Hospital-acquired Pneumonia and Ventilator-associated Pneumonia

Recent Advances in Epidemiology and Management

François Barbier; Antoine Andremont; Michel Wolff; Lila Bouadma


Curr Opin Pulm Med. 2013;19(3):216-228. 

In This Article

The Alarming Situation of Bacterial Resistance

The bacterial epidemiology of VAP ( Table 2 )[54] depends on a panel of factors including mechanical ventilation duration, length of hospital and ICU stays, previous exposure to antimicrobials, local epidemiology and potential epidemic phenomenon in a given ICU.[1] Rapid changes in the oropharyngeal flora of intubated patients (even in the absence of antibiotic exposure) represent a key determinant,[55] as microaspirations of pharyngeal secretions constitute the leading physiopathological mechanism of VAP. Early-onset VAP (within the first 4 days of mechanical ventilation) usually involve respiratory pathogens from the normal, community-acquired oropharyngeal microbiota ( Table 3 ), whereas late-onset VAP (occurring on day 5 of mechanical ventilation or later) mostly involve hospital-acquired and potentially MDR pathogens as a combined result of antibiotic selective pressure, cross-transmission and colonization from in-ICU environmental sources.[1,53,54] However, MDR pathogens may be isolated in early-onset VAP when risk factors exist prior to ICU admission, and even when such risk factors are lacking [notably for Pseudomonas aeruginosa and methicillin-resistant Staphylococcus aureus (MRSA)],[53] enlightening the limits of this classification in the current context of bacterial resistance.

Resistance frequencies differ from one ICU to another and at the geographic scale, but trends converge across international surveys ( Table 4 ).[14,50,54] The recent description of plasmidic linezolid resistance in MRSA elicits significant concerns.[58,59] Resistance to third-generation and fourth-generation cephalosporins in Enterobacteriaceae strains mostly depends on the expression of acquired extended-spectrum β-lactamases (ESBLs) and/or AmpC β-lactamases.[56–60] The spread of carbapenemase-producing strains is even more alarming ( Table 4 ).[57] MDR isolates of P. aeruginosa are increasingly prevalent, whereas one-half to two-thirds of Acinetobacter baumannii strains causing VAP are currently carbapenem-resistant.[14,50] Polymyxins (mainly colistin) are more and more seen as a last-line therapeutic option to treat MDR Gram-negative bacilli (GNB).[61] Unfortunately, colistin resistance is now also on the rise in ICUs with high prevalence of carbapenems resistance and heavy colistin consumption.[62,63,64] The situation of bacterial resistance appears as critical when HAPs in nonintubated patients are considered ( Table 4 ).