Leishmania donovani is a microscopic parasite that causes a severe disease in humans. This single-celled organism belongs to a group of parasites known as trypanosomatids. Its presence in the human body can lead to significant health complications.
The parasite is responsible for a serious human illness, representing a complex health challenge in many parts of the world. Understanding this parasite’s nature helps to grasp the disease it causes.
Understanding Leishmania donovani
Leishmania donovani is an obligate intracellular protozoan parasite, meaning it must live inside the cells of another organism to survive and reproduce. It is a single-celled eukaryote. This parasite is associated with a severe form of leishmaniasis.
The parasite exists in two primary forms depending on its host. In sandflies, it takes on a flagellated, elongated shape known as a promastigote, which allows for movement within the insect vector.
When Leishmania donovani infects humans, it transforms into an amastigote form. These amastigotes are oval-shaped and lack an external flagellum, making them non-motile. They reside within the mononuclear phagocyte system, including cells of the spleen, liver, and bone marrow in humans.
The Life Cycle and Transmission
Leishmania donovani has a complex life cycle requiring two different hosts: humans and sandflies. Only female sandflies transmit the infection because they require blood meals for reproduction. The life cycle begins when an infected female sandfly bites a human or another mammal.
During the bite, the sandfly injects infective promastigotes into the human skin. These promastigotes are then taken up by macrophages and other mononuclear phagocytic cells. Inside these cells, the promastigotes transform into the amastigote form.
The amastigotes multiply within the macrophages, particularly in the spleen, liver, and bone marrow. As the infected cells rupture, new amastigotes are released to infect other macrophages, continuing the parasitic spread within the human host. The cycle continues when an uninfected female sandfly takes a blood meal from an infected human or animal, ingesting macrophages containing amastigotes.
Once inside the sandfly’s midgut, the ingested amastigotes transform back into promastigotes. These promastigotes multiply and migrate to the sandfly’s proboscis, ready to be injected into a new host during a subsequent blood meal. This completes the life cycle, perpetuating the transmission of Leishmania donovani between hosts.
Visceral Leishmaniasis (Kala-azar): Symptoms and Pathogenesis
Leishmania donovani is the causative agent of visceral leishmaniasis (VL), also known as kala-azar, meaning “black fever”. This is the most severe form of leishmaniasis and can be fatal if left untreated. The incubation period for the disease generally ranges from three to six months, though it can sometimes be as short as 10 days or over a year.
The parasite primarily targets cells of the mononuclear phagocyte system, particularly in the spleen, liver, and bone marrow. This leads to the characteristic symptoms of VL, which often develop progressively over weeks or months. Common symptoms include prolonged fever, significant weight loss, and enlargement of the spleen (splenomegaly) and liver (hepatomegaly).
The unchecked multiplication of amastigotes within these mononuclear phagocytes causes the disease. The enlargement of the spleen and liver results from hyperplasia, an increase in the number of cells, due to the parasite’s proliferation. This parasitic activity can trigger a systemic inflammatory response, contributing to symptoms like fever and cachexia (wasting syndrome).
Anemia is another common symptom, resulting from the disease’s impact on bone marrow function and a systemic inflammatory response. In some cases, a darkening of the skin may also be observed, giving rise to the name “black fever”. If left untreated, the mortality rate for kala-azar is nearly 100%.
Diagnosis, Treatment, and Prevention
Diagnosing visceral leishmaniasis caused by Leishmania donovani involves various methods to confirm the presence of the parasite or antibodies against it. Direct detection of amastigotes through microscopic examination of tissue aspirates from bone marrow, spleen, or lymph nodes is considered a gold standard, though it can be invasive. Blood tests for antibody detection, such as the rK39 rapid diagnostic test, are also widely used and show high sensitivity in endemic areas.
Treatment for visceral leishmaniasis aims to prevent mortality and reduce morbidity. Medications like liposomal amphotericin B are commonly used and are approved for treating VL. Miltefosine is another oral drug approved for VL caused by Leishmania donovani. However, treatment faces challenges such as the high cost of drugs, potential toxicity, and the increasing problem of drug resistance.
Preventing Leishmania donovani infection focuses on controlling the sandfly vector and protecting individuals from bites. Vector control measures include the use of insecticide-treated bed nets and indoor residual spraying. Personal protection methods, such as applying insect repellents and wearing protective clothing, are also recommended to minimize exposure to sandfly bites. Early diagnosis and prompt treatment of infected individuals are also important to reduce the reservoir of parasites and limit further transmission.