Mycobacterium ulcerans Infection and Buruli Ulcer Disease: Emergence of a Public Health Dilemma

C. Harold King; Karen M. Dobos; David A. Ashford; Ellen A. Spotts Whitney; Pratima L. Raghunathan; Jeannette Guarner; Jordan W. Tappero

doi:10.1128/9781555816988.ch9

9 : Mycobacterium ulcerans Infection and Buruli Ulcer Disease: Emergence of a Public Health Dilemma

Authors: C. Harold King¹, Karen M. Dobos¹, David A. Ashford², Ellen A. Spotts Whitney², Pratima L. Raghunathan², Jeannette Guarner², Jordan W. Tappero³

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Affiliations: 1: Emory University School of Medicine, 69 Butler St. SE. Atlanta, GA 30303; 2: Centers for Disease Control and Prevention, 1600 Clifton Rd. NE, Atlanta, GA 30333; 3: Centers for Disease Control and Prevention, Atlanta, GA 30333; 4: The HIV/AIDS Collaboration, DMS 6 Building, Ministry of Public Health, Tivanon Rd., Nonthaburi 11000, Thailand

Content Type: Monograph

Publication Year: 2001

Category: Clinical Microbiology

Book DOI: 10.1128/9781555816988

Chapter DOI: 10.1128/9781555816988.ch9

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Abstract:

After tuberculosis and leprosy, Buruli ulcer disease (BUD) is the third most common mycobacterial disease among immunocompetent people in the tropical world. BUD caused by Mycobacterium ulcerans, is characterized by indolent, necrotizing ulcerations of the skin. M. ulcerans disrupts macrophages and adipose cell monolayers in vitro, in lieu of growing within these cells. One of the major goals of the WHO's Global Buruli Ulcer Initiative is to develop new diagnostic tests to identify patients infected with M. ulcerans prior to the development of advanced ulcerative disease. Because M. ulcerans is infrequently isolated, every well-characterized clinical isolate has the potential to add to the understanding of the molecular epidemiology of M. ulcerans. The main histopathologic feature during the nodule stage is the necrosis of the subcutaneous adipose tissues. Necrosis can be classified as coagulative since the tissue appears to maintain its architecture and shows intense eosinophilia due to loss of the normal basophilia imparted by cytoplasmic RNA. Surgery is the current recommended treatment for all stages of BUD. Ulcerative lesions require wide debridement followed by skin grafting, techniques requiring referral to specialized health care facilities. Currently, international efforts directed by the WHO Buruli Ulcer Initiative are targeted towards defining the worldwide burden of this disease, the source(s) and route(s) of transmission, improved diagnostic assays, the mechanisms of pathogenesis, less invasive treatment options, and improved public health control strategies.

Citation: Harold King C, Dobos K, Ashford D, Spotts Whitney E, Raghunathan P, Guarner J, Tappero J. 2001. Mycobacterium ulcerans Infection and Buruli Ulcer Disease: Emergence of a Public Health Dilemma, p 137-152. In Scheld W, Craig W, Hughes J (ed), Emerging Infections 5. ASM Press, Washington, DC. doi: 10.1128/9781555816988.ch9

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Buruli Ulcer: 0.4184144

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Mycobacterium ulcerans Infection and Buruli Ulcer Disease: Emergence of a Public Health Dilemma

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Figure 1.

Global distribution of BUD.

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Figure 1.

Global distribution of BUD.

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Figure 2.

Culture isolation. (A) Tissue preparation. Tissue samples are removed from transport tubes and superficial layers and scar tissue are aseptically removed with a sterile scalpel. (B) Tissue homogenization. Tissue (mostly dermis and subcutaneous fascia) is homogenized using a sterile plastic pestle and phosphate-buffered saline. (C) Decontamination. Tissue homogenate is decontaminated with HC1 and then neutralized with NaOH. (D) Sedimentation of bacilli. After decontamination, tissue homogenate is centrifuged; fatty tissue remains on the top layer, while bacteria settle to the bottom of the tube.

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Figure 2.

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Figure 3.

Western blot reactivity to MUCF. M, molecular size markers; lanes 1 to 6, representative BUD patient sera with reactivity to the MUCF; lanes 7 to 10, representative antibody reactivity in healthy persons from the area where the disease is endemic; lanes 11 and 12, serologic reactivities to the MUCF of two representative tuberculosis patients. Arrows indicate reactivity to the 70-, 38-, and 5-kDa antigens.

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Figure 3.

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Figure 4.

Two-dimensional gel electrophoresis (2D GE) mapping of the MUCF. (A) Silver-stain analysis. Fifty micrograms of MUCF protein was resolved by 2D GE using a pH gradient of 4 to 6.5 and discontinuous sodium dodecyl sulfate-15% polyacrylamide gel electrophoresis. (B) Western blot analysis. Fifty micrograms of MUCF was resolved by 2D GE as in panel A, transferred to nitrocellulose, and probed with BUD patient sera.

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Figure 4.

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Tables

Mycobacterium ulcerans Infection and Buruli Ulcer Disease: Emergence of a Public Health Dilemma

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Table 1

Candidate serodiagnostic proteins from M. ulcerans CF

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Table 1

Candidate serodiagnostic proteins from M. ulcerans CF