What are the clinical features of Hansen disease?

Clinical Features of Hansen Disease (Leprosy)

Hansen disease is a chronic bacterial infection caused by Mycobacterium leprae that primarily affects the skin, peripheral nerves, and upper respiratory mucosa, presenting as a clinical spectrum ranging from tuberculoid to lepromatous forms based on the host's cellular immune response. 1

Primary Affected Systems

• Skin involvement is the hallmark feature, with lesion characteristics varying dramatically across the disease spectrum 1, 2
• Peripheral nerve damage manifests as nerve swelling, thickening, and progressive neuropathy leading to anesthesia and weakness 1, 3
• Upper respiratory mucosa involvement can produce nasal symptoms and mucosal lesions 1, 2
• Eyes may be affected, causing pain or vision loss 3

Clinical Forms and Their Distinguishing Features

Tuberculoid (Paucibacillary) Form

• One or a few well-demarcated, hypopigmented skin lesions with sharp borders 1, 2
• Anesthetic lesions due to early nerve involvement 1, 2
• Active, spreading edges with clearing centers are characteristic 1
• Peripheral nerve swelling or thickening is frequently palpable 1, 2
• Represents a strong cellular immune response with minimal bacterial load 2, 4

Lepromatous (Multibacillary) Form

• Multiple erythematous papules and nodules distributed symmetrically 1, 2
• Infiltration of the face, hands, and feet in a bilateral pattern 1, 2
• Progressive skin thickening develops over time 1
• Lesions progress to cause facial disfigurement and leonine facies 3, 5
• High bacterial load with poor cellular immune response 4, 6

Borderline (Dimorphous) Form

• Mixed features combining characteristics of both tuberculoid and lepromatous disease 1, 2
• Most common histopathological subtype in clinical practice, particularly borderline tuberculoid 4, 6
• Clinical presentation varies along the spectrum depending on immune status 4, 6

Indeterminate Form

• Early lesions presenting as hypopigmented macules without fully developed features 1, 2
• Lacks definitive tuberculoid or lepromatous characteristics 1, 2
• May progress to other forms or resolve spontaneously 4, 6

Key Clinical Presentations

• Skin lesions with sensory loss (anesthesia to touch, pain, or temperature) is pathognomonic when present 3, 5
• Weakness and numbness in affected extremities from peripheral neuropathy 3, 5
• Bilateral and symmetrical distribution particularly in lepromatous disease 1
• Nerve thickening palpable on physical examination, especially ulnar, median, and peroneal nerves 3, 5

Immunologic Reactions (Critical Complications)

• Type 1 (reversal) reactions and Type 2 (erythema nodosum leprosum) reactions can occur before, during, or after treatment, causing acute worsening of symptoms 3
• These reactions represent immunologic phenomena requiring specific management while continuing antibacterial therapy 3

Diagnostic Confirmation

• Demonstration of acid-fast bacilli in skin or dermal nerve from full-thickness skin biopsy of lepromatous lesions provides laboratory confirmation 1, 2
• Clinical diagnosis combined with histopathology and bacteriological index (slit-skin smear) provides accurate classification 4, 6
• Clinico-histological correlation achieves concordance in approximately 63-65% of cases 4, 6

Common Pitfalls

• Early indeterminate lesions remain diagnostically challenging and may require repeat deeper punch biopsies for proper categorization 4
• Discordance between clinical and histopathological classification occurs most commonly between borderline tuberculoid and tuberculoid forms, and between borderline lepromatous and lepromatous forms, though this typically does not affect treatment decisions 4
• The disease affects predominantly younger individuals (peak 21-30 years) with a male predominance (1.66:1 ratio) 4