Immunoglobulin M Antibody Responses to<i>Mycobacterium ulcerans</i>Allow Discrimination between Cases of Active Buruli Ulcer Disease and Matched Family Controls in Areas Where the Disease Is Endemic

Okenu, Daniel M. N.; Ofielu, Lazarus O.; Easley, Kirk A.; Guarner, Jeannette; Whitney, Ellen A. Spotts; Raghunathan, Pratima L.; Stienstra, Ymkje; Asamoa, Kwame; Werf, Tjip S. van der; Graaf, Winette T.A. van der; Tappero, Jordan W.; Ashford, David A.; King, C. Harold

doi:10.1128/cdli.11.2.387-391.2004

Cited by 21 publications

(22 citation statements)

References 34 publications

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“…In tuberculosis (Tb) endemic areas, where BCG vaccination is common, the broad antigenic cross-reactivity of M. ulcerans antigens with M. tuberculosis and M. bovis antigens complicate the analysis of M. ulcerans specific immune responses substantially. In studies with M. ulcerans culture filtrates IgG antibody responses against the secreted M. ulcerans proteins were frequently found in BU patients, but also in Tb patients from BU non-endemic regions [75,76] . IgM responses of BU patients against the filtrate proteins were more distinct than those of healthy family members living in the same village [76] , indicative for B cell stimulation.…”

Section: Histopathologic Features Of Untreated Buruli Ulcer Lesionsmentioning

confidence: 98%

Immunosuppression and treatment-associated inflammatory response in patients withMycobacterium ulceransinfection (Buruli ulcer)

Schütte

Pluschke

2008

Expert Opinion on Biological Therapy

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Buruli ulcer is a necrotizing skin disease caused by Mycobacterium ulcerans . Major necrosis with abundant clusters of extracellularly replicating mycobacteria and only minor leukocyte infiltration are characteristic histopathologic features of the disease. Mycolactone, a cytotoxic macrolide exotoxin of M. ulcerans , plays a key role in the development of this pathology. Antimicrobial therapy, such as rifampicin/streptomycin that was recently introduced, seems to lead to phagocytosis of mycobacteria and massive leukocyte infiltration, which culminates in the development of ectopic lymphoid structures in the lesions. Whereas the curative effect of the antibiotic treatment may be supported by immune defense mechanisms, persisting mycobacterial antigens and immunostimulators occasionally also seem to cause apparent reactivation of the disease. This seems to be related to excessive immunostimulation rather than to incomplete killing of the pathogen.

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Section: Histopathologic Features Of Untreated Buruli Ulcer Lesionsmentioning

confidence: 98%

Immunosuppression and treatment-associated inflammatory response in patients withMycobacterium ulceransinfection (Buruli ulcer)

Schütte

Pluschke

2008

Expert Opinion on Biological Therapy

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“…The test should discriminate between immune responses against M. ulcerans and other mycobacteria, in particular M. tuberculosis and M. bovis BCG. Serological studies performed with complex antigen preparations have suggested that serological tests may be useful in the diagnosis and surveillance of Buruli ulcer (9,16,31). In view of the presence of species cross-reactive antibodies in sera of Africans living in regions where Buruli ulcer is endemic, thoroughly selected recombinantly expressed target antigens are required.…”

Section: Discussionmentioning

confidence: 99%

Use of the Immunodominant 18-Kilodalton Small Heat Shock Protein as a Serological Marker for Exposure to Mycobacterium ulcerans

Díaz

Döbeli

Yeboah-Manu

et al. 2006

Clin Vaccine Immunol

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While it is well established that proximity to wetlands is a risk factor for contracting Buruli ulcer, it is not clear what proportion of a population living in an area where the etiologic agent, Mycobacterium ulcerans, is endemic is actually exposed to this disease. Immunological cross-reactivity among mycobacterial species complicates the development of a specific serological test. Among immunodominant proteins recognized by a panel of anti-M. ulcerans monoclonal antibodies, the M. ulcerans homologue of the M. leprae 18-kDa small heat shock protein (shsp) was identified. Since this shsp has no homologues in M. bovis and M. tuberculosis, we evaluated its use as a target antigen for a serological test. Anti-18-kDa shsp antibodies were frequently found in the sera of Buruli ulcer patients and of healthy household contacts but rarely found in controls from regions where the infection is not endemic. The results indicate that only a small proportion of M. ulcerans-infected individuals contract the clinical disease.

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“…24,25 Strong IgM antibody responses to M ulcerans seem more frequent in patients with active Buruli ulcer than in healthy members of their families. 26 HIV infection Review has not been reported as a risk factor for Buruli ulcer 27 but severe clinical forms of the disease have been described in HIV-positive patients. 28 In three HIVpositive Buruli ulcer patients in Akoloninga, Cameroon, we observed that the healing process improved when the patients started antiretroviral treatment (EC, unpublished data).…”

Section: Figure 1: a Typical Buruli Ulcermentioning

confidence: 99%

Mycobacterium ulcerans infection: control, diagnosis, and treatment

Sizaire

Nackers

Comte

et al. 2006

The Lancet Infectious Diseases

186

145

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The skin disease Buruli ulcer, caused by Mycobacterium ulcerans, is the third most common mycobacterial disease after tuberculosis and leprosy and mainly affects remote rural African communities. Although the disease is known to be linked to contaminated water, the mode of transmission is not yet understood, which makes it difficult to propose control interventions. The disease is usually detected in its later stages, when it has caused substantial damage and disability. Surgery remains the treatment of choice. Although easy and effective in the early stages of the disease, treatment requires extended excisions and long hospitalisation for the advanced forms of the disease. Currently, no antibiotic treatment has proven effective for all forms of M ulcerans infection and research into a new vaccine is urgently needed. While the scientific community works on developing non-invasive and rapid diagnostic tools, the governments of endemic countries should implement active case finding and health education strategies in their affected communities to detect the disease in its early stages. We review the diagnosis, treatment, and control of Buruli ulcer and list priorities for research and development.

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Immunoglobulin M Antibody Responses toMycobacterium ulceransAllow Discrimination between Cases of Active Buruli Ulcer Disease and Matched Family Controls in Areas Where the Disease Is Endemic

Cited by 21 publications

References 34 publications

Immunosuppression and treatment-associated inflammatory response in patients withMycobacterium ulceransinfection (Buruli ulcer)

Immunosuppression and treatment-associated inflammatory response in patients withMycobacterium ulceransinfection (Buruli ulcer)

Use of the Immunodominant 18-Kilodalton Small Heat Shock Protein as a Serological Marker for Exposure to Mycobacterium ulcerans

Mycobacterium ulcerans infection: control, diagnosis, and treatment

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