Toxoplasma and Brain Tumors

Table of Contents

1. What the Presentation Said
2. What Toxoplasma Is
3. Country and Region Studies
4. Studies of Individual People
5. How the Parasite Might Be Involved
6. Reactivation During Cancer Treatment
7. When Toxoplasma Looks Like a Tumour
8. Weakened Toxoplasma as an Anti-Tumour Tool
9. How the Claim Compares With the Research
10. What Is Not Known
11. Connections
12. Key Research Papers
13. Featured Videos

What the Presentation Said

The presentation was a 2026 webinar on cancer and parasites given by the medical director of an integrative cancer clinic. It did not name Toxoplasma. It did, however, make several general points that bear directly on the parasite that brain-tumour researchers study most:

• The speaker said that parasites are not confined to the gut and can travel to any part of the body, including the brain, and showed a brain scan and a surgical case of a worm removed from a patient's brain as examples.
• The speaker said that, in a person with cancer, parasites are part of the tumour microenvironment — the mix of cells, blood vessels and signals that surrounds a tumour.
• The speaker described a chain of events said to lead from parasite infection to cancer: long-lasting inflammation, an immune system that can no longer detect the parasites and other microbes, oxidative stress that creates more mutations, and epigenetic changes (changes in which genes are switched on) that activate cancer genes. The speaker called this parasite-driven oncogenesis, meaning the formation of tumours driven by parasites.
• The speaker said that parasites suppress immune signalling, creating an environment where disease can flourish.
• Separately, the speaker linked parasites to depression, anxiety, mood change and memory loss, and said parasites release toxins that affect the nervous system. (That point has its own page in this series, listed under Connections.)

No study about Toxoplasma and brain tumours was cited in the presentation. This page therefore asks the question the presentation's general claims raise for the brain: does the most common brain parasite in humans have a measured link to brain tumours, and what does the research show about how it behaves around tumours and in people with cancer?

What Toxoplasma Is

Toxoplasma gondii is a protozoan — a single-celled organism, not a worm. The U.S. Centers for Disease Control and Prevention (CDC) states that cats play a key role in its spread and that it can last in human bodies, and those of other animals, for long periods, up to a lifetime.

How people catch it

The US Centers for Disease Control and Prevention (U.S. Centers for Disease Control and Prevention) lists the main routes as eating undercooked contaminated meat or shellfish or unwashed contaminated produce, accidentally swallowing the parasite from cat faeces or contaminated soil, and passage from a newly infected mother to her unborn child. The U.S. Centers for Disease Control and Prevention estimates that over 40 million people in the United States carry the parasite, and states that most people with healthy immune systems have no symptoms.

How common it is worldwide

A systematic review of 152 studies covering 648,010 apparently healthy people found an average seroprevalence of 25.7% (Molan and colleagues, 2019). Seroprevalence means the share of people whose blood carries antibodies to the parasite, a sign of past or present infection. The figure ranged from 0.5% to 87.7% between studies: highest on average in Africa (61.4%), and lowest in the USA and Canada (17.5%) and Asia (16.4%).

Why the brain matters

After the first infection the parasite changes into a slow-growing form that sits inside tissue cysts, mainly in the brain and muscles, often for life. In mice, a specialised group of immune cells that stay in the brain (brain-resident CD8 T cells) was enough to keep these cysts from reactivating even when circulating T cells were removed (Porte and colleagues, 2024). This lifelong presence in brain tissue is the reason researchers began asking whether the parasite could play any part in brain tumours (Dupont and colleagues, 2023).

Country and Region Studies

The first studies compared whole populations rather than individual people. These are called ecological studies: they show whether two things rise and fall together across places, not whether the people who carry the parasite are the ones who develop tumours.

• Across countries. Using national figures, researchers found that the prevalence of Toxoplasma explained 19% of the remaining variation in adult brain-cancer incidence between nations, after allowing for national wealth (richer countries detect more cancer) and latitude. Across the range of parasite prevalence in the data (4% to 67%), infection was associated with a 1.8-fold increase in brain-cancer risk. The authors described the results as correlational (Thomas and colleagues, 2012).
• Within France. A follow-up study used regional data inside a single country to reduce differences in cancer detection between nations. In adults aged 55 and over, regional brain-cancer death rates rose with local Toxoplasma seroprevalence, and the effect was particularly strong in men. The authors stated that the association does not demonstrate causation (Vittecoq and colleagues, 2012).

Ecological links can arise from many shared factors — diet, age structure, access to brain scans, how deaths are recorded — so these studies were presented by their own authors as reasons to study individuals, not as evidence that the parasite causes tumours.

Studies of Individual People

Blood taken years before diagnosis

The strongest design available so far tests blood that was stored long before anyone became ill, so the tumour cannot have caused the infection. Researchers did this in two prospective cohorts: an American cohort (37 people who later developed glioma, matched with 74 controls) and a Norwegian serum bank (323 glioma cases and 323 controls). Glioma is the most common type of malignant brain tumour.

• In the American cohort, people with Toxoplasma antibodies had an odds ratio for glioma of 2.70 (95% confidence interval 0.96–7.62).
• In the Norwegian cohort, the odds ratio was 1.32 (0.85–2.07).
• The link was stronger among people with high antibody levels against one parasite surface protein (sag-1): odds ratio 3.35 (0.99–11.38) in the American cohort and 1.79 (1.02–3.14) in the Norwegian one.

An odds ratio above 1 means the exposure was more common among people who developed the disease. A confidence interval that includes 1, as both main results do here, means chance cannot be ruled out. The authors called the result a suggestive increase in risk and the first prospective evidence of an association, and wrote that larger studies are needed to confirm it (Hodge and colleagues, 2021).

Pooling the case-control studies

A 2022 meta-analysis combined seven studies with 2,323 brain-tumour patients and 5,131 healthy controls. Evidence of infection was found in 24.2% of patients and 12.9% of controls, an overall odds ratio of 1.96 (1.37–2.80). By tumour type the odds ratios were 1.64 for glioma, 2.30 for meningioma (a usually benign tumour of the brain's coverings, with an interval of 1.0–5.27) and 2.19 for other brain tumours. The authors called this suggestive evidence and wrote that it needs confirming in well-designed cohort studies with strict control of confounders (Abdollahi and colleagues, 2022).

Children in Egypt

A study of 64 children with brain tumours and 92 healthy children in Egypt found antibodies in 62.5% of the children with tumours and 38% of the controls (odds ratio 2.7). Eating unwashed vegetables was a risk factor for infection. The authors reported that every glioma case in the group was seropositive, a figure drawn from a small subgroup (Hamouda and colleagues, 2024).

Why these numbers are hard to read

• Most studies took blood after the tumour was found. A brain tumour, its surgery, steroids or chemotherapy could change antibody levels or make infection more likely, which would produce a link running in the reverse direction.
• Antibodies show past contact with the parasite; they do not show where the parasite is or whether it is active.
• Most studies are small, and some come from regions where infection is very common, which affects how comparable they are.
• No study found for this page showed the parasite inside human brain-tumour cells in a way that shows it started the tumour.

How the Parasite Might Be Involved

Researchers who think a link is worth testing have proposed several ways it could work. These are hypotheses drawn mostly from laboratory work, not established facts about human brain tumours.

• Long-term inflammation. The parasite persists for years in brain tissue, and the authors of the country study based their prediction on the parasite's ability to provoke inflammation there (Thomas and colleagues, 2012).
• Blocking cell death. To survive inside a host cell, the parasite interferes with apoptosis (the cell's built-in self-destruct programme) and with the signals that control cell division. A 2023 review by French parasitologists presented these effects as the points that could underlie a causal link, while making clear it was a personal view calling for investigation (Dupont and colleagues, 2023).
• The opposite possibility. The same review literature notes that the parasite triggers a strong immune response, and that under some conditions this response attacks tumours rather than helping them (Li and colleagues, 2026). Which effect wins, if either does in people, is unknown.

These ideas overlap with the general mechanisms the presentation listed — inflammation and disturbed cell signalling — but for Toxoplasma and brain tumours none of them has been shown to operate in human patients.

Reactivation During Cancer Treatment

The best-documented connection between Toxoplasma and cancer is not about causing tumours. It is about what the parasite can do when cancer treatment weakens the immune system.

More common in people with cancer

A meta-analysis of 57 studies found antibodies in a pooled 30.8% of cancer patients, with an odds ratio of 3.1 (2.5–3.8) compared with people without cancer (Anvari and colleagues, 2019). Like the brain-tumour studies, this measures blood taken after diagnosis, so it cannot show which came first.

What chemotherapy can do

The U.S. Centers for Disease Control and Prevention lists people taking certain types of chemotherapy, people with human immunodeficiency virus (HIV) and recent organ-transplant recipients among those at risk of severe toxoplasmosis. In a cross-sectional study of 107 patients with solid tumours in northern Iran, 80.4% carried antibodies before treatment, and 28.92% showed a significant rise in antibody levels three weeks after chemotherapy began. The authors described this as a possible effect of chemotherapy in a subset of patients and wrote that its clinical meaning needs further research (Shekarriz and colleagues, 2026).

A fatal case

A Swiss case report describes a patient treated with chemotherapy for non-Hodgkin lymphoma who developed arm pain and spreading tingling six weeks after remission. A lymphoma relapse was suspected and steroids and radiation were started; the patient died five days later of multiple organ failure, and the autopsy found disseminated (body-wide) toxoplasmosis. The authors wrote that toxoplasmosis is described more rarely in cancer and chemotherapy than in human immunodeficiency virus, and that it is worth suspecting in patients with cancer, especially lymphoma, who develop unexplained nerve, lung or fever symptoms during or after chemotherapy (Herold and colleagues, 2009).

This is the clearest place where the presentation's general point about immune suppression and parasites matches the published record — but the direction is the reverse of the one described: here it is the cancer treatment that weakens immunity and lets a dormant parasite reawaken.

When Toxoplasma Looks Like a Tumour

Active toxoplasmosis in the brain (toxoplasmic encephalitis) forms rounded lesions with swelling around them. On a scan these can look very like a brain tumour or a brain lymphoma, and the two are treated in completely different ways.

• A case report from Japan describes a 25-year-old woman with human immunodeficiency virus whose largest brain mass took up a radioactive tracer in a pattern that suggested malignant lymphoma. A biopsy with a DNA test (polymerase chain reaction (PCR)) of the tissue identified Toxoplasma instead, and her scans improved dramatically after two weeks of sulfamethoxazole and trimethoprim. The authors stressed that careful pathology and DNA testing were needed to tell the two apart (Nakamura and colleagues, 2024).
• Case reports also describe the reverse problem. A 57-year-old man in Japan with daily contact with stray cats had several ring-shaped brain lesions; cerebral toxoplasmosis was suspected and treated with trimethoprim-sulfamethoxazole, but he worsened, and a second brain biopsy showed a glioblastoma, an aggressive brain tumour (Iwamoto and colleagues, 2025).

The presentation showed a brain scan and said imaging can reveal parasites that form cysts or lesions. Published case reports agree that parasite lesions and tumours can be confused on imaging, and they describe biopsy and laboratory tests as the way the two were distinguished. Decisions about cancer treatment and antiparasitic medicines belong with a clinician.

Weakened Toxoplasma as an Anti-Tumour Tool

An entirely different line of research uses Toxoplasma against tumours. The parasite provokes a strong “type 1” immune response, driven by the signalling molecules interleukin-12 and interferon-gamma, that activates killer T cells. Researchers have built weakened (attenuated) strains that cannot multiply normally, to borrow this response without causing disease. All of the results below are in mice.

• Pancreatic cancer in mice. A weakened strain that cannot make one of its own building blocks (a uracil auxotroph) was used to treat mice with spread-out pancreatic cancer and produced long-lasting immunity to the cancer, involving CD4 T cells and tumour-specific antibodies (Sanders and colleagues, 2016).
• Combined with a checkpoint inhibitor in mice. In another mouse model of pancreatic cancer, a weakened strain slowed tumour growth by activating dendritic cells and drawing CD8 T cells into the tumour. Combined with an anti-PD-1 antibody (a checkpoint-inhibitor drug type used in human cancer care), it controlled tumour growth better than either alone and reduced immune-suppressing cells in the tumour (Bahwal and colleagues, 2022).
• A brain tumour in mice. Most brain tumours contain few T cells, which is one reason immunotherapy works poorly against them. In a genetic mouse model of medulloblastoma (a childhood brain tumour), Toxoplasma infection drew T cells into the tumour and reprogrammed surrounding immune cells toward a state that supports T cells, without causing severe illness in the mice. The authors presented this as a foundation for future brain-tumour immunotherapy studies (Nguyen and colleagues, 2024).

What stands between this and patients

A 2026 review of this field listed the obstacles: strains differ in how harmful and how effective they are; live wild-type strains raise ethical and biosafety concerns; animal results transfer poorly to people; and the parasite may, under certain conditions, promote tumour formation rather than block it. Proposed workarounds include engineered strains, parasite-derived proteins, and using the parasite as a carrier to deliver drugs into brain tumours (Li and colleagues, 2026). No human clinical trial of Toxoplasma-based cancer therapy was found in the PubMed searches made for this page.

How the Claim Compares With the Research

Supported by the research

• Parasites can reach the brain: about a quarter of people worldwide carry antibodies to Toxoplasma (Molan and colleagues, 2019), and the parasite persists mainly in the brain (Dupont and colleagues, 2023).
• Parasites and immune suppression interact: published studies and case reports show that cancer treatment can let a dormant Toxoplasma infection reactivate, sometimes fatally (Herold and colleagues, 2009).
• Brain parasites can look like tumours on scans, and imaging alone did not settle the diagnosis in the published cases (Nakamura and colleagues, 2024).

Supported only in part

• A link between Toxoplasma and brain tumours exists in country-level data, case-control studies and one meta-analysis, and the only prospective study pointed the same way — but its main results did not reach statistical significance, and every author group described its findings as suggestive, correlational or needing confirmation.
• Inflammation and disturbed cell-death signalling are real effects of the parasite in laboratory studies, but they have not been shown to cause brain tumours in people.

Contradicted, or pointing the other way

• The presentation described parasites as suppressing immunity and favouring tumours. For Toxoplasma, much of the laboratory research shows the opposite effect in mice: the parasite's immune response attacked tumours and turned immune-poor tumours into immune-rich ones (Bahwal and colleagues, 2022; Nguyen and colleagues, 2024).
• In the reactivation research, it is cancer treatment that suppresses immunity and lets the parasite flourish, not the parasite that suppresses immunity and lets the cancer flourish.

No research found

• No study was found showing that Toxoplasma is present inside human brain-tumour tissue as a cause of the tumour.
• No trial was found testing whether treating Toxoplasma infection changes the risk or course of a brain tumour.

What Is Not Known

• Whether the link between Toxoplasma antibodies and glioma is real or the product of chance, confounding or reverse causation. Larger prospective studies using stored blood would be needed to answer it.
• Whether particular parasite strains, or a heavier or more recent infection, matter more than simple antibody status. The stronger link with high sag-1 antibody levels hints at this but is unconfirmed (Hodge and colleagues, 2021).
• Whether the parasite's effect on tumours in people resembles its anti-tumour effect in mice, its proposed pro-tumour effects, both, or neither.
• How often reactivated toxoplasmosis goes unrecognised in people having chemotherapy for solid tumours, and what a rise in antibody levels during treatment means clinically (Shekarriz and colleagues, 2026).
• Whether weakened Toxoplasma strains or parasite-derived proteins can be made safe and effective enough to test in human cancer trials.

Connections

• Cancer and Parasites
• Parasites Classified as Cancer-Causing Agents
• How Parasites Can Drive Cancer: The Mechanisms
• Parasites in the Brain
• Parasites, Mood and the Nervous System
• Toxoplasma — The Cause of Toxoplasmosis
• Toxoplasmosis in the Immunocompromised
• Antiparasitic Treatment for Toxoplasmosis
• Preventing Toxoplasmosis: Food Safety and Cat-Litter Precautions
• Toxoplasmosis
• Brain Cancer
• Primary Central Nervous System Lymphoma
• Lymphoma
• Pancreatic Cancer
• Human Immunodeficiency Virus/Acquired Immunodeficiency Syndrome
• Allison and Honjo: Checkpoint Immunotherapy

Key Research Papers

1. Thomas F, Lafferty KD, Brodeur J, Elguero E, Gauthier-Clerc M, Missé D. Incidence of adult brain cancers is higher in countries where the protozoan parasite Toxoplasma gondii is common. Biol Lett. 2012;8(1):101-3. PubMed PMID: 21795265
2. Vittecoq M, Elguero E, Lafferty KD, Roche B, Brodeur J, Gauthier-Clerc M, Missé D, Thomas F. Brain cancer mortality rates increase with Toxoplasma gondii seroprevalence in France. Infect Genet Evol. 2012;12(2):496-8. PubMed PMID: 22285308
3. Hodge JM, Coghill AE, Kim Y, Bender N, Smith-Warner SA, Gapstur S, Teras LR, Grimsrud TK, Waterboer T, Egan KM. Toxoplasma gondii infection and the risk of adult glioma in two prospective studies. Int J Cancer. 2021;148(10):2449-2456. PubMed PMID: 33427315
4. Abdollahi A, Razavian I, Razavian E, Ghodsian S, Almukhtar M, Marhoommirzabak E, Sartip B, Parsa H, Rostami A. Toxoplasma gondii infection/exposure and the risk of brain tumors: A systematic review and meta-analysis. Cancer Epidemiol. 2022;77:102119. PubMed PMID: 35152168
5. Hamouda MM, El-Saied AS, Zaher A, Khalil AF, ElBlihy AA, Nabih N, El-Beshbishi SN. Toxoplasma gondii: Seroprevalence and association with childhood brain tumors in Egypt. Acta Trop. 2024;251:107123. PubMed PMID: 38242223
6. Dupont D, Robert MG, Brenier-Pinchart MP, Lefevre A, Wallon M, Pelloux H. Toxoplasma gondii, a plea for a thorough investigation of its oncogenic potential. Heliyon. 2023;9(11):e22147. PubMed PMID: 38034818
7. Molan A, Nosaka K, Hunter M, Wang W. Global status of Toxoplasma gondii infection: systematic review and prevalence snapshots. Trop Biomed. 2019;36(4):898-925. PubMed PMID: 33597463
8. Porte R, Belloy M, Audibert A, Bassot E, Aïda A, Alis M, Miranda-Capet R, Jourdes A, van Gisbergen KPJM, Masson F, Blanchard N. Protective function and differentiation cues of brain-resident CD8+ T cells during surveillance of latent Toxoplasma gondii infection. Proc Natl Acad Sci U S A. 2024;121(24):e2403054121. PubMed PMID: 38838017
9. Anvari D, Sharif M, Sarvi S, Aghayan SA, Gholami S, Pagheh AS, Hosseini SA, Saberi R, Chegeni TN, Hosseininejad Z, Daryani A. Seroprevalence of Toxoplasma gondii infection in cancer patients: A systematic review and meta-analysis. Microb Pathog. 2019;129:30-42. PubMed PMID: 30708042
10. Shekarriz R, Azari Noor N, Hosseininezhad Z, Nazar E, Eslami Jouybari M, Zaboli E, Ghasemi M, Sharifpour A, Fakhar M. Sero-evidence of Latent Toxoplasma Gondii Infection in Cancer Patients Before and After Chemotherapy, Northern Iran. Acta Parasitol. 2026;71(1):28. PubMed PMID: 41661400
11. Herold MA, Kühne R, Vosberg M, Ostheeren-Michaelis S, Vogt P, Karrer U. Disseminated toxoplasmosis in a patient with non-Hodgkin lymphoma. Infection. 2009;37(6):551-4. PubMed PMID: 19499181
12. Nakamura S, Hara K, Kobayashi T, Sumitani R, Oura M, Maeda Y, Sogabe K, Yagi H, Takahashi M, Fujii S, Harada T, Bando Y, Abe M, Miki H. Toxoplasmic encephalitis with high (201)Tl uptake and retention mimicking malignant lymphoma in a patient with human immunodeficiency virus infection. Parasitol Int. 2024;101:102895. PubMed PMID: 38614255
13. Iwamoto M, Mori N, Shimatani Y, Yamamoto K, Imai Y, Ishihara H. [A case of multifocal glioblastoma with ring enhancement, mimicking cerebral toxoplasmosis with ring-enhanced lesions]. Rinsho Shinkeigaku. 2025;65(3):224-229. PubMed PMID: 40010714
14. Sanders KL, Fox BA, Bzik DJ. Attenuated Toxoplasma gondii therapy of disseminated pancreatic cancer generates long-lasting immunity to pancreatic cancer. Oncoimmunology. 2016;5(4):e1104447. PubMed PMID: 27141388
15. Bahwal SA, Chen JJ, E L, Hao T, Chen J, Carruthers VB, Lai J, Zhou X. Attenuated Toxoplasma gondii enhances the antitumor efficacy of anti-PD1 antibody by altering the tumor microenvironment in a pancreatic cancer mouse model. J Cancer Res Clin Oncol. 2022;148(10):2743-2757. PubMed PMID: 35556163
16. Nguyen YTM, Sibley L, Przanowski P, Zhao XY, Kovacs M, Wang S, Jones MK, Cowan M, Liu W, Merchak AR, Gaultier A, Janes K, Zang C, Harris T, Ewald SE, Zong H. Toxoplasma gondii infection supports the infiltration of T cells into brain tumors. J Neuroimmunol. 2024;393:578402. PubMed PMID: 38996717
17. Li J, El Shanawany EE, Hassan SE, Li PY, Sun JH, Li HM, Lu SH, Zhou XN, Zheng B. Toxoplasma gondii as a drug for anti-tumor immunotherapy: mechanisms, challenges, and perspectives. Parasite. 2026;33:4. PubMed PMID: 41641877

PubMed Topic Searches

1. Toxoplasma gondii and glioma
2. Toxoplasma gondii and brain tumour risk
3. Attenuated Toxoplasma in tumour immunotherapy
4. Toxoplasmosis reactivation during chemotherapy

Other Sources

1. CDC: About Toxoplasmosis

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