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Figure 1. Schematic representation of the Pseudomonas aeruginosa type III secretion needle that secrets exotoxins, including ExoS, ExoT, ExoU and ExoY. Exotoxins are introduced directly from the bacterial cytoplasm into the host cell cytoplasm where they contribute to VAP.11-12 The sketch of the type III secretion needle is drawn based upon its appearance in electron-microscopy images (see insert).

...that Pseudomonas aeruginosa expressing the type III secretion system is the most frequent cause of ventilator-associated pneumonia (VAP)? 

In the intensive care unit, a significant number of patients develop VAP after endotracheal ventilation [1]. One of the earliest concepts of endotracheal ventilation was derived from another invasive procedure known as tracheostomy, where a tube is placed in the trachea to mechanically ventilate the lung. Although the earliest account of tracheostomy can be traced back to 2000 BC Hindu scripts and 1500 BC Egyptian documents [2], the recent history of endotracheal ventilation refers to the seminal experiments of Andreas Vesalius, who in 1543 performed tracheal intubation in pigs [3]. For the next 366 years, endotracheal ventilation was considered extremely crude and technically underdeveloped for clinical use. However, in 1909 Meltzer and Auer developed a technique known as intratracheal insufflation, where endotracheal ventilation was used to deliver air into the lung and keep it in a steady, inflated state, with a stable heart rate and blood pressure [4]. This technique was modified to include a brief interruption in air flow for 2 or 3 minutes so that the lung could inflate and then deflate (known as rhythmic insufflation); rhythmic insufflation was translated into use in human patients in 1910 by Charles Elsberg with significant success [5]. Subsequent studies from 1910 to1950, including K.H. Giertz's studies from 1913 to 1916, established that rhythmic insufflation of the lungs using endotracheal ventilation was the safest ventilatory method [6]. Use of endotracheal ventilation became a standard method during the infamous polio epidemic of the 1950s and during the Vietnam War in the 1960s and 1970s.

The incidence of VAP paralleled the increased use of mechanical ventilation. VAP is the most common intensive care unit acquired infection that develops in patients with respiratory failure requiring endotracheal tube-delivered mechanical ventilatory support for ≥ 48 hours [7]. In 1967, Ian Phillips identified Pseudomonas aeruginosa as one of the principal causes of respiratory tract infections in patients receiving mechanical ventilation [8]. Pseudomonas aeruginosa is an antibiotic resistant Gram-negative bacillus that causes persistent or recurrent episodes of VAP. Frank and coworkers have recently discovered that the Pseudomonas aeruginosa possess a type III secretion system [9] which plays a major role in virulence of this organism [10]. The type III secretion system consists of a needle-like complex structure known as an 'injectisome'. The injectisome extends from the bacterial cytoplasm, through the bacterial periplasm and into the host cell's cytoplasm where it directly secretes exotoxins (Figure 1) [11-12]. While the mechanism(s) of action for type III secretion system toxins remain an area of intensive scientific investigation, we have come to recognize that Pseudomonas aeruginosa expressing the type III secretion system is the most frequent cause of virulent VAP.   

References:

  1. Chevret S, Hemmer M, Carlet J, Langer M. Incidence and risk factors of pneumonia acquired in intensive care units. Results from a multicenter prospective study on 996 patients. European Cooperative Group on Nosocomial Pneumonia. Intens Care Med. 1993; 19(5):256-64.
  2. Ezri T, Evron S, Hadad H, Roth Y. Tracheostomy and endotracheal intubation: a short history. Harefuah. 2005; 144(12):891-3, 908.
  3. Dobell AR. The origins of endotracheal ventilation. Ann Thorac Surg. 1994; 58(2):578-84.
  4. Meltzer SJ, Auer J. Continuous respiration without respiratory movements. J Exp Med. 1909; 11:622-625.
  5. Elsberg CA. Clinical experiences with intracheal insufflation (Meltzer), with remarks upon the value of the method for thoracic surgery, Ann Surg. 1910; 52:23-29.
  6. Crafoord C. Pulmonary ventilation and anesthesia in major chest surgery. J Thorac Surg. 1940; 9:237-253. 
  7. Park DR. The microbiology of ventilator-associated pneumonia. Respir Care. 2005; 50(6):742-63.
  8. Phillips I: pseudomonas aeruginosa respiratory tract infections in patients receiving mechanical ventilation. J Hyg (Camb) 1967; 65:229-235.
  9. Yahr TL, Mende-Mueller LM, Friese MB, Frank DW. Identification of type III secreted products of the Pseudomonas aeruginosa exoenzyme S regulon. J Bacteriol. 1997; 179(22):7165-8.
  10. Sawa T, Ohara M, Kurahashi K, Twining SS, Frank DW, Doroques DB, Long T, Gropper MA, Wiener-Kronish JP. In vitro cellular toxicity predicts Pseudomonas aeruginosa virulence in lung infections. Infect Immun. 1998; 66(7):3242-9.
  11. Galan JE, Collmer A. Type III secretion machines: bacterial devices for protein delivery into host cells. Science. 1999; 284(5418):1322-8.
  12. Stebbins CE, Galan JE. Priming virulence factors for delivery into the host. Nat Rev Mol Cell Biol. 2003; 4(9):738-43.

This article written by Nutan Prasain, July 2006. 

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