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Long Term Chronic Pseudomonas aeruginosa Airway Infection in Mice
Published on: March 17, 2014
Persistent infection with Pseudomonas aeruginosa in ventilator-associated pneumonia
Ali A El Solh1, Morohunfolu E Akinnusi, Jeanine P Wiener-Kronish
1Western New York Respiratory Research Center, Department of Medicine, State University of New York at Buffalo School of Medicine and Biomedical Sciences, Buffalo, New York 14215, USA. solh@buffalo.edu
Rationale:
Pseudomonas aeruginosa is one of the leading causes of gram-negative ventilator-associated pneumonia (VAP) associated with a mortality rate of 34 to 68%. Recent evidence suggests that P. aeruginosa in patients with VAP may persist in the alveolar space despite adequate antimicrobial therapy. We hypothesized that failure to eradicate P. aeruginosa from the lung is linked to type III secretory system (TTSS) isolates.
Objectives:
To determine the mechanism by which infection with P. aeruginosa in patients with VAP may evade the host immune response.
Methods:
Thirty-four patients with P. aeruginosa VAP underwent noninvasive bronchoalveolar lavage (BAL) at the onset of VAP and on Day 8 after initiation of antibiotic therapy. Isolated pathogens were analyzed for secretion of type III cytotoxins. Neutrophil apoptosis in BAL fluid was quantified by assessment of nuclear morphology on Giemsa-stained cytocentrifuge preparations. Neutrophil elastase was assessed by immunoenzymatic assay.
Measurements And Main Results:
Twenty-five out of the 34 patients with VAP secreted at least one of type III proteins. There was a significant difference in apoptotic rate of neutrophils at VAP onset between those strains that secreted cytotoxins and those that did not. Neutrophil elastase levels were positively correlated with the rate of apoptosis (r = 0.43, P < 0.01). Despite adequate antimicrobial therapy, 13 out of 25 TTSS(+) isolates were recovered at Day 8 post-VAP, whereas eradication was achieved in all patients who had undetectable levels of type III secretion proteins.
Conclusions:
The increased apoptosis in neutrophils by the TTSS(+) isolates may explain the delay in eradication of Pseudomonas strains in patients with VAP. Short-course antimicrobial therapy may not be adequate in clearing the infection with a TTSS secretory phenotype.
Insights
Pseudomonas aeruginosa with type III secretion systems (TTSS) causes persistent ventilator-associated pneumonia (VAP). TTSS strains increase neutrophil apoptosis, hindering bacterial eradication and potentially requiring longer antimicrobial therapy for VAP patients.
Area of Science:
- Infectious Diseases
- Microbiology
- Immunology
Background:
- Pseudomonas aeruginosa is a primary cause of gram-negative ventilator-associated pneumonia (VAP), carrying a high mortality rate.
- P. aeruginosa in VAP patients can persist in the lungs despite appropriate antibiotic treatment.
- The type III secretory system (TTSS) is hypothesized to play a role in this persistence.
Purpose of the Study:
- To investigate the mechanism by which P. aeruginosa VAP evades the host immune response.
- To determine if TTSS isolates are linked to the failure of bacterial eradication in VAP.
Main Methods:
- Bronchoalveolar lavage (BAL) samples were collected from 34 VAP patients at VAP onset and Day 8.
- Analysis included pathogen identification, type III cytotoxin secretion, neutrophil apoptosis quantification, and neutrophil elastase assessment.
Main Results:
- Twenty-five of 34 patients had P. aeruginosa isolates secreting type III proteins (TTSS+).
- TTSS+ strains showed a significant difference in neutrophil apoptosis rates compared to non-secretors.
- Neutrophil elastase levels correlated positively with apoptosis rates (r = 0.43, P < 0.01).
- Thirteen of 25 TTSS+ isolates persisted at Day 8, while all TTSS-negative isolates were eradicated.
Conclusions:
- Increased neutrophil apoptosis induced by TTSS+ P. aeruginosa may delay bacterial eradication in VAP.
- Short-course antimicrobial therapy might be insufficient for infections involving TTSS-secreting strains.
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