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Fig. 6.2 A, B. Multiple sinus tracts are a distinguishing feature of actinomycosis. A Actinomycosis affecting the angle of the mandible: the skin is tethered to the bone with some surrounding induration of the subcutaneous tissue and the sinuses are just beginning to appear. AMP 59-13732-1. B Multiple sinus tracts and abscesses in the foot, with the openings raised above the surface (due to A. madurae). (B from Bittencourt and Londero 1995)


Fig. 6.3 A-D. The histopathology of the actinomycetes. A This actinomycotic grain is almost 1.0 mm across and is visible without magnification. Around the perimeter is the Splendore-Hoeppli substance, giving the typical "ray" appearance. There are densely packed filaments centrally and the grain is surrounded by a neutrophil abscess and granulomatous reaction. Brown-Hopps Tissue Gram Stain, x 160. (Courtesy of Dr. D. H. Connor.) B Detail of the Splendore-Hoeppli phenomenon in a grain of Actinomadura madurae. C A fistulous tract within the epidermis with a large grain of S. somaliensis (arrow). There is an extensive abscess below it. H & E, x64. D Several other abscesses from the same fungus with multiple filaments around their periphery. H & E, x64. (B-D from Bittencourt and Londero 1995)



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Clinical Characteristics

Actinomycosis is divided by location into three main clinical varieties. Cervicofacial infections account for about 50% of all cases of actinomycosis, abdominal lesions for about 30%, and thoracic lesions for about 15%. Infection in other sites is uncommon.


The organisms, normally present in the mouth, may become invasive after injury to the mucosa, such as a dental extraction or trauma. The overlying skin becomes reddened and inflamed, with hard lumpy swelling either at the site of the infection or at the angle of the jaw. The swollen tissues become thickened, hard, and "woody" and eventually abscesses and sinuses are formed. As some of the sinus tracts heal, new ones form, or the older sinuses may reopen. Trismus is common, even though the site of infection is only slightly painful. The underlying maxilla or mandible may become infected and the infection may extend upwards to involve the meninges or form a brain abscess. The actinomycetes may enter the bloodstream and be carried by macrophages to form metastatic abscesses anywhere in the body. The most important clinical differentiation is from a neoplasm, and the presence of pus and characteristic sinuses is very significant.


The initial site of infection is usually in the cecum or appendix: only rarely is abdominal actinomycosis associated with cervicofacial actinomycosis. Clinical symptoms suggest appendicitis and there is often a palpable mass before the sinuses appear. This must be differentiated from a mass due to amebiasis, tuberculosis, or a helminthoma: the characteristic grains are not found in any of these other infections. Sinus formation may occur in amebiasis or tuberculosis, but it usually comprises a single tract and occurs late in the infection. There may be direct spread of actinomycosis from the cecal area into the liver or pelvic organs, and even to the urinary tract or pelvic bones: neglected intrauterine devices, left in situ for a long time, have caused uterine, tubo-ovarian actinomycosis. If the infection spreads through the portal system, jaundice may follow. The patient's symptoms may be due to actinomycotic cholecystitis, pyelonephritis, or cystitis. If there are no characteristic lumpy sinus tracts, biopsy may be necessary to establish the correct diagnosis.


Patients with pulmonary actinomycosis first complain of fever and cough, with yellow sputum: the initial diagnosis may be pneumonia. Abscess cavities in the lungs may suggest a bacterial or tuberculous etiology, but these causes become unlikely if the infection spreads to and through the chest wall and multiple sinuses develop, followed by bone infection and surrounding soft tissue fibrosis. Eventually there is restriction of chest movement. Pulmonary actinomycosis may develop when inhaled bacilli settle in part of a damaged lung, such as a hypoxic fibrotic cavity, bleb, or area of necrosis. It may also reach the lung by spreading through the diaphragm. The mediastinum and pericardium may be involved, causing dysphagia or constrictive pericarditis. Actinomycosis in the chest often seems to progress relentlessly, complicated by anemia and cachexia. Even if successfully treated, there is likely to be significant residual scarring of the lung and chest wall.


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