Development of a new myxozoan parasite Tetracapsula bryozoides gen. n. et sp. n. in the coelomic cavities of Cris-latella mucedo Cuvier is described. Uninucleate proliferative cells are formed within well-defined sacs, the wall of which is one cell thick. The sacs, of different sizes according to age, are free floating and are conspicuously moved about within the coelomic fluid by the ciliary movements of the host. Division of the proliferative cells produces spherical cells of different sizes with nuclei of commensurate size. The largest cells enter sporogony by dividing into ten cells. Four of these become capsulogenic cells arranged as an anterior group, each giving rise to a spherical polar capsule containing a polar filament, possibly without prior formation of an external tube or, at most, very transient formation of these. Four valvogenic cells enclose the two sporoplasms and overlie the capsulogenic cells except at the points of exit of the polar filaments from the polar capsules. The two uninucleate sporoplasms are packed with endoplasmic reticulum, numerous mitochondria with tubular cristae and sporoplasmosomes which are distributed peripherally. Both sporoplasms produce secondary cells. Typical myxosporean features of the wall cells of the sac and all stages within the sac are: nuclei with granular nucleoplasm and prominent nucleolus, gap junctions between cells consisting of thickened membranes with cross connections, and haplosporosomes. A new genus is established for the parasite, defined as having development limited to uninucleate pseudoplasmodia within a sac of parasite origin, each uninucleate sporogonie stage giving rise to one spore with tetraradial symmetry, composed of four shell valves, four anterior polar capsules and two uninucleate sporoplasms with secondary cells. No plasmodia are formed. The genus is placed within the order Multivalvuli-da, in a new family Saccosporidae, defined as having development within a sac of parasite origin and sporogony without external tube or microtubules during polar capsule formation.
We undertook a detailed ultrastructural investigation to gain insight into the early stages of development of the vermiform myxozoan, Buddenbrockia plumatellae Schröder, 1910 in two bryozoan hosts. Early cell complexes arise in the peritoneum after division and migration of isolated cells in the host body wall. The development of cell junctions linking the outer (mural) cells of the complex then produces a sac enclosing a mass of inner cells. Elongation to the vermiform stage (myxoworm) occurs during multiplication and reorganisation of the inner cells as a central core within the single-layered sac wall. The core cells develop into muscle and sporogonic cells separated from the mural cells by a basal lamina. Myogenesis occurs along the length of the myxoworm from cells that differentiate from the central core, and is independent of elongation. Four primary sporogonic cells maintain positions close to the basal lamina, between muscle cells, while giving rise to secondary sporogonic cells that eventually become free in the central cavity. At least some secondary sporogonic cells undergo meiosis. In view of the recent confirmation of the phylogenetic affinity of Buddenbrockia with the Cnidaria, we postulate how features observed in Buddenbrockia may be homologous with cnidarian structures. Finally we propose a new family name, Buddenbrockiidae, to replace Saccosporidae which was proposed previously in breach of the International Code of Zoological Nomenclature.
The microsporidium Trachipleistophora hominis Hollister, Canning, Weidner, Field, Kench et Marriott, 1996, originally isolated from human skeletal muscle cells, inhibited myotube formation from myoblasts when grown in a mouse myoblast cell line C2,C12. Uninfected cultures readily converted to myotubes. Albendazole, a drug with known antimicrosporidial activity, was tested against T. hominis in C2,C12 cells. The drug was added when infection had reached 75% of C2,C12 cells, a level comparable to that obtained in heavily infected muscle in vivo. Doses of 1 ng/ml and 10 ng/ml had no effect on merogony or sporogony. In cultures exposed to 100 ng/ml albendazole, the C2,C12 cells remained in good condition while infection levels dropped to 25% over 7 weeks. Drug doses of 500 ng/ml and 1,000 ng/ml were deleterious to the host cells but some spores retained viability and were able to establish new infections once albendazole pressure was removed. T. hominis meronts exposed to 100 ng/ml albendazole mostly lacked the normally thick surface coat and its reticulate extensions. Meronts were not seen in cultures exposed to higher drug doses. Albendazole at a concentration of 100 ng/ml and higher had a profound effect on spore morphogenesis. There was erratic coiling of the polar tube, often involving the formation of double tubes, and chaotic disposition of membranes which could have been those of polaroplast. The in vitro susceptibility of T. hominis to albendazole was low in comparison with in vitro susceptibility of other microsporidia of human origin.
Xenomas caused by Microgemma vivaresi Canning, Feist, Longshaw, Okamura, Anderson, Tsuey Tse et Curry, 2005 were found in liver and skeletal muscle of sea scorpions, Taurulus bubalis (Euphrasen). All muscle xenomas examined were in an advanced stage of destruction. In developing xenomas found in liver, parasites were restricted to the centre of the cell, separated from a parasite-free zone by a nuclear network formed by branching of the host cell nucleus. Although xenomas were able to reach a size of several hundred microns, the surface remained a simple plasma membrane. Host reactions took the form of penetration by phagocytes and isolation by fibroblasts. Once the xenoma had been attacked, the nuclear profiles became pycnotic and the barrier between parasitized and parasite-free zones was lost. Parasite antigens cannot be exposed at the surface of intact xenomas, as the host does not recognise the enlarging cell as foreign. Breaches in the plasma membrane of the xenoma and leakage of parasite antigens are thought to be the stimuli for phagocyte entry into the cell, its isolation by fibroblasts and eventual granuloma formation.