Larval nematodes from fish of the subfamily anisakinae and gastro-intestinal lesions in mammals

Abstract

The specificity of anisakine nematodes associated with gastric lesions in mammals is discussed and their suggested life-cycles are described. Mature grey seals, Halichoerus grypus, from the Orkney Islands were infected with adult Terranova decipiens and Contracaecum osculatum and with immature Terranova sp. and Contracaecum sp. Yearling grey seals from eastern Scotland had these species and also a few adult Anisakis typica and many immature Anisakis sp. Many seals had lesions in the fundic stomach associated with dense groups of immature Contracaecum sp. and Anisakis sp. Porpoises, Phocaena phocaena, from eastern Scotland were infected with mature Anisakis typica and larvae of Anisakis sp. and had associated stomach lesions similar to those in the grey seals, mostly in the first stomach. All lesions were parasitic eosinophilic granulomata and the associated larval nematodes usually had an eosinophilic substance surrounding their heads with an adjacent layer of necrotic host tissue. Cast cuticles with adherent macrophages, leucocytes and giant cells were also present in the apparent absence of nematodes as deep as the muscularis externa in encapsulated areas which were often calcified. Laboratory rats were infected with larval Anisakis sp. and Terranova sp. from the mesenteries of herring and the muscles of cod respectively. Larvae of Anisakis sp. penetrated mainly in the stomach wall and had passed through by three days. At four days the host response was an eosinophilic and lymphocytic infiltration with associated fibroblasts and macrophages. Second doses three and 14 days after the first infection induced many more inflammatory cells. Larvae of Terranova sp. penetrated only to the muscularis mucosa and their front ends were surrounded by a few eosinophils and a layer of necrotic host tissue whilst the submucosa showed a haemorrhagic eosinophilic and lymphocytic infiltration. It was concluded that the gastric lesion described by previous authors in mammalian hosts, and those described in the present paper from grey seals and porpoises are caused by the repeated penetration in one area of large numbers of the associated anisakine larvae.