Vibrio cholerae O1, the bacterium that causes cholera infections, is capable of persisting in low-nutrient aquatic environments for decades, and while many studies have analyzed the bacteria’s effect on the body, how they survive in nature is less well understood.
In a study published in Frontiers in Microbiology, University of Florida researchers found that after long-term persistence in nutrient-poor aquatic conditions, toxigenic V. cholerae O1 bacteria sustained a mutation that rendered them unable to move independently while also supporting connection to other bacteria in the form of a biofilm. The authors suggest that this biofilm allows the bacteria to survive, and when heavy rainfall brings an influx of necessary nutrients into the water, the bacteria can grow and reproduce more extensively. They propose that the increase in cholera transmission after monsoons, hurricanes and other intense weather phenomena is likely due to runoff from agricultural lands into nearby lakes and streams.
“In countries where cholera-causing bacteria persist in rivers, lakes and other aquatic reservoirs, fertilizers and other types of agricultural runoff help these bacteria increase from small doses to infectious doses,” said Dr. Shrestha Sinha-Ray, a research scholar working with Dr. Afsar Ali in the University of Florida College of Public Health and Health Professions and the primary author of the study. Dr. Ali is the senior author on the study, a research associate professor in the department of environmental and global health and a member of the Emerging Pathogens Institute.
In nutrient-rich conditions such as the human body, V. cholerae bacteria are motile — using their flagella to move independently toward nutrients.
Dr. Sinha-Ray found that when chitin, phosphate and other necessary nutrients were lacking in filter-sterilized lake water, however, a mutation within the cholera bacteria caused them to lose their flagellar motility after persisting in the water for 700 days.
Given the rapid changes V. cholerae faces in dynamic aquatic reservoirs, the authors assume this process also takes place under natural conditions, allowing the bacteria to better persist in aquatic reservoirs.
Dr. Sinha-Ray and Dr. Ali found out that the mutation of the flagellar regulatory gene, flrA, which led to the loss of flagellar motility in V. cholerae, enhanced biofilm formation only in nutrient-poor lake water conditions. The integrity of the biofilm was maintained by mannose sensitive hemagglutinin pili, or MSHA, pili. These pili are small, hair-like appendages found on the surface of many bacteria that help them attach both to surfaces and to each other.
By deleting the mshA gene responsible for creating MSHA pili in the now non-flagellated bacteria, Dr. Sinha-Ray rendered the bacteria incapable of producing biofilm; this change resulted in very few cells surviving in her water sample.