Monday, November 28, 2011


Pneumonia is an important cause of morbidity and mortality in adults and children. It results from the host inflammatory response to infection of the distal airways and the lung alveoli (Schutter et.al, 2011). The most useful classification is based on the site of acquisition: community-acquired (CAP) or hospital-acquired pneumonia (HAP) (Esperatti and Marti, 2008).
Hospital-associated pneumonia (HAP) is the second most common nosocomial infection (after urinary tract infection) and the most common nosocomial infection acquired in the intensive care unit (ICU). HAP associated with mechanical ventilation is called ventilator-associated pneumonia (VAP) (Franzetti et.al., 2010). VAP has an estimated incidence of 8–28% and is associated with an excess of ICU stay, increased costs, and attributable mortality (Safdar et.al., 2005).
The term atypical pneumonia was originally used to describe an unusual presentation of pneumonia. It is now more widely used in reference to either pneumonia caused by a relatively common group of pathogens, or to a distinct clinical syndrome the existence of which is difficult to demonstrate (Murdoch and Chambers, 2009).
The “atypical pathogen” group includes Mycoplasma pneumoniae; Legionella; Chlamydia pneumoniae; Coxiella burnettii; and the respiratory viruses, especially
Introduction and Aim of the Work
influenza A and B, parainfluenza 1, 2, and 3, respiratory syncytial virus (RSV) and Epstein-Barr virus (EBV) (Lieberman, 2005).
The diagnosis of pneumonia in the hospitalized patient is even more challenging than the diagnosis of CAP (Richards et.al., 2000). Clinical findings alone are not sufficient for a definitive diagnosis. Therfore, a variety of noninvasive and invasive tests have been proposed as guides for diagnosis and treatment of hospital-acquired pneumonia. Methods include sputum Gram stain and culture, serologic studies, antigen detection tests, and nucleic acid amplification methods (Carroll, 2002).
Many patient- and disease-specific factors contribute to the pathophysiology of HAP, particularly in the surgical population. Risk-factor modification and inpatient prevention strategies can have a significant impact on the incidence of HAP (Kieninger and Lipsett, 2009).

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