with monoclonal antibody against dengue type 2. After the initial isolate was identified, subsequent isolates were made by testing with the dengue monoclonal antibodies directly after acetone fixation.

Outbreaks of dengue-like disease have occurred several times in East Africa, but when viral agents have been isolated, they have been unrelated to the four dengue serotypes. Chikungunya virus was implicated in an outbreak of febrile illness in Tanganyika in the 1950s, and a closely related alphavirus, o'nyong-nyong virus, was responsible for a large epidemic that swept through eastern Africa between 1959 and 1963. Dengue virus antibodies have been detected in human serum in East Africa, but cross-reactivity within the flaviviruses makes implicating specific virus serotypes difficult. The recent rate of dengue virus isolation, considering the small number of acute samples (three positive of 15 tested), suggests considerable virus activity in East Africa. No striking increase in the number of febrile cases seen at coastal hospitals has been noted, but the number of cases diagnosed as "clinical malaria" appears to be higher this year than previously, possibly due to increased mosquito populations caused by exceptionally heavy rainfall in 1982. A proportion of these fever cases are likely to be dengue infections. Reported by BK Johnson, PhD, D Ocheng, A Gichogo, PM Tukei, MB, Virus Research Centre, S Musoke, MB, PH Rees, MRCP, The Nairobi Hospital, L Cartwright-Taylor, PhD, Medical School, University of Nairobi, A Githere, MB, Malindi District Hospital, Malindi, T arap Siongok, MD, Div of Disease Control and Epidemiology, Ministry of Health, Nairobi, Kenya; Vector-Borne Diseases Div, Virology Div, Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: The first published clinical account of dengue in Africa is that of Christie (1), who observed an outbreak in 1870 in Zanzibar. Subsequent reports of dengue-like illness in East Africa, without laboratory confirmation, have been reported; confusion exists because of the presence of chikungunya and other viruses producing similar clinical illness. In fact, Carey (2) suggested that the original report in 1870 more closely described chikungunya virus than dengue fever. Dengue virus (types 1 and 2) has been isolated only in West Africa (Nigeria, Ivory Coast, Upper Volta, Senegal). However, documented dengue type 2 epidemics occurred in the Seychelles islands in 1976-1977 and 1978-1979 (3,4). The Seychelles outbreaks and the appearance of dengue type 2 in Somalia and Kenya in 1982 may be the result of the frequent trade among India (where dengue is endemic (5)), the islands of the Indian Ocean, and East Africa. Another possibility, however, is extension of dengue from an enzootic transmission cycle involving forest Aedes and nonhuman primates; "jungle dengue" (analagous to jungle yellow fever) is known to occur in Malaysia and Senegal.

Aedes aegypti, including domestic and peridomestic forms which feed readily on humans in and around houses, is abundant in coastal Somalia and Kenya, and is the most likely vector of dengue in this region. Water storage is common, providing breeding sites for A. aegypti. Other Aedes (Stegomyia) species (such as simpsoni and metallicus) are also prevalent and must be considered potential vectors. A better definition of the transmission cycle in this region is needed.

In addition to the cases of dengue reported above, CDC has made serologic diagnoses in several Americans who visited Mogadisho, Somalia, in early 1982. Travelers to Somalia and coastal Kenya should be aware of the possibility of acquiring dengue and should take precautions to avoid mosquito bites.


  1. Christie J. On epidemics of dengue fever; their diffusion and etiology. Glasgow Medical Journal 1881;16:161-76.

  2. Carey DE. Chikungunya and dengue: a case of mistaken identity? J Hist Med 1971;26:243-62.

  3. Metselaar D, Grainger CR, Oei KG, et al. An outbreak of type 2 dengue fever in the Seychelles, probably transmitted by Aedes albopictus (Skuse). Bull WHO 1980;58:937-43.

  4. Calisher CH, Nuti M, Lazuick JS, Ferrari JD, Kappus KD. Dengue in the Seychelles. Bull WHO 1981;59:619-22.

  5. Myers RM, Varkey MJ, Reuben R, Jesudass ES, Benjamin B. The 1968 outbreak of dengue in Vellore, Southern India. Am J Public Health 1971;61:1379-91.

Disclaimer   All MMWR HTML documents published before January 1993 are electronic conversions from ASCII text into HTML. This conversion may have resulted in character translation or format errors in the HTML version. Users should not rely on this HTML document, but are referred to the original MMWR paper copy for the official text, figures, and tables. An original paper copy of this issue can be obtained from the Superintendent of Documents, U.S. Government Printing Office (GPO), Washington, DC 20402-9371; telephone: (202) 512-1800. Contact GPO for current prices.

**Questions or messages regarding errors in formatting should be addressed to

Page converted: 08/05/98


Safer, Healthier People

Morbidity and Mortality Weekly Report
Centers for Disease Control and Prevention
1600 Clifton Rd, MailStop E-90, Atlanta, GA 30333, U.S.A


Department of Health
and Human Services

This page last reviewed 5/2/01