Epidemiology, pathogenesis, microbiology, and diagnosis of hospital-acquired and ventilator-associated pneumonia in adults - UpToDate.pdf

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Epidemiology, pathogenesis, microbiology, and diagnosis of hospit…cquired and ventilator-associated pneumonia in adults - UpToDate
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Epidemiology, pathogenesis, microbiology, and
diagnosis of hospital-acquired and ventilator-
associated pneumonia in adults
Author: Michael Klompas, MD, MPH
Section Editor: Thomas M File, Jr, MD
Deputy Editor: Milana Bogorodskaya, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Mar 2022. | This topic last updated: Sep 10, 2021.
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 diagnosis, 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".)
DEFINITIONS
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
●

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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 during a hospitalization within the past three
months [1]. 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 IDSA/ATS 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 [9].
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 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 United States Centers for Disease Control and
Prevention (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 [12]:
admission and did not appear to be incubating at the time of admission.
VAP is a type of pneumonia that develops ≥48 hours after endotracheal intubation.
●
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.
●

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Awareness of local resistance patterns is critical for decisions regarding empiric therapy
for HAP and VAP [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) [10].
EPIDEMIOLOGY
HAP is one of the most common and morbid hospital-acquired infections [14]. Most cases
of HAP occur in nonventilated patients [14]. However, the highest risk for HAP is in
patients on mechanical ventilation (ie, VAP), in whom the entity has been best studied.
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 [15,16]. 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 [17].
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) [18].
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].
VAP is associated with long hospital stays and significant costs [10]. 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 [20,21].
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'.)

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PATHOGENESIS
The pathogenesis of HAP (or nosocomial pneumonia) and 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) [22]. Approximately
45 percent of healthy subjects aspirate during sleep and an even higher proportion of
severely ill patients aspirate routinely [23,24]. Although frequently regarded as partially
protective, the presence of an endotracheal tube facilitates aspiration of oropharyngeal
secretions and bacteria into the lungs [24]. 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 [22,23,25]. An additional mechanism of inoculation in mechanically
ventilated patients is direct contact with environmental reservoirs, including respiratory
devices and contaminated water reservoirs [26,27]. 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 [28]. 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
HAP (or nosocomial pneumonia) and VAP may be caused by a wide variety of pathogens
and can be polymicrobial. Common pathogens include aerobic gram-negative bacilli (eg,
Escherichia coli, Klebsiella pneumoniae, Enterobacter spp, Pseudomonas aeruginosa,

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Acinetobacter spp) and gram-positive cocci (eg, Staphylococcus aureus, including methicillin-
resistant S. aureus [MRSA], Streptococcus spp) [29,30]. 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 [31,32].
Among 8474 cases of VAP reported to the United States Centers for Disease Control and
Prevention from 2009 to 2010, the distribution of pathogens associated was S. aureus
(24.1 percent), P. aeruginosa (16.6 percent), Klebsiella species (10.1 percent), Enterobacter
species (8.6 percent), Acinetobacter baumannii (6.6 percent), and E. coli (5.9 percent) [33].
Similar findings have been observed in other surveillance studies [29].
There is a paucity of data regarding whether and how the pathogens that cause HAP in
nonventilated patients differ from those that cause VAP. One prospective observational
study evaluated 158,519 patients admitted to the University of North Carolina Hospital
over a four-year period [34]. A total of 327 episodes of VAP and 261 episodes of HAP in
nonventilated patients were identified:
These findings are largely similar to those observed in a meta-analysis of 24 studies
performed during the development of the 2016 Infectious Diseases Society of
America/American Thoracic Society HAP/VAP guidelines to determine the prevalence of
micro-organisms causing HAP [10]. 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
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 nonventilated patients with 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).
●

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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 [35]. 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 MDR pathogens [10]. 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 [10]. 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.
Risk factors for MDR VAP are summarized in the following table ( table 2). Risk factors
for MDR HAP (as well as risk factors for increased mortality) are summarized in the
following table ( table 3).
DIAGNOSIS
The clinical diagnosis of HAP and VAP is difficult in part because the clinical findings are
nonspecific. The 2016 Infectious Diseases Society of America/American Thoracic Society
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 [10].
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 [36,37]. 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

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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) [36].
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) [10].
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 [38-40].
Although there are limitations regarding the sensitivity and specificity of these tests (eg,
colonization or true pathogen) [40,41], they offer the potential for more rapid
identification of pathogens and resistance patterns (eg, methicillin resistance for S. aureus
[42], carbapenemase presence for Enterobacteriaceae), 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 [43].
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

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SUMMARY
th th
th
th
Basics topic (see "Patient education: Hospital-acquired pneumonia (The Basics)")
●
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.
•
Ventilator-associated pneumonia (VAP) is a type of pneumonia that develops ≥48
hours after endotracheal intubation.
•
HAP is among the most common and morbid hospital-acquired infections. (See
'Epidemiology' above.)
●
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.)
●
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.)
●

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ACKNOWLEDGMENT
We are saddened by the death of John G Bartlett, MD, who passed away in January 2021.
UpToDate gratefully acknowledges his tenure as the founding Editor-in-Chief for
UpToDate in Infectious Diseases and his dedicated and longstanding involvement with the
UpToDate program.
Use of UpToDate is subject to the Terms of Use.
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●
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Topic 7020 Version 34.0

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GRAPHICS
Pneumonia terminology
Term Definition
Classification by site of acquisition
Community-acquired
pneumonia (CAP)
An acute infection of the pulmonary parenchyma acquired
outside of health care settings
Nosocomial
pneumonia
An acute infection of the pulmonary parenchyma acquired in
hospital settings, which encompasses hospital-acquired
pneumonia and ventilator-associated pneumonia
Hospital-acquired
pneumonia (HAP)
Pneumonia acquired ≥48 hours after hospital admission; includes
both HAP and VAP
Ventilator-associated
pneumonia (VAP)
Pneumonia acquired ≥48 hours after endotracheal intubation
Health care-associated
pneumonia (HCAP)
Retired term, which referred to pneumonia acquired in health
care facilities (eg, nursing homes, hemodialysis centers) or after
recent hospitalization*
Classification by etiology
Atypical pneumonia Pneumonia caused by "atypical" bacterial pathogens including
Legionella spp, Mycoplasma pneumoniae, Chlamydia pneumoniae,
Chlamydia psittaci, and Coxiella burnetii
Aspiration pneumonia Adverse pulmonary consequences due to entry of gastric or
oropharyngeal fluids, which may contain bacteria and/or be of
low pH, or exogenous substances (eg, ingested food particles or
liquids, mineral oil, salt or fresh water) into the lower airways
Chemical pneumonitis Aspiration of substances (eg, acidic gastric fluid) that cause an
inflammatory reaction in the lower airways, independent of
bacterial infection
Bacterial aspiration
pneumonia
An active infection caused by inoculation of large amounts of
bacteria into the lungs via orogastric contents
* The term HCAP was used to identify patients at risk for infection with multidrug-resistant
pathogens. This categorization may have been overly sensitive, leading to increased,
inappropriately broad antibiotic use.
¶ The origin of the term "atypical" is a matter of debate. The term may refer to the fact that
¶

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these organisms are not "typical" bacteria that cannot be identified by standard microbiologic
techniques. Others suggest that atypical refers to the mild nature of the pneumonia caused by
some of these organisms compared with pneumonia caused by Streptococcus pneumoniae.
Graphic 130821 Version 2.0

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Ventilator-associated pneumonia: Risk factors for multidrug-resistance
in adults
Risk factors for MDR pathogens:
IV antibiotic use within the previous 90 days
Septic shock at the time of VAP
ARDS preceding VAP
≥5 days of hospitalization prior to the occurrence of VAP
Acute renal replacement therapy prior to VAP onset
Risk factors for MDR Pseudomonas and other gram-negative bacilli:
Treatment in an ICU in which >10 percent of gram-negative isolates are resistant to an
agent being considered for monotherapy
Treatment in an ICU in which local antimicrobial susceptibility rates are not known
Colonization with OR prior isolation of MDR Pseudomonas or other gram-negative bacilli
Risk factors for MRSA:
Treatment in a unit in which >10 to 20 percent of Staphylococcus aureus isolates are
methicillin resistant
Treatment in a unit in which the prevalence of MRSA is not known
Colonization with OR prior isolation of MRSA
MDR: multidrug resistant; IV: intravenous; VAP: ventilator-associated pneumonia; ARDS: acute
respiratory distress syndrome; ICU: intensive care unit; MRSA: methicillin-resistant S. aureus.
Adapted from: Kalil AC, Metersky ML, Klompas M, et al. Management of adults with hospital-acquired and ventilator-
associated pneumonia: 2016 clinical practice guidelines by the Infectious Diseases Society of America and the
American Thoracic Society. Clin Infect Dis 2016; 63:e61.

20/04/2022, 16:17
Page 17 of 18
Hospital-acquired pneumonia: Risk factors for MDR pathogens and/or
increased mortality in adults
Risk factors for increased mortality:
Ventilatory support for HAP
Septic shock
Risk factor for MDR Pseudomonas, other gram-negative bacilli, and MRSA:
IV antibiotics within the past 90 days
Risk factors for MDR Pseudomonas and other gram-negative bacilli:
Structural lung disease (bronchiectasis or cystic fibrosis)
A respiratory specimen Gram stain with numerous and predominant gram-negative
bacilli
Colonization with OR prior isolation of MDR Pseudomonas or other gram-negative bacilli
Risk factors for MRSA:
Treatment in a unit in which >20 percent of Staphylococcus aureus isolates are methicillin
resistant
Treatment in a unit in which the prevalence of MRSA is not known
Colonization with OR prior isolation of MRSA
MDR: multidrug resistant; HAP: hospital-acquired pneumonia; MRSA: methicillin-resistant S.
aureus; IV: intravenous.
Adapted from: Kalil AC, Metersky ML, Klompas M, et al. Management of adults with hospital-acquired and ventilator-
associated pneumonia: 2016 clinical practice guidelines by the Infectious Diseases Society of America and the
American Thoracic Society. Clin Infect Dis 2016; 63:e61.

20/04/2022, 16:17
Page 18 of 18
Contributor Disclosures
Michael Klompas, MD, MPH No relevant financial relationship(s) with ineligible companies to
disclose. Thomas M File, Jr, MD Grant/Research/Clinical Trial Support: Pfizer[Pneumococcal
vaccination]. Consultant/Advisory Boards: Nabriva Therapeutics[Community-acquired pneumonia]. All
of the relevant financial relationships listed have been mitigated. Milana Bogorodskaya, MD No
relevant financial relationship(s) with ineligible companies to disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these
are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of all
authors and must conform to UpToDate standards of evidence.
Conflict of interest policy

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