Emanuel Hanski, a microbiologist at Hebrew University in Jerusalem, and colleagues have found that the success of Group A Streptococcus is due in part to a protein that blocks the immune system's distress calls. The findings, published in the October 4, 2006, issue of the EMBO Journal, could lead to new strategies for treating necrotizing fasciitis and halting its rapid destruction of tissue. The paper was published in advance online.
The bacterium, group A Streptococcus, wreaks destruction on muscle and skin tissue in the form of necrotizing fasciitis, which kills roughly 30 percent of its victims and leaves the rest disfigured. Antibiotics and surgical interventions, the known treatments, often fail. Necrotizing fasciitis is a serious but rare infection of the skin and the tissues beneath it.
The work began two years ago, when Hanski developed a mouse model for necrotizing fasciitis. After injecting the mice with a virulent strain of Streptococcus of a type known as M14, isolated from a necrotizing fasciitis patient, the team noticed that unlike most Strep infections, in which white blood cells swarm invading bacteria to clear them from the body, few white blood cells appeared at the M14 infection site. A similar phenomenon had been observed in patients with necrotizing fasciitis but did not receive sufficient attention at the time.
"We knew that the pathology of the disease in people was typified by various degrees of a lack of white blood cells," said Hanski. After publishing their findings in the British medical journal The Lancet in 2004, the team began to search for the factor that blocked the recruitment of white blood cells during M14 infection.
They focused on the gene for a Streptococcus peptide called SilCR, after finding that the gene product
Source:Howard Hughes Medical Institute