ABSTRACT
Leprosy (also called Hansen’s disease, HD) is a chronic granulomatous disease of the skin and peripheral nervous system. Currently two bacteria – M. leprae and M. lepromatosis comprise a so-called “Mycobacterium leprae complex”. In this chapter, we focus on Mycobacterium leprae as the most frequent causative agent of leprosy.
M. leprae is a member of the Mycobacteriaceae family. It is an acid-fast obligate intracellular gram-positive bacillus that requires the environment of the host macrophage for survival and propagation by binary fission. It shows preferential tropism toward macrophages and Schwann cells that surround the axons of nerve cells. The bacilli resist intracellular degradation by macrophages, possibly by escaping from the phagosome into the cytoplasm and preventing fusion of the phagosome with lysosomes, and through the impairment of autophagy and antimicrobial peptide expression. Host immune responses to M. leprae differ for tuberculoid (TT) and lepromatous (LL) types of leprosy, with a prevalence of either T-cell immunity (TT) or antibody production (LL). Intermediate forms can revert to the less severe form of the disease, but LL is irreversible and presents as erythema nodosum leprosum (ENL).
The initial symptoms of leprosy are not demonstrative and often go unnoticed. Most often, patients start to lose sensation to heat and cold years before skin lesions occur followed by the lost sensation of touch, pain, and pressure, particularly in hands and feet. However, the disease is often recognized through the development of dermal eruptions. Diagnosis of leprosy is mainly clinical, assisted by skin biopsy, serologic and PCR tests. Leprosy control includes early detection of the disease, adequate treatment of patients, effective care for the prevention of disabilities, and patient rehabilitation. All forms and stages of newly diagnosed leprosy are treated with rifampicin, clofazimine, minocycline, ofloxacin, and dapsone as a part of a standard multidrug therapy (MDT) recommended by the WHO.
