Cholera has historically occurred in periodic epidemics, with the most severe epidemics limited to a few countries, namely Bangladesh, India, and countries in Africa and South America. During the past three decades, however, this disease has occurred in geographical areas from which it had seemingly disappeared almost a century ago (35). Including these new appearances, epidemics have been reported in over 75 countries in South America, Africa, and Asia during the past decade (38). In addition, each year sporadic cases are reported in other countries around the world (38).Interestingly, cholera is one of the few bacterial diseases known for its pandemicity, and until 1992, all epidemics of cholera were caused by Vibrio cholerae serogroup O1. In the latter part of 1992, a newly recognized O139 serogroup was isolated in areas surrounding the Bay of Bengal and was linked to major epidemics, first in Madras on the eastern coast of India and then in the southern part of Bangladesh. Later it was detected in neighboring countries and has continued to persist in that geographic region (6, 28).In 1992 in Bangladesh during a 12-week period, there were approximately 220,000 cases of cholera caused by serotype O139, with over 8,000 deaths, more deaths than in all of Latin America that same year (31,35). Cholera is known to be a disease with a high mortality (Ϸ60% if untreated); with adequate treatment (intravenous and oral rehydration therapy, supplemented with appropriate antibiotics) the mortality drops to Ͻ1.0% (5, 26). The large numbers of deaths indicate that adequate therapy was not available to the many persons who died (6,35).In the recent history of cholera, most major epidemics originated in coastal regions, including both the South American epidemic that began in the coastal regions of Peru, spreading to 21 countries, including Mexico, and the new O139 outbreak in India and Bangladesh. In Dhaka City and a rural area of Bangladesh, Matlab, cholera occurs year-round, with a distinct pattern of two peaks of disease, one in the spring and the other in the fall (16,30).The presence of V. cholerae O1 year-round via its commensal association with plankton was established by Colwell and coworkers using direct detection methods (17). It is still not certain what triggers the continuing seasonal epidemics of cholera in Bangladesh and what determines the persistence and multiplication of V. cholerae O1 and O139 in the choleraendemic regions of the world. However, coexistence of V. cholerae O1 and O139 serogroups in association with plankton has

A longitudinal study of diarrhea was carried out from May 1988 to April 1989 by household surveillance of 705 children less than 5 years old in rural Bangladesh. Stool samples were examined for enteric pathogens at the beginning of each diarrheal episode. For persistent episodes, stool examination was repeated on days 15-17 of the illness. For each case of persistent diarrhea, stool samples from age-matched acute diarrheal and healthy controls were examined. Compared with healthy controls, cases of diarrhea were associated with Shigella species (P = .07) and rotavirus (P less than .05). Diffusely adherent Escherichia coli (P less than .05) and cryptosporidia (P = .07) were the only enteropathogens associated with persistent diarrhea in comparison with acute diarrhea. No more than 15% of children had the same class of pathogen identified from stool on both days 1-3 and days 15-17, indicating that persistent infection was uncommon. However, a different enteropathogen was frequently found on days 15-17, suggesting that sequential infection may be a cause of persistent diarrhea.

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Despite nearly 200 years of study, the mechanisms contributing to the maintenance of endemic cholera and the causes of periodic epidemics remain poorly understood. To investigate these patterns, cholera data collected over 33 years (1966-1998) in Matlab, Bangladesh, were analyzed. Time-lagged autocorrelations were stratified by Vibrio cholerae serogroup, serotype, and biotype. Both classical and El Tor biotypes alternated and persisted between 1966 and 1988; the classical biotype disappeared by 1988, and the O139 serogroup first appeared in 1993. Both the Ogawa and Inaba serotypes circulated the entire time. The autocorrelations revealed that both Inaba and Ogawa epidemics were followed 12 months later by epidemics of the same serotype. Ogawa epidemics, however, were also followed by further Ogawa epidemics only 6 months later. Thus, epidemics of Inaba may selectively confer short-term population-level immunity for a longer period than those of Ogawa. These observations suggest that the Inaba antigen should be maximized in cholera vaccine designs.