Kala-azar, or Visceral Leishmaniasis (VL), is a parasitic disease that poses a public health challenge in tropical and subtropical regions. The name “Kala-azar” translates to “black fever” in Hindi, referring to the darkening of the skin sometimes seen in affected individuals. Caused by a protozoan parasite, it is the second-largest parasitic killer worldwide, surpassed only by malaria. If left without medical intervention, the disease is associated with a fatality rate exceeding 95%. It is highly endemic in parts of East Africa, Brazil, and the Indian subcontinent, with an estimated 50,000 to 90,000 new cases occurring annually.
The Parasite and Transmission Cycle
The disease is primarily caused by the protozoan parasite Leishmania donovani, which is transmitted to humans through the bite of an infected female phlebotomine sand fly. The sand fly acts as the vector, requiring a blood meal to produce its eggs. During this feeding process, the insect can ingest the parasite from an infected human or animal reservoir.
Once inside the sand fly, the parasite multiplies and transforms into an infective stage, called the metacyclic promastigote, which then moves to the insect’s mouthparts. When the infected fly subsequently bites a new mammalian host, it regurgitates the parasites, along with its saliva, into the skin. The parasites then migrate and target internal organs, hosted within the macrophages of the human body. The geographical distribution of Kala-azar is linked to the habitat of the specific species of sand fly that transmits the parasite. In the Indian subcontinent, transmission is anthroponotic, meaning humans are the primary reservoir, while in other regions, animals like dogs or rodents can also maintain the parasite’s life cycle.
Recognizing the Signs and Diagnosis
The symptoms of Kala-azar often develop progressively over a period of weeks to months following the sand fly bite. The most characteristic signs are a prolonged, irregular fever that can persist for weeks and significant, unexplained weight loss. The parasite’s migration to the internal organs causes them to swell substantially.
A physical examination will often reveal splenomegaly (enlargement of the spleen) and hepatomegaly (enlargement of the liver). The infection damages the bone marrow, leading to pancytopenia, which includes progressive anemia, a low white blood cell count, and a low platelet count. The anemia contributes to fatigue and weakness, while the low white blood cell count compromises the immune system, making the patient susceptible to secondary infections.
Diagnosis begins with a clinical suspicion based on the characteristic signs and a patient’s travel history to an endemic area. Serological tests are frequently used in the field, particularly the rapid diagnostic test (RDT) based on the rK39 antigen, which detects circulating antibodies against the parasite. For definitive confirmation, a microscopic examination is performed to visualize the parasite’s amastigote form within tissue aspirates, such as those taken from the bone marrow or spleen. While splenic aspiration offers high diagnostic sensitivity, it is an invasive procedure that carries a risk of fatal bleeding and must be performed by experienced medical staff.
Treatment Pathways and Recovery
Prompt treatment is necessary for recovery, as the disease is nearly always fatal without intervention. The specific drugs used can vary based on the geographic region, the species of parasite, and the prevalence of drug resistance. Current first-line therapies often involve injectable liposomal amphotericin B, which is highly effective and generally administered in a single-dose regimen in some endemic areas.
Other treatment options include the oral drug miltefosine and the injectable drug paromomycin, which may be used individually or in combination regimens. Treatment often requires hospitalization for proper administration of injectable medications and monitoring for adverse effects. The duration of therapy can range from a single infusion to courses lasting several weeks, depending on the drug and the patient’s condition.
Even after successful treatment, a subset of patients, particularly those in the Indian subcontinent and East Africa, may develop a complication called Post-Kala-azar Dermal Leishmaniasis (PKDL). PKDL manifests as a rash of macular, papular, or nodular lesions on the skin, often appearing months to years after the initial infection has resolved. Although not typically life-threatening, PKDL lesions act as a reservoir for the parasite, making the affected individual a potential source of transmission.
Prevention and Control Strategies
Control efforts for Kala-azar focus on a multi-pronged approach that targets the parasite, the vector, and the human host. A core strategy is the early diagnosis and prompt treatment of all cases, including PKDL, which reduces the human reservoir and breaks the transmission cycle. Public health campaigns concentrate on active case finding in endemic villages to identify and treat infected individuals who might otherwise go undiagnosed.
Vector control measures are important to minimize contact between the sand fly and humans. Indoor Residual Spraying (IRS) involves applying insecticides to the inner walls of homes and cattle sheds, where the sand flies rest. This has proven effective in reducing the sand fly population and halting transmission in elimination programs. Using long-lasting insecticide-treated bed nets (LLINs) is a practical and effective measure, especially since sand flies are most active during the night. Other behavioral changes include limiting outdoor activities during the peak biting hours of the sand fly, which typically occur from dusk to dawn.