Study of the 2 cases of cutaneous leishmaniasis

Study of the 2 cases of cutaneous leishmaniasis Mittal A, Pandya V, Parmar KS, Bilimoria F E - Indian J Dermatol

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Year : 2005 | Volume : 50 | Issue : 4 | Page : 233-235

Study of the 2 cases of cutaneous leishmaniasis

Amita Mittal, Vishvabhavan Pandya, Kirti S Parmar, FE Bilimoria
Department of Dermatology, Civil Hospital and BJ Medical College, Ahmedebad-16., India

Correspondence Address:
Amita Mittal
Department of Dermatology, Civil Hospital and BJ Medical College, Ahmedebad-16.
India

Abstract

Two cases of cutaneous leishmaniasis are presented here because of its rare association with HIV infection

Keywords: Leishmaniasis, Cutaneous Leishmaniasis, HIV infection.

How to cite this article:
Mittal A, Pandya V, Parmar KS, Bilimoria F E. Study of the 2 cases of cutaneous leishmaniasis. Indian J Dermatol 2005;50:233-5

How to cite this URL:
Mittal A, Pandya V, Parmar KS, Bilimoria F E. Study of the 2 cases of cutaneous leishmaniasis. Indian J Dermatol [serial online] 2005 [cited 2014 Mar 7];50:233-5. Available from: http://www.e-ijd.org/text.asp?2005/50/4/233/19753

Introduction

Leishmaniasis is the result of infection with intracellular protozoan parasites belonging to the genus Leishmania . The vector responsible is sandfly belonging to the genus Phlebotomus or Lutzomyia. The infection causes a wide spectrum of clinical changes. We report two cases of leishmaniasis because of its rarity and association with HIV infection.

Case Reports

Case 1

A 35 years old patient from Rajasthan reported to us with skin lesions of 13 month duration. Lesions were papules to begin with which first started from tip of the nose then spreading to the rest of the body. Later they turned into crusted plaques and nodules of varying size.

On examination, there were multiple crusted plaques and nodular lesions which were chiefly asymptomatic. Many of them were accompanied by satellite lesions. There was no lymphadenopathy or

hepato-splenomegaly.

Interestingly there were nodular lesions on the dorsa of the tongue. AFB smear for lepra bacilli, serum VDRL in serial dilution and m0 antoux test were negative. Patient was reactive for HIV with latest CD4 count 224.

A biopsy, both from cutaneous lesions as well as from tongue was performed for H & E stain. Multiple amastigotes of leishmania organism were observed intracellularly, chiefly in dermal macrophages along with lymphocytic infiltrations.

Case 2

A 42 year old farmer from Bihar presented to us with multiple nodular lesions of one and half year duration. Lesions were asymptomatic and insidious to develop. He also had past history of visceral kala-azar ten years back.

On examination, the lesions were papulo-nodular mainly on dorsum of both hands. There was no lymphadenopathy. Liver and spleen were moderately enlarged.

Specific investigations were undertaken to rule out leprosy, cutaneous tuberculosis and syphilis. Histopathological examination of a punch biopsy specimen showed the typical changes of cutaneous dermal leishmaniasis showing the large number of intracellular leishmania organism.

Treatment :- Both the cases were given ketoconazole 400mg/day. Case-1 was also given ART. (AZT300mg BD+ Lamivudinel 50mg BD + Nevirapine200mg OD) with the other prophylactic drugs for other opportunistic infections (Septran, INH).

Discussion

The infection causes a wide spectrum of clinical changes that divide leishmaniasis into four broad divisions based on the extent and severity of involvement in the human host: cutaneous leishmaniasis (CL), diffuse cutaneous leishmaniasis (DCL), mucocutaneous leishmaniasis (MCL), and visceral leishmaniasis (VL).

CL is a zoonosis found in widely scattered parts of Asia, Africa, and Europe, largely in tropical and subtropical zones, and in much of the Middle East, especially Iran, Iraq, eastern Saudi Arabia, the Jordan Valley (of Israel and Jordan) and the Sinai Peninsula.[3]

The disease begins as a small erythematous papule, which may appear immediately after the bite of the sandfly but usually appears 2 to 4 weeks later. The papule slowly enlarges in size (2 cm or more) over a period of several weeks and assumes a more dusky violaceous hue.

Eventually the lesion becomes crusted at the center. When the crust is removed, a shallow ulcer is found, often with a raised and somewhat indurated border. In some cases the central part of the nodule becomes hyperkeratotic, and a firmly adherent horn develops over the lesion. Small satellite papules may also be found at the periphery of the lesion. Occasionally subcutaneous nodules develop along the course of the proximal lymphatics.[4]

In acute CL the epidermal changes are highly variable and can range from atrophy or ulceration to hyperplasia, which may be pseudoepitheliomatous. The most constant feature is a diffuse dermal inflammatory cell infiltrate composed of varying proportions of histiocytes, lymphocytes, plasma cells, and neutrophils. Specific diagnosis requires identification of amastigotes within the cytoplasm of dermal macrophages.[5]

In chronic CL the dermal infiltrate is nodular and is characterized by tuberculoid-type histiocytic granulomas with lymphocytes and plasma cells surrounding them. Amastigotes are usually not detectable. Necrosis rarely occurs. This histology generates a differential diagnosis that includes other causes of tuberculoid type granulomas such as lupus vulgaris, tuberculoid leprosy and granulomatous rosacea. A specific diagnosis at this stage requires clinicopathological correlation.[5]

Gujarat is a non-endemic region for the leishmaniasis. Case-I was reported from Rajasthan which is also a non-endemic region. This uncommon presentation led us to think about some state of compromised immuner status and later it was confirmed to be HIV positive. The case-2 was from Bihar which is quite an endemic place for an cutaneous leishmaniasis. He had a clear past history of visceral Kalazar 10 years back.[6]

Both the cases are now in our regular follow-up in which the case-2 improved to a great extent but case-1 only improved a little.

References

1.	Walters LL, Modi GB, Tesh RB, Ultrastructural biology of Leishmania (viannia panamensis=Leishmania brazillensis panamesis) in Lutzomyia gomezi (Diptera:Psychodidac): a natural host-parasite association. Am J Trop Med Hyg 1989; 40: 19-39.
2.	Mon talban CK, Martinez-Fernandez R, Calleja JL, et al. Visceral leishmaniasis (kala-azar) as an opportunistic infection in patients infected with the human immunodeficiency virus in spain. Rev Infect Dis 1989;11: 655-60.
3.	Bryceson ADM. Immunological aspects of cutaneous leishmaniasis. Essays on Tropical Dermatology1972: 230.
4.	Sidney N. Klaus, Shoshana Frankenburg, A. Damian Dhar, et al. Leishmaniasis and othe Protozoan Infection. In: IM Freedberg AZ Eisen, Klaus Wolff, et al., eds. Fitzpatrick's Dermatology in General Medicine. 6th end. McGraw Hills, 2003; 2(6): 2215-20.
5.	Sengupta PC, Bhattacharjee B. Histopathology of post kala-azar dermal leishmaniasis. J Trop Med Hyg 1953;56: 110-6.
6.	Rashid JR, Chunge CN, Oster CN, et al. Post kala-azar dermal leishmaniasis occurring after long cure of visceral leishmaniasis in Kenya. E Afr Med J 1986;63:365-71.