The association of PCT with morbidity and mortality may be of clinical importance not primarily for outcome prediction but to monitor success of therapy. Current data support the hypothesis that a drop in PCT levels represents an adequate antimicrobial therapy and may actually define a time point where antibiotic treatment can be safely withdrawn [20, 21] . Recently, this has been Continuous data are given as median (interquartile range) or mean ± standard deviation. CAP, community acquired pneumonia; HAP, hospital acquired pneumonia; ICU, intensive care unit; PCT, procalcitonin; n.s., not significant; SOFA, sequential organ failure assessment; VAP, ventilator associated pneumonia. demonstrated in ICU patients with suspected bacterial infection at admission or during their ICU stay [22] . More than 70% of these patients had pulmonary infections. Unsuccessful source control and poor outcome is associated with persistently elevated PCTs which should negatively affect outcome [14, 34] . Thus, increasing PCT or persistently elevated PCT values should trigger a change in antimicrobial therapy. In this study of severe pneumonia in mechanically ventilated patients, there was no difference in PCT levels between culture positive and culture negative pneumonia. In another study on patients with severe pneumonia as defined by a high Pneumonia Severity Index (PSI), PCT correlated with outcome but could not differentiate between bacterial and nonbacterial etiology of pneumonia [35] . In 72 children with CAP, Moulin et al. found PCT levels > 2 ng/ml in all 10 patients with blood culture positive for S. pneumoniae; PCT concentration was greater than 1 ng/ml in 86% of patients with bacterial infection, with the highest percentage being in those with positive blood culture [36] . This PCT-threshold was more sensitive and specific than CRP, IL-6, or white blood cell count for differentiating bacterial and viral causes of pneumonia. Likewise, Boussekey et al. found higher PCT levels in microbiologically documented CAP (median 4.9 ng/ml vs 1.5 ng/ml if no bacteria were found), but PCT levels could not discriminate between specific bacterial agents [33] . Duflo et al. identified VAP based on a positive quantitative culture of 10 3 colony-forming units/ml or more obtained via a mini-bronchoalveolar lavage. Median PCT values of VAP survivors at baseline were 0.6 ng/ml in this study. This low PCT value questions the validity of currently used VAP diagnostic criteria. Luyt et al. found a similar low PCT of about 0.5 ng/ml in VAP survivors and doubted the usefulness of this parameter for diagnosis of VAP [19, 37] . The 28-day mortality of 8.2% in patients with VAP in our study was very low. The Canadian Critical Care Trials group recorded an overall 28 days mortality rate of 18.7% in a large cohort of patients where VAP was diagnosed using similar criteria as in our study [5] . However, mortality rates between 9.8 and 93.3% have been observed depending on the presence of risk factors such as coexisting diseases, presence of bacteremia, arterial hypotension, or ARDS [38] . The low mortality rate of VAP patients and low PCT-values in the VAP survivors in this study may reflect the uncertainty in correctly diagnosing VAP despite the requirement for a positive Gram stain of respiratory secretion. Although VAP is the most frequent cause of death in hospital for patients with respiratory failure [39, 40] , the diagnosis of VAP is difficult. The optimal invasive procedure for diagnosing HAP or VAP remains poorly defined [9, 10] . Indeed, one study demonstrated that 29% of clinically suspected VAP cases were disproved by autopsy results [41] . In this study, microbiological proof of infection was possible in about 67% of the patients. This is in good agreement with findings in large sepsis trials where microbiological proof was possible in 41 to 51% of the patients with airway infections [42, 43] .