A 20-year-old man belonging to a moderately endemic leprosy area in the Terai region of Nepal presented in our clinic as a referred patient from a teaching hospital with the history of 2 years. On clinical examination, a solitary hypopigmented, anaesthetic lesion was present on his left thigh extending to his knee. The surface of the lesion was dry and it had a length of approximately 15 cm with raised edge as shown in Figure 1. No other lesions were noted over the entire body. There was no peripheral nerve thickening. No history of contact with leprosy could be elicited. Furthermore, the rapid lateral flow test (supplied by Linda Oskam, KIT Biomedical Research, The Netherlands and Ray Cho, Yonsei University, Korea) for anti-Phenolic glycolipid-I (PGL-I) antibody of M. leprae was positive. Blood count was normal and the standard nerve function measurements by voluntary muscle testing and sensory test (VMT/ST) of the hand and feet were within normal limits. His slit skin smear and biopsy were sent for laboratory investigations.
His clinical presentation was consistent with tuberculoid leprosy (TT) and paucibacillary (PB) multidrug treatment (MDT) was initiated immediately comprising 600 mg of Rifampicin once a month and 100 mg of Dapsone daily. The patient was under PB MDT for a week; however, once the slit skin smear report was obtained, this prompted the clinician to change treatment from 6 months PB to 24 months multibacillary (MB) MDT regimen comprising Rifampicin 600 mg once a month, Clofazimine 300 mg once a month followed by 50 mg daily and Dapsone 100 mg daily.
Slit skin smear examination for M. leprae from the lesion revealed a Bacterial Index (BI) of 4+ (10-100 acid fast bacilli per oil immersion microscopic field on Ridley's logarithmic scale) as shown in Figure 2 while it was negative from the routine sites of the ear lobes, thigh and arm. The Morphological Index was 0%. On histopathological examination, the biopsy from the lesion revealed skin and subcutaneous tissue. There was an epidermal atrophy with mild orthokeratosis. Small aggregates of histocytes and lymphocytes were seen around vessels and skin adnexa and in and around nerves. The granuloma fraction was about 5%. Solid acid fast bacilli were seen in some of the granulomas, singly and in small clusters of 3 to 5 bacilli; the BI of the granuloma was 2+. Based on the smear results and histopathological report, the patient was classified as borderline tuberculoid (BT) in the spectrum of Ridley and Jopling's classification.
Five months after commencement of MB MDT, the patient developed a Type 1 or reversal reaction. This time, there was palpable enlargement of a nerve and evidence of nerve function impairment was observed. Again, we assessed the patient for clinical, bacteriological and immunological investigations. Clinically, the patient still had the same single lesion. Bacteriologically, the routine sites were still negative and the BI of the lesion was 1+. The lateral flow for anti-PGL-I antibody was positive with lesser intensity than the test done on his first visit indicating a lower bacterial load. The standard nerve function measurements by VMT/ST were normal on both feet and hands but some weakness was observed on the left foot which concurs with enlargement of the left lateral popliteal nerve.
Blood count was normal at this time and a whole blood interferon gamma (IFN-gamma) test was also performed to measure the cell mediated immune responses towards Mycobacterium tuberculosis purified protein derivative (MTB PPD), M. leprae soluble antigen devoid of lipoarabinomannan (MLSA-LAM) and M. leprae cell wall antigen (MLCwA), which were free of endotoxin and M. leprae lipoarabinomannan, supplied by Professor Patrick J. Brennan, Colorado State University, Fort Collins under NIH contract NO1-AI-25469. These were tested by QuantiFERON-CMI (Cellestis, Australia). IFN-gamma production levels were generated in response to stimulation with Cellestis mitogen but no detectable levels of IFN-gamma were obtained against these antigens in our patient.
The reversal reaction was treated with 12 weeks of oral prednisolone in a tapering dose and MDT was continued unaltered during this period. Initially, the prednisolone was prescribed at a dose of 40 mg per day for a 2-week period, then decreased to 30 mg per day for 2 weeks, 20 mg per day for 2 weeks, 15 mg per day for 2 weeks, 10 mg per day for another 2-week period and finally 5 mg per day for 2 weeks.