Microsporidia are a group of obligate intracellular eukaryotic parasites, which are able to infect a wide range of animals, including humans. Four genotypes of Encephalitozoon cuniculi have been found to date. The different courses of microsporidiosis described in humans, which are dependent on immunological status of the host and genotype of E. cuniculi, have been successfully imitated in murine models. In the present study, we quantified the microsporidial burden in individual organs of a murine experimental model, using qPCR and we compared the parasitic load of two genotypes of E. cuniculi, namely genotype II and III (EC II and EC III). While the extent of microsporidiosis caused by EC II gradually increased over 35 days post infection (DPI) in both immunocompetent and immunodeficient mice and caused death in the latter at 28 DPI, EC III had spread into all host organs by seven DPI and was not lethal for either mouse strain during the experimental time period. Moreover, EC III persisted in many organs until termination of the experiment. The number of microsporidial spores in individual organs was ten times higher in EC III-infected animals compared to those infected with EC II. EC II infection also progressively shifted towards organs outside the gastrointestinal tract (GIT) in both monitored mouse strains; whereas, EC III infection equally remained in both the GIT and organs outside the GIT. With the increasing use of molecular methods in diagnostics, it is important to better understand the pathophysiology of microsporidia, including its ability to escape from the immune system and persist in host organisms. Our results indicate that pathogenicity is not directly connected to spore burden, as infection caused by E. cuniculi genotype II is less extensive and spreads more slowly within the host organism than infection caused by E. cuniculi genotype III, but which caused the earlier death of immunodeficient mice.

• MeSH
• Arvicolinae MeSH
• Cercopithecus aethiops MeSH
• Encephalitozoon cuniculi klasifikace   genetika   růst a vývoj   fyziologie   MeSH
• encephalitozoonóza parazitologie   MeSH
• gastrointestinální trakt parazitologie   MeSH
• genotyp MeSH
• imunokompetence MeSH
• kvantitativní polymerázová řetězová reakce MeSH
• Microsporidia fyziologie   MeSH
• modely nemocí na zvířatech MeSH
• myši inbrední BALB C MeSH
• myši SCID MeSH
• myši MeSH
• parazitární zátěž MeSH
• spory hub MeSH
• Vero buňky MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• srovnávací studie MeSH

This study revises our understanding of the effectiveness of cell-mediated adaptive immunity and treatment against microsporidia using molecular detection and quantification of microsporidia in immunocompetent C57Bl/6 and immunodeficient CD4-/-and CD8-/-mice for the first time. We demonstrate an intense dissemination of microsporidia into most organs within the first weeks post-infection in all strains of mice, followed by a chronic infection characterized by microsporidia persistence in CD4-/-and C57Bl/6 mice and a lethal outcome for CD8-/-mice. Albendazole application reduces microsporidia burden in C57Bl/6 and CD4-/-mice, whereas CD8-/-mice experience only a temporary effect of the treatment. Surprisingly, treated CD8-/-mice survived the entire experimental duration despite enormous microsporidia burden. On the basis of our results, we conclude that microsporidia survive despite the presence of immune mechanisms and treatments that are currently considered to be effective and therefore that CD8 T lymphocytes represent a major, but not sole effector mechanism controlling microsporidiosis. Furthermore, the survival of mice does not correspond to spore burden, which provides new insight into latent microsporidiosis from an epidemiological point of view.

• MeSH
• adaptivní imunita imunologie   MeSH
• albendazol terapeutické užití   MeSH
• anthelmintika terapeutické užití   MeSH
• buněčná imunita imunologie   MeSH
• CD4-pozitivní T-lymfocyty imunologie   MeSH
• CD8-pozitivní T-lymfocyty imunologie   MeSH
• Encephalitozoon cuniculi růst a vývoj   imunologie   MeSH
• encephalitozoonóza imunologie   mikrobiologie   MeSH
• lymfopenie imunologie   MeSH
• myši inbrední C57BL MeSH
• myši knockoutované MeSH
• myši MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH

• MeSH
• aktivace makrofágů MeSH
• buněčné linie imunologie   parazitologie   MeSH
• Encephalitozoon cuniculi patogenita   růst a vývoj   účinky léků   MeSH
• financování organizované MeSH
• interferon gama farmakologie   MeSH
• peritoneální makrofágy imunologie   účinky léků   MeSH
• protilátky protozoální MeSH
• Publikační typ
• techniky in vitro MeSH

• MeSH
• Encephalitozoon cuniculi patogenita   růst a vývoj   MeSH
• encephalitozoonóza epidemiologie   etiologie   MeSH
• kultivované buňky MeSH
• myši MeSH
• oportunní infekce parazitologie   MeSH
• spory fyziologie   MeSH
• teplota MeSH
• virulence MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• zvířata MeSH
• Publikační typ
• techniky in vitro MeSH