eMedicine Specialties > Pulmonology > Infectious Lung Diseases

Lung Abscess

Author: Nader Kamangar, MD, FACP, FCCP, FAASM,, Associate Professor of Clinical Medicine, Director of Hospitalist/Intensivist Program, Division of Pulmonary, Critical Care and Sleep Medicine, David Geffen School of Medicine at University of California Los Angeles; Associate Director, Combined Pulmonary and Critical Care Fellowship Program, Cedars-Sinai/Olive View-UCLA/West Los Angeles Veterans Affairs Medical Center
Coauthor(s): Curtis C Sather, MD, Fellow, Divison of Pulmonary/Critical Care Medicine, Cedars-Sinai Medical Center; Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital
Contributor Information and Disclosures

Updated: Aug 19, 2009

Introduction

Background

Lung abscess is defined as necrosis of the pulmonary tissue and formation of cavities containing necrotic debris or fluid caused by microbial infection. The formation of multiple small (<2 cm) abscesses is occasionally referred to as necrotizing pneumonia or lung gangrene. Both lung abscess and necrotizing pneumonia are manifestations of a similar pathologic process. Failure to recognize and treat lung abscess is associated with poor clinical outcome.
 
In the 1920s, approximately one third of patients with lung abscess died; Dr David Smith postulated that aspiration of oral bacteria was the mechanism of infection. He observed that the bacteria found in the walls of the lung abscesses at autopsy resembled the bacteria noted in the gingival crevice. A typical lung abscess could be reproduced in animal models via an intratracheal inoculum containing, not 1, but 4 microbes, thought to be Fusobacterium nucleatum, Peptostreptococcus species, a fastidious gram-negative anaerobe, and, possibly, Prevotella melaninogenicus.
 
Lung abscess was a devastating disease in the preantibiotic era, when one third of the patients died, another one third recovered, and the remainder developed debilitating illnesses such as recurrent abscesses, chronic empyema, bronchiectasis, or other consequences of chronic pyogenic infections. In the early postantibiotic period, sulfonamides did not improve the outcome of patients with lung abscess until the penicillins and tetracyclines were available. Although resectional surgery was often considered a treatment option in the past, the role of surgery has greatly diminished over time because most patients with uncomplicated lung abscess eventually respond to prolonged antibiotic therapy.
 
Lung abscesses can be classified based on the duration and the likely etiology. Acute abscesses are less than 4-6 weeks old, whereas chronic abscesses are of longer duration. Primary abscess is infectious in origin, caused by aspiration or pneumonia in the healthy host; secondary abscess is caused by a preexisting condition (eg, obstruction), spread from an extrapulmonary site, bronchiectasis, and/or an immunocompromised state. Lung abscesses can be further characterized by the responsible pathogen, such as Staphylococcus lung abscess and anaerobic or Aspergillus lung abscess.

A thick-walled lung abscess.

A thick-walled lung abscess.

A thick-walled lung abscess.

A thick-walled lung abscess.

Pathophysiology

Most frequently, the lung abscess arises as a complication of aspiration pneumonia caused by mouth anaerobes. The patients who develop lung abscess are predisposed to aspiration and commonly have periodontal disease. A bacterial inoculum from the gingival crevice reaches the lower airways, and infection is initiated because the bacteria are not cleared by the patient's host defense mechanism. This results in aspiration pneumonitis and progression to tissue necrosis 7-14 days later, resulting in formation of lung abscess.
 
Other mechanisms for lung abscess formation include bacteremia or tricuspid valve endocarditis, causing septic emboli (usually multiple) to the lung. Lemierre syndrome, an acute oropharyngeal infection followed by septic thrombophlebitis of the internal jugular vein, is a rare cause of lung abscesses. The oral anaerobe F necrophorum is the most common pathogen.
 
Microbiology
 
Because of the difficulty obtaining material uncontaminated by nonpathogenic bacteria colonizing the upper airway, lung abscesses rarely have a microbiologic diagnosis.
 
Published reports since the beginning of the antibiotic area have established that anaerobic bacteria are the most significant pathogens in lung abscess. In a study by Bartlett et al in 1974, 46% of patients with lung abscesses had only anaerobes isolated from sputum cultures, while 43% of patients had a mixture of anaerobes and aerobes.1 The most common anaerobes are Peptostreptococcus species, Bacteroides species, Fusobacterium species, and microaerophilic streptococci.
 
Aerobic bacteria that may infrequently cause lung abscess include Staphylococcus aureus, Streptococcus pyogenes, Streptococcus pneumoniae (rarely), Klebsiella pneumoniae, Haemophilus influenzae, Actinomyces species, Nocardia species, and gram-negative bacilli.
 
Challenging current expert opinion, a study by Wang et al suggested that the bacteriologic characteristics of lung abscess have changed.2 In a series of 90 patients with community-acquired lung abscess in Taiwan, anaerobes were recovered from just 28 patients (31%); the predominant bacterium was K pneumoniae, in 30 patients (33%). Another significant finding was that the rate of resistance of anaerobes and Streptococcus milleri to clindamycin and penicillin increased compared with previous reports.
 
Nonbacterial and atypical bacterial pathogens may also cause lung abscesses, usually in the immunocompromised host. These microorganisms include parasites (eg, Paragonimus and Entamoeba species), fungi (eg, Aspergillus, Cryptococcus, Histoplasma, Blastomyces, and Coccidioides species), and Mycobacterium species.

Frequency

United States

The frequency of lung abscess in the general population is not known.

Mortality/Morbidity

Most patients with primary lung abscess improve with antibiotics, with cure rates documented at 90-95%.
 
Host factors associated with a poor prognosis include advanced age, debilitation, malnutrition, human immunodeficiency virus infection or other forms of immunosuppression, malignancy, and duration of symptoms greater than 8 weeks.3 The mortality rate for patients with underlying immunocompromised status or bronchial obstruction who develop lung abscess may be as high as 75%.4
 
Aerobic organisms, frequently hospital acquired, are associated with poor outcomes. A retrospective study reported the overall mortality rate of lung abscesses caused by mixed gram-positive and gram-negative bacteria at approximately 20%.5

Sex

A male predominance for lung abscess is reported in published case series.

Age

Lung abscesses likely occur more commonly in elderly patients because of the increased incidence of periodontal disease and the increased prevalence of dysphagia and aspiration. However, a case series from an urban center with high prevalence of alcoholism reported a mean age of 41 years.6

Clinical

History

Symptoms depend on whether the abscess is caused by anaerobic or other bacterial infection.

  • Anaerobic infection in lung abscess
    • Patients often present with indolent symptoms that evolve over a period of weeks to months.
    • The usual symptoms are fever, cough with sputum production, night sweats, anorexia, and weight loss.
    • The expectorated sputum characteristically is foul smelling and bad tasting.
    • Patients may develop hemoptysis or pleurisy
  • Other pathogens in lung abscess
    • These patients generally present with conditions that are more emergent in nature and are usually treated while they have bacterial pneumonia.
    • Cavitation occurs subsequently as parenchymal necrosis ensues.
    • Abscesses from fungi, Nocardia species, and Mycobacteria species tend to have an indolent course and gradually progressive symptoms.

Physical

The findings on physical examination of a patient with lung abscess are variable. Physical findings may be secondary to associated conditions such as underlying pneumonia or pleural effusion. The physical examination findings may also vary depending on the organisms involved, the severity and extent of the disease, and the patient's health status and comorbidities.

  • Patients with lung abscesses may have low-grade fever in anaerobic infections and temperatures higher than 38.5°C in other infections.
  • Generally, patients with in lung abscess have evidence of gingival disease.
  • Clinical findings of concomitant consolidation may be present (eg, decreased breath sounds, dullness to percussion, bronchial breath sounds, course inspiratory crackles).
  • The amphoric or cavernous breath sounds are only rarely elicited in modern practice.
  • Evidence of pleural friction rub and signs of associated pleural effusion, empyema, and pyopneumothorax may be present. Signs include dullness to percussion, contralateral shift of the mediastinum, and absent breath sounds over the effusion.
  • Digital clubbing may develop rapidly.

Causes

The bacterial infection may reach the lungs in several ways. The most common is aspiration of oropharyngeal contents.

  • Patients at the highest risk for developing lung abscess have the following risk factors:
    • Periodontal disease
    • Seizure disorder
    • Alcohol abuse
    • Dysphagia
  • Other patients at high risk for developing lung abscess include individuals with an inability to protect their airways from massive aspiration because of a diminished gag or cough reflex, caused by a state of impaired consciousness (eg, from alcohol or other CNS depressants, general anesthesia, or encephalopathy).
  • Infrequently, the following infectious etiologies of pneumonia may progress to parenchymal necrosis and lung abscess formation:
    • Pseudomonas aeruginosa
    • K pneumoniae
    • S aureus (may result in multiple abscesses)
    • Streptococcus pneumoniae
    • Nocardia species
    • Fungal species
  • An abscess may develop as an infectious complication of a preexisting bulla or lung cyst.
  • An abscess may develop secondary to carcinoma of the bronchus; the bronchial obstruction causes postobstructive pneumonia, which may lead to abscess formation.

More on Lung Abscess

Overview: Lung Abscess
Differential Diagnoses & Workup: Lung Abscess
Treatment & Medication: Lung Abscess
Follow-up: Lung Abscess
Multimedia: Lung Abscess
References

References

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  2. Wang JL, Chen KY, Fang CT, Hsueh PR, Yang PC, Chang SC. Changing bacteriology of adult community-acquired lung abscess in Taiwan: Klebsiella pneumoniae versus anaerobes. Clin Infect Dis. Apr 1 2005;40(7):915-22. [Medline].

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Further Reading

Keywords

lung abscess, lung abscesses, necrotizing pneumonia, lung gangrene, necrosis of pulmonary tissue, lung cavities, aspiration pneumonia, periodontal disease, bacteremia, tricuspid valve endocarditis

Contributor Information and Disclosures

Author

Nader Kamangar, MD, FACP, FCCP, FAASM,, Associate Professor of Clinical Medicine, Director of Hospitalist/Intensivist Program, Division of Pulmonary, Critical Care and Sleep Medicine, David Geffen School of Medicine at University of California Los Angeles; Associate Director, Combined Pulmonary and Critical Care Fellowship Program, Cedars-Sinai/Olive View-UCLA/West Los Angeles Veterans Affairs Medical Center
Nader Kamangar, MD, FACP, FCCP, FAASM, is a member of the following medical societies: American Academy of Sleep Medicine, American Association of Bronchology, American College of Chest Physicians, American College of Physicians, American Lung Association, American Medical Association, American Thoracic Society, California Thoracic Society, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Curtis C Sather, MD, Fellow, Divison of Pulmonary/Critical Care Medicine, Cedars-Sinai Medical Center
Curtis C Sather, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, and American Thoracic Society
Disclosure: Nothing to disclose.

Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital
Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Stephen P Peters, MD, PhD, Professor, Department of Medicine, Wake Forest University
Stephen P Peters, MD, PhD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Association of Immunologists, American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic Society, and Sigma Xi
Disclosure: See below for list of all activities None None

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Disclosure: eMedicine Salary Employment

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,, Kathy Roarty Placeholder
Disclosure: Nothing to disclose.

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
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Chief Editor

Zab Mosenifar, MD, Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center; Professor of Medicine, David Geffen School of Medicine at UCLA
Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society
Disclosure: Nothing to disclose.

 
 
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