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Cutaneous Leishmaniasis
 
Sangeeta B Kulkarni (Bhide)*, Ila M Vora**, Rajiv Rajmohanan***
 
Leishmaniasis is a parasitic infection caused by species leishmaniae, which can produce two types of manifestations-visceral and cutaneous. In India visceral leishmaniasis is more common than cutaneous leishmaniasis. A case of primary cutaneous leishmaniasis from a veterinary doctor is presented for its rarity.
 
Introduction

Leishmaniasis is a parasitic infection caused by species leishmania which belongs to family Trypanosomatidae, which can cause two types of manifestations- visceral and cutaneous.1-3 In India more commonly visceral type of Leishmaniasis caused by Leishmania Donovani is seen.2 Visceral Leishmaniasis (VC) also known as ‘Kala azar’ is a systemic disease. Since Leishmania Donovani infects and proliferates in the reticuloendothelial system, organs like bone marrow, spleen, lymph node, liver etc. are commonly evaluated for demonstration of parasite.1,3

A case of primary cutaneous leishmaniasis is presented here due to its rarity.

 
Case History

A 45-year-old male veterinarian doctor working in the Middle East presented with a boil in the right shoulder for more than six months duration. The boil was 1.0 X 1.0 cm in size, yellowish white in colour and was slowly increasing in size. There was no history of pain and tenderness. The boil did not discharge any secretions. The rest of the skin was normal. He had no history of fever, weight loss or weakness. There was no other systemic complaint. On clinical examination, he had no significant abnormality. On investigations, chest X-ray did not show any abnormality. Routine investigations were within normal limits. An excision biopsy of the lesion was done and routine histopathological examination was done.

Gross examination showed two firm tissue bits measuring 1.0 X 1.0 cm covered by skin. Cut surface was grey-white.

Microscopically, sections studied showed skin with subcutaneous tissue. Epidermis was lined by stratified squamous epithelium. Dermis showed heavy lympho-histiocytic and plasmacytic infiltration. There were few neutrophils and foci of lymphoid follicles. There were extensive areas of granulomas consisting of histiocytes or macrophages and occasional multinucleate giant cells, resembling Langhan’s type of cells (Fig. 1). At places some of them showed central area of minimal necrosis. No typical epithelioid cells were seen.

The histiocytes showed round to oval organisms resembling Leishmania intracellularly. Similar organisms were seen extracellularly also.

Giemsa stain showed organisms having rounded bodies with nucleus and a small kinetoplast resembling Leishmania. (Fig. 2)

PAS and GMS were done and was negative ruling out Histoplasmosis. Zeihl Neelsen stain was negative for Acid fast bacilli.

The diagnosis of cutaneous leishmaniasis was made. Bone marrow examination was suggested, which did not show any leishmania donovani bodies.


Fig. 1 : Photomicrograph showing granulomatous reaction and lymphocytes at periphery. (Haematoxylin and Eosin - X 160)

Fig. 2 : Photomicrograph showing lymphohistiocytic infiltration and Leishmania                 Donovani bodies intracellularly as well as extracellularly.
(Arrows) (Giemsa stain - X 400)
 
Discussion

The cutaneous leishmaniasis is divided into the OLD WORLD and NEW WORLD cutaneous leishmaniasis.3,4

The old world cutaneous leishmania (OWCL) comprise three species – Leishmania tropica, Leishmania major and Leishmania aethiopica.3,4 The areas of disease are Middle East, Northern Africa, Sub Saharan Africa, East Asia and Southern Europe.3,4

The species of cutaneous leishmaniae of the NEW WORLD are more numerous and more difficult to classify. They produce disease that are more chronic than old world. The species are – Leishmania braziliensis, Leishmania Mexica, Leishmania guyanensis, Leishmania panamensis, Leishmania peruviana. The areas of disease are South America and the Carribean Islands where the preferred term is ‘Tegumentary’ or mucocutaneous leishmaniasis.

Morphologically and histologically the cutaneous leishmania of the old and new world are similar.3 Transmission of disease to humans occurs through the bite of an infected sandfly.3,4, In general they produce a benign, limited disease in the exposed parts of skin with a tendency to heal spontaneously and leave the host with resistance to reinfections by the same species.3 The infection begins as a reddish papule at the site of the bite progressing to induration and ulceration often called as tropical sore.1-4 This patient presented with a boil on the right shoulder.

In diffuse cutaneous leishmaniasis, which is rare form of dermal infection begins as single skin nodule and spreads until the entire body is covered by bizarre nodular lesions.4

The diagnosis of cutaneous leishmaniae is usually made on clinical grounds like endemic area, clinical presentation and origin of the patient.3 This disease is diagnosed by demonstrating organisms from smears prepared from materials aspirated with a syringe or scrapings from bottom of the ulcer or biopsy of an ulcer.1,3,5,6

The smears are stained by Giemsa stain at pH – 7.2 which bring out the Leishnania Donovani (LD) bodies prominently.1,3,5,6 In positive smears the amastigotes are found intracellulary in macrophages.

The initial lesion is studded with the organisms with no granulomatous reaction. As the lesion progresses to chronicity for more than six months to 1–2 years, it shows less or no organisms and may show granulomatous reaction.1,4,7 In this case histopathological findings were similar to chronic lesion.

Cultures are optional and are not required for diagnosis unless species infecting the patient needs to be identified.3
Highly sensitive noninvasive molecular and antigen detection methods are evaluated and made available routinely, still tissue demonstration of Leishmaniae Donovani bodies remains the method of choice.5,6,8

In summary, primary cutaneous Leishmaniasis is a rare disease and the diagnosis can be made on clinical grounds, characteristic appearance of Leishmania organism on histopathology and Giemsa stain.

 
References
1. Jacob M, George R, George S, Kuruvillas S. Diseases caused by parasitic worms and protozoa. In : Valia RG, Valia AR, editors. Textbook and Atlas of Dermatology. 1st ed. Bombay: Bhalani publishing house, 1994; 1: 311-50.
2. Chatterjee KD. Subphylum Sarcomastigophora. In: Chatterjee KD, editor. Parasitology, Protozoology and Helminthology in relation to clinical medicine. 12th ed. Calcutta: Chatterjee Medical Publishers, 1980; 14-69.
3. Gutierrez Y, Lichtenberg FV. Protozoal diseases. In: Damjanov L, Linder J, editors. Anderson’s Pathology. 10th ed. St Louis: Mosby-year book, Inc., 1996;1: 985-1011.
4. Samuelson J, Lichtenberg FV. Infectious diseases. In : Cortan RS, Kumar V, Robbins SL, editors. Robbins Pathologic basis of disease, 5th ed. Philadelphia: W.B. Saunders Company, 1994; 305-77.
5. Giudice PD, Marty P, Lacour JP , Perin C, Pratlog F et al. Cutaneous Leishmaniasis due to Leishmania infantum. Arch Dermatol 1998; 134 : 193-98.
6. Shahi SK Ranga S, Thakur P, Khurana SK, Talib VH. Laboratory diagnosis of Viscral Leishmaniasis. Indian J Pathol Microbiol 1998; 41(3) : 361–72.
7. S. Lucas. Pathology of tropical infections. In : McGee JO’D, Isaacson PG, Wright NA editors. Oxford textbook of Pathology. 1st ed. New York: Oxford University Press, 1992; 2b : 2189-2254.
8. Anand M, Kumar R, Malhotra OP, Sing S. Amastigote forms of Leishmania Donovani in peripheral blood. Indian J Pathol Microbiol 2004; 47(2) : 307.