following infection with the same parasite i.e. xenomas per gill filament in chinook salmon was 8 to 33 times greater than in rainbow trout, showing differences in host cell susceptibility. Once a host cell is infected with the microsporidian (or protist) parasite, a complete restructuring of the host cell ensues. This occurs as the parasite seeks to take control of the metabolism of the cell, in order to survive and exploit the host cell's resources and reproduction. It provides the parasite with optimal growth conditions and protection from the host's immune response. The parasite proliferates within the host cell where its mass replaces most of the host cell's cytoplasm, with the rest being taken up by microvillus structures and rhizoids. Other structures may be present inside the infected host cell including vesicles, fat globules and bundles of fibril. The nucleus may be in varying locations including the centre of the cell and may also vary in structure i.e. lobed, branched or divided into multiple fragments, but it will always be hypertrophic. The host also commonly envelops the proliferating parasite and the host cell itself in layers of membranes and cells. In microsporidian xenomas the whole life cycle is restricted to the xenoma; this however differs between different protists. The life cycle predominantly follows a simple life cycle consisting of merogony followed by sporogony. Occasionally the endoplasmic reticulum associates with meronts, which are formed during merogony, and is lost once sporogony ensues. The time it takes for a xenoma to develop varies entirely on the host organism and cell as well as the infecting parasite. It can vary, however it usually starts to form after a few weeks following infection, depending on the life cycle of the parasite. The size of xenomas also varies with the type of parasite and host organism, and can range from a few micrometres to several millimetres. While it is generally accepted that the xenoma prevents spread of the parasite throughout the host organism, it is not entirely accurate. As the species that cause xenomas are spore-forming, it is possible that their spores may release their sporoplasms which penetrate the xenoma wall, infiltrating and infecting surrounding cells. In microsporidia this is mediated by a unique and highly specialised protein: the polar tube. This specialised protein is found inside the spore and is in contact with the sporoplasm. Specific environmental stimulation causes the spore to discharge the