INTRODUCTION — Hospital-acquired (or nosocomial) pneumonia (HAP) and ventilator-associated pneumonia (VAP) remain important causes of morbidity and mortality despite improvements in prevention, antimicrobial therapy, and supportive care.
The epidemiology, pathogenesis, and microbiology of HAP and VAP will be reviewed here. The risk factors, prevention, and treatment of HAP and VAP are discussed separately. (See "Clinical presentation and diagnostic evaluation of ventilator-associated pneumonia" and "Risk factors and prevention of hospital-acquired and ventilator-associated pneumonia in adults" and "Treatment of hospital-acquired and ventilator-associated pneumonia in adults".)
Pneumonia types — Pneumonia is frequently categorized based on site of acquisition (table 1).
●HAP (or nosocomial pneumonia) is pneumonia that occurs 48 hours or more after admission and did not appear to be incubating at the time of admission. HAP includes both VAP (ventilator-associated pneumonia) and NV-HAP (non-ventilator-associated pneumonia).
●VAP is a type of pneumonia that develops in a patient who has been intubated for ≥48 hours or within 48 hours following extubation.
The concept of health care-associated pneumonia (HCAP) was included in the 2005 American Thoracic Society/Infectious Diseases Society of America (ATS/IDSA) guidelines and referred to pneumonia acquired in health care facilities such as nursing homes, hemodialysis centers, outpatient clinics, or following a hospitalization within the preceding three months . This category was used to identify patients at risk for infection with multidrug-resistant (MDR) pathogens depending upon each patient's specific risk factors and severity of illness. However, this categorization may have been overly sensitive and may have led to increased, inappropriately broad antibiotic use. Although patients with recent contact with health care facilities are at increased risk for infection with MDR pathogens, this risk is small for most patients and the overall incidence is low [2-8]. Thus, the category of HCAP was purposefully not included in the 2016 ATS/IDSA guidelines. For similar reasons, the combined 2017 European and Latin American guidelines on the management of HAP and VAP did not categorize HCAP as a distinct type of pneumonia .
Of note, the concepts of ventilator-associated conditions and infection-related ventilator-associated complications introduced by the United States Centers for Disease Control and Prevention (CDC) in 2013 are not discussed here because they are designed for surveillance and quality improvement purposes at the population level and not to aid in diagnosis and treatment of individual patients [10,11].
Antimicrobial resistance — The CDC and the European Centre for Disease Prevention and Control (ECDC) have developed standard terminology for antimicrobial-resistant gram-negative bacilli, which are important causes of HAP and VAP :
●Multidrug-resistant (MDR) refers to acquired nonsusceptibility to at least one agent in three different antimicrobial classes.
●Extensively drug-resistant (XDR) refers to nonsusceptibility to at least one agent in all but two antimicrobial classes.
●Pandrug-resistant (PDR) refers to nonsusceptibility to all antimicrobial agents that can be used for treatment.
Awareness of local resistance patterns is critical for decisions regarding empiric therapy for HAP and VAP [10,13]. All hospitals should regularly create and disseminate a local antibiogram, ideally one that is specific to the different units in the hospital (although small numbers of cases per unit may preclude this) .
EPIDEMIOLOGY — Hospital-acquired (or nosocomial) pneumonia (HAP) is one of the most common and morbid hospital-acquired infections . The risk for HAP is greatest in patients on mechanical ventilation but most cases of HAP occur in nonventilated patients (NV-HAP) by virtue of their greater numbers [14,15]. The risk of HAP is about 10-fold higher in ventilated versus non-ventilated patients.
According to the United States Center for Disease Control and Prevention's National Healthcare Safety Network (NHSN), there has been a steady decline in reported VAP rates in the United States; between 2006 and 2012, in medical intensive care units (ICUs), the reported incidence of VAP per 1000 ventilator-days decreased from 3.1 to 0.9 and, in surgical ICUs, the reported incidence decreased from 5.2 to 2.0 [16,17]. Because the NHSN definition of VAP includes qualitative criteria (eg, increased secretions or worsening oxygenation), it is unclear whether the reported decrease in VAP incidence represents a true decline or reflects stricter application of these subjective criteria [18,19].
Notwithstanding the drop in cases reported to NHSN, independent audits of data from the Medicare Patient Safety Monitoring System (limited to patients ≥65 years of age) suggest that the rate of VAP remained stable among ventilated patients between 2005 and 2013 (10.8 percent during 2005 to 2006 versus 9.7 percent during 2012 to 2013) . A follow-up study using the same methodology found that VAP rates have continued to remain stable through 2019 . The differences between the rates reported to NHSN and this independent audit reflect the lack of definitive criteria for VAP and the subjectivity of surveillance [19,22].
Crude mortality rates for VAP and NV-HAP are similar and range between 15 to 30 percent [23,24]. Determining the fraction of these deaths attributable to pneumonia versus patients' underlying conditions is complicated but most estimates are relatively low [25,26].
VAP and NV-HAP are also associated with long hospital stays and significant costs . Two studies estimated that VAP prolongs the length of mechanical ventilation by 7.6 to 11.5 days and prolongs hospitalization by 11.5 to 13.1 days compared with similar patients without VAP; the excess cost associated with VAP has been estimated at approximately USD $40,000 per patient [23,27-29].
The prognosis of HAP and VAP is discussed separately. (See "Treatment of hospital-acquired and ventilator-associated pneumonia in adults" and "Treatment of hospital-acquired and ventilator-associated pneumonia in adults", section on 'Prognosis'.)
PATHOGENESIS — The pathogenesis of hospital-acquired (or nosocomial) pneumonia (HAP) and ventilator-associated pneumonia (VAP) is related to the number and virulence of micro-organisms entering the lower respiratory tract and the response of the host (eg, mechanical, humoral, and cellular host defenses). The primary route of infection of the lungs is through microaspiration of organisms that have colonized the oropharyngeal tract (or, to a lesser extent, the gastrointestinal tract) . Approximately 45 percent of healthy subjects aspirate during sleep and an even higher proportion of severely ill patients aspirate routinely. Although frequently regarded as partially protective, the presence of an endotracheal tube facilitates aspiration of oropharyngeal secretions and bacteria into the lungs . Depending upon the number and virulence of organisms reaching the lung and the host response, pneumonia may ensue.
Hospitalized patients often become colonized with microorganisms acquired from the hospital environment, and as many as 75 percent of severely ill patients will be colonized within 48 hours [30,32]. An additional mechanism of inoculation in mechanically ventilated patients is direct contact with environmental reservoirs, including respiratory devices and contaminated water reservoirs [33,34]. Disposable tubing used in respiratory circuits or tracheostomy or endotracheal tubes may become contaminated in the process of routine nursing care or via the (contaminated) hands of hospital personnel. Such contamination can occur despite rigorous cleaning of ventilator equipment.
In addition, the near sterility of the stomach and upper gastrointestinal tract may be disrupted by alterations in gastric pH due to illness, medications, or enteric feedings. For this reason, much attention has been paid to the possible adverse effect of ulcer prophylaxis regimens that raise the gastric pH [35,36]. Less frequently, pneumonia results from inhalation of infectious aerosols or from bacteremia originating in a distant focus. (See "Risk factors and prevention of hospital-acquired and ventilator-associated pneumonia in adults", section on 'Role of gastric pH'.)
MICROBIOLOGY — Ventilator-associated pneumonia (VAP) and non-ventilator-associated pneumonia (NV-HAP) may be caused by a wide variety of pathogens and can be polymicrobial. The most common organisms are Staphylococcus aureus (including methicillin-resistant S. aureus) and Pseudomonas aeruginosa. Other common causes include other aerobic gram-negative bacilli (eg, Escherichia coli, Klebsiella pneumoniae, Enterobacter spp, Acinetobacter spp) and gram-positive cocci (eg, Streptococcus spp) [37,38]. There is increasing recognition that a substantial fraction of nosocomial pneumonias may be due to viruses in general medical and surgical patients and both viruses and fungi in immunocompromised patients [39-41].
Among 9266 cases of VAP reported to the United States Centers for Disease Control and Prevention (CDC) from 2015 to 2017, the distribution of pathogens associated was S. aureus (28.8 percent), P. aeruginosa (12.9 percent), Klebsiella species (10.1 percent), Enterobacter species (8.4 percent), Haemophilus influenzae (5.9 percent), Streptococcus (5.7 percent), E. coli (5.6 percent), and Acinetobacter baumannii (3.2 percent) . Similar findings have been observed in other surveillance studies .
The pathogens that cause NV-HAP are generally similar to those that cause VAP. As an example, one prospective observational study evaluated 158,519 patients admitted to the University of North Carolina Hospital over a four-year period . A total of 327 episodes of VAP and 261 episodes of HAP in nonventilated patients were identified:
●The infecting flora in patients with VAP included methicillin-susceptible S. aureus (MSSA; 9 percent), MRSA (18 percent), P. aeruginosa (18 percent), Stenotrophomonas maltophilia (7 percent), Acinetobacter spp (8 percent), and other species (9 percent).
●The infecting flora in NV-HAP was similar, except non-Enterobacteriaceae gram-negative bacilli (P. aeruginosa, Acinetobacter, and S. maltophilia) were less likely. Specifically, it included MSSA (13 percent), MRSA (20 percent), P. aeruginosa (9 percent), S. maltophilia (1 percent), Acinetobacter spp (3 percent), and other species (18 percent).
These findings are largely similar to those observed in a retrospective analysis of 17,819 patients with culture-confirmed HAP  and a meta-analysis of 24 studies performed during the development of the 2016 Infectious Diseases Society of America/American Thoracic Society (IDSA/ATS) HAP/VAP guidelines . In this analysis, the prevalence of S. aureus infections were lower, with MRSA accounting for 10 percent of isolates and MSSA for 6 percent; Pseudomonas species accounted for 13 percent, enteric gram-negative bacilli for 16 percent, and Acinetobacter species for 4 percent.
A frequent criticism of such studies is that they may underestimate the prevalence of certain pathogens (eg, anaerobes) because special culturing techniques are required to identify them. However, a study that performed anaerobic cultures using protective brush specimens and bronchoalveolar lavage fluid from 185 patients with possible VAP identified only one anaerobic organism, nonpathogenic Veillonella spp . This finding and the history of success treating VAP using regimens that do not include anaerobic coverage suggests that anaerobes may play a relatively minor role in the pathogenesis of VAP.
Differences in host factors and in the hospital flora of an institution also influence the patterns of pathogens seen.
MDR risk factors — The etiology of HAP and VAP depends in large part upon whether the patient has risk factors for multidrug-resistant (MDR) pathogens . The frequency of specific MDR pathogens varies among hospitals, within hospitals, and between different patient populations. Prolonged hospitalization and recent exposure to antibiotics are two of the most important risk factors for MDR pathogens . An awareness of the susceptibility patterns of the nosocomial pathogens within a given health care setting is important to inform the selection of appropriate empiric antimicrobial therapy.
DIAGNOSIS — The clinical diagnosis of hospital-acquired (or nosocomial) pneumonia (HAP) and ventilator-associated pneumonia (VAP) is difficult in part because the clinical findings are nonspecific. The 2016 Infectious Diseases Society of America/American Thoracic Society (IDSA/ATS) guidelines for the management of HAP and VAP recommend a clinical diagnosis based upon a new lung infiltrate plus clinical evidence that the infiltrate is of infectious origin, which includes the new onset of fever, purulent sputum, leukocytosis, and decline in oxygenation .
While the clinical features described above support the diagnosis of HAP or VAP, no individual sign or symptoms nor any combination of signs and symptoms have been found to be highly sensitive or specific for diagnosis [22,46]. As an example, the presence of a new or progressive radiographic infiltrate plus at least two of three clinical features (fever >38ºC, leukocytosis or leukopenia, and purulent secretions) has a 69 percent sensitivity and 75 percent specificity for VAP, corresponding to a positive likelihood ratio of 2.5 (95% CI 1.3-4.8) and negative likelihood ratio of 0.06 (95% CI 0-0.87) .
Cultures of pulmonary secretions (sputum, endotracheal aspirates, bronchoalveolar lavage) are also prone to false positives and false negatives. When compared with histology, quantitative endotracheal aspirate cultures had a pooled sensitivity of 48 percent (95% CI 38-57 percent) and positive predictive value of 81 percent (95% CI 67-91 percent); quantitative bronchoalveolar lavage cultures had a sensitivity of 75 percent (95% CI 58-88 percent) and positive predictive value of 77 percent (95% CI 66-85 percent) .
Molecular diagnostic tests for detection of respiratory pathogens are being developed and offer promise for more rapid identification of the causes of HAP or VAP [47-49]. Although there are limitations regarding the sensitivity and specificity of these tests (eg, colonization or true pathogen) [49,50], they offer the potential for more rapid identification of pathogens and resistance patterns (eg, methicillin resistance for S. aureus , carbapenemase presence for Enterobacteriaceae, and influenza and other respiratory viruses), which may result in better selection of active empiric regimens and more rapid tailoring of directed antibiotic regimens. As an example, a multiplex polymerase chain reaction assay, which detects an array of respiratory bacterial pathogens including Streptococcus pneumoniae and several antibiotic-resistance genes, is approved for the diagnosis of pneumonia using bronchoalveolar lavage specimens in the United States but is not yet widely available . Future studies to assess the utility of these tests will ideally evaluate whether and how they affect antibiotic utilization and patient outcomes. (See "Treatment of hospital-acquired and ventilator-associated pneumonia in adults", section on 'Tailoring therapy'.)
The diagnostic approach to VAP is also discussed in more detail separately. (See "Clinical presentation and diagnostic evaluation of ventilator-associated pneumonia".)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Hospital-acquired pneumonia and ventilator-associated pneumonia in adults".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or email these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: Hospital-acquired pneumonia (The Basics)")
●Definitions – The following types of nosocomial pneumonia have been defined (see 'Definitions' above):
•Hospital-acquired pneumonia (HAP) is pneumonia that occurs 48 hours or more after admission and did not appear to be incubating at the time of admission. HAP can be divided into non-ventilator hospital acquired pneumonia (NV-HAP) and ventilator-associated pneumonia (VAP).
•VAP is a type of pneumonia that develops ≥48 hours after endotracheal intubation.
●Epidemiology – HAP is among the most common and morbid hospital-acquired infections. (See 'Epidemiology' above.)
●Pathogenesis – The pathogenesis of HAP and VAP is related to the numbers and virulence of micro-organisms entering the lower respiratory tract and the response of the host. The primary route of infection of the lungs is through microaspiration of organisms that have colonized the oropharyngeal tract (or to a lesser extent the gastrointestinal tract). (See 'Pathogenesis' above.)
●Microbiology – HAP and VAP may be caused by a wide variety of pathogens, can be polymicrobial, and may be due to multidrug-resistant (MDR) pathogens. (See 'Microbiology' above.) Staphylococcus aureus and Pseudomonas aeruginosa are the most common pathogens.
●MDR risk factors – MDR bacteria are most common in patients who have been hospitalized for prolonged periods (≥5 days) and/or who have received antibiotics within the preceding 90 days. (See 'MDR risk factors' above.)
●Diagnosis – The diagnosis of HAP and VAP should be suspected in patients with new onset of fever, purulent sputum, leukocytosis, and decline in oxygenation. (See 'Diagnosis' above.)
ACKNOWLEDGMENT — UpToDate gratefully acknowledges John G Bartlett, MD (deceased), who contributed on earlier versions of this topic and was a founding Editor-in-Chief for UpToDate in Infectious Diseases.
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