Viral, bacterial or both? Regardless, we need to treat infection in COPD

Abstract

@ERSpublications Specific prevention of infective exacerbations of COPD is required http://ow.ly/vdIIh Guidelines indicate that pharmacological treatment of chronic obstructive pulmonary disease (COPD) is based on bronchodilators with the addition of inhaled corticosteroids (ICS) in frequent exacerbators [1]. Although this recommendation is in accordance with the best evidence available, it does not take into account that more than half of the exacerbations are infective and infections are not adequately prevented or treated by ICS. In fact, no pharmacological treatment has been able to suppress all exacerbations and, on the contrary, the long-term use of ICS has been associated with higher airway bacterial load in stable COPD [2], and increased risk of pneumonia [3] and tuberculosis [4].Clinicians have always been aware that not all exacerbations of COPD are alike. Some must be treated with anti-infective agents while others respond better to systemic corticosteroids. Markers such as sputum colour and C-reactive protein levels are useful to differentiate exacerbations and guide therapy [5,6]. Recent studies have further characterised these different types of exacerbations, and identified bacterial, viral, inflammatory (eosinophilic) and pauci-inflammatory phenotypes of exacerbations, with the majority (59%) of exacerbations being bacterial or viral. Interestingly, the phenotype of the exacerbation remains constant in a given patient [7]. However, despite these different phenotypes of exacerbations, no studies have attempted to investigate whether different treatments would be more effective in preventing one type of exacerbation or another.Both the high bacterial load in the airways in stable COPD and an increased frequency of exacerbations have been associated with a more rapid decline in lung function and an impairment in quality of life [8][9][10]. More recently, the presence of bronchiectasis in patients with COPD [11] and the persistent colonisation by unusual microorganisms [12] have also been associated with increased mortality. These findings justify the identification of an ''infective phenotype'' that is usually a frequent exacerbator with mucous hypersecretion producing dark sputum during the stable state that is more abundant during exacerbations, and who requires frequent courses of antibiotics and probably demonstrates cylindrical bronchiectasis on computed tomography [13]. Treatment with bronchodilators and ICS never fully prevents infective exacerbations in this phenotype of patients.In order to treat patients with frequent infective exacerbations better, we need to understand the pathogenesis of acute and chronic bronchial infection in COPD. GEORGE et al. [14] studied sputum samples from 77 patients with COPD during the stable state and exacerbations, and used real-time quantitative PCR for both human rhinovirus (HRV) and usual respiratory bacteria. They found that HRV prevalence and load during exacerbation were significantly higher than in the stable state and no HRV was found 1 month after ...

C-reactive protein level and microbial aetiology in patients hospitalised with acute exacerbation of COPD

“…Although previous studies have demonstrated more severe respiratory symptoms, prolonged recovery times and higher levels of serum interleukin-6 levels in patients with virus-induced exacerbation compared to non-virus-induced exacerbations [9,26], our study is the first to show that CRP levels are strongly associated with viral rather than bacterial detection. Several other studies have examined CRP levels in § : despite a p-value of <0.1 on univariate analysis, this variable could not be added to the multivariate models due to the small number of outcomes (i.e.…”

Impact of baseline symptoms and health status on COPD exacerbations in the FLAME study

“…Therefore, whilst the present analysis has reaffirmed both the strong relationship between disease severity and exacerbation frequency, and the importance of dyspnoea in COPD patients, it appears that the intensity of other stable state symptoms is not a key driver of exacerbation symptom severity. This may be because exacerbation severity is largely driven by exacerbation triggers such as respiratory viruses and bacteria [37].…”

Role of infection in exacerbations of chronic obstructive pulmonary disease

“…There is enough evidence to suggest that a change in bacterial strain is associated with the initiation of an exacerbation, and that viral infection is associated with exacerbation and subsequent bacterial infection. It is possible that viral infection can lead to an infection by a new bacterial strain and both mechanisms could coexist in a given patient, but apparently both can initiate an exacerbation by themselves [6].…”

“…These bacteria contribute to chronic airway inflammation leading to COPD progression [2,4,5] and may be associated with exacerbations when they increase in concentrations in the airways, when there is a change in these strains or after a viral respiratory infection. These different mechanisms may be responsible for the development of a bacterial exacerbation of COPD [6].…”