nerve damage are the main clinical features of the disease. Blindness may develop, resulting either from destruction of peripheral nerves within ocular tissues or from direct bacillary corneal invasion. Some patients—particularly those with lepromatous leprosy (see below)—may be affected by bacillary infiltration into the mucosa of the upper respiratory tract, bones, and testes. Diagnosis of leprosy is mostly clinical and symptomatic, based on the presence of a few cardinal signs: hypopigmented or reddish-copper patches with definite sensory loss, with or without thickened nerves, and positive skin smears.
The social consequences for those affected with leprosy and for their families can be devastating.
figure-1: Photomicrograph of Mycobacterium leprae Taken from a Leprosy Skin Lesion
The disease occurs in a wide spectrum of forms, which stem from the varying host immune response to the pathogen. Individuals with tuberculoid leprosy display a strong cell-based immune response that controls bacterial proliferation and lesions, whereas patients with lepromatous leprosy lack specific cellular immunity, ending up with high mycobacterial loads and severe clinical manifestations. Most patients have borderline forms. After the age of puberty, leprosy has a male to female ratio of 1.5–2.0 to 1. Britton and Lockwood have pointed out that this male preponderance is real—it is not related to underdiagnosis in women, although in some countries it is accentuated by delayed presentation by female patients, which results in higher rates of deformity.
The impairment of nerve function is due both to involvement of nerves by the primary infection, and to the acute immunological phenomena known as reversal reactions or type-1 leprosy reactions. These reactions occur in a third of patients with borderline forms of disease, are caused by spontaneous increases in T-cell reactivity to mycobacterial antigens, and are associated with the infiltration of interferon γ and TNFα-secreting CD4-positive lymphocytes in skin lesions and nerves, resulting in oedema and painful inflammation. Sensory loss makes affected patients prone to inadvertent injury, leading to severe disabilities and visible deformities (Figure 2).
