BACKGROUND
Individuals with cystic fibrosis (CF) have decreased quantity and/or function of cystic fibrosis transmembrane conductance regulator (CFTR) protein located in cell membranes.1 This defect results in abnormal movement of sodium, chloride, and water across epithelial surfaces throughout the body. In the lungs, abnormal airway surface liquid leads to a vicious cycle of inflammation, obstruction, and infection. Infection with methicillin-susceptibleStaphylococcus aureus (MSSA) and methicillin-resistantStaphylococcus aureus (MRSA) tend to predominate early in life but infection shifts with age so that the majority people with CF eventually become infected with chronic Pseudomonas aeruginosa(PA).1,2 Antimicrobial therapy is essential in managing acute and chronic CF lung infections.3
CF-specific airway pathophysiology and chronic and/or frequent acute antimicrobial exposure lead to clinical challenges when managing infection. Chronic infections and hypoxia increase inflammatory processes which may result in progressive lung damage.4-5 CF lung infection is usually polymicrobial and interactions between microorganisms increase the risk of antimicrobial resistance. 4 Pseudomonas aeruginosa has increased virulence in CF lung infection secondary to the development of a mucoid phenotype, alginate biofilms and adaptive resistance mechanisms.5-6 These adaptive resistance mechanisms include modifications in targeted binding sites, efflux pumps, and the production of inactivating enzymes.7Additionally, studies have demonstrated there are limitations of oropharyngeal sampling and the challenges associated with this sampling method compared to expectorated sputum.8 This may contribute to variability with isolate surveillance and resistance trends over time. The combination of bacterial and host factors decreases the efficacy of treatments by impeding drug delivery, altering pharmacokinetics and increasing the risk of antimicrobial resistance.4,9,10
Empiric antibiotic selection for the management of pulmonary exacerbations is generally based on hospital-wide antibiograms (HWA). However, most HWA exclude culture antimicrobial susceptibility data from CF isolates. This creates challenges in determining appropriate empiric antibiotic therapy and monitoring for changes in susceptibility patterns over time. This work demonstrates why CF care centers should develop independent CF-specific antibiogram (CFA) for use in clinical practice.