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Epidemic Cholera -- Burundi and Zimbabwe, 1992-1993

The current cholera pandemic reached sub-Saharan Africa in 1970 and spread rapidly throughout the continent (1). Since then, epidemic cholera has persisted or reemerged in many African countries. This report summarizes cholera outbreaks in Burundi and Zimbabwe and the efforts to control these outbreaks. Rumonge, Burundi

During February 7-May 10, 1992, an epidemic of cholera caused by Vibrio cholerae O1, serotype Ogawa, affected 1044 persons in Western Burundi, a small country in central Africa (Figure 1). Index patients resided in a region bordering Lake Tanganyika, Zaire, and Rwanda. The epidemic spread southward among the provinces bordering the lake, reaching Bujumubura in March and Rumonge in April.

During February, the Burundi Ministry of Health (BMOH) formed a team of health professionals to plan and implement control measures. A surveillance system of daily reporting of suspected cholera cases and deaths was established to identify affected areas, and to evaluate control efforts.

By late April, the number of new cholera cases reported weekly had decreased when an outbreak was reported in Rumonge (1990 population: 12,000), located on Lake Tanganyika. The BMOH established a cholera ward at the local hospital, and trained health workers in rehydration therapy. To identify risk factors for cholera, the BMOH conducted a case-control study in Rumonge from May 5 through May 10. A case-patient was defined as any person aged greater than 5 years admitted to the Rumonge cholera treatment ward during May 5-9. Two controls were selected for each case-patient and matched by age, sex, and neighborhood of residence.

Case-patients were significantly more likely than neighborhood controls to have drunk untreated water from (odds ratio {OR}=2.7; 95% confidence interval {CI}=1.1- 6.4) or bathed in (OR=5.0; 95% CI=1.1-22.3) Lake Tanganyika during the 3 days before onset of illness. Because of a shortage of potable water and an insufficient number of functioning water taps in Rumonge, untreated lake water was often used for domestic purposes. Access to a functioning water tap during the 3 days before onset of illness was protective (OR=0.4; 95% CI=0.2-1.0, p=0.05).

On May 4, the Rumonge port was closed and access to the lake prohibited, and potable water was transported daily to the neighborhood most affected by the outbreak. The number of case-patients began to decrease on May 5, and by May 10, the outbreak ended (Figure 2). Six (2.7%) of 272 patients died during the Rumonge outbreak. In mid-June, both the Rumonge port and the lakeshore were reopened. Since May 10, 1992, no new cases of cholera have been reported in Burundi. Chadereka, Zimbabwe

From January 1 through February 8, 1993, 133 persons with cholera were identified in Chadereka (1992 population: 4029) in northeastern Zimbabwe (Figure 1) -- an attack rate of 3.3%. Most patients (123) were identified through an emergency cholera treatment facility established by the Zimbabwe Ministry of Health and Child Welfare on January 24; 10 were identified by patients of the clinic.

The median age of the 133 patients was 41 years (range: 3 weeks-92 years); 51% were male. Of 20 deaths (case-fatality rate=15%), 16 occurred before the cholera treatment center was established; mean age of patients who died was 65.5 years (range: 2-92 years). V. cholerae O1 was identified from rectal swabs of four of five persons with acute clinical cholera.

To identify risk factors and potential control measures, trainees in the University of Zimbabwe Master of Public Health and Field Epidemiology Training Program, in collaboration with members of the university's Department of Community Medicine and national and local health officials, conducted a case-control study. A case was defined as the occurrence of five or more episodes of acute watery nonbloody diarrhea during a 24-hour period, with onset from January 1 through February 8 in a person residing in Chadereka village. Because of the need for rapid identification of risk factors, a convenience sample (i.e., the first patients who could be located) of 56 of the 133 case-patients was interviewed for the study. Controls were identified through interviews with village residents during work and evening hours in the neighborhoods of case-patients and were matched by sex and 10-year age group. Only one case or one control was selected per household, and controls were excluded if they, or any household member, had had diarrhea since January 1.

The 56 case-patients selected for the study were similar in age and sex distribution to the 133 case-patients. Case-patients and controls had similar sources of water; 89% of both groups obtained water from a subterranean borehole well, and 25% reported obtaining water from a nearby river. Water was often stored for longer than 24 hours before consumption. Case-patients were more likely than controls to have noted contact of a household member's hands with water and were less likely to have reported boiling water; however, these findings were not statistically significant. No specific food -- including dried fish, cucumbers, meat, or sadza (a cooked cereal-based staple food) -- was associated with an increased risk of illness.

Although a specific source of the outbreak was not identified, one food appeared to be protective. Ten (18%) of 55 case-patients and 27 (50%) of 54 controls reported consumption of mahewu (matched OR=0.2; 95% CI=0.1-0.5), a porridge-like drink made of fermented cooked grain. Mahewu is made from porridge that is combined with malted sorghum flour and fermented for at least 12 hours before consumption. The resulting food is a thick liquid usually consumed the following day. Mahewu prepared in a Harare household and allowed to ferment for 18 hours had a pH of 3.8. Mahewu drinkers and nondrinkers did not differ significantly in consumption of other foods nor in source of drinking water.

Reported by: N Ndayimirije, MD, E Maregeya, MD, D Nshimirimana, MD, S Nkurikiye, MD, Ministry of Health, Burundi. C Dzuda, S Chigumira, MBChB, D Matanhire, K Mwenye, MBChB, S Mashayamombe, MBChB, Master of Public Health and Field Epidemiology Training Program, C Todd, MBBCh, M Bassett, MD, Dept of Community Medicine, Univ of Zimbabwe, Harare; R Munochiveyi, Provincial Medical Director, Mashonoland Central, Office of the Permanent Secretary, Ministry of Health and Child Welfare, Harare. S Grady, Tulane Univ, New Orleans. Technical Support Div, International Health Program Office; International Br, Div of Field Epidemiology, Epidemiology Program Office; Foodborne and Diarrheal Diseases Br, Div of Bacterial and Mycotic Diseases, National Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: In 1991, 21 African countries reported 153,367 cholera cases and 13,998 cholera-related deaths to the World Health Organization, representing 26% of all reported cases and 73% of cholera-associated deaths (2). However, surveillance data are incomplete in many countries, and the number of cases and deaths may be substantially underestimated. The 1991 cholera case-fatality rate of approximately 9% reported in Africa was lower than rates of 30%-50% reported in the 1970s but higher than the rate of 1% in Latin America.

Improving cholera surveillance and developing a coordinated response for epidemic cholera are high public health priorities in Africa. The first priority is to prevent cholera-associated deaths by providing vigorous rehydration therapy to affected persons (3). As of 1991, all African countries, except the Republic of South Africa, had developed a national plan to promote oral rehydration therapy for diarrheal illness (4 ). The proportion of childhood diarrheal episodes being treated with oral rehydration increased from an estimated 4% in 1984 to 40% in 1991 (4). The case-fatality rate of 2.7% reported from Rumonge suggests that rapid surveillance and aggressive and coordinated response by public health authorities to deliver adequate treatment to affected areas can prevent cholera-associated deaths.

Determination of the routes of cholera transmission is important in developing effective prevention measures. Because waterborne transmission of cholera in Africa has been associated with drinking untreated water from rivers and shallow wells (5-7), one strategy for preventing cholera is the provision of disinfected drinking water to persons residing in areas at risk. Boiling water is effective but consumes scarce fuel wood and is difficult to sustain. Chlorination is the most widely used method for purifying municipal water supplies. Providing safe, treated water supplies also may prevent other waterborne diseases (e.g., typhoid fever, hepatitis, and other diarrheal illnesses in children).

Cholera also has been transmitted by the foodborne route in Africa. Because V. cholerae O1 is rapidly inactivated at acid pH levels, recipes that acidify food can be protective. Transmission has been documented through consumption of contaminated moist cooked grains that were held for several hours before eating (5,7,8) and through contaminated shellfish (9). The findings in Zimbabwe that mahewu was protective suggest that it was less likely to transmit foodborne cholera than other foods available in the community. In laboratory studies, mahewu has inactivated a variety of enteric bacterial pathogens (10). The demonstrated safety of some traditional foods suggests prevention measures that can be recommended and implemented immediately and have particular relevance where fermented gruels are used as traditional weaning foods for young children.

Efforts to control cholera epidemics in Africa and elsewhere by mass chemoprophylaxis, vaccination campaigns, roadblocks, and broad embargoes on commodities have been ineffective and have diverted scarce resources away from the critical activities of providing treatment and improving the safety of water and food supplies. Adequate surveillance can guide the rational distribution of treatment and prevention supplies. Rapid and thorough investigation of outbreaks can identify unsuspected sources of the infection, can assess the adequacy of treatment, and are essential to development of future prevention efforts.


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  2. World Health Organization. Cholera in 1991. Wkly Epidemiol Rec 1992;67:253-60.

  3. World Health Organization. Guidelines for cholera control. Geneva: World Health Organization, Programme for Control of Diarrhoeal Disease, 1992; publication no. WHO/CDD/SER/80.4, rev. 4.

  4. World Health Organization. Programme for control of diarrhoeal disease: 8th programme report, 1990-1991. Geneva: World Health Organization, 1992.

  5. Tauxe RV, Holmberg SD, Dodin A, Wells JV, Blake PA. Epidemic cholera in Mali: high mortality and multiple routes of transmission in a famine area. Epidemiol Infect 1988;100:279-89.

  6. Sinclair GS, Mphahlele M, Duvenhage H, Nichol R, Whitehorn A, Kustner HG. Determination of the mode of transmission of cholera in Lebowa; an epidemiological investigation. S Afr Med J 1982;62:753-5.

  7. Swerdlow DL, Malanga G, Begokyian G, et al. Epidemic of antimicrobial resistant Vibrio cholerae O1 infections in a refugee camp -- Malawi {Abstract no. 529}. In: Program and abstracts of the 31st Interscience Conference on Antimicrobial Agents and Chemotherapy. Washington, DC: American Society of Microbiology, 1991:187.

  8. St. Louis ME, Porter JD, Helal A, et al. Epidemic cholera in West Africa: the role of food handling and high-risk foods. Am J Epidemiol 1990;131:719-28.

  9. Shaffer N, Mendes P, Costa CM, et al. Epidemic cholera in Guinea-Bissau: importance of foodborne transmission {Abstract no. 1459}. In: Program and abstracts of the 28th Interscience Conference on Antimicrobial Agents and Chemotherapy. Washington, DC: American Society of Microbiology, 1988:370.

  10. Simango C, Rukure G. Survival of bacterial enteric pathogens in traditional fermented foods. J Appl Bacteriol 1992;73:37-40.

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