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The distribution of Toxoplasma gondii genotypes varies from one geographic area to another. The present study aimed to determine T. gondii genotypes associated with human infection in Egypt. Individuals seropositive for anti-toxoplasma IgG and IgM (group I, n = 50) or for specific IgG only (group II, n = 50) were enrolled. Of the participants, 75 % were asymptomatic pregnant women. The others presented with lymphadenitis (n = 21), chorioretinitis (n = 3), and unexplained hepatomegaly (n = 1). Using nested PCR, T. gondii GRA6-coding fragment was amplified from DNA extracted from blood samples of participants. Amplification was successful in 12 samples with nonsignificant difference between both groups but with a significant association with the presence of toxoplasmosis-related manifestations. Restriction fragment length polymorphism analysis of these samples revealed the presence of type I in seven samples and atypical types in five samples. Both typical and atypical strains were detected in individuals of both groups with no bias towards specific clinical presentation.

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Background: Hashimoto’s thyroiditis (HT) is a common autoimmune disorder that causes significant morbidity. Interleukin (IL)-17 was identified as a major contributing factor in the pathogenesis of HT. Blastocystis hominis (BH) is a very common infection and has been shown to be associated with several diseases. Our aim was to determine serum IL-17 level in HT patients with and without BH infection and the effect of eradicating BH in patients with HT. Methods: A prospective cohort study was conducted on 20 HT patients not infected with BH (group I), 20 HT patients infected with BH (group II), and 20 healthy patients (group III). Serum free triiodothyronine (FT3), free thyroxine (FT4), thyroid stimulating hormone (TSH), thyroid peroxidase antibodies (anti-TPO), and IL-17 were performed by ELISA method and were repeated in group II after 6 weeks of eradication of BH. Results: Patients with HT showed a significantly higher serum IL-17 compared with controls. IL-17 was significantly higher in HT patients infected with BH compared with HT patients not BH infected (mean 6.93 ± 2.83 pg/ml versus 3.25 ± 1.55 pg/ml, p = 0.003). After BH eradication TSH, anti-TPO, and IL-17 were significantly decreased (mean 14.76 ± 11.11 µIU/ml versus 9.39 ± 7.11 µIU/ml, p < 0.001; mean 308 ± 175.6 IU/ml versus 295.4 ± 167.1 IU/ml, p = 0.006; and mean 6.93 ± 2.83 pg/ml versus 6.45 ± 2.48 pg/ml, p < 0.001), respectively. Multivariate analysis after treating BH infection showed that IL-17 was significantly negatively correlated with FT3 (adjusted p = 0.002) and significantly positively correlated with anti-TPO (adjusted p = 0.045). Conclusion: Treatment of BH infection ameliorates HT through reduction in IL-17, anti-TPO, and TSH. Clinical trial registration number: PACTR201909495111649

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