for treating buruli ulcer, but can be prohibitively expensive in low-resource settings. prevention buruli ulcer can be prevented by avoiding contact with aquatic environments in endemic areas, although this may not be possible for people living in these areas. the risk of acquiring it can be reduced by wearing long sleeves and pants, using insect repellent, and cleaning and covering any wounds as soon as they are noticed. there is no specific vaccine for preventing buruli ulcer. the bcg vaccine typically given to children to protect against tuberculosis offers temporary partial protection from buruli ulcer. epidemiology cases of buruli ulcer reported to the world health organization in 2018. color indicates case number: yellow, (1–150) dem. rep. congo, gabon, guinea, togo; orange (151–300), benin, cameroon, côte d'ivoire; light red (301–450), liberia, nigeria; dark red (451+), ghana. not shown are australia (358), papua new guinea (12) and japan (3). buruli ulcer is relatively rare, with 2,713 cases reported to the world health organization in 2018. most countries do not report data on buruli ulcer to the world health organization, and the extent of its spread is unknown. in many endemic countries, health systems likely do not record each case due to insufficient reach and resources, and so the reported numbers probably underestimate the true prevalence of the disease. buruli ulcer is concentrated in west africa and coastal australia, with occasional cases in japan, papua new guinea and the americas. in west africa, the disease is predominantly reported from remote, rural communities in benin, côte d'ivoire, cameroon, and ghana. other countries in the region also have buruli ulcer to some degree; a 2019 systematic review of prevalence studies found a clear consensus that it is present in the democratic republic of the congo, gabon, liberia, nigeria, togo, and south sudan, as well as "strong" or "very strong" evidence of the disease in the republic of the congo, sierra leone, the central african republic, guinea, and uganda. buruli ulcer is regularly reported from australia, where it occurs in coastal clusters—two in queensland (near rockhampton and north of cairns) and two in victoria (near bairnsdale and melbourne). it is more rarely reported from japan, papua new guinea, and the americas. japan reports a few locally acquired cases per year scattered across the main island, honshu. papua new guinea sporadically reports cases to the world health organization, typically less than a dozen per year. in the americas, most buruli ulcer is reported from french guiana, with few cases described in surrounding countries. a 2019 review found "strong" evidence for the presence of buruli ulcer in french guiana and peru, and "moderate" evidence in brazil, mexico and suriname. within affected countries, buruli ulcer tends to occur in rural areas near slow-moving or stagnant water. in particular, the disease tends to appear near water that has experienced human intervention, such as the building of dams or irrigation systems, flooding, or deforestation. within endemic communities, few characteristics predict who will acquire buruli ulcer. males and females are equally likely to be infected. ulcers can appear in people of all ages, although infections are most common among children between 5 and 15 years in west africa, and adults over 40 in australia and japan. other animals a common ringtail possum with an ulcer caused by m. ulcerans. m. ulcerans infection can cause buruli ulcer-like lesions in some non-human animals. natural non-human infections have only been described in coastal victoria, near melbourne. there, m. ulcerans-positive lesions have been described in koalas, common ringtail possums, and common brushtail possums, with lesions typically on the face, limbs, and tail. ulcers have also been reported on domesticated animals, namely dogs, horses, alpacas, and a cat. in laboratories several species of animals have been infected with m. ulcerans in an attempt to model the course of buruli ulcer. injection of m. ulcerans can cause ulcers in several rodents (mice, guinea pigs, greater cane rats and common african rats), larger mammals (nine-banded armadillos, common brushtail possums, pigs, and cynomolgus monkeys), and anole lizards. society and culture in endemic areas, particularly rural communities in africa, people may be aware of buruli ulcer's association with the environment, yet simultaneously associate it with witchcraft or other supernatural causes. this dual understanding of disease—combined with poor access to conventional medicine—drives many to seek traditional healers for primary care. traditional healers often treat buruli ulcer with two simultaneous approaches: herbs and sometimes burning or bleeding to treat the physical wound; and confession, ritual purification, and prohibitions on food, interpersonal contact, or sex to treat the spiritual component of the disease. those with buruli ulcer report feeling shame and experiencing social stigma that could affect their relationships, school attendance, and marriage prospects. buruli ulcer is known by several other names in different parts of the world. in southeastern australia, it was originally called "searls' ulcer" after the physician j. r. searls who saw the first australian patients at the bairnsdale clinic and sent material to peter maccallum's group for further examination. the disease later became more generally known as "bairnsdale ulcer" after the district where it was described. in northeastern australia, north of cairns, the disease is called "daintree ulcer" or "mossman ulcer" after the nearby daintree river and the town of mossman. in papua new guinea, the disease is called "kumusi ulcer" after the kumusi river along which villages with buruli ulcer were originally described. history albert r. cook (center) at mengo hospital in 1897. cook was the first to describe buruli ulcer. the first written description of buruli ulcer is credited to a british missionary doctor, albert r. cook. in 1897, at mengo hospital in uganda, cook noted several patients with slow-healing ulcers. the cause of these slow-healing ulcers was identified 50 years later in 1948, when peter maccallum, jean tolhurst, glen buckle, and h. a. sissons at the alfred hospital's baker institute described a series of cases from bairnsdale, victoria, isolated the causative mycobacterium, and showed it could cause ulcers in laboratory rats. over the following decades, more cases were described in africa. a particularly high prevalence in uganda's buruli county led to the disease becoming more widely known as "buruli ulcer". in 1998, the world health organization started the global buruli ulcer initiative with the aim of coordinating global efforts to control the disease. this was followed in 2004 by world health organization resolution wha57.1 calling upon member countries to support the global buruli ulcer initiative and increase research on buruli ulcer diagnostics and treatment. interest in buruli ulcer has been encouraged by its branding as a "neglected tropical disease", first in a 2005 plos medicine article, and later by both the world health organization and plos neglected tropical diseases. from the time the disease was described, buruli ulcer was treated with surgery to remove all affected tissue, followed by prolonged wound care. this treatment regimen was expensive, sometimes disfiguring, and often ineffective, ulcers recurring in up to a third of cases. treatment dramatically improved in 2004, when the world health organization recommended an eight-week course of daily oral rifampicin and injected streptomycin. the introduction of antibiotics reduced the rate of ulcer recurrence to fewer than 2% of cases. however, streptomycin can be toxic to the ears and kidneys, and administering daily injections is challenging in low-resource settings. in 2017, the world health organization updated its recommendation to replace streptomycin with the oral antibiotic clarithromycin. research buruli ulcer has been the subject of scientific research since the description of m. ulcerans in 1948, and the demonstration that the bacteria could cause ulcers in laboratory animals. while several animals are susceptible to m. ulcerans ulcers, mice (particularly balb/c and c57bl/6 mice) are most commonly used to model buruli ulcer in modern laboratories. since m. ulcerans can only grow in relatively cool temperatures, mice are typically infected in furless parts of the body: the ear, tail, or footpad. after injection into the mouse, bacteria double every three to four days, and the first signs of skin disease appear after three to four weeks. this mouse model of buruli ulcer has primarily been used to test antibiotics. the antibiotic combinations, dose frequencies, and treatment durations currently in use were first tested in laboratory-infected mice. some vaccine platforms have been tested in m. ulcerans-infected mice, mostly based on the mycobacterium bovis strain used in the bcg vaccine. the bcg vaccine and versions of the vaccine that also express m. ulcerans antigens prolong the survival of mice after m. ulcerans infection. as of 2019, no vaccine tested completely protects mice from infection. m. ulcerans can be grown in laboratory media, although its slow growth makes it challenging to study. bacteria plated on laboratory media can take up to three months to form visible colonies. strains of m. ulcerans used in laboratories are less standardized than the mice they infect; different laboratories use different strains based on convenience and accessibility. three m. ulcerans strains are particularly common, each isolated from an infected person: "cu001" from adzopé, côte d'ivoire in 1996; "mu1615" from malaysia in the 1960s; and "s1013" from cameroon in 2010.