Phylum Apicomplexa. Toxoplasma gondii
Toxoplasma gondii, the apicomplexan that lives inside our cells, its three infective forms and the apical complex it enters cells with, its life cycle between cats and every other warm-blooded animal, and toxoplasmosis, in the healthy, in pregnancy and when immunity fails.
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- Checked 27 Oct 2026
Point at a name or a part to light it.
Toxoplasma gondii has three infective forms. The tachyzoite, 4 to 8 µm long and 2 to 3 µm wide, invades almost any nucleated cell with its apical complex and multiplies fast in a vacuole of its own. Bradyzoites multiply slowly inside tissue cysts, 5 to 50 µm, mainly in the brain and muscle, for the life of the host. The oocyst, 10 to 12 µm, comes from the cat and, once sporulated, holds 2 sporocysts of 4 sporozoites each.
Simplified: not to scale: the tachyzoite drawn far larger than the forms beside it, and the oocyst drawn as large as the tissue cyst, which can be several times its size; only the apical complex, the nucleus and the apicoplast drawn in the tachyzoite: its single mitochondrion, Golgi body, endoplasmic reticulum and the inner membrane complex under its surface left out; the rosette drawn with eight tachyzoites; there can be many more, and most groups lie at random, a rosette forming only when they divide in step; the tissue cyst drawn with a few dozen bradyzoites, where it can hold hundreds, and without the host cell it lies in; the tachyzoite's flex played slowly, in one place; it glides forward in life.
Contents4 sections
At a glance
- Toxoplasma gondii is an apicomplexan: a protozoan that lives inside cells and enters them with the apical complex at its front end, the conoid, rhoptries and micronemes.
- It has three infective forms: the tachyzoite, which multiplies fast in almost any cell; the bradyzoite, which waits in tissue cysts in brain, eye and muscle for life; and the sporozoite, inside the oocyst that a cat passes.
- Cats and other felids are the only definitive hosts. People are infected by swallowing oocysts in food, water or soil, by eating tissue cysts in undercooked meat, or across the placenta.
- Most infections in healthy people cause no symptoms or a mild illness with swollen lymph nodes. A first infection in pregnancy can cause congenital toxoplasmosis; when immunity fails, the cysts reactivate as encephalitis.
- Diagnosis is mostly by serology. Treatment, when it is needed, is pyrimethamine with sulfadiazine and folinic acid; spiramycin is used early in pregnancy.
Apicomplexa and Toxoplasma
The phylum Apicomplexa takes its name from the apical complex, the set of organelles at the front end of the cell with which the parasite enters the cells of its host. All of them live inside cells, and they include the causes of malaria (Plasmodium), cryptosporidiosis and toxoplasmosis. Most also carry an apicoplast, a small plastid with four membranes, a relic of an alga their ancestors took in.
Toxoplasma gondii is one of the most common infections of people in the world. About a quarter of adults in the UK have been infected, a third to a half in much of Central and Southern Europe, though the numbers are falling.
The three forms
| Tachyzoite | Bradyzoite | Sporozoite | |
|---|---|---|---|
| Where | in almost any nucleated cell, in a parasitophorous vacuole | in tissue cysts, mostly in brain, eye and muscle | in the oocyst, two sporocysts of four sporozoites |
| What it does | multiplies fast; the acute infection, and the form that crosses the placenta | multiplies slowly; the latent infection, for life | infects whoever swallows the sporulated oocyst |
| Size | 4 to 8 µm long, 2 to 3 µm wide, crescent-shaped | slimmer, its nucleus toward the back; cysts 5 to 50 µm | oocyst 10 to 12 µm |
The tachyzoite's parts to know:
- The apical complex, at its tapered anterior end: the conoid, a short, hollow cone of spirally wound fibres; eight to ten club-shaped rhoptries, their necks running into the conoid; and small, rod-like micronemes, mostly near the front.
- Dense granules, round secretory organelles through the cell.
- The nucleus, near the middle of the cell, with the apicoplast just in front of it.
There is no flagellum. The parasite glides, and enters a cell actively, in a fixed order: the micronemes release adhesive proteins as it touches the cell, the rhoptries empty theirs as it pushes in, and the dense granules shape the parasitophorous vacuole it ends up in, made from the host cell's own membrane, where it is not digested. Inside the vacuole it multiplies by endodyogeny, two daughters forming within each parent, sometimes in a neat rosette, until the cell bursts and the tachyzoites move on.
As immunity takes hold, tachyzoites turn into bradyzoites inside a thin, elastic tissue cyst wall. A cyst can hold hundreds of them and lasts for the life of the host, out of the immune system's reach and untouched by the drugs.
The life cycle
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Toxoplasma's sexual cycle runs only in cats, which pass oocysts in their faeces. Almost any warm-blooded animal, people included, can be infected by swallowing sporulated oocysts, or by eating tissue cysts in another animal's meat. In people the tachyzoites spread and then settle as tissue cysts for life; a first infection in pregnancy can cross the placenta, and the cysts reactivate if immunity fails.
Simplified: a map, not anatomy: the hosts drawn as icons and the parasites drawn small, nothing to scale; the other animals drawn as one panel with a mouse; in them, as in the patient, tachyzoites come before the tissue cysts; the stages inside the cat's gut left out, cats infected by swallowing oocysts not drawn, and infection by transplant or transfusion only named.
Cats and other felids are the only definitive hosts. A cat that eats prey with tissue cysts, or more rarely swallows oocysts, is infected in the lining of its gut, where the parasite forms male and female gametes. The fertilised cells become oocysts, which the cat passes in its faeces for one to three weeks, often in huge numbers. They are not yet infective: in soil or water they sporulate in one to five days and then stay infective for a long time.
Almost any warm-blooded animal can be an intermediate host, people included. Rodents and birds swallow oocysts from the soil, and tissue cysts form in their brain and muscle; a cat eats them, and the cycle closes. Sheep, pigs, goats and game are infected the same way, and carry tissue cysts in their meat.
People are infected:
- by eating tissue cysts in undercooked meat, which in Europe accounts for a third to almost two-thirds of infections;
- by swallowing sporulated oocysts, on unwashed vegetables and fruit, in water, from soil or a cat's litter;
- across the placenta, mostly when a woman is first infected during pregnancy;
- rarely, from a transplanted organ or a blood transfusion.
Toxoplasmosis
In healthy people
Toxoplasmosis in a healthy person usually passes unnoticed. About 10 to 20 per cent have symptoms: swollen lymph nodes, mostly in the head and neck, with fever, aching muscles and tiredness, which settle by themselves, though the nodes and tiredness can last for months. Rarely there is hepatitis, pneumonia or myocarditis.
The eye can be affected, as a retinochoroiditis, an inflamed patch at the back of the eye, after a congenital infection or one caught later. It can recur from cysts left in the retina, and can threaten sight.
In pregnancy: congenital toxoplasmosis
Almost always, it is a first infection during pregnancy, or just before it, that puts the fetus at risk; rarely, the old cysts of a mother whose immunity fails, or reinfection with a different strain, can do so too. Tachyzoites in the mother's blood can cross the placenta, and the later in pregnancy, the more likely they are to pass, but the milder the damage:
| Mother infected in | Passed to the fetus | Damage |
|---|---|---|
| first trimester | under 10 per cent | the heaviest: miscarriage, or a severely affected baby |
| second trimester | about 30 per cent | between |
| third trimester | 60 to 70 per cent | usually none visible at birth |
A severely affected baby can have hydrocephalus or microcephaly, calcifications in the brain and retinochoroiditis, with seizures and delayed development. Most infected babies look well at birth, but without treatment many later develop eye lesions, some only in their teens or twenties.
When immunity fails
In people with advanced HIV infection, above all once the CD4 count falls below 100 cells per µL, or on strong immunosuppressive treatment, old tissue cysts can break open and the infection reactivates, most often in the brain, sometimes in the eye or lungs. After a transplant the same can happen, or a patient never infected before can be infected by cysts in a donor's organ, above all a heart, and the infection then often spreads through the body. Cerebral toxoplasmosis brings fever, headache, confusion, seizures and focal weakness, and a scan shows several ring-enhancing lesions. It is the most common cause of a mass in the brain in AIDS.
Diagnosis
- Serology is the main test. IgG shows an infection at some time and lasts for life; IgM points to a recent one, but can persist for a year or more, so a positive IgM alone does not date the infection; a negative IgM all but rules out a recent one. In pregnancy, the IgG avidity helps: high avidity means the infection began more than about 4 months before, while low avidity does not prove it is recent.
- PCR on amniotic fluid, from about 16 to 18 weeks and at least 4 weeks after the mother's infection, shows whether the fetus is infected: a positive result is reliable, but a negative one does not rule infection out, so the baby is still tested at birth. On blood, eye fluid or cerebrospinal fluid it helps when immunity is weak and serology may mislead.
- In cerebral toxoplasmosis, the diagnosis rests on the scan and on the response to treatment: improvement on the scan within about 3 weeks confirms it, and lymphoma is the main alternative. The IgG is positive in most, though not all, and a single lesion makes toxoplasmosis unlikely.
Treatment and prevention
- Healthy people rarely need treatment.
- Severe disease, eye disease and cerebral toxoplasmosis: pyrimethamine with sulfadiazine and folinic acid, which protects the bone marrow from pyrimethamine. Clindamycin replaces sulfadiazine in those allergic to sulphonamides. Treatment lasts at least 6 weeks; eye disease often also needs a corticosteroid for the inflammation.
- In pregnancy: spiramycin, to make passage to the fetus less likely, when the mother is infected before about 18 weeks and the fetus is not known to be infected. Pyrimethamine with sulfadiazine and folinic acid is given when the fetus is infected, and often for an infection caught later in pregnancy; pyrimethamine is avoided in the first trimester. How much any of this helps is not certain.
- Infected newborns are treated with pyrimethamine, a sulphonamide and folinic acid for 12 months.
- People with HIV: those with Toxoplasma IgG whose CD4 count falls below 100 cells per µL take trimethoprim-sulfamethoxazole, which also prevents Pneumocystis pneumonia. After cerebral toxoplasmosis, a lower dose continues until antiretroviral therapy has restored immunity.
The drugs act on tachyzoites only; the tissue cysts remain.
There is no vaccine for people. Prevention, above all for pregnant women who have never been infected and for people with weak immunity, means cooking meat well, or freezing it deeply for several days, which kills the tissue cysts; washing vegetables and fruit; drinking only treated water, as chlorine does not kill oocysts; wearing gloves for gardening and washing hands after handling raw meat or soil; and leaving the cat litter to someone else, or changing it every day with gloves, so the oocysts are removed before they become infective.
Check yourselfAnswer, then say how sure you were: a lucky guess still counts as a weak point.
1In which animal does Toxoplasma gondii reproduce sexually?
2Which form of Toxoplasma crosses the placenta to infect a fetus?
3How do the risk and the severity of congenital toxoplasmosis change through pregnancy?
4A man with untreated HIV infection has fever, headache and a weak left arm. A brain scan shows several ring-enhancing lesions, and his Toxoplasma IgG is positive. What is the next step?
5What do the rhoptries of the apical complex do?
6A pregnant woman who has never had toxoplasmosis asks how to avoid it. Which advice is right?