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1

Mortier, Emmanuel, Anne Grasland, Raluca Sterpu, Comlan Affo, and Isabelle Mahé. "Ulcère creusant et indolore : ulcère de Buruli." La Presse Médicale 41, no. 9 (September 2012): 892–93. http://dx.doi.org/10.1016/j.lpm.2011.10.018.

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2

Souillac, G., F. N. Fitoussi, F. M. Fitoussi, G. F. Penneçot, and A. Bourrillon. "Ulcère de Buruli : une pathologie d’exportation." Archives de Pédiatrie 7, no. 12 (December 2000): 1311–15. http://dx.doi.org/10.1016/s0929-693x(00)00149-4.

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3

Yedomon, G. H., F. Guedenon, A. Chauty, H. Adegbidi, F. Atadokpede, and F. Do Ango-Padonou. "C044 - Ulcère de Buruli : huit cas avec rechute." Annales de Dermatologie et de Vénéréologie 134, no. 1 (January 2007): 50–51. http://dx.doi.org/10.1016/s0151-9638(07)89076-4.

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4

KNIPPER, P., R. ZILLIOX, C. JOHNSON, and P. ANTOINE. "Ulcère de Buruli et chirurgie plastique, au dispensaire." Annales de Chirurgie Plastique Esthétique 49, no. 3 (June 2004): 265–72. http://dx.doi.org/10.1016/s0294-1260(04)00057-3.

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5

Stoffel, V., B. Barthelmé, and Frédéric Chagué. "Écopathologie tropicale : ulcère de Buruli par monts et par vaux." Santé Publique 17, no. 2 (2005): 191. http://dx.doi.org/10.3917/spub.052.0191.

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6

Kouassi, Y. I., K. C. Ahogo, B. Vagamon, M. Kaloga, H. S. kourouma, E. J. Ecra, A. Sangaré, et al. "Ulcère de Buruli : multiples lésions céphaliques après instauration du traitement médical." Annales de Dermatologie et de Vénéréologie 140 (April 2013): S30—S31. http://dx.doi.org/10.1016/j.annder.2013.01.400.

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7

Azanmasso, H., B. Addy Lolla, N. S. Diagne, G. T. Kpadonou, E. Alagnide, F. Lmidmani, and A. El Fatimi. "Intérêt du suivi des enfants opérés pour ulcère de Buruli au Bénin." Annals of Physical and Rehabilitation Medicine 56 (October 2013): e282-e283. http://dx.doi.org/10.1016/j.rehab.2013.07.728.

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8

Gnassingbe, W., B. Saka, J. Teclessou, G. Mahamadou, S. Akakpo, A. Mouhari-Toure, E. Belei, Y. Elegbede, K. Kombaté, and P. Pitché. "F18 : Basidiobolomycose simulant un ulcère de Buruli chez un garçon de 5 ans." Annales de Dermatologie et de Vénéréologie 143, no. 4 (April 2016): S19. http://dx.doi.org/10.1016/s0151-9638(16)30125-9.

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9

Vagamon, B., K. C. Ahogo, B. R. Aka, A. Diabaté, Y. I. Kouassi, S. H. Kourouma, C. Traoré, et al. "Ulcère de Buruli à début bifocal : multiples lésions céphaliques après instauration du traitement médical." Annales de Dermatologie et de Vénéréologie 140, no. 2 (February 2013): 125–28. http://dx.doi.org/10.1016/j.annder.2012.11.010.

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10

Pradinaud, R. "C10 - L’infection à Mycobacterium ulcerans ne doit plus être restreinte à l’impropre appellation « ulcère de Buruli »." Annales de Dermatologie et de Vénéréologie 134, no. 1 (January 2007): 28–29. http://dx.doi.org/10.1016/s0151-9638(07)89031-4.

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11

Couppié, P., J. Dufour, D. Kottler, A. Fior, E. Sambourg, M. Lazar, and D. Sainte-Marie. "Réaction paradoxale au cours du traitement médicamenteux de l’infection à Mycobacterium ulcerans (ulcère de Buruli). Quatre observations." Annales de Dermatologie et de Vénéréologie 138, no. 12 (December 2011): A260. http://dx.doi.org/10.1016/j.annder.2011.10.324.

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12

Douine, M., R. Gozlan, M. Nacher, J. Dufour, Y. Reynaud, E. Elguero, M. Combe, et al. "L’infection à Mycobacterium ulcerans (ulcère de Buruli) en Guyane ; transition d’un profil épidémiologique africain vers un profil australien." Annales de Dermatologie et de Vénéréologie 144, no. 12 (December 2017): S74—S75. http://dx.doi.org/10.1016/j.annder.2017.09.066.

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13

Brou, Y., E. Elguero, R. Ruffine, J. Dufour, J. Bron, J. Faure, M. Nacher, C. Chevillon, J. Guégan, and P. Couppié. "Infection à Mycobacterium ulcerans (ulcère de Buruli) sur l’Ile de Cayenne : distribution spatiale et étude des déterminants géographiques associés à la maladie." Annales de Dermatologie et de Vénéréologie 138, no. 12 (December 2011): A258. http://dx.doi.org/10.1016/j.annder.2011.10.319.

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14

Sambourg, E., J. Dufour, S. Édouard, A. Morris, E. Mosnier, Y. Reynaud, D. Sainte-Marie, M. Nacher, J. F. Guégan, and P. Couppié. "Réponses et réactions paradoxales au cours du traitement médicamenteux de l’infection à Mycobacterium ulcerans (ulcère de Buruli). Quatre observations en Guyane française." Annales de Dermatologie et de Vénéréologie 141, no. 6-7 (June 2014): 413–18. http://dx.doi.org/10.1016/j.annder.2014.01.010.

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15

Saka, Bayaki, Waguena Gnassingbe, Garba Mahamadou, Sefako Akakpo, Julienne Teclessou, Aurel Abilogun-Chokki, Abas Mouhari-Toure, Koussake Kombate, and Palokinam Pitché. "Basidiobolomycosis Simulating a Mycobacterium ulcerans Infection in a Togolese Rural Child." Case Reports in Dermatological Medicine 2017 (2017): 1–3. http://dx.doi.org/10.1155/2017/6905783.

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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.
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16

Foulon, Mélanie, Amélie Pouchin, Jérémy Manry, Fida Khater, Marie Robbe-Saule, Amandine Durand, Lucille Esnault, et al. "Skin-specific antibodies neutralizing mycolactone toxin during the spontaneous healing of Mycobacterium ulcerans infection." Science Advances 6, no. 9 (February 2020): eaax7781. http://dx.doi.org/10.1126/sciadv.aax7781.

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Buruli ulcer, a neglected tropical infectious disease, is caused by Mycobacterium ulcerans. Without treatment, its lesions can progress to chronic skin ulcers, but spontaneous healing is observed in 5% of cases, suggesting the possible establishment of a host strategy counteracting the effects of M. ulcerans. We reveal here a skin-specific local humoral signature of the spontaneous healing process, associated with a rise in antibody-producing cells and specific recognition of mycolactone by the mouse IgG2a immunoglobulin subclass. We demonstrate the production of skin-specific antibodies neutralizing the immunomodulatory activity of the mycolactone toxin, and confirm the role of human host machinery in triggering effective local immune responses by the detection of anti-mycolactone antibodies in patients with Buruli ulcer. Our findings pave the way for substantial advances in both the diagnosis and treatment of Buruli ulcer in accordance with the most recent challenges issued by the World Health Organization.
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17

Gooding, Travis M., Paul D. R. Johnson, May Smith, Andrew S. Kemp, and Roy M. Robins-Browne. "Cytokine Profiles of Patients Infected with Mycobacterium ulcerans and Unaffected Household Contacts." Infection and Immunity 70, no. 10 (October 2002): 5562–67. http://dx.doi.org/10.1128/iai.70.10.5562-5567.2002.

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ABSTRACT Mycobacterium ulcerans, the cause of Buruli ulcer, is an environmental mycobacterium with a distinct geographic distribution. The reasons why only some individuals who are exposed to M. ulcerans develop ulcers are not known but are likely to reflect individual differences in the immune response to infections with this bacterium. In this study, we investigated cytokine profiles of peripheral blood mononuclear cells (PBMC) from 23 Buruli ulcer patients and 25 household contacts in a region of Australia where Buruli ulcer is endemic. The results showed that following stimulation with M. ulcerans or Mycobacterium bovis BCG, PBMC from Buruli ulcer patients mounted a Th2-type response, which was manifested by the production of mRNA for interleukin 4 (IL-4), IL-5, IL-6, and IL-10, whereas unaffected contacts responded mainly with the Th1 cytokines gamma interferon (IFN-γ) and IL-12. For example, mRNA for IL-4 was detected in 18 of 23 patients but in only 3 of 25 control subjects (P < 0.0001). By contrast, PBMC from 21 of 25 unaffected individuals produced IFN-γ compared with 3 of 23 patients (P < 0.0001). IFN-γ release following stimulation with mycobacteria was markedly reduced in affected subjects. Frequencies of antibodies to M. ulcerans in serum samples from affected and unaffected subjects were similar, indicating that many of the control subjects had been exposed to this bacterium. Together, these findings suggest that a Th1-type immune response to M. ulcerans may prevent the development of Buruli ulcer in people exposed to M. ulcerans, but a Th-2 response does not.
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18

Rufai, Tanko, Enoch Aninagyei, Samuel Oko Sackey, Ernest Kenu, and Edwin Andrew Afari. "Evaluation of Buruli Ulcer Disease Surveillance System in the Ga West Municipality, Ghana, 2011–2015." Journal of Tropical Medicine 2019 (November 12, 2019): 1–5. http://dx.doi.org/10.1155/2019/4721236.

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Background. Buruli ulcer (BU) is one of the most neglected tropical diseases caused by Mycobacterium ulcerans. M. ulcerans infection may manifest initially as a pre-ulcerative nodule, a plaque, or oedema which breaks down to form characteristic ulcers with undermined edges. The Ga West Municipality is an endemic area for Buruli ulcer, and we evaluated the BU surveillance system to determine whether the system is meeting its objectives and to assess its attributes. Materials and Methods. We used a checklist based on Centers for Disease Control and Prevention (CDC) updated surveillance evaluation guidelines, 2006. We reviewed records and dataset on Buruli ulcer for the period 2011–2015. The evaluation was carried out at the national, regional, district, and community levels using the Ga West Municipality of the Greater Accra Region as a study site. Interviews with key stakeholders at the various levels were done using an interview guide, and observations were done with a checklist. Data were entered and analyzed using Epi info 7. Results. A total of 594 cases of Buruli ulcer were reported from 2011 to 2015 in Ga West. The number of confirmed cases decreased from 109 in 2011 to 17 in 2015. The system was useful, fairly simple, flexible, representative, and fairly acceptable. The system was sensitive with a PVP of 45.3%. Although the data quality was good with 85% of case report forms completed, there was under-reporting (3.6%), some discrepancies of data at the district, regional, and national levels. The system was moderately stable, and timeliness of reporting was 30.7%. Conclusion. The Buruli ulcer surveillance system is meeting its set objectives, and the data generated are used to reliably describe the epidemiologic situation and evaluate the results for actions and plan future interventions. There is a need for timely submission of data. We recommend that the National Buruli Ulcer Control Program (NBUCP) provides logistical support to treatment centres.
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19

Tsukagoshi, S., and TCB Dehn. "Buruli ulcer in a nine-month-old boy." Annals of The Royal College of Surgeons of England 94, no. 7 (October 2012): e8-e9. http://dx.doi.org/10.1308/003588412x13373405385692.

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The diagnosis of Buruli ulcer should be considered in all painless undermined ulcers in the tropics. The diagnosis and treatment are a challenge in rural settings despite the well established tuberculosis programmes. Immediate commencement on rifampicin and streptomycin is essential to halt the progression of disease and to, hopefully, reverse it. Surgery is indicated in those with complex ulcers or with complications. We report the case of a nine-month-old boy presenting to visiting British surgeons in a district hospital in Uganda with multiple ulcers to the right forearm.
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20

Kwyer, Thomas A., and Edwin Ampadu. "Buruli Ulcers." Advances in Skin & Wound Care 19, no. 9 (November 2006): 479–86. http://dx.doi.org/10.1097/00129334-200611000-00005.

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21

Evans, Mark R. W., Harry S. Thangaraj, and Mark H. Wansbrough-Jones. "Buruli ulcer." Current Opinion in Infectious Diseases 13, no. 2 (April 2000): 109–12. http://dx.doi.org/10.1097/00001432-200004000-00003.

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22

Einarsdottir, Thorbjorg, and Kris Huygen. "Buruli ulcer." Human Vaccines 7, no. 11 (November 2011): 1198–203. http://dx.doi.org/10.4161/hv.7.11.17751.

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23

Wansbrough-Jones, Mark, and Richard Phillips. "Buruli ulcer." BMJ 330, no. 7505 (June 16, 2005): 1402–3. http://dx.doi.org/10.1136/bmj.330.7505.1402.

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24

Moyano, Luz M., Juan C. Chero, and Guillermo E. Gonzalvez. "Buruli Ulcer." American Journal of Tropical Medicine and Hygiene 79, no. 1 (July 1, 2008): 3. http://dx.doi.org/10.4269/ajtmh.2008.79.3.

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25

Portaels, Françoise, Manuel T. Silva, and Wayne M. Meyers. "Buruli ulcer." Clinics in Dermatology 27, no. 3 (May 2009): 291–305. http://dx.doi.org/10.1016/j.clindermatol.2008.09.021.

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26

Millogo, Anselme, Dezemon Zingue, Amar Bouam, Sylvain Godreuil, Michel Drancourt, and Nassim Hammoudi. "Confirming Autochthonous Buruli Ulcer Cases in Burkina Faso, West Africa." American Journal of Tropical Medicine and Hygiene 105, no. 3 (September 15, 2021): 627–29. http://dx.doi.org/10.4269/ajtmh.20-0895.

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ABSTRACT. Environmental Mycobacterium ulcerans causes a disabling skin disease called Buruli ulcer. Recent studies completed the knowledge of the evolving geographic extension and epidemiology of Buruli ulcer in West Africa, where Côte d’Ivoire is reporting the highest number of cases. We report seven polymerase chain reaction-documented patients in Burkina Faso, a neighboring country of Côte d’Ivoire, where previously Buruli ulcer cases were confirmed primarily using clinical arguments.
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Ogbuagu, Chukwuanugo, Ifeoma Enweani, Agu Maurice, Ekenechukwu Ogbuagu, and Obiageli Emelumadu. "PO 8369 BURULI ULCER: PATTERN OF PRESENTATION IN A NIGERIAN HOSPITAL." BMJ Global Health 4, Suppl 3 (April 2019): A29.3—A30. http://dx.doi.org/10.1136/bmjgh-2019-edc.76.

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BackgroundBuruli ulcer is one of the neglected tropical diseases. It is a chronic, debilitating, necrotising disease of the skin and soft tissue caused by Mycobacterium ulcerans. Most times, the pattern of presentation is neglected by the infected because it is regarded as a disease of the poor who have little or no access to healthcare. Living in rural often inaccessible areas and suffering from a triad of ignorance, stigma and poverty, this poor population fails to present early to a hospital.MethodsA retrospective review of patients who accessed care at the infectious disease clinic of Nnewi Diocesan Hospital, Nnewi, Southeast Nigeria, between 1 January to 31 December 2017. To achieve a complete inference, the results of laboratory wound swab culture of all patients were collated and matched with the clinical presentation. All cultures were done by a trained scientist of the German Leprosy and TB Relief Association (GLRA).ResultsReview of data showed a total of 10 120 patients of which 6402 were outpatients and 3718 were inpatients; they were between 1 and 86 years of age. There were 60 cases of limb ulcers of which wound swab culture was done. Fifty-four (54) were diabetic foot ulcers while five (5) were venous ulcers. Acid-fast bacilli were detected with Ziehl-Neelsen staining in one specimen and confirmed by the reference center.ConclusionMost of the Buruli ulcer patients are found incidentally following late presentation at hospitals with a questionable ulcer/wound with a high index of suspicion on clinical examination. If Buruli ulcer is to be eradicated, an intensive rural epidemiological identification programme must be implemented to isolate the infected. The vicious cycle of ignorance, stigma and poverty needs to be broken by massive awareness and education campaigns.
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28

Henry, Ronnie. "Etymologia: Buruli Ulcer." Emerging Infectious Diseases 26, no. 3 (March 2020): 504. http://dx.doi.org/10.3201/eid2603.et2603.

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29

Korman, Tony M., Paul D. R. Johnson, and John Hayman. "Etymologia: Buruli Ulcer." Emerging Infectious Diseases 26, no. 12 (December 2020): 3104. http://dx.doi.org/10.3201/eid2612.200744.

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30

Kumar, Satendra, Somprakas Basu, Satyanam Kumar Bhartiya, and Vijay Kumar Shukla. "The Buruli Ulcer." International Journal of Lower Extremity Wounds 14, no. 3 (August 18, 2015): 217–23. http://dx.doi.org/10.1177/1534734615599653.

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31

Yotsu, Rie R., Chiaki Murase, Mariko Sugawara, Koichi Suzuki, Kazue Nakanaga, Norihisa Ishii, and Kingsley Asiedu. "Revisiting Buruli ulcer." Journal of Dermatology 42, no. 11 (September 1, 2015): 1033–41. http://dx.doi.org/10.1111/1346-8138.13049.

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32

Chukwuekezie, Okechukwu, Edwin Ampadu, Ghislain Sopoh, Ange Dossou, Alexandre Tiendrebeogo, Lola Sadiq, Françoise Portaels, and Kingsley Asiedu. "Buruli Ulcer, Nigeria." Emerging Infectious Diseases 13, no. 5 (May 2007): 782–83. http://dx.doi.org/10.3201/eid1305.070065.

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33

Bahadoran, Philippe, Nassim Hammoudi, Alice Gaudart, Jamal Saad, Yoan Di Filippo, Michel Drancourt, and Raymond Ruimy. "Case Report: A New Mycobacterium ulcerans Genotype Causing Buruli Ulcer in Côte d’Ivoire." American Journal of Tropical Medicine and Hygiene 104, no. 5 (May 5, 2021): 1782–83. http://dx.doi.org/10.4269/ajtmh.20-1307.

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ABSTRACTMycobacterium ulcerans, the opportunistic pathogen causing Buruli ulcer, is reported to affect rural populations in 36 tropical countries. We report one case of Buruli ulcer in a peri-urban area in Côte d’Ivoire, confirmed by whole genome sequencing which indicated a M. ulcerans genotype previously unreported in Côte d’Ivoire.
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34

Marsollier, Laurent, Raymond Robert, Jacques Aubry, Jean-Paul Saint André, Henri Kouakou, Pierre Legras, Anne-Lise Manceau, Chetaou Mahaza, and Bernard Carbonnelle. "Aquatic Insects as a Vector for Mycobacterium ulcerans." Applied and Environmental Microbiology 68, no. 9 (September 2002): 4623–28. http://dx.doi.org/10.1128/aem.68.9.4623-4628.2002.

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ABSTRACT Mycobacterium ulcerans is an emerging environmental pathogen which causes chronic skin ulcers (i.e., Buruli ulcer) in otherwise healthy humans living in tropical countries, particularly those in Africa. In spite of epidemiological and PCR data linking M. ulcerans to water, the mode of transmission of this organism remains elusive. To determine the role of aquatic insects in the transmission of M. ulcerans, we have set up an experimental model with aquariums that mimic aquatic microenvironments. We report that M. ulcerans may be transmitted to laboratory mice by the bite of aquatic bugs (Naucoridae) that are infected with this organism. In addition, M. ulcerans appears to be localized exclusively within salivary glands of these insects, where it can both survive and multiply without causing any observable damage in the insect tissues. Subsequently, we isolated M. ulcerans from wild aquatic insects collected from a zone in the Daloa region of Ivory Coast where Buruli ulcer is endemic. Taken together, these results point to aquatic insects as a possible vector of M. ulcerans.
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35

Phillips, R., O. Adjei, S. Lucas, N. Benjamin, and M. Wansbrough-Jones. "Pilot Randomized Double-Blind Trial of Treatment of Mycobacterium ulcerans Disease (Buruli Ulcer) with Topical Nitrogen Oxides." Antimicrobial Agents and Chemotherapy 48, no. 8 (August 2004): 2866–70. http://dx.doi.org/10.1128/aac.48.8.2866-2870.2004.

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ABSTRACT Mycobacterium ulcerans disease (Buruli ulcer) is a serious ulcerating skin disease which is common in many tropical countries. Standard treatment, by extensive excision and skin grafting, is not available in rural communities where the disease is common. We evaluated the efficacy and safety of treatment with topical nitrogen oxides. Thirty-seven patients with a clinical diagnosis of Buruli ulcer caused by M. ulcerans disease were randomly assigned to one of two groups. In one group, two creams containing sodium nitrite (6%, wt/wt) or citric acid monohydrate (9%, wt/wt) were applied daily for 6 weeks, while the other group received a placebo. In the second 6 weeks, both groups received the nitrogen oxide-generating combination of creams. Treatment was continued for another 4 weeks for patients whose ulcers were not healed after 12 weeks. The ulcer surface area was monitored by weekly tracings made by assessors blinded to the treatment. In the first 6 weeks, patients on sodium nitrite and citric acid monohydrate (group I, active treatment) showed a rapid decrease in ulcer size from 28.6 ± 5.6 cm2 (mean ± standard error) to 12.6 ± 3.2 cm2, a decrease significantly greater than that in group II (from 15.3 ± 3.1 to 11.7 ± 3.7 cm2; P = 0.03). Five ulcers in the placebo group enlarged during this period, compared with one in the active group. In the second 6 weeks (both groups on active treatment), the rates of healing were similar for the two groups and there was a significant reduction in ulcer size in group II (previously on placebo) compared to the first 6 weeks. Yellow pigmentation of the skin, which disappeared 3 days after treatment was stopped, was the only side effect to date. We conclude that creams releasing nitrogen oxides increase the healing rate of ulcers caused by M. ulcerans infection with minimal adverse events. This is the first controlled trial of any form of therapy which demonstrates efficacy in treating this disease.
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36

Komenan, Kassi, Ecra J. Elidjé, Gbery P. Ildevert, Kouassi I. Yao, Kouame Kanga, Kouassi A. Kouamé, Sangaré Abdoulaye, Kourouma S. Hamdam, Yoboué P. Yao, and Kanga Jean-Marie. "Multifocal Buruli Ulcer Associated with Secondary Infection in HIV Positive Patient." Case Reports in Medicine 2013 (2013): 1–4. http://dx.doi.org/10.1155/2013/348628.

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Buruli ulcer is a chronic and infectious skin disease, caused byMycobacterium ulcerans. It leads to large skin ulceration and sometimes bone infection which is responsible for deformities. Here, we report a case of multifocal form of Buruli ulcer associated with secondary infection in a 46-year-old human immunodeficiency virus (HIV) positive woman. The antimycobacterial drugs combined to surgery allowed curing this multifocal case and rose up two relevant issues: the susceptibility of immune reconstitution inflammatory syndrome (IRIS) occurrence andMycobacteriumdissemination. The deep immune depression, the underline biological, and clinical disorders of the patient might contribute to IRIS occurrence and Buruli ulcer dissemination. Future investigations have to be conducted on the mechanism of IRIS on set and onMycobacterium ulceransdissemination after ARV drugs initiation and the patient related underline clinical or biological disorders.
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37

Montoro, Ernesto, Virginia Capó, María E. Rodríguez, Aroldo Ruíz, and Alina Llop. "Buruli Ulcer in Ghana." Memórias do Instituto Oswaldo Cruz 92, no. 1 (January 1997): 31–32. http://dx.doi.org/10.1590/s0074-02761997000100006.

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38

Schierle, Hanns P., Gottfried Lemperle, and Detlev Erdmann. "THE BURULI TYPE ULCER." Plastic and Reconstructive Surgery 109, no. 7 (June 2002): 2608. http://dx.doi.org/10.1097/00006534-200206000-00088.

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39

Johnson, Paul. "BEWARE THE BURULI ULCER." ANZ Journal of Surgery 77, no. 5 (May 2007): 310–11. http://dx.doi.org/10.1111/j.1445-2197.2007.04108.x.

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40

Debacker, Martine, Julia Aguiar, Christian Steunou, Claude Zinsou, Wayne M. Meyers, and Françoise Portaels. "Buruli Ulcer Recurrence, Benin." Emerging Infectious Diseases 11, no. 4 (April 2005): 584–89. http://dx.doi.org/10.3201/eid1104.041000.

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41

Muelder, K., and A. Nourou. "Buruli ulcer in Benin." Lancet 336, no. 8723 (November 1990): 1109–11. http://dx.doi.org/10.1016/0140-6736(90)92581-2.

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L. Zaenglein, Andrea, Kimberly F. Faldetta, Michael A. Santos, Joanne E. Smucker, and Scott A. Norton. "Buruli Ulcer: A Review." Global Journal of Dermatology & Venereology 2, no. 2 (November 30, 2014): 69–75. http://dx.doi.org/10.12970/2310-998x.2014.02.02.5.

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Brun, Luc V. C., Jean Jacques Roux, Ghislain E. Sopoh, Julia Aguiar, Miriam Eddyani, Wayne M. Meyers, Dirk Stubbe, Marie T. Akele Akpo, Françoise Portaels, and Bouke C. de Jong. "Subcutaneous Granulomatous Inflammation due to Basidiobolomycosis: Case Reports of 3 Patients in Buruli Ulcer Endemic Areas in Benin." Case Reports in Pathology 2018 (2018): 1–6. http://dx.doi.org/10.1155/2018/1351694.

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Background. Basidiobolomycosis is a rare subcutaneous mycosis, which can be mistaken for several other diseases, such as soft tissue tumors, lymphoma, or Buruli ulcer in the preulcerative stage. Microbiological confirmation by PCR for Basidiobolus ranarum and culture yield the most specific diagnosis, yet they are not widely available in endemic areas and with varying sensitivity. A combination of histopathological findings, namely, granulomatous inflammation with giant cells, septate hyphal fragments, and the Splendore-Hoeppli phenomenon, can confirm basidiobolomycosis in patients presenting with painless, hard induration of soft tissue. Case Presentations. We report on three patients misdiagnosed as suffering from Buruli ulcer, who did not respond to Buruli treatment. Histopathological review of the tissue sections from these patients suggests basidiobolomycosis. All patients had been lost to follow-up, and none received antifungal therapy. On visiting the patients at their homes, two were reported to have died of unknown causes. The third patient was found alive and well and had experienced local spontaneous healing. Conclusion. Basidiobolomycosis is a rare subcutaneous fungal disease mimicking preulcerative Buruli ulcer. We stress the importance of the early recognition by clinicians and pathologists of this treatable disease, so patients can timely receive antifungal therapy.
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Etuaful, S., B. Carbonnelle, J. Grosset, S. Lucas, C. Horsfield, R. Phillips, M. Evans, et al. "Efficacy of the Combination Rifampin-Streptomycin in Preventing Growth of Mycobacterium ulcerans in Early Lesions of Buruli Ulcer in Humans." Antimicrobial Agents and Chemotherapy 49, no. 8 (August 2005): 3182–86. http://dx.doi.org/10.1128/aac.49.8.3182-3186.2005.

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ABSTRACT Mycobacterium ulcerans disease is common in some humid tropical areas, particularly in parts of West Africa, and current management is by surgical excision of skin lesions ranging from early nodules to extensive ulcers (Buruli ulcer). Antibiotic therapy would be more accessible to patients in areas of Buruli ulcer endemicity. We report a study of the efficacy of antibiotics in converting early lesions (nodules and plaques) from culture positive to culture negative. Lesions were excised either immediately or after treatment with rifampin orally at 10 mg/kg of body weight and streptomycin intramuscularly at 15 mg/kg of body weight daily for 2, 4, 8, or 12 weeks and examined by quantitative bacterial culture, PCR, and histopathology for M. ulcerans. Lesions were measured during treatment. Five lesions excised without antibiotic treatment and five lesions treated with antibiotics for 2 weeks were culture positive, whereas three lesions treated for 4 weeks, five treated for 8 weeks, and three treated for 12 weeks were culture negative. No lesions became enlarged during antibiotic treatment, and most became smaller. Treatment with rifampin and streptomycin for 4 weeks or more inhibited growth of M. ulcerans in human tissue, and it provides a basis for proceeding to a trial of antibiotic therapy as an alternative to surgery for early M. ulcerans disease.
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Muleta, Anthony J., Rachael Lappan, Timothy P. Stinear, and Chris Greening. "Understanding the transmission of Mycobacterium ulcerans: A step towards controlling Buruli ulcer." PLOS Neglected Tropical Diseases 15, no. 8 (August 26, 2021): e0009678. http://dx.doi.org/10.1371/journal.pntd.0009678.

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Mycobacterium ulcerans is the causative agent of Buruli ulcer, a rare but chronic debilitating skin and soft tissue disease found predominantly in West Africa and Southeast Australia. While a moderate body of research has examined the distribution of M. ulcerans, the specific route(s) of transmission of this bacterium remain unknown, hindering control efforts. M. ulcerans is considered an environmental pathogen given it is associated with lentic ecosystems and human-to-human spread is negligible. However, the pathogen is also carried by various mammals and invertebrates, which may serve as key reservoirs and mechanical vectors, respectively. Here, we examine and review recent evidence from these endemic regions on potential transmission pathways, noting differences in findings between Africa and Australia, and summarising the risk and protective factors associated with Buruli ulcer transmission. We also discuss evidence suggesting that environmental disturbance and human population changes precede outbreaks. We note five key research priorities, including adoption of One Health frameworks, to resolve transmission pathways and inform control strategies to reduce the spread of Buruli ulcer.
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Marsollier, Laurent, Tchibozo Sévérin, Jacques Aubry, Richard W. Merritt, Jean-Paul Saint André, Pierre Legras, Anne-Lise Manceau, Annick Chauty, Bernard Carbonnelle, and Stewart T. Cole. "Aquatic Snails, Passive Hosts of Mycobacterium ulcerans." Applied and Environmental Microbiology 70, no. 10 (October 2004): 6296–98. http://dx.doi.org/10.1128/aem.70.10.6296-6298.2004.

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ABSTRACT Accumulative indirect evidence of the epidemiology of Mycobacterium ulcerans infections causing chronic skin ulcers (i.e., Buruli ulcer disease) suggests that the development of this pathogen and its transmission to humans are related predominantly to aquatic environments. We report that snails could transitorily harbor M. ulcerans without offering favorable conditions for its growth and replication. A novel intermediate link in the transmission chain of M. ulcerans becomes likely with predator aquatic insects in addition to phytophage insects. Water bugs, such as Naucoris cimicoides, a potential vector of M. ulcerans, were shown to be infected specifically by this bacterium after feeding on snails experimentally exposed to M. ulcerans.
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da Silva Junior, Raimundo Geronimo, Vitoria Castelo B. R. Ibiapina do Monte, and Thiago Assis Borges Morais. "Buruli Ulcer: A Case Report." Selcuk Tip Dergisi 3, no. 34 (September 1, 2018): 129–31. http://dx.doi.org/10.30733/std.2018.01069.

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Minime-Lingoupou, Fanny, Narcisse Beyam, Germain Zandanga, Alexandre Manirakiza, Alain N’Domackrah, Siméon Njuimo, Sara Eyangoh, et al. "Buruli Ulcer, Central African Republic." Emerging Infectious Diseases 16, no. 4 (April 2010): 746–48. http://dx.doi.org/10.3201/eid1604.090195.

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Kpadonou, G. T., E. Alagnidé, A. A. Hans Moevi, E. A. Fiossi-Kpadonou, and H. Azanmasso. "Outcome of Buruli ulcer patients." Annals of Physical and Rehabilitation Medicine 54 (October 2011): e26. http://dx.doi.org/10.1016/j.rehab.2011.07.885.

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Thangaraj, Harry S., Mark R. W. Evans, and Mark H. Wansbrough-Jones. "Mycobacterium ulcerans disease; Buruli ulcer." Transactions of the Royal Society of Tropical Medicine and Hygiene 93, no. 4 (July 1999): 337–40. http://dx.doi.org/10.1016/s0035-9203(99)90104-9.

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