ABSTRACT
The major three species of human taeniid cestodes, Taenia solium, T. saginata and T. saginata asiatica (= T. asiatica) which require humans as the definitive host are still not rare in developing countries. Among these, T. solium is the most serious with medical and economic importance. Neurocysticercosis (NCC) in humans is now recognized as the major cause of neurologic disease in the world. As these human taeniid cestodes obligatory require domestic animals such as swine, cattle and swine as the major intermediate host animals respectively, it is not easy to analyze the basic research in these domestic animals. In this brief review, we introduce experimental animal model for these three species in order to obtain fully developed metacestode stage in severe combined immunodeficiency (scid) mice. Non-obese diabetic scid (NOD-scid) mice are expected to be a satisfactory animal model and to have advantages for analysis by several view points of developmental biology with gene expression throughout development, antigenic homology of cyst fluid of these three species, evaluation of drug efficacy or metacestocidal drug designs, confirmation of unknown taeniid gravid segments for identification based on the morphology and DNA analysis of metacestodes. The animal model is not only available for human Taenia spp but can also be applied to other taeniid cestodes of economic importance or in veterinary parasitology.
Subject(s)
Animals , Cattle , Cysticercosis/parasitology , Disease Models, Animal , Disease Reservoirs , Female , Humans , Mice , Mice, Inbred NOD/parasitology , Mice, SCID/parasitology , Swine , Zoonoses/parasitologyABSTRACT
Features of Schistosoma mansoni infection in SCID mice, which lack functional T- and B-lymphocytes, were investigated. The retarded development of parasites as well as reduction of liver egg recovery in SCID mice was significantly lower than those in congenic counterpart C.B-17 mice. Furthermore, the rate of parasite recovery from SCID mice with primary infection was always lower than that from C.B-17 mice by 20%, showing the innate resistance to S. mansoni infection. SCID mice vaccinated with UV-attenuated S. mansoni cercariae did not show protective immunity against a homologous challenge infection. The present innate resistance exhibited in SCID mice is discussed in relation to cell mediated immunity of macrophage activation by IFN-gamma which would not involve T-lymphocytes but is initiated by IL-12 and TNF-alpha cytokines. SCID mice may provide novel information on the host-parasite relationship in schistosome infections.