The resistance and susceptibility to the intestinal pinworm Aspiculuris tetraptera, a natural parasite of the house mouse Mus musculus, is experimentally analysed using both the F1 from wild-type mice of the two subspecies (M. m. domesticus and M m. musculus) and the F1 from different laboratory inbred mice. The results show that: (i) the F1 from wild-type mice harbour a lower parasite load than the parental mice, suggesting a phenomenon of hybrid vigour; and (ii) the F1 from inbred mice harbour parasite loads similar to the resistant parent, suggesting that resistance is inherited as a dominant feature in these laboratory mice. This analysis supports the hypothesis that recombinations occurring between the two mouse genomes (i.e. M. m. domesticus and M. m. musculus) are responsible for the hybrid dysgenesis observed in the natural hybrid zone between the two mice subspecies.
Cyprinid fish from the Lergue and Lez rivers in Herault, southern France, were found to be parasitized by the microsporidian Pleistophora mirandellae Vaney & Conte, 1901. The parasite was found only in the gonads, forming cysts in the connective tissue between the seminiferous tubules of testes or occurring in the oocytes of the ovaries. Two types of uninuclear spores are produced. The synonomy of mierosporidia parasitizing the gonads of cyprinid fish is discussed.
Synaptinemal complexes have been demonstrated in 7 microsporidian species belonging to 6 different genera (Gurleya, Thelohania, Pleistophora, Tuzetia, Baculea, Glugea). Thus, it can be presumed that a meiosis and consequently a karyogamy occur during their life cycle. Meisis occurs at the beginning of sporogony; therefore, karyogamy, must occur between spore and merogany, i.e. during the poorly known part of the life cycle. In the microsporidian species studied, with uninucleate spores and diplokaryotic merogony (Thelohania for instance), the 2 joined nuclei, each of them containing meiotic chromosomes, not only fail to fuse, but actually separate at the beginning of sporogony; afterwards, each of them undergoes meiosis. Their separation is accompanied by the appearance of an organelle whose structure and function are poorly understood. However, its structure resembles that of the kinetic center. The Nosema species studied do not have synaptinemal complexes; thus, their life cycle is difficult to understand: either karyogamy and meiosis occur during the unobserved part of the life-cycle, or sexual phanomena are absent altogether. In the latter case, the Nosema-type life cycle might be limited to vegetative multiplication which could be explained by the dimorphism theory of Microsporidia. It is shown also in the present study that the life cycle of Microsporidia does not involve haploid organisms which it might be thought to contain by comparing it with the cycles of sporozoa.
The susceptibility to Aspiculuris tetraptera of European Mus musculus hybrids is thought to reflect the disruption of genomic co-adaptation through recombination of the parental genomes. Here, we compared the susceptibility to this parasite between parents and experimental hybrids (intersubspecific until F4, intrasubspecific F1, F2) to clarify the contributions of heterosis and subspecies incompatibility. F1 showed hybrid vigor. Unlike intrasubspecific F2, intersubspecific F2 were less resistant than F1, but revealed no increased susceptibility relative to the parents. Intersubspecific F3 and F4 showed the same hybrid vigor as F1. Heterosis contributed most to the resistance, but the differences between intra- and intersubspecific F2 suggested genomic incompatibilities between subspecies. However, the susceptibility did not increase through the recombination process, showing that disruption of co-adaptation does not directly affect resistance. Even if previous studies still support the selective role of parasites in the current hybrid zone, an alternative hypothesis on the origin of hybrid susceptibility is warranted.
A severe case of microsporidian infection was observed in farmed Pterophyllum scalareCurs & Valens, 1831& Valens, , in 1987 and resulted in the complete destruction of the stock. Juveniles were severely affected by the parasite; a milky degeneration of skeletal muscle was produced, in which developmental stages of the parasite could be observed. Adult fish appeared more resistant to infection and were only lightly infected. Light and electron microscope observations on developmental stages and spores of the causative agent were sufficient to identify the parasite as Heterosporis finki Schubert, 1969. This parasite had already been reported in P. scalare, but this is the first time that its pathogen~city and its clinical significance for intensive farming systems are clearly assessed.
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