Publications by authors named "Wayne M Meyers"

Background: Basidiobolomycosis is a rare subcutaneous mycosis, which can be mistaken for several other diseases, such as soft tissue tumors, lymphoma, or Buruli ulcer in the preulcerative stage. Microbiological confirmation by PCR for and culture yield the most specific diagnosis, yet they are not widely available in endemic areas and with varying sensitivity. A combination of histopathological findings, namely, granulomatous inflammation with giant cells, septate hyphal fragments, and the Splendore-Hoeppli phenomenon, can confirm basidiobolomycosis in patients presenting with painless, hard induration of soft tissue.

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We report our experience in managing 13 consecutive clinically suspected cases of Buruli ulcer on the face treated at the hospital of the Institut Médical Evangélique at Kimpese, Democratic Republic of Congo diagnosed during 2003-2007. During specific antibiotherapy, facial edema diminished, thus minimizing the subsequent extent of surgery and severe disfigurations. The following complications were observed: 1) lagophthalmos from scarring in four patients and associated ectropion in three of them; 2) blindness in one eye in one patient; 3) disfiguring exposure of teeth and gums resulting from excision of the left labial commissure that affected speech, drinking, and eating in one patient; and 4) dissemination of Mycobacterium ulcerans infection in three patients.

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Buruli ulcer (BU), caused by the environmental organism Mycobacterium ulcerans and characterized by necrotizing skin and bone lesions, poses important public health issues as the third most common mycobacterial infection in humans. Pathogenesis of M ulcerans is mediated by mycolactone, a necrotizing immunosuppressive toxin. First-line therapy for BU is rifampin plus streptomycin, sometimes with surgery.

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Buruli ulcer is a neglected infectious disease caused by Mycobacterium ulcerans and is characterized by necrotic cutaneous lesions induced by the exotoxin mycolactone. Despite evidence of Th1-mediated protective immunity, M. ulcerans infection has been associated with systemic immunosuppression.

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Background: The World Health Organization (WHO) advises treatment of Mycobacterium ulcerans disease, also called "Buruli ulcer" (BU), with a combination of the antibiotics rifampicin and streptomycin (R+S), whether followed by surgery or not. In endemic areas, a clinical case definition is recommended. We evaluated the effectiveness of this strategy in a series of patients with large ulcers of > or =10 cm in longest diameter in a rural health zone of the Democratic Republic of Congo (DRC).

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Purpose Of Review: After tuberculosis, leprosy (Mycobacterium leprae) and Buruli ulcer (M. ulcerans infection) are the second and third most common mycobacterial infections in humankind, respectively. Recent advances in both diseases are summarized.

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We report a case of under treated necrotizing fasciitis (NF) in a 65-year-old woman with diabetes misdiagnosed as Mycobacterium ulcerans infection. She came to the Institut Médical Evangélique (IME) with an extensive painful edematous ulcerated lesion on the dorsum of the right foot and ankle. The diagnosis of Buruli ulcer (BU) was based initially on clinical findings and place of residence (Songololo Territory, the largest known focus of BU in Bas-Congo province).

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Mycobacterium ulcerans infection is an emerging disease that causes indolent, necrotizing skin lesions known as Buruli ulcer (BU) and occasional contiguous or metastatic bone lesions. Buruli ulcer is named after Buruli County in Uganda (east Africa), where an epidemic occurred in the 1960s. Today, BU is most common in central and west Africa.

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Invasive punch or incisional skin biopsy specimens are currently employed for the bacteriological confirmation of the clinical diagnosis of Buruli ulcer (BU), a cutaneous infectious disease caused by Mycobacterium ulcerans. The efficacy of fine-needle aspirates (FNA) using fine-gauge needles (23G by 25 mm) for the laboratory confirmation of BU was compared with that of skin tissue fragments obtained in parallel by excision or punch biopsy. In three BU treatment centers in Benin, both types of diagnostic material were obtained from 33 clinically suspected cases of BU and subjected to the same laboratory analyses: i.

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Buruli ulcer is an indolent necrotizing disease of the skin, subcutaneous tissue, and bone that is caused by Mycobacterium ulcerans. Buruli ulcer is presently the third most common mycobacterial disease of humans, after tuberculosis and leprosy, and the least understood of the three. The disease remained largely ignored by many national public health programs, but more recently, it has been recognized as an emerging health problem, primarily due to its frequent disabling and stigmatizing complications.

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We report 3 patients with laboratory-confirmed Buruli ulcer in Kafufu/Luremo, Angola, and Kasongo-Lunda, Democratic Republic of Congo. These villages are near the Kwango/Cuango River, which flows through both countries. Further investigation of artisanal alluvial mining as a risk factor for Buruli ulcer is recommended.

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Mycobacterium ulcerans is an emerging infection that causes indolent, necrotizing skin lesions known as Buruli ulcer (BU). Bone lesions may include reactive osteitis or osteomyelitis beneath skin lesions, or metastatic osteomyelitis from lymphohematogenous spread of M. ulcerans.

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Background: Mycobacterium ulcerans disease, or Buruli ulcer (BU), is an indolent, necrotizing infection of skin, subcutaneous tissue and, occasionally, bones. It is the third most common human mycobacteriosis worldwide, after tuberculosis and leprosy. There is evidence that M.

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Article Synopsis
  • * His treatment included multiple surgeries and a two-month course of antibiotics, specifically rifampin and ciprofloxacin, which helped improve healing and minimized the need for extensive surgical removal.
  • * This case highlights the challenges in diagnosing and managing Buruli ulcer and emphasizes the need for quick referrals and training for healthcare professionals to recognize this disease early.
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Mycobacterium liflandii causes a fatal frog disease in captive anurans. Here we report, to our knowledge, the first epizootic of mycobacteriosis in a European colony of clawed frogs (Silurana tropicalis), previously imported from a United States biologic supply company. Our findings suggest the emerging potential of this infection through international trade.

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Buruli ulcer, caused by Mycobacterium ulcerans, is a destructive infection that most commonly affects the skin. Animal models for Buruli ulcer include guinea pigs, rats, mice, and armadillos, but each is limited in replicating the spectrum of human disease. Here, a cynomolgus monkey was infected with two concentrations of M.

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Mycobacterium ulcerans is the etiologic agent of Buruli ulcer (BU), an emerging tropical skin disease. Virulent M. ulcerans secretes mycolactone, a cytotoxic exotoxin with a key pathogenic role.

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In the southern and southeastern United States, the 9-banded armadillo is an important reservoir for Mycobacterium leprae, the causative agent of leprosy (Hansen's disease). Here, we describe a woman living in Georgia with borderline tuberculoid leprosy who worked for many years in a garden where armadillos burrowed or were buried. There was no history of foreign travel or known exposure to a person with leprosy.

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Buruli ulcer (BU), which is caused by Mycobacterium ulcerans, is an important disabling skin disease. Its prevalence is highest in west and central Africa. We report an apparent resurgence of BU in the Bas-Congo Province, Democratic Republic of Congo.

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Mycobacterium ulcerans causes Buruli ulcer, an ulcerative skin disease in tropical and subtropical areas. Despite restricted genetic diversity, mycobacterial interspersed repetitive unit-variable-number tandem repeat analysis on M. ulcerans revealed 3 genotypes from different African countries.

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Buruli ulcer (BU) is a devastating, necrotizing, tropical skin disease caused by infections with Mycobacterium ulcerans. In contrast to other mycobacterioses, BU has been associated with minimal or absent inflammation. However, here we show that in the mouse M.

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