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LUNG ABSCESS
H Koziel, Harvard Medical School, Boston, MA, USA
& 2006 Elsevier Ltd. All rights reserved.

Abstract
Lung abscess is a clinical condition characterized by focal suppurative necrosis of lung parenchyma. The incidence of lung abscess is unknown. Current concepts suggest that most lung abscesses occur as a complication of aspiration pneumonia and are often attributed to anaerobic organisms from the gingival crevices of the oral cavity. Patients typically present with indolent onset of fever, malaise, night sweats, weight loss, cough, pleurisy, and purulent sputum production, of several weeks duration and often with an antecedent history of loss of consciousness or aspiration. The chest radiograph typically demonstrates parenchymal radiolucency with surrounding thick wall, or a radiolucency with an airuid level, and may require chest CT to conrm the diagnosis. Anaerobic bacteria frequently account for the majority of community-acquired lung abscess cases (often polymicrobial), whereas anaerobes may account for most cases of hospital-acquired lung abscess (often a single pathogen). Evaluation of sputum is controversial and blood cultures are rarely positive, so isolating the etiological agent often requires invasive techniques. Treatment includes prolonged antimicrobial therapy, and in general, the prognosis is favorable. Surgical resection is reserved for patients with poor clinical responses. Techniques of percutaneous or endobronchial drainage may be effective alternatives for select patients with poor clinical responses who are considered high surgical risk.

Introduction
Lung abscess is a suppurative process often considered in the spectrum of anaerobic pleuropulmonary diseases that include aspiration pneumonia, necrotizing pneumonia, lung abscess and empyema. As abscesses can be of varied sizes, the distinction between necrotizing pneumonia (or pulmonary gangrene) and lung abscess is somewhat arbitrary as these entities represent a progression along a continuum of lung infections. Generally, lung abscess is often dened as X2 cm in diameter whereas abscesses o2 cm are considered necrotizing pneumonia. Lung abscess has been recognized since the ancient Greek times of Hippocrates. Anaerobic bacteria were rst identied in empyema uid in 1899, and subsequently determined in 1927 to be a critical component of lung abscess formation based on experimental animal data. The role of aspiration was appreciated in 1934 with the association of high rate of lung abscess complicating head and neck surgery performed in the upright sitting position. The benet of drainage of lung abscesses was realized in 1945,

and the introduction of penicillin was associated with an apparent reduction in the incidence (especially in persons o50 years of age) and mortality. The major role of anaerobes in lung abscess formation was conrmed during the 1970s through investigations using newly developed laboratory culturing techniques that allowed for improved isolation and culturing of anaerobic bacteria. The incidence of lung abscess is not known, although lung abscesses likely develop relatively infrequently and the incidence appears to have decreased since the introduction of antibiotics (especially penicillin). From 1943 to 1956, the Massachusetts General Hospital reported 1011 cases of lung abscess per 10 000 hospital admissions in the pre-antibiotic era compared to 12 cases per 10 000 admissions in the post-antibiotic era. The Beth Israel Deaconess Medical Centers experience during 198496 showed that lung abscesses represented approximately 0.2% of all cases of pneumonia requiring hospitalization. The decrease in cases of lung abscess is primarily attributed to early and broad use of effective antimicrobials, improved management of hospitalized unconscious patients, and improved management of patients undergoing anesthesia. Patients with lung abscess typically present with indolent onset of fever, malaise, night sweats, weight loss, cough, pleurisy, and purulent sputum production, of several weeks duration and often with an antecedent history of loss of consciousness or aspiration. The chest radiograph typically demonstrates parenchymal radiolucency with surrounding thick wall, or a radiolucency with an airuid level, and may require chest CT to conrm the diagnosis (Figure 1). Mortality for untreated lung abscess may approach 40%.

Etiology
Anaerobic bacteria are considered the most common pathogens in community-acquired lung abscess, reecting both pathogenic potential and representing the predominant component of normal ora of the upper airways (although any pathogen can create a lung abscess under the appropriate circumstances). Prior studies using transtracheal aspirates or transthoracic needle aspirates reported recovery rates of anaerobic bacteria from 85% to 93% of lung abscess cases. Anaerobes were the only isolates in up to 46% of cases, whereas 43% of cases had a mixture of aerobes and anaerobes (Table 1). Although anaerobic abscesses generally contain multiple anaerobic

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Table 1 Reported microbiology of lung abscess Anaerobic organisms (common)a Fusobacterium nucleatum Peptopstreptococcus species Prevotella melaninogenica Bacteroides species Clostridium species Eubacterium species Lactobacillus Propionibacteria Aeorobic organisms (common) Staphylococcus aureus Streptococcus pyogenes Klebsiella pneumoniae Pseudomonas aeruginosa Aeorobic organisms (uncommon) Escherichia coli Haemophilus inuenzae type B Other pathogens (rare) Nocardia asteroids Paragonimus westermani Legionella species Burkholdaria pseudomallei Burkholdaria mallei (glanders) Mycobacterium tuberculosis Mucoraceae species Aspergillus species Entameoba histolytica Organisms associated with lung abscess in immunocompromised hosts (including HIV) Pseudomonas aeruginosa Streptococcus pneumonia Pneumocystis jiroveci Klebsiella pneumoniae Staphylococcus aureus Haemophilus inuenzae Stenotrophomonoas maltophilia Legionella species (nonpneumophilia) Enterobacter species Streptococcus milleri Proteus mirabilis Cryptococcus neoformans Aspergillus species Mycobacteria (nontuberculous) Nocardia Rhodococcus Zygomycetes
a

Figure 1 Radiological demonstration of lung abscess development in a patient with necrotizing Staphylococcus aureus pneumonia. A 47-year-old HIV male admitted to the medical intensive care unit following an acute drug overdose and loss of consciousness. (a) Admission anteroposterior chest radiograph demonstrated a dense RUL inltrate, and bronchoscopy with quantitative BAL revealed Staphylococcus aureus; (b) chest CT scan on day 14 of hospitalization conrmed the interval development of a cavitary lesion in the posterior segment of the RUL despite appropriate antimicrobials.

isolates, occasionally lung abscesses may result from a single anaerobic organism recognized as highly virulent, such as Fusobacterium nucleatum or Peptopstreptococcus species. Anaerobes may also be in combination with aerobic or facultative anaerobic species such as microaerophilic streptococci. In contrast to community-acquired lung abscess, aerobic bacteria may be a more important etiological agent in hospital-acquired lung abscess. Nosocomial aspiration is often associated with Gram-negative bacteria and Staphylococcus aureus, including organisms with hospital-acquired antibiotic resistance patterns. Furthermore, the spectrum of microbiological agents responsible for lung abscess in

Mouth ora.

immunocompromised hosts may be quite different and distinct from that of immunocompetent patients. This is evident in the study of the Beth Israel Deaconess Medical Centers experience during 198496 in 34 cases of lung abscesses in adults. Aerobic bacteria were the most common isolates in both immunocompromised and non-immunocompromised patients. However, immunocompromised patients more often had multiple pathogens, and certain

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pathogens were exclusively isolated from the lung abscess of immunocompromised patients, including Pseudomonas aeruginosa, and Hemophilus spp. (non-inuenzae), Stenotrophomonas maltophilia, Haemophilus inuenza, Enterobacter spp., Klebsiella oxytoca, nonpneumophilia Legionella spp., Mycobacterium avium complex and Candida spp. Anaerobes were isolated in only 20% of the cases of non-immunocompromised patients, and not isolated in any specimens from immunocompromised patients. Other reports of lung abscess in HIV patients demonstrate bacteria in 65% of isolates, followed by fungi (9%), and mixed infections (16%), although despite effective treatment, high relapse (36%) and mortality (19%) rates were experienced. More recent data suggest that the microbiology of lung abscess may be evolving, perhaps in part in response to external pressures induced by the indiscriminate use of broad-spectrum antimicrobials, development of bacterial resistance, presence of multiple or complex medical comorbidities in patients, and the expanding population of immuosuppressed individuals. As the microbiology of communityacquired pneumonia changes (e.g., the expanding role of methicillin-resistant Staphylococcus aureus), the agents responsible for community-acquired lung abscess are likely to change. Although certain genetic diseases that result in chronic lung disease (e.g., cystic brosis, Kartangeners syndrome) or chronic infection (e.g., Mycobacterium tuberculosis) may predispose to lung abscess formation, there are no known specic genetic markers that identify persons at risk for the development of lung abscess.

Table 2 Predisposing conditions or risk factors to development of lung abscessa Primary lung abscessb Alcoholism Seizure disorder General anesthesia Drug abuse Esophogeal lesions Neurological deficits (e.g., CVA, bulbar disease) Insulin-treated diabetes mellitus Secondary lung abscessc Pulmonary embolism with infarction Septic emboli with pulmonary infarction Endobronchial obstruction by neoplasm (benign or malignant) Obstruction by foreign body Bronchiectasis Cryptogenic lung abscess Absence of identiable risk factor 1015% of patients with lung abscess may not have obvious risk factor. b Symptoms often indolent over weeks. c Symptoms often abrupt over days.
a

Pathology
Lung abscess is dened as a pus-containing necrotic lesion of the lung parenchyma. The cardinal histologic change in all abscesses is suppurative destruction of the lung parenchyma within the central area of cavitation. Lung abscess can be of any size, from a few millimeters to several centimeters, often manifest as a single lesion (e.g., as a complication of aspiration pneumonia), but can develop multiple foci (e.g., as a complication of right-sided endocarditis). Lung abscesses are often infected and generally develop after inammation and produce tissue necrosis with cavitation. In the absence of communication with an airway, the abscess cavity may be lled with suppurative debris. However, when the abscess cavity communicates with an airway, the contents may be partially drained to create an air-containing cavity. In cases of pre-existing cavitary lung disease (such as that associated with emphysema or prior

Mycobacterium tuberculosis infection), infection of the cavity may proceed without overt necrosis. The abscess cavity may become lined with regenerated lung epithelium, and in cases of chronic lung abscess, broblastic proliferation may result in a brinous wall. Early autopsy observations that bacteria in the walls of the lung abscess at autopsy were similar to the bacteria found in the oral gingival crevice (between the tooth and gum tissue) prompted investigators to hypothesize that aspiration was the major mechanism in disease pathogenesis. Acute lung abscess is arbitrarily dened as o4 weeks duration, whereas chronic lung abscess is 44 weeks duration, although the clinical implications of this distinction are not clearly established. Abscess formation as a consequence of aspiration and pneumonia in a relatively normal host are dened as primary lung abscess (Table 2). In contrast, abscess formation as a consequence of central airway obstruction, bronchiectasis, immunocompromised state, or due to hematogenous spread from a distant site is dened as secondary lung abscess. Cases with no recognized or identiable risk factors are termed cryptogenic lung abscesses. Approximately 80% of cases of lung abscesses are primary lung abscess.

Clinical Features
Lung abscess is suspected from the history and physical exam, but requires radiographic conrmation. Clinical suspicion for lung abscess should be heightened in persons with a recognized pre-existing

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condition that increases risk for development of lung abscess (Table 2). In primary lung abscess, symptoms of lung abscess are similar to other anaerobic lung infections, and include indolent (13 weeks) development of fever, cough, pleurisy, dyspnea, sweats, weight loss, and sputum production (often foulsmelling). Sputum production may be absent in the absence of a communication of the abscess cavity and the airways. Most patients present with fever (median T 39.11C) and leukocytosis (median peripheral WBC 15 000 cells mm 3). The production of putrid sputum occurs in approximately 49% of the cases, and is generally considered diagnostic of anaerobic infection (as aerobic bacteria are generally not capable of producing this characteristic odor). In patients with chronic sputum production (such as bronchiectasis or chronic bronchitis), a change in the character, quality, or quantity of sputum should raise suspicion of a new lung infection or development of lung abscess. In secondary lung abscess, the development of symptoms may be more rapid, evolving over days, and may include localized symptoms that provide a clue to the underlying condition predisposing to rapid lung abscess formation (such as endobronchial tumor or endocarditis with multiple septic emboli). Radiographic appearances include a radiolucency surrounded by a visible irregular thick wall, or an airuid level within an area of pneumonia. Chest radiographs generally reveal cavity formation distributed in dependent lung segments. In recumbent patients, these include the superior segments of the lower lobes and posterior segments of the upper lobes. In patients who aspirate in the upright position, the basilar segments of the lower lobes are favored. For all patients, the right lung is more often involved in aspiration events due to the more direct vertical takeoff of the right mainstem bronchus compared to the angulated takeoff of the left mainstem bronchus. A solitary lung cavity is generally associated with primary lung abscess, whereas multiple small cavities suggest secondary lung abscess associated with hematogenous spread of infection. Peripheral parenchymal lung abscess near the chest wall may require chest CT to distinguish an abscess from a loculated empyema with bronchopleural stula. Chest CT scan is more sensitive than a routine chest radiograph, and may detect small cavities, demonstrate obstructing endobronchial lesions, or distinguish lung abscess from airuid levels in the pleural space. Cavitary lung lesions may represent lung abscess, but also represent noninfectious causes of cavitary lung lesions including pulmonary infarction, neoplasm, septic emboli, vasculitis, bullae or cystic

bronchiectasis, pulmonary sequestration, or sarcoidosis. These conditions represent conditions that may become secondarily infected with the subsequent development of a lung abscess. Complications of lung abscess include extension into the pleural space, hemorrhage, and septic emboli (brain abscess or meningitis). In an aspiration-prone patient with gingival disease presenting with a subacute illness, foul-smelling sputum, and a cavitary lesion on chest radiograph, a putative diagnosis of anaerobic lung abscess can be made without further microbiological studies. In other cases, the major challenges to establishing the bacterial diagnosis of lung abscess requires sampling the cavity without contamination by other oropharyngeal microbes (to distinguish pathogenic from colonizing bacteria) and sampling prior to the administration of antimicrobials (which may reduce the ability to cultivate bacteria from lung specimens). Generally, most patients receive antecedent antimicrobials as treatment for a pneumonitis, prior to the development of lung abscess. Techniques used to obtain relatively uncontaminated specimens include transtracheal aspirates (rarely used in current times) or quantitative cultures following bronchoalveolar lavage or protected brush specimens using beroptic bronchoscopy. Quantitative culture of lower respiratory specimens using bronchoscopy may improve the diagnostic yield for aerobes, whereas the detection of anaerobic bacteria by these methods is less well studied. In addition to sampling techniques, proper specimen storage, rapid transportation, and appropriate processing by the clinical laboratory are essential to optimizing isolation of etiological agents, especially anaerobes. As laboratory isolation of pathogens and in vitro sensitivity testing may require several days, empirical antimicrobial selection is necessary for initial treatment in patients with lung abscess. Gram-stain of expectorated sputum may provide initial guidance to the selection of antimicrobials, based on characteristic ndings of polymicrobial ora or the unique morphological features of certain Gram-negative anaerobic organisms and may provide clues as to the presence of anaerobic infection. Furthermore, selection of empirical antimicrobials should also consider the environmental exposures and immune status of the host, and whether the abscess is primary or secondary.

Pathogenesis
Aspiration of oropharyngeal contents is considered the main mechanism for the development of lung abscess (Figure 2). The association of peridontal

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Pathogenesis of lung abscess Aspiration of oral flora (especially anaerobes)* Large inoculum Altered host defense Aspiration pneumonia Pathogen virulence factors Anatomical abnormalities Necrotizing pneumonia

Lung abscess * Increased risk in persons with peridontal disease and predisposing factor for aspiration
Figure 2 Predominant mechanism for the development of lung abscess.

disease with lung abscess formation underscores the importance of anaerobic pathogens and aspiration. The bacteria implicated in anaerobic lung infections represent the normal ora of the oral cavity, and concentrations of anaerobic bacteria in the gingival crevice may approach 1012 organisms per gram, especially in the context of gingivitis. Lung abscess is rare in edentulous persons. Although aspiration of oropharyngeal materials may occur in 45% of healthy individuals during sleep, these occult aspirations may be of relatively small volume and normal host defense and clearance mechanisms allow spontaneous resolution preventing the development of clinical disease. However, clinically significant aspiration of these organisms occurs in persons with compromised consciousness or dysphagia. Predisposing conditions require compromised host defense mechanisms that protect the lower airways (such as cough, glottic closure, or mucocilliary clearance), and an infectious inoculum sufcient to induce disease (such as a large inoculum that overwhelms defenses, induction of a host inammatory response, or direct toxicity to the host) or a combination of these factors. The decisive factor for the development of lung complications following aspiration may depend on the frequency of aspiration events, volume of the aspirate, and character of the aspirated inoculum. Conditions that promote stasis or necrosis of tissue also predispose to anaerobic lung abscess including pulmonary infarction, obstruction due to endobronchial carcinoma, obstruction due to foreign body, and bronchiectasis. Aspiration of substances such as gastric acid pHo 2.5 (Mendelsons syndrome), milk and mineral oil, and volatile hydrocarbons are directly toxic to the lower respiratory tract. The inammatory process

induced by these substances (especially acid) may predispose to bacterial superinfections and result in abscess formation. Based on serial radiographic studies in patients following a dened period of aspiration, lung cavity formation was observed in 714 days. Anaerobic virulence factors promote abscess formation. The propensity for tissue necrosis by anaerobic bacteria may relate in part to a specic family of capsular polysaccharide of anaerobic Gram-negative bacilli. Specic repeating oligosaccharides containing sugars with positively charged free amino acid groups and negatively charged carboxyl or phosphate groups mediate abscess formation in experimental animal models. In addition, metabolic production of short-chain fatty acids by anaerobic bacteria (which may be responsible for the putrid odor of anaerobic infections) may inhibit phagocytosis and bacterial killing by host cell at low pH levels. The pathogenesis of lung abscess is in part dependent on the nature of the specic organism. For example, amoebic lung abscess formation generally involves the right lower lobe by direct extension of the liver abscess through the diaphragm.

Animal Models
Development of a reliable animal model for lung abscess has been elusive. Validation of the hypothesis that aspiration of oral bacteria was the major mechanism for the development of lung abscess was demonstrated in the pre-antibiotic era by Smith in 1927. Inoculating the trachea of rabbits with human gingival crevice material resulted in pneumonitis followed by the development of lung abscess formation in 710 days. The bacteriologic studies of the gingival crevice inoculum revealed predominantly anaerobic bacteria, including Fusobacterium nuclatum, Prevotella melaninogenica, Peptostreptococcus, and an anaerobic spirochete. Interestingly, lung abscess formation required a combination of anaerobes, as lung abscess formation did not occur when animals were inoculated individually with these anaerobic bacteria. In 1929, Varneys inoculation of human abscess material into experimental dogs produced lung abscess, although the microbiology of the inoculum was not fully dened. More recent experiments using rabbits inoculated with well-characterized laboratory anaerobic bacterial isolates suggested an important role for Bacteroides fragilis, although the nature of the stored bacteria may not be clinically relevant. Murine models of lung abscess using Porphyromonas gingivalis and Treponema denticola are associated with a high mortality and thus of limited value.

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Management and Current Therapy

Antibiotics represent the main component of treatment for lung abscess (Table 3). However, most published trials of antimicrobials in the treament of lung abscess have been relatively small. Penicillin represented the main agent during 195075 as most patients responded to it positively, whereas patients who failed to respond were treated with tetracycline. More recent data indicate that approximately 1525% of anaerobic bacteria responsible for lung infections are resistant to penicillin, generally due to penicillinase production. Penicillin resistance is of particular importance with infections by Fusobacteria, Prevotella, and Bacteroides species, where 4060% of these organisms may produce b-lactamases. In small randomized trials, clindamycin is superior to penicillin in terms of clinical response rates, time to defervescence, radiological improvement, clearance of sputum, and relapse rates. Metronidazole monotherapy for the treatment of anaerobic lung infections is associated with poor response in 50% of patients (possibly due to the presence of aerobic or microaerophilic streptococci), but may be effective in combination with penicillin. Other regimens are limited to anecdotal experience or efcacy in treatment of anaerobic infections at other anatomical sites, including amoxicillinclavulanate, a combination of b-lactam with a b-lactamase inhibitor, chloremphenicol, imipenem, cefoxitin, and cefotetan. The efcacy of macrolides in the treatment of anaerobic lung infections has not been established. Vancomycin has effect against Gram-positive anaerobes. Aminoglycosides, quinolones, aztreonam, and trimethoprimsulfamethoxazole
Table 3 Recommended antimicrobial treatment regimens for lung abscessa Recommended treatment for community-acquired lung abscess Clindamycin, or 300600 mg every 8 h Penicillin G, plus 1 gm every 8 h Metronidazoleb 500 mg every 8 h Suggested alternative treatments Combination penicillin/b-lactamase inhibitors Combination b-lactam/b-lactamase inhibitors Carbapenems Quinilones (moxioxacin, gataoxacin) Recommended treatment for hospital-acquired lung abscess Agents directed at aerobes and facultative bacteria, with particular regards to major institutional pathogens (especially Staphylococcus aureus, Pseudomonas, and Enterobacteriaceae).
a Recommended 36 weeks duration, or until constitutional symptoms are resolved and radiographic appearance of abscess is resolved or stable. b Possible disulram-like reaction in persons with chronic alcoholism.

have no significant activity against anaerobes and are generally not recommended. The need for drainage of abscess is in part dependent on the clinical response. The absence of an airuid level suggests the absence of communication with a bronchus, and may require drainage. Radiological-guided percutaneous catheter drainage of lung abscess may be associated with contamination of the pleural space and associated morbidity and mortality. However, a series of small reports suggests that percutaneous drainage may be used effectively in selected patients. Although bronchoscopy is useful in dening unanticipated endobronchial ndings or the development of bacterial resistance in cases of poorly resolving lung abscess, the role of bronchoscopic drainage is controversial as clinical outcomes are not necessarily improved, and complications of spread of infection to other areas of the lung, development of ARDS, and death, limit the enthusiasm for this intervention. Recent data suggest that endobronchial drainage combined with catheter-instilled antimicrobials may represent a viable option for select patients with a nonresolving lung abscess. In general, most patients with lung abscess improve with medial management including antimicrobial therapy alone, with collapse of the abscess in approximately 90% of patients. Patients generally defervesce in 710 days. Radiographic improvement lags behind clinical improvement, and cavity closure can occur in a median of 4 weeks, but may take several months. The role of chest physiotherapy, postural drainage, and bronchodilators has not been established. Antibiotics reduce the overall mortality from lung abscess to o10% (primary or communityacquired lung abscess mortality of approximately 2%) and reduce the pulmonary complications such as recurrent infections, recurrent abscess, pleural empyema, chronic bronchitis, and bronchiectasis. The prognosis for special populations such as HIV patients with lung abscess remains worse despite effective treatment and is associated with high relapse rates (36%) and high mortality (19%). As lung abscesses generally drain spontaneously, surgical resection may only be necessary in 1015% of cases, including cases of failed medical therapy, rapidly progressive infection, abscess due to an obstructing endobronchial lesion, large lung abscess (48 cm), abscess due to resistant organisms (e.g., Pseudomonas aeruginosa), infarcted lung, poorly functioning lung, or in cases of rapidly progressive lung abscess formation in a compromised host. Surgical intervention generally requires lung resection, lobectomy, and less often, pneumonotomy. Lung abscess can be complicated by empyema in approximately 30% of cases. Increased mortality

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from lung abscess is associated with advanced age, systemic disability, immunocompromised state, abscess due to aerobic pathogens, large abscess (45 cm), progressive lung necrosis, presence of obstructing lesion, and delays in seeking medical attention. Mortality may exceed 65% in cases of lung abscess associated with obstructing airway lesions, impaired host defenses, or nosocomial acquisition. Furthermore, approximately 1015% of cases of lung abscess may be associated with malignancy.
See also: Bronchiectasis. Pleural Effusions: Parapneumonic Effusion and Empyema. Pneumonia: Community Acquired Pneumonia, Bacterial and Other Common Pathogens. Systemic Disease: Sarcoidosis. Upper Airway Obstruction. Upper Respiratory Tract Infection. Viruses of the Lung.

Further Reading
Bartlett JG (1991) Antibiotics in lung abscess. Seminars in Respiratory Infections 6: 103111. Bartlett JG (1993) Anaerobic bacterial infections of the lung and pleural space. Clinical Infectious Diseases 16: S248S255. Bartlett JG, Gorbach SL, Tally FP, et al. (1974) Bacteriology and treatment of primary lung abscess. American Review of Respiratory Diseases 109: 510518. Finegold SM and Fishman JA (1998) Empyema and lung abscess. In: Fishman AP (ed.) Fishmans Pulmonary Diseases and Disorders, vol. 1, pp. 20212033. New York, NY: McGraw-Hill.

Fraser RG, Pare JAP, Pare PD, Fraser RS, and Genereux GP (1988) Diagnosis of Diseases of the Chest, 3rd edn., vol. 1, pp. 458 684. Philadelphia, PA: Saunders. Furman AC, Jacobs J, and Sepkowitz KA (1996) Lung abscess in patients with AIDS. Clinical Infectious Diseases 22: 8185. Grifths JK and Snydman DR (1994) Anaerobic pleuropulmonary infections: aspiration pneumonia, abscess, and empyema. In: Niederman MS, Sarosi GA, and Glassroth J (eds.) Respiratory Infections: A Scientic Basis for Management, pp. 345357. Philadelphia, PA: Saunders. Hammond JMJ, Potgieter PD, Hanslo D, et al. (1995) The etiology and antimicrobial susceptability patterns of microorganisms in acute community acquired lung abscess. Chest 108: 937941. Herth F, Ernst A, and Becker HD (2005) Endoscopic drainage of lung abscesses: technique and outcome. Chest 127: 13781381. Hirshberg B, Sklair-Levi M, Nir-Paz R, et al. (1999) Factors predicting mortality of patients with lung abscess. Chest 115: 746750. Husain AN and Kumar V (2005) The lung. In: Kumar V, Abbas AK, and Fausto N (eds.) Robbins and Cotran Pathologic Basis of Disease, pp. 711772. Philadelphia, PA: Elsevier Saunders. Johnson CC and Finegold SM (1988) Pyogenic bacterial pneumonia, lung abscess and empyema. In: Murray JF and Nadel JA (eds.) Textbook of Respiratory Medicine, pp. 803855. Philadelphia, PA: Saunders. Lorger B (2005) Lung abscess. In: Mandell GL, Bennett JE, and Dolin R (eds.) Principles and Practice of Infectious Diseases, pp. 853857. New York, NY: Churchill Livingstone. Mansharamani NG, Balachandran D, Delaney D, et al. (2002) Lung abscess in adults: clinical comparison of immunocompromised to non-immunocompromised patients. Respiratory Medicine 96: 178185. Mansharamani NG and Koziel H (2003) Chronic lung sepsis: lung abscess, bronchiectasis and empyema. Current Opinion in Pulmonary Medicine 9: 181185.

LUNG ANATOMY (INCLUDING THE AGING LUNG)

R Harding, Monash University, Melbourne, VIC, Australia K E Pinkerton, University of California, Davis, CA, USA
& 2006 Elsevier Ltd. All rights reserved. and basement membrane deposition with focal increases in the interstitium also appear in the normal aging process, while the metabolic function of the lungs decreases with age. Environmental factors are likely to inuence changes during the aging process that may be associated with asthma, emphysema, and chronic obstructive pulmonary disease.

Abstract
The respiratory system undergoes a continual process of change with age. A number of similarities have been noted in the mouse, rat, dog, and human with distension of alveolar ducts immediately beyond terminal and respiratory bronchioles. This enlargement is typically observed in the form of ductasia with alveoli becoming stretched and shallow in affected regions. Although destruction of alveolar walls may occur with age in the normal lung, these changes reect in large measure an increase in the size and frequency of alveolar pores connecting adjacent alveoli. An increase in the number of alveolar macrophages in the lungs is a common nding with aging. Increased collagen

Introduction
This article briey reviews basic lung anatomy and changes associated with normal aging. The focus will be the human lung, but data are also presented from the mouse, rat, and dog. Within these species there are many structural features in aging that are common. We will consider separately the gas-exchanging regions of the lung (alveoli) and the conductive structures (bronchial tree) as both contribute to lung function.