The Prevalence and Source of Toxoplasma Infection in the Environment

Jackson, M. H.; Hutchison, W. M.

doi:10.1016/s0065-308x(08)60331-0

Cited by 116 publications

(80 citation statements)

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“…Toxoplasma gondii is a globally prevalent protozoan parasite affecting all warm-blooded animals (Miller, Frenkel & Dubey, 1972 ;Jackson & Hutchinson, 1989). It causes the disease toxoplasmosis which, although generally asymptomatic, can be life threatening in immunocompromised patients, such as those suffering from AIDS (Luft & Remington, 1992).…”

Section: Introductionmentioning

confidence: 99%

Toxoplasma gondii major surface antigen (SAG1): in vitro analysis of host cell binding

2004

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Article:Robinson, S.A., Smith, J.E. and Millner, P.A. (2004) SUMMARYPrevious studies have indicated that SAG1, the major surface molecule of the protozoan parasite Toxoplasma gondii,isan important attachment ligand for the host cell. However, the research data that supports this claim comes largely from studies investigating tachyzoite binding, and not SAG1 binding per se. In this study we successfully developed an in vitro attachment assay to directly evaluate the mechanism of SAG1-host cell binding. Competition experiments were then performed using SAG1 that had been pre-treated with the neoglycoprotein BSA-glucosamide or with antibody. Soluble BSA-glucosamide blocked SAG1 attachment to MDBK cells in a dose-dependent manner, implying that SAG1 binding is mediated, in part, via attachment to host cell surface glucosamine. Interestingly, pre-incubation of SAG1 in polyclonal sera from chronically infected mice failed to block binding. This challenges the assumption that anti-SAG1 antibodies block parasite attachment through the masking of SAG1 host cell binding domains. Taken together, this evidence presents new strategies for understanding SAG1-mediated attachment.

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Section: Introductionmentioning

confidence: 99%

Toxoplasma gondii major surface antigen (SAG1): in vitro analysis of host cell binding

2004

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“…Toxoplasma gondii is a coccidian parasite of felids and has, as intermediate hosts, many warm-blooded animals, including mammals and birds (reviewed by Jackson & Hutchison, 1989). An intermediate host may become infected either through the ingestion of infected meat or by ingesting faecal material from infected cats.…”

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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“…Toxoplasma gondii is a highly prevalent, obligate, intracellular protozoan parasite that infects nearly one-third of the human population (1,2). Since its recognition as the causative agent of toxoplasmosis in the late 1930s, many clinical manifestations have been attributed to T. gondii infections including lymphadenopathy, ileitis, encephalitis, and/or blinding ocular infections in both children and adults (1,(3)(4)(5)(6)(7)(8).…”

mentioning

confidence: 99%

“…Since its recognition as the causative agent of toxoplasmosis in the late 1930s, many clinical manifestations have been attributed to T. gondii infections including lymphadenopathy, ileitis, encephalitis, and/or blinding ocular infections in both children and adults (1,(3)(4)(5)(6)(7)(8). T. gondii infections can also be lethal to a developing fetus and immunocompromised, cancer, AIDS, and organ transplant patients.…”

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confidence: 99%

Structural and Functional Characterization of SporoSAG

Crawford

Lamb

Wasmuth

et al. 2010

Journal of Biological Chemistry

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Toxoplasma gondii, the etiological agent of toxoplasmosis, utilizes stage-specific expression of antigenically distinct glycosylphosphatidylinositol-tethered surface coat proteins to promote and establish chronic infection. Of the three infective stages of T. gondii, sporozoites are encapsulated in highly infectious oocysts that have been linked to large scale outbreaks of toxoplasmosis. SporoSAG (surface antigen glycoprotein) is the dominant surface coat protein expressed on the surface of sporozoites. Using a bioinformatic approach, we show that SporoSAG clusters with the SAG2 subfamily of the SAG1-related superfamily (SRS) and is non-polymorphic among the 11 haplogroups of T. gondii strains. In contrast to the immunodominant SAG1 protein expressed on tachyzoites, SporoSAG is non-immunogenic during natural infection. We report the 1.60 Å resolution crystal structure of SporoSAG solved using cadmium single anomalous dispersion. SporoSAG crystallized as a monomer and displays unique features of the SRS ␤-sandwich fold relative to SAG1 and BSR4. Intriguingly, the structural diversity is localized to the upper sheets of the ␤-sandwich fold and may have important implications for multimerization and host cell ligand recognition. The structure of SporoSAG also reveals an unexpectedly acidic surface that contrasts with the previously determined SAG1 and BSR4 structures where a basic surface is predicted to play a role in binding negatively charged glycosaminoglycans. Our structural and functional characterization of SporoSAG provides a rationale for the evolutionary divergence of this key SRS family member.

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The Prevalence and Source of Toxoplasma Infection in the Environment

Cited by 116 publications

References 231 publications

Toxoplasma gondii major surface antigen (SAG1): in vitro analysis of host cell binding

Toxoplasma gondii major surface antigen (SAG1): in vitro analysis of host cell binding

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

Structural and Functional Characterization of SporoSAG

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