DOI: 10.1148/radiol.2441041211
(Radiology 2007;244:309-313.)
© RSNA, 2007
Case 117: Actinomycosis of Left Kidney with Sinus Tracts1
Panuch Yenarkarn, MBBS2,
Ruedi F. Thoeni, MD and
Douglas Hanks, MD
1 From the Departments of Radiology (P.Y., R.F.T.) and Pathology (D.H.), San Francisco General Hospital, University of California San Francisco Medical School, Box 0628, San Francisco, CA 94143-0628. Received July 10, 2004; revision requested September 14; revision received October 8; accepted November 15; final version accepted January 21, 2005.
Correspondence: Address correspondence to R.F.T. (e-mail: Ruedi.Thoeni{at}radiology.ucsf.edu).
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HISTORY
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A 39-year-old Samoan man presented to the emergency department with fever, progressive weakness, and left flank pain of 1-month duration. For several months, he had also experienced progressive weight loss. There was no history of recent trauma, and he was not taking any medication. His medical history was notable for a large left groin abscess and left lower lobe pneumonia of unknown cause 1 year prior to the current admission. Furthermore, he had undergone exploratory laparotomy and gastric surgery for peptic ulcer disease approximately 10 years ago. Physical examination findings were positive for a tender firm mass in the left flank with no associated skin changes. Laboratory findings revealed an elevated white blood cell count of 18 x 109/L. The urine cultures were negative. A computed tomographic (CT) image obtained 1 year prior to the current admission was unremarkable. CT of the abdomen and pelvis (section thickness, 5 mm) was performed after ingestion of 900 mL of 2% diatrizoate meglumine and diatrizoate sodium (Gastrografin; Bracco Diagnostics, Princeton, NJ). A 150-mL dose of iohexol (300 mg of iodine per milliliter) (Omnipaque; Nycomed, New York, NY) was administered intravenously at a rate of 4 mL/sec with a 70-second scan delay. Unenhanced CT images (not shown) did not reveal any areas of high attenuation.
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IMAGING FINDINGS
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Abdominal CT images (Figure) showed enlargement of the left kidney due to an infiltrative process. Compared with unenhanced images (not shown), the masslike infiltration was enhanced and associated with marked perinephric infiltration. The left iliopsoas muscle was enlarged, and multiple ill-defined linear and oval areas of enhancement were visible. The left abdominal wall muscles were broadened and demonstrated regions of linear enhancement. The wall of the descending colon showed increased thickness and hyperenhancement. Sinus tracts extended from the colon to the left iliopsoas and abdominal wall muscles. A few subcentimeter lymph nodes were visible in the retroperitoneum.

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Figure a: Sequential contrast materialenhanced CT images obtained in the transverse plane (a) at the middle portion of the left kidney, (b) near the inferior portion of the liver, (c) near the lower pole of the left kidney, and (d) at the lower pole of the right kidney. (a) The left kidney is enlarged by a contrast-enhanced infiltrative process (arrows). Marked perinephric infiltration (arrowhead) is present. (b) The contrast-enhanced kidney mass (large arrow) is visible. Marked perinephric infiltration (arrowheads) extends from the renal parenchyma and reaches the hypervascular descending colon wall (small arrow). (c) Left psoas muscle and abdominal wall muscles are enlarged and show multiple areas of ill-defined linear enhancement (large white arrows). Wall of the descending colon shows increased thickness and hyperenhancement (black arrow). Sinus tracts (small white arrows) extend from the colon to the left iliopsoas and abdominal wall muscles. A few subcentimeter lymph nodes (arrowheads) are seen in the retroperitoneum. (d) The thickened descending colon (large arrow) and the sinus tract (arrowhead) extend to the left iliopsoas muscle and are clearly seen. The broadened iliopsoas muscle shows multiple areas of oval enhancement (small arrows).
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Figure b: Sequential contrast materialenhanced CT images obtained in the transverse plane (a) at the middle portion of the left kidney, (b) near the inferior portion of the liver, (c) near the lower pole of the left kidney, and (d) at the lower pole of the right kidney. (a) The left kidney is enlarged by a contrast-enhanced infiltrative process (arrows). Marked perinephric infiltration (arrowhead) is present. (b) The contrast-enhanced kidney mass (large arrow) is visible. Marked perinephric infiltration (arrowheads) extends from the renal parenchyma and reaches the hypervascular descending colon wall (small arrow). (c) Left psoas muscle and abdominal wall muscles are enlarged and show multiple areas of ill-defined linear enhancement (large white arrows). Wall of the descending colon shows increased thickness and hyperenhancement (black arrow). Sinus tracts (small white arrows) extend from the colon to the left iliopsoas and abdominal wall muscles. A few subcentimeter lymph nodes (arrowheads) are seen in the retroperitoneum. (d) The thickened descending colon (large arrow) and the sinus tract (arrowhead) extend to the left iliopsoas muscle and are clearly seen. The broadened iliopsoas muscle shows multiple areas of oval enhancement (small arrows).
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Figure c: Sequential contrast materialenhanced CT images obtained in the transverse plane (a) at the middle portion of the left kidney, (b) near the inferior portion of the liver, (c) near the lower pole of the left kidney, and (d) at the lower pole of the right kidney. (a) The left kidney is enlarged by a contrast-enhanced infiltrative process (arrows). Marked perinephric infiltration (arrowhead) is present. (b) The contrast-enhanced kidney mass (large arrow) is visible. Marked perinephric infiltration (arrowheads) extends from the renal parenchyma and reaches the hypervascular descending colon wall (small arrow). (c) Left psoas muscle and abdominal wall muscles are enlarged and show multiple areas of ill-defined linear enhancement (large white arrows). Wall of the descending colon shows increased thickness and hyperenhancement (black arrow). Sinus tracts (small white arrows) extend from the colon to the left iliopsoas and abdominal wall muscles. A few subcentimeter lymph nodes (arrowheads) are seen in the retroperitoneum. (d) The thickened descending colon (large arrow) and the sinus tract (arrowhead) extend to the left iliopsoas muscle and are clearly seen. The broadened iliopsoas muscle shows multiple areas of oval enhancement (small arrows).
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Figure d: Sequential contrast materialenhanced CT images obtained in the transverse plane (a) at the middle portion of the left kidney, (b) near the inferior portion of the liver, (c) near the lower pole of the left kidney, and (d) at the lower pole of the right kidney. (a) The left kidney is enlarged by a contrast-enhanced infiltrative process (arrows). Marked perinephric infiltration (arrowhead) is present. (b) The contrast-enhanced kidney mass (large arrow) is visible. Marked perinephric infiltration (arrowheads) extends from the renal parenchyma and reaches the hypervascular descending colon wall (small arrow). (c) Left psoas muscle and abdominal wall muscles are enlarged and show multiple areas of ill-defined linear enhancement (large white arrows). Wall of the descending colon shows increased thickness and hyperenhancement (black arrow). Sinus tracts (small white arrows) extend from the colon to the left iliopsoas and abdominal wall muscles. A few subcentimeter lymph nodes (arrowheads) are seen in the retroperitoneum. (d) The thickened descending colon (large arrow) and the sinus tract (arrowhead) extend to the left iliopsoas muscle and are clearly seen. The broadened iliopsoas muscle shows multiple areas of oval enhancement (small arrows).
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DISCUSSION
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The CT images demonstrated an aggressive infiltrative process of the left kidney that crossed anatomic boundaries. The differential diagnosis included invasive renal tumor, renal hemorrhage from trauma or anticoagulant therapy with superinfection, and renal chronic inflammation caused by tuberculosis, histoplasmosis, Crohn disease, or actinomycosis.
We concluded that renal tumor was an unlikely diagnosis on the basis of the patient's fever and normal abdominal CT findings obtained 1 year earlier. While aggressive tumors such as lymphoma or sarcoma can grow rapidly, they usually are masslike and exhibit other features of malignancy, such as marked adenopathy, or they spread to other sites. Also, the aggressive nature of the left renal process with involvement of the abdominal wall, iliopsoas, and colon is rare for a neoplastic condition, given that the left kidney appeared to be healthy on CT images obtained 1 year earlier. Even superinfection of a renal tumor would rarely manifest in this fashion. The lack of a clinical history of recent trauma or anticoagulant therapy was evidence against the diagnosis of renal hemorrhage. The patient's clinical history (fever, weight loss, and leukocytosis) and imaging findings made chronic renal infection the most likely diagnosis.
Tuberculosis may involve the genitourinary tract as a secondary site after hematogenous dissemination from the lung. CT findings include low-attenuation parenchymal lesions in the kidneys; scarring and various patterns of hydronephrosis depend on the stricture site (1). Perirenal extension or fistulas to adjacent organs, such as the colon and duodenum, or sinus tracts into the soft tissue may be seen. Renal calcifications occur in more than 50% of patients with genitourinary tuberculosis (2). Tuberculosis manifestations that can be seen on abdominopelvic CT images include marked thickening of the wall of the involved ureter and renal pelvis, peritonitis, psoas abscess, calcifications in the liver and spleen, lymphadenopathy, and infectious changes in the spine. Sinus tracts were seen in this patient, but the left kidney did not have findings typically present in patients with genitourinary tuberculosis; these findings include renal calcifications, parenchymal loss, extrarenal spread to the ureter and bladder, and calyceal dilatation without a hydropelvis. Thus, tuberculosis as the underlying cause of disease was deemed unlikely in this patient.
Histoplasmosis is a fungal infection caused by Histoplasma capsulatum, which is a yeastlike fungus. The risk of histoplasmosis infection is often related to living in endemic areas or to immunosuppression; however, with modern travel, the disease must be considered ubiquitous. The clinical course of histoplasmosis is similar to that of tuberculosis. Histoplasmosis frequently affects the lungs and regional lymph nodes and less frequently affects single or multiple organs because of hematogenous spread. Clinical findings are usually nonspecific. Genitourinary involvement is common in patients with disseminated histoplasmosis, but urogenital manifestations rarely are the only clinical signs in an otherwise healthy-appearing host. These manifestations include recurrent chronic abscesses, fistula formation (eg, pylocutaneous fistula), chronic inflamed organs with noncaseating granulomatous changes (3), and urine cultures positive for Histoplasma capsulatum. The absence of substantial lymphadenopathy, the negative urine cultures, and no history of recurring abscesses, fistula formation, or chronic inflamed organs with noncaseating granulomatous changes made histoplasmosis an unlikely diagnosis.
In 4%35% of patients with Crohn disease, genitourinary complicationsincluding retroperitoneal abscess formation, periureteral fibrosis, cystitis, urinary fistulas, and metabolic derangements such as urolithiasis and development of amyloidosishave been reported (4). Communication of the colon with the pelvicaliceal system (renocolic fistula) or ureter (ureterocolic fistula) can occur in individuals with Crohn disease; however, this occurs less frequently than fistulas due to chronic suppurative xanthogranulomatous pyelonephritis (5). Crohn disease is an idiopathic inflammatory bowel disease in which the terminal ileum is involved most frequently; therefore, direct extension to the right ureter with obstruction near the pelvic prim is the most common finding (4). Isolated Crohn disease in the descending colon with extension to the left kidney was considered an unlikely diagnosis because most fistuale result from chronic suppuration with urolithiasis, obstruction, or both.
The aggressive nature of the infiltrating renal mass crossing anatomic boundaries and the formation of a sinus tract, fistula tract, or both, in the muscles and colon in the absence of substantial lymphadenopathy made renal actinomycosis the most likely diagnosis. Actinomycosis is an uncommon suppurative disease caused by Actinomyces bacteria, usually Actinomyces israelii, that may mimic a neoplasm. Actinomyces organisms are Gram-positive anaerobic bacteria that exist as normal flora in the oral cavity, tonsilar crypts, and genitourinary tract (6,7). Actinomycosis generally is a polymicrobial infection and the companion bacteria act as copathogens that enhance the low invasiveness of the actinomycetes. Actinomycosis occurs worldwide, with greater prevalence internationally in populations with low socioeconomic status and poor dental hygiene; it rarely occurs in the United States (8,9). Improved dental hygiene and widespread use of antibiotics to treat various infections probably have contributed to the declining incidence of this disease. No racial predilection exists; however, for unknown reasons, with the exception of the pelvic form, actinomycosis affects men more frequently than it affects women (10). Actinomycosis can affect individuals of any age, but it predominantly affects individuals aged 2050 years (11). Actinomycosis usually occurs in immunocompetent people, but it may be seen in those with diminished host defenses.
Human actinomycosis occurs in three forms: cervicofacial, thoracopulmonic, and abdominopelvic (6). The cervicofacial form is the most common, with 50%70% of reported cases occurring in the face and neck (12). This form of actinomycosis produces abscesses and open draining sinuses. Common causes of cervicofacial actinomycosis are dental abscess or oral surgery. Trauma to the jaw can also lead to this disease. Once the integrity of the mucous membranes is compromised, Actinomyces bacteria form an abscess and produce a hard red or reddish-purple lump, often on the jaw, leading to the name "lumpy jaw." Thoracopulmonic actinomycosis accounts for 15%20% of actinomycosis cases (13). The mechanism of infection usually consists of aspiration of oropharyngeal secretions that contain actinomycetes (14). Occasionally, infection may occur owing to introduction of the organism by means of esophageal perforation, direct extension from the neck or abdomen, or hematogenous spread from a distant lesion. Thoracopulmonic actinomycosis manifests as a pulmonary airspace or mass. If left untreated, this disease can spread to the pleura, chest wall, or pericardium and lead to sinus tract formation.
Abdominopelvic actinomycosis accounts for 10%20% of reported actinomycosis cases (15). Its pathogenesis is not well understood, but destruction of the mucosal barrier by trauma, visceral perforation, recent abdominal surgery, or long-term use of an intrauterine device are recognized as predisposing factors. Typically, patients have a history of recent or remote bowel surgery (eg, perforated acute appendicitis or perforated colonic diverticulitis after abdominal trauma) or ingestion of foreign bodies (eg, chicken or fish bones) that led to introduction of actinomycetes into deep tissues. The ileocecal region, particularly the appendix, is involved most frequently. Classically, the disease manifests as a slowly growing tumor (16). Involvement of any abdominal organ, including the abdominal wall, can occur by means of direct spread and lead to eventual formation of draining sinuses. Actinomycosis of the pelvis most commonly occurs by way of the ascending route from the uterus in association with intrauterine contraceptive devices that have been in place for an average of 8 years (17). Genitourinary involvement is rare. Most reported cases of genitourinary actinomycosis manifested as renal or perirenal masses. Renal actinomycosis can result from ascending spread or hematogenous dissemination (18).
The infiltrative nature and rapid progression of actinomycosisas well as its tendency to invade normal anatomic barriers, cross facial planes, and invade multiple compartmentsmay be attributed to the proteolytic enzyme of Actinomyces israelii. The aggressive nature of the infection, including pus production and abscess formation followed by necrosis and extensive reactive fibrosis, is comparable to the nature of acute necrotizing pancreatitis (6,18,19). Draining sinuses and fistulas may develop in late stages of disease (7). Extensive sinus or fistula tracts frequently drain to the skin. In this patient, no sinus tracts to the skin were identified, but sinus tracts from the kidney to the colon and muscles were evident and demonstrated the invasive nature of this disease. Extensive scarring in the perinephric tissue and sinus tracts was confirmed by examining the surgical specimen. Clinical and laboratory findings are variable and nonspecific depending on the principal site of involvement and the duration of the disease. Occasionally, patients can develop fever, leukocytosis, and an elevated erythrocyte sedimentation rate, as seen in this patient (19).
CT is the preferred method with which to locate and evaluate the extent of abdominopelvic actinomycosis. Two patterns are seen with CT or ultrasonography (18): The first is that of predominantly solid masses with focal areas of low attenuation. Contrast enhancement of these lesions varies. Sometimes it is higher than that of muscles, but generally it is lower. The second pattern is that of predominantly cystic masses with thick enhancing walls. Sinus tracts and fistulas characteristic of actinomycosis are depicted well with CT. Actinomycosis usually is not spread by the lymphatic system; therefore, regional lymphadenopathy is uncommon and develops late in the course of the disease (6,19). CT revealed only subcentimeter lymph nodes in this patient. Usually, infection does not disseminate to the whole peritoneal cavity, and ascites is absent or minimal (6). Overall, hematogenous spread is rare (20); however, in this patient it was the suspected mode of dissemination to the kidney from the groin abscess, pneumonia, or abdominal surgery. Likewise, hematogenous spread to the liver and spleen usually occurs by the hematogenous route (21).
A definitive diagnosis of actinomycosis is made after histologic identification of sulfur granules in the biopsy specimen or aspirated pus and is confirmed with Gram-stained smears and anaerobic cultures. Histologically, actinomycetes are Gram-positive, branching filamentous hyphalike anaerobes with the suppurative area surrounded by fibrosis and inflammation (22). Aspiration biopsy of the renal mass performed after CT revealed typical sulfur granules in the aspirate and the presence of Actinomyces bacteria when examined with microscopy and analyzed with anaerobic cultures.
Treatment of actinomycosis requires administration of antibiotics. High doses of penicillin administered over a period of up to 1 year are preferred, but macrolidessuch as tetracycline or erythromycincan be used instead. Surgery may be needed for advanced forms of actinomycosis to treat abscesses and sinus tracts (22). Because of the extensive disease in this patient, left nephrectomy with segmental resection of the descending colon en bloc was performed, and the patient was discharged with instructions to continue treatment with penicillin for at least 6 months. Full recovery is expected after treatment.
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FOOTNOTES
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2 Current address: Department of Radiology, Bumrungrad International Hospital, Bangkok, Thailand.Authors stated no financial relationship to disclose. 
Authors stated no financial relationship to disclose.
| Part one of this case appeared 4 months previously and may contain larger images.
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References
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- Chouabe S, Perdu D, Deslee G, et al. Endobronchial actinomycosis associated with foreign body: four cases and a review of the literature. Chest 2002;121(6):20692072.[CrossRef][Medline]
- Pulverer G, Schutt-Gerowitt H, Schaal KP. Human cervicofacial actinomycoses: microbiological data for 1997 cases. Clin Infect Dis 2003;37(4):490497.[CrossRef][Medline]
- de Feiter PW, Soeters PB. Gastrointestinal actinomycosis: an unusual presentation with obstructive uropathyreport of a case and review of the literature. Dis Colon Rectum 2001;44:15211525.[CrossRef][Medline]
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- Smego RA Jr, Foglia G. Actinomycosis. Clin Infect Dis 1998;26:12551261.[Medline]
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- Horvath K, Porkolab Z, Palko A. Primary renal and retroperitoneal actinomycosis. Eur Radiol 2000;10:287289.[CrossRef][Medline]
- Ha HK, Lee HJ, Kim H, et al. Abdominal actinomycosis. AJR Am J Roentgenol 1993;161:791794.[Abstract/Free Full Text]
- Klaaborg KE, Kronborg O, Olsen H. Enterocutaneous fistulization due to Actinomyces odontolyticus: report of a case. Dis Colon Rectum 1985;28:526527.[Medline]
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Congratulations to the 38 individuals and two resident groups that submitted the most likely diagnosis (actinomycosis of left kidney with sinus tracts) for Diagnosis Please, Case 117. The names and locations of the individuals and resident groups, as submitted, are as follows:
Individual responses
- Skip Michael Alderson, MD, Abington, Pa
- Kenneth Francis Baliga, MD, Rockford, Ill
- Eric Leigh Bressler, MD, Minnetonka, Minn
- Antonio Albuquerque Cavalcanti, MD, São Paulo, Brazil
- Michael Harold Childress, MD, Silver Spring, Md
- Haris Chrysikopoulos, Corfu, Greece
- Neal Raymond Conti, MD, Seattle, Wash
- Johannes F.K. De Villiers, MBChB, MMed, Gisborne, New Zealand
- Irwin M. Freundlich, MD, Tucson, Ariz
- Francisco Jose Gonzalez, Santander, Spain
- Pramod Kumar Gupta, MD, Plano, Tex
- Kiriakos Kalampoukas, MD, Halandri, Greece
- James Francis Lally, MD, Wallingford, Pa
- David Anthony Lisle, MBBS, Brisbane, Australia
- Edward Lubat, MD, Englewood, NJ
- Alberto Antonio Marangoni, MD, Cordoba, Argentina
- Frank J. McKowne, MD, Vancouver, Wash
- Steven J. Michel, MD, Bellingham, Wash
- Utaroh Motosugi, MD, Yamanashi, Japan
- Mizuki Nishino, MD, Boston, Mass
- Laura Oleaga, Philadelphia, Pa
- Suresh K. Patel, MD, Chicago, Ill
- Yeliz Pekcevik, Izmir, Turkey
- Ivan Pilate, Brussels, Belgium
- Rubem Pochaczevsky, MD, Bronx, NY
- Claudio Prata Ramos, MD, Juiz de Fora, Brazil
- Daniel C. Rappaport, MD, Toronto, Ontario, Canada
- Manoel De Souza Rocha, MD, São Paulo, Brazil
- Tsutomu Sakamoto, MD, Tokyo, Japan
- Anthony J. Scuderi, MD, Johnstown, Pa
- Mustafa Secil, MD, Izmir, Turkey
- Matthew P. Shapiro, MD, Charlottesville, Va
- Ken Simmons, MD, Sydney, Australia
- Darrin S. Smith, MD, Visalia, Calif
- Kouichi Sugiyama, Numazu, Japan
- Ayako Tamura, MD, Tokyo, Japan
- Douglas L. Teich, MD, Brookline, Mass
- Joe Yut, Olathe, Kan
Resident group responses
- Baylor University Medical Center Radiology Residents, Dallas, Tex
- University of Pennsylvania Radiology Residents, Philadelphia, Pa