Hansen disease

Mycobacterium leprae has a predilection for cooler body tissues (skin, superficial nerves, anterior eye, testes, nasal mucosa) because it cannot survive at core body temperature and cannot be cultured in vitro (grown in mouse footpads or armadillos). The disease spectrum reflects the host's Th1 vs Th2 immune response:

- Tuberculoid leprosy: Strong Th1/cell-mediated immunity leads to few, well-demarcated hypopigmented, anesthetic skin lesions with granuloma formation; low bacterial load (paucibacillary). Nerve involvement causes localized sensory loss.

- Lepromatous leprosy: Weak cell-mediated immunity with predominant Th2 response leads to diffuse skin involvement, symmetric nerve damage, leonine facies, saddle nose deformity, loss of eyebrows (madarosis), and high bacterial burden (multibacillary) with numerous acid-fast bacilli visible on skin biopsy/slit-skin smear. Patients are infectious.

Glove-and-stocking sensory neuropathy occurs due to nerve damage, predisposing to painless injuries and secondary trauma/infections leading to digit resorption. Nerve involvement particularly affects the ulnar nerve.

Diagnosis: Skin biopsy showing acid-fast bacilli (Fite stain), slit-skin smears, PCR. Lepromin skin test can help classify disease (positive in tuberculoid, negative in lepromatous) but is not diagnostic.

Treatment: Multidrug therapy per WHO guidelines - dapsone, rifampin, and clofazimine, with duration and regimen depending on paucibacillary vs multibacillary classification. Treatment duration typically 6-12 months or longer.

Epidemiology: Endemic in parts of Asia, Africa, and South America. In the U.S., cases are often linked to armadillo exposure (natural reservoir) or immigration from endemic areas.

Key boards associations: acid-fast, cannot be cultured on artificial media, tropism for cool tissues, granulomatous inflammation, association with armadillos, spectrum disease based on immune response (Th1 vs Th2).