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EN
The pathogenesis of alveolar echonococcosis caused by the metacestode of Echinococcus multilocularis is a process involving the host-parasite interface with both local and distant systemic effects. The survival strategy of the parasite is to continuously subvert the host defenses just as the host responds to contain the infection. There is a complex of signal molecules mediating between parasite-elaborated factors and specific and non specific cellular immune responses behind the gross pathological picture of a space-occupying lesion. This paper attempts to summarize the relationship of experimental findings with the clinicopathological picture by outlining pathways that may be involved in the process of pathogenesis.
EN
The weight of the larval cyst mass (LCM), splenomegaly and the amount of splenic amyloid deposition, was shown to be dependant on a putative alveolar hydatid cyst (AHC) soluble component. The increase in LCM, spleen weight, and splenic amyloid was inversely proportional to the number of cyst washings during the preparation of the inoculum. A minimum of 8 washings were found necessary to induce significant reduction in parasite growth and amyloid deposition. With twenty four washings progressive phase of infection was aborted; while the restrictive phase was extended to 8 weeks. This finding was further confirmed by surgical transplantation of cysts obtained from infected mice at 12 weeks post infection to normal mice. The amount of splenic amyloid deposits, LCM and spleen weight after one week post-transplant was statistically not different from those in mice infected with AHC following 24 washings at 12 weeks post infection. The restrictive phase was eliminated following transplantation. AHC-extract (AHC-EXT) prepared from AHC before or after 24 washings was shown to retain its antigenicity and react with infected mice sera in the gel diffusion test. The reaction intensity and the number of bands seen were less after washing.
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