Lung abscess

Author: John G Bartlett, MD

Section Editor: Stephen B Calderwood, MD
Deputy Editors: Helen Hollingsworth, MD, Sheila Bond, MD

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is
complete.

Literature review current through: Aug 2020. | This topic last updated: Mar 12, 2020.

INTRODUCTION

Lung abscess is defined as necrosis of the pulmonary parenchyma caused by

microbial infection. Some authorities use the term "necrotizing pneumonia" or
"lung gangrene" to distinguish pulmonary necrosis with multiple small abscesses
from a larger cavitary lesion, but this actually represents a continuum of the same
process. Lung abscesses are usually polymicrobial infections caused by strictly
anaerobic and facultatively anaerobic bacteria that colonize the oral cavity, but a
range of pathogens can cause them.

The classification, clinical features, diagnosis, and treatment of lung abscess will
be reviewed here. Aspiration pneumonia, which may precede the development of a
lung abscess, is discussed separately. (See "Aspiration pneumonia in adults".)

CLASSIFICATION

The term "lung abscess" is often applied to reflect the clinical features that are
useful in management decisions, such as duration of prior symptoms, presence of
associated conditions, or microbial etiology.

● Lung abscesses can be classified as acute or chronic based upon the duration
of symptoms prior to presentation for medical care; symptoms present for one
 month or more are considered chronic.

● Lung abscess may be primary or secondary based upon the presence or

absence of common associated conditions. Abscesses in patients prone to
aspiration or patients who have been healthy previously are usually considered
primary; the term "secondary lung abscess" typically indicates an associated
bronchogenic neoplasm or systemic disease that compromises immune
defenses, such as human immunodeficiency virus (HIV) infection or organ
transplantation.

● Lung abscess can also be defined by the responsible microbial pathogen (eg,
Pseudomonas lung abscess, anaerobic bacterial lung abscess, or Aspergillus
lung abscess).

When no pathogen was recovered from expectorated sputum five decades ago,
the lesion was referred to as a "nonspecific lung abscess." It is now thought that
these infections were caused by anaerobic bacteria. Putrid lung abscess refers to
the offensive odor that is often found in patients with lung abscesses and is
considered diagnostic of anaerobic bacterial infection. A review of more than
1000 reported cases of lung abscess during the antibiotic era indicates that
approximately 80 percent were considered primary, 60 percent were putrid, 40
percent were "nonspecific," and 40 percent were chronic [1].

PATHOPHYSIOLOGY

Most lung abscesses arise as a complication of aspiration pneumonia and are

caused by species of anaerobes that are normally present in the gingival crevices
[2]. The typical patient has a predisposition to aspiration due to a reduced level of
consciousness (eg, alcoholism, drug abuse, general anesthesia, head trauma) or
dysphagia. These patients also frequently have periodontal disease, especially
gingivitis, with high concentrations of anaerobic bacteria in the gingival crevice as
high as 1011/mL, as many bacteria as can occupy a geometric space.
The first step in the development of a lung abscess is for the inoculum from the
gingival crevice to reach the lower airways, which usually occurs while the patient
is in the recumbent position. Infection is initiated either because the bacteria are
not cleared due to suppressed consciousness or because the inoculum size is
large due to a swallowing disorder. Pneumonitis arises first but, based upon the
usual mixture of organisms, progresses to tissue necrosis after 7 to 14 days. This
necrosis results in lung abscess and/or an empyema; the latter can be due to a
bronchopleural fistula or direct extension of infection into the pleural space.

One unique mechanism for the development of lung abscesses occurs in

Lemierre's syndrome, or jugular vein suppurative thrombophlebitis. This infection
begins in the pharynx (sometimes with an overt tonsillar or peritonsillar abscess)
but spreads to involve spaces in the neck and the carotid sheath, which contains
the internal jugular vein. Bacteremia due to Fusobacterium necrophorum and septic
emboli to the lung, which subsequently cavitate, are all characteristic
complications of this process once the vessels are involved. (See "Suppurative
(septic) thrombophlebitis".)

Tricuspid valve endocarditis, usually due to Staphylococcus aureus, also typically

causes septic emboli that are widely distributed in both lungs. This is a common
feature of endocarditis complicating injection drug use and an infrequent
complication of septic venous thrombosis in other settings. (See "Right-sided
native valve infective endocarditis" and "Suppurative (septic) thrombophlebitis".)

MICROBIOLOGY

Lung abscesses are usually polymicrobial infections. The discussion here focuses
on bacterial causes, especially those caused by strictly anaerobic and facultatively
anaerobic bacteria that colonize the oral cavity, although S. aureus, Klebsiella
pneumoniae, and many other pathogens need to be included in the differential
diagnosis.
The pathogens in lung abscess usually reflect the predominantly anaerobic flora of
the gingival crevice and are often associated with gingival crevice disease such as
gingivitis or periodontitis. The most common organisms are Peptostreptococcus,
Prevotella, Bacteroides (usually not B. fragilis), and Fusobacterium spp (table 1) [3-
8].

Many other bacteria can also cause lung abscesses but do so substantially less
commonly. Probably the most common non-anaerobes are Streptococcus
anginosus and other facultatively anaerobic streptococci. These streptococci can
cause monomicrobial lung abscess but most often are isolated in mixed
infections with anaerobes.

Other bacteria that can cause monomicrobial lung abscess include S. aureus
[9,10], K. pneumoniae [11,12], other gram-negative bacilli [13], Streptococcus
pyogenes [14], Burkholderia pseudomallei [15,16], Haemophilus influenzae type b,
Legionella [17,18], Nocardia, and Actinomyces. There have been occasional case
reports of lung abscess caused by Streptococcus pneumoniae, but the bacterial
etiology is disputed due to the possibility of superinfection by anaerobic bacteria
[19]. (See "Clinical manifestations of Staphylococcus aureus infection in adults",
section on 'Pulmonary infection' and "Clinical features, diagnosis, and treatment of
Klebsiella pneumoniae infection", section on 'Lung abscess' and "Clinical
manifestations and diagnosis of nocardiosis", section on 'Pulmonary' and "Clinical
manifestations and diagnosis of Legionella infection", section on 'Clinical
features'.)

The bacteriology of lung abscess may be different in Taiwan as illustrated in a

retrospective evaluation of 90 adults hospitalized with lung abscess from 1995 to
2003 [12]. Unlike earlier studies in which anaerobic organisms predominated,
gram-negative bacilli accounted for 36 percent of isolates. Other organisms
included anaerobes (34 percent), gram-positive cocci (26 percent), and gram-
positive bacilli (4 percent). Of the 118 pathogens identified, K. pneumoniae (25
percent) was the most commonly isolated pathogen, followed by S. anginosus
group (16 percent).

An accompanying editorial noted that the study might have been biased since 25
percent of the patients had received antibiotics prior to culture, making recovery of
anaerobes less likely [20]. In addition, the study may be limited due to selection
bias in terms of which patients got transthoracic aspiration, since only 90 of 336
cases of lung abscess (27 percent) had evaluable microbiologic studies. However,
the K1 strain of K. pneumoniae appears to be a more common pathogen in Taiwan
than in other areas. Patients in Taiwan with K. pneumoniae infection had a high
rate of bacteremia in association with pneumonia [21]. Higher rates of abscess
formation of other sites (eg, liver abscess) also appear to occur in patients in
Taiwan with K. pneumoniae infection compared with other regions. This is
discussed in greater detail separately. (See "Pyogenic liver abscess", section on
'Microbiology' and "Invasive liver abscess syndrome caused by Klebsiella
pneumoniae" and "Clinical features, diagnosis, and treatment of Klebsiella
pneumoniae infection".)

Selected nonbacterial pathogens can produce lung abscess, including many fungi
(eg, Aspergillus spp, Cryptococcus spp, Histoplasma capsulatum, Blastomyces
dermatitidis, Coccidioides spp, the agents of mucormycosis), Mycobacterium
tuberculosis, nontuberculous mycobacteria (eg, M. avium, M. kansasii), and
parasites (eg, Entamoeba histolytica, Paragonimus westermani). (See
"Epidemiology and clinical manifestations of invasive aspergillosis", section on
'Pulmonary aspergillosis' and "Cryptococcus neoformans infection outside the
central nervous system" and "Pathogenesis and clinical features of pulmonary
histoplasmosis" and "Clinical manifestations and diagnosis of blastomycosis",
section on 'Pulmonary involvement' and "Primary pulmonary coccidioidal
infection", section on 'Clinical manifestations' and "Mucormycosis (zygomycosis)",
section on 'Pulmonary mucormycosis' and "Clinical manifestations and
complications of pulmonary tuberculosis" and "Overview of nontuberculous
mycobacterial infections in HIV-negative patients" and "Clinical manifestations
and diagnosis of nocardiosis", section on 'Pulmonary' and "Extraintestinal
Entamoeba histolytica amebiasis", section on 'Pleuropulmonary infection' and
"Paragonimiasis", section on 'Pulmonary paragonimiasis'.)

Immunocompromised hosts — In the immunocompromised host, the most

common causes of lung abscess are Pseudomonas aeruginosa and other aerobic
gram-negative bacilli, Nocardia spp, and fungi (Aspergillus and Cryptococcus spp).
A number of other organisms can also cause lung abscess in
immunocompromised hosts, such as the agents of mucormycosis, Rhodococcus
equi, Mycobacterium tuberculosis, and nontuberculous mycobacteria (table 2).
(See "Pseudomonas aeruginosa pneumonia" and "Clinical manifestations and
diagnosis of nocardiosis" and "Epidemiology and clinical manifestations of
invasive aspergillosis" and "Cryptococcus neoformans infection outside the
central nervous system" and "Mucormycosis (zygomycosis)" and "Clinical features,
diagnosis, therapy, and prevention of Rhodococcus equi infections" and "Clinical
manifestations and complications of pulmonary tuberculosis" and "Overview of
nontuberculous mycobacterial infections in HIV-negative patients".)

Pneumocystis pneumonia (PCP) can be confused with lung abscess because it

can cause cysts. PCP typically occurs in patients with defects in cell-mediated
immunity. (See "Clinical presentation and diagnosis of Pneumocystis pulmonary
infection in HIV-infected patients", section on 'Chest radiographs'.)

An overview of pulmonary infections in immunocompromised patients is

presented separately. (See "Epidemiology of pulmonary infections in
immunocompromised patients".)

CLINICAL FEATURES

Most patients with lung abscesses, and nearly all patients with lung abscesses
due to anaerobic bacteria, present with indolent symptoms that evolve over a
period of weeks or months [1,6,7,22].

Anaerobic infection — The characteristic features suggest pulmonary infection,

including fever, cough, and sputum production. Evidence of chronic systemic
disease is usually present, with night sweats, weight loss, and anemia. Patients
may seek medical attention for these systemic symptoms, hemoptysis, or pleurisy.
Nearly all patients have fever, but virtually none have shaking chills or true rigors.
Most patients are aware of putrid or sour-tasting sputum. Lung abscesses due to
S. anginosus behave like anaerobic infections but are not associated with putrid
sputum unless strict anaerobes are also present.

Typical findings on physical examination are gingival crevice disease, associated

conditions that reduce consciousness or cause dysphagia, fever, and abnormal
lung sounds reflecting a pleural effusion and/or parenchymal disease.

Chest radiographs usually show infiltrates with a cavity, frequently in a segment of

the lung that is dependent in the recumbent position (eg, the superior segment of
a lower lobe or a posterior segment of the upper lobes) [23].

Other bacterial pathogens — Although the majority of lung abscesses are caused

by strictly anaerobic bacteria, bacteria such as streptococci (eg, S. anginosus), S.
aureus, and K. pneumoniae may also cause lung abscesses. The term "nonspecific
lung abscess" is sometimes used for cases with no clear pathogen identified. The
assumption is that these are caused by anaerobes based upon absence of a
pathogen with routine aerobic and mycobacterial cultures.

Staphylococcus aureus — The most characteristic form of pneumonia caused

by S. aureus is fulminant disease in young adults or adolescents with underlying
influenza infection [24]. The putative strains may be methicillin resistant and have
the Panton-Valentine leukocidin (PVL) gene. These patients often have a fulminant
course with shock, neutropenia, lung necrosis, and high mortality despite
appropriate antibiotic therapy [25,26]. This syndrome was initially reported in 2002
in 16 young adults (median age 15 years), most of whom had preceding influenza
and 6 of whom (37 percent) died [24]. Initially, it was thought that PVL was an
important virulence factor [27], but subsequent research refuted this theory [28].
The community-acquired strain of methicillin-resistant S. aureus (MRSA), known
as the USA 300 strain, has caused a global epidemic [29]. (See "Virulence
determinants of community-acquired methicillin-resistant Staphylococcus aureus",
section on 'Panton-Valentine leukocidin' and "Epidemiology, pathogenesis, and
microbiology of community-acquired pneumonia in adults", section on 'S. aureus'.)

Risk factors for MRSA are summarized in the following table (table 3) and are
discussed in greater detail separately. (See "Methicillin-resistant Staphylococcus
aureus (MRSA) in adults: Epidemiology", section on 'Risk factors'.)

Klebsiella pneumonia — As noted above, K. pneumoniae has been associated

with lung abscess, particularly in Taiwan. The course may be relatively rapid with
necrosis of tissue, high rates of bacteremia, and a slow response to antibiotics
[30]. (See "Clinical features, diagnosis, and treatment of Klebsiella pneumoniae
infection".)

Nocardia — Nocardia can cause lung abscess, particularly in

immunocompromised hosts receiving prolonged courses of glucocorticoids. (See
"Microbiology, epidemiology, and pathogenesis of nocardiosis" and "Clinical
manifestations and diagnosis of nocardiosis".)

Other pathogens — Pathogens that sometimes cause lung abscess include

mycobacteria and fungi. (See "Overview of nontuberculous mycobacterial
infections in HIV-negative patients" and "Clinical manifestations and
complications of pulmonary tuberculosis" and "Epidemiology and clinical
manifestations of invasive aspergillosis" and "Mucormycosis (zygomycosis)".)

DIFFERENTIAL DIAGNOSIS
A lung abscess is typically diagnosed when a chest radiograph reveals a
pulmonary infiltrate with a cavity, indicating tissue necrosis; an air-fluid level is
frequently present. Cavitary lung lesions can be caused by a diverse array of
pathogens, which are discussed above. (See 'Microbiology' above.)

There are also multiple noninfectious causes, including vasculitis (eg,

granulomatosis with polyangiitis), malignancy, aspirated foreign body, and
bronchostenosis (table 4). (See "Granulomatosis with polyangiitis and
microscopic polyangiitis: Clinical manifestations and diagnosis", section on
'Tracheal and pulmonary disease' and "Airway foreign bodies in adults", section on
'Clinical manifestations' and "Congenital anomalies of the intrathoracic airways
and tracheoesophageal fistula", section on 'Bronchial stenosis'.)

DIAGNOSIS

The most important component of the evaluation of a lung abscess is to define

the probable etiologic agent in order to select appropriate antibiotic therapy and to
detect associated conditions, such as malignancy. Most patients with "primary
lung abscess" do not have a pathogen defined. It is important to exclude an
underlying lesion such as a neoplasm.

Lung imaging — A chest radiograph will often demonstrate the pulmonary lesion
to the extent necessary for diagnosis and management. However, better anatomic
definition can be achieved with computed tomographic (CT) scans (image 1 and
image 2) [22,31]. CT scanning can be particularly helpful if there is a question of
cavitation that cannot be clearly delineated on the chest radiograph or if an
associated mass lesion is suspected. A CT will also distinguish between a
parenchymal lesion and a pleural collection, which are managed very differently
(image 3). However, distinguishing between lung abscess and empyema with an
associated air-fluid level can be challenging in some cases. This is discussed in
detail separately. (See "Imaging of pleural effusions in adults", section on
'Empyema'.)

Studies for microbiologic testing — When patients show a typical presentation

with indolent symptoms (cough, fever, night sweats for more than two weeks)
combined with a typical underlying condition that leads to aspiration or a cavity in
a dependent pulmonary segment, it is appropriate to suspect that anaerobic
bacteria are involved.

Routine Gram stain and aerobic culture of expectorated sputum for aerobes
should be performed, ideally before antibiotics have been started. Care must be
exercised in interpretation since most yield deceptive contaminants [32]. As an
example, K. pneumoniae, S. aureus, P. aeruginosa, or other aerobic bacteria may be
cultured from expectorated sputum in a patient with a putrid lung abscess, but
treatment still needs to be directed at anaerobes. In addition, specimens may
represent upper airway flora rather than lower airway pathogens or may be
negative if antibiotics have already been started. Interpretation of sputum cultures
in these cases must take into account the clinical features of the patient,
concentrations of the different organisms found in the culture and Gram stain, and
the antibiotics the patient has received. When S. aureus or a gram-negative
bacillus is the cause of lung abscess and an adequate sputum specimen has been
obtained, it is typically seen on Gram stain and has heavy growth in culture. (See
"Sputum cultures for the evaluation of bacterial pneumonia".)

The approach should include evaluation of the expectorated secretions for

evidence of putrid odor. If there is putrid sputum or empyema fluid, the diagnosis
of anaerobic bacterial infection is confirmed. It is difficult to isolate anaerobic
bacteria in these circumstances since most respiratory tract specimens (sputum
or bronchoscopy aspirates) are contaminated by upper airway flora and are
consequently inappropriate for anaerobic culture. However, empyema fluid is a
good specimen type for Gram stain and anaerobic culture as well as aerobic
culture. Note that this difficulty in obtaining specimens that are appropriate for
anaerobic culture and the challenge of anaerobic cultures may contribute
substantially to the substantial decrease in reported cases of anaerobic lung
infections since the 1980s [33]. Alternatively, there may simply be a decrease in
incidence.

The only methods available for obtaining uncontaminated specimens are

transtracheal aspirates (TTA), transthoracic needle aspirates (TTNA), culture of
pleural fluid, or blood cultures [32,34,35]; TTA and TTNA are rarely performed
currently. It is appropriate to obtain pleural fluid and blood cultures, but blood
cultures are rarely positive for anaerobic bacteria in patients with lung abscess
due to anaerobes. None of these specimens is likely to yield anaerobes after
effective antibiotics are started. Thus, in the present era, the only anaerobic lung
infections that are likely to have bacteriologic confirmation are those associated
with an empyema. The same limitations apply to facultatively anaerobic
streptococci.

A controversial alternative to TTA is bronchoscopic aspiration using a quantitative

brush catheter or quantitation of organisms obtained from bronchoalveolar lavage
(BAL) fluid [36]. Although bronchoscopy with quantitative cultures seems to have
documented benefit in determining pathogenic organisms in most pneumonia
cases caused by aerobes, the experience with anaerobic lung infections is limited
by the sparse number of cases that have been reported and by the number of
laboratories that are capable of isolating anaerobes, which are oxygen sensitive. It
should also be emphasized that none of these specimens is likely to yield
anaerobes after antibiotics have been administered.

Diagnosing other causes — For patients with a less classic presentation or in

whom the diagnosis of bacterial lung abscess is not clear, the differential
diagnosis is broader and includes both infectious and noninfectious etiologies for
the cavitary lesion. It is particularly important to exclude epidemiologically
important organisms such as M. tuberculosis; placing the patient on airborne
precautions is standard in such cases until tuberculosis has been excluded. A
more invasive procedure, such as bronchoscopy, to obtain material for culture and
cells to exclude a malignancy may be warranted under these circumstances.

Some patients with lung abscess have previously unrecognized underlying

conditions such as an aspirated foreign body, a pulmonary neoplasm, or bronchial
stenosis. At one time, it was recommended that all patients with lung abscess
undergo bronchoscopy to detect underlying lesions [37]. This recommendation is
now reserved for patients who have atypical presentations and for those who fail
standard therapy. (See "Airway foreign bodies in adults".)

The differential diagnosis is discussed in greater detail above. (See 'Differential

diagnosis' above.)

Immunocompromised hosts — As noted above, the differential diagnosis of lung

abscess in immunocompromised hosts is broad and includes a range of bacterial,
mycobacterial, and fungal pathogens (table 2). (See 'Immunocompromised hosts'
above.)

Early diagnosis and specific therapy of opportunistic infections is the cornerstone

of successful management in such patients. The general rule is to be aggressive
in pursuing a specific microbiologic diagnosis in immunocompromised patients.
Invasive diagnostic techniques (eg, bronchoscopy with bronchoalveolar lavage)
are often required.

TREATMENT

History — A classic review of 2114 cases of pyogenic lung abscess in the pre-
antibiotic era described the natural history of this condition [38]. Approximately
one-third of patients died, another one-third recovered, and the remainder
developed debilitating illness with recurrent abscesses, chronic empyema,
bronchiectasis, or other sequelae. Drainage via rigid bronchoscopy did not alter
the mortality rate in this study, suggesting that lung abscess, in contrast with most
other types of abscesses, does not require assisted drainage as long as the
process spontaneously drains via the bronchus as indicated by the air-fluid level.

An early study of 1560 cases of lung abscess after the introduction of

sulfonamides showed that these drugs had no important effect on the outcome of
the infection [39]. Resectional surgery and penicillin were commonly used for the
treatment of lung abscess in the early 1950s, and the relative merits of surgery
versus antibiotics were often debated. Antibiotics then became favored, using
penicillin as the initial agent with tetracycline for those who did not respond
[1,7,40-44]. Patients who had persistent cavities at four to six weeks were defined
as having "delayed closure," and these patients were candidates for surgical
resection. An important study from Philadelphia General Hospital in the 1960s
showed that even patients with delayed closure eventually responded when
antibiotics were simply continued [41]. Since that time, surgery has been limited to
only approximately 5 to 10 percent of cases in most series [1].

Antimicrobial therapy

Empiric therapy — The antibiotic treatment of lung abscess is almost always

empiric, reflecting the difficulty of obtaining specimens that are appropriate for
anaerobic culture, the long time required to complete such cultures, and the fact
that susceptibility testing of anaerobes is performed infrequently. Furthermore, the
susceptibility pattern of anaerobes is usually predictable. There are few clinical
trials regarding the treatment of anaerobic lung abscesses, due to the infrequency
of their occurrence and the difficulty in establishing a microbial diagnosis.

Empiric regimens should penetrate the lung parenchyma and target both strict
anaerobes and facultatively anaerobic streptococci. Drugs that are reasonable to
use are any combination of a beta-lactam–beta-lactamase inhibitor (eg, ampicillin-
sulbactam 3 g intravenously [IV] every six hours) or a carbapenem (eg, imipenem,
meropenem); these choices are also supported by in vitro data [45], and modest
experience with these agents is favorable. (See "Combination beta-lactamase
inhibitors, carbapenems, and monobactams".)

Standard treatment for an anaerobic lung infection was formerly clindamycin (600
mg IV every eight hours, followed by 150 to 300 mg orally four times daily) based
upon two trials that demonstrated superiority of this agent compared with
parenteral penicillin in the response rates and speed of defervescence [46,47].
However, we prefer the agents suggested above to avoid the risk of Clostridioides
(formerly Clostridium) difficile infection with clindamycin. Clindamycin remains an
appropriate agent for those with beta-lactam allergy.

One of the reasons that an alternative to penicillin was originally tested was
because more anaerobes began producing beta-lactamase and, thus, were
resistant to penicillin. Examples of beta-lactamase–producing anaerobes involved
in lung abscess include Bacteroides ruminicola, black-pigmenting strains of
Prevotella (formally Bacteroides melaninogenicus group), Bacteroides gracilis,
Bacteroides ureolyticus, Fusobacteria, and others [8,48,49]. Other data suggest that
up to 40 percent of Fusobacteria and 60 percent of Bacteroides spp other than B.
fragilis produce penicillinase [50].

The experience with metronidazole monotherapy for putrid lung abscess has been
extremely disappointing, with an approximate 50 percent failure rate [45,49-53].
This is best explained by the concurrent presence of facultatively anaerobic
streptococci that presumably contribute to the pathogenesis of these infections in
a substantial number of cases. Although metronidazole is probably the most
active drug available against strictly anaerobic bacteria since it is uniformly active
against oxygen-sensitive strains and has a time-kill profile that is unique compared
with other drugs, it has no activity against streptococci. If metronidazole is used, it
should be combined with penicillin. (See "Metronidazole: An overview".)

Targeted therapy — When streptococci (ie, oral flora) are detected from a good
quality sputum specimen from a patient with lung abscess, antibiotics should be
selected that are active against both the pathogens that were detected and
anaerobes. Most drugs used for strict anaerobes are also active against
facultatively anaerobic streptococci, with the exception of metronidazole. The
empiric regimens discussed above are appropriate choices for patients with a
mixed anaerobic and streptococcal lung abscess. (See 'Empiric therapy' above.)

When a single pathogen that is not a typical part of the oral flora is detected, it is
often appropriate to tailor the regimen to target that pathogen. An exception is
that if the sputum is putrid, then anaerobes are likely to be playing a role and the
antimicrobial regimen should target not only the organism that was isolated but
also anaerobes. The rationale for this is that anaerobes are difficult to culture and
are likely to be present when the sputum is putrid. (See 'Empiric therapy' above.)

The appropriate antibiotic for aerobic gram-negative bacilli (eg, K. pneumoniae)

should be selected based upon the results of in vitro susceptibility testing. A risk
factor that makes a monomicrobial S. aureus lung abscess more likely is recent
influenza infection. (See "Epidemiology, pathogenesis, and microbiology of
community-acquired pneumonia in adults", section on 'S. aureus'.)

For methicillin-susceptible S. aureus, the agents of choice are cefazolin (2 g IV

every eight hours), nafcillin (2 g IV every four hours), or oxacillin (2 g IV every four
hours). For methicillin-resistant S. aureus (MRSA), we prefer linezolid (600 mg IV
every 12 hours) with a switch to oral linezolid at the same dose when the patient is
afebrile and stable [54]. The main alternative to linezolid is vancomycin (15 mg/kg
IV every 12 hours, adjusted to a trough concentration of 15 to 20 mcg/mL and for
renal function). Other options are ceftaroline, trimethoprim-sulfamethoxazole, and
telavancin. Ceftaroline is active in vitro against virtually all strains of MRSA [55],
but it has not been approved by the US Food and Drug Administration (FDA) for
MRSA pneumonia because the experience is too limited. Daptomycin should not
be used for pulmonary infections due to inadequate activity in the lung [29].
Duration and switch to oral therapy — The duration of therapy is controversial.
Some treat for three weeks as a standard and others treat based upon the
response. Our practice is to continue antibiotic treatment until the chest
radiograph shows a small, stable residual lesion or is clear. This generally requires
several months of treatment, most of which can be accomplished with an oral
regimen on an outpatient basis. Appropriate oral regimens will depend upon the
infecting pathogen. For patients with a mixed anaerobic and streptococcal
infection, amoxicillin-clavulanate is an appropriate regimen [56], but the choice of
regimen should be guided by susceptibility results when available.

There has also been interest in using moxifloxacin because early studies showed
good in vitro activity against anaerobes, and a small trial has shown benefit for
aspiration pneumonia and primary lung abscess [57]. However, moxifloxacin has
not been studied adequately to recommend it as a first-line agent for lung
abscess, and the rate of resistance of anaerobes to this drug is increasing [58].

The rationale for extended treatment is the anecdotal experience with five patients
who relapsed after therapy was discontinued despite receipt of antibiotics for
more than eight weeks [59].

Surgical intervention — Surgery is rarely required for patients with uncomplicated

lung abscess. The usual indications are failure to respond to medical
management (which is often merely a subjective impression), suspected
neoplasm, or hemorrhage. However, several predictors of a slow response or no
response are abscesses associated with an obstructed bronchus, an extremely
large abscess (>6 cm in diameter), and abscesses involving relatively resistant
organisms, such as P. aeruginosa. The usual procedure in such cases is a
lobectomy or pneumonectomy.

Alternative approaches for patients who are considered to be poor operative risks
include percutaneous and endoscopic drainage [60-69]. Percutaneous procedures
require special care to prevent contamination of the pleural space. Bronchoscopy
may be done as a diagnostic procedure, especially to detect an underlying lesion,
but this procedure is of relatively little use to facilitate drainage and can result in
spillage of abscess contents into the airways [70]. Endoscopic drainage, which
requires an experienced operator, is performed by placing a pigtail catheter into
the abscess cavity under bronchoscopic visualization, leaving the catheter in place
until the cavity has drained [65].

Response to therapy — Patients with putrid lung abscesses usually show clinical

improvement with decreased fever within three to four days after beginning
antibiotic treatment. Defervescence is expected in 7 to 10 days [1,3,4,71-73].
Persistent fevers beyond this time indicate delayed response, and such patients
should undergo further diagnostic tests to better define the underlying anatomy
and microbiology of the infection.

Cultures of expectorated sputum are not likely to be useful at this juncture except
for detecting nonbacterial pathogens such as mycobacteria and fungi. Serial
radiographs have limited use because there is often initial radiographic
progression even in patients with a good clinical response [23]. Major
considerations in patients with a delayed response include:

● An associated condition that precludes response, such as obstruction with a

foreign body or neoplasm.

● Erroneous microbiologic diagnosis with infection due to bacteria,

mycobacteria, or fungi that have not have been suspected and are not being
treated.

● Large cavity size (usually >6 cm in diameter) that may require unusually
prolonged therapy or empyema, which necessitates drainage. Empyema can
have an air-fluid level that is mistaken for a parenchymal abscess; the two can
be distinguished by computed tomography (CT) scan.
 ● An alternative, nonbacterial cause of cavitary lung disease, such as cavitating
neoplasm, vasculitis, or pulmonary sequestration.

● Other causes of persistent fever, such as drug fever or C. difficile–associated

colitis. (See "Drug fever" and "Clostridioides (formerly Clostridium) difficile
infection in adults: Clinical manifestations and diagnosis".)

Patients who fail to respond or have delayed response should be evaluated for an
alternative diagnosis or for a predisposing obstructing lesion, such as a foreign
body, cancer, or bronchial stenosis. The usual evaluation includes bronchoscopy
and imaging, if not already done. (See "Nonresolving pneumonia".)

OUTCOMES

Associated disease in the host is the most important factor in determining the
outcome of a lung abscess. Patients with primary lung abscess (including
alcoholics and injection drug users) with typical putrid lung abscesses generally
do well with cure rates using antibiotic treatment of 90 to 95 percent [1,4]. Patients
with underlying diseases such as immunocompromised patients and those with
bronchial obstructions have mortality rates reported to be as high as 75 percent
[73].

In one retrospective series of 75 patients with lung abscess from Israel, the overall
mortality was 20 percent [74]. The mortality rate was higher among those with
more than one underlying condition compared with one or no underlying disease.
Patients with P. aeruginosa, S. aureus, and Klebsiella spp also had a higher death
rate. The mean length of hospitalization in this study was 25.7 days (range 5 to 94
days).

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and
"Beyond the Basics." The Basics patient education pieces are written in plain
language, at the 5th to 6th grade reading level, and they answer the four or five key
questions a patient might have about a given condition. These articles are best for
patients who want a general overview and who prefer short, easy-to-read
materials. Beyond the Basics patient education pieces are longer, more
sophisticated, and more detailed. These articles are written at the 10th to 12th
grade reading level and are best for patients who want in-depth information and
are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We
encourage you to print or e-mail these topics to your patients. (You can also locate
patient education articles on a variety of subjects by searching on "patient info"
and the keyword(s) of interest.)

● Basics topic (see "Patient education: Aspiration pneumonia (The Basics)")

SUMMARY AND RECOMMENDATIONS

● Lung abscess is defined as necrosis of the pulmonary parenchyma caused by
microbial infection. Some authorities use the term "necrotizing pneumonia" or
"lung gangrene" to distinguish pulmonary necrosis with multiple small
abscesses from a larger cavitary lesion, but this actually represents a
continuum of the same process. (See 'Introduction' above.)

● Most lung abscesses arise as a complication of aspiration pneumonia and are

caused by species of anaerobes that are normally present in the gingival
crevices. The most common anaerobic organisms implicated in lung
abscesses are Peptostreptococcus, Prevotella, Bacteroides (usually not B.
fragilis), and Fusobacterium spp (table 1). Many other bacteria can also cause
lung abscesses but do so with substantially less frequency. Probably the most
common pathogens other than strict anaerobes are Streptococcus anginosus
 and other oral streptococci; these often cause mixed infections with
anaerobes. Other pathogens that cause lung abscess include Staphylococcus
aureus (especially methicillin-resistant S. aureus [MRSA]) and various gram-
negative bacilli (especially the K1 strain of Klebsiella pneumoniae). The most
common agents in the immunocompromised host are Pseudomonas
aeruginosa and other aerobic gram-negative bacilli, Nocardia, and fungi (eg,
Aspergillus and Cryptococcus spp). (See 'Pathophysiology' above and
'Microbiology' above.)

● Most patients with lung abscesses, and nearly all with lung abscesses due to
anaerobic bacteria, present with indolent symptoms that evolve over a period
of weeks or months. The characteristic features of anaerobic lung abscesses
suggest pulmonary infection, including fever, cough, and sputum production.
Evidence of chronic systemic disease is usually present, with night sweats,
weight loss, and anemia. Patients may seek medical attention for these
systemic symptoms, hemoptysis, or pleurisy. Nearly all patients have fever, but
virtually none have shaking chills or true rigors. Most patients are aware of
putrid or sour-tasting sputum. (See 'Clinical features' above.)

● A lung abscess is typically diagnosed when a chest radiograph reveals a

pulmonary infiltrate with a cavity, indicating tissue necrosis; an air-fluid level is
frequently present. However, multiple pathogens are associated with this
radiographic finding as well as numerous other conditions (table 4). Better
anatomic definition can be achieved with computed tomographic (CT) scans
than with chest radiographs (image 1 and image 2). (See 'Differential
diagnosis' above and 'Diagnosis' above.)

● When patients show a typical presentation with indolent symptoms (cough,

fever, night sweats for more than two weeks) combined with typical underlying
conditions that lead to aspiration or a cavity in a dependent pulmonary
segment, it is appropriate to suspect that anaerobic bacteria are involved. If
 there is putrid sputum or empyema fluid, the diagnosis of anaerobic bacterial
infection is confirmed. (See 'Studies for microbiologic testing' above.)

● Routine Gram stain and aerobic culture of expectorated sputum for aerobes
should be performed, but care must be exercised in interpretation since most
yield deceptive contaminants. In addition, specimens may represent upper
airway flora rather than lower airway pathogens or may be negative if
antibiotics have already been started. (See 'Studies for microbiologic testing'
above.)

● It is difficult to isolate anaerobic bacteria since most respiratory tract

specimens (sputum or bronchoscopy aspirates) are contaminated by upper
airway flora and are consequently inappropriate for anaerobic culture. The only
methods available for obtaining uncontaminated specimens are transtracheal
aspirates (TTA), transthoracic needle aspirates (TTNA), culture of pleural fluid,
and blood cultures; TTA and TTNA are rarely performed currently. It is
appropriate to obtain pleural fluid and blood cultures, but blood cultures are
rarely positive for anaerobic bacteria. In the present era, the only anaerobic
lung infections that are likely to have bacteriologic confirmation are those
associated with an empyema. (See 'Studies for microbiologic testing' above.)

● Empiric regimens should target both strict anaerobes and facultatively

anaerobic species (ie, streptococci). For empiric treatment of a lung abscess,
we suggest any combination of a beta-lactam–beta-lactamase inhibitor (eg,
ampicillin-sulbactam 3 g intravenously every six hours) or a carbapenem (eg,
imipenem, meropenem) (Grade 2C). (See 'Empiric therapy' above.)

● When a single pathogen that is not a typical part of the oral flora is detected, it
is often appropriate to tailor the regimen to target that pathogen. An exception
is that if the sputum is putrid, then anaerobes are likely to be playing a role and
the antimicrobial regimen should target not only the organism that was
 isolated but also anaerobes (which are difficult to culture). (See 'Targeted
therapy' above.)

● We suggest continuing antibiotic treatment until the chest radiograph shows a

small, stable residual lesion or is clear. This generally requires several months
of treatment, most of which can be accomplished with an oral regimen on an
outpatient basis. For patients with a mixed strictly anaerobic and facultatively
anaerobic infection, amoxicillin-clavulanate is an appropriate regimen, but the
choice of regimen should be guided by susceptibility results when available.
(See 'Duration and switch to oral therapy' above.)

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