Hospital-Acquired Pneumonia (Nosocomial Pneumonia) and Ventilator-Associated Pneumonia



The term healthcare-associated pneumonia (HCAP) was defined as pneumonia in nonhospitalized patients who had significant experience with the healthcare system. Such contact could include (1) intravenous therapy for wound care within the preceding 30 days, (2) residence in a long-term care facility, (3) hospitalization in an acute-care hospital within the preceding 90 days, and/or (4) outpatient treatment in a hospital or hemodialysis clinic within the preceding 30 days. These individuals were believed to be at an increased risk for infection with multidrug-resistant (MDR) organisms because of such contact.[1] However, more recent studies have indicated that many individuals who met the criteria for HCAP were not infected with MDR pathogens.[2] The risk of infection with MDR organisms appears to depend much more on specific risk factors of the given patient than on contact with various aspects of the healthcare system. Patients who would have met the criteria for HCAP should not be empirically treated with antibiotics to cover MDR bacteria unless they have valid risk factors for acquiring MDR organisms (see below).[3, 4]

Pneumonia is defined as "new lung infiltrates plus clinical evidence that the infiltrate is of an infectious origin, which include the new onset of fever, purulent sputum, leukocytosis, and decline in oxygenation."[5] Hospital-acquired pneumonia (HAP), or nosocomial pneumonia, is a lower respiratory infection that was not incubating at the time of hospital admission and that presents clinically 2 or more days after hospitalization. Pneumonia that presents sooner should be regarded as community-acquired pneumonia. Ventilator-associated pneumonia (VAP) is defined as pneumonia that presents more than 48 hours after endotracheal intubation.

Clinicians should understand that many of these findings are often shared with mimics of nosocomial pneumonia, such as congestive heart failure (CHF), pulmonary emboli, pulmonary hemorrhage, primary or metastatic lung carcinomas, leukemias/lymphomas, pulmonary drug reactions, and radiation pneumonitis, among others. VAP refers to nosocomial pneumonia that develops among patients on ventilators.[5, 1]

View Image

Typical chest radiograph of a patient with nosocomial pneumonia.

HAP is a common nosocomial bacterial infection and is most prevalent in medical and surgical intensive care units (ICUs). As such, HAP adds significantly to the cost of hospital care and to the length of hospital stays.

There is increasing evidence that non-ICU–acquired pneumonia (NIAP) should be called out as a separate epidemiological niche regarding management.[6]

Patients with HAP develop fever and leukocytosis. These findings are a requisite for its presumptive diagnosis. Respiratory tract symptoms include an increase in respiratory rate and shortness of breath.

Go to Mycoplasma Pneumonia, Bacterial Pneumonia, and Viral Pneumonia for more complete information on this topic.


Inhalation, aspiration, and hematogenous spread are the 3 main mechanisms by which bacteria reach the lungs. The primary route by which organisms enter the lower airways is aspiration of oropharyngeal secretions into the trachea.

Primary inhalation pneumonia develops when these organisms bypass normal respiratory defense mechanisms or when the patient inhales aerobic gram-negative organisms that colonize the upper respiratory tract or respiratory support equipment.

Aspiration pneumonia is due to the aspiration of colonized upper respiratory tract secretions.

The stomach appears to be an important reservoir of gram-negative bacilli that can ascend and colonize the respiratory tract. A prospective observational study found that patients who used acid-suppressive medications were more likely to develop hospital-acquired pneumonia (HAP) than were patients who did not (5% vs 2%). The risk for pneumonia was significantly increased with proton pump inhibitors, but not with histamine 2–blocking agents.[7]

Hematogenously acquired infections originate from a distant source and reach the lungs via the bloodstream.


The development of hospital-acquired pneumonia (HAP) represents an imbalance between normal host defenses and the ability of microorganisms to colonize and then invade the lower respiratory tract.

Because aerobic gram-negative bacilli (eg, Pseudomonas aeruginosa) are the major pathogens associated with HAP, the pathophysiology of nosocomial pneumonia relates to the destructive effect on lung tissue. Aerobic gram-negative pathogens may be divided into 2 categories. The first category includes organisms that cause necrotizing pneumonia with rapid cavitation, microabscess formation, blood-vessel invasion, and hemorrhage (eg, P aeruginosa).[8] Alternatively, other nonnecrotizing gram-negative bacilli (eg, Serratia marcescens) may be responsible for nosocomial pneumonia.

Common causes of hospital-acquired pneumonia

Common bacteria involved in hospital-acquired pneumonia (HAP) include the following:[9]

Acinetobacter species commonly colonize respiratory tract secretions in patients in the ICU. HAP caused by Acinetobacter species or B cepacia may be associated with outbreaks.

Streptococcus pneumoniae and Haemophilus influenzae are recovered only in early-onset HAP.

Less-common pathogens associated with hospital-acquired pneumonia

The following are less-common pathogens implicated in nosocomial pneumonia clusters/outbreaks:

Nosocomial Legionella pneumonia occurs often in outbreaks or clusters.

Influenza A, RSV, hMPV, or HPIV-3 may cause hospital-acquired pneumonia (HAP) from person-to-person spread.

Organisms associated with ventilator-associated pneumonia

Organisms associated with ventilator-associated pneumonia (VAP) include the following:

These organisms are commonly recovered from respiratory secretions in patients with VAP.[10] The recovery of a respiratory pathogen from respiratory secretions does not establish it as the cause of nosocomial pneumonia. MSSA/MRSA frequently colonize respiratory secretions in intubated patients but rarely, if ever, cause nosocomial pneumonia/VAP. In contrast, MSSA/MRSA may cause community-acquired pneumonia (CAP) in those with influenza. Anaerobic organisms are not important pathogens in nosocomial pneumonia. (See Differentials in Nosocomial Pneumonia.)

Risk factors

The stomach appears to be an important reservoir of gram-negative bacilli that can ascend and colonize the respiratory tract. A prospective observational study found that patients who used acid-suppressive medications were more likely to develop hospital-acquired pneumonia (HAP) than were patients who did not (5% vs 2%).

Further evaluation by drug class showed that the risk for pneumonia was significantly increased with proton pump inhibitors, but not with histamine 2–blocking agents.[7]

Epidemiology of Nosocomial Pneumonia

Incidence in the United States

The combination of hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP) constitutes the most common cause of death among all hospital-acquired infections, with mortality rates of up to 33%.

International incidence

The international incidence and prevalence of nosocomial pneumonia is similar to that in the United States, with comparable rates of responsible microorganisms.

Racial and sexual predilections

Nosocomial pneumonia has no racial or sexual predilection.

Age predilection

Nosocomial pneumonia is most common in elderly patients; however, patients of any age may be affected.

Morbidity and mortality in hospital-acquired pneumonia and ventilator-associated pneumonia

Intubation and ventilatory support bypass the normal host defense mechanisms, predisposing patients with ventilator-associated pneumonia (VAP) to infection.

In addition, hospital-acquired pneumonia (HAP)/VAP that develops in ICU patients is associated with high morbidity and mortality rates, because these patients are already critically ill.

Compromised cardiac and lung function may further decrease their cardiopulmonary reserve.

Ventilator-associated barotrauma often decreases already compromised lung function. In addition, it may alter chest radiographic appearances.

As mentioned above, early-onset HAP/VAP pneumonia (ie, hospital onset of CAP) expectedly has a better prognosis than late-onset nosocomial pneumonia because the latter tends to be associated with multidrug-resistant (MDR) organisms.[11, 12, 13, 14, 15]

Patient Prognosis

The prognosis in patients with hospital-acquired pneumonia (HAP) depends primarily on preexisting underlying cardiopulmonary function and host defenses.

In HAP/ventilator-associated pneumonia (VAP), outcomes usually depend on risk factors/comorbidities rather than on the initial empiric therapy.[16, 17, 18]

Differential Diagnoses of Nosocomial Pneumonia

All patients with presumed nosocomial pneumonia should undergo testing to rule out conditions that mimic nosocomial pneumonia. The diagnosis of nosocomial pneumonia is difficult because it may present in a very nonspecific fashion. A summary of management strategies is available through a recently released practice guideline provided by the Infectious Diseases Society of America (IDSA) and American Thoracic Society (ATS).[3]

The wide list of differential diagnoses presents a major challenge in diagnosing nosocomial pneumonia. Many conditions other than nosocomial pneumonia mimic pulmonary infiltrates (eg, fluid, atelectasis) on chest radiographs.

Any disorder that results in leukocytosis with variable degrees of left shift may be included in the differential diagnoses. Noninfectious inflammation may produce fever.

Consider all of these differential diagnoses carefully before settling on a diagnosis and embarking on a course of antimicrobial therapy.

The most common causes of infiltrates in ventilated patients with fever and/or leukocytosis include the following conditions:

ARDS is usually readily diagnosable based on the appearance of small lung volumes due to microatelectatic changes on the chest radiograph and the progressive and severe hypoxemia. Little or no fever accompanies ARDS, unless it is due to acute pancreatitis.

Electrocardiography (ECG) and ventilation-perfusion scans help to exclude pneumonia mimics. ECGs, cardiac enzymes, and Swan-Ganz readings may rule out left ventricular failure caused by exacerbation of heart failure or new myocardial infarction.

Obtain other tests that are related to the possible underlying causes of the pulmonary infiltrates; for example, if lupus pneumonitis is suspected, ask the patient about a history of systemic lupus erythematosus (SLE) pneumonitis. Afterward, serologic tests should be performed to assess for SLE.

Diagnostic Concerns

Below is a summary of the recommendations of the recent IDSA/ATF guidelines for the management of hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP).[3]

Microbiologic approach to diagnosing hospital-acquired pneumonia

If at all possible, patients should not be treated empirically. Antibiotic choice should be based on culture of sputum that is noninvasively obtained—spontaneously or by induction of sputum via nasotracheal suctioning or endotracheal aspiration in a patient who has been intubated because of HAP. Blood cultures should always be obtained, since blood culture findings are positive in a significant minority of HAP cases.

When no respiratory secretions can be obtained and blood cultures are negative, bronchoalveolar lavage should be considered in patients who are not responding to initial antibiotic therapy.[19]

Microbiologic approach to diagnosing ventilator-associated pneumonia

Obtaining sputum via noninvasive methods with semiquantitative cultures is preferred over invasive techniques with quantitative cultures or noninvasive approaches with quantitative cultures. Noninvasive techniques include collection of spontaneously expectorated samples, sputum production, and nasotracheal suctioning. Endotracheal aspiration in a patient with VAP is considered noninvasive. Invasive approaches include bronchoalveolar lavage, protected specimen brush, and blind bronchial sampling.

Biomarkers, such as procalcitonin, soluble triggering receptor expressed on myeloid cells (obtained via bronchoalveolar lavage), or C-reactive protein combined with clinical criteria should not be used to diagnose HAP/VAP. Such diagnoses should be based on clinical criteria alone. The biomarker procalcitonin (PCT) is usually unhelpful in the diagnosis of nosocomial pneumonia in ICU patients, who often have elevated PCT levels due to hypotension, renal failure, hepatic insufficiency, pancreatitis, drug reactions, or lung cancer, among others.[20, 21]

The use of the Modified Clinical Pulmonary Infection Score combined with clinical criteria should not be used to diagnose HAP/VAP. These diagnoses should be based on clinical criteria alone.

Physical Examination

Physical findings in nosocomial pneumonia relate to the pneumonia’s distribution in the chest. Physically, lobar lesions caused by nosocomial pneumonia mimic those caused by any other type of pneumonia (eg, rales in the location of the pneumonic process).

White Blood Cell Count and Blood Cultures

The WBC count may be normal or elevated in nosocomial pneumonia or disorders that mimic nosocomial pneumonia/ventilator-associated pneumonia (VAP). A left shift reflects the stress and neither rules out nor confirms infection. The degree of left shift indicates the degree of stress in the host. Neither leukocytosis nor a normal WBC count favors the diagnosis of nosocomial pneumonia over the diseases that mimic nosocomial pneumonia, as these can produce similar elevations.

Obtain blood cultures as early as possible, although they are infrequently positive, except in cases of hematogenous nosocomial pneumonia. The recovery of MSSA/MRSA in blood cultures in patients with nosocomial pneumonia/VAP without the clinical findings of MSSA/MRSA pneumonia (eg, rapid cavitation, high fevers, cyanosis) is likely due to skin contamination of blood cultures.


Serial chest radiography is most useful in ruling out progression of the pneumonia and serves as an indicator of the efficacy of appropriate antimicrobial therapy. Serial imaging is not indicated in documenting infection resolution since radiographic improvement lags far behind microbiological cure, often by several months.

View Image

Typical chest radiograph of a patient with nosocomial pneumonia.

Computed tomography (CT) scanning or spiral CT scanning may be useful in differentiating mimics from actual nosocomial pneumonia. For example, blood cultures that are positive for MSSA/MRSA in a febrile intubated patient are not diagnostic of MSSA/MRSA nosocomial pneumonia/ventilator-associated pneumonia (VAP). The diagnosis of MSSA/MRSA community-acquired pneumonia/nosocomial pneumonia is based on the clinical presence of fever, cyanosis, hypotension, and rapid cavitation of infiltrates (< 72 hours) on chest radiographs plus MSSA/MRSA in respiratory secretions.

Since only approximately 25% of changes documented on portable chest radiographs of ventilated patients represent an infectious process, follow-up CT scanning should be obtained in this situation.

Go to Imaging Atypical Pneumonia and Imaging Typical Pneumonia for more complete information on these topics.

Bronchoscopic Techniques

These techniques have variable sensitivities and specificities, although there are accepted criteria for semiquantitative cultures to improve the diagnostic reliability of bronchoscopically derived cultures.

Protected brush/cultures from bronchoalveolar lavage (BAL) reflect airway colonization (eg, Aspergillus, MSSA/MRSA, P aeruginosa) rather than nosocomial pneumonia/ventilator-associated pneumonia (VAP) pathogens in the lung parenchyma.

Multiple organisms as a cause of nosocomial pneumonia

Multiple pathogens obtained via nontissue biopsy culture methods usually indicate lower airway colonization.

Histologic Findings

Histologic study of lung tissue reveals either necrotizing or nonnecrotizing pneumonia, depending on the pathogen. P aeruginosa produces a necrotizing pneumonia with vessel invasion, local hemorrhage, and microabscess formation.[8] Other aerobic gram-negative bacilli produce a polymorphonuclear response at the site of invasion, but microabscess formation and vessel invasion are absent.

Other Tests

Electrocardiograms (ECGs) and ventilation-perfusion scans help to eliminate pneumonia mimics. ECGs, cardiac enzymes, and Swan-Ganz readings may rule out left ventricular failure caused by exacerbation of heart failure or new myocardial infarction.

Obtain other tests that are related to the possible underlying causes of the pulmonary infiltrates; for example, if lupus pneumonitis is suspected, ask the patient about a history of SLE pneumonitis. Afterward, serologic tests should be performed to assess for SLE.

ABG studies are useful in assessing the degree of severity of lung dysfunction but not in determining the specific etiology. In general, bacterial nosocomial pneumonia/ventilator-associated pneumonia (VAP) have low A-a gradients (< 35).

Treatment Considerations

Guidelines on management of adults with hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP) by the Infectious Diseases Society of America and the American Thoracic Society are as follows:[3]

Recent studies have addressed the emergence of MDR pathogens and treatment approaches, as well as the role of biomarkers in diagnosis and length of therapy.[22]

Antimicrobial therapy

Traditionally, nosocomial pneumonias have been treated for 7-14 days. However, ventilator-associated pneumonia (VAP) (except due to nonfermenting gram-negative rods [eg, P aeruginosa]) can be successfully treated in 7 days). If the patient receives appropriate antimicrobial therapy for 2 weeks and does not respond (ie, improved infiltrates findings on chest radiograph), initiate a diagnostic workup to detect nonbacterial infections (eg, herpesvirus type 1 [HSV-1] pneumonitis) or noninfectious disease mimics (eg, bronchogenic carcinomas).

The specific pathogen that causes a given case of nosocomial pneumonia is usually unknown. Therefore, empiric antimicrobial therapy is the only practical approach. These regimens should be based on the local profile of organisms associated with hospital-acquired pneumonia (HAP) and their antibiotic sensitivities.[23]

Initial and definitive treatment of hospital-acquired pneumonia

MSSA should be covered unless the patient has risk factors for MRSA, including intravenous antibiotic use within the preceding 90 days, exposure to a hospital unit where more than 20% of S aureus isolates are MRSA, or a high risk of death (eg, need for ventilatory support due to septic shock). Vancomycin or linezolid should be used to empirically cover MRSA.

For empiric coverage of MSSA, piperacillin-tazobactam cefepime, levofloxacin, imipenem, or meropenem is preferred. In cases of proven MSSA infection, oxacillin, nafcillin, or cefazolin is favored.

Double coverage against P aeruginosa should be provided in the empiric treatment of individuals with HAP who are likely to have Pseudomonas and other gram-negative infections or who are at a high risk of mortality (need for ventilatory support and/or septic shock). For all other cases, single coverage of P aeruginosa is indicated.[11]

Initial and definitive treatment of ventilator-associated pneumonia

Empiric treatment of VAP should include coverage of S aureus, P aeruginosa, and other gram-negative bacilli.

MRSA should be covered empirically in patients with any of the following risk factors for antibiotic resistance:

The preferred antibiotics for treatment of MRSA infections include vancomycin and linezolid.

The recommended antibiotics for the treatment of suspected MSSA infections include piperacillin-tazobactam, cefepime, levofloxacin, imipenem, and meropenem. When the pathogen is confirmed as MSSA, the patient should be switched to oxacillin, nafcillin, or cefazolin.

The preferred antibiotics for treatment of MRSA VAP include vancomycin and linezolid.

A single antibiotic with activity against P aeruginosa should be administered, except in patients with risk factors for multidrug-resistant (MDR) organisms, including the following:

In general, aminoglycosides should be avoided in the treatment of VAP. This also holds true for colistin. This recommendation is most likely based on poor penetration of these agents in the lung tissue, in addition to the potential nephrotoxicity of aminoglycosides and the challenge in achieving therapeutic blood levels in patients with fluctuating renal function.

In cases of HAP and VAP, antibiotics should be administered by either extended or continuous infusion. Dosing needs to be based on an antibiotic blood levels and should also be weight-based, when applicable.

The use of inhaled antibiotic therapy should be generally limited to cases of VAP produced by gram-negative bacilli that are sensitive only to aminoglycosides, colistin, or polymyxin B. These antibiotics should also be administered systemically.[24]

Double-drug coverage of P aeruginosa should combine agents with a high degree of antipseudomonal activity and low resistance potential. Optimal combinations include meropenem or doripenem plus either levofloxacin or aztreonam or amikacin.

A carbapenem or ampicillin/sulbactam should be used in treating Acinetobacter HAP/VAP. If there is resistance to these agents, inhaled and intravenous colistin should be substituted. The guidelines recommend against the use of tigecycline in the treatment of Acinetobacter VAP.


An important caveat is to differentiate P aeruginosa colonization from actual lung infection. P aeruginosa pneumonia is characterized by fever, cyanosis, hypotension, and rapid cavitation (< 72 hours) on chest radiography. Sputum recovered from these cases is typically greenish due to the pyocyanin pigment that is produced by the organism when it invades tissue. This is usually accompanied by an almond odor.

Enterobacter species do not typically cause hospital-acquired pneumonia (HAP)/ventilator-associated pneumonia (VAP). S maltophilia and B cepacia are common colonizers of respiratory secretions, but they rarely, if ever, cause nosocomial pneumonia in otherwise healthy hosts. However, they are colonizers/potential pathogens in patients with bronchiectasis or cystic fibrosis.

When the final culture and sensitivity results are available, the empiric broad-spectrum regimen should be converted to more narrow and specific coverage.

S aureus (MSSA/MRSA) commonly colonizes respiratory secretions (30%-50%) but rarely, if ever, causes necrotizing cavity nosocomial pneumonia. Oropharyngeal anaerobes are unimportant from a therapeutic standpoint.

Duration of therapy

In general, for both hospital-acquired pneumonia (HAP) and VAP, 7 days of treatment with appropriate antibiotics/antibiotics is recommended. This duration may be shortened or lengthened depending on the clinical response of the individual. Normalization of PCT levels may provide useful corroboration of clinical judgment in deciding to stop antibiotic therapy.

Patient Consultations

Consult an infectious disease specialist to assess the microbiology of the specimens obtained from the patient, to rule out the mimics of nosocomial pneumonia, and to administer empiric or specific antimicrobial therapy.

Consult a pulmonologist to help with mechanical ventilation (often required in patients with nosocomial pneumonia).

Other consultations include the following, if indicated:

Diet, Activity, and Deterrence

Many patients with nosocomial pneumonia have significant nutritional deficiencies. Early (within 48 hours) enteral nutrition appears to decrease infectious complications. Parenteral nutrition does not seem to have this effect and should be considered only in patients with a contraindication to enteral replacement.[25, 26]

Beds that permit some degree of patient turning may decrease the likelihood of hospital-acquired pneumonia (HAP)/ventilator-associated pneumonia (VAP) in at-risk patients. Decontamination of the mouth and gut may affect the risk of producing MDR organisms.[27]

Complications in Nosocomial Pneumonia

Failure to successfully wean the patient from the respirator (possibly because of a lack of cardiopulmonary function or a superimposed process [eg, HSV-1 pneumonitis]) is a common problem following intubation for nosocomial pneumonia.

HSV-1 pneumonitis develops in intubated patients who have unchanging or persistent pulmonary infiltrates after 2 weeks of antimicrobial therapy. These patients usually have low-grade fevers with variable degrees of leukocytosis. Demonstrating HSV-1 in samples of respiratory secretions may establish the diagnosis.

Start treatment with acyclovir in patients diagnosed with HSV-1 infection; acyclovir decreases hypoxemia and subsequently permits weaning of the patient from the respirator.

What is healthcare-associated pneumonia (HCAP)?What is hospital-acquired pneumonia (HAP)?Which conditions may mimic the findings of hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP)?Where is hospital-acquired pneumonia (HAP) most prevalent?How should non-ICU–acquired pneumonia (NIAP) be considered?What are the symptoms of hospital-acquired pneumonia (HAP)?How is bacterial infection transmitted in hospital-acquired pneumonia (HAP)?What is the pathogenesis of primary inhalation hospital-acquired pneumonia (HAP)?What is the pathophysiology of aspiration hospital-acquired pneumonia (HAP)?What factors increase the risk for developing hospital-acquired pneumonia (HAP)?What is the pathophysiology of hematogenous hospital-acquired pneumonia (HAP)?What causes hospital-acquired pneumonia (HAP) to develop?What is the role of aerobic gram-negative bacilli in the etiology of hospital-acquired pneumonia (HAP)?Which bacteria are common etiological agents of hospital-acquired pneumonia (HAP)?Which pathogens are less-causes of nosocomial pneumonia?Which organisms are etiologic agents of ventilator-associated pneumonia (VAP)?What are the risk factors for developing hospital-acquired pneumonia (HAP)?What is the mortality rate of nosocomial pneumonia in the US?What is the global prevalence of nosocomial pneumonia?What are the racial and sexual predilections of nosocomial pneumonia?What is the age predilection of nosocomial pneumonia?What is the morbidity and mortality associated with hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP)?What is the prognosis of hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP)?What guidelines are available for management of nosocomial pneumonia?Which conditions may be included in the differential diagnosis for nosocomial pneumonia?What are the most common causes of infiltrates in ventilated patients?Which tests are performed to exclude differential diagnoses of hospital-acquired pneumonia (HAP)?How are the underlying causes of pulmonary infiltrates determined in nosocomial pneumonia?What are the IDSA/ATF recommendations for the diagnosis of hospital-acquired pneumonia (HAP)?What are the IDSA/ATF recommendations for the diagnosis of ventilator-associated pneumonia (VAP)?Which physical findings are characteristic of nosocomial pneumonia?What is the role of WBC count in the evaluation of nosocomial pneumonia?What is the role of blood culture in the evaluation of nosocomial pneumonia?What is the role of radiography in the evaluation of nosocomial pneumonia?What is the role of CT scanning in the evaluation of nosocomial pneumonia?What is the role of bronchoscopy in the evaluation of nosocomial pneumonia?What does a nontissue biopsy finding of multiple pathogens indicate in the evaluation of nosocomial pneumonia?What are histologic findings characteristic of nosocomial pneumonia?Which tests may be indicated to exclude differential diagnoses in the evaluation of nosocomial pneumonia?What are the IDSA/ATS treatment guidelines for hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP) in adults?When is antimicrobial therapy indicated for nosocomial pneumonia?How is hospital-acquired pneumonia (HAP) treated?How is ventilator-associated pneumonia (VAP) treated?Which antibiotics are used for the treatment of MRSA nosocomial pneumonia?In which patients is a single antibiotic with activity against P aeruginosa contraindicated?What is the role of aminoglycosides in the treatment of ventilator-associated pneumonia (VAP)?How should antibiotics be administered in treatment of hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP)?What is the role of inhaled antibiotic therapy for nosocomial pneumonia?What are the optimal combination drug therapies for nosocomial pneumonia?How should Acinetobacter hospital-acquired pneumonia (HAP) or ventilator-associated pneumonia (VAP) be treated?What are the important considerations in treatment selection for nosocomial pneumonia?What is the duration of therapy for nosocomial pneumonia?Which specialists should be consulted in the treatment of hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP)?What is the role of nutrition in the treatment of nosocomial pneumonia?What may decrease the likelihood of hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP) in at risk patients?What are complications of nosocomial pneumonia?


Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

John L Brusch, MD, FACP, Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance

Disclosure: Nothing to disclose.


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Typical chest radiograph of a patient with nosocomial pneumonia.

Typical chest radiograph of a patient with nosocomial pneumonia.

Typical chest radiograph of a patient with nosocomial pneumonia.