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QJM. 2016 May; 109(5): 347–348.
Published online 2016 January 21. doi:  10.1093/qjmed/hcw005
PMCID: PMC4888333

Visceral Leishmaniasis: Kala-azar

R.V. Nampoothiricorresponding author
Department of Internal Medicine, Post Graduate Institute of Medical Education and Research, Chandigarh 160012, India
S. Sreedharanunni
Department of Hematopathology, Post Graduate Institute of Medical Education and Research, Chandigarh 160012, India

A 30-year-old male from rural northwest India presented to our hospital with fever of 4 weeks duration associated with abdominal pain. He was a farmer by occupation and gave history of sleeping in the open. General physical examination showed pallor and subcentimetric cervical lymphadenopathy. Abdominal examination revealed massive splenomegaly (14 cm below left costal margin). Liver was palpable 4 cm below right costal margin with a span of 15 cm. Investigations revealed pancytopenia, with hemoglobin of 6.2 g/dl (13.3–16.2 g/dl), total leukocyte count of 3500/cu mm (4000–11 000 cells/µl) and platelet count of 68 000/µlitre (150 000–400 000 platelets/µl). Polyclonal hypergammaglobinemia was noted with globulin fraction—5.3 g/dl (2.0–3.5 g/dl). Liver function tests and renal function tests were normal. Routine bacteriological cultures were sterile and chest radiography was normal. A bone marrow examination done, showed characteristic features (Figure 1A and B) which clinched the diagnosis.

Figure 1.
(A) Bone marrow aspirate smears showing amastigote forms of Leishmania Donovani (May-Grunwald-Giemsa, 100×). The kinetoplasts are highlighted by black arrows. (B) Bone marrow trephine biopsy showing intracellular amastigotes (Hematoxylin and eosin; ...

Visceral Leishmaniasis (Kala-azar) is a vector borne tropical infection caused by protozoans belonging to the genus Leishmania. The vector for transmission of the disease is the sandfly (Phleobotomus and Lutzomyia species). The disease is endemic in rural India, Nepal, Bangladesh, Sudan and Brazil.1

In visceral leishmaniasis, the protozoan infects the fixed and circulating phagocytic cells (macrophages and monocytes) involved in the immune response of the patient. The flagellate promastigote form is transmitted by the bite of the sandfly which transforms into the aflagellate amastigote form after phagocytosis by the macrophages of the liver, spleen and bone marrow. The intracellular amastigote form, also called the Leishman–Donovan (LD) body is oval, 2–5 µm in length and can be identified on microscopy by the presence of a nucleus and the extranuclear densely staining kinetoplast.2

Principal method of diagnosis is by the demonstration of amastigotes, i.e. LD bodies, either in the bone marrow or splenic aspirate. Demonstration of amastigotes within the splenic/bone marrow smear carries a specificity of 100%. Bone marrow aspiration is the preferred method of demonstrating amatigotes but its sensitivity is about 60–85%. Splenic aspirate, although having a sensitivity exceeding 95%, is not preferred due to the lack of expertise in most centres and the risk of fatal hemorrhage in a thrombocytopenic setting that is prevalent in most patients of visceral leishmaniasis.3 A rapid immunochromatographic test to detect antibodies against the K39 antigen, found in amastigote forms of all Leishmania species, can be performed as a screening test.4 rK39 is the recombinant K39 antigen cloned in Escherichia coli.

Liposomal amphotericin B is the only drug approved by the U.S. Food and Drug Administration (FDA) for the treatment of visceral leishmaniasis. The dose of the liposomal preparation is 3 mg/kg for 7 days (days 1–5, 14 and 21). In view of its high cost, amphotericin B deoxycholate and sodium stibogluconate are the first choice agents in India and other endemic areas, respectively. Other drugs that have been tried with moderate success include paramomycin and oral miltefosine.5

Our patient improved on treatment with Liposomal amphotericin B using the above-mentioned regimen and was discharged in 3 weeks following complete resolution of symptoms.

Conflict of interest: None declared.


1. Murray HW. Kala-azar–progress against a neglected disease. N Engl J Med 2002; 347:1793–4. [PubMed]
2. Varma N, Naseem S. Hematologic changes in visceral leishmaniasis/kala azar. Indian J Hematol Blood Transfus 2010; 26:78–82. [PMC free article] [PubMed]
3. Sundar S, Rai M. Laboratory diagnosis of visceral leishmaniasis. Clin Diagn Lab Immunol 2002; 9:951–8. [PMC free article] [PubMed]
4. Boelaert M, Verdonck K, Menten J, Sunyoto T, van Griensven J, Chappuis F., et al. Rapid tests for the diagnosis of visceral leishmaniasis in patients with suspected disease. Cochrane Database Syst Rev 2014; 6:Cd009135. [PMC free article] [PubMed]
5. Meyerhoff A. US. Food and Drug Administration approval of AmBisome (liposomal amphotericin B) for treatment of visceral leishmaniasis. Clin Infect Dis 1999; 28:42–8. discussion 9-51. [PubMed]

Articles from QJM: An International Journal of Medicine are provided here courtesy of Oxford University Press