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After the discovery of penicillin in the 1940’s, infections due to S. aureus began to decline. However, by 1961 resistance was discovered in nosocomial isolates of S. aureus (ref, Jevons). The prevalence of methicillin-resistant S. aureus is on the rise in all populations. Many studies describe MRSA infections in CF patients {Ren, 2007 #149}. In children with CF, it was found that a MRSA infection did not affect lung function, but it had the potential to affect lung growth and these patients received significantly more courses of intravenous antibiotics and had worse chest x-rays (ref, Miall). CA-MRSA has been reported {Elizur, 2007 #150} in this population, but the impact of the CA strain has yet to be determined. 
Like the HA strain, CA-MRSA carry the mecA gene which codes for methicillin resistance. The HA-MRSA strain is often SCCmec type II while the CA-MRSA strain is type IV. Unlike the HA strain, CA-MRSA produces the PVL toxin.  PVL is a two component pore forming toxin complex encoded by two co-transcribed genes (lukS-PV and lukF-PV) that cause tissue necrosis and leukocyte destruction (Finck-Barbancon et al., 1993; Supersac et al., 1993; Prevost et al., 1995). Recent studies have shown that PVL is a key virulence factor in pulmonary infections and as demostrated in a murine model, it was sufficient enough to cause necrotizing pneumonia (ref, Labandeira-Rey).
Although, CA-MRSA strains are more susceptible to antibiotics than HA-MRSA, CA-MRSA often produce more toxins and are more virulent. Since CF patients are often treated with long-term therapy and there is often clonal spread of organisms among the population, it is useful to know which MRSA strain is present.