Differences in the intensity of infection caused by Encephalitozoon cuniculi genotype II and III - Comparison using quantitative real-time PCR
Language English Country United States Media print-electronic
Document type Comparative Study, Journal Article
PubMed
30075234
DOI
10.1016/j.exppara.2018.07.019
PII: S0014-4894(18)30216-9
Knihovny.cz E-resources
- Keywords
- BALB/C, Encephalitozoon cuniculi genotypes II and III, Microsporidiosis, SCID, qRT-PCR,
- MeSH
- Arvicolinae MeSH
- Chlorocebus aethiops MeSH
- Encephalitozoon cuniculi classification genetics growth & development physiology MeSH
- Encephalitozoonosis parasitology MeSH
- Gastrointestinal Tract parasitology MeSH
- Genotype MeSH
- Immunocompetence MeSH
- Real-Time Polymerase Chain Reaction MeSH
- Microsporidia physiology MeSH
- Disease Models, Animal MeSH
- Mice, Inbred BALB C MeSH
- Mice, SCID MeSH
- Mice MeSH
- Parasite Load MeSH
- Spores, Fungal MeSH
- Vero Cells MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Comparative Study MeSH
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.
References provided by Crossref.org
Chronic Infections in Mammals Due to Microsporidia
Encephalitozoon cuniculi Genotype II Concentrates in Inflammation Foci