Clin J Gastroenterol (2013) 6:434–437 DOI 10.1007/s12328-013-0427-5
CASE REPORT
Multiple splenic nodules with fever: a case of splenic abscess due to Propionibacterium acnes Sho Kiritani • Junichi Kaneko • Taku Aoki Yoshihiro Sakamoto • Kiyoshi Hasegawa • Yasuhiko Sugawara • Norihiro Kokudo
•
Received: 14 May 2013 / Accepted: 11 September 2013 / Published online: 10 October 2013 Ó Springer Japan 2013
Abstract A 64-year-old man with a history of chronic lymphocytic leukemia (CLL) presented in the hematology department due to remarkable leukocytosis and progressing anemia. Ultrasound confirmed splenomegaly and plain computed tomography revealed multiple hypoattenuating areas in the large spleen. Following a clinical diagnosis of relapse of CLL, he underwent treatment with fludarabine, cyclophosphamide, and rituximab (FC-R). After five cycles of FC-R treatment, his leukocyte count and hemoglobin level were normalized, and the size of the spleen also decreased. He began to have intermittent high fever (38 °C), however, approximately 6 months after the initiation of FC-R treatment. The results of an interferongamma release assay were positive. 18F-fluoro-2-deoxy-Dglucose positron emission tomography showed multiple areas of high-uptake in the spleen, which was unclear in other radiologic modalities. We performed a splenectomy for the high fever and to confirm the diagnosis. Tissue cultures of the infarcted area of spleen were positive for Propionibacterium acnes. After splenectomy, the patient’s condition improved and there were no further episodes of fever. Until recently, three cases of splenic abscess caused by Propionibacterium acnes were reported. Here we present a fourth case of splenic abscess due to Propionibacterium acnes and review the literature.
S. Kiritani J. Kaneko T. Aoki Y. Sakamoto K. Hasegawa Y. Sugawara N. Kokudo (&) Hepato-Biliary-Pancreatic Surgery, Artificial Organ and Transplantation Division, Department of Surgery, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan e-mail: [email protected]
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Keywords Splenic abscess Splenectomy Propionibacterium acnes Chronic lymphocytic leukemia Positron emission tomography
Introduction Propionibacterium acnes (P. acnes) is gram-positive, anaerobic, and part of the normal flora of human skin, oral cavity, large intestine, conjunctiva, and external ear canal [1, 2]. P. acnes infections infrequently occur as postoperative and device-related infections [2, 3]. Until recently, three cases of splenic abscess caused by P. acnes were reported [4–6]. Here we present a fourth case of splenic abscess due to P. acnes and review the literature.
Case report A 64-year-old man with a history of chronic lymphocytic leukemia (CLL) presented in the hematology department due to remarkable leukocytosis (163,600/mm3) and progressing anemia. Lymphocytes accounted for 68 % of the white blood cells (WBC). The peripheral blood lymphocytes were CD5-positive. Lymphocytes accounted for more than 30 % of the bone marrow. Ultrasonography confirmed splenomegaly (height 9 length 9 width 20 9 17 9 8 cm). Although he did not complain of abdominal pain, plain computed tomography (CT) revealed multiple hypoattenuating areas in the large spleen (Fig. 1a). Following a clinical diagnosis of relapse of CLL, he underwent treatment with fludarabine, cyclophosphamide, and rituximab (FC-R). After five cycles of FC-R treatment, his leukocyte count and hemoglobin level were normalized, and the size of the
Clin J Gastroenterol (2013) 6:434–437
Fig. 1 Contrast enhanced computed tomography revealed multiple hypoattenuating areas in the enlarged spleen (a, arrowhead). The multiple hypoattenuating areas were unclear when the size of the spleen had decreased (b), 18F-fluoro-2-deoxy-D-glucose positron
435
emission tomography showed multiple areas of high-uptake in the spleen (c). Histopathologic findings revealed wedge-shaped white infarct lesions of the spleen (d)
Fig. 2 Magnified view of histopathologic findings revealed white infarct areas with liquefactive necrosis (a, arrowhead). Microscopic findings revealed overt neutrophil infiltration in the surrounding areas of necrosis (b, arrowhead). No granuloma was detected
spleen also decreased (16 9 15 9 5 cm) without multiple hypoattenuating areas (Fig. 1b). He began to have intermittent high fever (38 °C), however, approximately 6 months after the initiation of FC-R treatment. Physical examination revealed no lymphadenopathy and the spleen was not palpable. The WBC count was 6,700/mm3 and the C-reactive protein level was 5.8 mg/dL. Peripheral blood flow cytometry revealed no relapse of CLL. No bacteria were found in 10 sets of blood culture and 2 sets of urine
culture. The sputum culture showed normal flora. The procalcitonin level was not elevated and blood/urine/sputum cultures were all negative. Antinuclear antibodies; beta-D-glucan; and Cryptococcus, Aspergillus, and Candida antigen tests were all negative. He underwent several examinations for fever of unknown origin with levofloxacin administration. Chest and abdominal X-ray were unremarkable. No sites of inflammation or malignant tumor were found on contrast CT. The intermittent fever
123
436
continued for more than 3 months. Although sputum, urine, gastric juice, and bone marrow cultures were negative for Mycobacterium tuberculosis, the results of an interferon-gamma release assay (QuantiFERON, Cellestis Ltd., Chadstone, Australia) were positive. 18F-fluoro-2deoxy-D-glucose positron emission tomography (FDGPET) showed multiple areas of high-uptake in the spleen (Fig. 1c), which was unclear in other radiologic modalities. The maximum standardized uptake value was 12.4. We tentatively diagnosed the patient with CLL invading the spleen and/or splenic tuberculosis. We performed a splenectomy for the high fever and to confirm the diagnosis. The surgical duration was 3 h 55 min. The spleen adhered strongly and was greatly enlarged (14.8 9 10.0 9 4.5 cm, 448 g). Histopathologic findings revealed wedge-shaped white infarct lesions of the spleen without significant vascular disease (Fig. 1d). The histopathologic findings also revealed white infarct areas with liquefactive necrosis (Fig. 2a). Microscopy findings revealed overt neutrophil infiltration in the surrounding areas (Fig. 2b). No granuloma was seen. The CLL had not invaded the spleen and Mycobacterium tuberculosis was negative. Tissue cultures of the infarcted area were positive for P. acnes. After splenectomy, the patient’s condition improved and there were no further episodes of fever.
Discussion Splenic abscess is uncommon, with a frequency of 0.1–0.7 % in an autopsy series [7, 8]. Nelken and colleagues [7] classified splenic abscess into 5 causes as follows: metastatic infection, contiguous infection, trauma, immunodeficiency, and embolic events with subsequent infection. The etiology in our patient was not clear. Antopolsky and colleagues [9] suggested that circulatory disturbances causing infarcted areas in the spleen occur during rapid progression of splenomegaly when patients have acute general inflammation or hematologic malignancy, including CLL. Our patient had splenomegaly before the initial FC-R chemotherapy and the spleen already showed multiple lowdensity areas on the initial CT. Splenectomy is the treatment option of choice for splenic abscess. CT-guided abscess drainage was also recently reported [10]. Our patient required a precise diagnosis and we therefore decided to perform the splenectomy. Fever of unknown origin is classically defined as fever higher than 38.3 °C on several occasions for at least 3 weeks with uncertain diagnosis after a number of obligatory tests [11]. Although our patient has CLL, the clinical condition was similar to the definition of fever of unknown origin. Fever of unknown origin remains a clinical challenge as no diagnosis can be made in up to 50 % of
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Clin J Gastroenterol (2013) 6:434–437
the cases [11]. FDG-PET may be a sensitive diagnostic technique for evaluating fever of unknown origin. According to a Japanese multi-center study of FDG-PET for the diagnosis of fever of unknown origin, none of the 81 patients had a splenic abscess [12]. In our patient, FDGPET was key to diagnosing the splenic abscess. P. acnes causes invasive deep infections with reports of endocarditis, osteomyelitis after lumbar puncture, mediastinitis or discitis after surgery, spondylodiscitis following epidural catheterization, infection of intraocular lenses, ventro-peritoneal shunts, orthopedic implants, silicone implants, and artificial heart valve [2, 13]. In a recent report, P. acnes was found as a pathogen of sarcoidosis [14]. The etiology of splenic abscess due to P. acnes remains unclear. P. acnes may directly invade from the skin through an injection site or skin wound [2, 15]. Gekowski and colleagues [4] suggested that a patient in their study may have become inoculated with P. acnes during insulin administration, resulting in an inapparent subcutaneous focus of infection. Infection in our patient might have had a similar cause because high fever developed after 5 cycles of chemotherapy administered via intravenous injection. Our patient had underlying CLL. Two of the previously reported cases of P. acnes splenic abscess also had underlying disease: one with diabetes mellitus and the other with drug addiction [4, 5]. Whether or not the third patient had underlying disease is unknown. FC-R chemotherapy alone has a high risk for infection. According to a previous report, O’Brien and colleagues [16] suggest that 25 % of patients undergoing FC-R chemotherapy develop sepsis or pneumonia. A literature search using the terms ‘‘splenic infection’’ and ‘‘splenic abscess’’ was conducted using PubMed [National Library of Medicine (NLM), Bethesda, MD, USA) at the end of 2012. There were 834 cases of splenic abscess [7, 8, 10, 17]. Among these, anaerobic bacteria was the pathogen in 57 cases, Propionibacterium species was the pathogen in 6 cases, and P. acnes was the pathogen in 4 cases, including the present report. In previous reports, the most common pathogenic bacterium in splenic abscess was Staphylococcus aureus [18], Klebsiella pneumoniae [6], Streptococcus viridians [10], and Mycobacterium tuberculosis [19]. Although P. acnes splenic abscess is rare, P. acnes might be passed over unnoticed. The main reason is that P. acnes is anaerobic and difficult to detect in aerobic cultures. Another reason is that P. acnes is usually considered a contamination on blood culture as a normal inhabitant [20]. P. acnes recently received attention as an etiologic link to sarcoidosis [21], but no granuloma was detected in our patient. With regard to contamination during handling of the spleen specimen, we suspected tuberculosis at first, and therefore the spleen was opened in a sterilized and enclosed environment for infection control.
Clin J Gastroenterol (2013) 6:434–437
P. acnes is relatively easy to treat with antibiotics. Penicillin, cephem, carbapenem, and fluoroquinolone antibiotics are used [22, 23]. Although levofloxacin was administered to our patient, his high fever continued. Splenectomy was an effective treatment.
Conclusion We reported a case of a patient with splenic abscess due to P. acnes. Acknowledgments The authors would like to thank Masako Sugimoto, Yasuhiko Kamikubo, Mineo Kurokawa of Department of Hematology, Graduate School of Medicine, The University of Tokyo, Yukako Shintani, Masashi Fukayama of Department of Pathology, Graduate School of Medicine, The University of Tokyo, Junichi Shindoh, Yoshikuni Kawaguchi, Kiyohiko Omichi, Hepato-BiliaryPancreatic Surgery, Artificial Organ and Transplantation Division, Department of Surgery, Graduate School of Medicine, The University of Tokyo for their important contributions to the diagnosis. Disclosures Conflict of Interest: The authors declare that they have no conflict of interest. Human/Animal Rights: All procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional and national) and with the Helsinki Declaration of 1975, as revised in 2008(5). Informed Consent: Informed consent was obtained from all patients for being included in the study.
References 1. Levy PY, et al. Propionibacterium acnes postoperative shoulder arthritis: an emerging clinical entity. Clin Infect Dis. 2008; 46(12):1884–6. 2. Perry A, Lambert P. Propionibacterium acnes: infection beyond the skin. Expert Rev Anti Infect Ther. 2011;9(12):1149–56. 3. Harris AE, et al. Postoperative discitis due to Propionibacterium acnes: a case report and review of the literature. Surg Neurol. 2005;63(6):538–41 (discussion 541). 4. Gekowski KM, et al. Splenic abscess caused by Propionibacterium acnes. Yale J Biol Med. 1982;55(1):65–9.
437 5. Gangahar DM, Delany HM. Intrasplenic abscess: two case reports and review of the literature. Am Surg. 1981;47(11):488–91. 6. Chang KC, et al. Clinical characteristics and prognostic factors of splenic abscess: a review of 67 cases in a single medical center of Taiwan. World J Gastroenterol. 2006;12(3):460–4. 7. Nelken N, et al. Changing clinical spectrum of splenic abscess. A multicenter study and review of the literature. Am J Surg. 1987;154(1):27–34. 8. Chun CH, et al. Splenic abscess. Medicine (Baltimore). 1980;59(1):50–65. 9. Antopolsky M, et al. Splenic infarction: 10 years of experience. Am J Emerg Med. 2009;27(3):262–5. 10. Lee WS, Choi ST, Kim KK. Splenic abscess: a single institution study and review of the literature. Yonsei Med J. 2011;52(2): 288–92. 11. Vanderschueren S, et al. From prolonged febrile illness to fever of unknown origin: the challenge continues. Arch Intern Med. 2003;163(9):1033–41. 12. Kubota K, et al. FDG-PET for the diagnosis of fever of unknown origin: a Japanese multi-center study. Ann Nucl Med. 2011;25(5): 355–64. 13. Niazi SA, et al. Propionibacterium acnes and Staphylococcus epidermidis isolated from refractory endodontic lesions are opportunistic pathogens. J Clin Microbiol. 2010;48(11):3859–69. 14. Ishige I, et al. Quantitative PCR of mycobacterial and propionibacterial DNA in lymph nodes of Japanese patients with sarcoidosis. Lancet. 1999;354(9173):120–3. 15. Jakab E, et al. Severe infections caused by Propionibacterium acnes: an underestimated pathogen in late postoperative infections. Yale J Biol Med. 1996;69(6):477–82. 16. O’Brien SM, et al. Results of the fludarabine and cyclophosphamide combination regimen in chronic lymphocytic leukemia. J Clin Oncol. 2001;19(5):1414–20. 17. Ooi LL, Leong SS. Splenic abscesses from 1987 to 1995. Am J Surg. 1997;174(1):87–93. 18. Ferraioli G, et al. Management of splenic abscess: report on 16 cases from a single center. Int J Infect Dis. 2009;13(4):524–30. 19. Llenas-Garcia J, et al. Splenic abscess: a review of 22 cases in a single institution. Eur J Intern Med. 2009;20(5):537–9. 20. Park HJ, et al. Clinical significance of Propionibacterium acnes recovered from blood cultures: analysis of 524 episodes. J Clin Microbiol. 2011;49(4):1598–601. 21. Eishi Y, et al. Quantitative analysis of mycobacterial and propionibacterial DNA in lymph nodes of Japanese and European patients with sarcoidosis. J Clin Microbiol. 2002;40(1):198–204. 22. Roberts SA, et al. Antimicrobial susceptibility of anaerobic bacteria in New Zealand: 1999–2003. J Antimicrob Chemother. 2006;57(5):992–8. 23. Kawada A, Aragane Y, Tezuka T. Levofloxacin is effective for inflammatory acne and achieves high levels in the lesions: an open study. Dermatology. 2002;204(4):301–2.
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CASE REPORT
Multiple splenic nodules with fever: a case of splenic abscess due to Propionibacterium acnes Sho Kiritani • Junichi Kaneko • Taku Aoki Yoshihiro Sakamoto • Kiyoshi Hasegawa • Yasuhiko Sugawara • Norihiro Kokudo
•
Received: 14 May 2013 / Accepted: 11 September 2013 / Published online: 10 October 2013 Ó Springer Japan 2013
Abstract A 64-year-old man with a history of chronic lymphocytic leukemia (CLL) presented in the hematology department due to remarkable leukocytosis and progressing anemia. Ultrasound confirmed splenomegaly and plain computed tomography revealed multiple hypoattenuating areas in the large spleen. Following a clinical diagnosis of relapse of CLL, he underwent treatment with fludarabine, cyclophosphamide, and rituximab (FC-R). After five cycles of FC-R treatment, his leukocyte count and hemoglobin level were normalized, and the size of the spleen also decreased. He began to have intermittent high fever (38 °C), however, approximately 6 months after the initiation of FC-R treatment. The results of an interferongamma release assay were positive. 18F-fluoro-2-deoxy-Dglucose positron emission tomography showed multiple areas of high-uptake in the spleen, which was unclear in other radiologic modalities. We performed a splenectomy for the high fever and to confirm the diagnosis. Tissue cultures of the infarcted area of spleen were positive for Propionibacterium acnes. After splenectomy, the patient’s condition improved and there were no further episodes of fever. Until recently, three cases of splenic abscess caused by Propionibacterium acnes were reported. Here we present a fourth case of splenic abscess due to Propionibacterium acnes and review the literature.
S. Kiritani J. Kaneko T. Aoki Y. Sakamoto K. Hasegawa Y. Sugawara N. Kokudo (&) Hepato-Biliary-Pancreatic Surgery, Artificial Organ and Transplantation Division, Department of Surgery, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan e-mail: [email protected]
123
Keywords Splenic abscess Splenectomy Propionibacterium acnes Chronic lymphocytic leukemia Positron emission tomography
Introduction Propionibacterium acnes (P. acnes) is gram-positive, anaerobic, and part of the normal flora of human skin, oral cavity, large intestine, conjunctiva, and external ear canal [1, 2]. P. acnes infections infrequently occur as postoperative and device-related infections [2, 3]. Until recently, three cases of splenic abscess caused by P. acnes were reported [4–6]. Here we present a fourth case of splenic abscess due to P. acnes and review the literature.
Case report A 64-year-old man with a history of chronic lymphocytic leukemia (CLL) presented in the hematology department due to remarkable leukocytosis (163,600/mm3) and progressing anemia. Lymphocytes accounted for 68 % of the white blood cells (WBC). The peripheral blood lymphocytes were CD5-positive. Lymphocytes accounted for more than 30 % of the bone marrow. Ultrasonography confirmed splenomegaly (height 9 length 9 width 20 9 17 9 8 cm). Although he did not complain of abdominal pain, plain computed tomography (CT) revealed multiple hypoattenuating areas in the large spleen (Fig. 1a). Following a clinical diagnosis of relapse of CLL, he underwent treatment with fludarabine, cyclophosphamide, and rituximab (FC-R). After five cycles of FC-R treatment, his leukocyte count and hemoglobin level were normalized, and the size of the
Clin J Gastroenterol (2013) 6:434–437
Fig. 1 Contrast enhanced computed tomography revealed multiple hypoattenuating areas in the enlarged spleen (a, arrowhead). The multiple hypoattenuating areas were unclear when the size of the spleen had decreased (b), 18F-fluoro-2-deoxy-D-glucose positron
435
emission tomography showed multiple areas of high-uptake in the spleen (c). Histopathologic findings revealed wedge-shaped white infarct lesions of the spleen (d)
Fig. 2 Magnified view of histopathologic findings revealed white infarct areas with liquefactive necrosis (a, arrowhead). Microscopic findings revealed overt neutrophil infiltration in the surrounding areas of necrosis (b, arrowhead). No granuloma was detected
spleen also decreased (16 9 15 9 5 cm) without multiple hypoattenuating areas (Fig. 1b). He began to have intermittent high fever (38 °C), however, approximately 6 months after the initiation of FC-R treatment. Physical examination revealed no lymphadenopathy and the spleen was not palpable. The WBC count was 6,700/mm3 and the C-reactive protein level was 5.8 mg/dL. Peripheral blood flow cytometry revealed no relapse of CLL. No bacteria were found in 10 sets of blood culture and 2 sets of urine
culture. The sputum culture showed normal flora. The procalcitonin level was not elevated and blood/urine/sputum cultures were all negative. Antinuclear antibodies; beta-D-glucan; and Cryptococcus, Aspergillus, and Candida antigen tests were all negative. He underwent several examinations for fever of unknown origin with levofloxacin administration. Chest and abdominal X-ray were unremarkable. No sites of inflammation or malignant tumor were found on contrast CT. The intermittent fever
123
436
continued for more than 3 months. Although sputum, urine, gastric juice, and bone marrow cultures were negative for Mycobacterium tuberculosis, the results of an interferon-gamma release assay (QuantiFERON, Cellestis Ltd., Chadstone, Australia) were positive. 18F-fluoro-2deoxy-D-glucose positron emission tomography (FDGPET) showed multiple areas of high-uptake in the spleen (Fig. 1c), which was unclear in other radiologic modalities. The maximum standardized uptake value was 12.4. We tentatively diagnosed the patient with CLL invading the spleen and/or splenic tuberculosis. We performed a splenectomy for the high fever and to confirm the diagnosis. The surgical duration was 3 h 55 min. The spleen adhered strongly and was greatly enlarged (14.8 9 10.0 9 4.5 cm, 448 g). Histopathologic findings revealed wedge-shaped white infarct lesions of the spleen without significant vascular disease (Fig. 1d). The histopathologic findings also revealed white infarct areas with liquefactive necrosis (Fig. 2a). Microscopy findings revealed overt neutrophil infiltration in the surrounding areas (Fig. 2b). No granuloma was seen. The CLL had not invaded the spleen and Mycobacterium tuberculosis was negative. Tissue cultures of the infarcted area were positive for P. acnes. After splenectomy, the patient’s condition improved and there were no further episodes of fever.
Discussion Splenic abscess is uncommon, with a frequency of 0.1–0.7 % in an autopsy series [7, 8]. Nelken and colleagues [7] classified splenic abscess into 5 causes as follows: metastatic infection, contiguous infection, trauma, immunodeficiency, and embolic events with subsequent infection. The etiology in our patient was not clear. Antopolsky and colleagues [9] suggested that circulatory disturbances causing infarcted areas in the spleen occur during rapid progression of splenomegaly when patients have acute general inflammation or hematologic malignancy, including CLL. Our patient had splenomegaly before the initial FC-R chemotherapy and the spleen already showed multiple lowdensity areas on the initial CT. Splenectomy is the treatment option of choice for splenic abscess. CT-guided abscess drainage was also recently reported [10]. Our patient required a precise diagnosis and we therefore decided to perform the splenectomy. Fever of unknown origin is classically defined as fever higher than 38.3 °C on several occasions for at least 3 weeks with uncertain diagnosis after a number of obligatory tests [11]. Although our patient has CLL, the clinical condition was similar to the definition of fever of unknown origin. Fever of unknown origin remains a clinical challenge as no diagnosis can be made in up to 50 % of
123
Clin J Gastroenterol (2013) 6:434–437
the cases [11]. FDG-PET may be a sensitive diagnostic technique for evaluating fever of unknown origin. According to a Japanese multi-center study of FDG-PET for the diagnosis of fever of unknown origin, none of the 81 patients had a splenic abscess [12]. In our patient, FDGPET was key to diagnosing the splenic abscess. P. acnes causes invasive deep infections with reports of endocarditis, osteomyelitis after lumbar puncture, mediastinitis or discitis after surgery, spondylodiscitis following epidural catheterization, infection of intraocular lenses, ventro-peritoneal shunts, orthopedic implants, silicone implants, and artificial heart valve [2, 13]. In a recent report, P. acnes was found as a pathogen of sarcoidosis [14]. The etiology of splenic abscess due to P. acnes remains unclear. P. acnes may directly invade from the skin through an injection site or skin wound [2, 15]. Gekowski and colleagues [4] suggested that a patient in their study may have become inoculated with P. acnes during insulin administration, resulting in an inapparent subcutaneous focus of infection. Infection in our patient might have had a similar cause because high fever developed after 5 cycles of chemotherapy administered via intravenous injection. Our patient had underlying CLL. Two of the previously reported cases of P. acnes splenic abscess also had underlying disease: one with diabetes mellitus and the other with drug addiction [4, 5]. Whether or not the third patient had underlying disease is unknown. FC-R chemotherapy alone has a high risk for infection. According to a previous report, O’Brien and colleagues [16] suggest that 25 % of patients undergoing FC-R chemotherapy develop sepsis or pneumonia. A literature search using the terms ‘‘splenic infection’’ and ‘‘splenic abscess’’ was conducted using PubMed [National Library of Medicine (NLM), Bethesda, MD, USA) at the end of 2012. There were 834 cases of splenic abscess [7, 8, 10, 17]. Among these, anaerobic bacteria was the pathogen in 57 cases, Propionibacterium species was the pathogen in 6 cases, and P. acnes was the pathogen in 4 cases, including the present report. In previous reports, the most common pathogenic bacterium in splenic abscess was Staphylococcus aureus [18], Klebsiella pneumoniae [6], Streptococcus viridians [10], and Mycobacterium tuberculosis [19]. Although P. acnes splenic abscess is rare, P. acnes might be passed over unnoticed. The main reason is that P. acnes is anaerobic and difficult to detect in aerobic cultures. Another reason is that P. acnes is usually considered a contamination on blood culture as a normal inhabitant [20]. P. acnes recently received attention as an etiologic link to sarcoidosis [21], but no granuloma was detected in our patient. With regard to contamination during handling of the spleen specimen, we suspected tuberculosis at first, and therefore the spleen was opened in a sterilized and enclosed environment for infection control.
Clin J Gastroenterol (2013) 6:434–437
P. acnes is relatively easy to treat with antibiotics. Penicillin, cephem, carbapenem, and fluoroquinolone antibiotics are used [22, 23]. Although levofloxacin was administered to our patient, his high fever continued. Splenectomy was an effective treatment.
Conclusion We reported a case of a patient with splenic abscess due to P. acnes. Acknowledgments The authors would like to thank Masako Sugimoto, Yasuhiko Kamikubo, Mineo Kurokawa of Department of Hematology, Graduate School of Medicine, The University of Tokyo, Yukako Shintani, Masashi Fukayama of Department of Pathology, Graduate School of Medicine, The University of Tokyo, Junichi Shindoh, Yoshikuni Kawaguchi, Kiyohiko Omichi, Hepato-BiliaryPancreatic Surgery, Artificial Organ and Transplantation Division, Department of Surgery, Graduate School of Medicine, The University of Tokyo for their important contributions to the diagnosis. Disclosures Conflict of Interest: The authors declare that they have no conflict of interest. Human/Animal Rights: All procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional and national) and with the Helsinki Declaration of 1975, as revised in 2008(5). Informed Consent: Informed consent was obtained from all patients for being included in the study.
References 1. Levy PY, et al. Propionibacterium acnes postoperative shoulder arthritis: an emerging clinical entity. Clin Infect Dis. 2008; 46(12):1884–6. 2. Perry A, Lambert P. Propionibacterium acnes: infection beyond the skin. Expert Rev Anti Infect Ther. 2011;9(12):1149–56. 3. Harris AE, et al. Postoperative discitis due to Propionibacterium acnes: a case report and review of the literature. Surg Neurol. 2005;63(6):538–41 (discussion 541). 4. Gekowski KM, et al. Splenic abscess caused by Propionibacterium acnes. Yale J Biol Med. 1982;55(1):65–9.
437 5. Gangahar DM, Delany HM. Intrasplenic abscess: two case reports and review of the literature. Am Surg. 1981;47(11):488–91. 6. Chang KC, et al. Clinical characteristics and prognostic factors of splenic abscess: a review of 67 cases in a single medical center of Taiwan. World J Gastroenterol. 2006;12(3):460–4. 7. Nelken N, et al. Changing clinical spectrum of splenic abscess. A multicenter study and review of the literature. Am J Surg. 1987;154(1):27–34. 8. Chun CH, et al. Splenic abscess. Medicine (Baltimore). 1980;59(1):50–65. 9. Antopolsky M, et al. Splenic infarction: 10 years of experience. Am J Emerg Med. 2009;27(3):262–5. 10. Lee WS, Choi ST, Kim KK. Splenic abscess: a single institution study and review of the literature. Yonsei Med J. 2011;52(2): 288–92. 11. Vanderschueren S, et al. From prolonged febrile illness to fever of unknown origin: the challenge continues. Arch Intern Med. 2003;163(9):1033–41. 12. Kubota K, et al. FDG-PET for the diagnosis of fever of unknown origin: a Japanese multi-center study. Ann Nucl Med. 2011;25(5): 355–64. 13. Niazi SA, et al. Propionibacterium acnes and Staphylococcus epidermidis isolated from refractory endodontic lesions are opportunistic pathogens. J Clin Microbiol. 2010;48(11):3859–69. 14. Ishige I, et al. Quantitative PCR of mycobacterial and propionibacterial DNA in lymph nodes of Japanese patients with sarcoidosis. Lancet. 1999;354(9173):120–3. 15. Jakab E, et al. Severe infections caused by Propionibacterium acnes: an underestimated pathogen in late postoperative infections. Yale J Biol Med. 1996;69(6):477–82. 16. O’Brien SM, et al. Results of the fludarabine and cyclophosphamide combination regimen in chronic lymphocytic leukemia. J Clin Oncol. 2001;19(5):1414–20. 17. Ooi LL, Leong SS. Splenic abscesses from 1987 to 1995. Am J Surg. 1997;174(1):87–93. 18. Ferraioli G, et al. Management of splenic abscess: report on 16 cases from a single center. Int J Infect Dis. 2009;13(4):524–30. 19. Llenas-Garcia J, et al. Splenic abscess: a review of 22 cases in a single institution. Eur J Intern Med. 2009;20(5):537–9. 20. Park HJ, et al. Clinical significance of Propionibacterium acnes recovered from blood cultures: analysis of 524 episodes. J Clin Microbiol. 2011;49(4):1598–601. 21. Eishi Y, et al. Quantitative analysis of mycobacterial and propionibacterial DNA in lymph nodes of Japanese and European patients with sarcoidosis. J Clin Microbiol. 2002;40(1):198–204. 22. Roberts SA, et al. Antimicrobial susceptibility of anaerobic bacteria in New Zealand: 1999–2003. J Antimicrob Chemother. 2006;57(5):992–8. 23. Kawada A, Aragane Y, Tezuka T. Levofloxacin is effective for inflammatory acne and achieves high levels in the lesions: an open study. Dermatology. 2002;204(4):301–2.
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