From MicrobeWiki, the student-edited microbiology resource


Leishmania major by E. Draberova. Image from Academy of Sciences of the Czech Republic.


Higher order taxa:

Eukaryota; Euglenozoa; Kinetoplastida; Trypanosomatidae; Leishmania


Leishmania major, L. donovani, L. braziliensis

Description and Significance

Leishmania is a parasite which causes human leishmaniasis. The genus Leishmania is unique among parasites in that its species are divided based not on the form and structure of the cells, but rather on the pathology and symptoms of the disease they cause. Leishmania may infect many vertebrates, but in human hosts the infection most frequently stems from the bites of sand fly vectors or, in the case of Leishmania major, from gerbils and other small rodent vectors. Leishmaniasis can take three forms: dermal cutaneous leishmaniasis, visceral leishmaniasis, and mucocutaneous leishmaniasis. Dermal cutaneous leishmaniasis, generated by Leishmania major, causes sores on the human host's skin, which range in appearance and degree of discomfort. The sores are treatable with antibiotics and preventable with vaccination. Visceral leishmaniasis, produced by Leishmania donovani, is identified by an enlargement of the liver and spleen; symptoms include breathing difficulties, edema, diarrhea, and bleeding mucus membranes. If untreated for an extended period of time, visceral leishmaniasis may result in death. Mucocutaneous leishmaniasis, caused by Leishmania braziliensis, initially yields topical sores at the time of the vector bite, however secondary infections may lead to permanently disfiguring ulcerations in the mucus cavities of the mouth and nose.

Genome Structure

Leishmania major's genome Friedlin has been sequenced, and is found to have a 32.8mb genome with 36 chromosomes and a G+C content of approx. 63%. For a complete table of sequenced data of the Leishmania major genome Friedlin, click here.

Cell Structure and Metabolism

Life cycle. When Leishmania invades the sand fly vector, the promastigote form settles in the midgut and reproduces asexually. The promastigotes are transmitted to the vertebrate host when the sand fly vector bites. Once inside the vertebrate host, Leishmania invades the host's cells, where it morphs into its amastigote form after losing its flagella to the macrophages of the host's immune system. In the cells of the host the amastigote multiplies and eventually kill the cell, upon which the amastigotes are released to other cells. Human leishmaniasis' symptoms are the effects of these amastigotes destruction of cells. Image from Kinetoplastid Biology and Disease.

Leishmania 's promastigote form (found in the vector) is similar to the amastigote, but possesses a prominent flagella. The surface membrane has binding site molecules such as glycoproteins, and manose receptors have also been detected. These are important in the uptake of the promastigotes by macrophages in the host cell. Antibodies in the host serum bind to the promastigotes and facilitate uptake and entry into the macrophage. The macrophages have Fc receptors on their surface. Upon losing the flagella (see life cycle, below) Leishmania's amastigote form (found in the cells of the vertebrate host) is spherical and is contained within a parasitophorus vacuole within a macrophage. There is a prominent nucleus and kinetoplast, and the vacuolated cytoplasm contains lysosomes. The outer membrane has a polysaccharide component but there is no surface coat.Once inside the host cell, Leishmania is able to protect itself from powerful host immunities by using several unique defense mechanisms, including its rapid cell division. Leishmania is a heterotophic organism whose prominent flagella may allow it to puncture host cells, allowing the promastigote to consume nutrients and obtain energy from the cell sap.


The Leishmania parasite is found in 88 countries, in Central and South America, Mexico, southern Europe (very rarely), the Middle East, parts of Asia, and primarily eastern and northern Africa. Its habitat ranges from tropical rainforests to arid regions, depending on the type of vector (predominantly insect or rodent) each particular species inhabits. Leishmania is transported between vertebrate hosts through vector bites and causes cell disruption and subsequent illness in its host.




Drâberova, E.. Leishmania major. Molecular and Cellular Immunology.

"Geographic Distribution of Cutaneous Leishmaniasis." Map.

"Geographic Distribution of Visceral Leishmaniasis." Map.

Graphic Images of Parasites . Ohio State University College of Biological Sciences.

Ouaissi, A. "Molecular basis of Trypanosoma cruzi and Leishmania interaction with their host(s): exploitation of immune and defense mechanisms by the....." Abstract. PubMed.

Parasitic Disease Information . Centers for Disease Control and Prevention.

Ponte-Sucre, Alicia. "Physiological consequences of drug resistance in Leishmania and their relevance for chemotherapy." Kinetoplastid Biology and Disease 2 (2003).

Smith, James. Parasitism and Symbiosis - 177-345A. McGill University.

Totals for genome sequencing of Leishmania major Friedlin . The Wellcome Trust Sanger Institute.

For more information on parasites similar to Leishmania, see Trypanosoma.