ABSTRACT
Lungworm infection is caused by a Dictyocaulus filaria nematode parasitizing the bronchi and bronchioles of sheep and goats. Various anthelmintics, including albendazole, levamisole, fenbendazole, ivermectins, and others, are used to treat the animals. The aim of this investigation was to study the impact of lungworm infestation on the biochemical parameters of animals during combination treatment with albendazole and T- and B-activin. Experiments were carried out in 20 uninfected mongrel lambs aged 4-5 months. Infectious D.filaria larvae were given with water to 15 lambs once orally at a dose of 1000 larvae per head. 5 uninfected lambs served as a control group. The time course of changes in serum bio- chemical parameters was studied in animals. Treatment with Albena in combination with T- and B-activin in lambs ex- perimentally infested with lungworm was found to restore their biochemical reactivity. After sheep treatment with Albena alone, biochemical parameters were noted to tend to normalize, but their normal full recovery did not take place.
Subject(s)
Anthelmintics/administration & dosage , Dictyocaulus Infections/drug therapy , Sheep Diseases/drug therapy , Albendazole/administration & dosage , Animals , Dictyocaulus/pathogenicity , Dictyocaulus Infections/parasitology , Feces/parasitology , Fenbendazole/administration & dosage , Levamisole/administration & dosage , Sheep/parasitology , Sheep Diseases/parasitologyABSTRACT
Genetic resistance to malaria is associated with various genetic factors, including erythrocytic variability and variability of the genes involved into the pathogenetic process. Some genetic anomalies resulted from selective malaria pressure, which brought into existence different forms of hemoglobinopathies, glucose-6-phosphate dehydrogenase deficiency, and no Duffy antigens, and ovalocytosis, etc., which ensured varying malaria resistance. Cell adhesion is a major factor in the pathogenesis of malaria. Adhesion molecules express on the cellular membranes of the endothelium, platelets, macrophages, red blood cells and serve as binding receptors for membrane proteins PFRMP-1 of P. falciparum. Polymorphism of the CD36, ICAM-1, and PECAM1 genes can lower binding to blood vessel endothelial cells, which reduces the number of clinical forms of malaria. The high serum TNF-alpha level that is caused by mutation in the promoter of the TNF-alpha gene is associated with cerebral malaria. TNF-alpha enhances the endothelial expression of adhesion molecules, by increasing the adhesion of infected erythrocytes, including that in cerebral capillaries, by inducing in patients local thrombosis and inflammation with release of the cytokines--TNF-alpha. The products of inflammatory infiltrates attack the endothelium, by leading to the imbibition of plasma and erythrocytes in brain tissue and causing a cerebral form of malaria.
Subject(s)
Genetic Predisposition to Disease , Malaria/genetics , CD36 Antigens/genetics , CD36 Antigens/metabolism , Duffy Blood-Group System/genetics , Elliptocytosis, Hereditary , Glucosephosphate Dehydrogenase/genetics , Hemoglobins/genetics , Humans , Intercellular Adhesion Molecule-1/genetics , Intercellular Adhesion Molecule-1/metabolism , Malaria, Cerebral/blood , Malaria, Cerebral/genetics , Mutation , Platelet Endothelial Cell Adhesion Molecule-1/genetics , Platelet Endothelial Cell Adhesion Molecule-1/metabolism , Polymorphism, Genetic , Promoter Regions, Genetic/genetics , Receptors, Cell Surface/deficiency , Receptors, Cell Surface/genetics , Tumor Necrosis Factor-alpha/blood , Tumor Necrosis Factor-alpha/geneticsABSTRACT
The paper shows a high infection of some species of nonhuman primates with blastocysts. Lower rates of infection with this pathogen were observed in younger animals. The blastocysts isolated from Macaca mulatta were microscopically analyzed. The findings indicate a great morphological similarity between the blastocysts of primates and those of man (Blastocystis hominis).
