Biomedical Engineering Reference
In-Depth Information
significant duration and concluded that antibiotic therapy offered a small
but significant benefit in outcome in acute exacerbations (48).
Recent studies have re-examined the effects of bacteria at acute exacer-
bation with more detailed evaluation of the nature of the COPD exacerba-
tion and bacterial culture. Stockley et al. (49) showed that COPD
exacerbations associated with purulent sputum are more likely to produce
positive bacterial cultures than exacerbations where the sputum production
was mucoid. Sethi et al. (50) have shown that exacerbations associated with
H. Influenzae and B. catarrhalis are associated with significantly higher levels
of airway inflammatory markers and neutrophil elastase, compared to
pathogen-negative exacerbations. Miravitlles et al. (51) also showed that
the patients with a highest degree of functional impairment were more likely
to have P. aeruginosa and H. influenzae isolated, though this group of
patients also are more likely to have airway bacterial colonization. However,
the degree of airway bacterial load may be a more important determinant of
airway infection at exacerbation rather than the type of bacteria isolated, as
different types of bacteria and different strains may be present in individual
patients at exacerbation, especially those with more severe COPD. With anti-
biotic therapy, bacterial load and airway inflammation decrease and the rate
of resolution of the airway inflammatory changes and thus exacerbation
recovery has been related to the clearance of bacteria from the sputum (52).
Bandi et al. (53) have reported that different strains of H. influenzae
were recovered from the upper and lower airway in patients with chronic
bronchitis. At exacerbation, there was a low recovery of H. influenzae in
the lower airway due to early administration of antibiotics but, in 87% of
biopsies taken from acute exacerbations in intubated patients, H. influenzae
could be detected intracellularly. Thus, during an exacerbation, there is
intracellular invasion of H. influenzae and this will contribute to the
increased airway inflammation associated with exacerbation. However, in
view of the presence of airway bacterial colonization, detection of bacteria
at exacerbation does not prove the bacterial etiology of the exacerbation
and important virus-bacterial interactions may exist and require further
study. Recently, Sethi et al. (54) have suggested that isolation of a new
bacterial strain in COPD patients who were regularly sampled was
associated with an increased risk of an exacerbation, though this also does
not conclusively prove that bacteria are direct causes of exacerbations.
V. OTHER INFECTIVE AGENTS—CHLAMYDIA PNEUMONIAE
There has been some controversy about the role of C. pneumoniae at COPD
exacerbation. Using IgM and IgG antibody titres, C. Pneumoniae has been
identified as the etiologic factor in 5% of COPD exacerbations in outpatients
(55). This is similar to the results obtained by Blasi et al. (56) who identified
