International Notes Dengue Epidemic -- Ecuador, 1988

A large dengue 1 (DEN-1) epidemic occurred in Guayaquil, Ecuador, from late February through April 1988. The Virology Laboratory, Ecuadorian National Institute of Hygiene, detected antidengue hemagglutination-inhibition antibody in serum specimens from persons with viral syndromes who had visited local health centers in Guayaquil during February and March. Dengue infection was subsequently confirmed by CDC through serologic testing and isolation of DEN-1 virus from nine specimens.

From May 14 to May 19, 1988, a population-based cluster serosurvey was conducted in eight of Guayaquil's 14 parishes, representing 72% of the city's population. Serum collected from 1340 persons in 280 households was tested for antidengue IgM antibody using an IgM-capture, enzyme-linked immunosorbent assay (MAC-ELISA). Before DEN-1 was recognized as the infecting serotype of the epidemic, approximately half the specimens were screened using a mixed (DEN 1-4) antigen. Specimens from this group with equivocal results and all subsequent samples were then tested using DEN-1 antigen. Based on the resulting area-specific seropositivity rates, an estimated 420,000 individuals were infected with dengue during the epidemic.

Responses to a standard clinical questionnaire from a subsample of 106 IgM-seropositive persons reflected a pattern of illness consistent with classic dengue fever. Fever was reported by 105 (99%) of this group. More than 50% of the subsample reported one or more of the following symptoms: headache, chills, pruritus, rash, myalgias, and arthralgias; 12 (11%) persons reported hemorrhagic manifestations. Review of data at the National Institute of Hygiene and discharge records from a major tertiary hospital for severe dengue illness detected only one case of severe hemorrhagic disease and no deaths.

In an entomologic survey done concurrently with the serosurvey, the highest Aedes aegypti indices (container, 8.1% and 8.7%; house, 13.5% and 18.7%; and Breteau, 23.1 and 26.3) were in two of the parishes with the highest dengue attack rates. In another parish with high seropositivity, however, low mosquito indices were detected, probably as a consequence of intensive larval mosquito-control efforts implemented after infections had occurred but before the entomologic survey.

Weekly surveillance data from public clinics indicated that the number of patients with acute febrile illness increased during March and peaked during the week ending April 2. Most onsets of illness reported by IgM-positive persons in Febres Cordero and Letamendi parishes occurred in mid-April (Figure 1). At the time of the entomologic and serologic surveys, few persons reported current dengue-like illness. Thus, the epidemic appeared to have subsided by mid-May. An intradomiciliary fumigation campaign for Ae. aegypti control, involving approximately 350,000 houses, was conducted from May 27 to July 29, after the epidemic had subsided. Reported by: National Institute of Hygiene, National Malaria Eradication Service and Region II Epidemiology Office, Ministry of Health; Guayas Provincial Health Department, Guayaquil, Ecuador. Dengue Br, Div of Vector-Borne Viral Diseases, Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: In 1948, an Ae. aegypti eradication program for yellow fever control was initiated in Ecuador in collaboration with the Pan-American Health Organization (PAHO); by 1958, the country was declared free of this mosquito. As in many other countries in the Americas, however, surveillance declined, and reinfestation occurred. Ae. aegypti was detected in a province north of Guayaquil in 1977 and 1981 and in central Guayaquil in 1985. No dengue transmission was reported in Guayaquil from 1958 until 1988, although unreported transmission may have occurred before 1958 (1).

In response to the 1988 epidemic, mosquito-control efforts by the Ecuadoran National Malaria Eradication Service included 1) vehicle-applied, ultralow-volume (ULV) insecticide (malathion) spraying, 2) source reduction by elimination of larval habitats, and 3) treatment of water-holding containers with temephos insecticide. These measures may have contributed to decreasing transmission, although their effect cannot be evaluated retrospectively. Given the high seropositivity rates in areas heavily infested with Ae. aegypti, the epidemic probably ended because much of the population had become immune.

This epidemic and others in Brazil (2), Bolivia, and Paraguay (PAHO, unpublished data) illustrate the increasing problem of dengue fever in tropical America. The epidemics also demonstrate the vulnerability of many large urban centers in Central and South America to explosive dengue epidemics. Increased travel between countries in the Americas and other regions of the world heightens the risk for repeated introduction of different virus strains and serotypes. These factors, in turn, increase the risk for dengue epidemics, and possibly for epidemics of dengue hemorrhagic fever and urban yellow fever.

In the absence of Ae. aegypti eradication, large dengue and yellow fever epidemics can be prevented only through programs that combine surveillance with integrated vector-control programs. While ground-applied ULV insecticide has been recommended to control epidemic dengue (3), recent studies in Trinidad (4), Suriname (5), and Puerto Rico (CDC, unpublished data) suggest that these measures are ineffective in reducing adult Ae. aegypti densities. Ultimately, control of this mosquito must be community-based and directed toward larval source reduction (6).

References

1. Carbo-Noboa JM. Etiologia del dengue. Ann Soc Medico-Cirug del Guayas, Guayaquil, Ecuador 1924;4:326.

2. Schatzmayr HG, Nogueira RM, Travassos da Rosa AP. An outbreak of dengue virus at Rio de Janeiro-1986. Mem Inst Oswaldo Cruz 1986;81:245-6.

3. CDC. Biology and control of Aedes aegypti. Vector topics No. 4, September 1979.

4. Chadee DD. An evaluation of malathion ultralow volume spraying against caged and natural populations of Aedes aegypti in Trinidad, West Indies. Cah Orstom ser Ent med et Parasitol 1985;23:71-4.

5. Hudson JE. The 1982 emergency ultralow volume spray campaign against Aedes aegypti adults in Paramaribo, Suriname. PAHO Bull 1986;20:294-303.

6. Gubler DJ. Aedes aegypti and Aedes aegypti-borne disease control in the 1990s: top down or bottom up. Am J Trop Med Hyg 1989;40 (in press).

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.

Page converted: 08/05/98

HOME  |  ABOUT MMWR  |  MMWR SEARCH  |  DOWNLOADS  |  RSS |  CONTACT POLICY  |  DISCLAIMER  |  ACCESSIBILITY

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