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Buruli Ulcer Disease

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Buruli Ulcer Disease
Buruli ulcer is an emerging disease that has been found in over 30 countries worldwide, predominately in humid tropical areas of Asia, Latin America and Africa. (Infection, 2003) The disease may also occur in temperate climates like those found in the coastal regions of southeastern Australia. It is the third most common mycobacterial infection in immunocompetent people in the endemic regions. There are an increasing number of cases in West Africa, where the disease has surpassed leprosy and tuberculosis in some regions. Buruli ulcer is caused by an infection with Mycobacterium ulcerans that involves the skin and subcutaneous adipose tissue that mainly affects children between the ages of 5 and 15. (Wansbrough-Jones & Phillips, 2006). It typically presents itself as a painless subcutaneous nodule that ulcerates approximately 70-100% of the time. (World Health Organization, 2007) There are other pre-ulcerative forms of the disease such as papules that affect the skin, plaques, which are large, firm, painless raised lesions and oedema, which is the severe form of the disease.
The first reported case of Buruli ulcer is thought to have been as far back as 1897 in Uganda. Sir Albert Cook described cases of chronic ulceration in Africa at that time but the disease was not published until 1948. It was then reported in two Australian children and four adults in an area in Bairnsdale, Victoria that demonstrated the lesions in several different stages of infection. (Wansbrough-Jones & Phillips, 2006) It was not until 1965 that it was discovered that there was no inflammation around the acid-fast bacilli in the necrotic tissue of the lesions that suggested that Mycobacterium ulcerans secretes a toxin that causes tissue damage.
According to the World Health Organization (WHO) there are four methods that are used to substantiate Mycobacterium ulcerans infection: direct smear examination, PCR, culture and histopathology. Although PCR is currently considered the “gold standard” it is not widely used due to the remoteness of the endemic areas and cost of the testing. PCR has proven to be 98% sensitive with swabs obtained from ulcers or tissue biopsies. A culture of Mycobacterium ulcerans is approximately 40-43% sensitive when using Lowenstein –Jenson slopes when incubated at 32oC for 6-8 weeks or more. Histopathology requires tissue biopsies and has a 90% sensitivity and can be used for a differential diagnosis when the other methods are negative. The simplest way to differentiate Mycobacterium ulcerans is by a direct smear examination for acid-fast bacilli from a swab using Ziehl-Neelsen stain. The direct smear examination is currently the most widely used method for identification of Mycobacterium ulcerans because it is easy to perform at a local level, does not require expensive materials or equipment and gives you rapid results. (Van Der Werf, et al., 2005)
It has been known for some time that Buruli ulcer transmission is associated with tropical, humid areas in Africa usually where there are areas of stagnant ground water or slow moving rivers. The bacterium has been found in the environment, wild animals, water bugs and fish. Although it has been found in these areas the exact mode of transmission is not known. It is thought that it is spread through the bite of an infected water bug, such as Naucoris flavicollis or Belostoma cordofna or by some other type of penetrating injury with contaminated vegetation.
Mycobacterium ulcerans Is similar to M. marinum strains but produces a polyketide toxin mycolactone. (Nienhuis, et al., 2010) Microlactones are secreted and diffuse into the infected tissues and surrounding areas inducing apoptosis and necrosis. For several years the primary treatment was surgical excision of the lesion with primary closure or skin grafting following excision. In the last few years the World Health Organization has recommended the use of oral antibiotic therapy. The use of rifampicin and intramuscular streptomycin is currently being used along with or without surgical intervention. The drug therapy is recommended for 8 weeks. Because of poor access to healthcare in endemic regions and the belief of traditional ways of healing treatment is usually delayed. Delay of treatment usually leads to extensive destruction of skin and tissue and long-term functional disabilities from scarring and joint immobility.
With the inability to control Mycobacterium ulcerans the current focus is aimed at reducing prolonged suffering, disabilities and the socioeconomic burden caused by the disease. The World Health Organization held a Global Buruli Ulcer Initiative to establish a strategy to fight this disease by: early detection of cases at the community level, training of healthcare workers, case management (combination of antibiotics, surgery, and prevention of disability/rehabilitation), laboratory confirmation of cases, standardized recording and reporting, strengthening of health facilities and monitoring and evaluation of control activities. (Van Der Werf, et al., 2005)
Despite the many difficulties presented by Mycobacterium ulcerans researchers are still hopeful that with continued research they will yield promising results to combat Buruli Ulcer Disease and that the current wave of interest will give this disease more attention to help attract the much needed resources for new tools for diagnosis, treatment and prevention.

Works Cited
Infection. (2003, May 9). Weekly Epidemiological Record. Retrieved October 2010, from ProQuest Medical Library: http://www.proquest.com
Nienhuis, W., Steinstra, Y., Thompson, W., Awuah, P., Abass, M., Tuah, W., et al. (2010, February 4). Antimicrobrial treatment for early, limited Mycobacterium ulcerans infection. Retrieved October 2010, from The Lancet: http://www.thelancet.com
Silva, M., & Portaels, F. P. (2009, November Vol 9). Pathogenic mechanisms of the intercellular parasite Mycobacterium ulcerans leading to Buruli ulcer. Retrieved October 2010, from The Lancet: http://www.thelancet.com/infection
Van Der Werf, T., Steinstra, Y., Johnson, C., Phillips, R., Adjei, O., Fleischer, B., et al. (2005, October 83 (10)). Public Health Reviews: Bulletin of theWorld Health Organization. Retrieved October 2010, from World Health Organization International: http://www.who.int
Van Der Werf, T., Stinear, T., Steinstra, Y., Van Der Graaf, W., & Small, P. (2003). Rapid Review: Mycolactones and Mycobacterium ulcerans disease. Retrieved October 2010, from The Lancet: http://www.thelancet.com
Wansbrough-Jones, M., & Phillips, R. (2006, June 3). Buruli ulcer: emerging from obscurity. Retrieved October 2010, from The Lancet: http://www.thelancet.com
World Health Organization. (2007). Guidence on sampling techniques for laboratory-confirmation of Mycobacterium ulcerans infection. Retrieved October 2010, from World Health Organization International: http://www.who.int

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