P030 From nerve to nodules: the unexpected progression of pure neuritic leprosy to lepromatous leprosy with erythema nodosum leprosum

Abstract Leprosy, a chronic infectious disease caused by Mycobacterium leprae, manifests across a clinical spectrum, with nerve involvement being a hallmark. Pure neuritic leprosy (PNL) is a rare subtype characterized by isolated peripheral nerve damage without skin lesions, often delaying diagnosis and treatment. In this report, we present a rare case of PNL that unexpectedly transformed into lepromatous leprosy (LL), the most severe and disseminated form, complicated by erythema nodosum leprosum (ENL). A 35-year-old man presented with progressive numbness, muscle weakness and sensory deficits in both hands and feet. On clinical examination there was absence of skin lesions. However, nerve conduction studies revealed multiple mononeuropathies. Finally, the nerve biopsy confirmed PNL with acid-fast bacilli (AFB) 3+ with macrophages in August 2022. The patient was started on World Health Organization-recommended multidrug therapy with rifampicin, dapsone and clofazimine for 12 months. Nine months after completing the treatment, the patient presented with numerous painful erythematous nodules on his face, trunk and extremities, along with fever, malaise, ankle joint pain and pedal oedema. There was atrophy of small muscles of the hand, and a partial claw hand. A slit skin smear was advised, which was negative for AFB. Skin biopsy revealed positive lepromin stain, with the bacillary load confirming the transformation to LL with ENL. The patient was started on a regimen of monthly pulsed rifampicin, minocycline and moxifloxacin for 12 months. Thalidomide was started to manage the severe ENL reaction. At the 6-month follow-up, the patient had responded favourably to the treatment, with no new complaints and an improvement in sensation and deformity. This case illustrates the intricate clinical challenges associated with leprosy, particularly how PNL can progress into severe forms, such as LL. While type 1 reactions are documented in PNL, only a single instance of a type 2 reaction has been recorded. This case holds importance as this transformation to LL occurred after complete treatment with multidrug therapy. Persistent bacterial load, immune modulation, host factors and drug resistance can contribute to this shift, necessitating vigilant monitoring even after treatment completion. Persistent and resistant bacilli are believed to contribute significantly to atypical leprosy presentations, necessitating drug sensitivity testing in such cases. To conclude, while type 1 reactions are known to occur in PNL, patients with high bacillary load and lepromatous involvement of the nerves can be predisposed to develop type 2 reaction. Only one such case has been previously reported. This emphasizes the need for early diagnosis, vigilant follow-up and awareness of potential disease transformations, particularly in endemic areas.