Protozoa. Phylum Sarcomastigophora. Subphylum Mastigophora (Flagellata). Trypanosoma brucei gambiense, Trypanosoma brucei rhodesiense. Trypanosoma cruzi
What protozoa are and how the classic scheme sorts them, the flagellates and their four body forms, and the two trypanosomes that cause sleeping sickness in Africa and Chagas disease in Latin America.
- 12 min read
- 6 questions
- Checked 27 Oct 2026
Point at a name or a part to light it.
Trypanosoma brucei’s trypomastigote, the form in a patient’s blood, drawn large: 14 to 33 µm long, with its posterior end on the left. The four forms below differ in where the kinetoplast lies relative to the nucleus and in how much of the flagellum runs along the body. Leishmania lives as amastigotes in our macrophages and as promastigotes in the sand fly; T. cruzi lives as amastigotes in our cells, and both trypanosomes as epimastigotes in their insects and trypomastigotes in our blood.
Simplified: not to scale: the amastigote, 1 to 5 µm long, drawn far larger beside the other forms than it is, and the membrane and coat drawn thicker; the cell drawn large after T. brucei’s slender form, though the species takes several shapes, and T. cruzi’s trypomastigote is C-shaped in stained blood films, with a larger kinetoplast; most organelles and the flagellar pocket left out; the coat drawn on the cell body only; the kinetoplast drawn as a plain bar, though it is a network of interlocked DNA rings; the mitochondrion drawn as a plain tube, without its cristae; the four forms drawn without their mitochondrion or coat; the beat played far slower than life, as one simple wave drawn flat on the page; the real beat, and the way the cell turns as it swims, are more complex.
14 sources
- Centers for Disease Control and Prevention. DPDx: Trypanosomiasis, African. Last reviewed 6 March 2019.
- Centers for Disease Control and Prevention. DPDx: Trypanosomiasis, American. Last reviewed 16 June 2021.
- Centers for Disease Control and Prevention. DPDx: Leishmaniasis. Last reviewed 5 June 2024.
- Zeledón RA. Hemoflagellates. In: Baron S, editor. Medical Microbiology. 4th ed. Galveston (TX): University of Texas Medical Branch; 1996. Chapter 82.
- Yaeger RG. Protozoa: structure, classification, growth, and development. In: Baron S, editor. Medical Microbiology. 4th ed. Galveston (TX): University of Texas Medical Branch; 1996. Chapter 77.
- Wheeler RJ, Gluenz E, Gull K. The limits on trypanosomatid morphological diversity. PLoS One. 2013;8(11):e79581.
- Jensen RE, Englund PT. Network news: the replication of kinetoplast DNA. Annu Rev Microbiol. 2012;66:473–491.
- Kinetoplast. Wikipedia. Accessed 27 October 2026.
- Hoffmann A, Käser S, Jakob M, et al. Molecular model of the mitochondrial genome segregation machinery in Trypanosoma brucei. Proc Natl Acad Sci U S A. 2018;115(8):E1809–E1818.
- Sullenberger C, Hoffman B, Wiedeman J, Kumar G, Mensa-Wilmot K. Casein kinase TbCK1.2 regulates division of kinetoplast DNA, and movement of basal bodies in the African trypanosome. PLoS One. 2021;16(4):e0249908.
- Bílý T, Sheikh S, Mallet A, et al. Ultrastructural changes of the mitochondrion during the life cycle of Trypanosoma brucei. J Eukaryot Microbiol. 2021;68(3):e12846.
- Schimanski B, Aeschlimann S, Stettler P, et al. p166 links membrane and intramitochondrial modules of the trypanosomal tripartite attachment complex. PLoS Pathog. 2022;18(6):e1010207.
- Godar S, Oristian J, Hinsch V, et al. Light chain 2 is a Tctex-type related axonemal dynein light chain that regulates directional ciliary motility in Trypanosoma brucei. PLoS Pathog. 2022;18(9):e1009984.
- Mugnier MR, Stebbins CE, Papavasiliou FN. Masters of disguise: antigenic variation and the VSG coat in Trypanosoma brucei. PLoS Pathog. 2016;12(9):e1005784.
Contents4 sections
At a glance
- Protozoa are single-celled eukaryotes. The classic scheme puts the flagellates (Mastigophora) and the amoebae (Sarcodina) together in the phylum Sarcomastigophora.
- Between them, the trypanosomes and Leishmania take four body forms, told apart by where the kinetoplast lies and how far the flagellum runs along the body: amastigote, promastigote, epimastigote and trypomastigote.
- Trypanosoma brucei, carried by the tsetse fly, causes sleeping sickness in Africa. It lives outside cells throughout and dodges antibodies by switching its surface coat.
- T. b. gambiense in west and central Africa causes a chronic disease and most cases; T. b. rhodesiense in the east and south an acute one.
- Trypanosoma cruzi, passed in the faeces of triatomine bugs, causes Chagas disease in Latin America. It multiplies inside cells, and decades later it can damage the heart and gut.
Protozoa
Protozoa are microscopic, single-celled eukaryotes: one cell with a nucleus in its envelope, mitochondria and the other organelles, which still feeds, moves and reproduces like an animal. Most of the 50,000 or so species live freely in water and soil; a few live in us. Most parasitic protozoa are under 50 µm long, and the smallest, which live inside our cells, only 1 to 10 µm.
- Their outer layer. The plasma membrane covers the cell and its organs of movement. In some, the trypanosomes and Giardia among them, a stiffer layer under it, the pellicle, keeps a set shape that can still bend and twist.
- Their cytoplasm. In most it is a clear outer ectoplasm and a granular inner endoplasm that holds the organelles, plainest in the amoebae.
- Their stages. The trophozoite is the stage that feeds, moves and multiplies, and causes disease. Many also make a cyst, a resting stage inside a protective wall, which survives outside the host and passes the infection on.
- How they multiply. Mostly by binary fission: the organelles are copied and the cell splits in two, lengthwise in the flagellates. Some divide many times at once, and the Apicomplexa also reproduce sexually.
- How they feed. On ready-made organic matter, taken up in solution or as particles, as animals do.
How the syllabus classifies them
The syllabus follows the scheme the Society of Protozoologists published in 1985, which sorted protozoa into six phyla by what they look like under the light and electron microscopes. Three hold the parasites in this chapter:
| Phylum | Subphylum | How it moves | In this chapter |
|---|---|---|---|
| Sarcomastigophora | Mastigophora (Flagellata) | one or more flagella | Trypanosoma, Leishmania, Trichomonas, Giardia |
| Sarcomastigophora | Sarcodina | pseudopodia, the cell flowing into them | Entamoeba |
| Apicomplexa | no organ of movement; a complex of organelles at its tip to enter cells | Toxoplasma, Plasmodium | |
| Ciliophora | many short cilia | Balantidium |
The flagellates
The Mastigophora move with flagella. Some live in the gut or the genital tract (Giardia, Trichomonas); the haemoflagellates, Trypanosoma and Leishmania, live in the blood and tissues and pass between people by blood-sucking insects. In the figure, a trypanosome is drawn large with its parts:
- A single flagellum grows from a basal body near the posterior end, leaves the cell through the flagellar pocket and runs forward along the edge of the undulating membrane, a fold of the body that ripples as it beats. Past the anterior end it is free. Its beat is a wave that runs from the tip back to the base, the reverse of nearly all other flagella, and drives the cell forward.
- One long mitochondrion runs through the cell. At its posterior end it holds the kinetoplast, a disc of the mitochondrion's own DNA, tied to the basal body.
- The nucleus lies in the middle.
Four body forms
As they pass between their insect and us, the haemoflagellates change shape. The forms differ in where the kinetoplast lies relative to the nucleus, and in how much of the flagellum runs along the body:
| Form | Kinetoplast | Flagellum | Where it is found |
|---|---|---|---|
| Amastigote | beside the nucleus | only a stub, inside the cell | Leishmania and T. cruzi inside our cells |
| Promastigote | near the anterior end | free from the anterior end | Leishmania in the sand fly |
| Epimastigote | just in front of the nucleus | along a short undulating membrane, then free | both trypanosomes in their insects |
| Trypomastigote | behind the nucleus, near the posterior end | along an undulating membrane the length of the body, then free | both trypanosomes in our blood, and the infective stage the insect passes on |
Trypanosoma brucei: sleeping sickness
Human African trypanosomiasis, sleeping sickness, is caused by two subspecies of Trypanosoma brucei that look the same under the microscope. Both are carried by tsetse flies (Glossina), which bite by day and live only in sub-Saharan Africa. They differ in where they live and how fast they kill:
| T. b. gambiense | T. b. rhodesiense | |
|---|---|---|
| Where | 24 countries of west and central Africa | 13 countries of eastern and southern Africa |
| Share of reported cases | 92 per cent | 8 per cent |
| Tsetse flies | of riverine areas | of the open savannah |
| Kept in | mainly people; animals carry it too | cattle and wild game, so a zoonosis |
| Course | chronic: months or years before the brain is reached | acute: weeks |
| Chancre at the bite | seldom | often |
Its life cycle
Point at a name to light its pathway.
Both trypanosomes pass between an insect and a mammal and change form at each step. Trypanosoma brucei, the cause of sleeping sickness, lives outside cells throughout and multiplies in the patient’s blood; its fly passes it on with its bite. T. cruzi, the cause of Chagas disease, multiplies in the patient only inside cells, as amastigotes, and its trypomastigotes in the blood do not divide; its bug passes it on with its faeces, which must be rubbed into the bite or a mucous membrane, so not every bite infects.
Simplified: a map, not anatomy: the insects and the patient drawn as icons, nothing to scale; each stage’s form drawn small and the same size; T. brucei’s three kinds of trypomastigote drawn alike, and T. cruzi’s blood form C-shaped, as it looks in a stained blood film; T. brucei’s bloodstream forms drawn as one: the long slender forms that multiply turn into short stumpy ones, which do not, and it is these that go on in a fly; T. b. gambiense and T. b. rhodesiense drawn as one cycle, which they share; only the cycle through the insect: both also pass from mother to child and by laboratory accident, and T. cruzi by blood transfusion, organ transplant and food or drink soiled by the bugs; the animals that also carry the parasites left out; the insects named only as vectors; some textbooks also call the insect the intermediate host and the mammal the definitive host, and the genera named for the bug are the commonest of several.
8 sources
- Centers for Disease Control and Prevention. DPDx: Trypanosomiasis, African. Last reviewed 6 March 2019.
- Centers for Disease Control and Prevention. DPDx: Trypanosomiasis, American. Last reviewed 16 June 2021.
- Zeledón RA. Hemoflagellates. In: Baron S, editor. Medical Microbiology. 4th ed. Galveston (TX): University of Texas Medical Branch; 1996. Chapter 82.
- World Health Organization. Trypanosomiasis, human African (sleeping sickness). Fact sheet, 2 May 2023.
- World Health Organization. Chagas disease (also known as American trypanosomiasis). Fact sheet, 8 April 2026.
- Nascimento JF, Souza ROO, Alencar MB, et al. How much (ATP) does it cost to build a trypanosome? A theoretical study on the quantity of ATP needed to maintain and duplicate a bloodstream-form Trypanosoma brucei cell. PLoS Pathog. 2023;19(7):e1011522.
- Tsetse fly. Wikipedia. Accessed 27 October 2026.
- Díaz EV, Fiad FG, Gigena GV, et al. Environmental and dispersal-related drivers of color morph distribution in Triatoma infestans (Klug, 1834) (Hemiptera, Reduviidae). Insects. 2025;16(11):1103.
A tsetse fly injects metacyclic trypomastigotes into the skin as it feeds. They reach the blood through the lymph, become bloodstream trypomastigotes and multiply by binary fission in blood, lymph and other body fluids, later the cerebrospinal fluid. T. brucei never enters cells: every stage lives outside them. A fly that bites takes up bloodstream forms. In its midgut they become procyclic trypomastigotes and multiply, then move on to the salivary glands as epimastigotes, multiply again and become metacyclic trypomastigotes, ready for the next bite. The cycle in the fly takes about three weeks. The parasite can also cross the placenta, and laboratory workers have been infected by needles.
In the blood the parasites vary in shape and length. Long, slender forms divide; as their numbers rise they turn into short, stumpy forms that no longer divide but are ready to develop in a fly that takes them up.
How it escapes the immune system
About ten million copies of one variant surface glycoprotein (VSG) coat each parasite. Its genome holds more than a thousand VSG genes, most of them incomplete, and only one is read at a time. As the patient's antibodies clear the parasites wearing one VSG, the few that have switched to another survive and take over. This antigenic variation is why the parasites rise and fall in waves in the blood, and why no vaccine has worked. The constant fresh antigens also drive very high levels of IgM antibody in the blood.
The disease
- 1
At the bite
A swollen trypanosomal chancre can form where the fly fed and last for weeks, common in rhodesiense infection and rare in gambiense.
- 2
First, haemolymphatic stage
The parasites multiply in the blood and lymph: bouts of fever, headache, enlarged lymph nodes, joint pains and itching, with an enlarged spleen. Swollen nodes at the back of the neck, Winterbottom's sign, are typical of gambiense disease.
- 3
Second, meningoencephalitic stage
The parasites cross the blood–brain barrier. Behaviour changes, confusion, sensory disturbances and poor coordination follow, and the sleep cycle is disturbed, giving the disease its name. Coma follows.
Untreated, sleeping sickness is usually fatal. Rhodesiense disease runs its course quickly; gambiense disease can take years to reach the brain, while the patient carries parasites a fly can pick up.
Diagnosis and treatment
Diagnosis takes three steps. For gambiense, serological screening finds people who may be infected; no such test exists for rhodesiense. The parasite is then seen under the microscope in blood, a lymph node aspirate or fluid from the chancre. Finally, where needed, a lumbar puncture stages the disease by examining the cerebrospinal fluid, and the choice of drug depends on it: more than 5 white cells per microlitre or trypanosomes in it mean the second stage, and 100 or more white cells a severe second stage.
| Drug | Given | Used for |
|---|---|---|
| Fexinidazole | by mouth | from 6 years and 20 kg: gambiense, first stage and second stage that is not severe; rhodesiense, both stages, since WHO's 2024 guidelines |
| Pentamidine | into a muscle | gambiense, first stage, mainly in young children |
| Nifurtimox with eflornithine (NECT) | nifurtimox by mouth, eflornithine into a vein | gambiense, severe second stage, and second stage in children under 6 years or 20 kg; eflornithine does not work against rhodesiense |
| Suramin | into a vein | rhodesiense, first stage, where fexinidazole cannot be given |
| Melarsoprol | into a vein | rhodesiense, second stage, where fexinidazole cannot be given, as in children under 6 |
| Acoziborole | one dose by mouth | gambiense, both stages, from 12 years and 40 kg: given a positive EMA opinion in February 2026, for use outside the EU, and approved in the Democratic Republic of the Congo in June 2026 |
Melarsoprol is an arsenical: about 5 to 10 per cent of patients develop an encephalopathy, and about half of them die. Safer drugs, NECT and then fexinidazole, have largely replaced it. There is no test of cure, so treated patients are followed for up to two years in case the disease returns.
Sleeping sickness has fallen to under 1,000 reported cases a year since 2018, most of them in the Democratic Republic of the Congo. By 2030 WHO aims to stop the transmission of gambiense disease altogether, down to zero cases. Rhodesiense disease, kept in animals, is aimed only at elimination as a public health problem, since stopping it would take treating the animals too.
Trypanosoma cruzi: Chagas disease
Chagas disease, American trypanosomiasis, infects about 8 million people, mostly in Latin America, and has been found in 44 countries as people have moved.
How it spreads
T. cruzi is carried by triatomine bugs, the kissing or cone-nosed bugs (Triatoma, Rhodnius, Panstrongylus), which live in the cracks of mud walls and thatched roofs and feed at night, often on the face. The bug defecates as it feeds, and the parasites are in its faeces, not its saliva: they enter when the sleeper rubs the faeces into the bite, another break in the skin, an eye or the mouth. Not every bite infects. Opossums, armadillos, rodents and dogs are reservoirs. The parasite also passes:
- from mother to child, in pregnancy or at birth, now the main route of new infections worldwide;
- in food or drink soiled by the bugs, which causes outbreaks;
- in blood transfusions and organ transplants, and by laboratory accidents.
Its life cycle
The metacyclic trypomastigotes invade cells near where they entered and become amastigotes, which multiply by binary fission until the cell is full, a pseudocyst. They turn back into trypomastigotes, burst the cell and enter the blood, where they invade new cells, especially muscle. In the blood they do not divide: unlike T. brucei, T. cruzi multiplies in us only inside cells, and it does not switch its coat. A bug that feeds takes up the blood forms; in its midgut they become epimastigotes and multiply, and in its hindgut they become metacyclic trypomastigotes, passed with its faeces. In stained blood films the trypomastigote is typically C-shaped, with a large kinetoplast.
The disease
The acute phase lasts about two months, with many parasites in the blood. Most people have no symptoms or a mild fever. Where the parasite entered, a swelling of the skin, a chagoma, or a swelling of both eyelids of one eye, Romaña's sign, may form, with swollen nearby lymph nodes. Some develop a large liver and spleen, myocarditis or, in young children, meningoencephalitis.
Most then carry the parasite for life with no symptoms, the indeterminate form. One to three decades after infection:
- Up to a third develop heart disease. It starts with conduction defects, right bundle branch block and left anterior fascicular block, and can go on to arrhythmias and a dilated cardiomyopathy, sometimes with an aneurysm at the apex and clots in it. It can kill suddenly, through an arrhythmia, or slowly, through heart failure.
- Up to one in ten develop disease of the gut (or, less often, of the nerves): a megaoesophagus that makes swallowing hard, or a megacolon with severe constipation, seen mainly in some regions of South America. Some have both heart and gut disease.
The damage comes from inflammation round the pseudocysts in muscle and the loss of the parasympathetic nerve cells in the heart and the wall of the gut, perhaps with an autoimmune reaction on top.
Diagnosis and treatment
In the acute phase the parasites are seen in a blood film or found by PCR, or grown in culture, or by xenodiagnosis: clean, laboratory-bred bugs feed on the patient and their faeces are examined later. In the chronic phase there are too few to find reliably, so the diagnosis rests on antibodies to the parasite (serology), confirmed by at least two different tests. In people whose immunity fails, with HIV or after a transplant, a chronic infection can flare up again; PCR finds this reactivation.
Benznidazole and nifurtimox, each taken by mouth for 60 days, cure the infection when given early, in the acute phase or soon after birth, and work less well the longer the infection has lasted. Acute, congenital and reactivated infections and infected children are always treated, and so are girls and women who could become pregnant, to keep the parasite from passing to a baby. Treatment is strongly recommended for adults up to 50. Treatment cannot undo an established cardiomyopathy or megaoesophagus.
- Side effects are common, in up to 40 per cent of adults, and worse with age: rashes and nerve damage with benznidazole, loss of appetite and weight with both.
- Neither drug is given in pregnancy, nor to people with kidney or liver failure, and nifurtimox not to people with a history of neurological or psychiatric illness.
There is no vaccine. Spraying houses with insecticide has been the best prevention in Latin America, with better housing, screening of donated blood and organs, and testing of the babies of infected mothers.
Check yourselfAnswer, then say how sure you were: a lucky guess still counts as a weak point.
1In which body form does the kinetoplast lie behind the nucleus, with an undulating membrane running the length of the body?
2Which form of Trypanosoma cruzi multiplies in the patient?
3A traveller develops fever and a sore, crusted lesion two weeks after a safari in East Africa. Which parasite is most likely?
4How does Trypanosoma brucei survive the antibodies its host makes against it?
5How does Trypanosoma cruzi usually enter a person bitten by an infected triatomine bug?
6What marks the second stage of sleeping sickness?