Microbiology · Year 2 · from Microbiology
Case 3: Leprosy (Hansen's Disease)
Presentation
A 38-year-old man originally from Brazil presents with multiple skin lesions and numbness in his hands that have been present for over a year. He has noticed progressive weakness in his hands and difficulty gripping objects. Examination reveals numerous hypopigmented macules and plaques on the trunk, face, and extremities. Several lesions are anesthetic when tested with a monofilament. Bilateral ulnar nerve enlargement is palpable. He has loss of the outer third of his eyebrows (madarosis) and early claw hand deformity.
Clinical Image
Clinical photograph showing hypopigmented skin lesions with sensory loss, thickened peripheral nerves, and early claw hand deformity characteristic of leprosy.
Image Source: Lecture image - Mycobacterium leprae infection
Questions
- What is the diagnosis, and where does this patient fall on the clinical spectrum?
- Why do skin lesions in this disease demonstrate sensory loss?
- What causes the peripheral nerve enlargement and hand deformities?
- What is the appropriate treatment regimen for this patient?
Answers
- Diagnosis and spectrum: The diagnosis is leprosy (Hansen's disease) caused by Mycobacterium leprae. Based on the numerous skin lesions, bilateral nerve involvement, and systemic signs (madarosis), this patient falls toward the lepromatous (LL) end of the clinical spectrum - representing multibacillary disease. The spectrum ranges from tuberculoid leprosy (TT, paucibacillary, strong cell-mediated immunity) to lepromatous leprosy (LL, multibacillary, anergic immune response).
- Sensory loss mechanism: M. leprae has a unique predilection for cooler body tissues, preferring temperatures of 27-30°C rather than core body temperature. Skin lesions demonstrate sensory loss because the organism directly infects and destroys cutaneous nerves within the lesions. The resulting damage to small nerve fibers causes anesthesia over the affected skin areas - this association of hypopigmented lesions with anesthesia is virtually pathognomonic for leprosy.
- Nerve enlargement and deformities: M. leprae infects Schwann cells of peripheral nerves, particularly those in cooler anatomic locations (ulnar nerve at elbow, median nerve at wrist, lateral popliteal nerve, facial nerve). The resulting inflammation causes palpable nerve enlargement. Progressive damage leads to sensory loss, motor weakness, and autonomic dysfunction. The claw hand deformity results from ulnar nerve damage causing weakness of the intrinsic hand muscles and imbalance between flexors and extensors.
- Treatment regimen: This patient has multibacillary leprosy and requires the WHO multidrug therapy regimen:
- Dapsone daily
- Rifampin monthly (supervised)
- Clofazimine daily plus monthly supervised dose
- Duration: 12 months
Patients must be monitored for leprosy reactions: Type 1 (reversal) reactions cause acute inflammation of existing lesions and nerves (treated with corticosteroids), while Type 2 (erythema nodosum leprosum) causes systemic inflammation with skin nodules (treated with thalidomide or corticosteroids). Nerve damage during reactions can be irreversible if not treated promptly.