Allergic Reactions to Anisakis simplex Parasitizing Seafood

Moreno-Ancillo, A; Caballero, Teresa; Cabañas, Rosario; Contreras, J; Martín-Barroso, Juan-Antonio; Paredes, Pilar; López-Serrano, M C

doi:10.1016/s1081-1206(10)63009-8

Cited by 82 publications

(62 citation statements)

References 8 publications

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“…Furthermore, HLA DRB1*1502, DQB1*0601, and DRB I *0404 are significantly overrepresented (and hence probable genetic risk factors) in subjects allergic to A. simplex (239). The newly characterized allergens Ani s 2 and Ani s 3 ( (190,192) are showing that allergy in Europe is not confined to the Basque Country but is also in Japan, where more cases have also been diagnosed (152). However, Italian and Portuguese cases are similar to those of the Basque Country because they involve true allergy with cooked fish, and reports from other parts of Spain (Madrid and its surrounding provinces) appear to describe gastroallergic cases caused by raw or undercooked fish (71,99).…”

Section: Human Susceptibility Factorsmentioning

confidence: 99%

Anisakis simplex: from Obscure Infectious Worm to Inducer of Immune Hypersensitivity

2008

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SUMMARY Infection of humans with the nematode worm parasite Anisakis simplex was first described in the 1960s in association with the consumption of raw or undercooked fish. During the 1990s it was realized that even the ingestion of dead worms in food fish can cause severe hypersensitivity reactions, that these may be more prevalent than infection itself, and that this outcome could be associated with food preparations previously considered safe. Not only may allergic symptoms arise from infection by the parasites (“gastroallergic anisakiasis”), but true anaphylactic reactions can also occur following exposure to allergens from dead worms by food-borne, airborne, or skin contact routes. This review discusses A. simplex pathogenesis in humans, covering immune hypersensitivity reactions both in the context of a living infection and in terms of exposure to its allergens by other routes. Over the last 20 years, several studies have concentrated on A. simplex antigen characterization and innate as well as adaptive immune response to this parasite. Molecular characterization of Anisakis allergens and isolation of their encoding cDNAs is now an active field of research that should provide improved diagnostic tools in addition to tools with which to enhance our understanding of pathogenesis and controversial aspects of A. simplex allergy. We also discuss the potential relevance of parasite products such as allergens, proteinases, and proteinase inhibitors and the activation of basophils, eosinophils, and mast cells in the induction of A. simplex-related immune hypersensitivity states induced by exposure to the parasite, dead or alive.

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Section: Human Susceptibility Factorsmentioning

confidence: 99%

Anisakis simplex: from Obscure Infectious Worm to Inducer of Immune Hypersensitivity

2008

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“…Allergies to L3 infection have previously been diagnosed by positive skin prick tests, specific IgE production, and total elevation of IgE levels Moreno-Ancillo et al, 1997;Lopez-Serrano et al, 2000;Moneo et al, 2000;Purello-D'Ambrosio et al, 2000). Daschner et al (2002) has elucidated in detail the time course of IgE production in human L3-dependent allergies.…”

Section: Specific Immunoglobulin E Production and Allergy To L3mentioning

confidence: 99%

Immune reactions and allergy in experimental anisakiasis

Cho

Lee

2006

Korean J Parasitol

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Abstract:The third-stage larvae (L3) of the parasitic nematode, Anisakis simplex, have been implicated in the induction of hyperimmune allergic reactions in orally infected humans. In this work, we have conducted a review of an investigation into immune reactions occurring in animals experimentally infected with A. simplex L3. The patterns of serum antibody productions in the experimental animals against excretory-secretory products (ESP) of A. simplex L3 contributed to our current knowledge regarding specific humoral immune reactions in humans. In our review, we were able to determine that L3 infection of experimental animals may constitute a good model system for further exploration of immune mechanisms and allergy in anisakiasis of humans. worldwide (Mattiucci et al., 1997;Shih, 2004;Ugland et al., 2004). Many epidemics have been reported in Japan and Spain (Chai et al., 2005). Increasing reports of L3 infection in fish have been documented in South Korea, in which the consumption of raw marine fish is also popular (Chai et al., 1992;Im et al., 1995;Song et al., 1995Song et al., , 1999. Easy access to endoscopes and enhanced awareness of anisakiasis among clinicians has resulted in better reporting of morbidity resultant from L3 infection. L3 infection induces the production of specific antibodies and cytokines (Kennedy et al., 1988;Daschner et al., 2001;Nieuwenhuizen et al., 2006). Antibodies can be detected 2 weeks after infection, consistent with the time courses associated with other microorganisms. Analyses of specific antibody levels are generally irrelevant to the differential diagnosis of an acute state in cases of L3 infection, because the profound pain associated with L3 penetration begins only a few hours after the consumption of infected raw fish. However, antibody level measurements are helpful both in the differentiation of tumors from the granulomas formed by infiltrating L3 and in investigations of allergic diseases (Gutierrez and Cuellar, 2002;Kim et al., 2006).The production of IgE tends to increase during parasite infections, but the ultimate effects of IgE vary considerably, depending on the host-parasite relationships. Hyperimmune allergic reactions have been closely associated with IgE production. The infection of a parasite into its normal host tends to reduce the development of allergic responses, despite the associated upshift in IgE production (van den Biggelaar et al., 2000;Yazdanbakhsh et al., 2002). By contrast, the infection of T. canis in humans, an abnormal host, induces increased allergic reactions (Sharp and Olson, 1962;Sharghi et al., 2001). A. simplex L3 has also been shown to induce allergic diseases at a high rate, principally due to the fact that humans are not a regular host of this parasite (Audicana et al., 2002;Klimpel et al., 2004).Through investigations of allergic responses to L3 for a period of more than 10 years, several shared features have been identified, which indicate that immune reactions to L3 infection evidence similar patterns in humans and experimental...

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“…In recent years it has been recognised that the manifestations of infection with Anisakid parasites may be dominated by an allergic response [18]. Sensitisation may occur to both live parasites, or to parasitised food in which worms have been killed by cooking or pasteurisation.…”

Section: Anisakidosismentioning

confidence: 99%