Visceral leishmaniasis (VL) or kala-azar, caused by Leishmania donovani, L. chagasi or L. infantum, is endemic in 62 countries (1). An estimated 500,000 cases per year and over 90 per cent of cases of VL occur in five countries: India, Bangladesh, Nepal, Sudan, and northeastern Brazil (1,2). India has about 50 per cent of the global burden of VL, and eastern states Bihar, Jharkhand, East Uttar Pradesh and West Bengal are endemic for the disease, though sporadic cases occur across the country (3). About 90 per cent of these patients are poor and live in the rural areas of Bihar State (3,4). It is reported that the incidence and prevalence of this diseases remain high in these areas probably due to low socio-economic status of the inhabitants (4,5). Low socio-economic status has wide repercussions on the societal and personal health of the individuals including the malnutrition, which ultimately leads to compromised host immune status (6,7). Malnutrition as such is a complex condition involving deficiency of protein and energy with superimposed deficits of other essential trace elements and nutrients. It alters the innate immune response and is reported to be the most frequent cause of immunodeficiency (8). Epidemiological and experimental studies have documented an increased risk for VL, in the malnourished hosts (6,9). Although, information about the possible mechanisms for immunity in human VL is limited, it is well documented that for establishment of the infection L. donovani evades both the innate and adaptive arms of the immune system. It is also increasingly being recognized that humoral immunity is largely ineffective in containment of the disease and cell mediated immunity is essential (6,10). A strong correlation has been shown between disease outcome and the nature of the T cell response. In an experimental study Leishmania infection in murine model resulted in the development of Th1/Th2 paradigm polarization of immunity (11).