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To the Editor: Leprosy rates in Australia are low (less than one case per million population)1 and predominantly occur in Indigenous Australians and immigrants from leprosy-endemic areas.2
A 21-year-old pregnant Burundian woman had migrated to Australia in 2005 from a refugee camp in Tanzania. In the year before her arrival, she had received intermittent courses of steroids for an undefined illness characterised by fever, nightsweats and painful symmetrical peripheral polyarthritis. Three months after arriving in Australia, the patient presented to a rural hospital with a recurrence of the previous symptoms.
The symptoms improved on recommencement of prednisolone treatment. The patient was transferred to the Royal North Shore Hospital, where examination revealed bilateral peripheral sensory neuropathy (confirmed by nerve conduction studies); bilateral, enlarged, tender ulnar nerves; and tender hyperpigmented 2–3 cm nodules on the upper arms, but no other skin lesions or infiltrations. Skin biopsy revealed features consistent with erythema nodosum leprosum (ENL), but no acid-fast bacilli (AFB) were detected. Slit-skin smears were also negative for AFB. Leprosy was confirmed by histopathological examination of a sural nerve biopsy, which showed AFB and granulomatous changes of leprosy. The patient commenced multidrug therapy for multibacillary leprosy, with prednisolone for ENL.
Leprosy is a chronic granulomatous infection of skin and peripheral nerves with Mycobacterium leprae. Host immune responses determine the spectrum of clinical presentations. Leprosy is classified into either multibacillary disease (≥ 6 skin lesions and/or skin smears positive for AFB) or paucibacillary disease (< 6 skin lesions, with no bacilli on skin smears).3 Type 1 (reversal) reactions are delayed-type hypersensitivity reactions and manifest as neuritis and increased inflammation of pre-existing skin lesions. Type 2 reactions (ENL) are a systemic response to immune complex deposition and manifest with multiple tender nodules, fevers, neuritis, arthritis and iritis.4,5 ENL occurs exclusively in multibacillary disease in 10%–20% of patients, and negative slit-skin smears (as in our patient) are unusual. Possible explanations include undisclosed diagnosis and treatment of leprosy in Tanzania or the combination of steroid therapy and immune changes that occur during pregnancy.6 Multidrug therapy is well established and regarded as safe for pregnant women.
Diagnosis of infections that are uncommon in Western countries, especially leprosy, is often delayed.7 For refugees living in remote areas, access to expertise and support may be limited. Therefore, doctors, especially those involved in refugee health, should be aware of “exotic” infections and their varied presentations. Furthermore, effective referral networks should be encouraged, as this resulted in a swift positive outcome in our case.
Department of Microbiology and Infectious Diseases, Royal North Shore Hospital, Sydney, NSW.
Correspondence: vanhalATiprimus.com.au
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©The Medical Journal of Australia 2006 www.mja.com.au PRINT ISSN: 0025-729X ONLINE ISSN: 1326-5377