As previously stated, the lack of uniformly accepted diagnostic criteria for VAP has led to variability in publically reported rates, difficulty in determining accurate causes, epidemiology, prevention measures, and effective treatment. The Infectious Disease Society of America (IDSA) and American Thoracic Society (ATS) define VAP as pneumonia that develops more than 48 to 72 hours after initiation of ventilation via an endotracheal tube (EET) or tracheostomy tube.6,7 Pneumonia is suggested by a new or progressive infiltrate on chest X-ray associated with signs or symptoms of infection (fever, leukocytosis, and purulent sputum) and worsening oxygenation. Chest X-ray findings are integral to the clinical diagnosis, wrought as they are with subjectivity, and difficulties in interpretation in the ICU setting due to the presence of overlying lines and tubes, as well as frequently abnormal baseline radiographs in patients admitted for respiratory failure due to pneumonia and acute respiratory distress syndrome. This constellation of clinical criteria possesses high sensitivity but low specificity. The addition of a lower respiratory tract specimen is recommended as it can improve diagnostic accuracy and guide antimicrobial use. This microbiologic approach, however, is also contentious with regards to how the specimen should be collected (protected specimen brush, bronchoscopically, tracheal aspirate, or mini-bronchoalveolar lavage) and how it should be analyzed (quantitatively or qualitatively). Regardless of the microbiology, the principle of VAP diagnosis according to these professional guidelines focuses on clinical criteria and initiation of empiric antimicrobial therapy pending clinical improvement. The original CDC surveillance definition for VAP also began with chest radiograph interpretation, this time specifying serial X-rays, distinguishing findings on whether the patient had an abnormal X-ray at baseline. After meeting radiographic criteria, innumerable combinations from an extensive menu of signs and symptoms of infection (including subjective assessments of character and quantity of sputum, findings on auscultation, and respiratory symptoms such as dyspnea and cough), worsening gas exchange, and laboratory data could arrive one at a diagnosis of VAP on clinical grounds alone or by virtue of positive culture results.8 The wide array of diagnostic possibilities may have been intended to provide the infection preventionist (someone trained in the field of infection control) with a menu of all the possible observed phenomena that could occur as a result of VAP; however, in practice, this was burdensome, impractical, and easily manipulated.