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.