1 table omitted
In 1986, when the World Health Assembly first adopted a resolution calling for the eradication of dracunculiasis (Guinea worm disease), an estimated 3.5 million persons in 20 countries had the disease, and approximately 120 million persons were at risk for infection.1,2 By December 2001, annual incidence of dracunculiasis had decreased approximately 98%, and seven countries (Cameroon, Chad, India, Kenya, Pakistan, Senegal, and Yemen) in which dracunculiasis had been endemic previously had eliminated the disease.3 This report describes the status of the global Dracunculiasis Eradication Program (DEP)* as of June 2002. The findings indicate that DEP has succeeded in reducing incidence of dracunculiasis substantially; the disease can be eradicated if the remaining 13 countries in which it is endemic detect and contain transmission from the final cases.
For surveillance purposes, village-based health-care workers search for infected persons in each village in which disease is endemic and complete a register that provides a basis for monthly zonal, district, and national surveillance reports.3 During 2001, dracunculiasis was endemic in 13 African countries (Benin, Burkina Faso, Central African Republic, Côte d'Ivoire, Ethiopia, Ghana, Mali, Mauritania, Niger, Nigeria, Sudan, Togo, and Uganda) (2002 population: 353.5 million). These countries reported 63,717 cases from 6,122 villages4; 3,921 (64%) of these villages were in Sudan, which reported 49,471 (78%) cases.
During January-June 2002, a total of 21,164 cases were reported, including 14,986 (71%) from Sudan. In countries other than Sudan, 6,158 indigenous cases were reported during January-June 2002, a decrease of 26% from the 8,349 cases those countries reported during the same period in 2001 and 53% from the 13,142 cases reported during the same period in 2000.5 During January-June 2002, Ghana (3,076 cases) and Nigeria (1,993 cases) accounted for 82% of the cases reported outside of Sudan; 2,005 (33%) cases were reported from five districts in Ghana's northern region. A total of 27 cases were exported from one country to another, including 16 from Sudan, five from Togo, four from Ghana, one from Nigeria, and one from Burkina Faso. Mauritania has reported two indigenous cases of dracunculiasis, Uganda has reported four cases, Benin and Ethiopia appear close to interrupting transmission, and dracunculiasis is now confined to relatively restricted areas in Côte d'Ivoire and Mali. In addition, the World Health Organization (WHO) is verifying the occurrence of endemic transmission of dracunculiasis and the extent of the disease in the Central African Republic. During January-June 2002, the incidence of dracunculiasis in southeastern Nigeria, the country's most highly endemic zone, declined 80% compared with the same period in 2001.
Interventions in all 13 countries, including those parts of Sudan not affected by the civil war, have been intensified since mid-2000. For example, cloth filters were distributed in 13 countries to all households in 63% of villages in which the disease is endemic and in 85% of such villages excluding Sudan.5,6 During January-June 2002, external advisors provided programs with 176 person-months of in-country supervisory assistance compared with 88 person-months during 2000. To prevent further transmission of the infection, some national eradication programs (e.g., in Togo and Ghana) are emphasizing the voluntary physical isolation of patients in health facilities or temporary structures when worms are emerging.
The Carter Center, Atlanta, Georgia. World Health Organization Collaborating Center for Research, Training and Eradication of Dracunculiasis; Div of Parasitic Diseases, National Center for Infectious Diseases, CDC.
Dracunculiasis is a parasitic infection caused by Dracunculus medinensis. Persons become infected by drinking water from ponds contaminated by copepods (water fleas) that contain immature forms of the parasite. A year after entering the infected person, adult worms 1-meter (approximately 40 inches) long emerge through skin lesions, usually on the lower limbs, which frequently develop severe secondary bacterial infections. No effective treatment or vaccine for the disease exists, and infected persons do not become immune to future infections by the parasite. However, dracunculiasis can be prevented by filtering drinking water through a finely woven cloth, by treating contaminated water with the larvicide Abate® (temephos), by educating persons to avoid entering water sources when worms are emerging from their bodies, and by providing clean water from bore-hole wells or from protected hand-dug wells.
During January-June 2002, dracunculiasis continued to decline; the two major remaining endemic foci of the disease are in southern Sudan and northern Ghana. Increased efforts to stop transmission of dracunculiasis in northern Ghana are being carried out by the government and its partners (i.e., The Carter Center, United Nations Children's Fund [UNICEF], WHO, U.S. Peace Corps, Ghana Red Cross Society, and various bilateral donors and nongovernment organizations involved with providing safe sources of drinking water). These efforts are expected to result in reductions similar to those recorded in southeast Nigeria. In southern Sudan, the 19-year-old civil war is the main reason for the high rate of disease. If the intensified political negotiations now under way between the two sides in Sudan succeed in ending hostilities, full access to the final areas of endemic dracunculiasis in southern Sudan might be possible soon. After the war ends and health-care workers gain access to this area, at least 4-5 years will be required to eliminate dracunculiasis, given the extent to which the disease is endemic and southern Sudan's enormous size, geographic barriers, and poor infrastructure and communications networks. With the devotion of sufficient resources and the resolution of civil conflict, Sudan and the other countries in which dracunculiasis is endemic can eradicate this disease.
Progress Toward Global Dracunculiasis Eradication, June 2002. JAMA. 2002;288(22):2817-2818. doi:10.1001/jama.288.22.2817-JWR1211-3-1