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Key Mechanism to Emergence of Strep Bacteria

Researchers at the University of California, San Diego (UCSD) School of Medicine and the University of Wollongong in Australia have discovered that, 30 years ago, a virus infected the strep bacteria creating a deadly strain of flesh-eating bacteria that has evolved to produce serious human infections worldwide.

The incidence of serious strep infections has risen dramatically in the last three decades, and this increase is largely attributed to the spread around the globe of a single strain of strep known as the invasive M1T1 clone.

Just like a computer virus might come in and reprogram your hard drive, this virus reprogrammed the genetic machinery of the M1T1 strep into a more virulent form, said senior author Victor Nizet, M.D., UCSD Professor of Pediatrics and Pharmacy.

The consequences of this event on human health are still being felt three decades later.The research, reported in the July 15 advance online publication of the journal Nature Medicine, focuses on the major human pathogen group A Streptococcus (strep.)

Among the most important of all human infectious disease agents, strep is responsible for a wide range of diseases, ranging from simple throat and skin infections to life-threatening invasive conditions such as necrotizing fasciitis (flesh-eating disease) and toxic shock syndrome.

Strep is estimated to cause over 700 million infections each year; over 650,000 of these are dangerous invasive forms.

The UCSD-Australian research team sought to identify what special characteristics make the invasive M1T1 strep clone so virulent for humans. They observed that during the early stages of a simple skin infection, a small subpopulation of the strep bacteria hijack a protein called plasminogen from the human bloodstream.

The bacteria attach the protein to their own surface, and then activate it into a protease an enzyme that digests proteins and is capable of destroyin
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