<unk>  is caused by infection of the skin with the bacterium Mycobacterium ulcerans. M. ulcerans is a mycobacterium, closely related to Mycobacterium marinum which infects aquatic animals and, rarely, humans. It is more distantly related to other slow-growing mycobacteria that infect humans, such as Mycobacterium tuberculosis, which causes tuberculosis, and Mycobacterium leprae, which causes leprosy.<unk>  typically occurs near slow-moving or stagnant bodies of water, where M. ulcerans is found in aquatic insects, mollusks, fish, and the water itself. How M. ulcerans is transmitted to humans remains unclear,<unk> t somehow bacteria enter the skin and begin to grow. Ulceration is primarily caused by the bacterial toxin mycolactone. As the bacteria grow, they release mycolactone into the surrounding tissue. Mycolactone diffuses into host cells and blocks the action of Sec61, the molecular channel that serves as a gateway to the endoplasmic reticulum. When Sec61 is blocked, proteins that would normally enter the endoplasmic reticulum are mistargeted to the cytosol, causing a pathological stress response that leads to cell death by apoptosis. This results in tissue death at the site of infection, causing the open ulcer characteristic of the disease. At the same time, Sec61 inhibition prevents cells from signaling to activate the immune system, leaving ulcers largely free of immune cells. Immune cells that do reach the ulcer are killed by mycolactone, and tissue examinations of the ulcer show a core of growing bacteria surrounded by debris from dead and dying neutrophils (the most common immune cell). Transmission alt= A house in a swampy area. It is not known how M. ulcerans is introduced to humans.<unk>  does not spread from one person to another. In areas endemic for<unk> , disease occurs near stagnant bodies of water, leading to the long-standing hypothesis that M. ulcerans is somehow transmitted to humans from aquatic environments. M. ulcerans is widespread in these environments, where it can survive as free-living or in association with other aquatic organisms. Live M. ulcerans has been isolated from aquatic insects, mosses, and animal feces; and its DNA has been found in water, soil, mats of bacteria and algae, fish, crayfish, aquatic insects, and other animals that live in or near water. A role for biting insects in transmission has been investigated, with particular focus on mosquitoes, giant water<unk> gs, and Naucoridae. M. ulcerans is occasionally found in these insects, and they can sometimes transmit the bacteria in laboratory settings. Whether these insects are regularly involved in transmission remains unclear. Pre-existing wounds have been implicated in disease transmission, and people who immediately wash and bandage open wounds are less likely to acquire<unk> . Wearing pants and long-sleeved shirts is associated with a lower risk of<unk> , possibly by preventing insect bites or protecting wounds. Genetic susceptibility While<unk>  is not contagious, susceptibility sometimes runs in families, suggesting genetics could play a role in who develops the disease. Severe<unk>  in a Beninese family was attributed to a loss of 37 kilobases of chromosome 8 in a region that included a long non-coding RNA and was near the genes for beta-defensins, which are antimicrobial peptides involved in immunity and wound healing. Broader studies have focused on genes involved in susceptibility to other mycobacterial infections, finding susceptibility to<unk>  may be linked to variants in six immunity-related genes: SLC11A1, PRKN, NOD2, ATG16L1, iNOS, and IFNG, as well as in two long non-coding RNAs. A genome-wide association study linked resistance to<unk>  to a variant of ATG16L1 associated with susceptibility to Crohn's disease.
Buruli ulcer
Lichen planus
Callous ulcer
Lichen sclerosus
Kangri ulcer
Lipschütz ulcer
Stercoral ulcer
Melanosis coli