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Diffuse Cutaneous Leishmaniasis in HIV

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Diffuse Cutaneous Leishmaniasis in HIV
Vandana Mehta MD DNB1, C Balachandran MD1, Raghavendra Rao MD1, Sumeet Kaur Dil MD2, Laxmi Indusri MD1
Dermatology Online Journal 15 (4): 9

1. Dept of Skin and STD, Kasturba Hospital, Manipal, Karnataka, India.
2. Dept of Pathology, Kasturba Hospital, Manipal, Karnataka, India


Cutaneous leishmaniasis is caused by the intracellular protozoan parasite belonging to the genus leishmania and is characterized by a myriad of clinical lesions including papules, nodules, and ulcers. Diffuse cutaneous forms of leishmaniasis are rare. We report a rare case from South India of diffuse cutaneous leishmaniasis masquerading as lepromatous leprosy in the context of HIV infection.


Cutaneous leishmaniasis is caused by an intracellular protozoan parasite belonging to the genus leishmania and is transmitted by the bite of a female sandfly. Diffuse cutaneous forms of leishmaniasis are rare. We report an HIV positive paitent with the unusual presentation of diffuse cutaneous leishmaniasis that was initially diagnosed as lepromatous leprosy leprosy, a more common disease in South India.

Case history

Figure 1Figure 2

A 30-year-old male driver from South India, diagnosed to be HIV positive for the past 8 years (being treated with ART), presented with an asymptomatic skin-colored eruption that had first appeared on his face 18 months prior. Before visiting us, this patient had received treatment with dapsone and fluconazole for about 1 year from several dermatologists in and around Kerala. However, there was only a temporary improvement and the papules and plaques subsequently increased in number and size and gradually spread to his ears, upper extremities, and lower extremities. There was no history of prior trauma, ulceration, systemic symptoms, or travel outside his state (Kerala) located in Southern India. Cutaneous examination revealed erythematous scaly infiltrated plaques over the forehead, malar area, and ears (Fig. 1). Small tiny skin-colored papules were seen infiltrating the moustache area and chin; a few umbillicated papules were present on the nape of the neck and dorsa of the hands (Figs. 2, 3, 4).

Figure 3Figure 4

Figure 5Figure 6

Multiple discrete, skin-colored, non- tender nodules were present bilaterally and symmetrically on the extensor forearms, knees, and elbows (Figs. 5, 6). The palms, soles and mucosa surfaces were unaffected. He had no systemic complaints and physical exam revealed neither pulmonary abnormalities nor organomegaly. The diagnosis of lepromatous leprosy, which is commonly encountered in India, was initially suspected. His complete blood count, urinalysis, hepatic and renal function tests, chest X-ray, ultrasound of abdomen, and lipid profile were within normal limits. CD4 T cell count was 684 cells/mm³. Slit skin smear for AFB was negative, but showed the presence of numerous macrophages harboring leishmania amastigotes (Fig. 7).

Figure 7Figure 8

Figure 9Figure 10

Biopsies from an unbillicated papule, nodule, and infiltrated plaque on the face revealed a dense dermal histiocytic infiltrate with round cytoplasmic microgranules of 1-2 microns in size admixed with an infiltrate of lymphocytes, plasma cells, and eosinophils (Figs. 8, 9, 10). Periodic acid-Schiff (PAS) stain revealed the presence of a dot-like structure reminiscent of a kinetoplast, confirming the diagnosis of cutaneous leishmaniasis. Treatment was commenced with rifampicin 600 mg daily and levamisole 300 mg weekly. ART was continued and the patient was advised to start on injections of Sodium Stibogluconate IM daily for 3 weeks. However, the medication is not available in India and due to the difficulty of obtaining the medication, it was not started. He experienced initial improvement on the rifampin and levamisole, but then some flaring was noted after which he was lost to follow-up.


Leishmaniasis is one of the top five diseases targeted by the WHO Special Program for Research and Training in Tropical Diseases. About 1.5 million new cases are documented each year and over 350 million people live in areas of active parasite transmission. Diffuse cutaneous leishmaniasis (DCL) is a rare anergic variant of localized cutaneous leishmaniasis in which the lesions are disseminated, resembling lepromatous leprosy (LL). The disease usually begins with an initial primary lesion and then subsequently disseminates to involve other areas of the body. Unlike LL, nerve involvement does not occur. Histologically there is a superabundance of parasites in the cutaneous nodules with a predominance of Leishman Donovan bodies. Internal organ involvement is not seen and the disease responds only partially to treatment; relapses are frequent and the condition generally becomes chronic [1]. In the New world, DCL has been associated with Leishmania pifanoi, L. amazonensis, L. mexicana and L. venezuelensis. However, in the in the Old world it has been associated with L. aethiopica, L. major and L. tropica [2].

Cutaneous leishmaniasis forms, in which a large number of lesions occur at several anatomically different sites, are usually secondary to an underlying deficiency in cellular immunity. Leishmania species can cause a wide spectrum of cutaneous lesions in HIV positive patients: localized cutaneous, mucosal, muco-cutaneous, diffuse cutaneous, or post-kala-azar leishmaniasis (PKDL). Several authors suggest that the dissemination of lesions in DCL is more determined by the immunogenetic background of the patient than by the virulence of the species involved [3]. It has been postulated that the antigen-specific immunosuppression observed in DCL and the resulting clinical picture could partially be due to the ability of the infecting parasite to induce a predominance of interleukin-10 over interferon gamma [4]. Our case was HIV positive and this probably increased the disease severity and morbidity. Lepromatous leprosy and PKDL are endemic in India. LL in our patient was ruled out by the absence of hypoaesthesia and a negative Ziehl's stain. In PKDL, cutaneous lesions accompany or follow visceral leishmaniasis caused by L. donovani. Post-kala-azar leishmaniasis was ruled out in our patient because he hailed from an area non-endemic for kala azar, there was no history of kala azar in the past, and there were no hypopigmented macules, hepatosplenomegaly, lymphadenopathy, or any other sign of visceral leishmaniasis.

Systemic pentavalent antimonials (sodium stibogluconate and meglumine antimoniate) have been used as the standard first-line treatment for cutaneous leishmaniasis since 1929. However, they are available only parentally and the injections are painful, toxic, and unaffordable in most endemic areas. In addition, leishmanial resistance to antimonials has been reported; several courses of treatment may be necessary. Apart from antimonials, only anecdotal reports exist about use of liposomal Amphotericin B, miltefosine, and itraconazole in the treatment of CL. Diffuse cutaneous forms have a chronic relentless course and are usually refractory to treatment [5, 6]. This was also evident in our case; the lesions initially had reduced with treatment, only to flare up once again. To conclude, DCL should be suspected in areas where both HIV and leishmania infection are endemic and effective treatment will likely require simultaneous treatment of the two infections.


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