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Updated: Oct 18, 2026
3-D Imaging and Analysis of Neurons Infected In Vivo with Toxoplasma gondii
Published on: December 9, 2014
Toxoplasma serology: Breaking the diagnostic boundary of schizoaffective disorder? Insights from a comparative
Bruno Romeo1, Juliette Jeannin2, Valentine Lestra1
1APHP, Paul Brousse Hospital, Department of Psychiatry and Addiction medicine, Villejuif, F-94800, France; Unité de recherche UR Psychiatrie-Comorbidités-Addictions PSYCOMADD Université Paris Saclay, France.
Background:
Toxoplasma gondii (T. gondii) infection has been implicated in the pathophysiology of psychiatric disorders, yet no study has compared its seroprevalence between schizoaffective disorder (SZA) and other psychiatric conditions. This study aimed to compare T. gondii seroprevalence between patients with SZA, schizophrenia (SZ), and bipolar disorder (BD), and to examine whether seropositivity differentially affects innate immune markers across these diagnoses.
Methods:
Overall 144 patients were included in this cross-sectional study. T. gondii seroprevalence was determined and leukocyte counts and derived immune ratios were compared across diagnostic groups according to T.gondii seroprevalence.
Results:
T. gondii seroprevalence was significantly higher in SZA (68.8%) as compared to BD (44.2%; p = 0.02), but did not differ significantly from SZ (52.2%; p = 0.2). Relative to SZA, higher neutrophil (p < 0.01) and monocyte (p = 0.02) levels were associated with greater odds of BD, while higher NLR was associated with both BD (p = 0.04) and SZ (p = 0.02), and higher MLR with SZ (p = 0.02). However, none of these associations remained significant after Bonferroni correction. We observed a significant interaction between basophil counts and T. gondii in SZA versus BD (padj < 0.01) and SZ (padj < 0.01), indicating a diagnosis-specific immune modulation.
Conclusion:
Our findings suggest that T. gondii seroprevalence in SZA is closer to SZ than BD. However, seropositivity appears to affect innate immune markers differently in SZA, without inflammatory activation. This immune profile suggests a unique pathophysiological signature in SZA and warrants further investigation.
