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PubMed1986

Spleen and lymph node cell populations, in vitro cell proliferation and interferon-gamma production during the primary immune response to Toxoplasma gondii.

An animal model for the study of transient lymphadenopathy-splenomegaly during toxoplasmosis is presented. Injection of CBA/J mice with the low virulent, cyst-forming strain of Toxoplasma gondii (Pe strain) induces a three to four fold increase in weight and cellularity of spleen and lymph nodes with peak changes at 30-50 days after infection. The spleen displays marked haemopoiesis, a 30 fold increase in mononuclear phagocytes, and a two fold increase in Lyt2+ lymphocytes. Lymph nodes show a five fold increase in mononuclear phagocytes and a four and a half fold increase in Lyt2+ T cells. The increase in mononuclear phagocytes significantly alters T cell/macrophage ratios and this is associated with decreases in in vitro cell proliferation to mitogen and toxoplasma antigen. The relationship between alterations in cell balance of mononuclear phagocytes and T cell subsets and the expression of transient immune dysfunction can now be examined by modulating changes in these cell types.

Animals↗
PubMed1986

The immunodominant epitope of the major membrane tachyzoite protein (P30) of Toxoplasma gondii.

Several physicochemical characteristics of the repeated epitope of the major surface protein (P30) of Toxoplasma gondii were investigated with an anti-P30 mAb by two different methods: a one-site/inhibition assay that detects molecules containing single or multiple epitopes and a two-site/one antibody radiometric assay that is only effective with antigenic molecules containing two or more identical epitopes. Using both techniques, the repeated epitope within purified P30 was stable after 1 h at 63 degrees C, but labile at 100 degrees C. It was also resistant to successive freezing and thawing, and not affected after one year at -70 degrees C. Lyophilization and acidic or basic treatment had no effect. This epitope was also resistant to 20% trichloroacetic acid precipitation (activity recovered in the pellet) and to precipitation with cold acetone. To investigate the immunodominance of this repeated epitope during the humoral immune response against T. gondii, competition binding assays between anti-P30 mAb and polyclonal antibodies, from rabbits immunized with either purified P30 or total Toxoplasma extract and from patients with toxoplasmosis, have been used. We found that the mAb inhibited 50-95% of the binding of the IgG antibodies from both rabbits to purified P30. In addition, the binding of both human IgG and IgM antibodies to P30 was significantly inhibited by the mAb. It appears, therefore, that a single region of P30 contains most of the immunogenic activity.

Animals↗
PubMed1987

Isolation and characterization of a monoclonal anti-P30 antibody resistant mutant of Toxoplasma gondii.

Of the possible iodine-labelled Toxoplasma gondii surface proteins, P30 (apparent Mr 30,000) is the principal one recognized by acute and convalescent anti-toxoplasma sera. This protein which comprises from 3 to 5% of the total parasite protein was used to raise a panel of parasiticidal monoclonal anti-P30 antibodies. One of these monoclonal antibodies was able to select a resistant mutant from a large population of chemically mutagenized wild-type P strain parasites. This mutant retained the wild type sensitivity to other non-P30 parasiticidal monoclonal antibodies as well as polyclonal anti-P30 rabbit sera. Analysis of surface radioiodinated wild type and mutant parasites showed that the mutant had a quantitative reduction in the amount of P30. A comparison of surface biotin labelled wild type and resistant parasites by two dimensional electrophoresis showed that the mutant lacked one and possibly two of several proteins that make up wild type P30. Western blot analysis indicated that the mutant was devoid of antigenically reactive P30. These findings further support the hypothesis that antigenic variants of T. gondii can be induced and may involve the major surface membrane antigens of the parasite.

Animals↗
PubMed2006

Acute infection of Toxoplasma gondii and cytomegalovirus reactivation in a pediatric patient receiving liver transplant.

A 7-year-old Mexican boy with end-stage cirrhosis underwent liver transplantation and was maintained with cyclosporine and prednisolone. No specific data about Toxoplasma gondii or cytomegalovirus (CMV) infections in the cadaver donor were available. The recipient was seronegative for Toxoplasma, but CMV-IgG positive before transplantation. Ganciclovir was administered for prophylaxis during 3 months, but 5 months later he presented with icterus and increased transaminases. Acute transplant rejection was ruled out by biopsy. A seroconversion for T. gondii IgM and IgG and a small increase in CMV-IgM antibodies were observed, although the CMV-polymerase chain reaction (PCR) was negative. Ganciclovir was re-started, and the patient improved, but 6 months later he relapsed, and chorioretinitis lesions compatible both with T. gondii and CMV infections appeared. Pyrimethamine, sulfadiazine, folinic acid, and ganciclovir were administered. The boy showed favorable clinical improvement and remained stable for 12 months. Then, new retinal CMV lesions appeared in both eyes and the PCR for CMV became positive; therefore, the patient received a new regimen of ganciclovir, and clinically improved. From these data we concluded that the child presented a reactivation of CMV and a primary infection with T. gondii after transplantation.

Animals↗
PubMed2005

Use of PCR to diagnose Toxoplasma gondii chorioretinitis in eyes with severe vitritis.

Two cases are reported of intraocular inflammation in which severe vitritis hampered the fundal view, making an accurate clinical diagnosis impossible, and vitreous analysis using conventional techniques was unhelpful. PCR for Toxoplasma gondii was positive in both cases and provided the only way of confirming the diagnosis. Other ocular samples also underwent PCR for Toxoplasma DNA and the specificity of this approach is demonstrated.

Animals↗
PubMed2001

Seroprevalence of varicella zoster virus, parvovirus B19 and Toxoplasma gondii in a Melbourne obstetric population: implications for management.

At an antenatal clinic at a Melbourne obstetric hospital, 308 women were questioned about a known past history of infection with varicella zoster virus (VZV), human parvovirus B19 and Toxoplasma gondii. Immunoglobulin G (IgG) concentrations were determined for the 3 infectious agents and a recalled history of infection was compared with the presence of specific antibody. Exactly 66% of women recalled being infected with chickenpox (VZV) and 94% showed serological evidence of past exposure. Although 64% of women had parvovirus specific IgG, only one gave a definite history of past parvovirus infection. None of the 23% of women with evidence of previous exposure to Toxoplasma gondii recalled a past infection. The proportion of antenatal women at risk in this study was used to estimate the potential burden of disease from congenital infections in Australia and to examine implications for management of pregnancies complicated by these 3 infections.

Adolescent↗
PubMed1982

Toxoplasma, Toxocara, and epilepsy.

The presence of positive antibody titres to Toxoplasma and Toxocara in an adult epileptic population has been examined in relation to other observations of aetiological importance. With Toxoplasma, and more particularly with Toxocara, a higher incidence of positive antibody titres was recorded than in nonepileptic populations. Comparison with previous studies in childhood epilepsy indicate that the incidence of positive titres increased with age throughout adult life. Despite attention to the age of onset of epilepsy, presumed aetiological factors, and electroencephalographic and clinical observations, no causal relationship between parasitic infection and the aetiology of epilepsy was established.

Antibodies↗
PubMed1978

Effect of immunization of cats with Isospora felis and BCG on immunity to reexcretion of Toxoplasma gondii oocysts.

The effect of pretreatment with Isospora felis and bacillus Calmette-Guérin (BCG) on the reexcretion of Toxoplasma gondii oocysts was studied in 16 coccidia-free cats. The following conclusions were drawn: (A) Chronically T. gondii-infected cats reexcreted T. gondii oocysts after superinfection with I. felis, and this reexcretion was prevented in cats infected with I. felis before T. gondii infection. (B) Administration of BCG before Toxoplasma infection had no apparent effect on the outcome of the infection.

Animals↗
PubMed1981

Histological and ultrastructural studies of the interaction of Toxoplasma gondii Tachyzoites with mouse omentum in experimental infection.

Mouse omentum was studied after intraperitoneal challenge with tachyzoites of Toxoplasma gondii. Parasites inhabit omental histiocytes, fibroblasts, mesothelial cells, and free peritoneal macrophages. Recently infected cells showed enhanced metabolic and functional activity. Villous projections of the parasitophorous vacuole wall appeared, usually opposite the anterior pole of the parasite. In mesothelial cells, projections formed terminal swellings not observed in other infected cells. Activation of host cells was followed by reduction of the density of the cytoplasmic matrix, autophagosome formation, and intracellular edema, indicating the damage. The wall of the parasitophorous vacuole loses the supporting host cell endoplasmic reticulum that was attached to the vacuole just after entrance of the parasite into the cell. Then lysis of the parasitophorous vacuole and complete cell destruction occurs. The growth of parasites in undamaged cells does not coincide with the inflammatory response. Inflammation of the peritoneum develops only after the start of mass destruction of infected cells. Thus tachyzoites of Toxoplasma exert significant pathogenic effects by their ability to activate the host cell, causing lysis of the parasitophorous vacuole and subsequent destruction of the entire cell.

Animals↗
PubMed1983

Monoclonal antibodies to Toxoplasma cell membrane surface antigens protect mice from toxoplasmosis.

Groups of mice were given an intraperitoneal injection of one of six monoclonal antibodies to Toxoplasma gondii, a mixture of equal amounts of five monoclonal antibodies to T. gondii, or the murine myeloma protein MOPC 21, and challenged with either a highly virulent or moderately virulent parasite strain. Two monoclonal antibodies (FMC 19 and FMC 22) conferred total protection against the moderately virulent challenge, with all mice surviving, whereas 90% of control mice died. FMC 19 and FMC 22 also conferred significant protection against the highly virulent challenge as indicated by a prolonged mean time to death (MTD) of immunized compared with control groups of mice. One monoclonal antibody (FMC 23) and the mixture of five antibodies gave significant protection against the moderately virulent challenge only. Passive immunization with dilutions of FMC 22 antibody indicated that the lowest serum titer needed to confer significant protection to mice against a moderately virulent Toxoplasma challenge was 1/640. Mice challenged with highly virulent tachyzoites that had been preincubated with FMC 22 had a significantly longer MTD than mice challenged with highly virulent tachyzoites that had been preincubated with MOPC 21 or phosphate buffered saline, pH 7.2 (PBS). Immunoprecipitation and autoradiography of radiolabeled tachyzoites confirmed that FMC 19 was directed against a 35,000 molecular weight (mol. wt.) antigen and FMC 22 was directed against a 14,000 mol. wt. fraction. The potential for use of single antigens as protective immunogens in preventing toxoplasmosis is raised.

Animals↗
PubMedDate not supplied

Effect of extracellular ions on motility and cell entry in Toxoplasma gondii.

Toxoplasma gondii tachyzoites were quiescent in mouse peritoneal fluid or in K2SO4 buffer at pH 8.2. They became consistently motile when K+ was replaced by other monovalent or divalent cations at a constant pH (pH = 8.2). They also became motile when Cl- was substituted for SO4(2-). Nitrate or SCN-, can also be substituted for Cl- to a certain extent. Tachyzoites showed independent movement for more than 15 min in KCl, and for about 5 min in the other buffers at pH 8.2 after which they were exhausted and stopped. These tachyzoites could not then be further stimulated to motility by renewal of the suspension buffer. Infection of monolayer cells was demonstrated only with parasites which were motile during inoculation. The highest infectivity was thus obtained either with freshly collected tachyzoites or with those preincubated in K2SO4 buffer for 30 min at 37 degrees C at alkaline pH and thus not yet exhausted for motility. Approximately 34 to 38% of these latter organisms were seen to enter cells when they were inoculated into cultures immediately after being resuspended in MEM for 30 min at 37 degrees C. Conversely, those whose motility had been exhausted by the preincubation in buffers other than K2SO4, pH 8.2 could not enter monolayer cells. Additionally, parasites were unable to enter cells when inoculated into cultures in K2SO4 buffer at alkaline pH; instead they remained quiescent on the surface of the monolayer cells, suggesting that Toxoplasma enters the host cells by active invasion.

Animals↗
PubMedDate not supplied

Pyrimidine salvage pathways in Toxoplasma gondii.

Pyrimidine salvage enzyme activities in cell-free extracts of Toxoplasma gondii were assayed in order to determine which of these enzyme activities are present in these parasites. Enzyme activities that were detected included phosphoribosyltransferase activity towards uracil (but not cytosine or thymine), nucleoside phosphorylase activity towards uridine, deoxyuridine and thymidine (but not cytidine or deoxycytidine), deaminase activity towards cytidine and deoxycytidine (but not cytosine, cytidine 5'-monophosphate or deoxycytidine 5'-monophosphate), and nucleoside 5'-monophosphate phosphohydrolase activity towards all nucleotides tested. No nucleoside kinase or phosphotransferase activity was detected, indicating that T. gondii lack the ability to directly phosphorylate nucleosides. Toxoplasma gondii appear to have a single non-specific uridine phosphorylase enzyme which can catalyze the reversible phosphorolysis of uridine, deoxyuridine and thymidine, and a single cytidine deaminase activity which can deaminate both cytidine and deoxycytidine. These results indicate that pyrimidine salvage in T. gondii probably occurs via the following reactions: cytidine and deoxycytidine are deaminated by cytidine deaminase to uridine and deoxyuridine, respectively; uridine and deoxyuridine are cleaved to uracil by uridine phosphorylase; and uracil is metabolized to uridine 5'-monophosphate by uracil phosphoribosyltransferase. Thus, uridine 5'-monophosphate is the end-product of both de novo pyrimidine biosynthesis and pyrimidine salvage in T. gondii.

Animals↗
PubMed2001

Removal of Toxoplasma gondii oocysts from sea water by eastern oysters (Crassostrea virginica).

Toxoplasma gondii infections have been reported in a number of marine mammals. Presently it is not known how these animals acquire T. gondii from their aquatic environment. The eastern oyster, Crassostrea virginica, has been shown to remove Cryptosporidiwn oocysts from seawater and a similar phenomenon may be occurring with T. gondii oocysts and marine invertebrates. The present study was done to determine if eastern oysters could remove and retain T. gondii oocysts from seawater. Oocysts of the VEG strain of T. gondii (1 x 10(6) oocysts) were placed in seawater (32 ppt NaCl) containing live eastern oysters. The infected seawater was removed one day postinoculation (PI) and replaced with fresh seawater. Selected oysters were removed at 1, 3 and 6 days PI. Hemolymph, gill washes, and oyster tissue were collected separately at each observation time. The oyster tissue was homogenized and all 3 samples fed separately to mice. Toxoplasma gondii positive mice were observed at each time period. The results indicate that T. gondii oocysts can be removed from seawater by eastern oysters and retain their infectivity. Contaminated raw oysters may serve as a source of T. gondii infection for marine mammals and humans.

Animals↗
PubMed1995

Peritoneal macrophages from C57BL/6 mice orally immunized with Toxoplasma gondii antigens in association with cholera toxin possess an enhanced ability to inhibit parasite multiplication.

Gamma-interferon (IFN-gamma) has been reported to be a major mediator of resistance to toxoplasma infection, mainly through macrophage activation. Cholera toxin used as oral adjuvant induces enhanced protection. Following oral immunization of C57BL/6 mice with a Toxoplasma gondii sonicate (TSo), in association with either cholera toxin (CT) or its B subunit (CTB), the ability of primed sensitized peritoneal macrophages (PM phi) to prevent T. gondii intracellular proliferation in vitro was examined both with and without rIFN-gamma activation. Under these conditions, the inhibition of T. gondii multiplication was greatly enhanced in PM phi from mice immunized with a TSo and CT as an oral adjuvant. In contrast, PM phi from mice immunized with a TSo in association with CTB showed a decrease in their microbiostatic activity towards T. gondii. This negative effect on IFN-gamma-treated PM phi was cancelled out by the addition of a small amount of CT in association with TSo and CTB in the immunization regimen. These data suggest that CT could act as an oral adjuvant in vaccination against toxoplasmosis by increasing the microbiostatic activity of M phi activated with IFN-gamma. Further studies, using intestinal effector cells such as enterocytes, are needed to confirm the value of CT for enhancing this major mechanism of protection against T. gondii infection.

Adjuvants, Immunologic↗
PubMed1993

Development of an in vitro model of Toxoplasma gondii cyst formation.

Toxoplasma gondii tissue cyst reactivation is a major pathogenic mechanism in ocular toxoplasmosis, disease associated with AIDS and organ transplantation. The mechanisms associated with cyst formation and reactivation have not been elucidated. The complexity of studying these issues in animal models has led to the development of in vitro tissue culture strategies for cyst formation. In the present study we have adopted the human embryonic lung fibroblast (HEL) as the host cell and have compared the cyst forming abilities of eight clinical isolates. We describe by transmission electron microscopy and quantitative light microscopy the development of cysts in vitro. The numbers of in vitro cysts increased with time for all isolates. Cyst cultures were stabilised by manipulation of the free parasite load, an observation not previously recorded. Thus, in this paper we describe a viable model for the analysis of the mechanisms of Toxoplasma cyst development.

Animals↗
PubMed1999

MPS1: a small, evolutionarily conserved zinc finger protein from the protozoan Toxoplasma gondii.

Within the expressed sequence tag (EST) dataset of Toxoplasma gondii we have identified several ESTs encoding a protein similar to the small zinc finger protein MPS1. In human it is suggested that MPS1 plays a role as a transcriptional mediator in response to various growth factors and it is used as a tumour marker in sera from cancer patients. However, in rat a cDNA sequence homologous to MPS1 encodes ribosomal protein S27. To further characterise MPS1 in T. gondii we transformed tachyzoites with a c-Myc-tagged version of the Toxoplasma MPS1 cDNA, flanked by SAG1 sequences. Western blot analysis showed that the Myc-MPS1 was only poorly expressed in the stable transformants. In contrast, Northern blot analysis demonstrated that the Myc-MPS1 mRNA was abundantly transcribed and that the endogenous level of MPS1 mRNA was not affected.

Amino Acid Sequence↗
PubMed2000

Expression of a cDNA encoding a Toxoplasma gondii protein belonging to the heat-shock 90 family and analysis of its antigenicity.

A cDNA clone (Tgzy85d11.r1) obtained from the Toxoplasma Expressed Sequence Tag project was chosen due to its homology with proteins of the heat shock 90 family. The cDNA encodes 137 amino acids of the C-terminal portion of the Toxoplasma Hsp90 protein (TgHsp90). Serum samples obtained from orally infected BALB/c and C57BL/6 mice showed reactivity against a recombinant TgHsp90 (rTgHsp90) after 8 weeks postinfection. Isotype analysis showed an anti-rTgHsp90 IgG2a/IgG3 response in infected BALB/c and anti-rTgHsp90 IgG1/IgG2a/IgG2b response in infected C57BL/6 mice. Serum samples from individuals chronically and putative acutely infected with T. gondii showed a similar anti-rTgHsp90 IgG response. Our work identifies TgHsp90 as a novel parasite antigen that seems to elicit a higher relation of anti-TgHsp90/anti-T. gondii IgGs during chronic infection in comparison with the acute stage.

Amino Acid Sequence↗
PubMed1999

Signaling during the invasion of host cells by Toxoplasma gondii.

Invasion of host cells is essential for the pathogenicity of Toxoplasma gondii. This review examines the signal transduction pathways that lead to the internalization of T. gondii. We demonstrate that extra- and intracellular Ca(2+) mobilization, Ca(2+)-calmodulin complex and phospholipase A(2) activities are required for T. gondii entry. T. gondii also causes the activation of mitogen-activated protein kinase in infected cells and modifies its ionic environment during its intracellular state. Thus, many of the signaling systems found in other eukaryotes are operative in Toxoplasma invasion.

Animals↗