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Differences in the intensity of infection caused by Encephalitozoon cuniculi genotype II and III - Comparison using
Michaela Kotková1, Bohumil Sak2, Martin Kváč1
1Institute of Parasitology, Biology Centre, Czech Academy of Science, České Budějovice, Czech Republic; Faculty of Agriculture, University of South Bohemia in České Budějovice, České Budějovice, Czech Republic.
Abstract:
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.
Insights
Encephalitozoon cuniculi (E. cuniculi) genotype III spreads faster and has a higher spore burden than genotype II in mice. However, genotype II infection was more pathogenic, causing earlier death in immunodeficient mice.
Area of Science:
- Parasitology
- Immunology
- Molecular Biology
Background:
- Microsporidia are obligate intracellular parasites infecting diverse hosts, including humans.
- Encephalitozoon cuniculi (E. cuniculi) has multiple genotypes, influencing disease course.
- Murine models effectively replicate human microsporidiosis, varying with host immunity and parasite genotype.
Purpose of the Study:
- To quantify and compare the organ-specific parasitic burden of E. cuniculi genotypes II and III in a murine model.
- To investigate the dissemination patterns and pathogenicity of different E. cuniculi genotypes.
Main Methods:
- Quantitative Polymerase Chain Reaction (qPCR) was used to measure microsporidial DNA in individual organs.
- Immunocompetent and immunodeficient mice were experimentally infected with E. cuniculi genotype II or III.
- Parasitic load and organ distribution were monitored over 35 days post-infection.
Main Results:
- E. cuniculi genotype III exhibited rapid dissemination to all organs by 7 days post-infection (DPI) with a ten-fold higher spore burden than genotype II.
- E. cuniculi genotype II infection progressed slower, with increasing burden over 35 DPI, and caused mortality in immunodeficient mice at 28 DPI.
- Genotype II infection spread beyond the gastrointestinal tract, while genotype III remained in both gastrointestinal and extra-gastrointestinal sites.
Conclusions:
- Pathogenicity of E. cuniculi is not solely determined by spore burden; genotype II, despite lower burden, caused earlier mortality in immunodeficient hosts.
- Understanding E. cuniculi genotype-specific pathophysiology is crucial for diagnostics and treatment, especially concerning immune evasion and persistence.
- The study highlights distinct dissemination and virulence strategies between E. cuniculi genotypes II and III.
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