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Genetic Approach Boosts Yeast Infection Treatment
Date:10/27/2008

Inhibiting protein could yield new drug targets for mucosal fungus found in most people

MONDAY, Oct. 27 (HealthDay News) -- A new genetic approach to improve treatment of common infections caused by the yeast Candida albicans has been successfully tested by researchers at Georgetown University Medical Center.

The results confirm that inhibition of a protein produced by the Ssk1 gene could offer a new drug target against the yeast. The yeast resides in the mucous membranes of most people and causes problems such as diaper rash, vaginitis, oral infections, and invasive, blood-borne and life-threatening infections, the researchers said.

In laboratory tests, the researchers found that when the Ssk1 gene was deleted from Candida albicans, triazole drugs currently used to treat Candida-related infections were much more effective.

"This is a genetically intelligent approach to target identification and drug design," study lead author Richard Calderone, professor and chairman of the department of microbiology and immunology, and co-director of the doctoral program in the global infectious disease program at the medical center, said in a school news release.

The study was to be presented Oct. 27 at the ICAAC/IDSA annual meeting, in Washington, D.C.

"Candida infections are often treatable; however, in patients that are immunocompromised following cancer chemotherapy, bone marrow transplantation, or surgery, diagnosis is often delayed, postponing therapy," Calderone said. "Also, when drug-resistant yeast pathogens cause the infection, clinical management of the patient becomes a problem."

Candida invasive, blood-borne infections are the fourth most common hospital-acquired infection in the United States, costing the health-care system about $1.8 billion each year, Calderone said.

More information

The U.S. Centers for Disease Control and Prevention has more about Candida infections.



-- Robert Preidt



SOURCE: Georgetown University Medical Center, news release, Oct. 27, 2008


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