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Cystic Fibrosis is the most common inherited disease among Caucasians.  CF is an autosomal recessive disease caused by a mutation in the gene that codes for the cystic fibrosis transmembrane regulator (CFTR) located on chromosome 7.   The CFTR is a channel that transports Cl- ions across cell membranes. A missing or malfunctioning CFTR can cause major problems in sweat production, the lungs, the pancreas and the passageways of other organs.mo
The airway secretions of individuals with CF are thick and viscous resulting in chronic bacterial lung infection that is difficult to eradicate.  CF patients are often infected with Pseudomonas aeruginosa, Burkholdaria cepacia, but S. aureus was the first pathogen recognized in CF patients.  As the first invader on the scene, S. aureus binds this thick mucosa and continues to infect its host by adherence to respiratory epithelium and its ability to produce a variety of virulence factors which aid in the evasion of immune response (ref, Gilligan). This initial infection caused by S. aureus sets the stage for subsequent infections caused by other pathogens such as, P. aeruginosa. Before the discovery of antibiotics , lung infections due to S. aureus was the major cause of death in pediatric CF patients {Miller, 2003 #147} .  
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}, and CA-MRSA has been reported {Elizur, 2007 #150} in this population, but the impact of the CA strain has yet to be determined.