Buruli ulcer

Buruli ulcer is an infectious disease caused by Mycobacterium ulcerans. The early stage of the infection is characterised by a painless nodule or area of swelling. This nodule can turn into an ulcer. The ulcer may be larger inside than at the surface of the skin, and can be surrounded by swelling. As the disease worsens, bone can be infected. Buruli ulcers most commonly affect the arms or legs; fever is uncommon.A typical Buruli ulcer on the left hand of a 17-year-old boy in NigeriaHealed Buruli ulcer lesions in a Ghanaian womanEar of an 18-month-old with confirmed Buruli ulcerBuruli ulcer in a long-term traveler to Senegal Buruli ulcer is an infectious disease caused by Mycobacterium ulcerans. The early stage of the infection is characterised by a painless nodule or area of swelling. This nodule can turn into an ulcer. The ulcer may be larger inside than at the surface of the skin, and can be surrounded by swelling. As the disease worsens, bone can be infected. Buruli ulcers most commonly affect the arms or legs; fever is uncommon. M. ulcerans releases a toxin known as mycolactone, which decreases immune system function and results in tissue death. Bacteria from the same group also cause tuberculosis and leprosy (M. tuberculosis and M. leprae, respectively). How the disease is spread is not known. Sources of water may be involved in the spread. As of 2018 there is no effective vaccine. The Bacillus Calmette–Guérin (BCG) vaccine has demonstrated limited protection. If people are treated early, antibiotics for eight weeks are effective in 80% of cases. The treatment often includes the medications rifampicin and streptomycin. Clarithromycin or moxifloxacin are sometimes used instead of streptomycin. Other treatments may include cutting out the ulcer. After the infection heals, the area typically has a scar. About 2,000 cases are reported a year. Buruli ulcers occur most commonly in rural sub-Saharan Africa and Australia with fewer cases in South America and the Western Pacific. Children are most commonly infected in Africa, while adults are most commonly affected in Australia. Cases have been reported in 33 countries. The disease also occurs in animals other than humans, though no link between animal and human infection has been established. Albert Ruskin Cook was the first to describe buruli ulcers in 1897. It is classified as a neglected tropical disease. The infection, in most instances, presents as a painless lump or swelling and is often unaccompanied by fever. In southern Australia, the presentation is more often as a pimple in the skin (dermis) rather than under it and may be confused with an insect bite. The infection is mostly in the limbs, most often in exposed areas, but not on the hands or feet. In children, all areas may be involved, including the face or abdomen. The oedematous form of infection produces diffuse swelling of a limb, which, unlike the papule or nodule, can be painful and accompanied by low-grade fever. Infection may follow physical trauma, often minor trauma such as a small scratch. The disease is caused by Mycobacterium ulcerans. It often occurs in close proximity to water bodies, but no specific activities that bring people into contact with water have been identified (i.e. fetching of water, fishing, rice farming, washing, bathing, etc.). The mode of transmission of Buruli ulcer is not entirely known. Recent evidence suggests insects may be involved in the transmission of the infection. These insects are aquatic bugs belonging to the genus Naucoris (family Naucoridae) and Diplonychus (family Belostomatidae). Trauma is probably the most frequent means by which M. ulcerans is introduced into the skin from surface contamination. The initial trauma can be a mild skin wound such as scratch. Other studies have suggested aerosol spread but these are not proven. In Australia, animals such as koalas and possums are naturally infected. Epidemiological evidence has not clearly supported person-to-person transmission. However, Muelder & Nourou found that 10 out of 28 patients had relatives who had also had the disease, and cautioned against the dismissal of person-to-person transmission. Given the number of patients who shed large numbers of bacilli from their wounds and live in very close contact with relatives, more cases should have been observed. The cases reported by Muelder & Nourou could perhaps have been exposed to a common source of infection, and there might also be genetic component to sensitivity to the disease. After considering the various suspected agents, Portaels et al. proposed the hypothesis that human beings, as well as domestic and wild animals, could be contaminated or infected by biting insects such as water bugs. Aquatic bugs are cosmopolite insects found throughout temperate and tropical regions especially rich in freshwater. They represent about 10% of all species of Hemiptera associated with water and belong to two series of the suborder Heteroptera: the Nepomorpha, which include four superfamilies whose members spend most of their time under water, and the Naucoroidea, which include a single family, the Naucoridae, whose members are commonly termed creeping water bugs. Whether found in temperate countries like France or tropical ones like Ivory Coast, aquatic bugs exhibit the same way of life, preying, according to their size, on mollusks, snails, young fish, and the adults and larvae of other insects that they capture with their raptorial front legs and bite with their rostrum. These insects can inflict painful bites on humans as well. In the Ivory Coast, where Buruli ulcer is endemic, the water bugs are present in swamps and rivers, where human activities such as farming, fishing, and bathing take place. Present findings describing the experimental transmission of M. ulcerans from water bugs to mice are in good agreement with the possibility of this mode of transmission to humans by bites. Also in strong support of this hypothesis was the localization of M. ulcerans within the salivary glands of Naucoridae. Local physiological conditions of this niche appear to fit the survival and the replication needs of M. ulcerans but not those of other mycobacteria. Surprisingly, infiltration of the salivary glands of Naucoridae by M. ulcerans does not seem to be accompanied by any tissue damage similar to the ulcerative skin lesions developed by bitten individuals and mediated by the cytotoxic activity of the mycolactone and other toxins produced by M. ulcerans. The inactivation of the latter toxins could be the result of salivary enzymatic activities, which remain to be determined.