Buruli Ulcer Clinical Presentation

  • Author: Aaron Z Hoover, MD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Apr 13, 2010
 

History

  • The incubation period ranges from a few weeks to months.
  • Lesions usually begin as a single, painless, occasionally pruritic, dermal papule or subcutaneous nodule.
  • Suppuration and ulceration occur within 1-2 months.
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Physical

  • Approximately 90% of lesions occur on the limbs, with 60% occurring on the lower limbs.
  • In the preulcerative stage, Buruli ulcer manifests initially as firm, nontender, subcutaneous nodules 1-2 cm in diameter. Less common presentations include a dermal papule, indurated plaque, or a more aggressive edematous variant that rapidly causes diffuse swelling, which can involve an entire extremity and results in the formation of a very large ulcer.
  • The ulcerative stage occurs days to weeks later with the formation of an ulcer with undermined edges. The necrosis along the panniculus may extend several centimeters beyond the edge of the ulcer; therefore, the lesion appears smaller than its actual size. Characteristic lesions have a scalloped border and a sloughing, necrotic base. Ulcerations are generally painless unless complicated by secondary infection. The Buruli ulcers may destroy nerves, appendages, and blood vessels and may invade bone. A few studies have shown relatively high frequencies of bone involvement (15% of patients). Metastatic lesions may occur in skin, soft tissue, or bone via spread through the vasculature or lymphatics.
  • Healing is a slow process that often results in cosmetically disfiguring scars and functional disabilities.
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Causes

  • M ulcerans are slow-growing mycobacteria and are the causative agent of Buruli ulcer.
  • M ulcerans is an environmental pathogen that has been isolated from biofilms and small aquatic animals of slow-moving or stagnant bodies of water.[12, 13, 14, 15] Although the exact mode of transmission is unknown, M ulcerans most likely causes infection through contamination of a traumatic wound.[16] A role in transmission via the bites of Australian salt marsh mosquitoes and African biting water insects (Naucoridae and Belostomatidae) has been suggested.[17] Human-to-human transmission has rarely been reported.
  • A plasmid-encoded polyketide toxin called mycolactone is responsible for the extensive destruction and suppressed host response in Buruli ulcers. A total of 4 variants have been identified. Mycolactones A and B are the more virulent variates and are found in Africa. Mycolatone C is found in Australia, and Mycolatone D is found in Asia.
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Contributor Information and Disclosures
Author

Aaron Z Hoover, MD  Staff Dermatologist/Dermatopathologist, San Antonio Uniformed Services Health Education Consortium (SAUSHEC); Assistant Professor of Dermatology, Uniformed Services University of the Health Sciences

Aaron Z Hoover, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, Christian Medical & Dental Society, and International Society of Dermatopathology

Disclosure: Nothing to disclose.

Specialty Editor Board

Franklin Flowers, MD  Chief, Division of Dermatology, Professor, Department of Medicine and Otolaryngology, Affiliate Associate Professor of Pediatrics and Pathology, University of Florida College of Medicine

Franklin Flowers, MD, is a member of the following medical societies: American College of Mohs Micrographic Surgery and Cutaneous Oncology

Disclosure: Nothing to disclose.

Richard P Vinson, MD  Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association

Disclosure: Nothing to disclose.

Paul Krusinski, MD  Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine

Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Catherine M Quirk, MD  Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania

Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

The author and editors of eMedicine gratefully acknowledge the contributions of the following previous authors, Brian P. Green, DO, MS, PA-C, Sean T. Gunning, MD, and Mary K. Mather, MD, to the development and writing of this article. The author and editors of eMedicine would also like to thank Wayne M. Meyers, MD, for his clinical images from his article with Douglas S. Walsh, MD, in Transactions of the Royal Society of Tropical Medicine and Hygiene.[3] The authors and editors of eMedicine gratefully acknowledge the contributions of previous Chief Editor, William D. James, MD, to the development and writing of this article.

References

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  2. World Health Organization. Buruli ulcer disease (Mycobacterium ulcerans infection). World Health Organization. Available at http://www.who.int/mediacentre/factsheets/fs199/en/. Accessed December 3, 2008.

  3. Walsh DS, Portaels F, Meyers WM. Buruli ulcer (Mycobacterium ulcerans infection). Trans R Soc Trop Med Hyg. Oct 2008;102(10):969-78. [Medline].

  4. Wansbrough-Jones M, Phillips R. Buruli ulcer: emerging from obscurity. Lancet. Jun 3 2006;367(9525):1849-58. [Medline].

  5. George KM, Chatterjee D, Gunawardana G, et al. Mycolactone: a polyketide toxin from Mycobacterium ulcerans required for virulence. Science. Feb 5 1999;283(5403):854-7. [Medline].

  6. Pimsler M, Sponsler TA, Meyers WM. Immunosuppressive properties of the soluble toxin from Mycobacterium ulcerans. J Infect Dis. Mar 1988;157(3):577-80. [Medline].

  7. Walsh DS, Meyers WM, Portaels F, et al. High rates of apoptosis in human Mycobacterium ulcerans culture-positive buruli ulcer skin lesions. Am J Trop Med Hyg. Aug 2005;73(2):410-5. [Medline].

  8. Stienstra Y, van der Werf TS, Oosterom E, et al. Susceptibility to Buruli ulcer is associated with the SLC11A1 (NRAMP1) D543N polymorphism. Genes Immun. Apr 2006;7(3):185-9. [Medline].

  9. Guedenom A, Zinsou C, Josse R, et al. Traditional treatment of Buruli ulcer in Benin. Arch Dermatol. Jun 1995;131(6):741-2. [Medline].

  10. Aiga H, Amano T, Cairncross S, Adomako J, Nanas OK, Coleman S. Assessing water-related risk factors for Buruli ulcer: a case-control study in Ghana. Am J Trop Med Hyg. Oct 2004;71(4):387-92. [Medline].

  11. Meyers WM, Tignokpa N, Priuli GB, Portaels F. Mycobacterium ulcerans infection (Buruli ulcer): first reported patients in Togo. Br J Dermatol. Jun 1996;134(6):1116-21. [Medline].

  12. Eddyani M, Ofori-Adjei D, Teugels G, et al. Potential role for fish in transmission of Mycobacterium ulcerans disease (Buruli ulcer): an environmental study. Appl Environ Microbiol. Sep 2004;70(9):5679-81. [Medline].

  13. Marsollier L, Severin T, Aubry J, et al. Aquatic snails, passive hosts of Mycobacterium ulcerans. Appl Environ Microbiol. Oct 2004;70(10):6296-8. [Medline].

  14. Marsollier L, Stinear T, Aubry J, et al. Aquatic plants stimulate the growth of and biofilm formation by Mycobacterium ulcerans in axenic culture and harbor these bacteria in the environment. Appl Environ Microbiol. Feb 2004;70(2):1097-103. [Medline].

  15. Raghunathan PL, Whitney EA, et al. Risk factors for Buruli ulcer disease (Mycobacterium ulcerans Infection): results from a case-control study in Ghana. Clin Infect Dis. May 15 2005;40(10):1445-53. [Medline].

  16. Meyers WM, Shelly WM, Connor DH, Meyers EK. Human Mycobacterium ulcerans infections developing at sites of trauma to skin. Am J Trop Med Hyg. Sep 1974;23(5):919-23. [Medline].

  17. Johnson PD, Azuolas J, Lavender CJ, et al. Mycobacterium ulcerans in mosquitoes captured during outbreak of Buruli ulcer, southeastern Australia. Emerg Infect Dis. Nov 2007;13(11):1653-60. [Medline].

  18. Phillips R, Horsfield C, Kuijper S, et al. Sensitivity of PCR targeting the IS2404 insertion sequence of Mycobacterium ulcerans in an Assay using punch biopsy specimens for diagnosis of Buruli ulcer. J Clin Microbiol. Aug 2005;43(8):3650-6. [Medline].

  19. Rondini S, Mensah-Quainoo E, Junghanss T, Pluschke G. What does detection of Mycobacterium ulcerans DNA in the margin of an excised Buruli ulcer lesion tell us?. J Clin Microbiol. Nov 2006;44(11):4273-5. [Medline].

  20. Siegmund V, Adjei O, Nitschke J, et al. Dry reagent-based polymerase chain reaction compared with other laboratory methods available for the diagnosis of Buruli ulcer disease. Clin Infect Dis. Jul 1 2007;45(1):68-75. [Medline].

  21. Leigheb G, Cammarota T, Zavattaro E, et al. Ultrasonography for the monitoring of subcutaneous damage in Mycobacterium ulcerans infection (Buruli ulcer). Ultrasound Med Biol. Oct 2008;34(10):1554-63. [Medline].

  22. Chauty A, Ardant MF, Adeye A, et al. Promising clinical efficacy of streptomycin-rifampin combination for treatment of buruli ulcer (Mycobacterium ulcerans disease). Antimicrob Agents Chemother. Nov 2007;51(11):4029-35. [Medline].

  23. Etuaful S, Carbonnelle B, Grosset J, et al. Efficacy of the combination rifampin-streptomycin in preventing growth of Mycobacterium ulcerans in early lesions of Buruli ulcer in humans. Antimicrob Agents Chemother. Aug 2005;49(8):3182-6. [Medline].

  24. World Health Organization. Provisional guidance on the role of specific antibiotics in the management of Mycobacterium ulcerans disease (Buruli ulcer). World Health Organization. Available at http://www.who.int/buruli/information/antibiotics/en/. Accessed December 3, 2008.

  25. Johnson PD, Hayman JA, Quek TY, et al. Consensus recommendations for the diagnosis, treatment and control of Mycobacterium ulcerans infection (Bairnsdale or Buruli ulcer) in Victoria, Australia. Med J Aust. Jan 15 2007;186(2):64-8. [Medline].

  26. [Best Evidence] Nienhuis WA, Stienstra Y, Thompson WA, et al. Antimicrobial treatment for early, limited Mycobacterium ulcerans infection: a randomised controlled trial. Lancet. Feb 20 2010;375(9715):664-72. [Medline].

  27. Meyers WM, Shelly WM, Connor DH. Heat treatment of Mycobacterium ulcerans infections without surgical excision. Am J Trop Med Hyg. Sep 1974;23(5):924-9. [Medline].

  28. Krieg RE, Wolcott JH, Confer A. Treatment of Mycobacterium ulcerans infection by hyperbaric oxygenation. Aviat Space Environ Med. Oct 1975;46(10):1241-5. [Medline].

  29. Phillips R, Adjei O, Lucas S, Benjamin N, Wansbrough-Jones M. Pilot randomized double-blind trial of treatment of Mycobacterium ulcerans disease (Buruli ulcer) with topical nitrogen oxides. Antimicrob Agents Chemother. Aug 2004;48(8):2866-70. [Medline].

  30. Nackers F, Dramaix M, Johnson RC, et al. BCG vaccine effectiveness against Buruli ulcer: a case-control study in Benin. Am J Trop Med Hyg. Oct 2006;75(4):768-74. [Medline].

  31. van der Werf TS, Stienstra Y, Johnson RC, et al. Mycobacterium ulcerans disease. Bull World Health Organ. Oct 2005;83(10):785-91. [Medline].

  32. Bretzel G, Siegmund V, Racz P, et al. Post-surgical assessment of excised tissue from patients with Buruli ulcer disease: progression of infection in macroscopically healthy tissue. Trop Med Int Health. Nov 2005;10(11):1199-206. [Medline].

  33. Minutilli E, Orefici G, Pardini M, et al. Squamous cell carcinoma secondary to buruli ulcer. Dermatol Surg. Jul 2007;33(7):872-5. [Medline].

  34. Connor DH, Meyers WM, Kreig RE. Infection by Mycobacterium ulcerans. In: Binford CH, Connor DH, eds. Pathology of Tropical and Extraordinary Diseases. Washington, DC: Armed Forces Institute of Pathology; 1976:226-35.

  35. Health Section of the Secretariat of the League of Nations. Buruli ulcer disease. Wkly Epidemiol Rec. May 14 2004;79(20):194-9. [Medline].

  36. Meyers WM. Atypical mycobacteria skin infections. In: Strickland GT, ed. Hunter's Tropical Medicine. Philadelphia, Pa: WB Saunders; 1991:495-6.

  37. Prevot G, Bourreau E, Pascalis H, et al. Differential production of systemic and intralesional gamma interferon and interleukin-10 in nodular and ulcerative forms of Buruli disease. Infect Immun. Feb 2004;72(2):958-65. [Medline].

  38. Stienstra Y, van der Werf TS, van der Graaf WT, et al. Buruli ulcer and schistosomiasis: no association found. Am J Trop Med Hyg. Sep 2004;71(3):318-21. [Medline].

  39. Wagner D, Young LS. Nontuberculous mycobacterial infections: a clinical review. Infection. Oct 2004;32(5):257-70. [Medline].

 
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Buruli ulcer can extend to 15% of a person's skin surface and may destroy nerves and blood vessels. Metastatic bone lesions may develop.
An edematous Buruli ulcer in a 9-year-old Togolese girl. Courtesy of Wayne M. Meyers, MD.
Photo of Tongolese girl taken 5 years after the Buruli ulcer had been excised and repaired with autologous split-skin graft by G.B. Priuli, MD. Courtesy of Wayne M. Meyers, MD.
Table. Categories of Treatment
CategoryForm of DiseaseTreatmentPrimary AimSecondary Aimlevel of Health Care SystemDiagnosis
ISmall early lesion (eg, nodules, papules, plaques, ulcers < 5 cm in diameter)For papules and nodules, if immediate excision and suturing is possible, start antibiotics at least 24 hours before surgery and continue for 4 weeks. Otherwise, treat all lesions in this category with antibiotics for 8 weeks. Cure without surgery except for simple removal of dead tissueReduce or prevent recurrenceCommunity health centers and district hospitalsClinical and laboratory
IINonulcerative and ulcerative plaque and edematous forms



Large ulcerative lesions (>5 cm in diameter)



Lesions in the head and neck region, particularly the face



Treat with antibiotics for at least 4 weeks, then surgery (if necessary), followed by another 4 weeks of antibiotics.Reduce extent of the surgical excisionReduce or prevent recurrenceDistrict and tertiary hospitalsClinical and laboratory
IIIDisseminated/mixed forms (eg, osteitis, osteomyelitis, joint involvement)Treat with antibiotics for at least 1 week before surgery and continue for a total of 8 weeks.Reduce M ulcers infection and dissemination before and after surgeryReduce or prevent recurrence; reduce extent of surgical excisionDistrict and tertiary hospitalsClinical and laboratory
From " Provisional guidance on the role of specific antibiotics in the management of Mycobacterium ulcerans disease (Buruli ulcer). "[24]
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