Anaerobic Pneumonia & Lung Abscess
Aspiration pneumonitis and lung abscess generally involve anaerobic bacteria, which normally colonize the upper respiratory passages.
Aspiration of small amounts of oropharyngeal secretions occurs during sleep in normal individuals but rarely causes disease. Sequelae of aspiration of larger amounts of material include nocturnal asthma, chemical pneumonitis, mechanical obstruction of airways by particulate matter, bronchiectasis, and pleuropulmonary infection.
Individuals predisposed to disease induced by aspiration include those with depressed levels of consciousness due to drug or alcohol use, seizures, general anesthesia, or central nervous system disease; those with impaired deglutition due to esophageal disease or neurologic disorders; and those with tracheal or nasogastric tubes, which disrupt the mechanical defenses of the airways.
Periodontal disease and poor dental hygiene, which increase the number of anaerobic bacteria in aspirated material, are associated with a greater likelihood of anaerobic pleuropulmonary infection.
Aspiration of infected oropharyngeal contents initially leads to pneumonia in dependent lung zones, such as the posterior segments of the upper lobes and superior and basilar segments of the lower lobes. Body position at the time of aspiration determines which lung zones are dependent. The onset of symptoms is insidious. By the time the patient seeks medical attention, necrotizing pneumonia, lung abscess, or empyema may be apparent.
In most cases of aspiration and necrotizing pneumonia, lung abscess, and empyema, multiple species of anaerobic bacteria are causing the infection. Most of the remaining cases are caused by infection with both anaerobic and aerobic bacteria. Prevotella melaninogenica, Peptostreptococcus, Fusobacterium nucleatum, and Bacteroides species are commonly isolated anaerobic bacteria.
Symptoms and Signs
Patients with anaerobic pleuropulmonary infection usually present with constitutional symptoms, such as fever, weight loss, and malaise. Cough with expectoration of foul-smelling purulent sputum suggests anaerobic infection, though the absence of productive cough does not rule out such an infection. Dentition is often poor. Patients are rarely edentulous; if so, an obstructing bronchial lesion is usually present.
The different types of anaerobic pleuropulmonary infection are distinguished on the basis of their radiographic appearance. Lung abscess appears as a thick-walled solitary cavity surrounded by consolidation. An air-fluid level is usually present. Other causes of cavitary lung disease (tuberculosis, mycosis, cancer, infarction, granulomatosis with polyangiitis [formerly Wegener granulomatosis]) should be excluded. Necrotizing pneumonia is distinguished by multiple areas of cavitation within an area of consolidation. Empyema is characterized by the presence of purulent pleural fluid and may accompany either of the other two radiographic findings. Ultrasonography is of value in locating fluid and may also reveal pleural loculations.
Medications of choice are clindamycin (600 mg intravenously every 8 hours until improvement, then 300 mg orally every 6 hours) or amoxicillin-clavulanate (875 mg/125 mg orally every 12 hours).
Penicillin (amoxicillin, 500 mg every 8 hours, or penicillin G, 1–2 million units intravenously every 4–6 hours) plus metronidazole (500 mg orally or intravenously every 8–12 hours) is another option.
Penicillin alone is inadequate treatment for anaerobic pleuropulmonary infections because an increasing number of anaerobic organisms produce beta-lactamases, and up to 20% of patients do not respond to penicillins.
Antibiotic therapy for anaerobic pneumonia should be continued until the chest radiograph improves, a process that may take a month or more; patients with lung abscesses should be treated until radiographic resolution of the abscess cavity is demonstrated.
Anaerobic pleuropulmonary disease requires adequate drainage with tube thoracostomy for the treatment of empyema. Open pleural drainage is sometimes necessary because of the propensity of these infections to produce loculations in the pleural space.