Leishmania donovani. Leishmania tropica. Leishmania braziliensis

Leishmania, a flagellate that lives inside our macrophages and is carried by sand flies, its two body forms and its life cycle, and the three diseases its species cause in the skin, the mucosa of the nose and mouth, and the organs.

10 min read
6 questions
Checked 27 Oct 2026

Leishmania: the amastigote and the promastigote

Point at a name or a part to light it.

Leishmania takes two forms. In our macrophages it is the amastigote, 1 to 5 µm long, round to oval, with a large nucleus, a prominent kinetoplast and no free flagellum; it multiplies inside them until they burst. In the sand fly it is the promastigote, about 10 to 12 µm long, with its kinetoplast near the anterior end and its flagellum free from there, which the fly injects with its bite. The species that cause skin, mucosal and visceral disease look the same.

Simplified: not to scale: the two forms drawn large beside the macrophage, and its amastigotes far larger in it than they are; most organelles, the flagellar pocket and the macrophage’s own organelles left out; each amastigote drawn in a vacuole of its own, as in Leishmania donovani; some species share one large vacuole; the kinetoplast drawn as a plain bar, though it is a network of interlocked DNA rings; the beat played far slower than life, as one simple wave drawn flat on the page.

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Contents7 sections

At a glance

Leishmania is a flagellate, a kinetoplastid like the trypanosomes, carried by female phlebotomine sand flies.
It takes two forms: the round amastigote, which multiplies inside our macrophages, and the promastigote, with a free flagellum, which multiplies in the sand fly's gut.
The species look alike under the microscope but cause different diseases: cutaneous (L. tropica, L. major), mucocutaneous (L. braziliensis) and visceral, kala-azar (L. donovani, L. infantum).
Visceral leishmaniasis brings fever, weight loss, a huge spleen and low blood counts, and untreated it kills more than 95 per cent of those who develop it. In the Mediterranean, Greece included, it is kept in dogs.
Cell-mediated immunity decides the outcome: Th1 cells and interferon-γ arm the macrophages to kill the parasite.

Leishmania and its two forms

Leishmania is a haemoflagellate, like the trypanosomes: a single cell with one nucleus, one long mitochondrion and, in that mitochondrion, a kinetoplast of its own DNA. More than 20 species cause disease in people. All of them look the same, so they are told apart by where they were caught, the disease they cause and, in the laboratory, by their DNA or enzymes.

It takes two of the four body forms of the haemoflagellates:

	Amastigote	Promastigote
Where	inside macrophages and other mononuclear phagocytes, in us and other mammals	in the sand fly's gut, and in culture
Shape and size	round to oval, 1 to 5 µm long	slender, about 10 to 12 µm long
Nucleus	large	in the middle
Kinetoplast	prominent, beside the nucleus	near the anterior end
Flagellum	a short stub, inside the cell, rarely seen by light microscopy	free from the anterior end, often longer than the body

In a Giemsa-stained smear the amastigotes are the Leishman–Donovan bodies: small pale cells, inside a macrophage or freed from it, each with two dark dots, the large nucleus and the smaller, rod-shaped kinetoplast. In the promastigote the flagellum grows from a basal body beside the kinetoplast and leaves through the anterior tip, with no undulating membrane.

The macrophage takes the promastigote up to destroy it. Instead, the parasite turns into an amastigote in the parasitophorous vacuole, the phagosome after it has fused with lysosomes, survives the acid and the enzymes there and divides by binary fission until the cell bursts. The freed amastigotes are taken up by new macrophages.

The sand fly and the life cycle

Leishmania is carried by female phlebotomine sand flies: Phlebotomus in the Old World, Lutzomyia in the New. Over 90 species can carry it. Only the females take blood. They are about a quarter the size of a mosquito, silent, and bite mostly from dusk to dawn, often without the bite being felt.

Leishmania: the life cycle

Point at a name to light its pathway.

Leishmania passes between a female sand fly and a mammal. The fly injects promastigotes with its bite; in the patient they live and multiply only inside macrophages, as amastigotes, and a fly takes these up with its next blood meal. Which disease follows depends on the species and on the patient’s immunity: sores on the skin, destruction of the nose and mouth, or a visceral disease of the spleen, liver and bone marrow, kala-azar, which is fatal untreated.

Simplified: a map, not anatomy: the sand fly and the patient drawn as icons, nothing to scale; each stage’s form drawn small; in the fly the promastigotes go through more forms than the two shown; one species named for each disease, though several cause each: L. major and L. aethiopica sores on the skin, L. infantum kala-azar, and L. donovani sometimes a rash on the skin after kala-azar; only the bite drawn; Leishmania also passes, rarely, by shared needles, blood transfusions and from mother to child; the sand fly named only as the vector; it is also called the intermediate host, and the mammal the definitive host; dogs, rodents and other mammals are reservoir hosts.

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A sand fly that bites an infected person or animal takes up macrophages full of amastigotes. In its gut the amastigotes turn into promastigotes and multiply, attached by their flagella to the gut wall. They become slender, infective metacyclic promastigotes and move forward to the mouthparts; a fly can be so blocked by them that it struggles to feed and passes them on as it probes. With its next bite the fly injects them into the skin, macrophages take them up, and they turn into amastigotes and multiply.

Where they go next depends mainly on the species: they stay in the skin, spread to the mucosa of the nose and mouth, or spread through the body to the macrophages of the spleen, liver, bone marrow and lymph nodes. The host's immune response decides how far they get, and whether the infection makes the person ill at all.

Some species pass from person to person through the fly, with people their reservoir (anthroponotic); most are kept in animals, people infected by chance (zoonotic). More rarely, Leishmania passes in shared needles, blood transfusions or from mother to baby.

Three diseases, by species

Leishmaniasis is found in about 100 countries, in the tropics and subtropics and in southern Europe, with an estimated 700,000 to 1 million new cases a year.

Disease	Main species	Where	Kept in
Cutaneous (oriental sore)	L. tropica	towns of the Middle East and Central Asia; sporadic in Greece	people
Cutaneous	L. major	North Africa, the Middle East, Central Asia	rodents
Cutaneous, then mucocutaneous (espundia)	L. braziliensis	Central and South America	forest animals
Visceral (kala-azar)	L. donovani	the Indian subcontinent, East Africa	people; in parts of East Africa perhaps also animals
Visceral, sometimes only cutaneous	L. infantum	the Mediterranean, Greece included; the Middle East, Central Asia, Latin America	dogs

Cutaneous leishmaniasis

Cutaneous leishmaniasis is the commonest form, with 600,000 to 1 million new cases a year. Weeks to months after the bite, a small papule appears where the fly fed, often on the face or the arms. It slowly grows, hardens and usually ulcerates, into a painless or painful ulcer with a raised edge round a central crater, like a volcano. Several bites give several sores. Most heal on their own over months to a year or more, leaving a depressed scar for life, which on the face can be disfiguring.

Where the cell-mediated response fails, as with L. aethiopica in East Africa and L. amazonensis in South America, the parasites spread through the skin as many nodules full of parasites, with no ulcers: diffuse cutaneous leishmaniasis, which looks like lepromatous leprosy and heals poorly.

Mucocutaneous leishmaniasis

In some patients infected with L. braziliensis the parasites spread from the skin to the mucosa of the nose, mouth and throat, often years after the skin sore has healed. Mucocutaneous leishmaniasis, espundia, destroys the nasal septum, the palate and the lips, and can spread to the pharynx and larynx. It does not heal on its own and needs treatment. Over 90 per cent of cases are in Bolivia, Brazil, Peru and Ethiopia, where L. aethiopica causes it.

Visceral leishmaniasis, kala-azar

Visceral leishmaniasis, kala-azar ("black fever" in Hindi), comes from parasites that spread through the whole mononuclear phagocyte system. Most infections cause no symptoms. In those who become ill, weeks to months after the bite:

fever, often irregular, for weeks, with weakness and weight loss;
a very large spleen and a large liver, as the macrophages in them multiply;
pancytopenia, anaemia, few white cells and few platelets, as parasitised macrophages fill the bone marrow;
very high levels of immunoglobulin in the blood, which do not protect.

Untreated, visceral leishmaniasis kills more than 95 per cent of those who develop it, often through bleeding or another infection on top. About 50,000 to 90,000 new cases a year, most in Brazil, East Africa and India. In the Mediterranean it is caused by L. infantum and is seen mostly in young children and in adults whose immunity is weakened.

People with HIV are far more likely to develop visceral disease once infected, to relapse after treatment and to die of it; antiretroviral treatment lowers all three. In southern Europe many adult cases of visceral leishmaniasis have been in people with HIV.

Why some people heal

Leishmania lives inside macrophages, so cell-mediated immunity, not antibody, decides the outcome. Th1 cells release interferon-γ, which activates the infected macrophages to kill the amastigotes inside them: the sore heals and the patient is protected, usually for life, against that species. A Th2 response leaves the parasites to multiply. The spectrum runs from a single self-healing sore with a granuloma of lymphocytes and macrophages, through diffuse cutaneous disease, where the macrophages are full of parasites, to kala-azar, where the T cells hardly respond to the parasite until it is treated.

The old Montenegro skin test showed this: an injection of parasite antigen into the skin raises a hard lump after 48 to 72 hours in people with a cell-mediated response. It is positive in cutaneous leishmaniasis, negative in diffuse cutaneous disease and in active kala-azar, and turns positive after kala-azar is cured.

Diagnosis

The diagnosis rests on seeing the parasite, or its DNA:

Cutaneous and mucosal disease: a scraping, aspirate or biopsy from the raised edge of the sore, where the parasites are, stained with Giemsa to show the amastigotes. Grown in culture, on a blood agar medium such as NNN, they turn into promastigotes. PCR is more sensitive and names the species, which can decide the treatment. Antibody tests are of little use.
Visceral disease: amastigotes in an aspirate of the spleen, bone marrow or a lymph node. A spleen aspirate finds them most often, at a small risk of bleeding; bone marrow is safer. Unlike cutaneous disease, kala-azar makes plenty of antibody, so serology helps, including a rapid strip test for antibody to the parasite antigen rK39, used where kala-azar is common.

Treatment

Leishmaniasis can be treated and cured. Which drug depends on the form of the disease, the species, where it was caught and the patient's immune state:

Drug	Given	Used for
Liposomal amphotericin B	into a vein	visceral disease: the treatment of choice in Europe and North America, and as a single infusion in South Asia; with miltefosine, in people with HIV; also mucosal disease
Miltefosine	by mouth	visceral, cutaneous and mucosal disease; with paromomycin, now the first choice for kala-azar in East Africa in people without HIV
Pentavalent antimonials: sodium stibogluconate, meglumine antimoniate	into a vein or muscle, or injected into a skin sore	for decades the mainstay; still used in many countries where the disease is common
Paromomycin	into a muscle, or as an ointment on a skin sore	kala-azar, with miltefosine or an antimonial; cutaneous sores

Miltefosine harms the unborn child: it is never given in pregnancy, and women must avoid pregnancy during treatment and for months after it, five after a standard 28-day course.
The antimonials are toxic, to the heart among other organs, and resistance has made them useless in parts of India.
WHO's July 2026 guidelines suggest, for kala-azar in East Africa in people without HIV, a 14-day course of miltefosine by mouth with paromomycin injections, in place of 17 days of injections of an antimonial with paromomycin. The antimonial combination remains for patients who cannot take miltefosine, such as pregnant women.
A small, uncomplicated cutaneous sore that is healing may be left to heal, or treated locally, by freezing, heat or injections into the sore. Sores caught in Central or South America, where the species may spread to the mucosa, are usually treated with drugs given by mouth or injection.

Prevention

There is no vaccine or drug to prevent leishmaniasis in people. Prevention means avoiding the bite: staying inside from dusk to dawn, covering the skin, insect repellent, and fine-mesh bed nets treated with insecticide, since a sand fly can pass through the holes of an ordinary mosquito net. Where the cycle runs through people, spraying houses with insecticide and finding and treating patients, including those with PKDL, break it; where it runs through dogs, insecticide collars protect them, and vaccines exist for dogs, though none for people. India, Nepal and Bangladesh have pushed kala-azar down by these means, and in 2023 Bangladesh became the first country validated by WHO as having eliminated it as a public health problem.

Check yourselfAnswer, then say how sure you were: a lucky guess still counts as a weak point.

1Which form of Leishmania is found in a patient's tissues?

2What identifies a Leishmania amastigote in a Giemsa-stained smear?

3A man treated for a skin ulcer after a stay in the Brazilian rainforest returns years later with a destroyed nasal septum. Which species is most likely?

4Which picture fits visceral leishmaniasis?

5Where does Leishmania infantum, the cause of visceral leishmaniasis in Greece and the rest of the Mediterranean, mainly live between human cases?

6Which immune response clears a Leishmania infection?

See on the map

01Leishmania and its two forms

02The sand fly and the life cycle

03Three diseases, by species