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• W2296939458 abstract "After tuberculosis and leprosy, Buruli ulcer (BU) which is caused by Mycobacteriumulcerans, is the most common mycobacterial infection in immuno-competent humans.Since the 1980s BU has gained significant public health importance in the tropicsespecially in West Africa, including Ghana. The establishment of control measures ishampered as a result of the scarcity of understanding of many features of the disease.Priority areas for research defined by WHO include: understanding the mode oftransmission, development of simpler methods for early diagnosis, development ofeffective antibiotic treatment, and the understanding of protective immune responses tosupport vaccine development.The availability of M. ulcerans isolates from endemic areas is necessary for detailedtransmission studies and the analysis of efficacy of antibiotics for the treatment of BU.However, cultivation of M. ulcerans from clinical specimens is burdensome; reportedrecovery rates are as low as 20%. We evaluated four different decontamination methodsand one non-decontamination procedure in combination with four egg-based media forthe primary isolation of M. ulcerans from tissue specimens excised from BU lesions.Oxalic acid decontamination and culture on LJ medium supplemented with glycerol wasthe most efficient procedure and achieved a recovery rate of 75.6%. The success ofcultivation depended also on a good sampling procedure. The use of the optimisedcultivation method has allowed the production of a large isolate collection.For efficient case management and confirmation of epidemiological data, it is necessaryto reconfirm clinical diagnosis by laboratory procedures. We used culture together withPCR and direct AFB staining to establish a system of reconfirming cases clinicallydiagnosed at the Amasaman Health Centre, Ghana. All three methods showed acomparable sensitivity and the laboratory analysis demonstrated a high accuracy ofclinical judgment by an experienced clinician.Current recommendation by the WHO requires that BU patients be treated with acombination of rifampicin and streptomycin for 8 weeks before surgical excision. Inmany infectious diseases, the development of drug resistance has a serious impact onpatient management. It is therefore essential to monitor the drug susceptibility of M.ulcerans. We analysed the susceptibility of 28 isolates to rifampicin, streptomycin isoniazid and ethambutol and identified both streptomycin and rifampicin resistant strainsin Ghana. Findings from this study call for reconsideration of the current treatmentguidelines.Currently, micro-epidemiological studies aiming to reveal transmission chains cannot bedone in BU. This is due to the low degree of genetic polymorphism in M. ulceransrevealed by routinely used genetic fingerprinting procedures. We used VNTR typingbased on a newly identified polymorphic locus designated ST1 and the previouslydescribed locus MIRU 1 to detect genetic diversity in isolates from Ghana. Analysisrevealed three different genotypes in isolates from Ghana, demonstrating for the first timegenetic diversity among M. ulcerans isolates in an African country.Ex vivo ELISpot analysis of IFN-γ secreting cells was carried out by stimulating PBMCsfrom BU patients with PPD, IPP and IRIV. Data from the study demonstrated for the firsttime that M. ulcerans infection-associated systemic reduction in IFN-γ responses is notconfined to stimulation with live or dead mycobacteria and their products but extends toother antigens. We also showed that the immune suppression reversed after surgicaltreatment and that the suppression is not related to reduction in IL-12 secretions. Thisindicates that the observed systemic immunosuppression was not the consequence of agenetic defect in T cell function predisposing for BU but is rather related to the presenceof M. ulcerans bacteria.In a longitudinal study, we compared recovery of immediate effector function of Vγ2Vδ2T cells in surgically treated BU patients to that of TB patients under chemotherapy. Atthe time of diagnosis, systemic production of IFN-γ after IPP stimulation was suppressedin both disease states but reverses after treatment. Restoration of Vγ2Vδ2 reactivity wasslow such that an optimum response was not yet achieved by two months in bothpopulations. Our result demonstrates that immunosuppression in BU may not be causedby the terpenoid toxin of M. ulcerans (mycolactone) alone." @default.
• W2296939458 created "2016-06-24" @default.
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• W2296939458 date "2006-01-01" @default.
• W2296939458 modified "2023-09-24" @default.
• W2296939458 title "Bacteriological and immunological studies towards effective control of Mycobacterium ulcerans disease (Buruli ulcer)" @default.
• W2296939458 doi "https://doi.org/10.5451/unibas-004112947" @default.
• W2296939458 hasPublicationYear "2006" @default.
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