New clinical and experimental insights into Old World and neotropical ocular toxoplasmosis
Retinal lesions or other ocular manifestations are serious consequences of infection with the protozoan parasite Toxoplasma gondii. Whilst classically considered a consequence of congenital transmission, recent screening studies estimated that 2% of T. gondii seropositive persons in Europe and North...
- Autores:
- Tipo de recurso:
- Fecha de publicación:
- 2014
- Institución:
- Universidad del Rosario
- Repositorio:
- Repositorio EdocUR - U. Rosario
- Idioma:
- eng
- OAI Identifier:
- oai:repository.urosario.edu.co:10336/24331
- Acceso en línea:
- https://doi.org/10.1016/j.ijpara.2013.09.007
https://repository.urosario.edu.co/handle/10336/24331
- Palabra clave:
- Disease
Gene
Genetic marker
Parasite
Parasite transmission
Protein
Protozoan
Virulence
Europe
Genetic marker
Genetic variability
Geographic distribution
Host parasite interaction
Host susceptibility
Human
Immune response
Immunogenetics
Nonhuman
North america
Parasite incidence
Parasite load
Parasite prevalence
Parasite virulence
Pathophysiology
Review
South america
Toxoplasmosis
South america
Protozoa
Toxoplasma gondii
Human studies
Inflammation
Mouse models
Ocular toxoplasmosis
Parasite strains
South america
Toxoplasma gondii
Americas
Animals
Europe
Eye diseases
Humans
Toxoplasmosis
Human studies
Inflammation
Mouse models
Ocular toxoplasmosis
Parasite strains
South america
Toxoplasma gondii
- Rights
- License
- Abierto (Texto Completo)
Summary: | Retinal lesions or other ocular manifestations are serious consequences of infection with the protozoan parasite Toxoplasma gondii. Whilst classically considered a consequence of congenital transmission, recent screening studies estimated that 2% of T. gondii seropositive persons in Europe and North America have retinal lesions, most of them persisting unnoticed. The situation is more dramatic in South America, probably due to the predominance of virulent strains. Some of these strains seem to exhibit ocular or neuronal tropism and are responsible for severe ocular lesions. Despite the medical importance, the physiopathological mechanisms have only recently begun to be elucidated. The particular immune-privileged situation in the eye has to be considered. Studies on French patients showed low or undetectable ocular parasite loads, but a clear Th1/Th17 type immune reaction. Suitable mouse models have appeared in the last few years. Using such a model, IL-17A proved to impair parasite control and induce pathology. In contrast, in South American patients, the parasite seems to be much less efficiently controlled through a Th2 type or suppressive immune response that favors parasite replication. Finally, several host genetic markers controlling immune response factors have been associated with ocular involvement of T. gondii infection, mainly in South America. © 2013 Australian Society for Parasitology Inc. |
---|