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A case of Hansen Disease presenting as tinea versicolor

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A case of Hansen Disease presenting as tinea versicolor
Shelley Yang1 BS, Maryanne Makredes2 MD, Patrick O’Donnell3 DO, Nikki A Levin2 MD PhD
Dermatology Online Journal 19 (4): 7

1. University of Massachusetts Medical School, Worcester, Massachusetts
2. Division of Dermatology, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts
3. Department of Pathology, University of Massachusetts Medical School, Worcester, Massachusetts


Hansen Disease (leprosy) is an infectious disease that targets macrophages and Schwann cells, caused by the acid fast intracellular organism, Mycobacterium leprae. Clinically, it presents with a spectrum of findings that may include hypopigmented macules, erythematous plaques and nodules, and thickened or tender peripheral nerves. The most feared complication is mutilating damage to facial structures or digits resulting from loss of sensation in affected skin. In non-endemic areas, the diagnosis of leprosy is frequently delayed because it may mimic other more common skin conditions. We present a case of borderline/lepromatous leprosy in an otherwise healthy young Brazilian man that was initially diagnosed as tinea versicolor, but did not respond to appropriate treatment. This case highlights the importance of having a high index of suspicion for leprosy in patients from endemic areas who present with lesions that could be consistent with this disease.


Leprosy, also known as Hansen Disease, is a gradually progressive infectious disease caused by Mycobacterium leprae, an acid-fast obligate intracellular bacterium. It is endemic in tropical and subtropical areas, with the highest prevalence in India, followed by Brazil. Leprosy has a broad spectrum of clinical presentations that are dependent on the host immune response, ranging from a single macular lesion to widespread nodules and plaques. In addition, a spectrum from minimal involvement of the peripheral nervous system to significant hypoesthesia and other neurological deficits may be present. M. leprae has a predilection for cool areas of the body, explaining the tendency of leprosy lesions to occur on the extremities, nose, and ears. In countries where leprosy is non-endemic, diagnosis is frequently delayed and patients may present to multiple specialists before obtaining the correct diagnosis [1]. We report the case of a Brazilian man who presented with what appeared to be typical tinea versicolor, but did not respond to appropriate treatment; he was eventually diagnosed with lepromatous leprosy after a skin biopsy was performed.

Case report

A 24-year-old healthy Brazilian man presented to a free medical clinic for evaluation of an asymptomatic rash that had been present for 2 years. He was previously healthy and did not have any significant medical history. Physical examination revealed hypopigmented macules symmetrically distributed over the upper trunk, coalescing in some areas to form larger patches. The clinical impression was suggestive of tinea versicolor, and the patient was empirically treated with two doses of oral ketoconazole 400 mg one week apart and selenium sulfide 2.5 percent lotion used as a body wash daily for 10 days. He was instructed to return to the clinic in two months if his eruption did not clear.

One year after his original presentation, the patient returned to the free clinic stating that his eruption was no better. He reported that when the eruption had not cleared after his initial treatment, he had taken a 30-day course of oral ketoconazole and a 10-day course of oral fluconazole, sent by his mother from Brazil. This regimen also failed to improve his eruption. He also reported that he was concerned that his left arm was becoming numb; he had sustained multiple burns on the left arm in the previous year without experiencing pain.

Figure 1Figure 2
Figure 1a. Hypopigmented macular lesions symmetrically distributed over the upper chest, abdomen, and back, coalescing in some areas to form larger patches. Figure 1b. Closer view of right upper back.

Figure 2. Multiple scars and post-inflammatory hyperpigmentation on the patient’s left arm. He had sustained multiple burns on the arm without experiencing pain.

Upon examination, the patient was now found to have widespread symmetrically distributed hypopigmented macules and patches on his chest, back, abdomen, and bilateral proximal upper extremities (Figure 1). There was decreased hair growth on the hypopigmented truncal areas and he was noted to have multiple scars and associated post-inflammatory hyperpigmentation on his left arm (Figure 2). On crude sensory testing, he had hypoesthesia on the dorsal aspect of his left arm extending from the mid-upper arm to the mid-forearm following a radial nerve distribution. There was no apparent loss of sensation over the areas of hypopigmentation on the trunk or shoulders. A potassium hydroxide preparation of scale from the hypopigmented patches was negative for spores or hyphal forms.

Figure 3Figure 4
Figure 3a. Specimen from the right chest shows a perivascular, periadnexal, and perineural mononuclear inflammatory infiltrate of lymphocytes, foamy histiocytes, and mast cells in the superficial and deep dermis. (H&E x40). Figure 3b. Higher magnification (x400) shows focally perineural mononuclear inflammatory infiltrate.

Figure 4. Affected skin from the left arm demonstrates numerous mycobacterial organisms within macrophages. (Fite stain x1000)

Punch biopsies were taken from affected areas of the chest and left arm. Histology revealed a perivascular, periadnexal, and focally perineural mononuclear inflammatory infiltrate of lymphocytes, foamy histiocytes, and mast cells in the superficial and deep dermis (Figure 3). The epidermis was unremarkable and a PAS stain was negative for fungal elements. A Fite stain revealed numerous mycobacterial organisms within macrophages (Figure 4). No well-formed granulomas were seen. The histopathological findings in combination with the clinical presentation were considered to be consistent with a diagnosis of Hansen disease (leprosy), classified as between the borderline and lepromatous types.

The patient was referred to a regional Hansen’s Disease Clinic, where in July 2012 he began a course of Rifampin (600 mg once daily), Clofazamine (50 mg once daily), and minocycline (100 mg once daily). Minocycline was chosen over dapsone because the patient was noted to have a glucose-6-phosphate dehydrogenase deficiency on pre-treatment blood testing. As of his most recent follow up in January 2013, his response to treatment had been very good, with fading of his multiple hypopigmented lesions and resolution of the raised borders. He continued to have anesthesia in areas of the left arm, but had not developed any new areas of anesthesia or hypesthesia. The patient’s wife and two children were screened for evidence of Hansen disease, but since they did not have any skin lesions or hypesthesia, they did not require treatment. They will be followed long term to ensure nothing develops.


Despite great strides in controlling leprosy since the World Health Organization (WHO) began a campaign against this disease in the 1990s, leprosy remains a public health problem in numerous tropical and sub-tropical countries, notably India, Brazil, Indonesia, and Bangladesh. Although the disease is not easily transmitted, its long incubation period and requirement for months to years of antibiotic treatment make eradication difficult. In 2010, the WHO reported 169 new cases in the United States and 228,474 new cases of leprosy worldwide [2]. About 74 percent of new cases in the United States occur among immigrants [3] and it is believed that armadillos, a zoonotic reservoir for M. leprae, are the main source of disease in cases contracted in the United States [4]. Although the prevalence of leprosy has decreased over the last 15 years, the incidence has risen, which may be the result of increased case detection campaigns and the expansion of leprosy services in endemic countries [5].

Clinically, leprosy presents as a chronic disease affecting the skin and nerves, with the extent of the disease depending on a person’s immune status and genetic factors [6]. It has been estimated that 5 percent to 10 percent of the population is susceptible to developing leprosy, and this predisposition has been found to correlate with HLA types DQ1, DR2, and DR3 [7]. Diagnosis is primarily clinical and is complemented by skin bacilloscopy and histopathology. A case of leprosy has been defined by the WHO as an individual who has not completed a course of treatment and has one or more of the following: 1) hypopigmented or reddish skin lesions with loss of sensation, 2) involvement of the peripheral nerves as demonstrated by thickening and associated loss of sensation, 3) a skin-smear that is positive for acid-fast bacilli [8].

The mechanism of hypopigmentation in leprosy is not well understood, but it has been hypothesized to be due to a lack of tyrosine resulting from overuse of this amino acid by M. leprae [9]. Because tyrosine is the substrate for tyrosinase, which catalyzes the rate-limiting step in melanin production by melanocytes, a lack of tyrosine could lead to hypopigmentation. An alternative explanation for hypopigmentation in leprosy is the disrupted transfer of melanosomes to keratinocytes [10].

The differential diagnosis of hypopigmented lesions in leprosy includes vitiligo, idiopathic guttate hypomelanosis, pityriasis alba, tinea versicolor, tinea corporis, post-inflammatory hypopigmentation, hypopigmented mycosis fungoides, morphea, pityriasis lichenoides chronica, nevus depigmentosus, pinta, and sarcoidosis. Distinguishing tinea versicolor from leprosy solely on the basis of clinical examination may be problematic because both conditions can present as symmetrical coalescing hypopigmented macules and patches on the upper trunk [11], as was the case in our patient. He had not developed sensory alteration in his hypopigmented lesions at the time of examination. Furthermore, tinea versicolor may coexist with leprosy and our patient may have initially had both leprosy and tinea versicolor. There is a higher reported incidence of tinea versicolor in leprosy patients than in the general population [12] and the two conditions can also co-localize [13]. Skin scrapings for fungal hyphae and spores are generally positive in cases of tinea versicolor, whereas skin bacilloscopy or biopsy showing acid-fast bacteria would confirm a diagnosis of leprosy. Our patient’s skin scraping and potassium hydroxide preparation may have been negative owing to his recent treatment with a long course of oral antifungal agents.

We present this case to remind clinicians that leprosy remains a public health issue in the United States, especially in regions with large numbers of immigrants from countries in which leprosy is endemic. Many common skin conditions, including tinea versicolor, can mimic leprosy and the diagnosis of leprosy may be delayed for years. Early recognition and treatment of leprosy is vital in the prevention of progression to disability and disfigurement.


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