Interactions with the host cell

Normally microsporidia develop in the cytoplasm of the host cell, but occasionally intranuclear development, like in Nucleospora salmonis, has been observed (Hedrick et al. 1990). In the most simple cases the host cells are used up by the proliferating microsporidia, but no particular modifications of the host cells are visible, except that the cell, and often also the nucleus of the host cell, become hypertrophic. The microsporidium reproduces freely in the cytoplasm. In other cases the microsporidia are separated from the cytoplasm by an envelope formed by the host (parasitophorous vacuole). There are also well-known cases where the cytology of the host cell is reorganized under the influence of the microsporidia. Chytridiopsis species establish such close connection to the host nucleus that the developing microsporidium finally lies in a shallow invagination of the nucleus (Sprague et al. 1972). Another example is the close association between Buxtehudea scaniae and the mitochondria of the host cell which aggregate around the microsporidium (Larsson 1980).

In the infected tissue cell walls might be destroyed, transforming the tissue into a syncytium where the developmental stages of the microsporidium are floating among host nuclei. Microsporidia of fish sometimes induce the production of tumours. The best known example is the xenoma caused by Glugea anomala, a common skin parasite of sticklebacks. The microsporidium completely rules the infected epidermis cell, inducing nuclear fission, cell hypertrophy, and encapsulation processes (Canning et al. 1982). The final xenoma is a rounded body, a few millimetres in diameter, which contains hundreds, or even thousands, of host nuclei and millions of microsporidia. It is encapsulated by numerous layers of fibroblasts and material from the host cell surface coat.

The clinical aspects of microsporidiosis have been recently reviewed by Kotler and Orenstein (1999).

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