Lung Abscess 

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.

See the image below.

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.^[3]

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.^[4] The mortality rate for patients with underlying immunocompromised status or bronchial obstruction who develop lung abscess may be as high as 75%.^[5]

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%.^[6]

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.^[7]