Lung Abscess due to Clostridium barati in a Patient with Invasive Pulmonary Aspergillosis ACCEPTED
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1 JCM Accepts, published online ahead of print on 3 January 2008 J. Clin. Microbiol. doi: /jcm Copyright 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved. Lung Abscess due to Clostridium barati in a Patient with Invasive Pulmonary Aspergillosis Clostridial pleuro-pulmonary infections are rare, most of which are attributed to Clostridium perfringens [1] and none have been reported involving C. barati. We describe here a fatal case of C. barati lung abscess superimposed on invasive pulmonary aspergillosis. A 47-year-old man was diagnosed with myelodysplastic syndrome with refractory anemia and excess blasts in December The disease course was complicated by disseminated Mycobacterium avium complex infection and invasive pulmonary aspergillosis. The patient underwent allogeneic hematopoietic stem cell transplantation in May One year later, he was admitted for leukemia relapse associated with febrile neutropenia. Chest radiography and computed tomography (CT) displayed multiple small opacities on the right upper and lower, and left upper lung fields. Compared with chest CT one year before, only the lesion on the left upper lung increased in size (Figure 1A). Low grade fever persisted despite treatment with imipenem and voriconazole. Serum Aspergillus antigen [Platelia Aspergillus enzyme immunoassay; Bio-Rad Laboratories] was negative. The lesion on the right lung progressed rapidly within 1
2 one month (Figure 1B). Follow-up chest CT showed an abscess with a thick wall (Figures 1 C and D). In August 2007, the patient was admitted to the intensive care unit (ICU) because of acute respiratory failure. Sonography-guided trans-thoracic lung biopsy was performed on the 2 nd ICU day. Pathology examination of the lung biopsy disclosed narrow, dichotomous and septated hyphae compatible with Aspergillus spp. Cultures of the lung biopsy and aspirates of the lung abscess as well as blood cultures all yielded C. barati that was susceptible to penicillin, chloramphenicol, metronidazole, and cefmetazole but was resistant to clindamycin by disk diffusion test. The patient s hemodynamics deteriorated and died of multi-organ failure on the 12 th ICU day. The genus Clostridium has more than 150 species but fewer than 20 are associated with human diseases [2, 3]. Members of the genus are mainly natural inhabitants of the human intestinal tract and their disease spectra in humans are broad [3]. C. barati has attracted limited attention because its lack of overt pathogenesis and failure to produce lethal toxin. Its most striking clinical feature is its neuro-toxogenesis, the type F botulism in infants [4] and in adults [4, 5]. However, C. barati pulmonary infection in adults has never been reported in literature. We speculate that the development of C. barati lung abscess in this 2
3 case may be closely related to the patient s leukemia relapse with persistent neutropenia and invasive pulmonary aspergillosis. The hyphae of Aspergillus tends to invade blood vessels which in turn leads to local thrombosis and tissue infarction [6, 7]. Simultaneously, clostridial bacteremia originating from the disruption of the gastro-intestinal mucosa becomes seeding into the lung with subsequent formation of lung abscess. The infection is refractory to antimicrobials in the face of tissue infarction despite the use of antimicrobial agents with in-vitro activity against C. barati. In conclusion, among high-risk hosts, the rapid progression of fungal pneumonia into lung abscess may suggest a superimposed infection due to anaerobic bacteria such as C. barati. Chin-Chung Shu 1, Ming Yao 1, Chien-Ching Hung 1, Yih-Leong Chang 2, Shih-Chi Ku 1, and Chong-Jen Yu 1 Departments of Internal Medicine 1 and Pathology 2, National Taiwan University Hospital 3
4 REFERENCES 1. Bayer AS, Nelson SC, Galpin JE, Chow AW, Guze LB: Necrotizing pneumonia and empyema due to Clostridium perfringens. Report of a case and review of the literature. Am J Med 1975, 59(6): Hatheway CL: Toxigenic clostridia. Clin Microbiol Rev 1990, 3(1): Lorber B: Gas Gangrene and Other Clostridium-Associated Diseases. In: Principles and Practice of Infectious Diseases. Edited by Mandell B, & Dolin, 6th edn: Churchill Livingstone; 2005: 2828~ Harvey SM, Sturgeon J, Dassey DE: Botulism due to Clostridium baratii type F toxin. J Clin Microbiol 2002, 40(6): Gupta A, Sumner CJ, Castor M, Maslanka S, Sobel J: Adult botulism type F in the United States, Neurology 2005, 65(11): Fraser RS: Pulmonary aspergillosis: pathologic and pathogenetic features. Pathol Annu 1993, 28 Pt 1: Kamai Y, Chiang LY, Lopes Bezerra LM, Doedt T, Lossinsky AS, Sheppard DC, Filler SG: Interactions of Aspergillus fumigatus with vascular endothelial cells. Med Mycol 2006, 44 Suppl 1:S
5 FIGURE LEGENDS Figure 1. Computed tomography (CT) scan of the chest on admission showed a small faint patch at the left upper lung field (LULF) and old fibrotic changes at the right upper lung filed (RULF) (A). Follow-up chest radiography one month later disclosed a mass lesion at the LULF (B) and CT scan at the same period (C and D) revealed a mass with a fluid-retaining central cavity, thick irregular wall, and a rim enhancing a focal area of consolidation over the LULF. 5
6 Figure 1 6
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