From the Research
Leprosy, caused by Mycobacterium leprae, presents with diverse skin manifestations, including hypopigmented or erythematous patches, nodules, and plaques, and is associated with nerve involvement and distinct pathological findings, as described in the most recent study 1. The disease typically begins with hypopigmented or erythematous patches with reduced sensation, progressing differently along the leprosy spectrum.
- Tuberculoid leprosy features well-defined, anesthetic skin lesions with dry, scaly surfaces,
- while lepromatous leprosy presents with numerous symmetrical, shiny nodules and plaques.
- Borderline forms show intermediate characteristics. Nerve involvement is a hallmark of leprosy, with predilection for superficial nerves like the ulnar, median, radial, common peroneal, and facial nerves, leading to sensory loss, motor deficits, and deformities, as noted in 2. Pathologically,
- tuberculoid leprosy shows granulomatous inflammation with few bacilli,
- while lepromatous leprosy demonstrates numerous acid-fast bacilli within foamy macrophages (Virchow cells), as described in 3. The most recent and highest quality study 1 highlights the importance of early diagnosis and treatment to prevent permanent nerve damage and deformities, with regular monitoring for lepra reactions that may require additional anti-inflammatory therapy. Treatment requires multidrug therapy (MDT) with dapsone, rifampin, and clofazimine for 6-12 months depending on classification, as outlined in 4 and 5.
- Paucibacillary cases receive dapsone (100mg daily) and rifampin (600mg monthly) for 6 months,
- while multibacillary cases require additional clofazimine (50mg daily and 300mg monthly) for 12 months. The skin manifestations of leprosy can also include verrucous lesions, which are an uncommon finding and may be misdiagnosed, as reported in 1.