Actinomycosis is a chronic localized or hematogenous infection caused by Actinomyces israelii. Symptoms are a local abscess with multiple draining sinuses, a TB-like pneumonitis, and low-grade septicemia. Diagnosis is by the typical appearance combined with laboratory identification. Treatment is with prolonged antibiotics and surgery.

The causative organisms, Actinomyces sp and Propionibacterium sp (most commonly A. israelii), are often present commensally on the gums, tonsils, and teeth. However, many, if not most, infections are polymicrobial, with other bacteria (oral anaerobes, staphylococci, streptococci, or Enterobacteriaceae) frequently cultured from lesions.

Actinomycosis most often occurs in adult males and takes several forms. In the cervicofacial (lumpy jaw) form, the most common portal of entry is decayed teeth. In the thoracic form, pulmonary disease results from aspiration of oral secretions. In the abdominal form, disease presumably results from a break in the mucosa of a diverticulum or the appendix or during trauma. There is also a localized pelvic form of actinomycosis, a complication of certain types of intrauterine device (IUD) contraceptives. Spread from primary sites occurs rarely, presumably by hematogenous seeding.

Symptoms and Signs

The characteristic lesion is an indurated area of multiple, small, communicating abscesses surrounded by granulation tissue. Lesions tend to form sinus tracts that communicate to the skin and drain a purulent discharge containing “sulfur” granules (rounded or spherical, usually yellowish, and ≤ 1 mm in diameter). Infection spreads to contiguous tissues, but only rarely hematogenously.

Cervicofacial Actinomycosis

The cervicofacial form usually begins as a small, flat, hard swelling, with or without pain, under the oral mucosa or the skin of the neck, or as a subperiosteal swelling of the jaw. Subsequently, areas of softening appear and develop into sinuses and fistulas that discharge the characteristic sulfur granules. The cheek, tongue, pharynx, salivary glands, cranial bones, meninges, or brain may be affected, usually by direct extension.

In the abdominal form, the intestines (usually the cecum and appendix) and the peritoneum are infected. Pain, fever, vomiting, diarrhea or constipation, and emaciation are characteristic. One or more abdominal masses that cause signs of partial intestinal obstruction occur. Draining sinuses and intestinal fistulas may develop and extend to the external abdominal wall.

In the thoracic form, lung involvement resembles TB. Extensive invasion may occur before chest pain, fever, and productive cough appear. Perforation of the chest wall, with chronic draining sinuses, may result.

In the generalized form, infection spreads hematogenously to the skin, vertebral bodies, brain, liver, kidneys, ureters, and (in women) pelvic organs. Diverse symptoms, such as back pain, headache, and abdominal pain, related to these sites may occur. A local pelvic form may occur. Symptoms include vaginal discharge along with pelvic or lower abdominal pain.

Diagnosis

Diagnosis is suspected clinically and confirmed by x-rays and identification of A. israelii in sputum, pus, or biopsy specimen. In pus or tissue, the microorganism appears as the distinctive sulfur granules or as tangled masses of branched and unbranched wavy bacterial filaments, pus cells, and debris, surrounded by an outer zone of radiating, club-shaped, hyaline, and refractive filaments that take hematoxylin-eosin stain in tissue but are positive on Gram stain.

Nodules in any location may simulate malignant growths. Lung lesions must be distinguished from those of TB and cancer. Most abdominal lesions occur in the ileocecal region and are difficult to diagnose, except during laparotomy or when draining sinuses appear in the abdominal wall. Aspiration liver biopsy should be avoided because it can produce a persistent sinus.

Prognosis and Treatment

The disease is slowly progressive. Prognosis relates directly to early diagnosis. It is most favorable in the cervicofacial form and progressively worse in the thoracic, abdominal, and generalized forms, especially if the CNS is involved.

Most patients respond to antibiotics, although response is usually slow because of extensive tissue induration and the relatively avascular nature of the lesions. Therefore, treatment must be continued for at least 8 wk and occasionally for ≥ 1 yr, until signs and symptoms have resolved. High doses of penicillin G (eg, 3 to 5 million units IV q 6 h) are usually effective. Penicillin V (1 g po qid) may be substituted after about 2 to 6 wk. Tetracycline 500 mg po q 6 h may be given instead of penicillin. Minocycline, clindamycin, and erythromycin also have been successful. Antibiotic regimens may be broadened to cover other pathogens cultured from lesions. Anecdotal reports suggest that hyperbaric O₂ therapy is helpful.

Extensive and repeated surgical procedures may be required. Sometimes, small abscesses can be aspirated; large ones are drained, and fistulas are excised surgically.

Last full review/revision November 2005