No abstract

The relationship among (i ) the local incidence of cholera, (ii) the prevalence in the aquatic environment of Vibrio cholerae, and (iii) bacterial viruses that attack potentially virulent O1 and O139 serogroup strains of this organism (cholera phages) was studied in Dhaka, Bangladesh. Over nearly a 3-year period, we found that significantly more environmental water samples contained either a phage or a phage-susceptible V. cholerae strain than both (P < 0.00001). The number of cholera patients varied seasonally during this period and frequently coincided with the presence of pathogenic V. cholerae strains in water samples that otherwise lacked detectable cholera phages. Interepidemic periods were characterized by water samples containing cholera phages but no viable bacteria. Our data support the conclusion that cholera phages can influence cholera seasonality and may also play a role in emergence of new V. cholerae pandemic serogroups or clones.bacteriophage ͉ seasonality ͉ epidemiology ͉ emergence ͉ lysogeny E pidemics of cholera caused by toxigenic Vibrio cholerae belonging to the O1 or O139 serogroups are a major public health problem in many developing countries of Asia, Africa, and Latin America (1). Cholera epidemics occur with seasonal regularity in the Ganges delta region of Bangladesh and India. Epidemics usually occur twice during a year, with the highest number of cases just after the monsoon during September to December. A somewhat smaller peak of cholera cases also is observed during the spring, between March and May. Although V. cholerae is a human pathogen, these bacteria constitute part of the normal aquatic flora in estuarine environments, and water is clearly a vehicle for transmission of V. cholerae. Although the seasonality of cholera in Bangladesh and elsewhere has been temporally associated with numerous physical and biological parameters (2), these associations do not directly cause epidemics, nor do they end them. More than a century of public health experience has shown that toxigenic O1 and O139 V. cholerae cells cause cholera epidemics and that the elimination of these cells from drinking water ends cholera epidemics. The parameters that directly modulate the level of viable cells belonging to the pathogenic clones of V. cholerae O1 and O139 in the Ganges delta aquatic environment remain unknown. Furthermore, the fact that pathogenic strains of V. cholerae are clonally distinct from environmental, nonpathogenic V. cholerae strains (1) undermines proposed mechanisms of seasonality and pandemic spread that are based on data from studies measuring the abundance of all Vibrio species in the aquatic environment (2).Bacterial viruses (phages) are known to play a critical role in the evolution of pathogenic bacterial species, and V. cholerae in particular. For example, cholera toxin genes are transferred to nontoxigenic strains by means of a lysogenic filamentous phage, CTX⌽ (3). Here we show that the presence of bacterial viruses acting on V. cholerae O1 or O139 (cholera phages or vibriopha...

We present here quantitative evidence for an increased role of interannual climate variability on the temporal dynamics of an infectious disease. The evidence is based on time-series analyses of the relationship between El Niñ o͞Southern Oscillation (ENSO) and cholera prevalence in Bangladesh (formerly Bengal) during two different time periods. A strong and consistent signature of ENSO is apparent in the last two decades (1980 -2001), while it is weaker and eventually uncorrelated during the first parts of the last century (1893-1920 and 1920 -1940, respectively). Concomitant with these changes, the Southern Oscillation Index (SOI) undergoes shifts in its frequency spectrum. These changes include an intensification of the approximately 4-yr cycle during the recent interval as a response to the well documented Pacific basin regime shift of 1976. This change in remote ENSO modulation alone can only partially serve to substantiate the differences observed in cholera. Regional or basin-wide changes possibly linked to global warming must be invoked that seem to facilitate ENSO transmission. For the recent cholera series and during specific time intervals corresponding to local maxima in ENSO, this climate phenomenon accounts for over 70% of disease variance. This strong association is discontinuous in time and can only be captured with a technique designed to isolate transient couplings.