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Buruli Ulcer

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Question: 2 questions about Buruli ulcer (Mycobacterium ulcerans)? 1) Explain the pathology of Buruli ulcer. Describe 3 reasons why the disease is a much bigger problem in West African than in Australia. *I know that part of this is due to west africa being more hot and humid which leads to more aquatic insects which are a reservoir. I think a second reason may be a lack of health care in West Africa but i don't think that is a strong enough reason. * 2) Mycobacterium ulcerans is an environmental pathogen. What are some of the potential reservoir species? Develop a method for identification of the organism in the environment and describe the problems likely to be encountered. *I know the reservoirs include mollusks, fish, frogs, and aquatic insects but can't seem to come up with an identification scheme other than looking for the ulcers.

Answer: Background: Buruli ulcer is a chronic, indolent, necrotizing disease of the skin due to Mycobacterium ulcerans. It manifests initially as firm, nontender, subcutaneous nodules 1-2 cm in diameter at the sites of penetrating skin trauma (preulcerative stage). Within the next 1-2 months, these areas become fluctuant, followed by the formation of a painless, undermined ulceration (ulcerative stage.) Ulcerations can be extensive, involving as much as 15% of the patient's skin surface (see Image 1). The infection may destroy nerves, appendages, and blood vessels, and it occasionally invades bone. Most lesions eventually heal spontaneously, but they frequently result in chronic lymphedema and disfiguring scarring. It was first described by Sir Albert Cook in patients from Buruli County in Uganda. Pathophysiology: M ulcerans is a slow-growing mycobacterium affecting the skin and the mucous membranes. Inoculation into the skin occurs via trauma. The growing M ulcerans mycobacterium produces a soluble polyketide toxin called mycolactone. This toxin has been shown to have both immunosuppressive properties and cytotoxic properties, which explains the lack of host symptoms, such as fever, malaise, or adenopathy, and the extent of tissue undermining and destruction that is seen in Buruli ulcers. Mycolactone has been shown to induce apoptosis without inducing inflammation. Thus, M ulcerans does not cause the inflammation associated with other mycobacterial infections, such as Mycobacterium leprae and Mycobacterium tuberculosis. Frequency: In the US: Three cases have been diagnosed in the United States, all of which originated from outside the United States. Internationally: Worldwide, M ulcerans infection is the third most common mycobacterial disease of humans who are immunocompetent. Endemic areas include much of central and western Africa, such as Zaire, Congo, Cameroon, Nigeria, Benin, Ghana, Liberia, and the Ivory Coast. Cases of Buruli ulcer have been reported in contiguous countries completely across Africa from Uganda to Guinea. Other involved geographic areas include Australia, Southeast Asia, and sporadic cases in Central America and South America. Subtropics and/or swampy terrain are major endemic foci for M ulcerans. Mortality/Morbidity: Despite often extensive host involvement, little morbidity occurs with M ulcerans infection. Tissue necrosis may extend to muscle or bone, and metastatic bone lesions can develop. Healing with fibrosis may lead to significant deformity, with lymphedema, scarring, and contractures. Subclinical infections are common, as demonstrated by a positive burulin skin test. Race: No specific racial predilection is known. Sex: No differences in the rates of infection among males and females exist. Age: Cases most commonly occur in children younger than age 15 years, but the condition may affect person from any age group. One study found that swimming in rivers on a regular basis was the only significant risk factor for developing a Buruli ulcer. Because this behavior is more common among children, they develop the infection more often than adults.……… These are just 3 websites there are heaps if your but in the disease in the search area

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