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Histoid leprosy (HL) was originally described by Wade in 1963 and is regarded as a rare variant of lepromatous leprosy (LL). These characteristic clinical lesions are firm, deeply adhered nodules with features reminiscent of dermatofibromas or keloids in a background of apparently healthy skin. The main histopathological findings described are the presence of spindle cell histiocytes immersed in a richly collagenized background, usually forming a nodular pattern of infiltration with sharply delimitation and positive staining for acid-fast bacilli.

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Background: Histoid leprosy is a subtype of leprosy with distinct clinical presentation and histologic features. It accounts for <4% of leprosy cases. The exact location of histoid leprosy along the immune spectrum and its relation to other subtypes is unclear.

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Wade's histoid leprosy (HL) is a rare variant of multibacillary leprosy, with characteristic clinical, immunologic, histopathologic, and bacteriologic features. It is associated with resistance to sulfa drugs or polychemotherapy and is rarely observed in patients who have not undergone prior treatment. Clinically, HL resembles keloid or dermatofibroma.

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Article Synopsis
  • An 18-year-old man had a 4-year history of skin patches and later developed nodules and nerve issues, with a history of close contacts having leprosy.
  • Histopathological tests showed acid-fast bacilli, confirming the diagnosis of lepromatous leprosy, specifically the histoid variant.
  • He received multidrug therapy as per WHO guidelines, leading to significant improvement, highlighting the importance of early detection and treatment to prevent complications.
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Histoid leprosy is a rare multibacillary form that presents with disseminated papule-nodular cutaneous lesions. To study the inflammatory infiltrate of the histoid form and to compare it with other lepromatous forms, we performed histological and immunohistochemical analysis on skin biopsies. Fifteen patients were included for histopathological analysis (10 histoid and five lepromatous) via the haematoxylin-eosin and Ziehl-Neelsen-Faraco stains.

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