TL;DR: 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.
Abstract: 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
TL;DR: The problems and clinical implications associated with A. simplex, other related conditions, and the way in which disease manifestations vary from person to person are discussed.
TL;DR: The polymorphisms obtained by restriction fragment length polymorphisms have provided a new set of genetic markers for the accurate identification of sibling species and morphospecies.
TL;DR: The morphological and morphometric analyses revealed the presence of morphological features that differed among the 3 biological species, and the tree topologies support the finding that A. simplex (s.s.), A. pegreffii, and A. berlandi n.
Abstract: Numerous specimens of the 3 sibling species of the Anisakis simplex species complex (A. pegreffii, A. simplex (senso stricto)), and A. simplex sp. C) recovered from cetacean species stranded within the known geographical ranges of these nematodes were studied morphologically and genetically. The genetic characterization was performed on diagnostic allozymes and sequences analysis of nuclear (internal transcribed spacer [ITS] of ribosomal [r]DNA) and mitochondrial (mitochondrial [mt]DNA cox2 and rrnS) genes. These markers showed (1) the occurrence of sympatry of the 2 sibling species A. pegreffii and A. simplex sp. C in the same individual host, the pilot whale, Globicephala melas Traill, from New Zealand waters; (2) the identification of specimens of A. pegreffii in the striped dolphin, Stenella coeruleoalba (Meyen), from the Mediterranean Sea; and (3) the presence of A. simplex (s.s.) in the pilot whale and the minke whale, Balaenoptera acutorostrata Lacepede, from the northeastern Atlantic wa...
TL;DR: It is suggested that gastroallergic anisakiasis be considered a distinct clinical entity in which the predominant symptoms are hypersensitivity symptoms and inWhich the correct diagnosis is not only important in the management of the acute reaction but also in the prevention of further allergic episodes.
Abstract: Background: Human subjects can be parasitized by Anisakis simplex by eating raw or undercooked fish. Gastric anisakiasis is probably the most frequent clinical entity presenting with severe epigastric pain, vomiting, and diarrhea. In gastroallergic anisakiasis hypersensitivity symptoms predominate. Objective: We sought to describe clinical features, laboratory data, and gastroscopic findings in gastroallergic anisakiasis. Methods: We selected 40 patients presenting to the emergency department with an acute allergic reaction, and if we suspected acute parasitism by A simplex , a fiberoptic gastroscopy was performed. In 20 patients we could detect one or more nematodes; these patients are referred to as group A. Those in whom no worm could be found are referred to as group B (n = 20). A detailed history, clinical features, gastroscopic findings, laboratory data, and skin prick test responses were compared. Results: Long-time intervals of up to 26 hours between fish intake and onset of hypersensitivity symptoms were found (group A, 5.4 ± 6.3 hours; group B, 5.3 ± 2.6 hours). Patients in groups A and B did not differ with respect to allergic symptoms (urticaria, angioedema, erythema, bronchospasm, and anaphylaxis) or the mainly light abdominal symptoms (upper abdominal pain, nausea, vomiting, and diarrhea). No significant differences were found with respect to age, time interval between fish intake and onset of symptoms, white cell and eosinophil counts, specific IgE levels against A simplex , or total IgE levels. Conclusions: The peculiar sometimes long-time interval between fish intake and onset of allergic symptoms render the diagnosis difficult. An early gastroscopy can confirm the diagnosis and prevent complications. We suggest that gastroallergic anisakiasis be considered a distinct clinical entity in which the predominant symptoms are hypersensitivity symptoms and in which the correct diagnosis is not only important in the management of the acute reaction but also in the prevention of further allergic episodes. (J Allergy Clin Immunol 2000;105:178-81.)