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Actinomycotic tumor of the abdominal wall.

Abstract: We present the case of an elderly patient with abdominal pain, weight loss, and subjective fever in whom a magnetic resonance imaging study revealed a perihepatic abscess without invasion. After drainage, anaerobic cultures yielded Actinomycosis israelii. We discuss Actinomycosis species, with an emphasis on its pathology and multiple presentations.


Actinomycosis is a chronic, abscess-forming disease that affects multiple areas of the body. This disease is most commonly caused by Actinomycosis israelii, a Gram-positive anaerobic bacterium that is part of the normal flora of the oral cavity, gastrointestinal tract, and vagina. Current theories suggest that a breakdown in mucosal integrity allows for the transition from colonization to infection. In our patient, however, the site of the primary abscess was located far from any presumed disruption of the mucosal barrier, suggesting possible hematologic spread.


Actinomycosis is a chronic abscess-forming disease with three main pathologic presentations: cervicofacial (50% of cases), abdominal (20%), and thoracic (15%). (1) The remaining 15% of cases include pelvic actinomycosis, which may be linked to the presence of intrauterine devices, and other, less prominent sites, such as the central nervous system and the musculoskeletal system. The predominant causative agent of actinomycosis is Actinomyces israelii, which is a Gram-positive, anaerobic, filamentous bacterium that normally colonizes the oral cavity, the gastrointestinal tract, and the vagina. Human disease also may be caused by Actinomyces naeslundii, Actinomyces odontolyticus, Actinomyces viscosus, Actinomyces meyeri, and Propionibacterium propionicum. (2)

Although there is still some debate concerning the pathogenesis of actinomycosis, a key step is thought to be disruption of the mucosal barrier. The majority of cases of cervicofacial actinomycosis are preceded by a dental procedure or another form of oral trauma. Thoracic actinomycosis is thought to be secondary to aspiration of bacteria from the oral cavity. Abdominal actinomycosis is also frequently associated with a loss of mucosal integrity by gastrointestinal surgery, diverticulitis, appendicitis, or the presence of a foreign body. (3) In a significant proportion of cases, however, no obvious history of mucosal disruption can be found or the site of the primary abscess formation is not congruent with an area of known trauma. Hematogenous spread of the bacteria has been hypothesized in these cases. Lymphatic spread of the disease secondary to the lack of lymphatic involvement in the disease process itself is not currently suspected. (4) Patients who are immunosuppressed are known to be at a higher than normal risk for developing this disease. However, the mechanism by which the immune system combats this disease is not currently known. (5)


The classic symptoms of abdominal actinomycosis are diffuse abdominal pain, nausea, vomiting, and diarrhea. Weight loss and chronic low-grade fever are symptoms common to all of the different presentations of actinomycosis. This disease is thought to be underdiagnosed secondary to the nondescript nature of these complaints. Physical examinations may reveal a mass that can sometimes be palpated, with a purple or blue discoloration to the skin often noted.

The classic pathologic progression of actinomycosis involves the formation of a primary abscess, usually at the site of disruption of the mucosal barrier. The primary abscess enlarges and develops a fibrotic capsule that, after further growth, breaks down with the formation of sinus tracts. (2) Fistulae complicate approximately one-third of abdominal actinomycotic abscesses, which may allow for continuous spread. (6) The purulent material found in the abscesses contains sulfur granules in 50% of cases, which are highly suggestive of but not specific for this disease. (2) (3) CT may demonstrate a solid mass with focal areas of low attenuation or a cystic mass with a thickened wall.

Our case was an unusual presentation of actinomycosis in that the site of the primary abscess was located in the anterior abdominal wall. (7-11) The patient had undergone a dental procedure 3 weeks before developing symptoms and 6 weeks before admission. Despite the history of disruption of the oral mucosa, our patient did not develop any signs or symptoms of cervicofacial actinomycosis. Instead, he complained of a gradual onset of abdominal pain that eventually localized to the right upper quadrant. The patient also denied any history of diarrhea, nausea, or vomiting, which suggests a lack of intestinal involvement of the disease. No sinus tracts were seen on CT and MRI, which suggests that the abdominal wall abscess was primary in nature, with no evidence of contiguous spread.

Although difficult to diagnose, actinomycosis is relatively simple to treat. (3) Actinomyces israelii consistently responds well to antibiotic treatment. Penicillin, erythromycin, tetracycline, doxycycline, and clindamycin have been shown to be effective in extensive clinical experience. (2) Current debate stems from the length of time required to treat actinomycosis safely. (1) High-dose IV antibiotics are suggested for 1 month, followed by oral antibiotic treatment for a total of 6 to 12 months. With successful use of antibiotic regimens, surgical treatment has become less necessary. Although drainage of the abscess is recommended, extensive debridement is no longer required. (2)


Actinomycosis is a chronic abscess-forming disease that most commonly involves a cervicofacial presentation. The case reported here is unusual in that the primary abscess was located in the anterior abdominal wall. Hematologic dissemination from a prior dental procedure was suspected; however, actinomycosis usually develops at sites of mucosal disruption.

Key Points

* Actinomyces israelii is a Gram-positive anaerobic bacterium that is part of the normal flora of the oral cavity and the gastrointestinal and genitourinary tracts.

* A breakdown in mucosal integrity allows for the transition from colonization to infection.

* The majority of cases of actinomycosis are cervico-facial, thoracic, and abdominal.

* Abdominal wall actinomycotic abscess is a rare presentation of disease and may result from hematogenous spread.

Laughter is a form a internal jogging. It moves your internal organs around. It enhances respiration. It is an igniter of great expectation.

--Norman Cousins

Accepted December 9, 2002.

Copyright [c] 2004 by The Southern Medical Association



(1.) Cintron JR, Del Pino A, Duarte B, et al. Abdominal actinomycosis. Dis Colon Rectum 1996;39:105-108.

(2.) Russo TA. Agents of actinomycosis, Mandell GL, Bennett JE, Dolin R (eds): Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. Philadelphia, Churchill Livingstone, 2000, vol 2, ed 5, pp 2645-2654.

(3.) Weese WC, Smith IM. A study of 57 cases of actinomycosis over a 36-year period: A diagnostic "failure" with good prognosis after treatment. Arch Intern Med 1975;135:1562-1568.

(4.) Berardi RS. Abdominal actinomycosis. Surg Gynecol Obstet 1979;149:257-266.

(5.) Smego RA Jr, Foglia G. Actinomycosis. Clin Infect Dis 1998;26:1255-1263.

(6.) Piper MH, Schaberg DR, Ross JM, et al. Endoscopic detection and therapy of colonic actinomycosis. Am J Gastroenterol 1992;87:1040-1042.

(7.) Minocha VR, Sharma MM, Nair SK. Primary actinomycosis of the abdominal wall. Aust N Z J Surg 1975;45:66-68.

(8.) Puppala AR, Steinheber FU. Case report: Primary actinomycosis of external oblique muscle. Postgrad Med 1978;63:179-182.

(9.) Deodhar SD, Shirahatti RG, Vora IM. Primary actinomycosis of the anterior abdominal wall (a case report). J Postgrad Med 1984;30:133-134.

(10.) Lau WY, Boey J, Fan ST, et al. Primary actinomycosis of the abdominal wall. Aust N Z J Surg 1986;56:873-875.

(11.) Gupta SK, Shukla VK, Khanna S. Primary actinomycotic mycetoma of the anterior abdominal wall (a case report). J Postgrad Med 1990;36:175-177.


An 88-year-old man presented with a complaint of increasing abdominal pain during the course of 3 weeks. The pain was described as epigastric in the right upper quadrant. It was characterized as sharp and nonradiating and was exacerbated by movement or direct pressure. The patient denied any nausea, vomiting, or diarrhea. The patient did report subjective fever without chills or rigors during the previous 2 weeks, as well as a decreased appetite. He admitted to a 5-kg weight loss during the preceding month. His medical history was significant for chronic obstructive pulmonary disease, hypertension, coronary artery disease necessitating angioplasty 1 year before admission, peripheral vascular disease, and dental work 6 weeks before admission. His medications included oral albuterol, isosorbide mononitrate, atenolol, nifedipine, and hydrochlorothiazide/triamterene. His surgical history was significant for cholecystectomy 3 years earlier. His medical history also was significant for 210 packs per year cigarette smoking, no alcohol use, and no recent travel.

The physical examination revealed that the patient was afebrile with otherwise normal vital signs. Diffuse expiratory wheezing and a Grade III/VI systolic ejection murmur at the right upper sternal border were auscultated. The abdomen was tender in the right upper quadrant, with voluntary guarding and no rebound tenderness. There was palpable fullness without discernible mass on palpation of the right upper quadrant. The patient's liver size was estimated by percussion at 10 cm in the midclavicular line. There was no discoloration of the skin. No bruits were noted.

Laboratory studies showed a leukocyte count of 18 X 1[0.sup.3]/[micro]l, hemoglobin 14 g/dl, and platelet count of 621,000/[micro]l. The complete metabolic panel was normal other than blood urea nitrogen 28 mg/dl, [gamma]-glutamyl transpeptidase 94 IU/L, and albumin 3.1 g/dl. The patient's erythrocyte sedimentation rate was 58 mm/h. The remainder of the laboratory studies were normal.

The abdominal films and chest x-rays were unremarkable. However, computed tomography (CT) of the abdomen revealed a large, perihepatic, multiloculated, cystic mass (Fig. 1). Magnetic resonance imaging (MRI) of the abdomen disclosed a perihepatic abscess with a lack of invasion of the hepatic parenchyma. Percutaneous drainage with CT was performed, which yielded a milky, brown-colored fluid. Gram staining of the fluid demonstrated Gram-positive bacilli with beaded, branching filaments and a large number of leukocytes. Anaerobic cultures subsequently grew Actinomyces israelii. No other bacteria were cultured from the abscess drainage. The patient was treated with IV ampicillin/sulbactam for 1 month, followed by oral amoxicillin/clavulanic acid for an additional 4 months. The patient clinically improved with resolution of the CT findings.

Kristine Owen, MD, Michael T. Flannery, MD, Ahmed B. Elaini, MD, and Juan Rivera, MD

From the Department of Internal Medicine, University of South Florida, Tampa, FL.

Reprint requests to Michael T. Flannery, MD, FACP, Department of Internal Medicine, University of South Florida, 4 Columbia Drive, Harbourside Medical Tower, Suite 630, Tampa, FL 33606. Email:
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Article Details
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Title Annotation:Case Report
Author:Rivera, Juan
Publication:Southern Medical Journal
Date:Feb 1, 2004
Previous Article:Isolated gastrointestinal histoplasmosis: case report and review of the literature.
Next Article:Methimazole-induced cholestatic jaundice.

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