polar tube which penetrates the xenoma membrane and provides an exit route for the sporoplasm. This is thought to be a form of autoinfection. Rupture of the xenoma may also result in dispersal of the infectious spores. This can lead to the formation of other and more persistent forms of xenomas. Transmission of such pathogens occurs predominantly via oral administration when in contact or in the vicinity of diseased organisms via the release of infectious spores. However, there are reports of obtaining infection in some organisms through the skin. Experimentally inducing infection and xenoma formation can be performed intramuscularly, intravascularly and intraperitoneally. It is widely thought that the first site of entry for many of these parasites is in the gastrointestinal tract where enzymes such as pepsin or even an alkaline pH shift (caused by the mucous layer prominent in this area) induces polar tube discharge. Following this their migration from their initial release to their final destination in the host cell varies considerably, depending on the pathogen, the host organism and the host cell location. It was discovered through in situ hybridization that the microsporidia Loma salmonae enters the mucosal epithelium in the intestine and migrates to the lamina propria before arriving at the gills, where it eventually resides, via infecting blood cells. Other transport vehicles are thought to include T cells, lymphocytes, and other migratory cells including monocytes where they succumb to infection by means of either phagocytosis of the parasite in the lamina propria or by infiltration by sporoplasms using their polar tube. It is also very possible that these transport cells might themselves develop into a xenoma. Xenomas in fish Microsporidia is a common cause of disease in fish and so xenomas tend to be seen more frequently in fish than in other organisms. A paper published in 2002 listed 15 genera and 157 microsporidian species that cause disease in fish, however only ten of these genera induce xenoma formation. Microsporidia genera that cause xenomas can therefore be quite diverse and so are characterised more comprehensively into several groups depending on their morphology: Xenomas without a thick wall and where the complete volume of the original cell is not converted into a xenoma Xenomas without a thick wall and where the complete volume of the original cell is converted into a xenoma Xenomas with plasmalemma surrounded by host fibrils Xenomas with a thick wall Recently fish-infecting