Mycobacterial Skin Ulcers in Uganda

Clancey, J. K.; Dodge, O. G.; Lunn, H. F.; Oduori, M.L.

doi:10.1016/s0140-6736(61)90793-0

Cited by 111 publications

(66 citation statements)

References 5 publications

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“…3,32 In nearby Uganda, necrotizing skin ulcers containing M. ulcerans were seen in nearly epidemic proportions. 33 Because the condition was especially common in Buruli County (Uganda), the term Buruli ulcer arose. Although widely present in west and central Africa, especially in Benin, Ghana, and Ivory Coast, other known endemic regions include Malaysia, Mexico, Bolivia, Peru, French Guyana, and Papua New Guinea.…”

Section: Resultsmentioning

confidence: 99%

Transmission of Mycobacterium ulcerans to the nine-banded armadillo.

Walsh¹,

Meyers²,

Krieg³

et al. 1999

The American Journal of Tropical Medicine and Hygiene

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Abstract. Animal models for Mycobacterium ulcerans infections (Buruli ulcer) include guinea pigs, rats, and mice, but each has limitations in replicating the spectrum of human disease. Here, 19 adult nine-banded armadillos were inoculated intradermally with M. ulcerans. Injection sites were examined and skin samples obtained for histologic and microbiology studies. Necropsies were conducted to assess systemic involvement. In group 1 (n ϭ 4), 2 animals developed progressive skin ulcers with undermined borders at the injection sites within 6-10 weeks. Biopsies showed features similar to human disease including extensive necrosis in the deep dermis and subcutaneous fat, mixed cellular infiltrates, and acid-fast bacilli (AFB). In group 2 (n ϭ 15), 5 animals developed progressive skin ulcers, 3 had evanescent papulo-nodules, 3 died shortly after inoculation of unknown causes, and 4 showed no signs of infection. Lesion samples from 3 animals with progressive ulcers were culture positive for AFB. Our findings indicate that nine-banded armadillos are susceptible to M. ulcerans and may develop cutaneous lesions that closely mimic Buruli ulcer.In tropical countries, skin ulcers caused by infectious agents are common. Mycobacterium ulcerans, the causative organism of Buruli ulcer first isolated in Australia, is considered a public health threat, especially in Africa. [1][2][3][4][5][6][7][8][9][10] Recent observations suggest that environmental sources of M. ulcerans include swamps, with subsequent transmission by insects. 11 The clinical features of Buruli ulcer are variable. In uncomplicated disease, painless skin ulcers, typically on the extremities, develop without fever or malaise. 12,13 However, progressive lesions may result in large areas of ulceration, necrosis, and osteomyelitis. Many lesions tend to heal, but this may take years without medical intervention. Advanced disease requires surgical excision and skin grafts or amputation. Crippling contractures and lymphedema may accompany healing. Medical therapies include clofazimine, dapsone, rifampicin, phenytoin, cotrimoxazole, macrolide compounds, and heat. However, cure rates are generally low. [14][15][16][17][18][19] Understanding the pathogenesis of human M. ulcerans infections has been slowed by the lack of an animal model that develops features resembling human disease. Rats, mice, and guinea pigs are used as animal models for M. ulcerans infections, but each is limited in replicating the spectrum of features found in human disease. Rats and mice develop lesions after cutaneous inoculation with M. ulcerans, but lack the extensive ulceration characteristic of human disease. In the mouse footpad, the organisms multiply but necrosis without ulceration destroys the limb and causes death. 20,21 Guinea pigs develop inflammatory lesions at the inoculation sites that usually resolve without ulcer formation. 21,22 The nine-banded armadillo is highly susceptible to M. leprae and has been a useful animal model for leprosy. 23 Here, we report that armadillos are also s...

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Section: Resultsmentioning

confidence: 99%

Transmission of Mycobacterium ulcerans to the nine-banded armadillo.

Walsh¹,

Meyers²,

Krieg³

et al. 1999

The American Journal of Tropical Medicine and Hygiene

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“…In most endemic areas patients present late with ulcerated lesions; for such cases wide surgical excision was the treatment of choice. 2,4,11,12 Adjunctive skin grafting was usually required. 4,12,13 A clinical trial conducted in Ghana under the auspices of the World Health Organisation demonstrated that after daily treatment with rifampicin and streptomycin for at least four weeks MU could no longer be cultured from the lesions.…”

Section: Discussionmentioning

confidence: 99%

Surgical management of Buruli ulcer disease: A four year experience from four endemic districts in Ghana

Adu

Ampadu²,

Acheampong³

2011

Ghana Medical Journal

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“…Thirteen years after the first report, the etiological agent of the ulcer was determined to be Mycobacterium ulcerans, a previously unknown mycobacterium (5,14). During the 1960s, many M. ulcerans infections were reported in Uganda, especially in Buruli County, for which this disease was eventually named (3,32). It is a necrotizing disease of the skin that mostly affects children, producing massive ulcers and permanent, disabling scars.…”

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confidence: 99%

Nineteen Cases of Buruli Ulcer Diagnosed in Japan from 1980 to 2010

et al. 2011

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The etiology, clinical manifestations, and treatment of 19 sporadic cases of Buruli ulcer (BU) in Japan are described. The cases originated in different regions of Honshu Island, with no evidence of patient contact with an aquatic environment. The majority (73.7%) of cases occurred in females, with an average age of 39.1 years for females and 56.8 years for males. All patients developed ulcers on exposed areas of the skin (e.g., face, extremities). Most ulcers were <5 cm in diameter (category I), except in one severe progressive case (category II). Pain was absent in 10 of the 19 cases. Fourteen ulcers were surgically excised, and nine patients needed skin grafting. All cases were treated with various antibiotic regimens, with no reported recurrences as of March 2011. Mycobacterium ulcerans-specific IS2404 was detected in all cases. Ten isolates had identical 16S rRNA gene sequences, which were similar to those of M. ulcerans. However, the rpoB gene showed a closer resemblance to Mycobacterium marinum or Mycobacterium pseudoshottsii. PCR identified pMUM001 in all isolates but failed to detect one marker. DNA-DNA hybridization misidentified all isolates as M. marinum. The drug susceptibility profile of the isolates also differed from that of M. ulcerans. Sequence analysis revealed "Mycobacterium ulcerans subsp. shinshuense" as the etiologic agent of BU in Japan. Clinical manifestations were comparable to those of M. ulcerans but differed as follows: (i) cases were not concentrated in a particular area; (ii) there was no suspected connection to an aquatic environment; (iii) drug susceptibility was different; and (iv) bacteriological features were different.

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Mycobacterial Skin Ulcers in Uganda

Cited by 111 publications

References 5 publications

Transmission of Mycobacterium ulcerans to the nine-banded armadillo.

Transmission of Mycobacterium ulcerans to the nine-banded armadillo.

Surgical management of Buruli ulcer disease: A four year experience from four endemic districts in Ghana

Nineteen Cases of Buruli Ulcer Diagnosed in Japan from 1980 to 2010

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