Abstract

ABSTRACT The consumption of inadequately thermally treated fish is a public health risk due to the possible propagation of Anisakis larvae and their antigenic proteins, the causative agent of the zoonotic disease anisakidosis. The present study demonstrated the physiological and histopathological changes that accompanied an oral inoculation of crude extracts from fresh and thermally treated Anisakis Type II (L3) in Wistar albino rats. Nematode worms were isolated from the marine fish Dicentrarchus labrax. They were examined and taxonomically identified using light and scanning electron microscopy. The study was performed in 6 rat groups: a control group (I), a garlic oil (GO) inoculated group (II), a fresh L3 inoculated group (III), a thermally treated L3 inoculated group (IV), a fresh L3 + GO inoculated group (V), and a thermally treated L3 + GO inoculated group (VI). It was observed that rats inoculated with fresh and thermally treated L3 crude extracts showed abnormal oxidative stress markers associated with the destruction of normal architecture of spleen and thymus. GO produced a protective effect in rat groups inoculated with L3 extracts + GO administration via the amelioration of oxidative stress markers, which was confirmed by the marked normal structure of the organs’ histology. Cooking of L3 infected fish induced severe physiological and histopathological alterations compared to uncooked infected fish. The administration of garlic before and after fish eating is recommended to avoid the dangerous effect of anisakids, even if they are cooked.

Highlights

  • Anisakidosis is a vital fish-borne zoonotic disease caused by third or, infrequently, fourth larval stages of the nematode A. simplex, which live as encapsulated larvae embedded in the edible muscle of marine fish (Morsy et al, 2013)

  • Anisakis larvae pose a health risk to humans even when the fish is thoroughly cooked because dead or thermally treated L3 produce a number of physiological and histopathological changes in humans after fish ingestion, which lead to the concept of acute anisakiasis (Montalto et al, 2005)

  • For scanning electron microscopy (SEM), 10 worms were fixed in 3% phosphate-buffered glutaraldehyde for 3h, washed in the same buffer, and dehydrated in an ascending alcohol series according to Madden and Tromba (1976)

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Summary

Introduction

Anisakidosis is a vital fish-borne zoonotic disease caused by third or, infrequently, fourth larval stages of the nematode A. simplex, which live as encapsulated larvae embedded in the edible muscle of marine fish (Morsy et al, 2013). The life cycle begins when eggs are passed in the feces of marine mammals into water, where they hatch to release free-living larvae (L2), which are consumed by crustaceans and further develop into L3. When infected crustaceans are ingested by fish, the third larvae enter their body cavity and muscles (Kassem and Bowashi, 2015; Nieuwenhuizen, 2016). Anisakis larvae pose a health risk to humans even when the fish is thoroughly cooked because dead or thermally treated L3 produce a number of physiological and histopathological changes in humans after fish ingestion, which lead to the concept of acute anisakiasis (Montalto et al, 2005). Traditional medicines worldwide identified the benefits of plants in human health and have taken advantage of the empirical treatment of common human diseases

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