Altera??es Morfo-fisiol?gicas Em Biomphalaria glabrata Say, 1818 (Pulmonata, Planorbidae) Por Infec??o Experimental De Echinostoma paraensei Lie & Basch, 1967 (Trematoda, Echinostomatidae)

• Ano de defesa: 2012
• Autor(a) principal: Alves, Victor Menezes Tunholi
• Orientador(a): Rodrigues, Maria de Lurdes de Azevedo
• Banca de defesa: Brandoline, Solange Viana Paschoal Blanco, Vidigal , Teofania H. D. A.
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal Rural do Rio de Janeiro
• Programa de Pós-Graduação: Programa de P?s-Gradua??o em Ci?ncias Veterin?rias
• Departamento: Instituto de Veterin?ria
• País: Brasil
• Palavras-chave em Português: Biompalaria glabrata; Echinostoma paraensei; homeostase
• Palavras-chave em Inglês: Biompalaria glabrata; Echinostoma paraensei; homeostasis
• Área do conhecimento CNPq: Medicina Veterin?ria
• Link de acesso: https://tede.ufrrj.br/jspui/handle/jspui/3676

Parasites belonging to the Echinostoma genus are characterized by having a complex biological cycle, with two intermediate hosts and a final habitat restricted to the intestinal lumen of the definitive hosts. These hosts include aquatic birds, mammals (including humans) and occasionally some reptile and fish species. Their first intermediate hosts are freshwater snails, into which the miracidia actively penetrate for development of the next three stages (sporocysts, rediae and cercariae). Freshwater crustaceans, amphibians, fish and snails act as the second intermediate hosts, enabling the formation of metacercariae, the infective larval stage to the definitive host. In this work, Biomphalaria glabrata specimens were experimentally infected with different doses (5 or 50) of E. paraensei miracidia. The snails were dissected one, two, three and four weeks after infection to collect the hemolymph, shells and tissues (gonad-digestive gland complex- GDG). During this period, the snails? oviposition was observed. In the hemolymph, the concentrations of total proteins, urea, uric acid, cholesterol and triglycerides were measured, as well as the activities of the transaminases (ALT and AST). In the tissues, the levels of neutral lipids (fatty acids, triglyceride, cholesterol and esterified cholesterol) were measured, and in the shells the CaCO3 content was quantified. Significant differences were observed in the bioenergy state of the snails infected with both miracidium doses in relation to the control group (not infected), probably because of the intense formation of glucogenic amino acids from the protein catabolism in response to the stress generated by the parasites. Because of the high energy consumption of the infected snails, it is possible that the anaerobic metabolism becomes more active, culminating in the accumulation of organic acids that reduce the pH of the hemolymph, thus explaining the significant increase in calcemia. In parallel, accentuated decreases in the calcium levels in the shells were found in the snails infected by both miracidium doses (5 and 50), which coincided with the peak calcemia in these specimens. Drastic declines in the total protein concentration in the hemolymph were observed in the infected snails, related to the probable increase of the activities of the transaminases (ALT and AST), an effect also caused by the appearance of rediae and corroborated by the accumulation of uric acid and urea. Additionally, the significant alteration of the lipid profile of the infected snails indicates intense utilization of lipids as a substrate both by the intermediate host and the parasite, suggesting the probable participation of lipids in the energy and structural metabolism of both organisms. The results observed in this study indicate that infection with 5 or 50 E. paraensei miracidia caused considerable metabolic changes in B. glabrata, with the snails exposed to the higher number of miracidia suffering greater damage.