Fig. 4.

Schematic model for factors influencing seasonal epidemics of cholera. Events occurring in the environment are shown in circles, whereas those occurring in human cholera victims are shown in rectangles. 1, Seasonal conditions (e.g., floods or physical-chemical factors causing phage instability) lead to the reduction of viable lytic phages in the aquatic environment. 2, Other seasonal factors (e.g., elevated temperature or biological-cofactors) lead to a bloom of nonpathogenic and pathogenic Vibrio species in local water sources. 3, A favorable aquatic environment facilitates infection by a pathogenic V. cholerae strain (black vibrios), causing an asymptomatic or undetected symptomatic infection in an index case. 4, Amplification of the pathogenic clone in the index case seeds the environment. 5, An epidemic begins, triggered by the index case leading to host amplification of the pathogenic clone and massive environmental contamination. 6, Phages produced by environmental Vibrio species (e.g., through induction of lysogens or lytic growth) begin to amplify on the pathogenic clone in the environment. 7, Cholera victims increasingly ingest both the pathogenic clone and the lytic phage from environmental sources leading to amplification of the phage in vivo. 8, Environmental contamination with phage shed by cholera victims and further amplification of phage on the pathogenic clone within the environment lead to collapse of the epidemic. Factors contributing to the collapse of the epidemic include the decreasing concentration of the pathogenic clone in the environment coincident with a upsurge in environmental phage concentration that together contribute to a dramatic reduction in the rate of transmission of cholera in the interepidemic period.