Group A streptococcus (GAS) is a human pathogenic bacteria. Many people carry GAS asymptomatically in their upper respiratory tract and other anatomic sites. However, these bacteria can cause a variety of human diseases ranging from superficial skin and throat infections to highly invasive life-threatening diseases such as toxic shock and necrotizing fasciitis, commonly known as the flesh-eating bacteria. Along with the consequences of autoimmune complications of rheumatic fever and rheumatic heart diseases, a conservative estimate of 500,000 deaths per year globally due to GAS infections has been calculated, placing this bacterium as one of the top 10 infectious causes of mortality.
Little is known about what controls the conversion of the bacteria from a non-harming form to the pathogenic state in GAS infections. Since these bacteria generally exist as communities and not as solitary microorganisms, bacterial communication systems are key elements in determining host-bacterial interactions. Most communication between bacterial cells is done by signaling molecules secreted and sensed by the bacteria. When the level of the signaling molecules is high enough, they can activate the expression of genes that coordinate their behavior. This activation only takes place in the presence of a sufficient number (a quorum) of bacteria, giving this mechanism the name quorum-sensing.
A novel research, led by Professor Emanuel Hanski from the Department of Microbiology and Molecular Genetics at the Medical School of the Hebrew University of Jerusalem, (Belotserkovsky et al., PLoS Pathogens 5(11): e1000651; http://dx.plos.org/10.1371/journal.ppat.1000651), identified a new array of genes in GAS and in a close relative, Group G Streptococcus (GGS), usually considered a commensal that do not harm the host. These genes are activated by a quorum-sensing peptide termed SilCR. SilCR is not functional in highly invasive GAS strains, suggesting that this array of genes may be involved in colonization and establishment of commensal host-bacterial relationships. The researchers further show that GAS and GGS strains can sense their respective SilCR molecules, thus coordinating their pathogenicity, and comprising a novel communication system between these bacteria. The research was funded by the Chief Scientist Office of the Israeli Ministry of Health, under the framework of ERA-NET PathoGenoMics, a European Commission funded imitative aiming at advancing transnational research in genome-based research programs on human-pathogenic microorganisms.
"This study opens up exciting possibilities for controlling the pathogenicity of Streptococcus A, which can cause several invasive, life-threatening illnesses," said Dr. Marion Karrasch-Bott, Coordinator of ERA-NET PathoGenoMics. "The researchers not only identified a new genetic element that controls bacterial virulence, but also an array of genes regulated by this element. This will help in our understanding of how bacterial-host interactions can lead to mutual existence in some cases, or to violent infections in other cases, and will eventually lead to innovative drugs that could prevent the bacteria from making the wrong decision."