Prof. Emanuel Hanski of Hebrew University..
(photo credit: Courtesy)
Researchers from the Hebrew University of Jerusalem have just published their research in the journal Cell, which explains how a usually harmless pathogen turns deadly, opening the door to possible future treatments to halt this and other potentially fatal bacteria.
The bacteria called Group A Streptococcas (GAS) can live inside humans without causing any symptoms or any harm, but in some cases, it may trigger fatal diseases such as necrotizing fasciitis (also known as flesh-eating disease) and toxic-shock syndrome.
Until now, scientists had no clue what turns the harmless bugs into deadly ones.
The research was conducted by Prof. Emanuel Hanski of the Institute of Medical Research Israel Canada at the Hebrew University’s faculty of medicine.
Nectrotizing fasciitis is a rare infection of the deeper layers of skin and tissues under the skin, but usually don’t affect the muscle, easily spreading across the fascial plane within the subcutaneous tissue. It was first recognized in 1952.
Around the world, each year, GAS infections lead to about 500,000 deaths and cause severe consequences to those infected.
The flesh-eating disease, in particular, is an extremely vicious infection that moves quickly through the soft tissues of the body, often leaving doctors with little time to stop or delay its progress.
The main treatments include antibiotics and cutting out infected tissues. Yet despite prompt treatment, the bacteria spread and caused death in about one-quarter of all patients.
The majority of infections are caused by organisms that normally reside on the person’s skin. Necrotizing fasciitis progresses quickly, having greater risk of developing in the immuno-compromised, due to conditions such as diabetes or cancer.
The longer it takes to treat, the higher the risk of death.
Hanski and doctoral student Moshe Baruch, together with an international research team, discovered a novel mechanism that influences GAS virulence at the early steps of the infection.
They found that when GAS sticks to and infects the host’s cells, it delivers into these cells two streptolysin toxins.
These poisons impair the body’s mechanism for quality control of protein synthesis, triggering a defensive stress response that, among other things, also increases the production of the amino acid asparagine.
GAS senses the increased asparagine level and alters its gene expression profile and its rate of proliferation, which can be deadly in the host.