Hospital-acquired and ventilator-associated pneumonia: what's new in diagnosis and treatment?

Nosocomial infections are an important cause of morbidity and mortality in US hospitals [1]. The cost to the country is enormous, with $4.5 billion being spent annually on the treatment of patients with nosocomial pneumonia. According to the American Society of Microbiology, approximately 70% of nosocomial infections are caused by organisms resistant to 1 antimicrobial agent [2]. In addition to extended-spectrum -lactamase–producing Klebsiella pneumoniae and Escherichia coli, and vancomycin-resistant enterococci (VRE), other problems include vancomycinintermediate Staphylococcus aureus (VISA) and Staphylococcus epidermidis, penicillin-resistant Streptococcus pneumoniae, methicillin/oxacillin-resistant staphylococci, and multidrug–resistant Pseudomonas aeruginosa, Acinetobacter species, and Enterobacter species. Antimicrobial resistance is becoming 1 of the most important problems of the early 21st century, and it is imperative to find ways to reduce these problems. Urinary tract infection is the most common nosocomial infection, but it has minimal associated morbidity and mortality. Pneumonia and bacteremia are the 2 most prevalent serious nosocomial infections, representing 27% and 19% of all nosocomial infections, respectively [3] (Table 1). Nosocomial pneumonia is associated with a significant increased mortality rate. The Prevalence of Nosocomial Infections in European ICUs (EPIC) study documented that nosocomial pneumonia was an independent risk factor for increased mortality, with an odds ratio (OR) of 1.91. In that study, clinical sepsis (OR, 3.63) and bacteremia (OR, 1.61) were also independent risk factors for worse mortality [4]. The pathophysiology of hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP) usually requires that 2 important processes take place: (1) bacterial colonization of the aerodigestive tract, and (2) aspiration of contaminated secretions into the lower airway. These 2 processes ultimately lead to the development of bronchiolitis and subsequent development of focal or multifocal bronchopneumonia, with ultimate development of confluent bronchopneumonia.