scholarly journals A stepwise approach to the laboratory diagnosis of Buruli ulcer disease

2006 ◽  
Vol 0 (0) ◽  
pp. 061109085615002-??? ◽  
Author(s):  
G. Bretzel ◽  
V. Siegmund ◽  
J. Nitschke ◽  
K. H. Herbinger ◽  
W. Thompson ◽  
...  
2010 ◽  
Vol 5 (3) ◽  
pp. 363-370 ◽  
Author(s):  
Marcus Beissner ◽  
Karl-Heinz Herbinger ◽  
Gisela Bretzel

2010 ◽  
Vol 48 (10) ◽  
pp. 3732-3734 ◽  
Author(s):  
K.-H. Herbinger ◽  
M. Beissner ◽  
K. Huber ◽  
N.-Y. Awua-Boateng ◽  
J. Nitschke ◽  
...  

2009 ◽  
Vol 48 (8) ◽  
pp. 1055-1064 ◽  
Author(s):  
Karl‐Heinz Herbinger ◽  
Ohene Adjei ◽  
Nana‐Yaa Awua‐Boateng ◽  
Willemien A. Nienhuis ◽  
Letitia Kunaa ◽  
...  

2006 ◽  
Vol 11 (11) ◽  
pp. 1688-1693 ◽  
Author(s):  
G. Bretzel ◽  
V. Siegmund ◽  
J. Nitschke ◽  
K. H. Herbinger ◽  
R. Thompson ◽  
...  

Author(s):  
Samuel A. Sakyi ◽  
Samuel Y. Aboagye ◽  
Isaac Darko Otchere ◽  
Dorothy Yeboah-Manu

Background.Buruli ulcer (BU) is a necrotizing cutaneous infection caused byMycobacterium ulcerans.Early diagnosis is crucial to prevent morbid effects and misuse of drugs. We review developments in laboratory diagnosis of BU, discuss limitations of available diagnostic methods, and give a perspective on the potential of using aptamers as point-of-care.Methods.Information for this review was searched through PubMed, web of knowledge, and identified data up to December 2015. References from relevant articles and reports from WHO Annual Meeting of the Global Buruli Ulcer initiative were also used. Finally, 59 articles were used.Results.The main laboratory methods for BU diagnosis are microscopy, culture, PCR, and histopathology. Microscopy and PCR are used routinely for diagnosis. PCR targetingIS2404is the gold standard for laboratory confirmation. Culture remains the only method that detects viable bacilli, used for diagnosing relapse and accrued isolates for epidemiological investigation as well as monitoring drug resistance. Laboratory confirmation is done at centers distant from endemic communities reducing confirmation to a quality assurance.Conclusions. Current efforts aimed at developing point-of-care diagnostics are saddled with major drawbacks; we, however, postulate that selection of aptamers against MU target can be used as point of care.


2008 ◽  
Vol 14 (8) ◽  
pp. 1247-1254 ◽  
Author(s):  
M. Eric Benbow ◽  
Heather Williamson ◽  
Ryan Kimbirauskas ◽  
Mollie D. McIntosh ◽  
Rebecca Kolar ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Pius Agbenorku ◽  
Anthony Edusei ◽  
Margaret Agbenorku ◽  
Thomas Diby ◽  
Esenam Nyador ◽  
...  

Objectives. To describe trends and category of disabilities caused by Buruli ulcer disease. Design. This retrospective study was set up to quantify information on the disability trends caused by Buruli ulcer (BU) using data on patients attending BU and chronic ulcer clinics from 2004 to 2009, at Global Evangelical Mission Hospital, Apromase. Methods. Data was retrieved from the WHO BU1 form, case registry book, surgical theatre register, and BU patients' records book of the hospital. Disability was measured as the incapability of patients to perform one or more daily activities due to his/her state of BU disease before treatment. Results. A total of 336 positive BU cases comprising 181 males (53.9%) were recorded of which 113 (33.6%) cases of disabilities were identified. A mean age of 52.5 (±1.32) years was recorded. For the trend of disabilities, the year 2009 recorded the highest (N = 34, 31.0%). The lesions were mostly located at the lower limbs (N = 65, 57.5%) region of the patients. Lesions with diameter >15 cm were the major (59.3%) category of lesions. Conclusion. Trend of disability reveals proportional increase over the years from 2004 to 2009. Contracture at the knee and ankle joints was the commonest disability recorded.


2021 ◽  
Vol 12 ◽  
Author(s):  
Bruno Tello Rubio ◽  
Florence Bugault ◽  
Blandine Baudon ◽  
Bertrand Raynal ◽  
Sébastien Brûlé ◽  
...  

Mycolactone is a diffusible lipid toxin produced by Mycobacterium ulcerans, the causative agent of Buruli ulcer disease. Altough bacterially derived mycolactone has been shown to traffic from cutaneous foci of infection to the bloodstream, the mechanisms underpinning its access to systemic circulation and import by host cells remain largely unknown. Using biophysical and cell-based approaches, we demonstrate that mycolactone specific association to serum albumin and lipoproteins is necessary for its solubilization and is a major mechanism to regulate its bioavailability. We also demonstrate that Scavenger Receptor (SR)-B1 contributes to the cellular uptake of mycolactone. Overall, we suggest a new mechanism of transport and cell entry, challenging the dogma that the toxin enters host cells via passive diffusion.


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