Faruque, S. M. et al. PNAS. (2005).

"Seasonal epidemics of cholera inversely correlate with the prevalence of environmental cholera phages".

Reviewed: 11/10/11

Cholera epidemics in and around Dhaka, Bangladesh occur seasonally, typically twice a year. Cholera is a human disease that is caused by pathogenic strains of Vibrio cholerae, however the bacteria is a normal component of aquatic ecosystems. Aquatic transmission of the disease-causing bacteria was first noted approximately one hundred and fifty years ago and while many environmental and biological parameters have been associated with the temporally varying disease surges, none have been conclusively linked to the cause or finish of the epidemic (other than the obvious requirement of water). Bacteriophages have been shown to be linked to transmission of toxigenicity in V. cholerae. Data obtained from plaque assays, bacterial cultures, and stool samples randomly obtained from local hospitals were used to demonstrate that the abundance of cholera-inducing bacterial strains was inversely correlated with increases in their own pathogens' numbers.
If the presence of a host-specific bacteriophage was noted within any given water sample collected from local aquatic systems, than its target host was significantly less likely to be found. The percentage of co-occurrences of virus and target host was lower than one that could have been predicted by chance alone.
Cross comparison of monthly collection and analysis for phages in water samples with stool samples showing cholera disease in humans did in fact show an oscillating relationship between the bacteria strains and their viruses. Two strains of bacteria are primarily responsible for the disease in Bangladesh, and six phage types, which can actually be grouped into 4 genetically distinct groups, are associated with them. However, the life modes of these viral types are not all homogenous. The authors propose that the difference between lytic and lysogenic capable phages may be driving a lot of the seasonality of the cholera epidemics.
The model they present begins with epidemics arising during periods of low lytic phage concentrations as described above. Modularity in epidemics may come about from the presence of lysogenic bacteria because lysogeny can build up in bacterial populations via prophages. Prophages make the lysogenic bacteria resistant to superinfection by other viral types and concurrently drive other bacterial strain populations down because they do not have the resistance to the lytic-cycle-dominant phages still present in the system.
This difference in lysogeny or lytic cycle phages, if they are capable of only one cycle or both and what would induce them to choose lysis over lysogeny, is here shown to directly link to the basic pattern of the cholera epidemic.
Other studies have provided evidence on the elimination of a previously dominant V. cholerae strain due to differential infection patterns of a lysogenic virus. It seems that more information on what environmental conditions are necessary to induce a lysogenic pathway in the virus would be useful for researchers hoping to identify natural resevoirs for the virus, or inversely the bacteria. Nutritional treatments could easily be applied to cultures of bacteria and virus in a laboratory setting. Similar methods used to test for prophages as were used in this study (methods such as Southern blots and DNA probes) could potentially provide a lot of information on this globally pervasive disease and the bacteria that causes it.