Recurrent <i>Pseudomonas aeruginosa</i> Pneumonia in  Ventilated Patients

Rello, Jordi; Mariscal, Dolors; March, Francesca; Jubert, Paola; Sanchez, Ferran; Vallès, Jordi; Coll, Pere

doi:10.1164/ajrccm.157.3.9703014

Cited by 131 publications

(72 citation statements)

References 15 publications

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“…Thus, persistence of micro-organisms in the ETT occurred in several cases even after apparently successful treatment of the previous nosocomial pneumonia. While this series is far too small to make any definitive comment, it would be interesting to speculate that colonization of the ETT may precede nosocomial pneumonia in a number of patients or, more importantly, be a persistent source of organisms that may cause recurrent pneumonia, much in the same way as it has been suggested in recent studies that recurrent P. aeruginosa pneumonia may be due to persistence and relapse of these strains in the lower respiratory tract [22].…”

Section: Discussionmentioning

confidence: 78%

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The presence and sequence of endotracheal tube colonization in patients undergoing mechanical ventilation

Feldman

Kassel²,

Cantrell³

et al. 1999

Eur Respir J

217

139

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Endotracheal tube colonization in patients undergoing mechanical ventilation was investigated.In the first part of this prospective study, the airway access tube was examined for the presence of secretions, airway obstruction and bacterial colonization, in cases undergoing extubation or tube change. In the second part of the study, the sequence of oropharyngeal, gastric, respiratory tract and endotracheal tube colonization was investigated by sequential swabbing at each site twice daily for 5 days in consecutive noninfected patients.In the first part, it was noted that all airway access tubes of cases undergoing extubation had secretions lining the interior of the distal third of the tube which were shown on scanning electron microscopy to be a biofilm. Gram-negative micro-organisms were isolated from these secretions in all but three cases. In the second part, it was noted that the sequence of colonization in patients undergoing mechanical ventilation was the oropharynx (36 h), the stomach (36±60 h), the lower respiratory tract (60±84 h), and thereafter the endotracheal tube (60±96 h). Nosocomial pneumonia occurred in 13 patients and in eight cases identical organisms were noted in lower respiratory tract secretions and in secretions lining the interior of the endotracheal tube.The endotracheal tube of patients undergoing mechanical ventilation becomes colonized rapidly with micro-organisms commonly associated with nosocomial pneumonia, and which may represent a persistent source of organisms causing such infections. Eur Respir J 1999; 13: 546±551.

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Section: Discussionmentioning

confidence: 78%

“…While regular ETT changes may seem appropriate, recent studies have suggested that this may be associated with a higher incidence of nosocomial pneumonia [4,22]. The reasons for this are not entirely clear, but may relate to the passing of the airway access tube through areas (e.g.…”

Section: Discussionmentioning

confidence: 99%

The presence and sequence of endotracheal tube colonization in patients undergoing mechanical ventilation

Feldman

Kassel²,

Cantrell³

et al. 1999

Eur Respir J

217

139

View full text Add to dashboard Cite

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“…One explanation for the appearance of resistant clones in the absence of antimicrobial exposure could be cross-colonization with a new strain from another patient (41). We therefore determined whether resistant and susceptible clones were genotypically related by performing RAPD analysis on 27 isolates from patient A ( Table 1) and 35 isolates from patient B ( Table 2).…”

Section: Resultsmentioning

confidence: 99%

Development and Persistence of Antimicrobial Resistance in Pseudomonas aeruginosa : a Longitudinal Observation in Mechanically Ventilated Patients

Reinhardt¹,

Köhler²,

Wood³

et al. 2007

Antimicrob Agents Chemother

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Intubated patients frequently become colonized by Pseudomonas aeruginosa, which is subsequently responsible for ventilator-associated pneumonia. This pathogen readily acquires resistance against available antimicrobials. Depending on the resistance mechanism selected for, resistance might either be lost or persist after removal of the selective pressure. We investigated the rapidity of selection, as well as the persistence, of antimicrobial resistance and determined the underlying mechanisms. We selected 109 prospectively collected P. aeruginosa tracheal isolates from two patients based on their prolonged intubation and colonization periods, during which they had received carbapenem, fluoroquinolone (FQ), or combined ␤-lactam-aminoglycoside therapies. We determined antimicrobial resistance phenotypes by susceptibility testing and used quantitative real-time PCR to measure the expression of resistance determinants. Within 10 days after the initiation of therapy, all treatment regimens selected resistant isolates. Resistance to ␤-lactam and FQ was correlated with ampC and mexC gene expression levels, respectively, whereas imipenem resistance was attributable to decreased oprD expression. Combined ␤-lactam-aminoglycoside resistance was associated with the appearance of small-colony variants. Imipenem and FQ resistance persisted for prolonged times once the selecting antimicrobial treatment had been discontinued. In contrast, resistance to ␤-lactams disappeared rapidly after removal of the selective pressure, to reappear promptly upon renewed exposure. Our results suggest that resistant P. aeruginosa is selected in less than 10 days independently of the antimicrobial class. Different resistance mechanisms lead to the loss or persistence of resistance after the removal of the selecting agent. Even if resistant isolates are not evident upon culture, they may persist in the lung and can be rapidly reselected.

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“…Although a high incidence of antibiotic resistance among P. aeruginosa strains contributes to the excess mortality associated with this bacterium, its intrinsic virulence also likely plays a role. Even VAP patients treated with antimicrobial agents to which their P. aeruginosa isolates were susceptible had a relapse rate of 18% (42). This suggests that P. aeruginosa elaborates potent virulence determinants that are adept at neutralizing the host immune response, resulting in persistent bacterial infections with poor outcomes.…”

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confidence: 99%

Pseudomonas aeruginosa Induces Localized Immunosuppression during Pneumonia

et al. 2008

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Hospital-acquired bacterial pneumonia is a common and serious complication of modern medical care. Many aspects of such infections remain unclear, including the mechanisms by which invading pathogens resist clearance by the innate immune response and the tendency of the infections to be polymicrobial. Here, we used a mouse model of infection to show that Pseudomonas aeruginosa, a leading cause of hospital-acquired pneumonia, interferes with the ability of recruited phagocytic cells to eradicate bacteria from the lung. Early in infection, phagocytic cells, predominantly neutrophils, are recruited to the lungs but are incapacitated when they enter the airways by the P. aeruginosa toxin ExoU. The resulting paucity of functioning phagocytes allows P. aeruginosa to persist within the lungs and results in local immunosuppression that facilitates superinfection with less-pathogenic bacteria. Together, our results provide explanations for previous reports linking ExoU-secreting P. aeruginosa with more severe pulmonary infections and for the tendency of hospital-acquired pneumonia to be polymicrobial.Hospital-acquired pneumonia (HAP) is a common and frequently lethal complication of admission to an acute medical care facility. HAP infections occur in 0.5 to 2% of hospitalized patients (30,33) and are associated with mortality rates of approximately 30% (6,13,41,54). HAP is usually caused by bacterial pathogens, and in 26 to 67% of cases the etiology is polymicrobial (3,8,39). While the reasons for this are unclear, the coexistence of multiple species of bacteria within the lungs of patients may contribute to the high mortality associated with this disease.The gram-negative bacterium Pseudomonas aeruginosa is the leading cause of HAP in patients undergoing mechanical ventilation (referred to as ventilator-associated pneumonia [VAP]) (40). Interestingly, infection with P. aeruginosa, as opposed to infection with most other bacterial species, is an independent risk factor for death in patients with VAP (23). Although a high incidence of antibiotic resistance among P. aeruginosa strains contributes to the excess mortality associated with this bacterium, its intrinsic virulence also likely plays a role. Even VAP patients treated with antimicrobial agents to which their P. aeruginosa isolates were susceptible had a relapse rate of 18% (42). This suggests that P. aeruginosa elaborates potent virulence determinants that are adept at neutralizing the host immune response, resulting in persistent bacterial infections with poor outcomes.Despite the severity of HAP caused by P. aeruginosa, much remains unknown about the mechanisms by which this bacterium persists in the lungs and causes the tissue damage and inflammation associated with pneumonia. P. aeruginosa elaborates a number of virulence factors that may augment the disease process (12, 45), including a type III secretion system, which has been associated with more-severe disease in patients with HAP (18,44). Via a type III secretion system, some strains of P. aeruginosa injec...

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Recurrent Pseudomonas aeruginosa Pneumonia in Ventilated Patients

Cited by 131 publications

References 15 publications

The presence and sequence of endotracheal tube colonization in patients undergoing mechanical ventilation

The presence and sequence of endotracheal tube colonization in patients undergoing mechanical ventilation

Development and Persistence of Antimicrobial Resistance in Pseudomonas aeruginosa : a Longitudinal Observation in Mechanically Ventilated Patients

Pseudomonas aeruginosa Induces Localized Immunosuppression during Pneumonia

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