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SANTA BARBARA, CALIF. — Community-acquired methicillin-resistant Staphylococcus aureus is unlike its hospital-acquired cousin epidemiologically, clinically, and genetically, an infectious disease specialist explained.
“It is a different organism,” Dr. Paul Holtom said at the annual meeting of the California Society of Dermatology and Dermatologic Surgery.
For starters, the two forms of MRSA attack different populations.
Risk factors for hospital-acquired (HA) MRSA have not changed appreciably in the roughly 20 years since its emergence. The first risk factor, obviously, is hospitalization. Infections are most commonly seen in the ICU, although they are known to spread rapidly throughout institutions.
Within the hospitalized population, risk factors include use of fluoroquinolones, enteral feeding, surgery, previous hospitalization, and extended lengths of stay.
For community-acquired (CA) MRSA, early lists of potential risk factors included intravenous drug use, homosexuality (men having sex with men), homelessness or marginal housing, and being in a correctional institution.
Athletes with skin-to-skin contact were then added to the risk pool, but it soon became clear that the risk was widespread in the healthy population.
“The problem has moved far outside these original risk groups to almost everyone,” said Dr. Holtom, director of the infectious disease clinic fellowship program and hospital epidemiologist at the Los Angeles County Hospital/University of Southern California Medical Center.
For example, both his institution and the University of California, Los Angeles, Medical Center, which draw from profoundly disparate socioeconomic populations in Los Angeles, have CA-MRSA rates of greater than 70% in patients presenting to the emergency departments with skin and soft tissue infections.
Genetic testing reveals that CA-MRSA is indeed a distinct entity, rather than an HA-MRSA that has spread to the nonhospital world, Dr. Holtom said.
Hospital-acquired MRSA contains a special mecA gene that codes for penicillin-binding protein (PBP) 2a, which is an important binding site for penicillins and related antibiotic classes. Specifically, the staphylococcus cassette chromosome (SCC) mec types found in HA-MRSA are types I, II, and III, with type II dominating.
It's a different story for CA-MRSA, which is characterized by SCCmec types IV and sometimes V, which carry genes for a variety of toxins that are not seen in HA-MRSA, including the Panton-Valentine leukocidin toxin known for generating a prolific inflammatory response and skin necrosis.
The genetic differences are not surprising, considering the disparate nature of the infections, Dr. Holtom said.
“The one thing that has been very interesting about HA-MRSA for all of these years is that it does not spread in the community setting,” he noted.
He theorized that other organisms may have a competitive advantage in non-health care settings, or that HA-MRSA may spread too slowly in the immunocompetent population.
ELSEVIER GLOBAL MEDICAL NEWS
SANTA BARBARA, CALIF. — Community-acquired methicillin-resistant Staphylococcus aureus is unlike its hospital-acquired cousin epidemiologically, clinically, and genetically, an infectious disease specialist explained.
“It is a different organism,” Dr. Paul Holtom said at the annual meeting of the California Society of Dermatology and Dermatologic Surgery.
For starters, the two forms of MRSA attack different populations.
Risk factors for hospital-acquired (HA) MRSA have not changed appreciably in the roughly 20 years since its emergence. The first risk factor, obviously, is hospitalization. Infections are most commonly seen in the ICU, although they are known to spread rapidly throughout institutions.
Within the hospitalized population, risk factors include use of fluoroquinolones, enteral feeding, surgery, previous hospitalization, and extended lengths of stay.
For community-acquired (CA) MRSA, early lists of potential risk factors included intravenous drug use, homosexuality (men having sex with men), homelessness or marginal housing, and being in a correctional institution.
Athletes with skin-to-skin contact were then added to the risk pool, but it soon became clear that the risk was widespread in the healthy population.
“The problem has moved far outside these original risk groups to almost everyone,” said Dr. Holtom, director of the infectious disease clinic fellowship program and hospital epidemiologist at the Los Angeles County Hospital/University of Southern California Medical Center.
For example, both his institution and the University of California, Los Angeles, Medical Center, which draw from profoundly disparate socioeconomic populations in Los Angeles, have CA-MRSA rates of greater than 70% in patients presenting to the emergency departments with skin and soft tissue infections.
Genetic testing reveals that CA-MRSA is indeed a distinct entity, rather than an HA-MRSA that has spread to the nonhospital world, Dr. Holtom said.
Hospital-acquired MRSA contains a special mecA gene that codes for penicillin-binding protein (PBP) 2a, which is an important binding site for penicillins and related antibiotic classes. Specifically, the staphylococcus cassette chromosome (SCC) mec types found in HA-MRSA are types I, II, and III, with type II dominating.
It's a different story for CA-MRSA, which is characterized by SCCmec types IV and sometimes V, which carry genes for a variety of toxins that are not seen in HA-MRSA, including the Panton-Valentine leukocidin toxin known for generating a prolific inflammatory response and skin necrosis.
The genetic differences are not surprising, considering the disparate nature of the infections, Dr. Holtom said.
“The one thing that has been very interesting about HA-MRSA for all of these years is that it does not spread in the community setting,” he noted.
He theorized that other organisms may have a competitive advantage in non-health care settings, or that HA-MRSA may spread too slowly in the immunocompetent population.
ELSEVIER GLOBAL MEDICAL NEWS
SANTA BARBARA, CALIF. — Community-acquired methicillin-resistant Staphylococcus aureus is unlike its hospital-acquired cousin epidemiologically, clinically, and genetically, an infectious disease specialist explained.
“It is a different organism,” Dr. Paul Holtom said at the annual meeting of the California Society of Dermatology and Dermatologic Surgery.
For starters, the two forms of MRSA attack different populations.
Risk factors for hospital-acquired (HA) MRSA have not changed appreciably in the roughly 20 years since its emergence. The first risk factor, obviously, is hospitalization. Infections are most commonly seen in the ICU, although they are known to spread rapidly throughout institutions.
Within the hospitalized population, risk factors include use of fluoroquinolones, enteral feeding, surgery, previous hospitalization, and extended lengths of stay.
For community-acquired (CA) MRSA, early lists of potential risk factors included intravenous drug use, homosexuality (men having sex with men), homelessness or marginal housing, and being in a correctional institution.
Athletes with skin-to-skin contact were then added to the risk pool, but it soon became clear that the risk was widespread in the healthy population.
“The problem has moved far outside these original risk groups to almost everyone,” said Dr. Holtom, director of the infectious disease clinic fellowship program and hospital epidemiologist at the Los Angeles County Hospital/University of Southern California Medical Center.
For example, both his institution and the University of California, Los Angeles, Medical Center, which draw from profoundly disparate socioeconomic populations in Los Angeles, have CA-MRSA rates of greater than 70% in patients presenting to the emergency departments with skin and soft tissue infections.
Genetic testing reveals that CA-MRSA is indeed a distinct entity, rather than an HA-MRSA that has spread to the nonhospital world, Dr. Holtom said.
Hospital-acquired MRSA contains a special mecA gene that codes for penicillin-binding protein (PBP) 2a, which is an important binding site for penicillins and related antibiotic classes. Specifically, the staphylococcus cassette chromosome (SCC) mec types found in HA-MRSA are types I, II, and III, with type II dominating.
It's a different story for CA-MRSA, which is characterized by SCCmec types IV and sometimes V, which carry genes for a variety of toxins that are not seen in HA-MRSA, including the Panton-Valentine leukocidin toxin known for generating a prolific inflammatory response and skin necrosis.
The genetic differences are not surprising, considering the disparate nature of the infections, Dr. Holtom said.
“The one thing that has been very interesting about HA-MRSA for all of these years is that it does not spread in the community setting,” he noted.
He theorized that other organisms may have a competitive advantage in non-health care settings, or that HA-MRSA may spread too slowly in the immunocompetent population.
ELSEVIER GLOBAL MEDICAL NEWS