Microbiology
Lung abscess—infection of the lung that results in necrosis of the pulmonary parenchyma—can be caused by a variety of microorganisms. The etiology depends, in part, on the characteristics of the host.
• Previously healthy pts are at risk for infection with bacteria (e.g., S. aureus, Streptococcus milleri, K. pneumoniae, group A Streptococcus) and parasites (e.g., Entamoeba histolytica, Paragonimus westermani, Strongyloides stercoralis).
• Aspiration-prone pts are at risk for infection with anaerobic bacteria; S. aureus, P. aeruginosa, and F. necrophorum (embolic lesions); endemic fungi; and mycobacteria.
• Immunocompromised pts are susceptible to M. tuberculosis, Nocardia asteroides, Rhodococcus equi, Legionella species, Enterobacteriaceae, Aspergillus species, and Cryptococcus species.
Clinical Manifestations
Nonspecific lung abscesses—typically presumed to be due to anaerobic organisms—present as an indolent infection with fatigue, cough, sputum production, fever, weight loss, and anemia. Pts may have foul-smelling breath or evidence of periodontal infection with pyorrhea or gingivitis.
Diagnosis
A chest CT is the preferred radiographic study to precisely delineate the lesion.
• Sputum samples can be cultured to detect aerobic bacteria but are unreliable for culture of anaerobic bacteria.
• Pleural fluid or bronchoalveolar lavage specimens may be helpful if they are processed promptly and appropriately for anaerobic bacteria.
TREATMENT
Treatment depends on the presumed or established etiology.
• Most infections caused by anaerobic bacteria should be treated initially with clindamycin (600 mg IV qid). Any β-lactam/β-lactamase inhibitor combination is an alternative.
• A transition from parenteral to oral therapy is appropriate once pts become afebrile and improve clinically.
• Although the duration of therapy is arbitrary, continuation of oral treatment is recommended until imaging shows that chest lesions have cleared or have left a small, stable scar.
• Fever persisting for 5–7 days after antibiotics have been started suggests failure of therapy and a need to exclude factors such as obstruction, complicating empyema, and involvement of antibiotic-resistant bacteria. – Clinical improvement with decreased fever usually occurs within 3–5 days, with defervescence in 5–10 days. – Pts with fevers persisting for 7–14 days should undergo bronchoscopy or other diagnostic tests to better define anatomic changes and microbiologic findings.
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