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.