Visceral Leishmaniasis

Synopsis

Visceral leishmaniasis (VL) is a systemic protozoal disease. It is considered one of the “neglected tropical diseases” by the World Health Organization (WHO). It is commonly called kala-azar (meaning “black fever” in Hindi) because some cases of VL, particularly in India, have been associated with generalized skin hyperpigmentation. It is also known as Dumdum fever and Assam fever.

The majority of cases (>90%) of VL are found in the following areas of the world: Eastern India, Nepal, Bangladesh, Sudan, South Sudan, Brazil, and Ethiopia. It disproportionately affects impoverished individuals.

Two species of Leishmania, Leishmania donovani and Leishmania infantum (known as Leishmania chagasi in South America), are causative agents for almost all cases of VL. The disease is transmitted by the bite of an infected sandfly. The parasite exists in 2 forms: the amastigote form (in humans) and the promastigote form (in sandflies). The amastigote form is a round or oval structure that consists of a nucleus and a DNA-containing body called the kinetoplast. The parasite has a predilection to infect the mononuclear phagocyte system (MPS), previously termed the reticuloendothelial system.

The incubation period varies from weeks to months. While the majority of infections tend to be subclinical, when symptomatic the disease often runs an insidious course and presents with fevers, weight loss, malnutrition, and hepatosplenomegaly. Lymphadenopathy is often seen in VL encountered in Sudan but is less common in India. Patients often appear emaciated, and children may present with growth retardation and severe wasting. VL may present acutely with high fevers, though this is not a common presentation.

Immunocompromised hosts such as HIV patients and organ transplant recipients are at increased risk for disseminated disease and multiorgan involvement. In fact, some cases of subclinical infection may surface when immunity wanes.

Look For

Clinical findings of fever, anemia, malnutrition, and emaciation are nonspecific but should raise suspicion of VL in endemic regions. As previously noted, skin hyperpigmentation may be seen in VL in India and could serve as a clue to the diagnosis.

Clinical signs and laboratory findings suggest involvement of the MPS. Splenomegaly, seen more often than hepatomegaly, may be moderate to severe and should heighten probability and suspicion in the right clinical setting. Lymphadenopathy is seen in VL in Sudan. Anemia, leukopenia, and thrombocytopenia are seen in the advanced stages of the disease.

Liver function tests are variably elevated. As in many other chronic diseases, there tends to be hypoalbuminemia and hypergammaglobulinemia, resulting in a decrease in albumin-globulin (A/G) ratio.

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