Leprosy

Leprosy is an extremely chronic, low-infectivity disease caused by Mycobacterium leprae, mainly affecting skin and peripheral nerves; severe cases cause disfigurement and limb deformity. China has basically achieved elimination of leprosy by the end of last century, with only a few residual cases in remote western and coastal mountain areas and virtually no new cases. Leprosy has been epidemic worldwide for nearly 3000 years; India, Egypt, and China are considered the three ancient foci, with India the earliest. Chinese leprosy has been epidemic for over 2000 years since the Spring and Autumn/Warring States periods, called lifeng, dafeng, or eji. The word leprosy comes from Hebrew zarrath (unclean) via Greek lepra. M. leprae was discovered by the Norwegian Hansen in 1873, hence also called Hansen disease.

Common Symptoms

Splenomegaly; macule; papule; weakness; lymphadenopathy; sensory disturbance; conjunctival congestion; bacteremia; testicular atrophy; muscle atrophy

Causes and Pathogenesis

Traditionally, transmission is via contact between bacillus-containing skin/mucosal lesions and broken skin/mucosa; currently, droplet nuclei from coughing/sneezing by carriers via the upper respiratory tract are considered the main route. Indirect contact (clothing, bedding) is rare. Host resistance is decisive; most contacts develop subclinical infection and specific immunity. Pathogenesis: M. leprae is weakly virulent and intracellular; disease mainly depends on cell-mediated immunity. Humoral immunity is basically normal; lepromatous patients overproduce antibodies against phospholipid antigens that cross-react with host tissues, causing ENL reactions. Cell-mediated immunity defects form a continuous spectrum: lepromatous (LL, extreme anergy, widespread lesions, abundant bacilli) at one end and tuberculoid (TT, strong immunity, limited lesions, few bacilli, focal neuritis) at the other, with borderline (BT/BB/BL) forms in between. Bacilli are phagocytosed by macrophages, with antigen presentation via HLA-DR/DP/DQ to T cells; defective recognition leads to widespread diffuse lesions with lepra (foam) cells. Histology: indeterminate (nonspecific infiltration, few/no bacilli); tuberculoid (dense lymphocytes, granulomas, epithelioid/Langhans cells, few bacilli, positive lepromin); borderline tuberculoid (more lesions, weaker reaction); borderline (subepidermal no-infiltration band, foamy cells, more bacilli, negative lepromin); lepromatous (foam cells packed with bacilli, diffuse lesions, systemic involvement, negative lepromin). Lepra reactions: (Type II, ENL) in multibacillary patients during chemotherapy due to immune complex deposition causing painful nodules, iridocyclitis, neuritis, glomerulonephritis; (Type I) in tuberculoid/borderline patients, reversal reactions (upgrading toward TT) or downgrading (toward LL) depending on immune changes; both can worsen damage and cause permanent deformity.

Treatment

Chemotherapy, drug therapy, supportive therapy, rehabilitation

Preventive Measures

No fully mature leprosy vaccine exists; low incidence and long incubation make vaccine evaluation difficult. Killed vaccine plus BCG trials have reduced incidence variably. Health education on transmission, early symptoms, and curability with multidrug therapy is vital. Household contacts, especially children under 16, should take prophylactic dapsone.

Department to Visit

It is recommended to visit the Infectious Diseases department; an appointment can be booked on this platform before the visit.

Warm reminder: The above information is for health science reference only and cannot replace professional medical diagnosis. If you have related symptoms, please seek medical attention at a regular hospital promptly.