eMedicine Specialties > Infectious Diseases > Lower Respiratory Tract Infections

Nosocomial Pneumonia

Author: 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
Contributor Information and Disclosures

Updated: May 28, 2009

Introduction

Background

According to recent American Thoracic Society (ATS) guidelines, nosocomial pneumonia (NP; also known as hospital-acquired pneumonia [HAP] or health care–associated pneumonia [HCAP]) is defined as pneumonia that occurs more than 48 hours after admission but that was not incubating at the time of admission. Ventilator-associated pneumonia (VAP) is defined as pneumonia that occurs after 48-72 hours of endotracheal intubation. Nosocomial pneumonia is the second-most-common nosocomial infection and is usually bacterial in origin. The disease adds significantly to the cost of hospital care and to the length of hospital stays.

Although most patients with nosocomial pneumonia develop fever and leukocytosis, these findings are not uniform and are not a requisite for the presumptive diagnosis of nosocomial pneumonia.

The ATS subdivides nosocomial pneumonia into early onset (usually within the first 4 d of the hospitalization) and late onset (usually occurring after the fifth hospital day). Early-onset nosocomial pneumonia tends to carry a better prognosis, whereas late-onset nosocomial pneumonia tends to be associated with multidrug-resistant organisms, meaning that it is associated with higher mortality rates.

Pathophysiology

The development of nosocomial pneumonia represents an imbalance between normal host defenses and the ability of microorganisms to colonize and then invade the lower respiratory tract. The primary route through which organisms enter the lower airways is via aspiration of oropharyngeal secretions into the trachea. Hematogenous spread to the lungs is an alternative but uncommon route of infection.

Because aerobic gram-negative bacilli are the major pathogens associated with nosocomial pneumonia, the pathophysiology relates to the destructive effect of these organisms on invaded lung tissue. Aerobic gram-negative pathogens may be divided into two categories. The first category includes organisms that cause necrotizing pneumonia with rapid cavitation, microabscess formation, blood-vessel invasion, and hemorrhage (eg, Pseudomonas aeruginosa). The second category consists of all other nonnecrotizing gram-negative organisms responsible for nosocomial pneumonia.

Frequency

United States

Nosocomial pneumonia is the second-most-common nosocomial infection in the United States and is usually bacterial in nature. It is one of the most common diagnoses made in medical and surgical intensive care units (ICUs) and is common in patients undergoing mechanical ventilation. Nosocomial pneumonia also occurs in patients in the general hospital wards who are not receiving mechanical ventilation.

International

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

Mortality/Morbidity

Because patients in ICUs are already typically critically ill, the mortality and morbidity rates associated with nosocomial pneumonia in these patients are high. Intubation and ventilatory support bypass the normal host defense mechanisms, predisposing to infection.

Race

Nosocomial pneumonia has no racial predilection.

Sex

Nosocomial pneumonia has no sexual predilection.

Age

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

Clinical

History

  • Symptoms of nosocomial pneumonia (NP; also known as hospital-acquired pneumonia [HAP] or health care–associated pneumonia [HCAP])
    • Respiratory tract symptoms, which may include an increase in respiratory rate, shortness of breath, and a productive cough
    • Fever (most cases)
  • Clinical diagnosis
    • In most cases, the diagnosis of nosocomial pneumonia is clinical, supported by appropriate cultures, which may include semiquantitative cultures from bronchoalveolar lavage (BAL) samples.
    • The definitive diagnosis of nosocomial pneumonia rests on tissue biopsy, which is rarely performed; therefore, the clinician is forced to grapple with various nonspecific findings that can mimic nosocomial pneumonia. This situation is particularly true of chest radiographic findings of pulmonary infiltrates, which may be caused by numerous conditions common in the critical care setting. The most common causes of infiltrates in ventilated patients with fever and/or leukocytosis include the following conditions:  

Physical

  • Physical findings in nosocomial pneumonia relate to the pneumonia 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).
  • In most cases, neither consolidation nor pleural effusions are features of nosocomial pneumonia. The presence of either should prompt consideration of an alternate diagnosis.
  • The presumptive diagnosis of nosocomial pneumonia is clinical and is based on nonspecific findings; therefore, it is not necessarily precise. Most patients in the ICU who have fever and pulmonary infiltrates probably do not have nosocomial pneumonia; nonetheless, therapy should be based on a clinical diagnosis since tissue-based biopsy methods are not used in most patients.
  • Several conditions mimic nosocomial pneumonia; therefore, incorporate the exclusion of these conditions as part of the clinical diagnosis.

Causes

Inhalation, aspiration, and hematogenous spread are the 3 main mechanisms by which bacteria reach the lungs.

Factors that predispose to infection include the following:

  • 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 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 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.1
  • Hematogenously acquired infections originate from a distant source and reach the lungs via the bloodstream. In bacteremic nosocomial pneumonia, blood culture results are frequently positive if obtained early in the disease process and if the patient is not already receiving antimicrobial therapy.

Microbiology of Nosocomial Pneumonia

Common causes of nosocomial pneumonia

Common bacteria involved in nosocomial pneumonia include the following:

Nosocomial pneumonia is mistakenly diagnosed in many cases; therefore, the differential diagnoses are important.

Less-common pathogens associated with nosocomial pneumonia

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

Influenza A virus, RSV, parainfluenza virus, and adenovirus, may cause HAP in the right clinical setting.

Extremely rare causes of nosocomial pneumonia

The following are rarely isolated in patients with nosocomial pneumonia:

Although these organisms may be very uncommon causes of nosocomial pneumonia, they have been recovered in patients with ventilator-associated pneumonia (VAP). The recovery from respiratory secretions of an organism that is typically pathogenic does not prove that it is pathogenic or the cause of nosocomial pneumonia. Anaerobic organisms are not typically isolated in nosocomial pneumonia.

Multiple organisms as a cause of nosocomial pneumonia

Multiple pathogens are proof of lower airway colonization obtained by nontissue biopsy culture methods.

More on Nosocomial Pneumonia

Overview: Nosocomial Pneumonia
Differential Diagnoses & Workup: Nosocomial Pneumonia
Treatment & Medication: Nosocomial Pneumonia
Follow-up: Nosocomial Pneumonia
Multimedia: Nosocomial Pneumonia
References

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Further Reading

Keywords

nosocomial pneumonia, NP, hospital-acquired pneumonia, HAP, healthcare-associated pneumonia, health care–associated pneumonia, HCAP, ventilator-associated pneumonia, VAP

Contributor Information and Disclosures

Author

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
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Medical Editor

Wesley W Emmons, MD, FACP, Assistant Professor, Department of Medicine, Thomas Jefferson University; Consulting Staff, Infectious Diseases Section, Department of Internal Medicine, Christiana Care, Newark, DE
Wesley W Emmons, MD, FACP is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and International AIDS Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Ronald A Greenfield, MD, Professor, Department of Internal Medicine, Section of Infectious Diseases, University of Oklahoma College of Medicine
Ronald A Greenfield, MD is a member of the following medical societies: American College of Physicians, American Federation for Medical Research, American Society for Microbiology, Central Society for Clinical Research, Infectious Diseases Society of America, Medical Mycology Society of the Americas, Phi Beta Kappa, Southern Society for Clinical Investigation, and Southwestern Association of Clinical Microbiology
Disclosure: Pfizer Honoraria Speaking and teaching; Gilead Honoraria Speaking and teaching; Ortho McNeil Honoraria Speaking and teaching; Wyeth Honoraria Speaking and teaching; Abbott Honoraria Speaking and teaching; Astellas Honoraria Speaking and teaching; Cubist  Speaking and teaching

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD, Professor, Stewart G Wolf Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center
Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physician Executives, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, Association of Professors of Medicine, Association of Program Directors in Internal Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, and Southern Society for Clinical Investigation
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