Assessment of the experimental infection by Echinostoma paraensei (Lie & Basch, 1967) (Trematoda: Echinostomatidae) in two Biomphalaria tenagophila (D’Orbigny, 1835) (Gastropoda: Planorbidae) isolates resistant and susceptible to Schistosoma mansoni (Sambon, 1907) (Trematoda: Schistosomatidae)

Different isolates of Biomphalaria tenagophila show a large spectrum of compatibility to the trematode Schistosoma mansoni, ranging from entirely refractory to highly susceptible. The aim of this study was to verify the pattern of compatibility of two B. tenagophila geographical isolates, resistant and susceptible to S. mansoni, when infected with Echinostoma paraensei. The snails were exposed to different numbers of miracidia, and mortality, histopathological characteristics and the number of cercariae released were evaluated. A correlation between the number of miracidia and the infectivity rate of B. tenagophila (TAIM) was observed. There was no correlation between the number of miracidia used and the number of cercariae released for both B. tenagophila isolates. Biomphalaria tenagophila (SJC) showed little susceptibility to the E. paraensei infection. The results demonstrate different degrees of compatibility for the two B. tenagophila isolates when infected with E. paraensei, and may contribute to studies about host-parasite relationships

Schistosomiasis and liver fibrosis

Submitted by Martha Silveira Berbert ([email protected]) on 2011-04-06T15:32:40Z No. of bitstreams: 1 Schistosomiasis and liver fibrosis.pdf: 438380 bytes, checksum: ce435588570007f540d1784bdba732a9 (MD5)Made available in DSpace on 2011-04-06T15:32:40Z (GMT). No. of bitstreams: 1 Schistosomiasis and liver fibrosis.pdf: 438380 bytes, checksum: ce435588570007f540d1784bdba732a9 (MD5) Previous issue date: 2009-08-04Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, BrasilSchistosoma mansoni infection invariably results in liver fibrosis of the host. This fibrosis may be represented by small focal areas of chronic inflammation and excess extracellular matrix deposited in periovular granulomas, distributed in variable numbers at the periphery of the portal vein system. This is the outcome of 90% of the infected population in endemic areas. Conversely, a minority of infected individuals develop extensive disease with numerous granulomas along the entire extension of the portal spaces. This latter situation is mainly dependent on special hemodynamic changes created by a heavy worm load, with the subsequent production of numerous eggs and represents a severe form of a peculiar chronic hepatopathy. Thus, host-parasite interactions in schistosomiasis help us to understand a number of important features of liver fibrosis: its initiation and regulation, the significance of accompanying vascular changes, the dynamics of fibrosis formation and regression with antiparasitic treatment; host genetic and immunological contributions, and the pathophysiology of portal hypertension