The oil of garlic, Allium sativum L. (Amaryllidaceae), as a potential protectant against Anisakis spp. Type II (L3) (Nematoda) infection in Wistar rats / O óleo de alho, Allium sativum L. (Amaryllidaceae), como potencial protetor contra Anisakis spp. Infecção tipo II (L3) (Nematoda) em ratos Wistar

Abstract The consumption of inadequately thermally treated fish is a public health risk due to the possible propagation of Anisakis larvae. 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 rats. Worms were isolated from a marine fish and examined and identified using light and scanning electron microscopy. The study was performed in 6 rat groups: control (I), garlic oil (GO) inoculated (II), fresh L3 inoculated (III), thermally treated L3 inoculated (IV), fresh L3 + GO inoculated (V), and a thermally treated L3 + GO inoculated (VI) groups. Rats inoculated with fresh and thermally treated L3 showed abnormal liver and kidney functions associated with the destruction of normal architecture. GO produced a protective effect in rat groups inoculated with L3 extracts + GO via the amelioration of liver and kidney functions, which was confirmed by the marked normal structure on histology. Cooking of L3-infected fish induced severe alterations compared to uncooked fish. The administration of garlic before and after fish eating is recommended to avoid the dangerous effect of anisakids, even if they are cooked.

Resumo O consumo de peixe inadequadamente tratado termicamente representa um risco para a saúde pública, com a possibilidade da propagação de larvas de Anisakis. O presente estudo demonstrou as alterações fisiológicas e histopatológicas acompanhadas de inoculação oral de extractos brutos de Anisakis tipo II (L3) frescos e termicamente tratados em ratos. Os vermes foram isolados de um peixe marinho, examinados e identificados por microscopia de luz e eletrônica de varredura. O estudo foi conduzido em 6 grupos de ratos: controle (I), óleo de alho (GO) inoculado (II), L3 fresco inoculado (III), L3 tratado termicamente inoculado (IV), L3 fresco + GO inoculado (V), e um grupo L3 + GO tratado termicamente inoculado (VI). Observou-se que ratos inoculados com L3 fresco e tratados termicamente mostraram funções hepáticas e renais anormais, associadas à destruição da sua arquitetura normal. GO produziu um efeito protector em grupos de ratos inoculados com extractos L3 + GO através da melhoria das funções do fígado e dos rins, o que foi confirmado pela estrutura normal marcada da sua histologia. A cozedura de peixes infectados com L3 induziu alterações mais graves do que os peixes não cozidos. Recomenda-se a administração de alho antes e depois do consumo de peixe, para evitar o efeito perigoso dos anisakids, mesmo que sejam cozidos.

Study of the correlation between Helicobacter pylori infection and Hepatic Encephalopathy in patients with Liver Cirrhosis

Background and study aim: Ammonia plays a major role in hepatic encephalopathy pathogenesis. Most of ammonia is known to be produced by the action of colonic bacteria which possess a urease enzyme activity. H. pylori which infects the stomach possesses a stronger urease activity which produce a large amount of ammonia that may precipitate hepatic encephalopathy (HE). The aim of the present study is to determine the correlation between Helicobacter pylori infection and HE in patients with liver cirrhosis.Patients and Methods: One hundred patients (50 patients of liver cirrhosis with hepatic encephalopathy and 50 patients of liver cirrhosis without hepatic encephalo-pathy) were evaluated for presence of H. pylori by stool antigen test (ELISA method) and for blood ammonia level estimation.Results: Prevalence of H. pylori infection in the study groups (patients of liver cirrhosis with and without hepatic encephalopathy) was 70% (liver cirrhosis with hepatic encephalopathy group (A) 80%, and liver cirrhosis without hepatic encephalopathy group (B) 60%). Mean blood ammonia levels were: 82.14± 47.9 mmol/l for group A (liver cirrhosis with hepatic encephalopathy) and 36.44± 17.9 mmol/l for group B (liver cirrhosis without hepatic encephalopathy). Prevalence of H. pylori and blood ammonia level were found significantly increasing with the severity and the degree of hepatic encephalopathy.Conclusion: There is a significant association between H. pylori and hepatic encephalopathy in patients with liver cirrhosis. There may be a role of anti-H. pylori therapy in patients of hepatic encephalopathy and should be investigated further