Microsporidia are pathogenic organism related to fungi. They cause infections in a wide variety of mammals as well as in avian, amphibian, and reptilian hosts. Many microsporidia species play an important role in the development of serious diseases that have significant implications in human and veterinary medicine. While microsporidia were originally considered to be opportunistic pathogens in humans, it is now understood that infections also occur in immune competent humans. Encephalitozoon cuniculi, Encephalitozoon intestinalis, and Enterocytozoon bieneusi are primarily mammalian pathogens. However, many other species of microsporidia that have some other primary host that is not a mammal have been reported to cause sporadic mammalian infections. Experimental models and observations in natural infections have demonstrated that microsporidia can cause a latent infection in mammalian hosts. This chapter reviews the published studies on mammalian microsporidiosis and the data on chronic infections due to these enigmatic pathogens.

• Klíčová slova
• Epidemiology, Infection, Latency, Mammals, Microsporidia, Recurrent infection, Transmission,
• MeSH
• Enterocytozoon * MeSH
• feces mikrobiologie   MeSH
• lidé MeSH
• Microsporidia * genetika   MeSH
• perzistentní infekce MeSH
• savci MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH

BACKGROUND: Microsporidia of the genus Encephalitozoon are generally connected with severe infections with lethal outcome in immunodeficient hosts. In immunocompetent hosts, microsporidiosis typically establishes a balanced host-parasite relationship that produces minimal clinically overt disease. Although the alimentary tract represents one of the main primary target tissues, the mechanisms of reaching other tissues during systemic microsporidian infections remain unclear. METHODS: In the present study, we tested the relation between inflammation induction in immunocompetent and immunodeficient mice and the presence of spores of E. cuniculi genotype II in selected organs and in fecal specimens by using molecular and histology methods. RESULTS: We reported the positive connection between inflammation induction and the significant increase of E. cuniculi genotype II occurrence in inflammation foci in both immunocompetent BALB/c and immunodeficient severe combined immunodeficient (SCID) mice in the acute phase of infection and the re-activation of latent microsporidial infection following inflammation induction in immunocompetent mice. CONCLUSION: The results imply possible involvement of immune cells serving as vehicles transporting E. cuniculi genotype II purposefully across the whole host body towards inflammation. With increasing number of records of infections, it is necessary to reconsider microsporidia as agents responsible for various pathologies. The elucidation of possible connection with pro-inflammatory immune responses represents an important challenge with consequences for human health and development of therapeutic strategies.

• Klíčová slova
• Encephalitozoon cuniculi, inflammation, targeted migration,
• Publikační typ
• časopisecké články MeSH

BACKGROUND: Microsporidia are obligate intracellular parasites causing severe infections with lethal outcome in immunocompromised hosts. However, these pathogens are more frequently reported as latent infections in immunocompetent individuals and raises questions about the potential risk of reactivation following induced immunosuppression. AIMS: To evaluate the possibility latent microsporidiosis, efficacy or albendazole, and reactivation, the authors monitored the course of E. cuniculi infection in immunocompetent BALB/c mice and immunodeficient SCID mice using molecular methods. METHODS: Mice were per orally infected with 10(7) spores of E. cuniculi. Selected groups were treated with albendazole, re-infected or chemically immunosuppressed by dexamethasone. The presence of microsporidia in the host's organs and feces were determined using PCR methods. Changes in numbers of lymphocytes in blood and in spleen after induction of immunosuppression were confirmed using flow cytometry analysis. RESULTS: Whereas E. cuniculi caused lethal microsporidiosis in SCID mice, the infection in BABL/c mice remained asymptomatic despite parasite dissemination into many organs during the acute infection phase. Albendazole treatment led to microsporidia elimination from organs in BALB/c mice. In SCID mice, however, only a temporary reduction in number of affected organs was observed and infection re-established post-treatment. Dexamethasone treatment resulted in a chronic microsporidia infection disseminating into most organs in BALB/c mice. Although the presence of E. cuniculi in organs of albendazole- treated mice was undetectable by PCR, it was striking that infection was reactivated by immunosuppression treatment. CONCLUSION: Our results demonstrated that microsporidia can successfully survive in organs of immunocompetent hosts and are able to reactivate from undetectable levels and spread within these hosts after induction of immunosuppression. These findings stress the danger of latent microsporidiosis as a life-threatening risk factor especially for individuals undergoing chemotherapy and in transplant recipients of organs originating from infected donors.

• MeSH
• albendazol terapeutické užití   MeSH
• Cercopithecus aethiops MeSH
• dexamethason MeSH
• Encephalitozoon cuniculi * MeSH
• encephalitozoonóza farmakoterapie   imunologie   MeSH
• feces mikrobiologie   MeSH
• modely nemocí na zvířatech * MeSH
• myši inbrední BALB C MeSH
• myši SCID MeSH
• myši MeSH
• počet lymfocytů MeSH
• polymerázová řetězová reakce MeSH
• průtoková cytometrie MeSH
• Vero buňky MeSH
• vnitřnosti mikrobiologie   MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• albendazol MeSH
• dexamethason MeSH

Microsporidia are eukaryotic, obligate, intracellular protists that are emerging pathogens in immunocompromised hosts, including AIDS patients and organ transplant recipients. The efficacy of gamma interferon (IFN-gamma) for the treatment of microsporidiosis caused by Encephalitozoon cuniculi was studied by means of adoptive transfer and IFN-gamma administration in SCID mice. While the adoptive transfer of CD4(+) T cells from immunocompetent mice prolonged survival of SCID mice infected perorally with E. cuniculi, survival was not improved by adoptive transfer of CD4(+) T lymphocytes from IFN-gamma-deficient mice. The protective effect of IFN-gamma was confirmed in cytokine therapy experiments in which SCID mice receiving IFN-gamma survived significantly longer than mice receiving mock injections. The administration of serum containing specific antibodies against E. cuniculi was found to prolong the survival of concurrently IFN-gamma-treated SCID mice. The data presented in this study suggest that IFN-gamma is potentially useful as a cytokine therapy for microsporidiosis, especially in CD4(+) T-cell-deficient patients.

• MeSH
• CD4-pozitivní T-lymfocyty imunologie   MeSH
• Encephalitozoon cuniculi imunologie   MeSH
• encephalitozoonóza imunologie   mortalita   parazitologie   terapie   MeSH
• imunoterapie MeSH
• interferon gama aplikace a dávkování   genetika   terapeutické užití   MeSH
• lidé MeSH
• modely nemocí na zvířatech MeSH
• monoklonální protilátky imunologie   terapeutické užití   MeSH
• myši inbrední BALB C MeSH
• myši knockoutované MeSH
• myši SCID MeSH
• myši MeSH
• převzatá imunita MeSH
• specificita protilátek * MeSH
• výsledek terapie MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• interferon gama MeSH
• monoklonální protilátky MeSH

The role of CD4+ and CD8+ T lymphocytes in the protection against intraperitoneally (i.p.) or perorally (p.o.) acquired Encephalitozoon cuniculi (Levaditi et al., C R Soc Biol Paris 89:984-986, 1923) infection was studied by means of reconstitution of severe combined immunodeficiency (SCID) mice with well-defined populations of naive CD8+ or CD4+ T lymphocytes. Adoptive transfer of pure CD8+ T lymphocyte subpopulation protects SCID mice against a lethal microsporidiosis caused by E. cuniculi. The protective effect of CD8+ T lymphocytes is manifested in both i.p. and p.o. infection. On the contrary, the host defense against peroral infection does not require CD8+ T cells. The protective role is not mediated by CD4+ T lymphocytes only. SCID mice reconstitution with pure CD4+ T cell subpopulation led to prolonged survival of perorally infected mice. However, these mice died due to lethal encephalitozoonosis caused by i.p. infection.

• MeSH
• CD4-pozitivní T-lymfocyty imunologie   MeSH
• CD8-pozitivní T-lymfocyty imunologie   MeSH
• Encephalitozoon cuniculi imunologie   MeSH
• encephalitozoonóza imunologie   MeSH
• myši inbrední BALB C MeSH
• myši MeSH
• převzatá imunita MeSH
• těžká kombinovaná imunodeficience imunologie   MeSH
• ústa MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

The possible role of humoral antibodies in the immune response to microsporidiosis was studied using a novel anti-exospore monoclonal antibody (MAb) P5/H1 which recognised Encephalitozoon cuniculi. The effect of the P5/H1 MAb on microsporidial growth in vitro resulted in a reduction of the numbers of E. cuniculi spores in a Vero E6 cell-line culture. This reduction in the number of infected cells and the decrease of intracellular spores in infected cells was found when MAb P5/H1 was present in cultures, compared to cultures with an irrelevant isotype control MAb. Moreover, the presence of P5/H1 MAb increased the number of phagocytosed spores in macrophage cultures, and increased the activation of macrophages measured by nitrite oxide production. These results suggest a possible partial role of specific humoral antibodies in the protection against E. cuniculi infection.

• MeSH
• antigeny protozoální imunologie   MeSH
• Cercopithecus aethiops MeSH
• Encephalitozoon cuniculi imunologie   fyziologie   MeSH
• interferon gama metabolismus   MeSH
• kultivované buňky MeSH
• makrofágy MeSH
• monoklonální protilátky imunologie   MeSH
• myši inbrední BALB C MeSH
• myši MeSH
• protilátky protozoální imunologie   MeSH
• senzitivita a specificita MeSH
• specificita protilátek MeSH
• spory protozoální imunologie   fyziologie   MeSH
• Vero buňky MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• antigeny protozoální MeSH
• interferon gama MeSH
• monoklonální protilátky MeSH
• protilátky protozoální MeSH