Infection with "Helicobacter pylori" was assessed through serum "H. pylori" IgG antibody in children with intellectual disabilities (ID). The sero-status of cytotoxin-associated gene A (CagA) was determined as a risk determinant for severe "H. pylori"-associated diseases. In total, 210 children with ID were included who were permanent resident of three institutes in Tehran. Medical history and demographic data were collected by reviewing the medical file records. The anti "H. pylori" IgG antibody was detected in serum of 74.8% of children using ELISA. Significant correlations were found between the rate of infection and age (P = 0.001) and duration of institutionalization (P = 0.018). The likelihood of "H. pylori" IgG positive response increased with age with the highest response in 15-18 years age group (OR = 6.66, 95% CI: 2.14-20.17; P = 0.001). Similarly, the average titers of "H. pylori" IgG antibody were increased with age. The institutionalization duration of more than 49 months affected the likelihood of "H. pylori" IgG positive response (OR = 2.437, 95% CI: 1.12-5.26; P = 0.023). Anti-CagA titers were higher than 5 arbU/ml in 92 (58.6%) children, indicating a positive response against CagA protein. The titer of "H. pylori" IgG was significantly higher in CagA-positive (mean [plus or minus] SE = 51.04 [plus or minus] 3.41) than in CagA-negative children (38.07 [plus or minus] 4.18; P = 0.017). In contrast to total "H. pylori" IgG titers, anti-CagA antibody had non-regular trend of alterations with age. The seropositivity rate of "H. pylori" infection in ID children was higher than other reports in healthy children from various regions of the country. The risk of "H. pylori" infection is increased with age and duration of institutionalization. The serostatus of CagA in children with IDs has not been reported so far. The regular monitoring of the CagA-positive carriers is recommended; since CagA positive cases carry the risk of progression of infection toward severe "H. pylori" associated sequels such as gastric cancer and duodenal ulcers. (Contains 1 figure and 4 tables.)