The Independent Evolution Of Healthcare-Associated And Community-Acquired MRSA

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CoNS=coagulase-negative staphylococci; MRSA=methicillin-resistant Staphylococcus aureus.
Figure 2. Example of a positive D-zone test result for detection of inducible clindamycin resistance. The organism shown is Staphylococcus aureus ATCC BAA 977 that contains ermC and demonstrates the induced macrolide, lincosamide, and group B streptogrami
CA-MRSA=community-acquired methicillin-resistant Staphylococcus aureus; HA-MRSA=healthcare-associated MRSA; ICU=intensive care unit; IV=intravenous; IVDA=intravenous drug abuser; LTC=long-term care; PVL=Panton-Valentine leukocidin; SAHM=sexually active ho
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Prevalence And Risk Factors For MRSA Infections
The incidence of Staphylococcus aureus has increased dramatically throughout the United States as a cause of nosocomial infections. Based on data reported to the National Nosocomial Infections Surveillance (NNIS) System from 1989 to 2003, there has been a dramatic 40% increase in the rate of methicillin-resistant S. aureus (MRSA) isolates from intensive care unit (ICU) patients during the study period.1 In 2003, 59.5% of ICU S. aureus isolates were MRSA.1 In addition, the incidence of community-acquired MRSA (CA-MRSA) is increasing at an alarming rate.2

CA-MRSA has been defined as an MRSA isolate recovered from a clinical culture from a patient with no established risk factors for MRSA infection. Established risk factors include: the isolation of MRSA 2 or more days after hospitalization; a history of hospitalization, surgery, dialysis, or residence in a long-term care (LTC) facility within 1 year before the MRSA culture date; the presence of a permanent indwelling catheter or percutaneous medical device at the time of culture; or previous isolation of MRSA.

No longer can MRSA be regarded as an exclusively nosocomial pathogen. Risk factors for developing a healthcare-associated MRSA (HA-MRSA) infection include: previous hospitalization, in particular, a length of stay greater than 8.4 days; surgery; enteral feeding; and prior antibiotics.3 Risk factors associated with MRSA in community-acquired skin and soft tissue infections (SSTIs) include: recent antimicrobial therapy; recent hospitalization or contact with a healthcare worker; frequent device use (ie, IV catheter, hemodialysis); high rates of MRSA in a nearby institution or the community; and previous MRSA colonization.4 Fluoroquinolones, in particular, levofloxacin and ciprofloxacin, are the most common antibiotics identified as risk factors for MRSA.3,5

Differentiating CA-MRSA And HA-MRSA Infections
Naimi and colleagues compared and contrasted some of the features of CA-MRSA and HA-MRSA infections.6 In a prospective cohort study of MRSA cases conducted in Minnesota in 2000, they found that 12% were CA-MRSA and 85% were HA-MRSA. Patients with HA-MRSA were older than patients with CA-MRSA (age 68 versus age 23) and had more underlying disease. SSTIs were more common among CA-MRSA patients (75%) than among HA-MRSA patients (37%). Respiratory tract infections were more common in HA-MRSA (22%) than in CA-MRSA (6%).6

CA-MRSA is prevalent in children, athletes, prisoners, soldiers, selected ethnic populations, IV drug abusers, and sexually active homosexual men. HA-MRSA is seen more in LTC facility residents, patients with diabetes, patients who have renal failure and are on dialysis, patients with prolonged hospitalization, ICU patients, and those with long-term indwelling IV catheters. The staphylococcal chromosomal cassette is mostly Type IV in the CA-MRSA strains and Types I, II, and III in the HA-MRSA strains.2

Antimicrobial resistance is mostly seen with the b-lactams in CA-MRSA while multidrug resistance is seen in the HA-MRSA strains.2 Another concern regarding CA-MRSA is inducible clindamycin resistance. CA-MRSA strains are reported to be resistant to erythromycin but susceptible to clindamycin. However, the possibility of emergence of clindamycin resistance during therapy exists. Simple laboratory testing using the erythromycin-clindamycin “D-zone” test can separate strains that have the genetic potential to become resistant during therapy from strains that are fully susceptible to clindamycin.

The D-zone test is performed by placing clindamycin and erythromycin at an edge-to-edge distance of 15 mm to 20 mm, and looking for flattening of the clindamycin zone nearest the erythromycin disk. A positive D-zone test suggests the presence of an erm gene that could result in constitutive clindamycin resistance and clinical failure.7,8

The Panton-Valentine leukocidin (PVL) toxin is present in approximately 77% of CA-MRSA strains and is rare in the HA-MRSA strains.6 The PVL toxin promotes lysis of human leukocytes and is associated with severe necrotizing hemorrhagic pneumonia and skin infections.

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