MEDICAL: DISEASES : MEDICAL: RESEARCH: Treatment for S. Aureus Skin Infection Works in Mouse Model
David P. Dillard
.
MEDICAL: DISEASES :
MEDICAL: RESEARCH:
Treatment for S. Aureus Skin Infection Works in Mouse Model
Date: Tue, 31 Aug 2010 10:45:09 -0400
From: "NIH OLIB (NIH/OD)" <ol...@od.nih.gov>
To: NIHP...@list.nih.gov
Subject: Treatment for S. Aureus Skin Infection Works in Mouse Model
U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Institute of Allergy and Infectious Diseases (NIAID)
http://www.niaid.nih.gov/
For Immediate Release: Tuesday, August 31, 2010
CONTACT:
Ken Pekoc
e-mail:
TREATMENT FOR S. AUREUS SKIN INFECTION WORKS IN MOUSE MODEL
Scientists from the National Institutes of Health and University of
Chicago have found a promising treatment method that in laboratory mice
reduces the severity of skin and soft-tissue damage caused by USA300, the
leading cause of community-associated Staphylococcus aureus infections in
the United States. By neutralizing a key toxin associated with the
bacteria, they found they could greatly reduce the damaging effects of the
infection on skin and soft tissue. Community strains of S. aureus cause
infection in otherwise healthy people and are considered extremely
virulent, as opposed to hospital strains that infect people who already
are weakened by illness or surgery.
While much recent attention has been focused on deaths caused by S. aureus
infection in the bloodstream-and those caused by methicillin-resistant S.
aureus in particular-the Centers for Disease Control and Prevention
estimates that in 2005, physicians treated 14 million non-lethal S. aureus
skin and soft-tissue cases in the United States.
In their study, now online in the Journal of Infectious Diseases,
scientists from NIH's National Institute of Allergy and Infectious
Diseases (NIAID) examined the effects of the bacterial toxin
alpha-hemolysin, or Hla, on S. aureus skin infections in laboratory mice.
In all aspects of the study where the Hla toxin was either removed from S.
aureus bacteria or neutralized through immunization, skin abscesses were
significantly smaller, mice recovered faster and there was little or no
skin destruction.
When S. aureus secretes Hla during infection in humans, the toxin pokes
holes in a variety of different host cells, killing them. Scientists who
have studied Hla for years have mainly focused on neutralizing the toxin
in cases of pneumonia-related S. aureus infection. Until now, no one had
tested how the absence of Hla would affect the severity of USA300 skin
infections and whether immunization against the toxin could neutralize Hla
and its contribution to the severity of skin disease.
"For cases of skin and soft-tissue infection caused by Staph aureus, this
study highlights the potential for antitoxin treatment to become an
effective alternative to traditional antibiotics, which we know have
limitations because of drug resistance," says NIAID Director Anthony S.
Fauci, M.D. Antitoxins prevent harm caused by a specific part of a
pathogen-such as Hla in S. aureus-rather than trying to kill the entire
pathogen, as antibiotics do.
The study, led by Frank DeLeo, Ph.D., of NIAID's Rocky Mountain
Laboratories in Hamilton, Mont., documented physical differences in mice
infected with different strains of S. aureus, including USA300 with or
without Hla. The second portion of the study tested what is known as
active and passive immunity, with mice being immunized with a non-lethal
version of the toxin or injected with Hla-specific antibodies,
respectively. Both types of immunization protected mice from skin lesions
that typically destroy skin and surrounding tissue.
The group noted that multiple S. aureus molecules must contribute to skin
infection because simply removing or neutralizing Hla did not completely
prevent the formation of skin abscesses, although the abscesses were
smaller in size.
Study collaborators from the University of Chicago, Olaf Schneewind, M.D.,
Ph.D., and Juliane Bubeck Wardenburg, M.D., Ph.D.,contributed the Hla
treatment concept, which they developed through their recent work on S.
aureus pneumonia. Dr. DeLeo's group adapted that work to their mouse model
of skin infection, which is a good indicator of how abscess size and skin
destruction could affect humans, according to the study investigators.
"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," says Dr. DeLeo. His group is continuing its
collaboration with Drs. Schneewind and Bubeck Wardenburg on the project.
NIAID conducts and supports research-at NIH, throughout the United States,
and worldwide-to study the causes of infectious and immune-mediated
diseases, and to develop better means of preventing, diagnosing and
treating these illnesses. News releases, fact sheets and other
NIAID-related materials are available on the NIAID Web site at
The National Institutes of Health (NIH) -- The Nation's Medical Research
Agency -- includes 27 Institutes and Centers and is a component of the
U.S. Department of Health and Human Services. It is the primary federal
agency for conducting and supporting basic, clinical and translational
medical research, and it investigates the causes, treatments, and cures
for both common and rare diseases. For more information about NIH and its
programs, visit
--------------------
REFERENCES:
A Kennedy et al.
Targeting of alpha-hemolysin by active or passive immunization decreases
severity of USA300 skin infection in a mouse model.
The Journal of Infectious Diseases.
DOI: 10.1086/655779 (2010).
J Bubeck Wardenburg et al.
Vaccine protection against Staphylococcus aureus pneumonia.
Journal of Experimental Medicine.
205:287-94 (2008).
J Bubeck Wardenburg et al.
Poring over pores: alpha-hemolysin and
Panton-Valentine leukocidin in Staphylococcus aureus pneumonia.
Nature Medicine.
13:1405-06 (2007).
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The HTML version of this release contains an image at:
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This NIH News Release is available online at:
http://www.nih.gov/news/health/aug2010/niaid-31.htm
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