Epidemiology
Etiology
Pathophysiology
- Tuberculoid leprosy
- Strong TH1-mediated response (interleukin IL-2, IFN-γ, and IL-12) in affected tissues, leading to the activation of macrophages that kill M leprae organisms, thereby limiting disease extent.
- However, this localized inflammation damages the skin and cutaneous nerves, leading to the development of a small number of hypopigmented, well-demarcated plaques with decreased sensation.
- Lepromatous leprosy
- More disseminated form of the disease characterized by an innate inability to recognize and mount a cellular immune response against M leprae antigens.
- Affected tissues show extensive accumulation of acid-fast bacilli within macrophages and often a TH2 cytokine profile (IL-4, IL-5, and IL-10).
- Patients with lepromatous leprosy develop more numerous, poorly demarcated plaques that are widespread across the body. Over time, the bacterial load increases and the nodular lesions coalesce, causing the development of leonine facies and degeneration and loss of the nose and digits.
Clinical features
Diagnostics
The lepromin skin test (in which M leprae antigens are injected intradermally) can be used to distinguish between tuberculoid and lepromatous leprosy. Patients with tuberculoid leprosy will develop an indurated nodule at the site of the injection (much like a positive PPD test for M tuberculosis). In contrast, the test is usually nonreactive in patients with lepromatous leprosy due to their weak TH1 cell-mediated immune response.