Fine-needle aspiration cytology of leishmanial lymphadenitis in an HIV-reactive patient: Report of a rare case.

Lymphatic leishmaniasis is a rare parasitic disease even in endemic region. It is usually associated with visceral and post-kala-azar dermal leishmaniasis. Leishmaniasis is being increasingly recognized in association with immunodeficient patients (HIV/AIDS). However, leishmanial lymphadenitis has been rarely diagnosed by fine-needle aspiration cytology (FNAC) of epitrochlear lymph node in an HIV patient. Cytological features of leishmanial lymphadenitis in an HIV-reactive patient have been rarely addressed in previous literature. We present the FNAC of a case of leishmanial lymphadenitis in epitrochlear lymph node in the case of an HIV-reactive patient with visceral leishmaniasis.

INTRODUCTION

Leishmaniasis is a parasitic disease caused by a protozoan called “Leishmania sp.” and it is transmitted by “sandfly.”[1] It is an endemic disease in the tropical and subtropical regions of South America, Southern Europe, as well as Eastern India.[23] Leishmaniasis is categorized under several manifestations – visceral, cutaneous, and mucosal.[1] The parasite affects the macrophages of mononuclear phagocyte system and increased incidence seen in malnutrition, immunosuppression, and HIV infection.[13] Leishmaniasis is an emerging opportunistic coinfection in HIV-positive patients in endemic areas.[4] Diagnosis of the cases often delayed due to lack of awareness and uncommon presentation.[4] Demonstration of Leishman–Donovan (LD) bodies in lymph node by fine-needle aspiration cytology (FNAC) has rarely been reported in visceral leishmaniasis.[5] We describe a rare case of cytology of leishmanial lymphadenitis involving epitrochlear lymph node in a case of HIV-reactive visceral leishmaniasis.

CASE REPORT

A 38-year-old male patient presented to the Medicine Department with a history of low-grade fever, weight loss, and anorexia for the past 6 weeks. General examination revealed mild pallor, splenomegaly, and mild hepatomegaly with discrete enlarged lymph nodes at the right epitrochlear area and right cervical region. He was advised for all necessary investigations including FNAC of the lymph nodes. All biochemical tests were within normal limits, except mild elevation of liver enzymes (serum glutamic pyruvic transaminase – 60 IU/L, serum glutamic oxaloacetic transaminase – 53 IU/L, lactic dehydrogenase – 370 IU/L). On hematological examination, he had a hemoglobin level of 10.2 g% and erythrocyte sedimentation rate (ESR) was elevated (ESR – 68 mm/h). On serology screening, he was reactive to HIV I.

FNAC was performed from both cervical and epitrochlear lymph nodes with a 24G needle attached with 20 cc syringe. The smears were stained with Leishman–Giemsa stain and Ziehl–Neelsen stain. The smears showed polymorphous cell population, comprised of reactive lymphoid cells, histiocytes, isolated epithelioid cells, many tangible body macrophages, and macrophages filled with leishmania amastigote form [Figures 1 and 2]. Subsequently, he had undergone bone marrow examination and the smears revealed high parasitic load of amastigote form of leishmania in the bone marrow smears (parasite load – [5+]). The diagnosis was established as visceral leishmaniasis with leishmanial lymphadenitis with HIV-reactive status. He was treated with stibogluconate for 28 days with antiretroviral therapy.

Figure 1

Cytology of lymph node showing polymorphous population of lymphoid cells, isolated epithelioid cells, and plenty of extra- and intracellular Leishman–Donovan bodies (Leishman and Giemsa stain, high-power view)

Figure 2

Cytology of the lymph node revealing intra- and extracellular Leishman–Donovan bodies and macrophages (Leishman and Giemsa, high-power view)

DISCUSSION

Visceral leishmaniasis is endemic in different areas of India and also in many Mediterranean countries.[1] It is a chronic infection of monocyte–macrophage system. Commonly, the patients of visceral leishmaniasis present with fever, abdominal pain, hepatosplenomegaly, cachexia, and pancytopenia.[13] However, concomitant visceral leishmaniasis presenting with lymphadenopathy with HIV infection is rare and rarely diagnosed by FNAC of the epitrochlear lymph node. Generalized lymphadenopathy is an important presenting feature of HIV infection and lymphadenopathy is also not uncommon in leishmaniasis. The causes of lymphadenopathy in HIV patients are multifactorial. Most often, lymphadenopathy is due to the disease itself, but secondary causes such as tuberculosis, fungal infections, and lymphoma are also common.[456] Microscopically, most of the leishmanial lymphadenopathy did not produce LD bodies. They exhibit reactive lymphoid hyperplasia or granulomatous reaction which can be misinterpreted as tuberculous origin. Kumar et al. found five types of cytological findings in leishmanial lymphadenitis cases: (i) acute inflammatory with giant cells, (ii) histiocytic granuloma, (iii) epithelioid granulomas, (iv) plasma cell types, and (v) mixed histioplasmacytic type.[7] Sah et al. found LD bodies in 90.47% (19 cases out of 21 cases) of lymphadenopathy cases in visceral leishmaniasis and post-kala-azar dermal leishmaniasis (PKDL).[5] In their series, the prevalence of lymphadenopathy was only 12.35% of visceral leishmaniasis and PKDL.[5] The presence of LD bodies in aspirate is pathognomonic of leishmanial lymphadenitis, which may or may not be associated with visceral leishmaniasis and PKDL.[5] Microscopically, LD bodies are small, round/ovoid structures of 2–5 μm (diameter) with fine membrane and central round nucleus and rod-shaped kinetoplast.[4] In FNAC smears, there will be intra- and extracellular LD bodies with nonnecrotic granulomatous reaction, histiocytes, plasma cells, and giant cell formation.[25]

Sometimes, other infectious agents such as Toxoplasma, Histoplasma, Paracoccidioides, and Cryptococcus may be morphologically misinterpreted as LD bodies in lymph node aspirates.[578] These differential diagnoses are important in cytological evaluation of lymph node aspirates in HIV patients.

Prognosis of leishmanial coinfection with HIV patients is poor (average survival reduced) than other HIV patients. Sodium stibogluconate is the first-line therapy. Amphotericin B has been found to be more effective and less toxic than others in the treatment of visceral leishmaniasis with immunosuppression.[8]

CONCLUSION

Leishmaniasis is a rare cause of lymphadenopathy but should be considered as a differential diagnosis, particularly in endemic region. Visceral leishmaniasis may be a secondary cause of lymphadenopathy and pyrexia of unknown origin in HIV patients. Cytology diagnosis is an excellent tool for the management of leishmanial lymphadenitis.

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Conflicts of interest

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