Actinomycosis is caused by members of the family Actinomycetaceae. The most important cause of disease in humans is A. israelii. This organism is characterized by its mycelial granules, which are usually called sulfur granules because of their yellow color. The organisms are normal inhabitants of the human oropharynx, especially in persons with poor oral hygine. In the majority of cases, disease is aquired by the direct spread of endogenous organisms from the oropharynx into the lung or into the gastrointestinal tract. Most infections occur in individuals who are not immunocompromised. Grossly, chronic pulmonary actinomycosis is characterized by multiple abscesses interconnected by granulating sinus tracts and surrounded by a variable amount of fibrous tissue. Histologically, the abscesses are composed of an outer rim of grannulation tissue surrounding masses of polymorphonuclear leukocytes that often contain typical sulfur granules. Surrounding lung parenchyma shows a variable degree of fibrosis and chronic inflammatory infiltrate.
The typical pattern in the acute variety of actinomycosis consists of airspace pneumonia, without recognizable segmental distribution, commonly in the periphery of the lung and with a predilection for the lower lobes. With appropriate therapy, most cases resolve without complications. Actinomycosis frequently presents roentgenographically as a mass that simulates pulmonary carcinoma. According to the many articles and textbook, extension across the pleural fissures and into the chest wall is common. But recent study for the radiologic findings of thoracic actinomycosis in SNUH (in press) revealed that all 22 patients showed no evidence of chest wall involvement. Chronic segmental air-space consolidation containing round to oval, peripherally enhancing low attenuation areas, adjacent pleural thickening were characteristic CT findings of thoracic actinomycosis. The low attenuation area represents microabscess or necrotic material containing ectatic bronchi.