Mycobacterium leprae is a slow-growing bacillus that causes leprosy. the infection may take two to ten years to incubate. While the exact mechanism of infection transmission is unknown, direct bacillus absorption through the nasal or respiratory mucosa and aerosolized nasal secretions are the most common theories. The bacteria is subsequently transported by the bloodstream to the peripheral nerves, where it can result in tissue damage from painless burns and ulcers as well as irreparable nerve damage that results in a loss of protective feeling.

One of the most common host cells that mycobacteria encounter is macrophages. The process of monocyte-derived macrophages phagocytosing M. leprae is controlled by protein kinase and can be facilitated by complement receptors CR1 (CD35), CR3 (CD11b/CD18), and CR4 (CD11c/CD18). A Th2 cytokine profile appears to be correlated with nonreactivity to M.Leprea.

The Ridley-Jopling classification (1962) divides leprosy into six forms: Tuberculoid (TT), Borderline Tuberculoid (BT), Borderline-borderline Mid-borderline (BB), Borderline-Lepromatous (BL), Subpolar Lepromatous (LLs), and Polar Lepromatous (LLp). These categories are based on clinical, histopathological, and immunological criteria. According to WHO, leprosy is classified into two groups: the paucibacillary (PB) and multibacillary (MB) types, to aid in treatment.

Leprosy is treated as an outpatient procedure using WHO-standardized regimens from 1982, which essentially consist of three first-line medications: clofazimine, rifampicin, and dapsone. This relationship is referred to as polychemotherapy, or MDT (PCT). With minimal bactericidal activity, sulfone (diaminodiphenyl sulfone, or DDS), commonly referred to as dapsone, primarily acts as a bacteriostatic agent.

It most likely functions as an antagonist of para- aminobenzoic acid (PABA), preventing M. leprae from using it to synthesize folic acid. It is well-tolerated and has a number of adverse effects, most of which do not require stopping treatment.

The primary bactericidal effect of rifampicin (RMP), a semi-synthetic derivative of rifamycin B, is observed. It functions by preventing the RNA-polymerase enzyme in the bacillus from growing. RMP has been used to treat leprosy since 1963. Most of the bacilli become non-viable after a few days of therapy, and its use is crucial in all clinical types of leprosy. Clofazimine (CLF) is an iminophenazine dye . It has a mild bactericidal action, acting slowly on M. leprae and destroying 99% of the bacteria in approximately five months. Its efficacy is similar to DDS. CLF has an important anti-inflammatory action.

With an estimated heritability of up to 57%, family studies and community epidemiological surveys have amply established the significant role that host genetics plays in an individual's vulnerability to leprosy.

RAB32 is a low molecular weight G protein belonging to the Ras superfamily. It is necessary for the production of autophagic vacuoles and the control of autophagy's removal of aggregated proteins. Rab32 may play a similar role in the pathogenesis of leprosy, according to a recent study that found the protein controls the recruitment of cathepsin D to phagosomes containing Mycobacterium tuberculosis.

Inclusion Criteria:

• Patients of both sexes with positive slit skin smear for m.leprae .

Exclusion Criteria:

• Contraindications to Multi drug therapy :
• Patients with hypersensitivity to sulfa .
• Patients with hypersensitivity to clofazimine or rifampcin.
• pregnant or lactating women.