paucibacillary

Paucibacillary leprosy lies on the tuberculoid end of the Ridley-Jopling spectrum for Hansen's disease, caused by Mycobacterium leprae (and M. lepromatosis). Patients mount a strong Th1-mediated cellular immune response with high IFN-gamma production, which limits bacterial proliferation but causes granulomatous tissue damage, including nerve involvement. Clinically, paucibacillary disease presents with one to five hypopigmented, anesthetic skin lesions, asymmetric peripheral nerve thickening, and a negative or scanty acid-fast bacilli count on slit-skin smear or biopsy (bacterial index <2). This contrasts with multibacillary leprosy (lepromatous end), which features numerous lesions, symmetric distribution, high bacterial loads, and a weak Th2-dominant immune response with poor cell-mediated immunity. The WHO classification system uses the paucibacillary/multibacillary distinction to guide treatment duration: paucibacillary leprosy is treated with a shorter multidrug regimen (rifampin and dapsone for 6 months), whereas multibacillary leprosy requires a longer regimen (rifampin, dapsone, and clofazimine for 12 months). Nerve damage in paucibacillary disease tends to be more localized but can still cause significant sensory loss, predisposing patients to trauma and secondary infections. Diagnosis involves clinical examination, skin smears, and sometimes nerve biopsy showing granulomas with few or no detectable bacilli. Understanding this classification is high-yield for USMLE Step 1 in the context of leprosy immunopathogenesis and for Step 2 in guiding appropriate antimicrobial therapy selection and duration.