S15 Detection of bacteria in sputum following experimental rhinovirus infection is more common in COPD than controls subjects

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Introduction and Objectives

There is increasing evidence that the majority of acute exacerbations of COPD (AECOPD) are caused by virus infection, and rhinoviruses are the most frequently identified species. Bacteria are also responsible for AECOPD but the relationship between these two is poorly understood. To investigate this further bacterial culture was performed in sputum samples collected from GOLD stage II COPD subjects (n=9) and non-obstructed smoking (n=10) and non-smoking (n=11) controls enrolled in a rhinovirus challenge study.


Rhinovirus infection was confirmed with quantitative PCR performed on nasal lavage and sputum samples collected at baseline and days 3, 5, 9, 12, 15, 21 and 42 post virus inoculation. Semi-quantitative bacterial detection was performed in sputum samples by a CPA-accredited microbiological laboratory. Any subject that had bacteria detected on or after day 9 was defined as “bacteria positive” and those with none detected were defined “bacteria negative”. Species frequently associated with respiratory illness were defined as pathogenic (S pneumoniae, H influenzae, M catarrhalis and S aureus) and any others as non-pathogenic.


No bacteria were detected in baseline sputum samples. Peak virus load occurred on day 9 with maximum bacterial colonies identified on day 15. There were significantly more bacteria positive subjects in the COPD group (67%) with the majority of control subjects (81%) being classified as bacteria negative, (Abstract S15 figure 1, χ2 p=0.04). COPD subjects with bacteria detected at any time point in the study had significantly more pathogenic species in their sputum samples (n=8/8) compared to controls (n=1/9), (χ2 p=0.0001). No non-pathogenic bacteria were detected in COPD subjects.


Detection of bacteria is common after rhinovirus infection, with the peak occurring 6 days after maximum virus load. COPD subjects are more likely to have pathogenic bacteria detected than controls following virus infection. Mechanisms responsible for this phenomenon merit further investigation.

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