Introduction The leading cause of COPD in developed nations is exposure to tobacco smoke. COPD is characterised by acute periods of exacerbation, which are often bacterial in aetiology. The direct effect of cigarette smoke on bacteria present in the COPD lung, and how this may drive disease progression, has not been determined. This preliminary study aimed to determine the effect of cigarette smoke extract (CSE) on the growth and antibiotic susceptibility of COPD bacterial lung pathogens.

Methods CSE was prepared as described previously. Briefly, smoke from one, two, three or four cigarettes was bubbled through 100 mls growth medium. Bacterial type strains (Pseudomonas aeruginosa, Moraxella catarrhalis, Streptococcus pneumoniae, Prevotella spp and Haemophilus influenzae) were inoculated into growth medium +/- CSE and incubated either aerobically or anaerobically (Prevotella spp). Total viable counts (TVC cfu/ml) were estimated from 0–48 hrs (aerobes) and 0–72 hrs (Prevotella spp). Changes in minimum inhibitory concentration (MIC) of antibiotics used in the treatment of respiratory infections were determined by E-Test®, in bacterial cultures exposed daily to CSE over 12 days.

Results The growth of P.aeruginosa, S. pneumoniae and H. influenzae were not completely inhibited by any concentration of CSE; however a reduction in growth rate at higher concentrations was observed. M. catarrhalis growth was completely inhibited by two cigarettes/100 ml growth medium. No difference in growth was observed between Prevotella spp +/- CSE. A marked increase in P.aeruginosa resistance to tetracycline and doxycycline was observed after repeated CSE exposure: resistance to tetracycline and doxycycline increased from 24 to >256 μg/ml, and 48- >256 μg/ml, respectively.

Conclusions The growth of principal bacteria isolated from COPD patients were not affected by concentrations of CSE utilised in this study, but changes in the susceptibility of P. aeruginosa to tetracyclines was observed. This increase in resistance may be mediated by efflux pump up-regulation, and may lead to cross-resistance with other antibiotics. Work currently underway aims to determine whether CSE induces other key phenotypic changes (virulence factor expression and/or biofilm production) which might enhance the pathogenicity of these bacteria in the presence of CSE and result in poorer outcomes for patients with COPD.