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Emerging staph strains found to be increasingly deadly and deceptive

A study of how the immune system reacts to strains of antibiotic-resistant Staphylococcus aureus bacteria--emerging strains that sicken otherwise healthy people, or so-called "community-acquired" infections--has shown for the first time that these strains are more deadly and better at evading human immune defenses than more common S. aureus strains that originate in hospitals and other health-care settings.

In a paper released today online in The Journal of Immunology, scientists from the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, describe how community-acquired S. aureus strains that survive treatment with the methicillin family of antibiotics can evade immune defenses. Infections from community-acquired methicillin-resistant S. aureus, or MRSA, are difficult to treat and are increasing nationally at an alarming rate, say experts.

Scientists at NIAID's Rocky Mountain Laboratories (RML) in Hamilton, MT, and colleagues examined the ability of MRSA strains to cause disease in mice and avoid destruction by human white blood cells called neutrophils. Neutrophils, which typically ingest and then kill harmful bacteria, make up about 60 percent of all white blood cells and are the first line of defense against bacteria. Scientists know that community-acquired strains differ from hospital strains, but they don't know why the community strains cause more serious infection in otherwise healthy people.

The work also identified specific S. aureus genes that potentially control the bacterium's escape from neutrophils. Among thousands of S. aureus genes analyzed in the five different strains used in the study, the scientists identified a large group of genes whose role in helping spread infection is unknown. RML's Frank DeLeo, Ph.D., the investigator who directed the study, and colleagues plan to determine if some of the unknown genes help promote disease. If they can learn which genes control t
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Source:NIH/National Institute of Allergy and Infectious Diseases


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