Differences in the intensity of infection caused by Encephalitozoon cuniculi genotype II and III - Comparison using quantitative real-time PCR

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60076658%3A12220%2F18%3A43898020" target="_blank" >RIV/60076658:12220/18:43898020 - isvavai.cz</a>

Alternative codes found

RIV/60077344:_____/18:00498718

Result on the web

<a href="http://dx.doi.org/10.1016/j.exppara.2018.07.019" target="_blank" >http://dx.doi.org/10.1016/j.exppara.2018.07.019</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.exppara.2018.07.019" target="_blank" >10.1016/j.exppara.2018.07.019</a>

Result language

angličtina

Original language name

Differences in the intensity of infection caused by Encephalitozoon cuniculi genotype II and III - Comparison using quantitative real-time PCR

Original language description

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 HI, but which caused the earlier death of immunodeficient mice.

Czech name

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Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

—

OECD FORD branch

40301 - Veterinary science

Project

<a href="/en/project/GA17-12871S" target="_blank" >GA17-12871S: Elucidation of different virulence and drug resistance of genotypes of Encephalitozoon cuniculi using murine model.</a><br>

Continuities

S - Specificky vyzkum na vysokych skolach

Publication year

2018

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

Experimental Parasitology

ISSN

0014-4894

e-ISSN

—

Volume of the periodical

192

Issue of the periodical within the volume

září

Country of publishing house

US - UNITED STATES

Number of pages

5

Pages from-to

93-97

UT code for WoS article

000444788600014

EID of the result in the Scopus database

2-s2.0-85053053119