Lung abscess

Author
John G Bartlett, MD
Section Editor
Stephen B Calderwood, MD
Deputy Editor
Anna R Thorner, MD
Contributor disclosures
All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Jul 2016. | This topic last updated: Jul 08, 2014.
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.
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 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 thought to be 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 compromised consciousness (eg,
alcoholism, drug abuse, general anesthesia) or dysphagia. These patients also frequently have

periodontal disease, especially gingivitis, with concentrations of bacteria in the gingival crevice as
high as 1011/mL.
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 dysphagia. 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 "Infective endocarditis in injection drug users" and "Suppurative (septic)
thrombophlebitis".)
MICROBIOLOGY Lung abscess is caused most frequently by bacteria, usually anaerobes. The
bacteria in lung abscess reflect the predominantly anaerobic flora of the gingival crevice. The most
common organisms arePeptostreptococcus, Prevotella, Bacteroides (usually not B. fragilis),
and Fusobacterium spp (table 1) [3-8].
Many other bacteria can also cause lung abscesses but do so with substantially less frequency.
Probably the most common nonanaerobes are Streptococcus milleri and other microaerophilic
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], Klebsiella
pneumoniae [10,11], other gram-negative bacilli [12], Streptococcus pyogenes [13], Burkholderia
pseudomallei [14,15], Haemophilus influenzae type b, Legionella [16,17], Nocardia,
and Actinomyces. There have been occasional case reports of lung abscess caused
by Streptococcus pneumoniae, but the bacterial etiology is in dispute due to the possibility of
superinfection by anaerobic bacteria [18].
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 [11]. 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,Klebsiella pneumoniae (25
percent) was the most common isolated pathogen, followed by Streptococcus milleri 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 [19]. 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 K-1 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 [20]. Higher rates of abscess formation of other sites (eg,
liver abscess) appear to occur in patients in Taiwan with K. pneumoniae infection compared with
other regions. This is discussed in 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 parasites (eg, Paragonimus
westermani and Entamoeba histolytica), many fungi (eg, Aspergillus spp, Cryptococcus
neoformans, Histoplasma capsulatum,Blastomyces dermatitidis, Coccidioides immitis),
and Mycobacteria spp. (See "Clinical manifestations and diagnosis of
nocardiosis" and "Extraintestinal Entamoeba histolytica amebiasis", section on 'Pleuropulmonary
infection'.)
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 andCryptococcus spp). A number of opportunistic organisms can also cause
lung abscess in immunocompromised hosts, such as Rhodococcus equi, Mycobacteria spp,
and Aspergillus spp (table 2). (See "Clinical features; diagnosis; therapy; and prevention of
Rhodococcus equi infections" and "Microbiology, epidemiology, and pathogenesis of
nocardiosis" and "Clinical manifestations and diagnosis of nocardiosis" and "Epidemiology and
clinical manifestations of invasive aspergillosis" and "Nontuberculous mycobacterial infections in
solid organ transplant candidates and recipients" and "Tuberculosis in solid organ transplant
candidates and recipients".)
CLINICAL FEATURES 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 [1,6,7,21].
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. milleri behave like anaerobic infections but do not have putrid sputum unless the organism
occurs in a mixed infection including anaerobes.
Typical findings on physical examination are gingival crevice disease, the stigma of associated
conditions that compromise consciousness or cause dysphagia, fever, and abnormal lung sounds
reflecting a pleural effusion and/orparenchymal 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) [22]. The approach
should include evaluation of the expectorated secretions for evidence of putrid odor.

Other bacterial pathogens Although the majority of lung abscesses are caused by anaerobic
bacteria, aerobic bacteria such as microaerophilic streptococci (eg, S. milleri), Staphylococcus
aureus, and Klebsiella pneumoniae may also cause lung abscesses.
Staphylococcus aureus The most characteristic form of pneumonia caused by Staphylococcus
aureus is fulminant disease in young adults or adolescents with underlying influenza infection [23].
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 [24,25]. This syndrome was initially reported in
2002 in 16 young adults (median age 15 years), most of whom had preceding influenza and six of
whom (37 percent) died [23]. Initially, it was thought that PVL was an important virulence factor [26],
but subsequent research refuted this theory [27]. The community-acquired strain of methicillinresistant S. aureus (MRSA), known as the USA 300 strain, has caused a global epidemic [28].
(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, Klebsiella 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 [29]. (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".)
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. However, as noted above, multiple pathogens are associated with this radiographic finding
as well as numerous other conditions (table 4).
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. A chest radiograph will generally 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 andimage 2) [21,30]. 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).
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'.)
Classic presentation 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. 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.
The only methods available for obtaining uncontaminated specimens are transtracheal aspirates
(TTA), transthoracic needle aspirates (TTNA), pleural fluid, or blood cultures [31-33]; TTA and TTNA
are rarely performed currently. It is realistic to obtain pleural fluid and blood cultures, but blood
cultures are rarely positive for anaerobic bacteria. 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 microaerophilic streptococci.
A controversial alternative to TTA is bronchoscopic aspiration using a quantitative brush catheter or
quantitation of organisms obtained from bronchoalveolar lavage (BAL) fluid [34]. 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.
Routine cultures of expectorated sputum for aerobes can be performed, but care must be exercised
in interpretation since most yield deceptive contaminants [31]. As an example, Klebsiella spp, S.
aureus, or P. aeruginosa may be cultured from expectorated sputum in a patient with a putrid lung
abscess, but treatment still needs to be directed at anaerobes. 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 the antibiotics the patient has received.
Less typical presentation For patients with a less classic presentation, 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 under respiratory precautions is standard in such cases until acid-fast bacilli
(AFB) smears are negative on three morning sputa. A more invasive procedure, such as
bronchoscopy, to obtain material for culture and cells to exclude a malignancy may be warranted
under these circumstances. A bronchoscopy specimen for AFB can substitute for one sputum
specimen in excluding the diagnosis of tuberculosis.
Some patients with lung abscess have previously unrecognized underlying conditions such as an
aspirated foreign body, a pulmonary neoplasm, or bronchostenosis. At one time, it was
recommended that all patients with lung abscess undergo bronchoscopy to detect underlying

lesions [35]. This recommendation is now reserved for patients who have atypical presentations and
for those who fail standard therapy. (See "Airway foreign bodies in adults".)
TREATMENT A classic review of 2114 cases of pyogenic lung abscess in the pre-antibiotic era
described the natural history of this condition [36]. 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 to 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.
History 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 [37]. 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 [1,7,3842]. 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 [39]. Since that time, surgery has
been limited to only approximately 5 to 10 percent of cases in most series [1].
Antimicrobial therapy Standard treatment for an anaerobic lung infection is clindamycin (600
mg intravenously [IV] every eight hours, followed by 150 to 300 mg orally four times daily) based
upon two published trials that demonstrated superiority of this agent compared with parenteral
penicillin in the number of patients who responded and the speed of defervescence following the
inception of treatment [43,44]. One of the reasons that an alternative to penicillin was tested was
because more anaerobes began producing beta-lactamase and, thus, were resistant to penicillin.
Examples of beta-lactamaseproducing anaerobes include Bacteroides ruminicola, blackpigmenting strains of Prevotella (formally B. melaninogenicus group), B. gracilis, B.
ureolyticus, Fusobacteria, and others [8,45,46]. Other data suggest that up to 40 percent
of Fusobacteria and 60 percent of Bacteroides spp other than B. fragilisproduce penicillinase [47].
Despite in vitro resistance of some of the anaerobic species, it should be emphasized that lung
abscesses are usually polymicrobial infections. It has never been clear that all components of such
mixed infections need to be specifically treated. A number of antibiotic regimens may be effective in
lung abscess (table 5). Available in vitro data also support the use of a combination of a beta-lactam
and beta-lactamase inhibitor, and a modest experience with these agents is favorable [48].
(See "Combination beta-lactamase inhibitors, carbapenems, and monobactams".)
The experience with metronidazole for putrid lung abscess has been extremely disappointing with
an approximate 50 percent failure rate [46-51]. This is best explained by the concurrent presence of
aerobic and microaerophilic 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 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
aerobic and microaerophilic streptococci. If metronidazole is used, it should be combined with
penicillin. (See"Metronidazole: An overview".)

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. Nevertheless,
other drugs that are reasonable to use are any combination of a beta-lactam beta-lactamase
inhibitor (eg, ampicillin-sulbactam 3 g IV every six hours) or a carbapenem. (See "Combination
beta-lactamase inhibitors, carbapenems, and monobactams".)
Lung abscess caused by organisms other than anaerobes is best treated with antibiotics that are
active against the infecting pathogen and penetrate the lung parenchyma. Most drugs used for
anaerobes are also active against aerobic and microaerophilic streptococci, except metronidazole.
The appropriate antibiotic for aerobic gram-negative bacilli should be selected based upon the
results of in vitro susceptibility testing.
For lung abscesses caused by methicillin-resistant Staphylococcus 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 [52]. 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 [53], but it has not been approved by the US Food and Drug
Administration (FDA) for MRSA pneumonia (because the experience is too limited). Telavancin is
not available in the United States. Daptomycin should not be used for pulmonary infections due to
inadequate lung penetration [28]. (See "Treatment of community-acquired pneumonia in adults who
require hospitalization", section on 'Community-acquired MRSA'.)
Duration of 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 oral agents on an outpatient
basis. 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
[54].
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 [55-63]. 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 [64]. 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
[60].

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 [1,3,4,65-67]. 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 roentgenographic progression even in patients with a good clinical
response [22]. 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 microbial 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 Clostridium difficileassociated colitis
(see "Drug fever" and "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.
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 [67]. In one retrospective series of 75 patients with lung abscess from Israel, the overall
mortality was 20 percent [68]. 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 10 th 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 information: 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
organisms 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 nonanaerobes
are Streptococcus milleri and other microaerophilic streptococci. Other pathogens that cause
lung abscess include Staphylococcus aureus (especially methicillin-resistant Staphylococcus
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
(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 'Classic presentation' 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), pleural

fluid, and blood cultures; TTA and TTNA are rarely performed currently. It is realistic 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 'Classic presentation' above.)
Standard treatment for an anaerobic lung infection is clindamycin (600 mg intravenously [IV]
every eight hours, followed by 150 to 300 mg orally four times daily). Other drugs that are
reasonable to use are any combination of a beta-lactam beta-lactamase inhibitor
(eg, ampicillin-sulbactam 3 g IV every six hours), penicillin plus metronidazole, or a
carbapenem. (See 'Antimicrobial therapy' above.)
For lung abscesses caused by methicillin-resistant Staphylococcus aureus, 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. 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, trimethoprimsulfamethoxazole, and telavancin.Daptomycin should not be used for pulmonary infections
due to inadequate lung penetration. (See 'Antimicrobial 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 oral agents on an outpatient basis. (See 'Duration of
therapy' above.)