5. Clinical appearances

Based on two types of extreme immune responses, two polar forms (tuberculoid at one end and lepromatous in the other) of the clinical presentation of the disease occur. The disease may present with a clinical picture representing severity, anywhere in the continuous/variable spectrum between these two polar forms (see Appendix No. IV for Ridley's general overview and Jopling Hardness classification on leprosy, in the form of a continuous spectrum and Appendix III for differential diagnosis leprosy). People with a "good" CMI response develop a milder and localized form of disease (tuberculoid) with fewer bacterial loads, whereas people with weak or absent CMI develop a widespread spread of disease (lepromatous) with a high bacterial load.

The transmission of leprosy exactly is still understood. The human being is the main reservoir of leprosy infection, although by history, transmission through African green monkeys and Armadillos has been reported [15]. Other dissemination routes were suspected, but their role in the transmission of leprosy was not clearly defined [16]. M. leprae has a tropism for the skin and Schwann cells of the peripheral nerves. The primary sign appears as sensory neuritis, but in untreated patients seeking medical treatment at a late phase with severe motor impairment. Plantar ulcers, lytic bone lesions and ulnar nerve paralysis or lagophthalmos are frequent complications in leprosy patients [16].

Leprosy diagnosis remain based clinical findings and easy make for health workers to treat patients. Various clinical signs can be known during the early phase of leprosy, defined as indeterminate phase, so that it is difficult to diagnose the disease.
