We carried out a comprehensive microbiological study of the upper and lower airways in patients with severe exacerbations of chronic obstructive pulmonary disease (COPD) requiring mechanical ventilation in order to describe microbial patterns and analyze their clinical significance. Quantitative cultures of tracheobronchial aspirates (TBAs), bronchoscopically retrieved protected specimen brush (PSB) and bronchoalveolar lavage fluid (BALF) at admission to the ICU and after 72 h, as well as serology for bacteria and respiratory viruses were performed. Fifty patients (mean age 68 +/- 8, 46 males) were studied prospectively. Potentially pathogenic microorganisms (PPMs) and/or a positive serology were present in 36 of 50 (72%) patients, including 12 (33%) polymicrobial cases. Only six (12%) had no pathogen in any sample in the absence of antimicrobial pretreatment. Microbial patterns corresponded to community-acquired pathogens (Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis) in 19 of 34 (56%) and to gram-negative enteric bacilli (GNEB), Pseudomonas, and Stenotrophomonas spp. in 15 of 34 (44%) of isolates. Chlamydia pneumoniae and respiratory viruses were found in 18% and 16% of investigations, respectively. Repeated investigation after 72 h in 19 patients with PPMs in the initial investigation revealed eradication of virtually all isolates of community-acquired pathogens and GNEB but persistence of three of five Pseudomonas spp. and both Stenotrophomonas spp. as well as the emergence of new GNEB, Pseudomonas and Stenotrophomonas spp. Clinical parameters neither predicted the presence of PPMs nor of GNEB and Pseudomonas/Stenotrophomonas spp. Nevertheless, severe pneumonia attributable to initially isolated pathogens occurred in two patients with severe COPD exacerbation. We conclude that pathogens were more frequently present than previously reported. The rate of GNEB and Pseudomonas/Stenotrophomonas spp. isolates was high. The presence of pathogens was clinically unpredictable. Thus, in this population of patients with severe exacerbations of COPD, it may be advisable to obtain respiratory samples and to treat according to diagnostic results. Further studies are warranted to clarify this issue.
The effect of bacterial colonization of the bronchi on the progress of airflow limitation is not well known. Therefore, the pattern of airway inflammation in smokers and patients with stable chronic obstructive pulmonary disease (COPD) and its relation to bronchial microbial colonization was assessed.Eight nonsmoking and 18 smoking controls as well as 52 patients with COPD (28 mild, 11 moderate and 13 severe) were studied. All subjects were investigated by means of flexible bronchoscopy including protected specimen brush and bronchoalveolar lavage (BAL) sampling. Differential cell counts, cytokine (interleukin (IL)-1b, IL-6, IL-8, IL-10 and tumour necrosis factor-a (TNF-a) concentrations and microbial patterns were determined in BAL fluid.Forced expiratory volume in one second (FEV1) % of the predicted value was inversely correlated with pack-yrs of cigarette smoking (r=-0.47, p<0.0001), the percentage of neutrophil (r=-0.56, p<0.0001) and IL-6 (r=-0.37, p=0.01) and IL-8 concentration (r=-0.43, p=0.004) in BAL fluid. Accordingly, pk-yrs of cigarette smoking (r=0.39, p=0.01) and IL-8 (r=0.69, p<0.0001) and TNFa (r=0.4, p<0.005) were positively correlated with the percentage of neutrophils in BAL fluid. Smoking controls and COPD patients were mainly colonized in the bronchial tree (33%) by community endogenous potentially pathogenic micro-organisms (PPMs). Colonization rates and patterns of PPMs were not affected by severity of airflow obstruction. The presence of PPMs was significantly associated with higher percentages of neutrophils (33.210.4% versus 10.13.5%, p=0.02) and TNF-a concentration (29.910.8 versus 6.32.1 pg . mL -1 , p=0.01) in BAL fluid.In conclusion, bronchial neutrophilia is a key inflammatory pattern in chronic obstructive pulmonary disease patients. Bronchial colonization with potentially pathogenic micro-organisms may represent an independent stimulus for additional airway inflammation.
In contrast to the healthy population, distal airway bacterial colonization may occur in patients with chronic lung diseases, who often have altered pulmonary defences. However, the information dealing with this issue is insufficient and is based mainly on nonspecific samples, such as sputum cultures.Using quantitative cultures of bronchoscopic protected specimen brush (PSB) and bronchoalveolar lavage (BAL) samples, we studied the bacterial colonization of distal airways in 16 healthy subjects, 33 patients with bronchogenic carcinoma, 18 with chronic obstructive pulmonary disease (COPD), 17 with bronchiectasis, and 32 with a long-term tracheostomy due to laryngeal carcinoma. All patients were without exacerbation, and free from antibiotic treatment at least 1 month before the study protocol. Thresholds for quantitative cultures to define colonization were ≥10 2 colony-forming units (cfu)·mL -1 for PSB and ≥10 3 cfu·mL -1 for BAL.Only one healthy subject was colonized by a potential pathogenic microorganism (PPM) (Staphylococcus aureus 4×10 2 cfu·mL -1 in a PSB culture). Colonization was observed in 14 (42%) bronchogenic carcinoma patients (19 non-PPMs, and 10 PPMs); in 15 (83%) COPD patients (22 non-PPMs and 7 PPMs); in 15 (88%) bronchiectasis patients (20 non-PPMs and 13 PPMs); and in 15 (47%) long-term tracheostomy patients (5 non-PPMs and 13 PPMs). The two most frequent nonPPMs isolated in all groups studied were Streptococcus viridans and Neisseria spp. Haemophilus spp., Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis were the most frequent PPMs isolated in bronchogenic carcinoma, COPD, bronchiectasis and long-term tracheostomized patients, respectively. Pseudomonas aeruginosa colonization was infrequent in all the groups.Our results show that distal airway bacterial colonization is a frequent feature in stable patients with chronic lung diseases and also in patients with long-term tracheostomy. However, the pattern of colonization differs among groups studied. The knowledge of different colonization patterns may be important for future antibiotic prophylactic strategies and for the empirical antibiotic regimens when exacerbations occur in these patients.
The aetiopathogenesis of ventilator-associated pneumonia (VAP) requires abnormal oropharyngeal and gastric colonization and the further aspiration of their contents to the lower airways. VAP develops easily if aspiration or inoculation of microorganisms occur in patients with artificial airways, in whom mechanical, cellular and/or humoral defences are altered.Well-known risk factors for gastric colonization include: alterations in gastric juice secretion; alkalinization of gastric contents; administration of enteral nutrition; and the presence of bilirubin. However, the role of the colonized gastric reservoir in the development of VAP remains debatable.Evidence in favour of the role of the stomach in the development of VAP comes mainly from randomized, controlled trials of selective gut decontamination and stress ulcer prophylaxis in the intensive care unit (ICU), in which reducing the bacterial burden of the stomach decreases the incidence of nosocomial respiratory infections. However, at least three studies of flora have found an absence of stomach origin of pneumonia occurring during mechanical ventilation.Prophylactic measures suggested to prevent VAP in relation to the gastric reservoir include: treatment for stress ulcers with sucralfate; prevention of duodenal reflux with metoclopramide; reduction of gastric burden and bacterial translocation by selective digestive decontamination; acidification of enteral feeding; and jejunal feeding. Gastro-oesophageal reflux can be prevented by using small bore nasogastric tubes and jejunal feeding. The aspiration of gastric contents can be reduced by positioning patients in a semirecumbent position, checking the patency of the tube cuff, and aspiration of subglottic secretions.The role of the stomach as a reservoir for microorganisms causing ventilatorassociated pneumonia is still controversial but despite the debate, there is major evidence in the literature in favour of the gastric origin of part of these pulmonary infections.
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