Kala Azar Associated With Malaria

A 22-year-old man presented with complaints of mild- to moderate-grade fever with chills and rigor, cough with scanty expectoration, and progressive weight loss of 1 month's duration. On examination, he was pale, febrile, and had normal vital signs. Multiple superficial lymph nodes in the cervical and axillary regions were palpable, varying from 1.5 to 2.5 cm in diameter. The glands were nontender, matted, firm, and mobile. Liver and spleen were enlarged 2 and 3 cm below the costal margin, respectively. Other systems were normal. A clinical diagnosis of disseminated tuberculosis was considered.

Laboratory investigations revealed the following values: hemoglobin, 5.2 g/dL; total leukocyte count, 3400/mm3, with a differential count of 57% polymorphs, 41% lymphocytes, and 2% monocytes. Erythrocyte sedimentation rate (Westergren) was 76 mm in the first hour, and the platelet count was 1 50 000/mm3. Peripheral blood smear showed normocytic hypochronic to macrocytic red cells, neutrophils with prominent toxic granules, and no malarial parasite. Results of a Mantoux test and sputum test for acid-fast bacilli were negative. Blood culture was sterile. Bone marrow aspirate revealed a hypercellular marrow with macronormoblastic reaction. Megakaryopoiesis was normal. Few giant myelocytes and metamyelocytes were seen. Leishman-Donovan (L-D) bodies were seen extracellularly (arrow), along with ring form of Plasmodium falciparum (Figure 1). Hemophagocytosis with hemophagocytosed L-D bodies (Figure 2, a) was also seen with gametocytes of P falciparum (Figure 2, b).

Fine-needle aspiration biopsy of left cervical lymph node showed multiple intracellular, as well as extracellular, L-D bodies in a polymorphous background. Results of kidney and liver function tests were within normal limits. The case was diagnosed as visceral leishmaniasis with leishmania lymphadenitis and coexistent falciparum malaria. The patient was treated with quinine, 10 mg/kg for 7 days. The fever decreased in intensity, but did not reach baseline. He received sodium stibogluconate, 20 mg/kg/d deep intramuscularly for 30 days, and 3 units of whole blood following quinine therapy. After the sixth day of sodium stibogluconate therapy, he was afebrile. At the end of the antimonial therapy, the bone marrow aspirate did not show any L-D bodies or malarial parasites, and there was no residual lymphadenopathy. Results of pretherapy and posttherapy renal function tests, and electrocardiographs performed before the treatment, during treatment, and during follow-up of the patient remained normal.

Kala azar caused by Leishmania donovani and malaria due to P falciparum and Plasmodium vivax are endemic in the Southern Terai (plain areas) of Nepal. Kala azar with chronic malaria in undernourished children was known as “malaria cachexia” in Imperial India. Despite high endemicity of both kala azar and malaria in India, Nepal, and elsewhere, concomitant infection of both these parasites is rarely reported these days.1,2 Kala azar and malaria have different immunologic spectra of illness. Chronic kala azar is known to cause CD4 lymphopenia and a low CD4-CD8 ratio, whereas the blood CD4-CD8 ratio remains unaltered during malarial paroxysms.2 Therefore, it seems kala-azar–mediated CD4 lymphopenia may have nullified the protective immunity against malaria in our case.

Infection-associated hemophagocytic syndrome in Western countries is commonly due to viral infections. Hemophagocytic syndrome associated with visceral leishmaniasis and P falciparum is common in other tropical countries. To our knowledge, only 2 cases of hemophagocytic syndrome induced by P falciparum have been reported to date.3 Indian kala azar is usually not accompanied by lymph node enlargement, although this is a common feature in Mediterranean countries, Africa, and China. Our patient had multiple enlarged lymph nodes in cervical and axillary regions. Fine-needle aspiration cytology of left cervical lymph node revealed L-D bodies.