Nieuwenhuizen, Natalie, Lopata, Andreas L. , Jeebhay, Mohamed F., Herbert, De'Broski R., Robins, Thomas G., and Brombacher, Frank (2006) Exposure to the fish parasite Anisakis causes allergic airway hyperreactivity and dermatitis. Journal of Allergy and Clinical Immunology, 117 (5). pp. 1098-1105.

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Abstract

Background Several case reports show allergy and anaphylactic reactions to the fish parasite Anisakis in the domestic and occupational setting. Further research is needed on the prevalence and mechanisms of disease.

Objective To determine the prevalence of Anisakis sensitization and related symptoms among workers in 2 fish-processing factories, and to use gene-deficient mice to determine the working mechanisms of Anisakis allergy.

Methods A modified version of the European Community Respiratory Health Survey was used to interview 578 South African fish-processing workers. Sensitization to Anisakis, seafood, and common aeroallergens was determined by skin prick test. Lung function was measured by spirometry and methacholine challenge. Serum eicosapentaenoic acid levels were used as an index of seafood consumption. Sensitized wild-type, IL-4, or IL-4 receptor α–deficient mice were challenged orally with Anisakis extract. Allergic reactions, lung pathology, antibodies, cytokines, mast cell proteases, and histamine were evaluated.

Results The prevalence of sensitization to Anisakis was higher than the prevalence of sensitization to fish (8% vs 6%). Anisakis-specific IgE reactivity was associated with bronchial hyperreactivity and dermatitis, and significantly increased with fish consumption. In mice, Anisakis infective larvae (L3) induced a striking TH2/type 2 response. Food-allergic–type reactions induced by oral challenge with Anisakis extract were absent in IL-4 receptor α knockout mice.

Conclusion Anisakis sensitization in fish-processing workers is associated with allergic symptoms and correlates with high levels of fish consumption. Anisakis proteins induce allergic reactions in sensitized mice by IL-4/IL-13–mediated mechanisms.

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