Toxoplasmosis, caused by the protozoan parasite Toxoplasma gondii (T. gondii), is a highly prevalent zoonotic disease, infecting approximately one-third of the global population (Bisetegn et al., 2023). Seroprevalence varies widely, from 10 % to over 90 % (Safarpour et al., 2020; Torgerson and Mastroiacovo, 2013). Transmission occurs primarily through ingestion of undercooked meat, contaminated water, or food with oocysts (Shapiro et al., 2019), as well as congenital transmission from mother to fetus (Pinto-Ferreira et al., 2019).
T. gondii infection is typically asymptomatic or causes mild flu-like symptoms in immunocompetent individuals but poses significant risks for immunocompromised patients and pregnant women (Teimouri et al., 2022). Congenital transmission can lead to fetal complications, such as abortion or malformations, with risks decreasing later in pregnancy (Khan and Khan, 2018). Emerging studies also link T. gondii to neurological and mental disorders, including schizophrenia and Alzheimer's disease (Kazemi Arababadi et al., 2024).
T. gondii infection in the central nervous system is controlled by immune responses that balance infection management and inflammation (Ghahremani et al., 2025; Wohlfert et al., 2017). Interferon-driven immunity typically converts acute infection into a latent state with tissue cysts containing bradyzoites (Matta et al., 2021), which persist in the brain, causing oxidative stress and localized inflammation (Matta et al., 2021; Schlüter and Barragan, 2019). These cysts may protect against reinfection but can reactivate into severe acute infection in immunocompromised individuals (Flegr, 2013).
Ischemic stroke is a sudden neurological disorder primarily caused by the blockage of blood vessels or brain bleeding (Johnston et al., 2009). Atheroma in large cerebral vessels or heart-originated blood clots commonly leads to ischemic strokes, whereas small cerebral vessel diseases can cause both ischemic stroke and cerebral hemorrhage (Greenberg, 2006). Stroke is a leading global cause of death and disability, with ischemic stroke accounting for 80 % of cases (Boysen and Truelsen, 2000). Inflammation and oxidative stress drive ischemic brain injury, triggering acute and sustained inflammatory responses that impact white blood cell function and clinical outcomes in patients (Anrather and Iadecola, 2016; Chavda et al., 2022). Infections and stroke exhibit bidirectional links: acute infections may trigger stroke, whereas post-stroke immunosuppression increases the risk of infection, exacerbating immune dysregulation and long-term cognitive decline, underscoring the relevance of these interactions (Elkind et al., 2020; Miller and Elkind, 2016).
T. gondii infection may influence ischemic stroke outcomes by modulating inflammation and oxidative stress. In mice with chronic T. gondii infection undergoing middle cerebral artery occlusion, smaller infarct sizes were observed, likely due to increased anti-inflammatory cytokines and reduced pro-inflammatory cytokines (Arsenijevic et al., 2007). Chronic infection may also promote neuroprotective factors, potentially improving post-ischemic outcomes (Lee et al., 2020).
While animal studies have indicated the potential neuroprotective effects of chronic T. gondii infection (Arsenijevic et al., 2007; Lee et al., 2020), there remains a notable gap in human research, specifically investigating the influence of this infection on outcomes in acute ischemic stroke (AIS) patients.
The complex relationship between T. gondii infection and the inflammatory processes involved in AIS underscores the need for further investigations. Understanding how these factors interact could shed light on potential therapeutic avenues and improve clinical outcomes for stroke patients. This study aimed to (1) assess the seroprevalence of T. gondii in patients diagnosed with AIS, (2) evaluate the potential influence of T. gondii infection on clinical outcomes, and (3) investigate the correlation between T. gondii seropositivity and stroke severity. We hypothesized that T. gondii seropositivity may be associated with altered clinical outcomes in patients with AIS. Understanding the relationship between T. gondii infection and AIS could provide insights into potential risk factors and management strategies for stroke patients.
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