Antibacterials
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Antibacterials Ototoxicity, peripheral neuropathy and leprosy unmasking due to type 1 leprosy immunological reaction: case report
A 25-year-old man developed ototoxicity during treatment with kanamycin, peripheral neuropathy secondary to cycloserine and linezolid, and unmasking of the leprosy due to type 1 leprosy immunological reaction during treatment with clofazimine and levofloxacin for multidrug-resistant tuberculosis (MDR-TB) [routes not stated]. The man, who presented with cough, fever, night sweats and right axillary lymphadenopathy with suppurative discharge, was eventually diagnosed with MDR-TB. No medical comorbidities were noted, and there was no previous history of TB or leprosy. Further evaluation revealed that he was resistant to rifampicin, isoniazid, streptomycin and ethionamide (MDR-TB), but was sensitive to pyrazinamide, ethambutol, ofloxacin, amikacin, kanamycin, capreomycin and cycloserine. He started receiving levofloxacin [LVX] 750mg once daily, kanamycin [KM] 600mg, pyrazinamide [PZA] 1500mg, cycloserine [CS] 500mg, clofazimine [clofazamine, CFZ] 100mg, linezolid [LZD] 600mg and pyridoxine 100mg. After 2 weeks of treatment, he started to develop symptoms of hearing impairment and progressive numbness of his feet and hands. Thus, kanamycin-related ototoxicity, and peripheral neuropathy secondary to cycloserine and linezolid was suspected. The man’s therapy with kanamycin was therefore suspended, and was substituted with bedaquiline. Additionally, cycloserine and linezolid were withheld due to the concern of progressive peripheral neuropathy, with addition of aminosalicylic acid. Two months into his treatment for MDR-TB, he was noted with the changes consistent with multibacillary leprosy with loss of eyebrows, a palpable thickened ulnar nerve of his left hand with reduced grasping power, a small depigmented skin lesion with anaesthesia on his left arm and bilateral partial foot drop. A slit skin smear test (taken from his ear lobe) was positive for acid-fast bacilli. Eventually, he was diagnosed with multibacillary leprosy co-infection with ulnar and likely bilateral peroneal nerve neuritis secondary to a type 1 leprosy immunological reaction. Based on the presentation, it was determined that the underlying leprosy was unmasked due to the type 1 leprosy immunological reaction during treatment with clofazimine and levofloxacin for MDR-TB. Immediately, he started receiving prednisolone and multidrug therapy with rifampicin and dapsone, which were added to the clofazimine and levofloxacin therapies. One month later, the foot drop had largely resolved and the weakness of his left hand had dramatically improved. He was then planned to receive 12 months of multidrug therapy for leprosy and 20 months of MDR-TB treatment. The death and breakdown of M. leprae organisms by clofazimine and levofloxacin likely precipitated the type 1 leprosy immunological reaction. Kama G, et al. Tuberculosis treatment unmasking leprosy: Management of drug-resistant tuberculosis and leprosy co-infection. Public Hea
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