Úlcera de Buruli

Boleira, Manuela; Lupi, Omar; Lehman, Linda; Asiedu, Kingsley; Kiszewski, Ana Elisa

doi:10.1590/s0365-05962010000300002

Cited by 22 publications

(11 citation statements)

References 46 publications

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“…BU pathogenesis is mediated by mycolactone, a potent polyketide-derived macrolide that triggers apoptotic cell death [ 2 ] and is associated with the necrotic nature of the disease [ 3 ]. BU mostly affects people in tropical countries in Africa [ 4 ], America [ 5 ], Asia [ 6 ] and Australia [ 7 ]. Although no official estimate of global incidence is available at present, West Africa is the main endemic area, with 1967 new cases reported by Côte d'Ivoire, Ghana, and Benin in 2013[ 8 ].…”

Section: Introductionmentioning

confidence: 99%

Clinical Epidemiology of Buruli Ulcer from Benin (2005-2013): Effect of Time-Delay to Diagnosis on Clinical Forms and Severe Phenotypes

Capela

Sopoh²,

Houézo³

et al. 2015

PLoS Negl Trop Dis

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Buruli Ulcer (BU) is a neglected infectious disease caused by Mycobacterium ulcerans that is responsible for severe necrotizing cutaneous lesions that may be associated with bone involvement. Clinical presentations of BU lesions are classically classified as papules, nodules, plaques and edematous infiltration, ulcer or osteomyelitis. Within these different clinical forms, lesions can be further classified as severe forms based on focality (multiple lesions), lesions’ size (>15cm diameter) or WHO Category (WHO Category 3 lesions). There are studies reporting an association between delay in seeking medical care and the development of ulcerative forms of BU or osteomyelitis, but the effect of time-delay on the emergence of lesions classified as severe has not been addressed. To address both issues, and in a cohort of laboratory-confirmed BU cases, 476 patients from a medical center in Allada, Benin, were studied. In this laboratory-confirmed cohort, we validated previous observations, demonstrating that time-delay is statistically related to the clinical form of BU. Indeed, for non-ulcerated forms (nodule, edema, and plaque) the median time-delay was 32.5 days (IQR 30.0–67.5), while for ulcerated forms it was 60 days (IQR 20.0–120.0) (p = 0.009), and for bone lesions, 365 days (IQR 228.0–548.0). On the other hand, we show here that time-delay is not associated with the more severe phenotypes of BU, such as multi-focal lesions (median 90 days; IQR 56–217.5; p = 0.09), larger lesions (diameter >15cm) (median 60 days; IQR 30–120; p = 0.92) or category 3 WHO classification (median 60 days; IQR 30–150; p = 0.20), when compared with unifocal (median 60 days; IQR 30–90), small lesions (diameter ≤15cm) (median 60 days; IQR 30–90), or WHO category 1+2 lesions (median 60 days; IQR 30–90), respectively. Our results demonstrate that after an initial period of progression towards ulceration or bone involvement, BU lesions become stable regarding size and focal/multi-focal progression. Therefore, in future studies on BU epidemiology, severe clinical forms should be systematically considered as distinct phenotypes of the same disease and thus subjected to specific risk factor investigation.

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Section: Introductionmentioning

confidence: 99%

Clinical Epidemiology of Buruli Ulcer from Benin (2005-2013): Effect of Time-Delay to Diagnosis on Clinical Forms and Severe Phenotypes

Capela

Sopoh²,

Houézo³

et al. 2015

PLoS Negl Trop Dis

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“… The recovery of infected individuals is assumed to occur both spontaneously and through treatment. Research has shown that localized lesions may spontaneously heal but, without treatment, most cases of Buruli ulcer result in physical deformities that often lead to physiological abnormalities and stigmas [ 4 ]. …”

Section: Methodsmentioning

confidence: 99%

On the transmission dynamics of Buruli ulcer in Ghana: Insights through a mathematical model

Nyabadza

Bonyah

2015

BMC Res Notes

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BackgroundMycobacterium ulcerans is know to cause the Buruli ulcer. The association between the ulcer and environmental exposure has been documented. However, the epidemiology of the ulcer is not well understood. A hypothesised transmission involves humans being bitten by the water bugs that prey on mollusks, snails and young fishes.MethodsIn this paper, a model for the transmission of Mycobacterium ulcerans to humans in the presence of a preventive strategy is proposed and analysed. The model equilibria are determined and conditions for the existence of the equilibria established. The model analysis is carried out in terms of the reproduction number . The disease free equilibrium is found to be locally asymptotically stable for The model is fitted to data from Ghana.ResultsThe model is found to exhibit a backward bifurcation and the endemic equilibrium point is globally stable when Sensitivity analysis showed that the Buruli ulcer epidemic is highly influenced by the shedding and clearance rates of Mycobacterium ulcerans in the environment. The model is found to fit reasonably well to data from Ghana and projections on the future of the Buruli ulcer epidemic are also made.ConclusionsThe model reasonably fitted data from Ghana. The fitting process showed data that appeared to have reached a steady state and projections showed that the epidemic levels will remain the same for the projected time. The implications of the results to policy and future management of the disease are discussed.

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“…Buruli ulcer (BU), a necrotic skin disease caused by Mycobacterium ulcerans , is the third most prevalent mycobacterial infection after tuberculosis and leprosy [1]. It has been reported in West Africa, Central Africa, East Africa, Australia, China, South America and Japan with West Africa being the most endemic region [2].…”

Section: Introductionmentioning

confidence: 99%

Experimental demonstration of the possible role of Acanthamoeba polyphaga in the infection and disease progression in Buruli Ulcer (BU) using ICR mice

et al. 2017

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The transmission of Buruli ulcer (BU), caused by Mycobacterium ulcerans (MU), remains puzzling although a number of hypothesis including through bites of infected aquatic insects have been proposed. We report the results of experiments using ICR mice that give credence to our hypothesis that Acanthamoeba species may play a role in BU transmission. We cocultured MU N2 and MU 1615 which expresses red fluorescent protein (RFP) and Acanthamoeba polyphaga (AP), and confirmed infected AP by Ziehl-Neelsen (ZN) staining. We tested for viability of MU inside AP and observed strong RFP signals inside both trophozoites and cysts after 3 and 42 days of coculturing respectively. ICR mice were topically treated, either on shaved intact or shaved pinpricked rumps, with one of the following; MU N2 only (2.25 x 106 colony forming units [CFU] / ml), MU N2:AP coculture (2.96 x 104 CFU: 1.6 x 106 cells/ml), AP only (1.6 x 106 cells/ml), PYG medium and sterile distilled water. Both MU N2 only and MU N2:AP elicited reddening on day (D) 31; edema on D 45 and D 44 respectively, and ulcers on D 49 at pinpricked sites only. To ascertain infectivity and pathogenicity of MU N2 only and MU N2:AP, and compare their virulence, the standard mouse footpad inoculation method was used. MU N2:AP elicited reddening in footpads by D 3 compared to D 14 with MU N2 only of the same dose of MU N2 (2.96 x 104 CFU). ZN-stained MU were observed in both thin sectioned and homogenized lesions, and aspirates from infected sites. Viable MU N2 were recovered from cultures of the homogenates and aspirates. This study demonstrates in ICR mice MU transmission via passive infection, and shows that punctures in the skin are prerequisite for infection, and that coculturing of MU with AP enhances pathogenesis.

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Úlcera de Buruli

Cited by 22 publications

References 46 publications

Clinical Epidemiology of Buruli Ulcer from Benin (2005-2013): Effect of Time-Delay to Diagnosis on Clinical Forms and Severe Phenotypes

Clinical Epidemiology of Buruli Ulcer from Benin (2005-2013): Effect of Time-Delay to Diagnosis on Clinical Forms and Severe Phenotypes

On the transmission dynamics of Buruli ulcer in Ghana: Insights through a mathematical model

Experimental demonstration of the possible role of Acanthamoeba polyphaga in the infection and disease progression in Buruli Ulcer (BU) using ICR mice

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