PO121 | IMMUNOTHROMBOSIS AND MULTIPLE-SITE VENOUS THROMBOEMBOLISM IN ACUTE TOXOPLASMOSIS: A CASE REPORT

A. Grembiale¹, A. Sabena¹, G. Dettori¹, C. Grendene¹, S. Grazioli¹, S. Venturini² | ¹SOC Medicina Interna 2 - Azienda Sanitaria Friuli Occidentale - Pordenone, Italy; ²SSD Malattie Infettive - Azienda Sanitaria Friuli Occidentale - Pordenone, Italy

Introduction. Immunothrombosis can limits pathogen dissemination and enhances antimicrobial activity at the microvascular level but this process can progress to pathological thrombosis (thromboinflammation). Infections can trigger venous thromboembolism (VTE) through crosstalk between inflammatory and coagulation pathways, a mechanism described mainly in viral illnesses but also reported in bacterial and parasitic infections. Multisite VTE work-up focuses on malignancy, inflammation, autoimmune issues, thrombophilia, and infections. Toxoplasmosis is a global parasitic disease, in healthy individuals, infection is usually asymptomatic or causes mild illness; organ involvement is rare. Immunocompromised patients may experience severe organ involvement (central nervous system CNS, lungs, liver, or other organs), especially if Toxoplasma reactivates from dormant cysts. VTE during acute Toxoplasma infection is extremely rare and documented only in isolated case reports.
Case Report. A 63-year-old male with psoriatic arthritis, receiving adalimumab and MTX therapy, presented with fever, pneumonia, and generalized seizures. Head CT demonstrated a right parietal hemorrhagic infarction, while brain MRI identified cerebral venous sinus thrombosis involving both transverse and sigmoid sinuses with extension to the internal jugular veins. Contrast-enhanced CT revealed severe consolidation in the right lung, multisite splanchnic thrombosis— with involvement of the splenic and superior mesenteric veins—and microinfarcts suggestive of embolic phenomena across multiple organs. DVT, endocarditis, and sinusitis were excluded; autoimmune panel and thrombophilia screening was negative, complement was normal. The patient was initiated on UFH, subsequently switched to warfarin. Whole-body PET/CT detected multiple hypermetabolic lymphadenopathies at thoracic and external iliac stations. Serological testing for Toxoplasma gondii indicated recent primary infection and PCR confirmed its presence in blood. Due to CNS and visceral organ involvement, oral trimethoprim–sulfamethoxazole was administered for six weeks, resulting in clinical improvement.
Conclusions. VTE at unusual sites represents a diagnostic challenge. In the present case, an extensive etiological workup for multisite/unusual-site VTE was unremarkable, with no alternative provoking factors identified; subsequent investigations were therefore guided by immune status and organ involvement. Experimental evidence indicates that the parasite can induce endothelial injury and promote coagulation at the neurovascular interface. The mechanisms underlying thrombosis associated with toxoplasmosis remain incompletely defined. T. gondii tachyzoites invade endothelial cells, leading to endothelial activation and disruption of barrier integrity within the microvasculature. This process results in upregulation of procoagulant pathways and adhesion molecules, thereby favoring local platelet–fibrin clot formation, consistent with infection-driven immunothrombosis. Concomitant cytokine release, further enhances endothelial permeability and promotes complement activation. Local reductions in blood flow may decrease the threshold for thrombosis. Collectively, these mechanisms provide a biologically plausible explanation for thrombotic events observed in primary toxoplasmosis. Our report identifies acute toxoplasmosis as a rare cause of thrombosis and supports targeted T. gondii testing in febrile patients with multisite VTE