The ultrastructural pathology of congenital murine toxoplasmic retinochoroiditis. Part I: the localization and morphology of Toxoplasma cysts in the retina

McMenamin, Paul G.; Dutton, Gordon N.; Hay, John; Cameron, Samuel J.

doi:10.1016/s0014-4835(86)80021-5

Cited by 44 publications

(13 citation statements)

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“…The localization of tissue cysts is strikingly similar in ocular toxoplasmosis. In murine congenital ocular toxoplasmosis, cysts are most frequently found in the inner retinal layers at the border of retinal scars or remote from scars in the absence of an in¯ammatory reaction (McMenamin et al 1986). …”

Section: Discussionmentioning

confidence: 99%

Canine neosporosis: clinical and pathological findings and first isolation of Neospora caninum in Germany

2000

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Neosporosis was diagnosed in an 11-week-old puppy of the breed Kleiner Münsterländer with progressive hindlimb paresis. Pathohistological and immunohistological examinations revealed a disseminated infection with Neospora caninum. Parasitic stages were demonstrated in the brain, spinal cord, retina, muscles, thymus, heart, liver, kidney, stomach, adrenal gland, and skin. Immunohistochemistry investigations were carried out using polyclonal rabbit antisera developed against N. caninum tachyzoites and the recombinant bradyzoite-specific antigen BAG-5 of Toxoplasma gondii, which is known to cross-react with N. caninum bradyzoites. BAG-5 antibodies recognized tissue cysts within the CNS and some protozoan stages that were not surrounded by a visible cyst wall. All parasite clusters in the retina and some in muscle tissue stained positively with the BAG-5 antiserum. N. caninum was isolated in cell culture and mice inoculated with brain and spinal cord of the puppy. The new isolate is the first reported in Germany and is designated NC-GER1.

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Section: Discussionmentioning

confidence: 99%

Canine neosporosis: clinical and pathological findings and first isolation of Neospora caninum in Germany

2000

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“…For this reason the development of a suitable laboratory model of congenital toxoplasmosis is essential to test the efficacy of putative vaccines. Such a model system has been studied in this laboratory, using outbred mice and has proven useful in studying ophthalmological, behavioural and neurological sequelea (Hay et al 1981(Hay et al , 1985Hutchison et al 1982;McMenamin et al 1986;Dutton et al 1986). However, the value of this model for immunological studies or vaccine design has never been assessed; indeed to analyse, dissect and characterize the nature of protective immunity as well as guaranteeing reproducibility of results, it is essential that the disease model should comprise the use of inbred mice.…”

Section: Introductionmentioning

confidence: 99%

Studies on a murine model of congenital toxoplasmosis: vertical disease transmission only occurs in BALB/c mice infected for the first time during pregnancy

Roberts

Alexander

1992

Parasitology

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This version is available at https://strathprints.strath.ac.uk/47342/ Strathprints is designed to allow users to access the research output of the University of Strathclyde. Unless otherwise explicitly stated on the manuscript, Copyright © and Moral Rights for the papers on this site are retained by the individual authors and/or other copyright owners. Please check the manuscript for details of any other licences that may have been applied. You may not engage in further distribution of the material for any profitmaking activities or any commercial gain. You may freely distribute both the url (https://strathprints.strath.ac.uk/) and the content of this paper for research or private study, educational, or not-for-profit purposes without prior permission or charge.Any correspondence concerning this service should be sent to the SUMMARYThe incidence of congenital toxoplasmosis was determined by an ELISA in the litters of BALB/c mice which had been infected 8 weeks before mating, on day 12 of pregnancy, or on both these occasions. Of those mice given the infection for the first time on day 12 of pregnancy, 5 out of 6 gave birth to infected litters with approximately 50 % of the individuals in each litter being infected. BALB/c mice which had been infected 8 weeks before mating did not give birth to infected litters, even if they were reinfected on day 12 of pregnancy. Following infection BALB/c mice were found to harbour significantly fewer tissue cysts than the congenic H-2 derivative BALB/K strain. However, chronically infected BALB/K mice also failed to produce infected litters, indicating that tissue cyst burden in the dam did not influence congenital infection at least on the BALB background. This study demonstrates that BALB/c dams chronically infected with Toxoplasma gondii, have immunity capable of protecting their embryos from congenital infection, even if the dams are reinfected during pregnancy. Our results demonstrate that the BALB/c mouse can be used as a model of human or ovine congenital T. gondii infection suitable for testing putative vaccines.

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“…The intensity of damage to the retina and choroid depends on the severity of the infection and the associated inflammatory reaction (11,13,20). Inflammatory cells, predominantly macrophages and lymphocytes, infiltrate the retina, the subretinal space, and the vitreous (6,11,20).…”

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confidence: 99%

“…Inflammatory cells, predominantly macrophages and lymphocytes, infiltrate the retina, the subretinal space, and the vitreous (6,11,20). In the severe form of T. gondii-induced uveitis, destruction of large segments of the outer retina and pigment epithelium is observed (6,9,13,24). Within the retina, lysosomal and other autolytic enzymes released by inflammatory cells are thought to contribute to the pathogenic mechanisms of retinal tissue damage (6,11).…”

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confidence: 99%

Toxoplasma gondii Infection Induces Gene Expression and Secretion of Interleukin 1 (IL-1), IL-6, Granulocyte-Macrophage Colony-Stimulating Factor, and Intercellular Adhesion Molecule 1 by Human Retinal Pigment Epithelial Cells

2000

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We have used human retinal pigment epithelial (HRPE) cultures to investigate the primary cellular responses of retinal resident cells to intracellular Toxoplasma gondii replication. At 4 days postinoculation, when all of the cells were infected, the secretion of interleukin 1␤ (IL-1␤), IL-6, granulocyte-macrophage colonystimulating factor (GM-CSF), and intercellular adhesion molecule 1 (ICAM-1) was augmented by 23-, 10-, 8-, and 5-fold, respectively, over the control. Northern and reverse transcriptase PCR analyses showed significant upregulation of steady-state levels of mRNA for IL-1␤, IL-6, GM-CSF, and ICAM-1. The secretion of these molecules by HRPE cells may play a critical immunoregulatory role in the pathophysiological processes associated with T. gondii-induced retinochoroiditis.Retinochoroiditis caused by Toxoplasma gondii during ocular toxoplasmosis results in inflammation and disorganization of the retina, occasionally leading to severe loss of vision (11,20,23,30). The intensity of damage to the retina and choroid depends on the severity of the infection and the associated inflammatory reaction (11,13,20). Inflammatory cells, predominantly macrophages and lymphocytes, infiltrate the retina, the subretinal space, and the vitreous (6,11,20). In the severe form of T. gondii-induced uveitis, destruction of large segments of the outer retina and pigment epithelium is observed (6, 9, 13, 24). Within the retina, lysosomal and other autolytic enzymes released by inflammatory cells are thought to contribute to the pathogenic mechanisms of retinal tissue damage (6, 11).Retinal pigment epithelium (RPE), an integral part of the neuroretina in the posterior pole of the eye, acts as a barrier between the highly vascularized choroid and the retina with a complex architecture of neuronal cells (2, 31). In addition to its role in the transport of metabolites between retina and choroid, the RPE phagocytose the shed outer segments of retinal rods and cones (2, 31). Many of these activities of the RPE are essential for the structural and functional integrity of the retina and choroid. The RPE, because of its critical location and physiological activities, is constantly subjected to contact with various infectious agents and inflammatory mediators (12,14).Tachyzoites of T. gondii injected into the peritonial cavities of mice were thought to reach the retina via both choroidal and retinal circulation (8,21,26). In a rabbit model, injection of tachyzoites into the suprachoroidal space resulted in outer retinal lesions and localized foci of retinal pigment epitheliosis within 48 h. This suggests the crossing of the parasite through the RPE-Bruchs membrane barrier from the choroid to the retina (27). Histopathological examination of the eyes of patients with toxoplasma-induced retinochoroiditis revealed the presence of free tachyzoites and cysts in the RPE and the retina (9,19,24). Hence, studies of the mechanisms of T. gondii replication within retinal cells and the responses of the host cells to parasite invasion would be ...

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The ultrastructural pathology of congenital murine toxoplasmic retinochoroiditis. Part I: the localization and morphology of Toxoplasma cysts in the retina

Cited by 44 publications

References 20 publications

Canine neosporosis: clinical and pathological findings and first isolation of Neospora caninum in Germany

Canine neosporosis: clinical and pathological findings and first isolation of Neospora caninum in Germany

Studies on a murine model of congenital toxoplasmosis: vertical disease transmission only occurs in BALB/c mice infected for the first time during pregnancy

Toxoplasma gondii Infection Induces Gene Expression and Secretion of Interleukin 1 (IL-1), IL-6, Granulocyte-Macrophage Colony-Stimulating Factor, and Intercellular Adhesion Molecule 1 by Human Retinal Pigment Epithelial Cells

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