[Dysphagia] pathogenesis of ventilator-associated pneumonia

[Paula.Leslie at newcastle.ac.uk (Paula leslie)]

This 1995 review article has just been thrown up by one of my abstract 
notifier things.  Might be of interest for ICU/ITU AND others?  I haven't 
critically reviewed the whole paper - yet.

Paula

Intensive Care Medicine (Historical Archive) 
ISSN: 0342-4642 (Paper) 1432-1238 (Online) 
Issue:  Volume 21, Number 4

Date:  April 1995 
Pages: 365 - 383  
Review Article
The pathogenesis of ventilator-associated pneumonia: I. Mechanisms of 
bacterial transcolonization and airway inoculation
R. J. Estes1, 2 and G. U. Meduri1

(1)  Division of Pulmonary and Critical Care Medicine, 956 Court Avenue, H314, 
38163 Memphis, TN, USA 
(2)  Present address: Knoxville Pulmonary Group, P. A., 1932 Alcoa Highway, 
Suite 480, 37920 Knoxville, TN, USA

Received: 11 May 1993  Accepted: 5 July 1994

Abstract  Ventilator-associated pneumonia (VAP) is an infection of the lung 
parenchyma developing in patients on mechanical ventilation for more than 48 
h. VAP is associated with a remarkably constant spectrum of pathogenic 
bacteria, most of which are aerobic Gramnegative bacilli (AGNB) and, to a 
lesser extentStaphyloccus aureus. Most authorities agree that VAP develops as 
a result of aspiration of secretions contaminated with pathogenic organisms, 
which appear to be endogenously acquired. These pathogens gain access to the 
distal airways by mechanical reflux and aspiration of contaminated gastric 
contents and also by repetitive inoculation of contaminated upper airway 
secretions into the distal tracheobronchial tree. Persistence of these 
organisms in the upper airways involves their successful colonization of 
available surfaces. Although exogenous acquisition can occur from the 
environment, the rapidity at which critically ill patients acquire AGNB in the 
upper airways in conjunction with the low rate of AGNB colonization of 
health-care workers exposed to the same environment favors the presence of 
endogenous proximate sources of AGNB and altered upper airway surfaces that 
are rendered receptive. Proximate sources of AGNB remain unclear, but 
potential sites harboring AGNB prior to illness include the upper 
gastrointestinal tract, subgingival dental plaque, and the periodontal spaces. 
Following illness or antibiotic therapy, competitive pressures within the 
oropharynx favor AGNB adherence to epithelial cells, which lead to 
oropharyngeal colonization. Similar dynamic changes in contiguous structures 
(oropharynx, trachea, sinuses, and the upper gastrointestinal tract) lead to 
the transcolonization of these structures with pathogenic bacteria. Following 
local colonization or infection, these structures serve as reservoirs of AGNB 
capable of inoculating the lower airways. As the oropharynx becomes colonized 
with AGNB, contaminated oropharyngeal secretions reach the trachea, 
endotracheal tube, and ventilator circuit. Contaminated secretions pooled 
above the endotracheal tube cuff gain access to the trachea and inner lumen of 
the endotracheal tube by traversing endotracheal tube cuff folds. Amorphic 
particulate deposits containing AGNB form along the endotracheal tube and are 
capable of being propelled into the distal airways by ventilator-generated 
airflow or by tubing manipulation. Bacteria embedded within this type of 
amorphous matrix are particularly difficult for the host to clear. If host 
defenses fail to clear the inoculum, then bacterial proliferation occurs, and 
the host inflammatory response progresses to bronchopneumonia. By 
understanding the mechanisms involved in the pathogenesis of VAP, new 
strategies may be developed to prevent this significant complication of 
mechanical ventilation.
Key words  Ventilator-associated pneumonia - Colonization - Aspiration defense 
mechanisms - Inflammatory response

Paula Leslie
Degree Programme Director
Surgical and Reproductive Sciences
Faculty of Medical Sciences
University of Newcastle
Newcastle upon Tyne
NE2 4HH
UK
T +44 (0) 191 222 6279
F +44 (0) 191 222 8988
http://www.ncl.ac.uk/sars/postgrad/MSc.htm