Abstract Rationale Ventilator-associated pneumonia (VAP) remains one of the most frequent and morbid hospital-acquired infections in the ICU. While individual microbial or host-response factors have been explored, the combined influence of microbiological, immunological, clinical, and biochemical characteristics on VAP development is not well defined. Objectives To identify and integrate microbiological pathogens, host immune responses, clinical risk factors, and biochemical biomarkers associated with the development of VAP in mechanically ventilated adults. The selected sample included adult patients admitted to the ICU of two hospitals in Chía, Colombia, who required invasive mechanical ventilation due to respiratory failure of non-infectious origin, without evidence of pneumonia at the time of admission, and who had approval to participate in the study. Methods We conducted a prospective cohort study of mechanically ventilated ICU patients without pneumonia at baseline. Serial lower respiratory tract cultures, plasma inflammatory markers, and routine biochemical panels were collected from intubation through day 7. Microbiological profiles were characterized using culture and PCR-based assays through either tracheal aspirates or bronchoalveolar lavage. Immunological assessment included measurements of arterial blood gases, procalcitonin, and CRP. Clinical variables included demographics, comorbidities, ventilator parameters, sedation practices, hemodynamic instability, and antibiotic exposure. Patients who developed VAP (CDC/NHSN criteria) were compared with those who did not. Results Among 141 patients, 33.3% developed VAP at 3 days after intubation (n = 23), 5 days (n = 10), and 7 days (n = 7). About 42.6% received empiric antibiotics, which mostly were cefazolin (n = 28), ceftriaxone (n = 15), ampicillin-sulbactam (n = 14), and vancomycin (n = 9). VAP cases were more likely to have demonstrated significantly higher levels of CRP preceding diagnosis with area under the curve 0.711 (p 0.01). Biochemically, elevated lactate at day 5 and worsening inflammatory indices were early markers of VAP onset. In multivariable models, prolonged mechanical ventilation were the strongest predictors of VAP. In-hospital mortality was not influenced by development of VAP in multivariable regression (aOR: 1.226 0.572-2.626). Conclusions The development of VAP is driven by a complex interplay of microbial colonization, heightened systemic inflammation, adverse clinical conditions, and early biochemical deterioration. Integrating these domains may improve early risk stratification and guide preventative strategies. Future work should validate a multidimensional prediction model to identify high-risk patients prior to clinical onset. This abstract is funded by: None
Asghar et al. (2026) studied this question.