Study of Leishmania – Classification, Life Cycle and Mode of Transmission

Study of Leishmania – Classification, Life Cycle and Mode of Transmission

Classification of Leishmania

Phylum : Protozoa
Subphylum : Sarcomastigophora
Class : Zoomastigophorea
Order : Kinetoplastida
Family : Trypanosomatidae
Genus : Leishmania


  • It is found as an intracellular parasite in Leucocytes and cells of liver, spleen, bone marrow, etc.

Morphology and Life Cycle of Leishmania

Study of Leishmania
  • Leishmania spp. are digenetic or heteroxenous parasites, whose life cycle involves two
  • Hosts, a vertebrate and an invertebrate, the sandfly
  • Hemoflagellates may have several morphological stages that differ from one another in the placement of the kinetoplast relative to the nucleus, as well as the location and origin of the flagellum
  • In Leishmania the life cycle stage in the vertebrate is the amastigote and in the insect, the promastigote. Leishmania exist in two basic body forms (a) The amastigote, the intracellular form in the vertebrate host, and (b) Promastigote, the extracellular form in the sandfly (Phleobotomus spp and Lutzomyia spp.) Vector
  • Amastigotes are taken up from the blood of an infected host when the female sandfly bites, and in the sandfly gut they develop into promastigotes where they multiply by binary fission; promastigotes move anteriorly into the proboscis, and are introduced into the vertebrate host when the sandfly bites again The promastigotes injected by the sandfly during feeding are phagocytized and develop in to intracellular amastigotes.
  • The amastigote, literally “without a flagellum,” is the intracellular, non-motile form in the vertebrate host, and it divides by longitudinal binary fission at 37 degree. Intracellular zamastigotes are 3-6 um in length and 1.5-3.0 um in width.7
  • The amastigote is also called the Leishman-Donovan (LD) body. The amastigote is not really devoid of a flagellum, it is simply that the flagellum does not protrude beyond the body surface and by light microscopy cannot be seen. The promastigote, literally the body form with “an anterior flagellum” is 15-30 mm in body length and 5mm in width.
  • it is extracellular, motile, and grows and divides by longitudinal binary fission at 27degree in the sand.
  • Promastigotes can be grown in vitro at 25 degree temperature on NNN medium, which has a solid phase of blood agar and a liquid phase containing a physiologic salt solution. Liquid media that support promastigote growth are also available.
  • Amastigotes usually are grown inside tissue culture cells and can also be grown extracellularly at 37 degree under special conditions

Leishmania donovani is a digenetic parasite passing its life cycle in two different hosts.

Definitive host

In humans the metacyclic promastigotes are injected by sandfly through the skin during its blood meal. When sandfly bites using its proboscis it rejects the parasites that are stored inside the hollow tube. Some promastigotes may enter the blood stream directly where some are destroyed by macrophagic cytolysis. But many are also taken up through phagocytosis by mononuclear phagocytes in liver, spleen and bone marrow. Inside the cells they undergo spontaneous transformation into oval-shaped amastigotes. Granulocytes selectively kill the promastigotes by oxidative mechanism; while amastigotes are resistant.

Then the surviving amastigotes undergo cell division using simple binary fission. Multiplication continues until the host cell can no longer hold and ruptures. In a fully congested cell there can be as many as 50 to 200 amastigotes, which are released into tissue cavities. Each individual amastigote is then capable of invading fresh cells. As a result, the entire tissue is progressively infected and destroyed. A number of free amastigotes then enters the blood stream where many are phagocytosed by macrophages. These free and phagocytosed amastigotes in peripheral blood are then sucked up by blood-feeding sandfly.

Intermediate host

L. donovani undergo further development only in the digestive tract of the female sandfly. Hence only females are responsible for transmitting the infection. Once the amastigotes are ingested, they enter the midgut of the sandfly. Then they undergo structural modification into flagellated promastigotes, becoming larger and considerably elongated. They get attached to the gut epithelial lining where they multiply rapidly by binary fission. (They are also capable of sexual reproduction by genetic hybridisation in the sandfly gut.)

They then migrate back towards the anterior part of the digestive system such as pharynx and buccal cavity. This process is known as anterior station development, which is unique in Leishmania. A heavy infection of pharynx can be observed within 6 to 9 days after initial blood meal. The promastigotes become infective only by this time, and the event is called the metacyclic stage the metacyclic promastigotes then enter the hollow proboscis where they accumulate and completely block the food passage. Immediately upon biting a human, the parasites are released, which invariably results in infection. The stages of development in sandfly can be described as follows:-

  1. Soon after entering the gut, the amastigotes get coated with peritrophic matrix, which is composed of chitin and protein complex. This protects the parasites from the digestive enzymes of the host.
  2. The amastigotes travel as far as the abdominal midgut and first transform into a weakly motile “procyclic promastigotes” on the gut wall within 1–3 days.
  3. The young promastigotes secrete a neuropeptide that stop peristalsis of the gut. The surface lipophosphoglycan (LPG) of the promastigote serves as an attachment to the gut epithelium. These factors prevent the expulsion of promastigotes during excretion of the insect.
  4. During 4–7 days the peritrophic matrix is degraded by the activity of chitinases. This release the more actively motile “nectomonad promastigotes” which migrate anteriorly until they reach the opening of the thoracic gut.
  5. Another transformation takes place by which they turn into “leptomonad promastigotes”. These are fully motile and capable of binary fission. Multiplication and migration towards thoracic midgut cause congestion of the pharynx and buccal cavity.
  6. Here they secrete promastigote secretory gel (PSG), which is composed of soluble acid phosphatase and phosphoglycoprotein.
  7. After 6–9 days the promastigotes become metacyclic. Some are also transformed into Non-replicating promastigotes, which also become metacyclic. The sandfly is able to regurgitate and eject the parasites from its proboscis with the help of PSG when it bites.

Reservoir host

Dogs are known to be susceptible to L. donovani infection. Especially in the New World, infection is a zoonotic disease, involving different canine species, including domestic dog and the two fox species, Lycalopex vetulus and Cerdocyon thous. In the Mediterranean region domestic dogs and the three fox species Vulpes vulpes, V. corsac and V. zerda are common reservoir hosts. In Africa and Brazil, some marsupials and rodents are also reported to harbour L. Donovan.

Symptoms of the Disease

Different species of Leishmania, diseases cause y them and the symptoms are:

  1. L.donovan: cause Kala Azar or dum dum fever: Darking of skin, enlargement of spleen and liver, fever and anaemia.
  2. L.tropica causes OrientalSores: disfiguration of ear, face, fore arms and legs.
  3. L.brasiliensis: Cause American Lishmaniasis: inflammation of mucous membrane of nose and throat and enlargmen of spleen and liver, spleen lymph nodes etc.

Mode of transmission

All species are transmitted by small blood-sucking sandflies, notably Phlebotomus spp. in the Old World and Lutzomyia spp. in the New World. Only the females feed on blood. Amastigotes ingested during feeding transform in the midget or hindgut into promastigotes which multiply by binary fission. The parasites migrate forward to the foregut and proboscis where some become swept away by saliva into the bite site when the fly feeds.


  • Some cutaneous infections require no treatment as lesions may heal within several months.
  • Systemic therapy with pentavalent antimonials (sodium stibogluconate or meglumine antimonate) is the treatment of choice for disfiguring and visceral infections.
  • The development of antimonial drug resistance, however, is a growing problem in many endemic areas, including South America, India and the Middle-East. Pentamidine or amphotericin B can be used if antimonials are ineffective, and miltefosine and aminosidine (paromomycin) have shown promise as treatment options, especially when combined with immunotherapy using the tumour-necrosis factor-alpha (TNF-?) inhibitor pentoxifylline.


  • Preventive measures include protection from sand fly bites but this can be difficult as they are so small that they can penetrate most mosquito nets. Reducing the size of reservoir host populations (especially dogs) has proven beneficial in many endemic urban areas.
  • Cutaneous infections, however, are acquired in forests away from human habitation, as the reservoir hosts are wild animals (esp. rodents). The prevention of sand fly bites in forest areas is almost impossible but may be minimized by the use of protective clothing, insect repellants and insecticidal sprays in houses.
  • Killing of reservoir hosts like infected street dogs.

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