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48 0.036 Chronic liver disease 5.63 2.20 to 14.39 < 0.001 8.99 2.91 to 27.77 < 0.001 Fever 0.49 0.24 to 1.01 0.053 - - - Pneumonia severity index IV to V 4.77 1.43 to 15.91 0.011 - - - Multilobar infiltration 2.28 1.13 to 4.60 0.021 - - - Number of pathogens identifiedb ? ? 0.055 - - - ???None 1 - - ? ? ? ???Monomicrobial 1.56 0.72 to 3.38 0.26 - - - ???Polymicrobial 3.31 1.25 to 8.77 0.016 - - - Inappropriate empiric treatment 11.23 4.44 to 28.38 < 0.001 10.79 3.97 to 29.30 < 0.001 aHosmer-Lemeshow goodness-of-fit test, P = 0.81. bThe P value <a href="https://www.selleckchem.com/products/MS-275.html">selleck chemicals</a> corresponds to differences between the three groups (none, one or more than one pathogen). The odds ratio and 95% confidence interval (CI) of monomicrobial and polymicrobial pneumonia are related to cases with no pathogen identified. Among these variables, age �� 65 years, neurological disease, chronic liver disease and inappropriate antimicrobial treatment were independently associated with increased hospital mortality in the multivariate analysis. Discussion Polymicrobial aetiology was found in 11% of all patients with CAP admitted to the ICU, 20% considering those with defined aetiology only. Although S. pneumoniae was the most frequent pathogen in both groups, we found MRSA, P. aeruginosa, GNEB, H. influenzae, M. catarrhalis and respiratory viruses more frequently identified in polymicrobial pneumonia than in monomicrobial pneumonia. Chronic respiratory disease and ARDS criteria <a href="https://en.wikipedia.org/wiki/CASK">CASK</a> were independent predictors of polymicrobial aetiology. Although an independent predictor of hospital mortality such as inappropriate treatment <a href="https://www.selleckchem.com/products/bay80-6946.html">PI3K inhibitor</a> was more frequent in the polymicrobial aetiology group, the trend for higher hospital mortality in patients from this group was not statistically significant. In general populations of hospitalised patients with CAP, we have previously reported lower rates of polymicrobial pneumonia (5%) [3, 12] than in this series of ICU patients. Other studies on patients with CAP found 5.7% and 38.4% rates of polymicrobial aetiology in their series [4, 5]. These wide variations might be explained by differences in the populations studied, epidemiological settings, rate of antimicrobial pretreatment, microbiological workup and definitions of aetiology. A typical limitation of many studies dealing with microbial aetiology in CAP is that not all microbiological tests are applied systematically for all patients. This issue means that the real frequency of polymicrobial aetiologies could possibly be higher if a complete microbiological investigation was performed in all cases. In view of these methodological problems, it seems difficult to indicate precisely the extent of the problem of polymicrobial aetiology. Analysing the potential impact of polymicrobial aetiology is therefore more important, particularly in the most severely ill patients and in those at highest risk of death. S.

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