The Effect of Toxoplasmosis
Although most people who are infected by the parasite experience mild symptoms (e.g., swollen lymph glands or muscle aches and pains), often resembling the flu, severe toxoplasmosis can occur in people with severely compromised immune systems, and infants with mothers who were infected with the parasite during pregnancy can be born with congenital birth defects. Recent studies have shown that T. gondii infection can be highly problematic and can contribute to changes in brain chemistry and neurological pathways.
T. gondii and glutamate
Studies have found evidence that links the protozoan infection with conditions such as epilepsy, schizophrenia and Parkinson’s disease. Researchers recently found that the T. gondii infection can contribute to the accumulation of glutamate – an amino acid involved in cognition, memory and learning – outside of cells. This buildup is similar to the buildup of glutamate outside of cells seen in patients with traumatic brain injury, neurodegenerative diseases such as Alzheimer’s disease, epilepsy and multiple sclerosis, and psychiatric conditions such as schizophrenia and mania. Increased glutamate concentration outside of cells is problematic because it can contribute to cell death and can change the chemistry and how cells communicate in the brain.
The T. gondii protozoan parasite was also recently linked to a chronic lifelong infection in the brain. Emma H. Wilson and her colleagues investigated the changes that occurred in the glutamate activity in the central nervous system (CNS) of mice that were infected with the T. gondii infection. The researchers hypothesized that the T. gondii infection would induce glutamate dysregulation in the CNS and contribute to heightened glutamate concentrations in the prefrontal cortex, an area of the brain that is important for anxiety and decision-making processes.
The researchers used microdialysis to collect extracellular (i.e., outside the cell) glutamate concentrations in the CNS from mice infected with the toxoplasma parasite. They found that the T. gondii infection produced heightened extracellular glutamate, which impairs the ability of glutamate transporters (i.e., GLT-1) to remove excess glutamate from outside the cells. While the results of this study provide evidence for the lifelong consequences and neural changes that result from infection of T. gondii, researchers also found that the treatment of the mice with ceftriaxone, an antibiotic commonly used to treat certain bacterial infections, was beneficial for reversing the negative effects that the infection had on glutamate transmission.
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About the author
Amanda Habermann is a writer for Sovereign Health. A graduate of California Lutheran University, she received her M.S. in clinical psychology with an emphasis in psychiatric rehabilitation. She brings to the team her background in research, testing and assessment, diagnosis and recovery techniques. For more information and other inquiries about this article, contact the author at firstname.lastname@example.org.