From the Research
Leprosy is caused by Mycobacterium leprae, a slow-growing bacterium that primarily affects the skin, peripheral nerves, upper respiratory tract, and eyes, with its pathogenesis determined by the host's immune response, ranging from tuberculoid to lepromatous leprosy, as described in the most recent study 1. The disease spectrum of leprosy depends on the host's immune response, with the most recent study 1 highlighting the importance of early detection and treatment to prevent irreversible damage and disabilities.
- The pathogenesis of leprosy begins when M. leprae enters the body, typically through respiratory droplets or skin contact with infected individuals, as noted in 1.
- After entry, the bacteria are phagocytosed by macrophages but resist destruction due to their waxy cell wall, as described in 2.
- The bacteria multiply slowly and have a preference for cooler body temperatures, explaining their predilection for peripheral tissues, as mentioned in 3.
- The disease spectrum depends on the host's immune response, ranging from tuberculoid leprosy (strong cell-mediated immunity with few bacteria) to lepromatous leprosy (poor cell-mediated immunity with numerous bacteria), as discussed in 4.
- In tuberculoid leprosy, T-helper cells activate macrophages to contain the infection, resulting in localized disease, while in lepromatous leprosy, the immune response is ineffective, allowing widespread bacterial multiplication, as explained in 2.
- Nerve damage, a hallmark of leprosy, occurs through direct bacterial invasion, immune-mediated inflammation, and reactive episodes called reactions, as noted in 5.
- Treatment requires multidrug therapy with dapsone, rifampin, and clofazimine for 6-12 months depending on disease classification, addressing both the infection and preventing resistance, as recommended in 1.