Volume 17, Supplement 2, 2009
Review
Bacteria and biofilm in respiratory tract infections
Drago Lorenzo
Biofilm is a structured community of bacterial cells included in a self-produced polymeric matrix adherent to an inert or living surface. The main property of biofilm consists of making microrganisms more resistant to exogenous insults. Antibiotic therapy typically resolves symptoms determined by planktonic cells released by biofilms but is not able to eradicate and completely clear biofilm. This is why infections sustained by biofilm-producer bacteria are often recurrent, making mandatory repeated antibiotic treatments. The typical conformation of biofilm, the phenotypical and genetical features existing among the different microrganisms confer a natural resistance to a number of antimicrobials so that it is necessary to test antimicrobial activity against the microbial species itself and also against biofilm, when it is present. Comparative studies, performed on quinolones and β-lactams, evidenced a significant activity against biofilm produced by pneumococci, haemophyli and pseudomonas as well.
Acute bacterial exacerbation of chronic obstructive pulmonary disease and biofilm
Legnani Delfino
The lower respiratory tract of patients affected by COPD is constantly colonized by pathogenic microrganisms such as H. influenzae, M. catarrhalis and S. pneumoniae. Role of bacterial colonization of big and small airways in patients affected by COPD is still unclear but it is likely to play a role in directly or indirectly maintaining the vicious circle of infection/inflammation.
Colonizer pathogens are capable to stimulate mucus production, to alter the ciliary function by inducing
dyskinesia and stasis; in addition, they represent a strong stimulus for neutrophils to come in the airways, which release elastase that, in turn, inhibit the mucus-ciliary function. The same pathogens are responsible for epithelial damage and chronic inflammation, by releasing neutrophilic elastase, leading to the damage progression and obstruction.
Recent studies have also shown that infection sustained by H. influenzae is not limited to bronchial mucosa, i.e. surface epithelial cells, but that the pathogen is capable to penetrate cells, so spreading the infection in sub-epithelial cellular layers.
In addition, the ability to produce biofilm is another possible defence mechanism which allows them to grow and colonise.
Such a mechanism could in part explain the lack of response to antimicrobials and contribute to stimulation of parenchymal inflammatory response, the cause of pathological-anatomic damage which occurs in COPD. The impossibility to eradicate chronic infection and bacterial exacerbations of COPD are likely the elements that prompt and worsen obstruction, so determining the disease’s progression.
