Microbiology

Using traditional culture techniques pathogenic microorganisms are isolated in 2/3 to ¾ of patients with bronchiectasis, although we now know from modern molecular techniques sequencing the 16s bacterial ribosomal RNA gene (16s rRNA) that a large and diverse bacterial community is present in the bronchiectasis airway even in patients without detectable bacteria on routine culture.[51,52] Bacterial infection drives the “vicious cycle” of bronchiectasis consisting of bacterial infection, airway inflammation and airway damage.[53] The most frequently isolated organisms in patients with non-CF bronchiectasis are Haemophilus influenzae, Pseudomonas aeruginosa, Moraxella catarrhalis, Streptococcus pneumoniae and Staphylococcus aureus.[12,37,54] Less frequently isolated pathogens include Aspergillus species, enteric gram negative organsisms, methicillin resistant Staphylococcus aureus and non-tuberculous mycobacteria as discussed previously. The frequency of pathogens isolated in selected studies of adults with bronchiectasis is shown in Table 3.

Table 2. Reported frequency of bacterial isolates in adult patients using culture based techniques in non-CF bronchiectasis. ND= not done. Dashes indicate data not reported. Some percentages may add up to more than 100% as frequently patients culture more than one organism.

Hi= Haemophilus influenzae, PA= Pseudomonas aeruginosa, Sa= Staphylococcus aureus, Sp= Streptococcus pneumonia, Mc= Moraxella catarrhalis, ASP= Aspergillus species, Myco= Mycobacterium , NP= no pathogens isolated.

Bacteria in the airway are the primary drivers of the neutrophil mediated airway inflammation that is characteristic of bronchiectasis. Neutrophils are by far the most numerous immune cell type found in the airway lumen. While neutrophils are required to control bacteria in the lung, their response also contributes directly and indirectly to lung damage.[42] Large numbers of neutrophils and evidence of neutrophil degranulation can be detected in patients with clinically stable bronchiectasis, [37,68] while numbers further increase during exacerbation. Activated neutrophils release large amounts of proteinases and toxic granule products including elastase into the airways.[37] Proteolytic damage is an important contributing factor in airway remodelling and overall progression of the disease and also contributes indirectly to bacterial infection by disabling neutrophil functions and other innate immune mechanisms.[42]