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article imageNew clue about cholera infection

By Tim Sandle     Sep 30, 2014 in Science
Houston - A new study has revealed how humans become infected with cholera. The infection is linked to RNA in the human body which triggers a rise in temperature. This rise in temperature signals to the contaminating bacterium to release a toxin.
Cholera is an acute infection caused by ingestion of food or water that is contaminated with the bacterium Vibrio cholerae. The main symptoms are watery diarrhea and vomiting. This may result in dehydration and in severe cases grayish-bluish skin. Cholera is common to the following parts of the world: sub-Saharan Africa, south and south-east Asia, the Middle East, and central America and the Caribbean. Mass outbreaks of cholera can occur in times of a natural disaster or war, as a result of overcrowding in poor living conditions and a lack of access to clean water.
Researchers have discovered that the Vibrio bacterium, which normally lives in oceans and rivers, senses a shift in temperature as it enters the human body. The bacterium enters the body via a mechanism termed the Ribonucleic Acid (RNA) thermometer. An RNA thermometer is a temperature-sensitive non-coding RNA molecule which regulates gene expression.
The RNA thermometer detects the higher body temperature of 98.6 degrees Fahrenheit, and then turns on the virulence factors that lead to cholera. The main factor is the release of a toxin. The researchers found that disrupting the thermometer can prevent the Vibrio from causing disease.
The research could lead to a new therapeutic mechanism to present cholera infections. When the RNA thermometer is prevented from working, Vibrio bacteria do not release their deadly toxin and simply pass through the mammalian body. This means that the disease does not take effect.
The study was carried out at UTSA's South Texas Center for Emerging Infectious Diseases. The findings have been published in the journal Proceedings of the National Academy of Sciences, in a paper titled “RNA thermometer controls temperature-dependent virulence factor expression in Vibrio cholerae.”
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