eMedicine Specialties > Pulmonology > Infectious Lung Diseases

Lung Abscess

Author: 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: May 8, 2006

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 1920s, approximately one third of patients with lung abscess died; Dr 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 not by one but with an inoculum containing 4 microbes, known as anaerobic spirochete: 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.

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, caused by septic emboli to the lung.

Microbiology

In lung abscesses, anaerobes are recovered in up to 89% of the patients. 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. The most common anaerobes are Peptostreptococcus, Bacteroides, Fusobacterium species, and microaerophilic streptococcus.

Other organisms 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.

Nonbacterial pathogens may also cause lung abscesses. These microorganisms include parasites (eg, Paragonimus, Entamoeba), fungi (eg, Aspergillus, Cryptococcus, Histoplasma, Blastomyces, Coccidioides), and Mycobacterium.

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% (Bartlett, 1992). The mortality rate for patients with underlying immunocompromised status or bronchial obstruction who develop lung abscess may be as high as 75% (Pohlson, 1985). A retrospective study (Hirshberg, 1995) reported the overall mortality rate of lung abscesses caused by mixed gram-positive and gram-negative bacteria at approximately 20%.

Age

These conditions occur more commonly in elderly patients because of the increased incidence of periodontal disease and the increased prevalence of microaspiration.

Clinical

History

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

  • Anaerobic infection
    • 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 bacterial pathogens
    • 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, and mycobacteria 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 may have low-grade fever in anaerobic infections and temperatures higher than 38.5°C in other infections.
  • Generally, evidence of gingival disease is present.
  • 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:
    • Poor dentition
    • Seizure disorder
    • Alcohol abuse
  • Other patients at high risk for developing lung abscess include the following:
    • Individuals with an inability to protect their airways because of an absent gag reflex, such as during coma, loss of consciousness, or general anesthesia and sedation
    • Patients with primary lung disorders, such as septic emboli from tricuspid endocarditis, vasculitic disorders, cavitating lung malignancies, and pulmonary cystic diseases
  • Infrequently, the following infectious etiologies of pneumonia may progress to parenchymal necrosis and lung abscess formation:
    • Pseudomonas aeruginosa
    • Klebsiella pneumoniae
    • Staphylococcus aureus (may result in multiple abscesses)
    • Streptococcal pneumonia
    • Nocardia species
    • Fungal species
  • An abscess may develop as an infectious complication of a preexisting bulla or lung cyst.
  • An abscess may occur secondary to carcinoma of the bronchus; the bronchial obstruction causes postobstructive pneumonia, which may lead to abscess formation.
  • A recent study by Wang et al from Taiwan suggested that the bacteriologic characteristics of lung abscess have changed. By performing transthoracic lung aspiration, they showed that anaerobes were recovered from just 28 patients (31%); the predominant bacterium was Klebsiella pneumoniae, in 30 patients (33%). This study concluded that K pneumoniae has become more common as a cause of lung abscess, and the antibiotic coverage should include this organism, anaerobes, and S milleri (Wang, 2005).

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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Further Reading

Keywords

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

Contributor Information and Disclosures

Author

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: Nothing to disclose.

Pharmacy Editor

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

Managing Editor

Robert S Crausman, MD, MMS, Chief Administrative Officer, Rhode Island Board of Medical Licensure and Discipline, Rhode Island Department of Health; Associate Professor, Department of Medicine, Brown University School of Medicine
Robert S Crausman, MD, MMS is a member of the following medical societies: American College of Chest Physicians and American College of Physicians
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
Disclosure: Nothing to disclose.

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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