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The investigators studied the high mortality figures in Pseudomonas VAP and evaluated causes of microbial persistence in the alveolar space despite adequate antimicrobial therapy.
Microbial persistence in respiratory airways of pathogens implicated in VAP, even with an appropriate antibiotic therapy, has been related to the lack of response to treatment and to the relapse of VAP [ 25, 26].
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Microbial persistence was detected in 9 (64%) patients with VAP.
Enterococcus faecalis Aggregation Substance (Asc10) protein enhances the severity of experimental endocarditis, where it has been implicated in formation of large vegetations and in microbial persistence during infection.
The bacteria most frequently implicated in microbial persistence were A. baumannii and P. aeruginosa (seven of the nine cases).
Biofilm stands as a pathogenic mechanism for microbial persistence, and impaired response to treatment in VAP.
In this situation, microbial persistence and impaired response to treatment (treatment failure and relapse) were more frequent (100% vs 29%, P = 0.021; 57% vs 14%, P = 0.133).
Bacterial survival in ETT biofilm can promote VAP microbial persistence and consequently affect patient prognosis.
The presence of autoantibodies and the evolution toward chronic liver inflammation in the absence of long-term microbial persistence suggested the possibility of an autoimmune origin to the liver disease.
However, no attempt has been performed in order to assess the relationship among biofilm, microbial persistence and outcome of the VAP episode.
Microbial persistence was defined as the persistence of the causative microorganism of the VAP episode in at least two successive respiratory samples, despite 72 hours of proper antibiotic therapy irrespective of colony counts [ 35].
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