Leishmania


 LEISHMANIA – THE PARASITIC FLAGELLATE

Leishmania occurs as an intracellular parasite in leucocytes or reticulo-epithelial or reticulo-endothelial cells of skin, liver, spleen, bone marrow, lymphatic glands etc. It causes a disease known as Kala-azar or leishmaniasis that results in fever, enlargement of spleen and reduction in the number of white blood corpuscles. It is transmitted through the bite of many species of sandflies (Phlebotomus). Leishmania donovani occurs in India, China, Africa, Southern Europe, South America, and Russia. It is common in Assam, Bengal, Bihar, Orissa, Madras and the eastern parts of Uttar Pradesh.

SPECIES OF LEISHMANIA

There are many species of Leishmania that cause different diseases in man and animals and are all transmitted by different species of sandfly but the following species are important in relation to man.

  • Leishmania donovani causes kala-azar or black fever or visceral leishmaniasis which is transmitted by Phlebotomus argentipes.
  • Leishmania chagasi causes American kala-azar in South America and is transmitted by Phlebotomus braziliensis.
  • Leishmania infantum causes infantile kala-azar in the Mediterranean Region and is transmitted by Phlebotomus orientalis and P. perniciosus.
  • Leishmania tropica causes oriental sore or cutaneous leishmaniasis in Arabian and Asian countries and is transmitted by Phlebotomus sergenti and P. papatasi.
  • Leishmania braziliensis causes Espundia of nose, mouth and throat in Mexico and South America and is transmitted by Phlebotomus intermedius.

Leishmania occurs in two different forms: Amastigote form in man and Promastigote form in sandfly.

Amastigote form or Leishmania form occurs inside the cells of the reticulo-endothelial system or macrophage of vertebrate hosts such as man, dog etc. This form is rounded or oval in shape, measuring 2 to 4 micron. Nucleus is oval or rounded and is usually situated in the middle of the cell. The extranuclear DNA, called the kinetoplast lies in the cytoplasm. A short flagellum emerges from the basal body but ends within the cytoplasm and does not emerge out of the pellicle. This stage multiplies by binary fission within the human cells continuously till the host-cells enlarge and rupture, releasing 50 to 200 parasites per cell that seek and invade fresh cells and the cycle is repeated again and again. When sand flies suck human blood the amastigote forms are sucked along and reach the stomach of sandfly where they change into promastigote forms.

Promastigote form or Leptomonad form occurs in the stomach of sandflies where the sucked blood is stored for digestion. This form is long and slender, spindle-shaped and measures 15-20 microns in length and 1-2 microns in width. Nucleus is situated in the centre of the cell and kinetoplast lies near the anterior end. The exposed part of flagellum may be equal to its body length and projects from the anterior end of its body. Flagellum is used for swimming about in the blood. The promastigote form multiplies repeatedly by longitudinal binary fission producing large number of flagellates in the mid-gut of the sand fly. This multiplication continues for 7-10 days in the stomach of sandfly after which the parasites migrate to the pharynx, buccal cavity and proboscis of the sand fly and wait there till they are injected into the host blood by the bite of sandfly. The food passage of such sandflies is blocked by the presence of large number of leptomonad forms and hence these sandflies are ever hungry and bite again and again, transmitting parasites to large number of hosts. When sandfly bites it has to inject saliva to prevent the blood from coagulating and this washes the parasite into the wound and eventually into the host blood. Some flagellates may be destroyed by the host phagocytes but some manage to take refuge inside the cells of the reticulo-endothelial system, where they transform into amastigote forms and start multiplication by binary fission.

Symptoms of Kala-azar include continuous fever, weakness and anaemia. Spleen enlargement is one of the most striking features along with the liver enlargement. In advanced stage, skin becomes dry, rough and often with dark patches. Hairs tend to be brittle and fall out. If left untreated, majority of the patients die in 2 years, more by the secondary infections by bacteria or viruses. Owing to the destruction of leucocytes, the defense mechanism of body becomes so weak that the patient is unable to resist opportunistic diseases.

Drugs for Kala-azar: Treatment of kala-azar is prolonged and the drugs which are mostly antimony compounds have to be injected into blood. The drugs are: sodium stibogluconate, Meglumine antimoniate, Amphotericin Miltefosine and Paromomycin.