| Autor: |
Nau J; Institute of Medical Microbiology and Hospital Hygiene, Medical Faculty, Heinrich-Heine-University Düsseldorf, Universitätsstraße 1, 40225 Düsseldorf, Germany., Eller SK; Institute of Medical Microbiology and Hospital Hygiene, Medical Faculty, Heinrich-Heine-University Düsseldorf, Universitätsstraße 1, 40225 Düsseldorf, Germany., Wenning J; Institute of Medical Microbiology and Hospital Hygiene, Medical Faculty, Heinrich-Heine-University Düsseldorf, Universitätsstraße 1, 40225 Düsseldorf, Germany., Spekker-Bosker KH; Institute of Medical Microbiology and Hospital Hygiene, Medical Faculty, Heinrich-Heine-University Düsseldorf, Universitätsstraße 1, 40225 Düsseldorf, Germany., Schroten H; Pediatric Infectious Diseases, Department of Pediatrics, Medical Faculty Mannheim, Heidelberg University, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany., Schwerk C; Pediatric Infectious Diseases, Department of Pediatrics, Medical Faculty Mannheim, Heidelberg University, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany., Hotop A; Institute for Medical Microbiology, University Medical Center, Kreuzbergring 57, 37077 Göttingen, Germany., Groß U; Institute for Medical Microbiology, University Medical Center, Kreuzbergring 57, 37077 Göttingen, Germany., Däubener W; Institute of Medical Microbiology and Hospital Hygiene, Medical Faculty, Heinrich-Heine-University Düsseldorf, Universitätsstraße 1, 40225 Düsseldorf, Germany. |
| Abstrakt: |
Porcine infections are currently not the state-of-the-art model to study human diseases. Nevertheless, the course of human and porcine toxoplasmosis is much more comparable than that of human and murine toxoplasmosis. For example, severity of infection, transplacental transmission, and interferon-gamma-induced antiparasitic effector mechanisms are similar in pigs and humans. In addition, the severe immunosuppression during acute infection described in mice does not occur in the experimentally infected ones. Thus, we hypothesise that porcine Toxoplasma gondii infection data are more representative for human toxoplasmosis. We therefore suggest that the animal model chosen must be critically evaluated for its assignability to human diseases. |
