WASHINGTON (Dow Jones)--Researchers may have found a promising alternative to
antibiotics when it comes to fighting skin damage caused by a certain strain of
Staphylococcus aureus, or Staph.
Instead of focusing on antibiotics, which can be a limiting treatment option
due to drug-resistance issues, the new method would involve neutralizing a cell-
killing toxin associated with the bacteria.
In their recently published study, scientists from the National Institutes of
Health and University of Chicago found that when mice were immunized with a non-
lethal version of a Staph toxin known as alpha-hemolysin (Hla) or injected with
certain antibodies, the skin damage that's typically-associated with Staph
infections was significantly reduced.
"Skin abscesses were significantly smaller, mice recovered faster and there
was little or no skin destruction," the NIH wrote in a press release this week.
The study is available online in The Journal of Infectious Diseases.
The study, led by Frank DeLeo of NIH's National Institute of Allergy and
Infectious Diseases, focuses on a particular strain of the bacteria known as
USA300. The strain is the leading cause of community-associated Staph infections
in the U.S. While hospital strains tend to infect patients grappling with
illness or recovering from procedures, community strains are often found in
healthy people.
The study is one of the first to evaluate the Hla toxin's impact on skin
infections. The toxin, which kills human cells when its secreted by the Staph
bacteria, has been studied in cases of pneumonia-related infections. But the
NIH-University of Chicago study is one of the first to examine skin and soft-
tissue damage and to test whether immunization against a key toxin could reduce
the severity of skin infections.
"This toxin is probably one of the most promising targets we currently have in
our efforts to develop therapeutics that protect against severe Staph aureus
skin infections," said DeLeo.
-By Maya Jackson Randall, Dow Jones Newswires; 202-257-6313, maya.jackson-
randall@dowjones.com
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09-01-10 1305ET
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