Ocular toxoplasmosis II: Clinical features, pathology and management
ABSTRACT The term, ocular toxoplasmosis, refers to eye disease related to infection with the parasite, Toxoplasma gondii. Recurrent posterior uveitis is the typical form of this disease, characterized by unilateral, necrotizing retinitis with secondary choroiditis, occurring adjacent to a pigmented retinochoroidal scar and associated with retinal vasculitis and vitritis. Multiple atypical presentations are also described, and severe inflammation is observed in immunocompromised patients. Histopathological correlations demonstrate focal coagulative retinal necrosis, and early in the course of the disease, this inflammation is based in the inner retina. For typical ocular toxoplasmosis, a diagnosis is easily made on clinical examination. In atypical cases, ocular fluid testing to detect parasite DNA by polymerase chain reaction or to determine intraocular production of specific antibody may be extremely helpful for establishing etiology. Given the high seroprevalence of toxoplasmosis in most communities, serological testing for T. gondii antibodies is generally not useful. Despite a lack of published evidence for effectiveness of current therapies, most ophthalmologists elect to treat patients with ocular toxoplasmosis that reduces or threatens to impact vision. Classic therapy consists of oral pyrimethamine and sulfadiazine, plus systemic corticosteroid. Substantial toxicity of this drug combination has spurred interest in alternative antimicrobials, as well as local forms of drug delivery. At this time, however, no therapeutic approach is curative of ocular toxoplasmosis. © 2012 The Authors. Clinical and Experimental Ophthalmology © 2012 Royal Australian and New Zealand College of Ophthalmologists.
- SourceAvailable from: Pilar Nannini
[Show abstract] [Hide abstract]
- "Substantial toxicity of this drug combination has spurred interest in alternative antimicrobials, as well as local forms of drug delivery. At this time, however, no therapeutic approach is curative of ocular toxoplasmosis  "
ABSTRACT: Infection with the protozoan Toxoplasma gondii is one of the most frequent parasitic infections worldwide and the common infection of the retina in the general population. We describe a case report of a chorioretinitis in an immunocompetent 8-year-old patient as a consequence of a underdiagnosed neonatal toxoplasmosis. The boy was successfully managed with pyrimethamine and sulfadiazine. The present case we would like to empathize the importance of considering toxoplasma gondii as a possible cause of chorioretinitis in children living in developed countries and we provide a detailed reviewed of the literature about treatment of Toxoplasma gondii infection.08/2014; 4(4):323–328. DOI:10.1016/S2222-1808(14)60582-X
[Show abstract] [Hide abstract]
- "Due to the very limited access to ocular tissue, pathophysiological studies on humans are rare. Some post-mortem examinations described histopathological features (Butler et al., 2013), but immunological investigations usually looked at immune mediators in the peripheral blood or genetic markers (see below). Therefore, we assessed cytokine concentrations in aqueous humor, taken by puncture at the same time as the diagnosis, as ocular fluids are the most reliable samples to test for the presence of Toxoplasma DNA and/or local specific antibody production (Villard et al., 2003). "
ABSTRACT: 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.International journal for parasitology 11/2013; 44. DOI:10.1016/j.ijpara.2013.09.007 · 3.40 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: Abstract Background: Treatment of ocular toxoplasmosis is aimed at stabilizing visual function and reducing recurrence rates. Methods: Small controlled studies indicate that available treatments do not affect visual outcome and recurrence rates, and no antibiotic in current use will kill bradyzoites. Results: Antiparasitic treatment is justified in center-involving lesions and in large aggressive lesions namely in South American patients. Antibiotic treatment is needed for disease in the immunosuppressed, and this needs to be systemic. There exists strong agreement that a monotherapy, using steroids, is contraindicated. Prophylactic antibiotics may reduce recurrence rates in endemic areas and immunosuppressed patients. Conclusion: An ideal therapeutic strategy includes the strain of parasite, localization of the lesion, and severity of the inflammatory response as a basis for therapeutic decision making. New treatments targeting aspects of the parasite s physiology are very promising. On a global scale, public health measures to prevent transmission from animals and to access potable water are required.Ocular immunology and inflammation 04/2013; 21(4). DOI:10.3109/09273948.2013.779724 · 1.44 Impact Factor