Short-course Fluoroquinolones in Acute Exacerbations of Chronic Bronchitis

Mark H Gotfried; Ronald F Grossman

Disclosures

Expert Rev Resp Med. 2010;4(5):661-672. 

In This Article

Etiology

Acute exacerbations of chronic bronchitis can be triggered by air pollutants, allergens, irritants (e.g., dust, cigarette smoke), temperature changes and infectious agents (viral and bacterial pathogens).[3,5,7,101] Bacterial and viral infections of the lower respiratory tract account for approximately 80% of all AECB episodes.[5,8] There is significant overlap between AECB and acute exacerbations of chronic obstructive pulmonary disease (COPD). Most antimicrobial intervention studies include patients with and without airflow obstruction that might be associated with COPD, but the two populations are not often clearly separated or identified. For this article, we have chosen to focus on AECB, consistent with the definitions used in the studies we have included, which did not provide baseline spirometry measurements for the study population. Furthermore, the distinction between colonization and infection are often not well defined in these studies. The distinction between the two is also not clear, as approximately 25% of patients with COPD are colonized, while about 50% of those with AECB are colonized. The etiology of AECB is shown in Figure 1.[5]

Figure 1.

Etiology of acute exacerbations of chronic bronchitis. The infectious causes, including Gm+ and Gm bacteria, respiratory viruses and atypical bacteria, as well as noninfectious causes of acute exacerbations of chronic bronchitis were identified in patients with acute exacerbations of chronic bronchitis.
Gm+: Gram-positive; Gm: Gram-negative.
Reproduced with permission from [5].

Bacterial pathogens, including common Gram-positive and Gram-negative bacteria and atypical respiratory pathogens, are estimated to account for 50–70% of infection-related acute exacerbations.[4] The predominant bacterial pathogens implicated in AECB are Haemophilus influenzae, which is present in 50% of all bacterial exacerbations, and Streptococcus pneumoniae and Moraxella catarrhalis, found in approximately a third of isolates.[9]Pseudomonas aeruginosa and other Gram-negative bacilli, such as Enterobacteriaceae, are more prevalent in patients with severe impairment of lung function.[4,10,11] Atypical pathogens, Mycoplasma pneumoniae and Chlamydophila pneumoniae, are identified in as many as 5–10% of AECB, although the role of Mycoplasma is questionable.[8] Viral causes of AECB account for 30–50% of cases.[9] The most commonly detected viral pathogen in AECB is rhinovirus, although influenza and parainfluenza are also implicated. In addition, many bacterial exacerbations are preceded by a viral infection.[4,12]

Many pathogens involved in AECB have developed resistance to commonly used antimicrobials, including β-lactams and macrolides.[5,13,14] β-lactamase-mediated resistance to amoxicillin and variable trimethoprim–sulfamethoxazole resistance by region were noted in H. influenzae.[5,14] High resistance of S. pneumoniae to penicillin, azithromycin (and other macrolides), cefuroxime and trimethoprim–sulfamethoxazole, and emerging resistance of M. catarrhalis to β-lactams, also have been observed in AECB.[5,14]

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