Background and study aim: With the eradication of poliomyelitis, GuillainBarré syndrome (GBS) is the most common cause of Acute Flaccid Paralysis (AFP) in children. The present study aimed at assessment of how far Toxoplasmosis contributes to the cases of Acute Flaccid Paralysis (AFP) among children in Sharqiya governorate, Egypt. Patient and Methods: Over years from April 2010 to September 2012, one hundred children with non-polio acute flaccid paralysis were selected, after their parent written consent, out of children monitored in Sharqiya Governorate by the Project of Acute Flaccid Paralysis (AFP) Surveillance, the Ministry of Health and Population, Egypt. As they underwent treatment by appropriate therapy for AFP, anti-Toxoplasma IgM and IgG antibodies, anti-Campylobacter jejuni IgM and IgG antibodies and tumor necrosis factor alpha (TNF-α) were sought quantitatively in their sera by ElISA. Results:Anti-Toxoplasma IgM and IgG were respectively detected among 3 (3%) and 42 (42%) of them. Anticampylobacter IgM and IgG were respectively detected among 25 (25%) and 54 (54%) of them. TNF-α absorbance values were 0.95±0.35 among 3 patients with symptomatic acute toxoplasmosis (positive IgM and IgG), 0.22 ±0.11 among 39 patients with chronic toxoplasmosis (with positive anti Toxoplasma IgG only), and 0.21±0.12 among patients without toxoplasmosis. The 3 cases of acute flaccid paralysis due to acute toxoplasmosis did not respond to the ordinary treatment of AFP treatment; but dramatically responded to Sulfadiazine and Pyrimethamine. Conclusion: These results may make the study hypothesize that Toxoplasma may exert its pathogenic effect on nerve myelin directly via TNF-α. Thus approaching Acute Flaccid Paralysis, higher index of suspicion is needed so as to do not miss cases with toxoplasmic etiology.