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

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.

Different syndromes due to CA-MRSA include: furuncles, impetigo, scalded skin syndrome, pneumonia, endocarditis, and toxic shock syndrome as well as septic arthritis and osteomyelitis. Prosthetic joint infections are an increasingly difficult management problem due to MRSA, and finally, necrotizing soft tissue infections due to CA-MRSA have been reported.9 HA-MRSA strains are mostly associated with nosocomial pneumonia, catheter-related urinary tract infections, IV catheters, bloodstream infections, and, less commonly, SSTIs.2

Table 1 illustrates the differences between CA-MRSA and HA-MRSA strains.2,10 It is important for clinicians to understand these differences in order to institute appropriate therapy.

Conclusion
CA-MRSA is increasing in prevalence at an alarming rate. This organism has spread throughout the entire United States in a matter of 2 or 3 years. Some of these infections are associated with increased severity, such as necrotizing infections, S. aureus, toxic shock syndrome, and fulminant necrotizing hemorrhagic pneumonia, particularly following influenza. In addition, CA-MRSA is resistant not only to methicillin but also to a number of other agents (such as erythromycin, fluoroquinolones, and clindamycin) that are commonly used to treat community-acquired SSTIs.