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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. After penicillins and tetracyclines became available,
outcomes improved. 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 abscesses
are infectious in origin, caused by aspiration or pneumonia in the healthy host. Secondary
abscesses are 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 abscesses and anaerobic
abscess or Aspergillus lung abscess.
See the image below.
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 714 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
Some geographic differences exist, with Streptoccous speciesbeing more prevelant in this study
(done in 1 hospital in Japan), compared to previous accounts of anaerobic bacterial species being
most predominant in Western populations. The study population notably had a 61% of
individuals with periodontal disease, 16.6% were considered alcoholic, and 22.9% had
significant diabetes mellitus. They were primarily Japanese, male (82%), smokers (75.6%), and
alcoholic (34%).[3]
To support the findings by Takayangi et al, a subsequent study done by Want et al 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.[2]
Both studies by Wang et al and Takayanagai suggest that aerobic organisms were more likely to
be found in individuals with diabetes mellitus and periodontal disease, both risk factors for
aerobic community acquired lung abscesses.
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.
Epidemiology
Frequency
United States
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 Grampositive and Gram-negative bacteria at approximately 20%.[6]
Sex
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]