Leprosy — expanded notes
Microbiology and transmission
Leprosy is caused by Mycobacterium leprae or M. lepromatosis, acid-fast organisms with tropism for macrophages and Schwann cells. The organisms prefer cooler body regions, explaining involvement of skin, superficial nerves, ears, nose, hands and feet. Transmission is associated with prolonged close contact with untreated multibacillary disease; casual contact does not usually transmit infection.
Immunological spectrum
The Ridley–Jopling spectrum reflects host cell-mediated immunity. Tuberculoid disease has strong cellular immunity, few bacilli and well-formed granulomas. Lepromatous disease has weak cellular immunity, high bacillary load and diffuse macrophage infiltration. Borderline forms lie between and may shift during reactions.
Nerve damage
M. leprae infects Schwann cells and provokes inflammation, causing sensory, motor and autonomic neuropathy. Loss of pain and temperature sensation leads to unnoticed injury; motor weakness causes clawing and foot drop; autonomic dysfunction causes dry skin and fissuring. Nerve impairment is a major cause of disability.
Diagnosis
Cardinal signs are a skin lesion with definite sensory loss, a thickened peripheral nerve with sensory/motor deficit, or acid-fast bacilli on slit-skin smear or biopsy. Fite-Faraco staining helps demonstrate bacilli. Biopsy pattern and bacillary index assist classification. Assess eyes, hands, feet and peripheral nerve function.
Reactions
Type 1 (reversal) reaction causes acute inflammation and swelling of existing lesions and nerves, risking rapid nerve-function loss. Type 2 erythema nodosum leprosum causes tender nodules and systemic inflammation in multibacillary disease. Reactions are immunological complications and do not necessarily indicate antimicrobial treatment failure.
Treatment and disability prevention
WHO multidrug therapy uses rifampicin, dapsone and clofazimine; duration depends on classification and national protocol. Monitor for hepatotoxicity, haemolysis, hypersensitivity and pigmentation. Treat neuritis/reactions promptly, commonly with corticosteroids for significant nerve inflammation. Provide protective footwear, daily inspection, wound care, physiotherapy and reconstructive referral where needed.