Most<unk>  complications are the result of nerve damage. The nerve damage occurs from direct invasion by the M. leprae bacteria and a person's immune response resulting in inflammation. The molecular mechanism underlying how M. leprae produces the symptoms of<unk>  is not clear, but M. leprae has been shown to bind to Schwann cells, which may lead to nerve injury including demyelination and a loss of nerve function (specifically a loss of axonal conductance). Numerous molecular mechanisms have been associated with this nerve damage including the presence of a laminin-binding protein and the glycoconjugate (PGL-1) on the surface of M. leprae that can bind to laminin on peripheral nerves. As part of the human immune response, white blood cell-derived macrophages may engulf M. leprae by phagocytosis. In the initial stages, small sensory and autonomic nerve fibers in the skin of a person with<unk>  are damaged. This damage usually results in hair loss to the area, a loss of the ability to sweat, and numbness (decreased ability to detect sensations such as temperature and touch). Further peripheral nerve damage may result in skin dryness, more numbness, and muscle weaknesses or paralysis in the area affected. The skin can crack and if the skin injuries are not carefully cared for, there is a risk for a secondary infection that can lead to more severe damage.
Leprosy
Sporotrichosis
Onychomycosis
Mumps
Tinea barbae
Tinea faciei
Trichinosis
Tinea manuum