Protozoa Parasites in MS: Part 6 MS is an Infectious Disease I Pam Bartha

Every day, people with multiple sclerosis (MS) are told that there’s no known cause for their disease. But what if the truth has been quietly overlooked for decades? What if some of the most dangerous culprits are invisible to the naked eye—microscopic parasites called protozoa?

 

What are Protozoa?

Most people picture worms or flukes when they think of parasites. But protozoa are single-celled organisms—tiny invaders capable of infiltrating our most sensitive tissues, including the brain. They can hijack the immune system, alter brain chemistry and trigger chronic inflammation. Some live harmlessly in the body, but others have been increasingly linked to neurodegenerative diseases, including MS. And yet, mainstream medicine continues to ignore them.

Protozoa are vastly underappreciated for their impact on human health. Unlike bacteria, which lack a nucleus, protozoa are eukaryotic—meaning they’re more structurally complex, more adaptive, and often more resilient. They thrive in water, soil, and living hosts. Many have clever ways to hide from the immune system, making them difficult to detect and even harder to treat.

Protazoa Linked to MS and Neurological Disease

Researchers have identified several protozoan parasites that may play a role in MS and other neurodegenerative conditions. Plasmodium, Toxoplasma gondii, and Babesia are some of those most commonly linked to MS.

Plasmodium Species That Cause Malaria

In the early 1900s, some doctors began to notice a surprising pattern: patients diagnosed with MS showed remarkable improvements when treated for malaria. These observations led to early theories that MS might actually be a chronic form of cerebral malaria. Though these insights have been lost from mainstream consideration, modern research is bringing it into focus again.

How it affects the body: Plasmodium infects red blood cells and can cause brain swelling in severe cases. It damages the blood-brain barrier (BBB) and triggers inflammation. Infected red blood cells stick to the lining of small blood vessels, leading to vascular blockages, lack of oxygen and immune activation.

Symptoms include: Fatigue, weakness, balance and coordination difficulties, seizures, headaches, cognitive impairments, depression, rapid heart rate or rapid breathing, cough and coma. In the eyes, it can cause floaters, blurry vision, retinopathy and optic neuritis.

Testing: Blood smears, rapid antigen tests, PCR and MRI.

Treatment: Antimalarial drugs like artemisinin, artesunate, quinine, and chloroquine.

Research Summary and Link to MS: From the late 1800s to the early 1900s, several physicians believed that MS might be caused by chronic cerebral malaria. MS patients treated with malaria medications during outbreaks showed significant improvements. Chronic cerebral malaria was thought to cause microbleeds in the brain and the deposition of iron rings around lesions, likely from red blood cell breakdown. These microbleeds were also noted to contain parasite forms, despite the difficulty in detecting them with traditional tests.

Modern studies support this vascular connection. A review titled, Vascular Multiple Sclerosis, discusses endothelial dysfunction, BBB breakdown, and immune infiltration in MS, aligning with mechanisms seen in malaria.

Another study found that people with MS have a 150% increased risk of cardiovascular death and a 350% increased risk of all-cause mortality, even after adjusting for confounding factors.

CLICK HERE to learn more about vascular abnormalities in MS.

Shared Vascular and Blood Abnormalities in MS and Malaria:

1. Red Blood Cell (RBC) Aggregation: Both MS and malaria show increased RBC clumping, which impairs microcirculation and oxygen delivery. RBC deformability is also reduced in both diseases.
2. Platelet Abnormalities: Platelets are abundant in MS lesions and are activated during flares. Malaria also influences platelet function and count, affecting disease progression.
3. Anemia: Common in both malaria and MS. MS patients with anemia have a 200% higher risk of developing the disease.
4. Reduced Blood Flow: Malaria causes vessel obstruction via sticky RBCs. MS is associated with CCSVI (chronic cerebrospinal venous insufficiency), impairing venous drainage.
5. High Blood Pressure: Seen in both MS and malaria survivors. Hypertension is a risk factor for severe malaria and is prevalent in up to 30% of MS patients.
6. Heart Failure: Malaria raises heart failure risk by 30%. MS is associated with a threefold increase in cardiovascular-related mortality.
7. Immune Suppression: Malaria suppresses T and B cell responses, similar to the immune dysfunction observed in MS. Lymphocyte levels normalize post-treatment.

Therapeutic Overlap:

• Hydroxychloroquine, an antimalarial drug, was shown in a 2021 University of Calgary study to significantly slow progression in patients with primary progressive MS.

These findings show a significant overlap in the disease process and treatment response, suggesting a strong link between MS and parasitic infections like malaria.

Click Here to learn more about the link between Malaria and MS.

Toxoplasma gondii

Toxoplasma gondii, another protozoan parasite, may be even more relevant—and far more widespread. It’s estimated that one-third of the global population is infected. Often contracted through undercooked meat, contaminated water, or contact with cat feces, T. gondii forms tissue cysts in the brain and muscles, where it can lie dormant for life. While often symptomless in healthy people, in those with a significant disruption to their microbiome, it can wreak havoc.

Toxoplasma gondii can significantly disrupt brain function. It interferes with critical neurotransmitters like glutamate and dopamine, leading to imbalances that affect mood, movement, and cognition. This parasite also triggers chronic brain inflammation and alters immune system regulation, creating a cascade of damage over time.

Symptoms:

• Cerebral toxoplasmosis: Seizures, confusion, cognitive dysfunction, headaches, dizziness, fatigue, lesions on MRI, poor coordination, muscle, weakness, muscle pain and encephalitis
• Neuropsychiatric: Depression, anxiety, schizophrenia, cognitive decline, increased suicide risk
• In the eyes: Retinochoroiditis (inflammation and damage to both the retina and choroid in the back of the eye), a sudden onset of floaters, vision loss, hazy vision, pain, and/or photophobia.

How it infects the CNS: T. gondii travels via infected immune cells that cross the blood-brain barrier. Once inside the CNS, it forms cysts in neurons and glial cells, particularly in regions tied to motor control, emotion, and cognition.

It can:

• Disrupt glutamate balance
• Trigger chronic grade inflammation
• Alter neural connectivity and function.

Causes immune dysfunction:

• Modulates host inflammation to evade detection
• Infects and uses immune cells (dendritic, macrophages) as Trojan horses
• Suppresses antigen presentation and induces T-cell exhaustion
• Increases host vulnerability to secondary infections and chronic illness.

Testing:

• Blood: IgG and IgM antibody testing, avidity assays
• Brain: MRI or CT scans for lesions, PCR for T. gondii DNA.

Treatment:

• Standard medical: Pyrimethamine + Sulfadiazine + Leucovorin, TMP-SMX, Clindamycin (as an alternative)
• Supportive care: Anti-inflammatory diet, glutamate regulation, antiparasitic herbs (Artemisia annual (sweet wormwood), turmeric, nutmeg, black cumin – blackseed oil, rosemary, red, sage, thyme oil.

Research Summary and Link to MS: A 2017 case-control study of 200 MS patients and 200 healthy controls found a significantly higher T. gondii seropositivity in MS patients (60.5%in MS vs. 28%in controls). A second study reported similar findings in a smaller cohort (44.2% in MS vs. 24.4% in controls), reinforcing the potential link. Both studies suggest that chronic toxoplasmosis may be an environmental risk factor for MS.

These findings are supported by the biological plausibility of CNS cyst formation, neurotransmitter disruption, immune dysfunction, and chronic inflammation—all of which are central to MS pathology. Despite its global prevalence and extensive evidence, T. gondii remains largely overlooked in MS diagnosis and treatment, representing a critical blind spot in mainstream medicine.

Emerging research increasingly links T. gondii infection to a wide range of neurological and psychiatric disorders—including multiple sclerosis (MS), Parkinson’s disease, Alzheimer’s, ALS, anxiety, depression, schizophrenia, and cognitive decline. These findings suggest that this overlooked parasite could play a key role in many chronic brain conditions.

CLICK HERE to learn more about how high glutamate in MS can be caused by Toxoplasmosis.

Babesia

Babesia is another protozoan parasite that deserves attention—particularly for patients diagnosed with MS. Babesia is spread by biting insects and, like malaria, it infects red blood cells.

Symptoms: Night sweats, air hunger, insomnia, anxiety, palpitations, dry cough, petechiae, fatigue, tinnitus, bruising, enlarged red blood cells, and headaches. These symptoms often fluctuate and are frequently misdiagnosed.

Testing: Diagnosis is difficult with conventional testing. Blood smears require expert analysis, and PCR and IFA tests can produce false negatives. Symptom patterns and energy testing by holistic practitioners are sometimes more reliable indicators.

Treatment:

• Diet and prep phase: Low-carb, anti-inflammatory diet; liver support; treatment of fungal and larger parasite infections.
• Herbal therapies: Artemisinin, Cryptolepis, and liposomal herbal combinations.
• Antibiotics: Atovaquone + Azithromycin is widely used; Clindamycin + Quinine is reserved for more severe cases. New drug Tafenoquine shows promise.
• Bioenergetic testing: Used to tailor treatment to the individual’s unique response.

According to Dr. Dietrich Klinghardt, a pioneer in Lyme and chronic illness research, patients with neurological diseases like MS, ALS, and Parkinson’s often harbor undetected Babesia infections. Conventional tests often miss it, and clinical symptoms are usually more telling than lab results.

The three parasites—Plasmodium, Toxoplasma gondii, and Babesia—share a powerful ability to disrupt brain and immune function. They cross the blood-brain barrier, suppress immune defenses and leave behind lesions and inflammation like what is seen in MS.

And yet, the expert panel responsible for defining how MS is diagnosed and treated continues to ignore this evidence. Doctors aren’t being trained to recognize or test for these infections. Researchers struggle to get funding to explore them. And patients are left to suffer while the medical community insists MS is simply an immune system malfunction.

CLICK HERE to learn more about the link between MS and Babesia.

It’s time for change!

The science is ample and the stories of real recovery—from those who treated the parasites and reclaimed their health—are too powerful to ignore.

We don’t need more years of mystery. We need doctors willing to challenge outdated models. We need testing that looks for infections. And patients must understand that their immune system is not broken. They are infected and recovery is possible.

This isn’t just a medical oversight, it’s a humanitarian crisis.

And the time for change is now!

There are real solutions to recover from parasites today!

To restore health, we must focus on treating the cause of inflammation, which are parasites. First, identify the enemy (parasites), then support the body and treat the parasites while following a holistic approach. When parasitic infections are treated effectively, we can overcome inflammation or disease.

If you’re frustrated with the fact that our standard of care STILL doesn’t offer a real solution for treating MS and other diseases, then click on the link below to watch Pam Bartha’s free masterclass training and discover REAL solutions that have allowed Pam and many others to live free from MS and other diseases.

CLICK Here to watch Pam’s masterclass training

References:

World Health Organization. (2023). Malaria Fact Sheet. Retrieved from https://www.who.int/news-room/fact-sheets/detail/malaria

MS Society of Canada. (2021). Hydroxychloroquine as a Potential Treatment for Primary Progressive MS. Retrieved from https://mscanada.ca/ms-research/latest-research/hydroxychloroquine-as-a-potential-treatment-for-primary-progressive-ms

University of Calgary. (2021). Hydroxychloroquine Delays Disability in MS. Retrieved from https://cumming.ucalgary.ca/news/study-finds-hydroxychloroquine-delays-disability-least-treatable-form-multiple-sclerosis

Caprio, Maria & Russo, Camilla & Giugliano, Antonio. (2016). Vascular Disease in Patients with Multiple Sclerosis: A Review. Journal of Vascular Medicine & Surgery. 04. 10.4172/2329-6925.1000259.https://www.researchgate.net/publication/303439403_Vascular_Disease_in_Patients_with_Multiple_Sclerosis_A_Review

DuBose, Noah G. et al. Vascular dysfunction in multiple sclerosis: Scoping review of current evidence for informing future research directions. Multiple Sclerosis and Related Disorders, Volume 78, 104936.  https://www.msard-journal.com/article/S2211-0348(23)00437-6/abstract

Cameron, D. (2020). Babesia microti in a Patient Diagnosed with Multiple Sclerosis. Retrieved from https://danielcameronmd.com/babesia-microti-multiple-sclerosis-patient/

Krause, P. J., et al. (1996).Concurrent Lyme disease and babesiosis. Evidence for increased severity and duration of illness, Jun 5;275(21):1657-60. https://pubmed.ncbi.nlm.nih.gov/8637139/

Gray, E. B., et al. (2023).Babesia microti Variant With Multiple Resistance Mutations Detected in an Immunocompromised Patient Receiving Atovaquone Prophylaxis. Open Forum Infectious Diseases, 10(3), ofad097. https://academic.oup.com/ofid/article/10/3/ofad097/705591

Kissler, H. (2001). Is multiple sclerosis caused by a silent infection with malarial parasites? Part I. Medical Hypotheses, 57(2), 180–187. https://pubmed.ncbi.nlm.nih.gov/11516218/

Kissler, H. (2001). Is multiple sclerosis caused by a silent infection with malarial parasites? A historico-epidemiological approach: Part II. Medical Hypotheses, 57(3), 292–301. https://doi.org/10.1054/mehy.2001.1277

Palladino, R., et al. (2020). Evaluating the Risk of Macrovascular Events and Mortality Among People With Multiple Sclerosis in England. JAMA Neurology, 77(7), 820–828. https://pmc.ncbi.nlm.nih.gov/articles/PMC7199174/

Rahnama, M., Asgari, M., Petramfar, P., & Solgi, R. (2020). The Role of Toxoplasma gondii Infection Among Multiple Sclerosis Patients Compared to Ordinary People in South of Iran: A Case-Control Study. Journal of Clinical Neuroscience, 79, 1–5. https://doi.org/10.1016/j.jocn.2020.07.004

Zakeri, Z., & Barani, A. (2013). The Relationship between Glutamate and Multiple Sclerosis. Iranian Biomedical Journal, 17(3), 123–130. https://ibbj.org/article-1-148-en.pdf

Azevedo, C. J., Kornak, J., Chu, P., Sampat, M., Okuda, D. T., Cree, B. A. C., Nelson, S. J., Hauser, S. L., & Pelletier, D. (2014). In Vivo Evidence of Glutamate Toxicity in Multiple Sclerosis. Annals of Neurology, 76(2), 269–278. https://escholarship.org/uc/item/2d0277ng

Stojanovic, I., Kostic, M., & Milosevic, M. (2020). The Role of Glutamate in the Pathogenesis of Multiple Sclerosis. ResearchGate. https://www.researchgate.net/publication/344088186_The_Role_of_Glutamate_in_the_Pathogenesis_of_Multiple_Sclerosis

Cader, S., Cifelli, A., Abu-Omar, Y., Palace, J., & Matthews, P. M. (2014). Memory in Multiple Sclerosis is Linked to Glutamate Concentration in Grey Matter Regions. Journal of Neurology, Neurosurgery & Psychiatry, 85(8), 833–839. https://jnnp.bmj.com/content/jnnp/85/8/833.full.pdf

Newcombe, J., Cammer, W., & Cotterell, D. (2000). Multiple sclerosis: altered glutamate homeostasis in lesions correlates with oligodendrocyte and axonal damage. Brain, 123(8), 1343–1352. https://pubmed.ncbi.nlm.nih.gov/11506399/

Pitt, D., Werner, P., & Raine, C. S. (2000). Glutamate excitotoxicity—a mechanism for axonal damage and oligodendrocyte death in Multiple Sclerosis? Annals of Neurology, 47(6), 739–749. https://pubmed.ncbi.nlm.nih.gov/11205156/

Gramsbergen, J. B. P., et al. (2013). Increased Concentrations of Glutamate and Glutamine in Normal-Appearing White Matter of Patients with Multiple Sclerosis and Normal MR Imaging Brain Scans. PLOS ONE, 8(5), e61817. https://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0061817

Hardy, T. L., & Reynolds, R. (2003). Altered expression patterns of group I and II metabotropic glutamate receptors in multiple sclerosis. Brain, 126(8), 1755–1766. https://pubmed.ncbi.nlm.nih.gov/12805104/

Pitt, D., & Lassmann, H. (2017). Glutamate, T cells and multiple sclerosis. Current Opinion in Immunology, 46, 103–108. https://pubmed.ncbi.nlm.nih.gov/28236206/

Srinivasan, R., Sailasuta, N., Hurd, R., Nelson, S., Pelletier, D., & Nelson, S. J. (2005). Evidence of Elevated Glutamate in Multiple Sclerosis Using Magnetic Resonance Spectroscopy at 3T. Brain, 128(5), 1016–1025. https://academic.oup.com/brain/article-abstract/128/5/1016/278496

Pitt, D., Nagelmeier, I. E., Wilson, H. C., & Raine, C. S. (2003). Glutamate Receptor Expression in Multiple Sclerosis Lesions. Brain, 126(8), 1755–1766. https://pubmed.ncbi.nlm.nih.gov/17924980/

David, C. N., Frias, E. S., Szu, J. I., Vieira, P. A., Hubbard, J. A., Lovelace, J., Michael, M., Worth, D., & Wilson, E. H. (2016). GLT-1-Dependent Disruption of CNS Glutamate Homeostasis and Neuronal Function by the Protozoan Parasite Toxoplasma gondii. PLOS Pathogens, 12(6), e1005643. https://pmc.ncbi.nlm.nih.gov/articles/PMC4900626/

Miranda, A. S., Vieira, L. B., Lacerda-Queiroz, N., Souza, A. H., Rodrigues, D. H., Vilela, M. C., et al. (2010). Increased Levels of Glutamate in the Central Nervous System are Associated with Behavioral Symptoms in Experimental Malaria. Brazilian Journal of Medical and Biological Research, 43(12), 1173–1177. https://www.scielo.br/j/bjmbr/a/Ncx4KXMKP3433zzhTJkKDMg/?lang=en

University of Virginia Health System. (2016). Scientists unpack how Toxoplasma infection is linked to neurodegenerative disease. EurekAlert. https://www.eurekalert.org/news-releases/922159