BURULI ULCER

BURULI ULCER
The Buruli ulcer (also known as the Bairnsdale ulceror Searls ulcer is an infectious disease caused by Mycobacterium ulcerans. The genus also includes the causative agents of tuberculosis and leprosy (M. tuberculosis and M. leprae, respectively). The early stage of infection is characterised by a painless nodule, with non-pyogenic, necrotising lesions developing in the skin, and occasionally in adjacent bone, as the disease progresses. M. ulcerans secretes a lipid toxin,mycolactone, which functions as an immune suppressant, necrotising agent and activator of cellularapoptosis in mammalian tissues.

James Augustus Grant, in his book A Walk across Africa(1864), describes how his leg became grossly swollen and stiff with later a copious discharge. This was almost certainly the severe oedematous form of the disease, and is the first known description of the infection Buruli ulcer disease was identified in 1897 by Sir Albert Cook, a British physician, at Mengo Hospital in Kampala,Uganda. A detailed description of the disease was written in 1948 by Professor Peter MacCallum and his colleagues, who were treating patients from the Bairnsdale district, near Melbourne, Australia. They were the first to identify Mycobacterium ulcerans as the pathogen causing it. The disease was so named after Buruli County in Uganda (now called Nakasongola District), because of the many cases that occurred there in the 1960s. The incidence of the disease has recently been rising in tropical Africa.

A 2008 study indicated that the disease is transmitted via aquatic areas rather than person to person. An international team of researchers led by University of Melbourne scientist Dr Tim Stinear has sequenced the entire genome of M. ulcerans.

The infection occurs in well defined areas throughout the world, mostly tropical areas - in several areas in Australia, in Uganda, in several countries in West Africa, in Centraland South America, in southeast Asia and New Guinea. It is steadily rising as a serious disease, especially in West Africa and underdeveloped countries, where it is the third leading cause of mycobacterial infection in healthy people, after tuberculosis and leprosy. In East Africa, thousands of cases occur annually and in these areas the disease has displaced leprosy to become the second most important mycobacterial disease of man (after tuberculosis).

§  The disease is more likely to occur where there have been environmental changes such as the development of water storages, sand mining and irrigation. (WIKIPEDIA)

PREVENTION

Bacillus Calmette-Guérin vaccine is said to prevent this kind of disease.

TREATMENT

Treatment is by surgical excision (removal) of the lesion, which may be only a minor operation and very successful if undertaken early. Advanced disease may require prolonged treatment with extensive skin grafting. Surgical practice can be dangerous and scarcely available in affected third world countries.

Antibiotics currently play little part in the treatment of Buruli ulcer. The WHO currently recommendrifampicin and streptomycin for eight weeks in the hope of reducing the need for surgery. The combination of rifampicin and clarithromycin has been used for many years in Australia. Rifampicin must never be used alone because the bacterium quickly becomes resistant.

There are a number of experimental treatments currently being investigated:

• Sitafloxacin and rifampicin is a synergistic combination that has only been trialled in mice.
• Rifalazil is a rifamycin antibiotic that appears to be more potent than rifampicin that has only been trialled in mice.
• Epiroprim and dapsone are synergistic when used in combination (in vitro studies only at present)
• Diarylquinoline shows high potency in vitro
• Application of French clay.^[10]

In a small series of eight patients, local heat at 40°C led to complete healing without surgery (except the initial removal of dead tissue).^[11]