Variable Number Tandem Repeat Profiling of Reveals New Genotypes in Buruli Ulcer Endemic Communities in Ghana and Côte d'Ivoire.

Buruli ulcer (BU), a necrotic skin disease caused by , is mainly prevalent in West Africa, but cases have also been reported in other tropical parts of the world. It is the second most common mycobacterial disease after tuberculosis in Ghana and Côte d'Ivoire. Heterogeneity among from different geographical locations has not been clearly elucidated, and some studies seem to suggest genetic differences between in humans and in the environment.

Non-tuberculous mycobacteria, not , are a significant cause of TB-like lesions observed in slaughtered cattle in Ghana.

Objectives: The aim was to isolate and identify the species of mycobacteria causing tuberculous-like (TB-like) lesions in cattle in Ghana.

Methods: Between 2019 and 2020, 68 bovine tissue samples with TB-like lesions, identified during post slaughter examination, were obtained from four major abattoirs close to border towns in Ghana. The samples were cultured on Lowenstein-Jensen medium.

Natural antioxidants attenuate mycolactone toxicity to RAW 264.7 macrophages.

produces a macrolide exotoxin, mycolactone which suppresses immune cells activity, is toxic to most cells and the key virulence factor in the pathogenesis of Buruli ulcer disease. Mycolactone is reported to mediate the production of reactive oxygen species in keratinocytes; cells that play critical role in wound healing. Increased levels of reactive oxygen species have been shown to disrupt the well-ordered process of wound repair; hence, the function of wound-healing cells such as macrophages, keratinocytes, and fibroblast could be impaired in the presence of the reactive oxygen species mediator, mycolactone.

Paradoxical reactions in Buruli ulcer after initiation of antibiotic therapy: Relationship to bacterial load.

Background: We investigated the relationship between bacterial load in Buruli ulcer (BU) lesions and the development of paradoxical reaction following initiation of antibiotic treatment.

Methods: This was a longitudinal study involving BU patients from June 2013 to June 2017. Fine needle aspirates (FNA) and swab samples were obtained to establish the diagnosis of BU by PCR.

IFN-γ and IL-5 whole blood response directed against mycolactone polyketide synthase domains in patients with infection.

Background: Buruli ulcer is a disease of the skin and soft tissues caused by infection with a slow growing pathogen, . A vaccine for this disease is not available but possesses a giant plasmid pMUM001 that harbours the polyketide synthase (PKS) genes encoding a multi-enzyme complex needed for the production of its unique lipid toxin called mycolactone, which is central to the pathogenesis of Buruli ulcer. We have studied the immunogenicity of enzymatic domains in humans with disease, their contacts, as well as non-endemic areas controls.

Clearance of viable Mycobacterium ulcerans from Buruli ulcer lesions during antibiotic treatment as determined by combined 16S rRNA reverse transcriptase /IS 2404 qPCR assay.

Introduction: Buruli ulcer (BU) caused by Mycobacterium ulcerans is effectively treated with rifampicin and streptomycin for 8 weeks but some lesions take several months to heal. We have shown previously that some slowly healing lesions contain mycolactone suggesting continuing infection after antibiotic therapy. Now we have determined how rapidly combined M.

Infection with Mansonella perstans Nematodes in Buruli Ulcer Patients, Ghana.

During August 2010-December 2012, we conducted a study of patients in Ghana who had Buruli ulcer, caused by Mycobacterium ulcerans, and found that 23% were co-infected with Mansonella perstans nematodes; 13% of controls also had M. perstans infection. M.