Short Communication Volume 14 Issue 1
Received: March 21, 2026 | Published: April 6, 2026
Citation: Hamad MNM. Zinc–iron dysregulation and fear processing in chronic toxoplasma gondii infection: a ZFT-centered hypothesis. J Microbial Exp. 2026;14(1):21-22. DOI: 10.15406/jmen.2026.14.00452
Toxoplasma gondii is an obligate intracellular protozoan parasite capable of establishing lifelong infection in approximately one third of the global human population. While acute infection is typically asymptomatic in immunocompetent individuals, chronic toxoplasmosis has been increasingly associated with subtle neurobiological, behavioral, and neuropsychiatric alterations. Acute infection follows a 48–72hour tachyzoite replication cycle and can disseminate widely, particularly in immunocompromised hosts. Transmission occurs via ingestion of tissue cysts in undercooked meat, food or water contaminated with oocysts, or vertical (congenital) transmission. Standard treatment of acute toxoplasmosis includes pyrimethamine, sulfadiazine, and leucovorin, while spiramycin is indicated in pregnant women to reduce fetal transmission risk. Experimental studies in rodents demonstrate parasite-induced disruption of innate fear responses, most notably the loss of aversion to predator odors (“fatal attraction”). Despite extensive documentation of these behavioral effects, the molecular mechanisms linking chronic infection to fear dysregulation remain incompletely understood. Evidence indicates that T. gondii infection disrupts host micronutrient homeostasis, particularly zinc and iron, alongside alterations in calcium signaling, antioxidant defenses, and hippocampal structure. This paper proposes a unifying hypothesis in which parasite-mediated sequestration of zinc and iron via a Zinc/Iron Transmembrane Transporter (ZFT) sustains chronic infection while indirectly destabilizing host neural circuits involved in fear learning and extinction.
Keywords: Toxoplasma gondii; acute toxoplasmosis; chronic toxoplasmosis; zinc deficiency; iron metabolism; calcium signaling; hippocampus; fatal attraction; micronutrients
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