# 11 - 132 Lung Abscess

### 132 Lung Abscess

community-acquired pneumonia in adults. Clin Infect Dis 44:S27, 
2007.
Martin-Loeches I et al: ERS/ESICM/ESCMID/ALAT guidelines for 

the management of severe community-acquired pneumonia. Eur 
Respir J 61:2200735, 2023.
Metlay JP et al: Diagnosis and treatment of adults with communityacquired pneumonia. An Official Clinical Practice Guideline of 
the American Thoracic Society and Infectious Diseases Society of 
America. Am J Respir Crit Care Med 200:e45, 2019.
Vacheron CH et al: Attributable mortality of ventilator-associated 
pneumonia among patients with COVID-19. Am J Respir Crit Care 
Med 206:161, 2022.
Rebecca M. Baron, Beverly W. Baron, 

Miriam Baron Barshak

Lung Abscess
Lung abscess represents necrosis and cavitation of the lung following 
microbial infection. Lung abscesses can be single or multiple but usu­
ally are marked by a single dominant cavity >2 cm in diameter.
PART 5
Infectious Diseases
■
■ETIOLOGY
The low prevalence of lung abscesses makes them difficult to study in 
randomized controlled trials. Although the incidence of lung abscesses 
has decreased in the antibiotic era, they are still a source of significant 
morbidity and mortality.
Lung abscesses usually are characterized as either primary (~80% of 
cases) or secondary. Primary lung abscesses generally arise from aspi­
ration, often are caused principally by anaerobic bacteria, and occur in 
the absence of an underlying pulmonary or systemic condition. 
Secondary lung abscesses arise in the setting of an underlying condi­
tion, such as a postobstructive process (e.g., bronchial foreign body, 
tumor) or a systemic process (e.g., HIV infection, another immuno­
compromising condition). Lung abscesses can also be characterized as 
acute (<4–6 weeks in duration) or chronic (~40% of cases).
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■EPIDEMIOLOGY
The majority of the existing epidemiologic information involves pri­
mary lung abscesses. In general, middle-aged men are more commonly 
affected than middle-aged women. The major risk factor for primary 
lung abscesses is aspiration. Patients at particular risk for aspiration, 
such as those with altered mental status, alcoholism, drug overdose, 
seizures, bulbar dysfunction, prior cerebrovascular or cardiovascular 
events, or neuromuscular disease, are most commonly affected. At 
additional risk are patients with esophageal dysmotility or esophageal 
lesions (strictures or tumors) and those with gastric distention and/or 
gastroesophageal reflux, especially those who spend substantial time in 
the recumbent position.
It is widely thought that colonization of the gingival crevices by 
anaerobic bacteria or microaerophilic streptococci (especially in 
patients with gingivitis and periodontal disease), combined with a risk 
of aspiration, is important in the development of lung abscesses. In 
fact, many physicians consider it extremely rare for lung abscesses to 
develop in the absence of teeth as a nidus for bacterial colonization.
The importance of these risk factors in the development of lung 
abscesses is highlighted by a significant reduction in abscess inci­
dence in the late 1940s that coincided with a change in oral surgical 
technique: beginning at that time, these operations were no longer 
performed with the patient in the seated position without a cuffed 
endotracheal tube, and the frequency of perioperative aspiration events 
was thus decreased. In addition, the introduction of penicillin around 

TABLE 132-1  Examples of Microbial Pathogens That Can Cause Lung 
Abscesses
CLINICAL CONDITION
PATHOGENS
Primary lung abscess 
(often with risk factors 
for aspiration)
Anaerobes (e.g., Peptostreptococcus spp., Prevotella 
spp., Bacteroides spp., milleri group streptococci), 
microaerophilic streptococci
Secondary lung 
abscess (often 
with underlying 
immunocompromise)
Staphylococcus aureus, gram-negative rods (e.g., 
Pseudomonas aeruginosa, Enterobacteriaceae), 
Nocardia spp., Aspergillus spp., Mucorales, 
Cryptococcus spp., Legionella spp., Rhodococcus equi, 
Pneumocystis jirovecii
Embolic lesions
Staphylococcus aureus (often from endocarditis), 
Fusobacterium necrophorum (Lemierre’s syndrome; see 
text for details)
Endemic infections 
(with or without 
underlying 
immunocompromise)
Mycobacterium tuberculosis (as well as 
Mycobacterium avium and Mycobacterium kansasii), 
Coccidioides spp., Histoplasma capsulatum, 
Blastomyces spp., parasites (e.g., Entamoeba 
histolytica, Paragonimus westermani, Strongyloides 
stercoralis)
Miscellaneous 
conditions
Bacterial pathogen (often S. aureus) after influenza or 
another viral infection, Actinomyces spp.
the same time significantly reduced the incidence of and mortality rate 
from lung abscess.
■
■PATHOGENESIS
Primary Lung Abscesses 
The development of primary lung 
abscesses is thought to originate when chiefly anaerobic bacteria (as well 
as microaerophilic streptococci) in the gingival crevices are aspirated 
into the lung parenchyma in a susceptible host (Table 132-1). Patients 
who develop primary lung abscesses usually carry an overwhelming 
burden of aspirated material or are unable to clear the bacterial load. 
Pneumonitis develops initially (exacerbated in part by tissue damage 
caused by gastric acid); then, over a period of 7–14 days, the bacteria 
produce parenchymal necrosis and cavitation whose extent depends on 
host–pathogen interaction (Fig. 132-1). Anaerobes are thought to pro­
duce more extensive tissue necrosis in polymicrobial infections in which 
virulence factors of the various bacteria can act synergistically to cause 
more significant tissue destruction.
Secondary Lung Abscesses 
The pathogenesis of secondary 
abscesses depends on the predisposing factor. For example, in cases 
of bronchial obstruction from malignancy or a foreign body, the 
A
B
FIGURE 132-1  Representative chest CT scans demonstrating development of lung 
abscesses. This patient was immunocompromised from underlying lymphoma and 
developed severe Pseudomonas aeruginosa pneumonia, as represented by a left 
lung infiltrate with concern for central regions of necrosis (panel A, black arrow). 
Two weeks later, areas of cavitation with air-fluid levels were visible in this region 
and were consistent with the development of lung abscesses (panel B, white 
arrow). (Images provided by Dr. Ritu Gill, formerly of the Division of Chest Radiology, 
Brigham and Women’s Hospital, Boston; with permission.)

obstructing lesion prevents clearance of oropharyngeal secretions, 
leading to abscess development. With underlying systemic conditions 
(e.g., immunosuppression after bone marrow or solid organ transplan­
tation), impaired host defense mechanisms lead to increased suscepti­
bility to the development of lung abscesses caused by a broad range of 
pathogens, including opportunistic organisms (Table 132-1).
Lung abscesses also arise from septic emboli, either in tricuspid 
valve endocarditis (often involving Staphylococcus aureus) or in 
Lemierre’s syndrome, in which an infection begins in the pharynx 
(classically involving Fusobacterium necrophorum) and then spreads 
to the neck and the carotid sheath (which contains the jugular vein) to 
cause septic thrombophlebitis.
■
■PATHOLOGY AND MICROBIOLOGY
Primary Lung Abscesses 
The dependent segments (posterior 
upper lobes and superior lower lobes) are the most common locations 
of primary lung abscesses, given the predisposition of aspirated materi­
als to be deposited in these areas. Generally, the right lung is affected 
more commonly than the left because the right mainstem bronchus is 
less angulated.
Primary lung abscesses often are polymicrobial, primarily including 
anaerobic organisms as well as microaerophilic streptococci (Table 132-1). 
The retrieval and culture of anaerobes can be complicated by the con­
tamination of samples with microbes from the oral cavity, the need for 
expeditious transport of the cultures to the laboratory, the need for early 
plating with special culture techniques, the prolonged time required for 
culture growth, and the need for collection of specimens prior to admin­
istration of antibiotics. When attention is paid to these factors, rates of 
recovery of specific isolates are reportedly as high as 78%.
Because it is not clear that knowing the identity of the causative 
anaerobic isolate alters the approach to treatment of a primary lung 
abscess, practice has shifted away from the use of specialized tech­
niques to obtain material for culture, such as transtracheal aspiration 
and bronchoalveolar lavage with protected brush specimens that allow 
recovery of culture material while avoiding contamination from the 
oral cavity. When no pathogen is isolated from a primary lung abscess 
(which occurs as often as 40% of the time), the abscess is termed a 
nonspecific lung abscess, and the presence of anaerobes is often pre­
sumed. A putrid lung abscess refers to cases with foul-smelling breath, 
sputum, or empyema; these manifestations are essentially diagnostic of 
an anaerobic lung abscess.
Secondary Lung Abscesses 
The location of secondary abscesses 
may vary with the underlying cause. The microbiology of second­
ary lung abscesses can encompass a broad bacterial spectrum, with 
infection by Pseudomonas aeruginosa and other gram-negative rods 
the most common. In addition, a broad array of pathogens can be 
identified in patients from certain endemic areas and in specific clini­
cal scenarios (e.g., a significant incidence of fungal infections among 
immunosuppressed patients following bone marrow or solid organ 
transplantation). Because immunocompromised hosts and patients 
without the classic presentation of a primary lung abscess can be 
infected with a wide array of unusual organisms (Table 132-1), it is of 
special importance to obtain culture material to target therapy.
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■CLINICAL MANIFESTATIONS
Clinical manifestations initially may be similar to those of pneumo­
nia, with fevers, cough, sputum production, and chest pain; a more 
chronic and indolent presentation that includes night sweats, fatigue, 
and anemia is often observed with anaerobic lung abscesses. A subset 
of patients with putrid lung abscesses may report discolored phlegm 
and foul-tasting or foul-smelling sputum. Patients with lung abscesses 
due to non-anaerobic organisms, such as S. aureus, may present 
with a more fulminant course characterized by high fevers and rapid 
progression.
Findings on physical examination may include fevers, poor denti­
tion, and/or gingival disease as well as amphoric and/or cavernous 
breath sounds on lung auscultation. Additional findings may include 
digital clubbing and the absence of a gag reflex.

■
■DIFFERENTIAL DIAGNOSIS
The differential diagnosis of lung abscesses is broad and includes other 
noninfectious processes that result in cavitary lung lesions, including 
lung infarction, malignancy, sequestration, cryptogenic organizing 
pneumonia, sarcoidosis, vasculitides and autoimmune diseases (e.g., 
granulomatosis with polyangiitis), lung cysts or bullae containing fluid, 
and septic emboli (e.g., from tricuspid valve endocarditis). Other less 
common entities can include pulmonary manifestations of diseases 
that usually present at locations other than the chest (e.g., inflamma­
tory bowel disease, pyoderma gangrenosum).

■
■DIAGNOSIS
Lung abscesses are documented by chest imaging. Although a chest 
radiograph usually detects a thick-walled cavity with an air-fluid level, 
CT permits better definition and may provide earlier evidence of 
cavitation. CT may also yield additional information regarding a pos­
sible underlying cause of lung abscess, such as malignancy, and may 
help distinguish a peripheral lung abscess from a pleural infection. This 
distinction has important implications for treatment because a pleural 
space infection, such as an empyema, may require urgent drainage.
As described earlier (see “Pathology and Microbiology,” above), 
more invasive diagnostics (such as transtracheal aspiration) were tra­
ditionally undertaken for primary lung abscesses, whereas empirical 
therapy that includes drugs targeting anaerobic organisms currently 
is used more often. While sputum can be collected noninvasively for 
Gram’s stain and culture, which may yield a pathogen, the infection is 
likely to be polymicrobial, and culture results may not reflect the pres­
ence of anaerobic organisms. Increasing use of molecular techniques 
for bacterial detection (e.g., 16S RNA gene amplification) may eventu­
ally yield more specific pathogen identification. As stated above, many 
physicians consider putrid-smelling sputum to be virtually diagnostic 
of an anaerobic infection.
CHAPTER 132
When a secondary lung abscess is present or empirical therapy fails 
to elicit a response, sputum and blood cultures are advised in addi­
tion to serologic studies for opportunistic pathogens (e.g., viruses and 
fungi causing infections in immunocompromised hosts). Additional 
diagnostics, such as bronchoscopy with bronchoalveolar lavage or 
protected brush specimen collection and CT-guided percutaneous 
needle aspiration, can be undertaken. Risks posed by these more 
invasive diagnostics include spillage of abscess contents into the other 
lung (with bronchoscopy) and pneumothorax and bronchopleural 
fistula development (especially with CT-guided needle aspiration). 
However, early diagnostics in secondary abscesses, especially in immu­
nocompromised hosts, are particularly important because the patients 
involved may be especially fragile, at risk for infection with a broad 
array of pathogens, and therefore less likely than other patients to 
respond to empirical therapy.
Lung Abscess
TREATMENT
Lung Abscess
The availability of antibiotics in the 1940s and 1950s established 
therapy with this drug class as the primary approach to the treat­
ment of lung abscess. Previously, surgery had been relied upon much 
more frequently. For many decades, penicillin was the antibiotic of 
choice for primary lung abscesses in light of its anaerobic cover­
age; however, because oral anaerobes can produce β-lactamases, 
clindamycin has proved superior to penicillin in clinical trials. For 
primary lung abscesses, the recommended regimens are (1) clindamy­
cin (600 mg IV three times daily; then, with the disappearance of 
fever and clinical improvement, 300 mg PO four times daily) or (2) 
an IV-administered β-lactam/β-lactamase combination, followed—
once the patient’s condition is stable—by orally administered 
amoxicillin-clavulanate. This therapy should be continued until 
imaging demonstrates that the lung abscess has cleared or regressed 
to a small scar. Treatment duration may range from 3–4 weeks to as 
long as 14 weeks, with some literature suggesting that a course of 
at least 6 weeks may be associated with better outcomes. One small