Microsporidia – Wikipedia

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The Microsporidia , also Microspora or Microsporea , are individual parasites and pathogens of microsporidiasis belonging to the mushrooms. You can reach a size of a few µm (2–12 µm). Microspora mostly parasitize intracellularly with representatives of many animal trunks, less often in other Protists from the SAR called eukaryotes. A transfer is carried out by absorbing individual spores (mostly orally, i.e. through the mouth).

Microsporidia are mandatory parasites. They live inside the cell of a cell of their host. Unlike many other cell parasites, they do not live in a separate vacuole, but directly in the cytoplasm. The infection takes place from a spore, the only stage found outside the host cell. The parasite’s cytoplasm (called sporoplasma) is separated from that of the host cell by its cell membrane, which often surrounds a shell, especially from complex carbohydrates, called glycocalyx. At this stage, the parasite does not noticeaize the host cell (occasionally there are functional restrictions in muscle fibers), it increases in parallel to the host cell through cell division (merogony), the stage will also be Meront called. Due to the position within the cell, it is invisible to the host’s immune system. The parasite cell is extremely reduced in its structure and completely depends on the host cell in basal cell functions. At first it contains only one cell nucleus (rarely doubled, dicaryon), densely packed ribosomes and various membrane components that are not organized for organelles, neither a Golgi apparatus nor functional mitochondria are recognizable. Organelle named mitosomes represent reduced relics of mitochondria in which only about 20 functional proteins are detectable (normal mitochondria contain around 1000). They no longer have an independent genome. The genome of the core of the microsporidia cell is also highly reduced. There are only about 2000 genes left, so that many metabolic products have to be adopted from the host cell. The genes for nucleotide synthesis and many essential components of the respiratory chain are missing. They are even partially dependent on the direct import of adenosintriphosphate (ATP) from the host cell for energy supply, the metabolism of which they heat up for this purpose. Although the ribosomes are also reduced in the range of functions, the parasite has a lot of them. These enable him to grow very quickly at the expense of his host. His ability to defend itself against infection by programmed cell death (apoptosis) is specifically sabotaged by signal substances. As a result, the infected host cell swells to many times its normal size. Some microsporidies (especially fish parasites) form huge inclusion bodies filled with spores, which are called Xenosoma, which are often merged into a syncytium.

Very quickly, often within three days of the infection, the microsporidies within the host cell begin with the production of new spores. The spore -forming stage within the cell is also Sport called. In the groups in which Meiosis occurs, this occurs immediately before the formation of spore. The spores of the microsporidia serve both to infect new cells within the host and to infection new hosts. You have developed a specific mechanism for the infection process. New cells are infected via a thin infection hose, which, compared to the cell length, can reach unusual length (up to over 100 micrometers). The infection hose can, like an injection syringe, penetrate into tissue and cells, where the spore content is transferred to the new host through a massive increase in pressure within the spore. There are usually two types of spore, one that quickly infected new cells, and another that only delays this time, with some microsporide types, these can also be distinguished morphologically.

The compactly built, mostly round, oval, pear or chopstick-shaped spore has a thick cell wall that is built in two layers. The inner (endospore) location consists of proteins and chitin, the exterior only in proteins. The inner situation probably serves above all to resist the extreme pressure that is built up during the infection (more than 7 megapascal is achieved), the exterior is used for cell contact, for example for host recognition. To do this, they often have spiky -like processes. In addition to the cell nucleus and little cytoplasm, the injection apparatus that forms the infection tube and a polarop load for membrane components is located inside the spore. The overpressure of the infection is generated by a vacuole in the rear section, which quickly increases in size and thus builds up pressure. The infection hose at the front of the spore has a thread -shaped effect, therefore also called the polarfish, it is usually rolled up like a loop. With bee parasites Nosema apis If the spore is 5 micrometers long, the injection hose (polar trial) reaches 300 micrometers in length inside. Instead, a fifth of the microsporidia genera have a short, stable injection hose that only reaches spore length. With them it is anchored in a mushroom -shaped structure, the polar cap. The main component of the infection hose is a PTP1 protein. This proves to be a strong antigen for hosts (also in humans), so that the immune response directed against it can resist the landlord against infections. During the infection process, the cell content is pressed into the hose by the expanding vacuole in the spore. The polaroplast, which consists primarily of folded membrane in the idle state, provides the necessary material for the new cell membrane in the hose. The infection hose penetrates adjacent tissue and other obstacles, including possible other microsporide spores that would be in the way.

Numerous types of microsporidia produce several spore forms, usually two (dimorphic), rarely three or more (polymorphic). Different forms either alternatively serve the fast infection within a host and the delayed germination for infection of new hosts, or different spore forms are trained in different types of hosts. In others, all spores look the same and differ only in the speed of germination. New hosts are infected by slowly germinating spores, usually after admission over the mouth and digestive tract (oral). In the case of water-living microsporidies, there are hyperparasitic species in which the infection tube penetrates the body or intestinal wall of the host in order to parasitize the parasites living inside.

The newly formed spores usually get through the faeces, the urine, or only after the host’s death. With many hosts, including most vertebrates, the infection is chronic, so that spores are excreted over long periods of time. In the case of insects, after delayed and often relatively symptomless start, there are also severe infections that can end with the death of the host. Even with the chronic infections, the lifespan and the general condition of the host types are usually affected.

Most microsporidia species are host-specific, they only affect one type or few closely related species. Within the host, you are usually specialized in certain fabrics. Microsporidia of the genus Nosema The pathogens of nosemosis are not only specialized in the genus honeybees Apis , but affect cells of the middle intestine in these exclusively. Often closely related host species have their own, equally related parasites (called “Ko-Kladogenesis”). In many cases, the host specificity is specified by environmental factors, i.e. H. Under experimental conditions, in the laboratory, species can also be infected in which this never occurs in the field. Other species have a wide host spectrum, e.g. B. all mammals that they use opportunistic.

Microsporidia infections are among the most common parasitic diseases in the animal kingdom. In about half of the tribes of the animal kingdom, microsporidia were registered as parasites. However, only the relatively few groups, in which the infection leads to economic or health damage that are significant for humans are better examined. It is therefore assumed that most of the species are still undetected and blank. Most known host types are among the insects and the crustaceans. Microsporidia can cause considerable damage: the Pébrine disease Nosema bombycis led around the mid-19th century to collapse the European silk caterpillar breeding. Other species, such as parasites of mosquitoes, also have positive effects for humans as regulators or in the context of biological pest control. Around 160 species from 17 genera infect fish species. 14 microsporidies were registered in humans as a host, not a single host -specific one. Types of genus Endoreticulatus are, for example, opportunistic pathogens that occur in both humans and others as well as in types of insects.

Important parasites and their hosts [ Edit | Edit the source text ]

Microsporidiosis is the generic term for clinical pictures by these organisms.

The nomenclatory status of the Microsporidia is not clear. They were treated as a tribe according to the international rules for the zoological nomenclature (ICZN) (at that time assigned the sporozoa), but there is ambiguity about the author citing. It is also questionable whether the name is valid according to the international code of the botanical nomenclature (ICN). The membership of the Microsporidia to the mushrooms and therefore the jurisdiction of the ICN resulted in 2007. The assignment to Balbiani (C. R. Acad. Sci Paris 95: p. 1168, 1882) is therefore temporary [first] , but still common.

Phylogenie [ Edit | Edit the source text ]

The department (or trunk, phylum) Microsporidia forms the genus with a clade of little -known organisms around the genus Rozella (referred to as rozellida or cryptomycota) and the aphelidea, a species -poor group of parasites of individual algae, a group that has been named opisthosporidia [2] [3] , It is classified in the classic system as a overstate (superphylum). The Opisthosporidia belong to the group of mushrooms (in a broader sense).

In the meantime, a number of Protists have been found that have numerous features in common with the Microsporidia, but deviates from them in some characteristics. Among other things, there are representatives with less reduced genome that also have functional mitochondria. This group includes the genera Mitosporidium , Paramicrosporidium and Nucleophaga . Another group, including Amphiamblys and Amphiacantha summarized as “Metechnikovelliden” are hyperparasites in, even parasitic, individuals of the Apicoplexa. Genetically similar are also numerous, previously still unknown organisms, of which only their base sequence obtained from environmental DNA is known without the associated organism and its biology so far known; Some of these are very common in environmental samples. Almost the entire group, often summarized as rozellomycota or cryptomycota, turned out to be closer to the microsporidia in recent analyzes Rozella Related so that an extended group of Microsporidia was proposed, including these groups. [4]

The structure of the microsporidia in groups is unclear according to the previous state of knowledge. A proposal to split it, also based on genetic data, in three classes of the Aquasporidia (especially in fresh water), Marinosporidia (especially Marin) and Terresporidia (especially in terrestrial habitats) [5] Ultimately, due to different recent data, it has not been accepted.

Research history [ Edit | Edit the source text ]

In the 1850s, the Pébrine disease devastated the European silk raupe. The Swiss researcher Carl Wilhelm von Nägeli discovered infectious “globules” in 1857, which he Nosema bombycis described. Her way of life was then informed in 1870, especially by the famous Louis Pasteur and recommended countermeasures, so that the industry recovered. Nägeli placed his find into the “split mushrooms” or schizomycetes, a summary of the “low” mushrooms and bacteria that are not related to each other. Édouard-Gérard Balbiani provided in 1882 Nosema And relatives in the group of sporozoa and shaped the term microsporidia (“microsporidies”). He set up a group of the “Cnidosporidia” for her, which also included some groups that have not been related to today’s knowledge, including the Myxozoa (nibrating according to today’s knowledge).

Further insights into the Microsporidia will only come after the invention of electron microscopy in the 1950s. Now it became clear that the Microsporidia lacks numerous characteristics that are otherwise almost universally common within the animals. There are no mitochondria nor a Golgi apparatus or peroxisomes in the cells, there are no bridging cells with flagellum or structures that can be derived from them in no life stage. Thomas Cavalier-Smith then develops the hypothesis that Microsporidia belonged to a (paraphylete) group of primeval eukaryotes who had split off from the common family tree before these structures were evaluated. This group called “Archezoa” was also well supported by the first genetic analyzes. In the mid -1990s, numerous working groups then discovered characteristics, especially of various protein families, who instead obtained a closer relationship between Microsporidia with the mushrooms. Ultimately, the support for the Archezoa proved to be a so-called “Long Branch Attraction” artifact through better genetic methods, in which DNA sequences from the sorting algorithm deviates very strongly and thus pretended a basal position. For a while it was now unclear whether the Microsporidia should be understood as a sister group of the mushrooms or whether they belonged to the mushrooms. The new position was only clarified after 2010, by further improved analysis methods and newly discovered organisms of the kinship group. [6]

  • Jiří Vávra, Julius Lukeš: Microsporidia and ‘The Art of Living Together’. Chapter 4 in D. Rollinson, D. (Editor): Advances in Parasitology 82. Academic Press (Elsevier), 2013. S 253–320. ISBN 978-0-12-407706-5.
  • Marianne Abele-Horn: Antimicrobial therapy. Decision aids for the treatment and prophylaxis of infectious diseases. With the collaboration of Werner Heinz, Hartwig Klinker, Johann Schurz and August Stich, 2nd, revised and expanded edition. Peter Wiehl, Marburg 2009, ISBN 978-3-927219-14-4, p. 292 f.
  • Heinz Mehlhorn: Floor plan of zoology; Chapter: tribes and blueprints. Spectrum Berlin reprint; P. 71 ff.
  • Alexander Mathis et al.: Zoonotic Potential of the Microsporidia . Clinical Microbiology Reviews, July 2005, p. 423–445, Vol. 18, No. 3 PMID 16020683
  • Eva Heinz et al. „The Genome of the Obligate Intracellular Parasite Trachipleistophora hominis: New Insights into Microsporidian Genome Dynamics and Reductive Evolution.“ In: PLoS Pathogens 8.10 (2012): e1002979. Doi: 10.1371/Journal.ppat.1002979
  • Louis M. Weiss, James J. Becnel (HRSG.): Microsporidia: Pathogens of Opportunity. [728-page reference work]. Wiley-Blackwell, 2014. ISBN 978-1-118-39522-6 (print); ISBN 978-1-118-39526-4 (eBook)
  1. ↑ D. S. Hibbett et al.: A higher-level phylogenetic classification of the Fungi . In: Mycological research , May 2007; 111 (5): 509-547. EPUB 2007 March 13, 2007. PMID 17572334
  2. ↑ Sergey A. Karpov, Maria A. Mamkaeva, Vladimir V. Aleoshin, Elena Nassonova, Osu Lilje Frank H. Gleason (2014): Morphology, phylogeny, and ecology of the aphelids (Aphelidea, Opisthokonta) and proposal for the new superphylum Opisthosporidia. Frontiers in Microbiology 5:112. Two: 10.3389/FMICB.2014.00112
  3. ↑ Sina M. Adl et al. (2018): Revisions to the Classification, Nomenclature, and Diversity of Eukaryotes. Journal of Eukaryotic Microbiology 66: 4–119. DOI: 10.1111/game. 12691
  4. ↑ David Bass, Lucas Czech, Bryony A. P. Williams, Cedric Berney, Micah Dunthorn, Frederic Mahe, Guifre Torruella, Grant D. Stentiford, Tom A. Williams (2018): Clarifying the Relationships between Microsporidia and Cryptomycota. Journal of Eukaryotic Microbiology 65: 773–782. DOI: 10.1111/game.12519
  5. ↑ Charles R. Vossbrinck & Bettina A. Debrunner-Vossbrinck (2005): Molecular phylogeny of the Microsporidia: ecological, ultrastructural and taxonomic considerations. Folia Parasitologica 52: 131–142.
  6. ↑ Abschnitt nach: Nicolas Corradi & Patrick J. Keeling (2009): Microsporidia: a journey through radical taxonomical revisions. Fungal Biology Reviews 23: 1-8. doi:10.1016/j.fbr.2009.05.001