Bacterial Lung Abscess

OVERVIEW: What every practitioner needs to know

Are you sure your patient has a bacterial lung abscess? What should you expect to find?

Presentation with fever and productive cough
History of subacute to chronic symptoms (weeks to months), including weight loss, night sweats, putrid sputum, hemoptysis, and clubbing
Most common in patients with high aspiration risk and underlying periodontal disease

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How did the patient develop a bacterial lung abscess? What was the primary source from which the infection spread?

A bacterial lung abscess is a localized area of suppuration of lung tissue leading to parenchymal destruction. Primary sources include:

Aspiration of oropharyngeal or gastric contents
Transdiaphragmatic spread from subphrenic or hepatic abscesses
Cavitating pneumonia commonly from Streptococcus pneumoniae, Staphylococcus aureus, or Klebsiella pneumoniae
Bacteremia from intravenous (IV) drug abuse resulting in septic pulmonary infarct
Trauma from penetrating chest wall injury

Which individuals are of greater risk of developing bacterial lung abscess?

Aspiration risk: history of impaired consciousness or gastric motility

alcoholism, seizures, illicit drugs, opiates, sedatives, or anesthesia
bulbar or esophageal dysfunction

Immunosuppression: Infection can present in multilobar distribution with aerobic organisms predominating.

HIV, diabetes mellitus, chronic corticosteroid use, chemotherapy

Pre-existing pulmonary disease: underlying structural lung disease

chronic obstructive pulmonary disease (COPD), asthma, bronchiectasis

Obstruction: impaired local defense mechanisms

bronchogenic carcinoma, post-obstructive pneumonia

Beware: there are other diseases that can mimic bacterial lung abscess:

Cavitary tuberculosis
Cavitating carcinoma
Non-tuberculous granulomatous disease
Fungal infections
Pulmonary infarct with cavitation
Infected pulmonary cysts or bullae

What laboratory studies should you order and what should you expect to find?

Results consistent with the diagnosis

Peripheral white blood cell (WBC) with differential may reveal leukocytosis with left shift.
Sputum gram stain showing many different bacterial organisms is consistent with the diagnosis.

Results that confirm the diagnosis

Uncontaminated lower airway specimens are preferred. They can be obtained through surgical drainage, bronchoalveolar lavage, fiberoptic bronchoscopy with protective brushings, transbronchial biopsy, or CT-guided needle aspiration
Expectorated sputum cultures confirm diagnosis. However, these are unreliable in diagnosing anaerobic lung abscesses, as the oral cavity is extensively colonized with anaerobes and may result in a false-positive results
Blood cultures confirm diagnosis.

What imaging studies will be helpful in making or excluding the diagnosis of bacterial lung abscess?

CXR: consolidation in segmental or lobar distribution with central cavitation and air-fluid level
CT scan: irregularly shaped, thick-walled lesion; differentiates cavitary lesions from a mass that is obstructive; delineates location, which is often posterior segments of upper lobes or superior segments of lower lobes (dependent locations when patient is supine)
Ultrasound: helpful for abscesses located peripherally or inside lung consolidation; reveals rounded, hypoechoic lesion with outer margin; Cavitation is marked by non-dependent hyperechoic signs from gas-tissue interface.

What consult service or services would be helpful for making the diagnosis and assisting with treatment?

If you decide the patient has a bacterial lung abscess, what therapies should you initiate immediately?

Therapies that should be initiated immediately include:

Pulmonary for bronchoscopy to obtain diagnostic specimen
Cardiothoracic Surgery or Interventional Radiology for possible drainage
Infectious Disease for diagnostic work-up, antimicrobial selection, and patient follow-up

Key principles of therapy include:

Antibiotics: Most bacterial lung abscesses are treated empirically for a duration of 4-8 weeks and typically until resolution of the lesion on CXR or presence of a small, stable lesion
Drainage: Percutaneous or surgical drainage can be performed for both diagnostic and therapeutic measures.
Surgical resection: This is rarely performed, but indicated when medical management fails. The procedure typically involves lobectomy or pneumonectomy.

1. Anti-infective agents

If I am not sure what pathogen is causing the infection what anti-infective should I order?

Empiric antimicrobial therapy (Table I):

Clindamycin + second or third generation cephalosporin
Ampicillin-sulbactam or amoxicillin-clavulante
Moxifloxacin
Penicillin G + Metronidazole: This should not be given for patients with suspected multi-drug resistant organisms.
Carbapenems: This is preferred for patients with suspected multi-drug resistant organisms (those with history of prior treatment with broad-spectrum antibiotics, known colonization with resistant organisms, or in whom hospital-acquired infection is suspected).

Table I.

Organism	Antibiotic	Dose	Alternative
Gram positive	Clindamycin	600mg IV q6-8h	Penicillin G 2 million units IV q4h
Gram positive + Gram negative	Clindamycin +2^nd or 3^rd generation cephalosporin(e.g., Cefoxitin or Ceftriaxone, Ceftazidime)	600mg IV q6-8h	Beta-lactam/ Beta-lactamase inhibitor ampicillin/sulbactam 1.5 to 3g IV q6h piperacillin/tazobactam 3.25g IV q6h ticarcillin/clavulanate 3 to 6g IV q6hMoxifloxacin 400mg PO/IV dailyPenicillin G 2 million units IV q4h + Metronidazole 500mg IV q6h
Multi-drug resistant organisms	Imipenem/ cilastatinMeropenem	0.5-1g IV q6-8h1g IV q8h	Ertapenem 1g IV q24h *should not be used in suspected cases of P. aeruginosa or Acinetobacter spp.
MRSA	Vancomycin	15-20mg/kg IV q 8-12h	Linezolid 600mg PO/IV q12h

2. Other key therapeutic modalities.

Chest physiotherapy for mobilization and drainage of secretions are helpful.

What complications could arise as a consequence of bacterial lung abscess?

What should you tell the family about the patient's prognosis?

90-95% is cured with appropriate medical management.
Risk factors for poor outcome include large cavity (>6 cm), prolonged symptoms (>8 weeks), old age, immunosuppression, necrotizing pneumonia, bronchial obstruction, aerobic bacterial infection (particularly Pseudomonas aeruginosa, Klebsiella pneumoniae, and Staphylococcus aureus).
Morbidity includes massive hemorrhage, sepsis, bronchopleural fistula, rupture into pleural cavity, spillage of purulent material into other lung, and malnutrition.
Mortality is 15-20% if no therapy is given.

How do you contract a bacterial lung abscess and how frequent is this disease?

Most common predisposing factors include male gender, age 50-59, smoking history, and alcoholism.

Incidence within the general population is unknown. Within the hospitalized population, it is uncommon, accounting for 4-5 cases per 10,000 hospital admissions.

Mode of spread is aspiration of oropharyngeal flora or gastric contents.

Lung abscess as a primary manifestation of a bacterial zoonosis has not been identified or well-described in the literature.

What pathogens are responsible for this disease?

Anaerobic or mixed anaerobic and aerobic infections present with subacute to chronic symptoms (weeks to months) of fevers, sweats, cough productive of foul-smelling and foul-tasting sputum, and weight loss.

Immunocompromised patients tend to present with aerobic infections as opposed to anaerobic infections.

Lung abscesses due to Methicillin-resistant Staphylococcus aureus (MRSA) are rare, but present in a more fulminant and lethal manner, often occurring in young, previously health adults or children.

Anaerobic bacteria include Peptostreptococcus species, Actinomyces species, Prevotella species (formerly Bacteroides melaninogenicus), Veillonella species, and Fusobacterium species.

Aerobic bacteria include Streptococcus spp., including S.mitis and S. milleri, Klebsiella pneumoniae, Staphylococcus aureus, Pseudomonas aeruginosa, Haemophilus spp.

How do these pathogens cause a bacterial lung abscess?

Bacterial lung abscess is typically a polymicrobial infection with anaerobic predominance. Inciting event is aspiration or translocation of oropharyngeal or gastric bacteria. These bacteria destroy segments of lobe by severe infection, resulting in impairment of microvascular supply, leading to tissue necrosis and suppuration. Cavitation of lung parenchyma and formation of putrid sputum tend to occur 8-14 days following the inciting event.

What other clinical manifestations may help me to diagnose and manage a bacterial lung abscess?

History includes fever, productive cough, hemoptysis, pleuritic chest pain, sweats, dyspnea, fatigue, and weight loss, or patient may be asymptomatic.

Physical Exam includes:

fever greater than 38°C
clinical findings of consolidation on auscultation of lungs, including decreased breath sounds, bronchial breath sounds, coarse inspiratory crackles
putrid sputum
periodontal disease
clubbing with chronic abscess

How can a bacterial lung abscess be prevented?

Aspiration precautions in patients who are high-risk including head of the bed elevation greater than 30°
Good dental hygiene

WHAT'S THE EVIDENCE for specific management and treatment recommendations?

Gudiol, F, Manresa, F, Pallares, R. “Clindamycin vs Penicillin for anaerobic lung infections. High rate of penicillin failures associated with penicillin-resistant bacteroides melaninogenicus”. Arch Internal Med. vol. 150. 1990. pp. 2525-9. (Thirty-seven patients with either necrotizing pneumonia (N=10) or lung abscess (N=27) presenting in Barcelona, Spain from 1984-1987 were randomized to receive clindamycin verses penicillin. Initial therapy was clindamycin 600mg IV q6h or PCN G 2 million Units IV q4h for at least 8 days until clinical and radiographic improvement were noted. Groups then received the antibiotic orally to complete a course of 4 weeks (Clindamycin 300mg PO q6h or PCN V 759mg PO q6h). Eight out of 18 patients randomized to penicillin group failed treatment compared to only 1 out of 19 patients in the clindamycin group. In addition, the group isolated a total of 47 different anaerobes through transthoracic aspiration or bronchoscopic protective brush specimens. Ten of these isolates were resistant to penicillin, including 9 bacteroides melaninogenicus. These findings suggest that penicillin-resistant bacteroides are common findings in anaerobic lung infections, and Clindamycin should be the preferred drug for empiric therapy.)

Allewelt, M, Schuler, P, Bolcskei, PL. “Ampicillin + sulbactam vs. clindamycin ± cephalosporin for the treatment of aspiration pneumonia and primary lung abscess”. Clin Microbiol Infect. vol. 10. 2004. pp. 163-70. (A multicenter trial in Germany demonstrated equivalent efficacy and tolerance in treatment of aspiration pneumonia, including primary lung abscesses with ampicillin+sulbactam or clindamycin+/-cephalosporin in 70 treated patients between 1995 and 1998. A second or third generation cephalosporin was combined with clindamycin in cases with known gram-negative involvement due to clindamycin's lack of activity verses gram negative organisms.)

Ott, SR, Alleweit, M, Lorenz, J. “Moxifloxacin vs ampicillin/sulbactam in aspiration pneumonia and primary lung abscess”. Infection. vol. 36. 2008. pp. 23-30. (This is another multicenter trial in Germany demonstrating equivalent efficacy in achieving clinical response and tolerance in treatment of aspiration pneumonia and primary lung abscesses in 48 patients treated in each group from 2001 to 2005. The group notes additional convenience in therapy with moxifloxacin as once daily dosing.)

Wang, JL, Chen, KT, Fang, CT, Hsueh, PR, Yang, PC, Chang, SC. “Changing bacteriology of adult community-acquired lung abscess in Taiwan: versus anaerobes”. Clin Infect Dis. vol. 40. 2005. pp. 915-22. (This is an analysis of 90 cases of community-acquired lung abscess presenting in Taiwan from 1996 to 2003 revealed Klebsiella pneumoniae as the most commonly occurring pathogen accounting for 21% of cases. Diabetes Mellitus was the most significant risk factor for developing lung abscess secondary to Klebseilla pnueumoniae. This study also identified increasing resistance to penicillin and clindamycin among Streptococcus milleri (now known as Strep anginosus) and anaerobes. Based on these results, the group recommends adding a beta-lactam/ beta-lactamase inhibitor or a second or third generation cephalosporin to empiric therapy with clindamycin or metronidazole.)

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