A xenoma (also known as a 'xenoparasitic complex') is a growth caused by various protists and fungi, most notably microsporidia. It can occur on numerous organisms; however is predominantly found on fish.
In most cases the host cell and nuclei suffers from hypertrophy resulting in a change in organisation of the cell and its structure and can result in polyploid nuclei. This outcome is due to the microsporidian parasite proliferating inside the host cell. This results in a 'symbiotic co-existence' between the parasite and the host cell. This forms the xenoparasitic complex. They tend to contain numerous cellular components as well as microsporidia at different developmental stages and spores.
Not all microsporidia infections result in the formation of xenomas; only a few microsporidia actually cause xenoma formation.
History
Xenoparasitic complex was the term initially devised in the early twentieth century to describe specific type 'tumours' found on various organisms, specific as the infections were caused by multiple subclasses of microsporidia. A paper published in 1922 by Weissenberg came up with the term 'xenon' for the xenoparasitic complexes he observed on sticklebacks caused by Glugea anomala, before eventually changing it to xenoma (xenon was already the name of a newly discovered chemical element).
Hypertrophy of cells caused by protists and fungi has been observed since the late nineteenth century. Scientists observed them in several organisms, of which the infection would have varied host cell specificity, ultimately leading to different cellular consequences. For example, the dinoflagellate protist Sphaeripara catenata induces hypertrophy, polyploid nuclei formation whilst forming a thick-walled hyposome where rhizoids extend into the cytoplasm for nutrient absorption in the appendicularian Fritillaria pellucida. This can be contrasted to the Microsporidium cotti infection of the testes of Taurulus bubalis where a dense microvillus layer is present for improved nutrient absorption.
Pathogenesis
Xenomas are provoked in various types of organisms, depending on the species of the parasite. Microsporidia are known to produce xenomas in oligochaetes, insects, crustaceans and fish. In addition to organism specificity, different species of parasite will have distinct host cell specificity, even if targeting the same organism. For example, Microsporidium chaetogastris infects solely connective and muscle tissue cells of the annelid Chaetogaster diaphanus, whereas other species of microsporidia will target other tissue types. Another example is microsporidial gill disease in different species of fish caused by Loma salmonae. It was found that certain species had a higher prevalence of xenoma formation 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.