New etiopathogenic concepts of ventilator-associated pneumonia.

Overview

Ventilator-associated pneumonia develops as a consequence of impaired host defenses and exposure to large numbers of potential pathogens. Both of these processes interact and allow colonization of the airways with enteric gram-negative bacteria to occur through the molecular mechanism of bacterial adherence. Bacterial adherence is a cell-cell interaction mediated by the following variables: (1) host receptors, (2) bacterial adhesins, and (3) the proper microenvironment on the respiratory mucosa. For gram-negative bacteria, an important adhesin may be the pili that project from the cell surface, and important epithelial receptors for adhesins may be glycoproteins contained in respiratory mucus. The proper microenvironment for adherence to take place is a mixture of exposed cell receptors, prolonged bacterial-epithelial cell contact, impaired airway defenses, presence of proteases, and an optimal pH. In some way, all of the risk factors discussed impact either directly or indirectly with this basic molecular process. Once adherence is accomplished, potential pathogens may begin to colonize the respiratory tract. Once colonization occurs, bacteria may proliferate on the respiratory mucosa. At this point, the general status of host defenses determines whether colonization progresses to overt parenchymal lung infection.