الفهرس 
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Abstract
The present work was carried out to study the haematological, biochemical and histopathological changes in rats experimentally infested witharichinella spiralis . One hundred and twenty rats were divided into
2 equal groups (groups 1 and 2). Group 1 was subdivided into 6 equal subgroups. Subgroups 1,2 and 3 were orally given 300 larvae of Trichinella spiralis, subgroups 4, 5 and 6 were control. Group 2 was subdivided into 6 equal subgroups. Subgroups 1,2 and 3 were infested with 300 larvae of Irichinella spiralis . Subrgroups. 1 and 2 were given 3 successive daily oral doses of thiabendazole (50 mg/kg. B.w) on the 2nd,
3 rd and 4 th days postinfection (subgroup 1- intestinal phase), and on the 7 th, 8 th and 9th days postinfection (subgroup 2 - migratory phase). Subgroup 3 was given 3 successive daily oral doses (300 mg/kg - B.w) on the 45 th, 46 th and 47 th days postinfection . Subgroups 4 and 5 were control . Subgroup 6 was given 3 oral successive doses (50mg/kg - B.w) thiabendazole) and sacrificed 3 days after the 3 rd dose. Subgroups 1 , 2 and 3 beside their control, in both groups, were sacrificed 4 (intestinal phase), 15 (migratory phase), and 60 (cystic phase) days postinfection respectively. The haematological findings showed severe leucocytosis, eosinophilia and lymphocytosis specially in gp.l-. Subgroups 2,3 (Migratory and;Cysiic phases). It was mild in gp.1 subgroup 1 (intestinal phase), gp.l subgroup 4, 5. Highly severe eosinophilia in gp.2 subgroup 6 could be due to the toxic effect and tissue reaction against the thiabend-azole The ’clinicobiochemicalanalysis,showed a picture of cholestatic hepatocellular Jaundice in all animals. This picture was manifested by highly increased leveles of -y .GTp, S. GOT, S. GPT and AP in addition to total, direct and indirect bilirubin specially in gp.l subgroup 2 and very highly increased levels in gp.l subgroup 3 and mild increased levels in gp. 1 Subgroup 1. The hepatocellular damage was manifested by
hypoglycaemia with the same degree in subgroups 1 and 2 with no chage in group 1 subgroup 3. Severe hypoalbuminaemia and hypercholesterolaemia were seen in gp.1 subgroups 2,3 with no affection in gp.l subgroup 1. The blood chemistry revealed muscle affection. This picture was manifested by highly increased levels of lactic dehydrognase and creatinine phosphokinase specially in gp.l subgroups 2 and 3 with mild changes in gp.l subgroup 1, . The renal function tests denoted the presence of chronic renal damage in all animals . The renal damage was manifested by very highly increased levels of 13.U.N and serum creatinine specially in gp.1 subgroup 2 and 3 with mild change in gp.2 subgroups 1,4,5,6. The serum electrolytes showed increased levels of phosphorus, potassium and decreased levels of chloride and calcium specially in gp. 1 subgroup 2 and 3 and mild change in gp.2 subgroups 1,4 and 5. The histopathological study confirmed our clinicopathological results. The liver showed congested blood vessels and sinusoids. The hepatic cells suffered cloudy swelling, vacuolar and hydropic degenerations, infiltration of the hepatic parenchyma with eosinophils, lymophocytes and macrophages. The kidneys showed congestion of renal blood vessels . The epithelium suffered cloudy swelling beside vacuolar and hydropic degenerations. The renal parenchyma was infiltrated with eosinophils, lymphocytes and macrophages . The muscles were edematous and infiltrated with eosinophils, lymphocytes and
macrophages.