[Fighting against Buruli ulcer: the Côte-d'Ivoire experience]. / La lutte contre l'ulcère de Buruli. experience de la Côte-d'Ivoire.

Caused by Mycobacterium ulcerans, Buruli ulcer is an infectious disease which leads to large cutaneous ulceration and is responsible for huge socio-economic consequences. Since 1997 the World Health Organization has started a global Buruli ulcer initiative in which African endemic countries are committed. After an epidemiological background of the disease in Côte-d'Ivoire and a description of the different clinical aspects, we report the main disease management actions carried out in the country by the National Program for Buruli ulcer control from 1998 to 2003. It seems that surgical team missions carried out in health center to treat cases, early detection and treatment of cases together with the implementation of a specific poly-chemotherapy lead to an effective control of the disease.

[Contribution of heparin therapy in the medical treatment of Buruli ulcer apropos of 1 case]. / L'apport de l'héparinothérapie dans le traitement médical de l'ulcère de Buruli à propos d'une observation.

Medical treatment of Buruli ulcer is mostly disappointing even if Mycobacterium ulcerans is susceptible to many antibacterial drugs. The inefficiency in vivo of the drugs may be due to the tissue vascularisation disorders caused by the toxin that Mycobacterium ulcerans produces. This toxin causes an endarteritis followed by a thrombosis of the dermal vessels responsible for an ischemia which prevents the antibacterial drugs from reaching the infected area. Removal or prevention of that thrombosis should allow the drugs to be more effective. To verify this assumption, we used a combined therapy with two gold standard medicines in an oedematous form of Buruli ulcer on the face which could not be surgically treated: heparin for its activity on thrombosis and rifampin for its bactericidal activity on Mycobacterium ulcerans. Rifampin was administered at 300 mg dose per day. Based on the management of envenomisation cases due to viper bites, we used standard heparin at 500 Ul dose per kg repeatedly administered by an electrical syringe releasing 1 cc per hour in the tubulure of isotonic glucose infusion. The results were encouraging. The dreadful oedema of the face started to reduce on the 15th day and disappeared on the 30th day. A small area at the temple dried. But we were obliged to stop the use of standard heparin due to an occurrence of Klebsiella oxytoca septicaemia from permanent vein route. Rifampin was still administered at the same dose. The face oedema reappeared quickly, followed by a full closure of the eyelids and an ulceration at the right temple level. The standard heparin was therefore substituted by low weight molecular heparin, enoxaparin, administered at 40 mg twice per day by subcutaneous route. 45 days later the oedema reduced and ulceration did not develop. After 90 days of treatment, usual signs of mycobacterial infection progression disappeared. We stopped therefore the use of enoxaparin but continued with rifampin until healing of the ulceration which occurred after 12 months of treatment. We observed no recurrence over a period of 16 months after complete healing. We can conclude that heparin combined with antimycobacterial drugs--which are active in vitro on Mycobacterium ulcerans--could provide an effective medical treatment for Buruli ulcer.