The principal pathology in the acute phase of trichinellosis starts with the release of histaminase enzyme, which is responsible for eosinophilia (type I hypersensitivity reaction), followed by increased levels of mast cells, eosinophils, and parasite-specific IgE production, leading to inducing Trichinella damage to the blood vessels which caused by eosinophil cationic protein, and eosinophil peroxidase [9]. This evidence concerns the gene IGHE and IgE responsiveness, atopic.