RESUMO
The authors utilized a recently developed DNA probe technique to obtain quantitative data on occurrence of Vibrio cholerae in samples collected monthly from 12 environmental sites in Lima, Peru, from November 1993 through March 1995. Peak V. cholerae counts ranged from 10(2)/ml to 10(5)/ml, with the highest counts in sewage-contaminated areas and irrigation water. With our methodology, no V. cholerae cases were detected at any site during the winter months of July through October. Counts were detectable in the environment before onset of cholera in the community, with counts at "cleaner" sites upriver correlating significantly with occurrence of community disease 2 and 3 months later. In sites with heavy sewage contamination, V. cholerae could still be detected before the onset of cases in the community; however, in contrast to upriver sites, counts at these latter sites correlated most closely with the number of concurrently occurring cholera cases. These data support a model of cholera seasonality in which initial increases in number of V. cholerae in the environment (possibly triggered by temperature) are followed by onset of illness in the community, with these human cases further amplifying the organism as the epidemic cycle proceeds.
PIP: A newly developed DNA probe technique was used to analyze the occurrence of Vibrio cholerae in samples collected from 12 environmental sites in metropolitan Lima, Peru, each month from November 1993 to March 1995. Epidemic V. cholerae cases were found in 69 (34.5%) of the 200 samples collected. This represents more than twice the number of cholera-positive samples correctly identified with traditional methods. The highest V. cholerae counts were recorded in sewage-contaminated areas and irrigation water. No V. cholerae cases were detected at any site during the winter months of July through October. At the relatively cleaner upriver sites, counts were detectable 2-3 months prior to the outbreak of disease in the community. In sites with heavy sewage contamination, counts were more closely correlated with the number of concurrently occurring cholera cases in the community. These findings provide evidence for a model of cholera seasonality, in which initial increases in number of V. cholerae in the environment (possibly triggered by temperature) are followed by an onset of illness in the community, with these human cases further amplifying the organism as the epidemic cycle proceeds. Enhanced understanding of the complex web of human and environmental interactions that lead to seasonal cholera outbreaks would facilitate the design of preventive interventions.