Buruli ulcer: Mycobacterium ulcerans infection

2020 ◽  
pp. 1167-1170
Author(s):  
Bouke de Jong ◽  
Françoise Portaels ◽  
Wayne M. Meyers
Keyword(s):  
Polymerase Chain Reaction ◽  
Subcutaneous Tissue ◽  
Buruli Ulcer ◽  
Central Africa ◽  
Skin Grafting ◽  
Surgical Excision ◽  
Mycobacterium Ulcerans ◽  
West And Central Africa ◽  
Cutaneous Nodule ◽  
Polymerase Chain

Buruli ulcer is caused by Mycobacterium ulcerans, which secretes a cytotoxic and immunosuppressive toxin, mycolactone. The disease is characterized by necrosis of skin, subcutaneous tissue, and bone, and is re-emerging as a potentially disabling affliction of inhabitants of tropical wetlands. Major foci are in West and Central Africa with an increasing focus in Australia, Mexico, South America, and Southeast Asia. It is not contagious; environmental sources include water, vegetation, and insects, with humans probably becoming infected by traumatic introduction of the bacillus into the skin from the overlying M. ulcerans-contaminated surface in most instances. Clinical presentation may be as a cutaneous nodule, undermined ulcer, plaque, or widely disseminated oedematous lesion. Clinical diagnosis is often accurate by experienced clinicians, and smears for acid-fast bacilli, culture, polymerase chain reaction assays, and histopathology are confirmatory. Treatment was formerly by wide surgical excision and skin grafting, yet antibiotics have now been found effective, including an all-oral regimen.

Buruli ulcer: Mycobacterium ulcerans infection

2010 ◽  
pp. 848-850
Author(s):  
Wayne M. Meyers ◽  
Bouke de Jong ◽  
Françoise Portaels
Keyword(s):  
South America ◽  
East Asia ◽  
Subcutaneous Tissue ◽  
Buruli Ulcer ◽  
Central Africa ◽  
Mycobacterium Ulcerans ◽  
South East Asia ◽  
Tropical Wetlands ◽  
West And Central Africa ◽  
Water Vegetation

Buruli ulcer is caused by Mycobacterium ulcerans, which secretes a cytotoxic and immunosuppressive toxin, mycolactone. The disease is characterized by necrosis of skin, subcutaneous tissue, and bone, and is re-emerging as a potentially disabling affliction of inhabitants of tropical wetlands. Major foci are in West and Central Africa, but there are minor endemic foci in Australia, Mexico, South America, and South-East Asia. It is not contagious; environmental sources include water, vegetation, and insects, with humans probably becoming infected by traumatic introduction of the bacillus into the skin from the overlying ...

scholarly journals Buruli Ulcer (Acha-ere): Pathogenesis and Manifestation

2019 ◽  
pp. 1-5
Author(s):  
Elendu C. Onwuchekwa ◽  
Uzochukwu G. Ekeleme ◽  
Oliver Onu-Osi ◽  
Okonudo P. Osezele
Keyword(s):  
Subcutaneous Tissue ◽  
Buruli Ulcer ◽  
Central Africa ◽  
Mycobacterium Ulcerans ◽  
Actin Dynamics ◽  
Tropical Regions ◽  
West And Central Africa ◽  
Chronic Skin ◽  
Pass Through ◽  
Syndrome Protein

Infection of subcutaneous tissue with Mycobacterium ulcerans can lead to chronic skin ulceration known as Buruli ulcer. It has been reported in over 33 countries around the world, the greatest burden of disease is in the tropical regions of West and Central Africa, Australia, and Japan. It primarily affects children aged 5-15 years. Buruli ulcers generally begin as a painless dermal papule or subcutaneous edematous nodule, which over a period of weeks to months, breaks down to form an extensive necrotic ulcer with undermined edges. The pathogenesis of this neglected tropical disease is dependent on a lipidlike toxin, mycolactone, which diffuses through tissue away from the infecting organisms and elucidate its cytotoxic and immunosuppressive properties. The underlying molecular targets for mycolactone are: First, it can target scaffolding proteins (such as Wiskott Aldrich Syndrome Protein), which control actin dynamics in adherent cells and therefore lead to detachment and cell death. Second, it prevents the co-translational translocation (and therefore production) of many proteins that pass through the endoplasmic reticulum for secretion or placement in cell membranes.  Treatment includes a prolonged course of antibiotics and surgical debridement. Early identification and treatment are key, as lesions heal with scarring that can be a significant source of morbidity.

scholarly journals Promising Clinical Efficacy of Streptomycin-Rifampin Combination for Treatment of Buruli Ulcer (Mycobacterium ulcerans Disease)

2007 ◽  
Vol 51 (11) ◽  
pp. 4029-4035 ◽  
Author(s):  
Annick Chauty ◽  
Marie-Françoise Ardant ◽  
Ambroise Adeye ◽  
Hélène Euverte ◽  
Augustin Guédénon ◽  
...  
Keyword(s):  
Treatment Initiation ◽  
Buruli Ulcer ◽  
Skin Grafting ◽  
Surgical Excision ◽  
Mycobacterium Ulcerans ◽  
Directly Observed Treatment ◽  
Stopping Treatment ◽  
One Year

ABSTRACT According to recommendations of the 6th WHO Advisory Committee on Buruli ulcer, directly observed treatment with the combination of rifampin and streptomycin, administered daily for 8 weeks, was recommended to 310 patients diagnosed with Buruli ulcer in Pobè, Bénin. Among the 224 (72%) eligible patients for whom treatment was initiated, 215 (96%) were categorized as treatment successes, and 9, including 1 death and 8 losses to follow-up, were treatment failures. Of the 215 successfully treated patients, 102 (47%) were treated exclusively with antibiotics and 113 (53%) were treated with antibiotics plus surgical excision and skin grafting. The size of lesions at treatment initiation was the major factor associated with surgical intervention: 73% of patients with lesions of >15 cm in diameter underwent surgery, whereas only 17% of patients with lesions of <5 cm had surgery. No patient discontinued therapy for side effects from the antibiotic treatment. One year after stopping treatment, 208 of the 215 patients were actively retrieved to assess the long-term therapeutic results: 3 (1.44%) of the 208 retrieved patients had recurrence of Mycobacterium ulcerans disease, 2 among the 107 patients treated only with antibiotics and 1 among the 108 patients treated with antibiotics plus surgery. We conclude that the WHO-recommended streptomycin-rifampin combination is highly efficacious for treating M. ulcerans disease. Chemotherapy alone was successful in achieving cure in 47% of cases and was particularly effective against ulcers of less than 5 cm in diameter.

Histopathological and polymerase chain reaction-based analyses of Buruli ulcer caused by Mycobacterium ulcerans subspecies shinshuense

2017 ◽  
Vol 86 (2) ◽  
pp. e39
Author(s):  
Toshifumi Takahashi ◽  
Noriki Fujimoto ◽  
Miho Kabuto ◽  
Takeshi Kato ◽  
Takeshi Nakanishi ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
Buruli Ulcer ◽  
Mycobacterium Ulcerans ◽  
Chain Reaction ◽  
Polymerase Chain

scholarly journals Genotyping Mycobacterium ulcerans and Mycobacterium marinum by Using Mycobacterial Interspersed Repetitive Units

2005 ◽  
Vol 187 (5) ◽  
pp. 1639-1647 ◽  
Author(s):  
Pieter Stragier ◽  
Anthony Ablordey ◽  
Wayne M. Meyers ◽  
Françoise Portaels
Keyword(s):  
Tandem Repeats ◽  
Central Africa ◽  
Mycobacterium Ulcerans ◽  
Pathogenic Species ◽  
Missing Link ◽  
Potential Value ◽  
Related Organism ◽  
Geographic Origins ◽  
West And Central Africa ◽  
Unique Genotype

ABSTRACT A novel category of variable tandem repeats (VNTR) called mycobacterial interspersed repetitive units (MIRUs) has been identified for Mycobacterium ulcerans (n = 39), M. marinum (n = 27), and one related organism. Fifteen MIRU loci were identified in the genome of M. marinum and were used to genotype M. ulcerans, M. marinum, and an M. marinum-like organism that is considered a possible missing link between M. marinum and M. ulcerans. Seven MIRU loci were polymorphic, and locus-specific PCRs for four of these loci differentiated seven M. ulcerans genotypes, four M. marinum genotypes, and a unique genotype for the missing link organism. The seven M. ulcerans genotypes were related to six different geographic origins of isolates. All isolates from West and Central Africa, including old and recent isolates, belonged to the same genotype, emphasizing the great spatiotemporal homogeneity among African isolates. Unlike the M. ulcerans genotypes, the four M. marinum genotypes could not be clearly related to the geographic origins of the isolates. According to MIRU-VNTR typing, all M. ulcerans and M. marinum isolates of American origin were closely related, suggesting a common American ancestor for these two pathogenic species on the American continents. MIRU typing has significant potential value for discriminating between reoccurrence and reinfection for M. ulcerans disease.

scholarly journals Mycobacterium ulcerans Population Genomics To Inform on the Spread of Buruli Ulcer across Central Africa

mSphere ◽  
2019 ◽  
Vol 4 (1) ◽  
Author(s):  
Koen Vandelannoote ◽  
Delphin Mavinga Phanzu ◽  
Kapay Kibadi ◽  
Miriam Eddyani ◽  
Conor J. Meehan ◽  
...  
Keyword(s):  
Disease Control ◽  
Population Genomics ◽  
Demographic History ◽  
Buruli Ulcer ◽  
Central Africa ◽  
Mycobacterium Ulcerans ◽  
Evolutionary Trajectory ◽  
Content Type ◽  
Mode Of Transmission ◽  
The Impact

ABSTRACT Buruli ulcer is a neglected tropical disease of skin and subcutaneous tissue caused by infection with the pathogen Mycobacterium ulcerans. Many critical issues for disease control, such as understanding the mode of transmission and identifying source reservoirs of M. ulcerans, are still largely unknown. Here, we used genomics to reconstruct in detail the evolutionary trajectory and dynamics of M. ulcerans populations at a central African scale and at smaller geographical village scales. Whole-genome sequencing (WGS) data were analyzed from 179 M. ulcerans strains isolated from all Buruli ulcer foci in the Democratic Republic of the Congo, The Republic of Congo, and Angola that have ever yielded positive M. ulcerans cultures. We used both temporal associations and the study of the mycobacterial demographic history to estimate the contribution of humans as a reservoir in Buruli ulcer transmission. Our phylogeographic analysis revealed one almost exclusively predominant sublineage of M. ulcerans that arose in Central Africa and proliferated in its different regions of endemicity during the Age of Discovery. We observed how the best sampled endemic hot spot, the Songololo territory, became an area of endemicity while the region was being colonized by Belgium (1880s). We furthermore identified temporal parallels between the observed past population fluxes of M. ulcerans from the Songololo territory and the timing of health policy changes toward control of the Buruli ulcer epidemic in that region. These findings suggest that an intervention based on detecting and treating human cases in an area of endemicity might be sufficient to break disease transmission chains, irrespective of other reservoirs of the bacterium. IMPORTANCE Buruli ulcer is a destructive skin and soft tissue infection caused by Mycobacterium ulcerans. The disease is characterized by progressive skin ulceration, which can lead to permanent disfigurement and long-term disability. Currently, the major hurdles facing disease control are incomplete understandings of both the mode of transmission and environmental reservoirs of M. ulcerans. As decades of spasmodic environmental sampling surveys have not brought us much closer to overcoming these hurdles, the Buruli ulcer research community has recently switched to using comparative genomics. The significance of our research is in how we used both temporal associations and the study of the mycobacterial demographic history to estimate the contribution of humans as a reservoir in Buruli ulcer transmission. Our approach shows that it might be possible to use bacterial population genomics to assess the impact of health interventions, providing valuable feedback for managers of disease control programs in areas where health surveillance infrastructure is poor.

scholarly journals Basidiobolomycosis Simulating a Mycobacterium ulcerans Infection in a Togolese Rural Child

2017 ◽  
Vol 2017 ◽  
pp. 1-3 ◽  
Author(s):  
Bayaki Saka ◽  
Waguena Gnassingbe ◽  
Garba Mahamadou ◽  
Sefako Akakpo ◽  
Julienne Teclessou ◽  
...  
Keyword(s):  
General Condition ◽  
Buruli Ulcer ◽  
Granulomatous Inflammation ◽  
Mycobacterium Ulcerans ◽  
Chain Reaction ◽  
Deep Mycosis ◽  
Sharp Edges ◽  
Polymerase Chain ◽  
The Right ◽  
Multiple Ulcers

Background. Basidiobolomycosis is a deep mycosis which preferentially affects rural young people in tropical countries. We report an atypical case, with multiple ulcers, simulating a Buruli ulcer. Case Report. A 5-year-old boy, living in a rural area, was seen for ulcers on the buttocks and at the back and right flank that had been in progress for 4 months. On examination, we found an infiltrated plaque with sharp edges, little painful, located on the buttocks, back, and the right flank. On this plaque, there were multiple ulcers with polycyclic contours and fibrinous bottom. There were inguinal inflammatory lymph nodes. The patient had an altered general condition. Examination of other organs was normal. The diagnosis of Buruli ulcer was evoked first; the search for Mycobacterium ulcerans by polymerase chain reaction was negative. Histology test performed revealed hypodermic granulomatous inflammation with predominant macrophage and eosinophils. The mycological culture was not done. The child was treated successfully with ketoconazole (10 mg/kg/day) during eight weeks. Discussion. Our observation shows great clinical and epidemiological similarities between basidiobolomycosis and Buruli ulcer. It confirms the efficacy of ketoconazole in severe basidiobolomycosis infection with alteration of general condition. Histopathology is very important for differential diagnosis between these two diseases.

scholarly journals Increasing Experience with Primary Oral Medical Therapy for Mycobacterium ulcerans Disease in an Australian Cohort

2016 ◽  
Vol 60 (5) ◽  
pp. 2692-2695 ◽  
Author(s):  
N. Deborah Friedman ◽  
Eugene Athan ◽  
Aaron L. Walton ◽  
Daniel P. O'Brien
Keyword(s):  
Medical Therapy ◽  
Subcutaneous Tissue ◽  
Buruli Ulcer ◽  
Skin Lesions ◽  
Antimicrobial Treatment ◽  
Mycobacterium Ulcerans ◽  
Content Type ◽  
Southeastern Australia ◽  
Observational Cohort ◽  
Stage 1

ABSTRACTBuruli ulcer (BU) is a necrotizing infection of subcutaneous tissue that is caused byMycobacterium ulceransand is responsible for disfiguring skin lesions. The disease is endemic to specific geographic regions in the state of Victoria in southeastern Australia. Growing evidence of the effectiveness of antibiotic therapy forM. ulceransdisease has evolved our practice to the use of primarily oral medical therapy. An observational cohort study was performed on all confirmedM. ulceranscases treated with primary rifampin-based medical therapy at Barwon Health between October 2010 and December 2014 and receiving 12 months of follow-up. One hundred thirty-two patients were managed with primary medical therapy. The median age of patients was 49 years, and nearly 10% had diabetes mellitus. Lesions were ulcerative in 83.3% of patients and at WHO stage 1 in 78.8% of patients. The median duration of therapy was 56 days, with 22 patients (16.7%) completing fewer than 56 days of antimicrobial treatment. Antibiotic-associated complications requiring cessation of one or more antibiotics occurred in 21 (15.9%) patients. Limited surgical debridement was performed on 30 of these medically managed patients (22.7%). Cure was achieved, with healing within 12 months, in 131 of 132 patients (99.2%), and cosmetic outcomes were excellent. Primary rifampin-based oral medical therapy forM. ulceransdisease, combined with either clarithromycin or a fluoroquinolone, has an excellent rate of cure and an acceptable toxicity profile in Australian patients. We advocate for further research to determine the optimal and safest minimum duration of medical therapy for BU.

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