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PubMed2001

Effect of testing for IgG avidity in the diagnosis of Toxoplasma gondii infection in pregnant women: experience in a US reference laboratory.

The usefulness of testing for IgG avidity in association with Toxoplasma gondii was evaluated in a US reference laboratory. European investigators have reported that high-avidity IgG toxoplasma antibodies exclude acute infection in the preceding 3 months. In this US study, 125 serum samples taken from 125 pregnant women in the first trimester were chosen retrospectively, because either the IgM or differential agglutination (AC/HS) test in the Toxoplasma serologic profile suggested or was equivocal for a recently acquired infection. Of 93 (74.4%) serum samples with either positive or equivocal results in the IgM ELISA, 52 (55.9%) had high-avidity antibodies, which suggests that the infection probably was acquired before gestation. Of 87 (69.6%) serum samples with an acute or equivocal result in the AC/HS test, 35 (40.2%) had high-avidity antibodies. Forty women were given spiramycin, to prevent congenital transmission, and 7 (17.5%) had high-avidity antibodies. These findings highlight the value of testing a single serum sample obtained in the first trimester of pregnancy for IgG avidity.

Animals↗

PubMed2002

Laboratory diagnosis of Toxoplasma gondii infection and toxoplasmosis.

For the past 40 years, the Toxoplasma Serology Laboratory at the Palo Alto Medical Foundation Research Institute (TSL-PAMFRI) has been dedicated to the laboratory diagnosis of Toxoplasma gondii infection and toxoplasmosis. TSL-PAMFRI is the "brain child" of Jack S. Remington. Jack's ceaseless devotion to objectivity and uncompromising excellence has made TSL-PAMFRI the Toxoplasma reference laboratory for the Centers for Disease Control and Prevention, the US Food and Drug Administration, and health care providers and clinical laboratories in the United States and other countries. Jack's leadership and vision created, defined, and significantly contributed to the development of laboratory methods for the diagnosis of the infection and diseases caused by T. gondii. A summary of the laboratory tests currently available at TSL-PAMFRI for the diagnosis of infection and disease caused by the parasite is presented here.

Animals↗

PubMed2002

Prevalence and predictors of Toxoplasma seropositivity in women with and at risk for human immunodeficiency virus infection.

We assessed the prevalence and predictors of latent Toxoplasma infection in a large group of human immunodeficiency virus (HIV)-infected and HIV-uninfected at-risk US women. The prevalence of latent Toxoplasma infection was 15% (380 of 2525 persons) and did not differ by HIV infection status. HIV-infected women aged > or =50 years and those born outside of the United States were more likely to have latent Toxoplasma infection, with prevalences of 32% and 41%, respectively.

AIDS-Related Opportunistic Infections↗

PubMed1980

Identification of the activator system for antibody to Toxoplasma as the classical complement pathway.

In view of the many recent advances in our understanding of the composition and function of the complement system, it was decided to apply this newer knowledge to an investigation of the heat-labile activator required for the action of antibody to Toxoplasma gondii in the neutralization and dye tests. With use of antibody-coated toxoplasma trophozoites in a diluent of 0.2% gelatin in 0.85% NaCl and alkaline methylene blue as indicator, various component-deficient sera were added to activate the antibody on the protozoan membranes. It was determined that the classical complement system is required for antibody activity and that the properdin system plays no role in the reaction. Human sera genetically deficient in C5, C6, C7, and C8 were shown to be inactive as activators of antibody to Toxoplasma. The addition of specific missing components immediately restored full activity to the deficient sera.

Animals↗

PubMed1999

Differential CD86/B7-2 expression and cytokine secretion induced by Toxoplasma gondii in macrophages from resistant or susceptible BALB H-2 congenic mice.

The influence of the intracellular parasite Toxoplasma gondii on macrophage expression of co-stimulatory molecules was studied. Unlike surface expression of CD80/B7-1, that of CD86/B7-2 is increased in mouse peritoneal macrophages 24 h following exposure to live toxoplasma in vitro. Most CD86 molecules are found on infected cells bearing a maximum parasite load. Consistent with the elevated membrane expression, the quantity of CD86 gene transcript is increased in macrophages infected by T. gondii in vitro or in vivo. CD86 up-regulation contributes to the augmented capacity of parasitized macrophages to present antigen to tuberculin-specific CD4+ T cells as demonstrated by blocking CD86 ligand interaction. T. gondii triggers up-regulation of CD86 in macrophages from BALB/c mice which are resistant to the development of toxoplasmic encephalitis. Infection of macrophages from the susceptible strain BALB.B, however, results in a decreased surface expression of CD86, although the parasite load and intracellular proliferation proved comparable in both macrophages. This differential host cell reaction correlates with disparate profiles in T. gondii-induced cytokine secretion. Upon challenge with toxoplasma, IL-1alpha and tumor necrosis factor (TNF)-alpha are released to a significantly higher extent by BALB/c than by BALB.B macrophages, whereas the latter secrete more IL-12 and IL-10. In BALB.B macrophages, T. gondii-induced IL-10 down-regulates surface expression of CD86, thus indicating an interference of parasite-dependent cytokine release and modulation of CD86. The biased secretory response in macrophages from the two congenic strains implies an MHC-dependent and dichotomous monokine induction by T. gondii. Up-regulation of CD86 seems to occur along the IL-1/TNF-inducing pathway and experimental evidence indicates that this enhances T cell activation by parasitized macrophages.

Animals↗

PubMed2004

Preliminary evaluation of one conventional nested and two real-time PCR assays for the detection of Toxoplasma gondii in immunocompromised patients.

Toxoplasma reactivation is a serious complication in patients receiving allogenic stem cell transplantation. Real-time PCR assays allow a rapid diagnosis of toxoplasma infection; however, no comparative data are available on the performance of real-time PCR protocols under routine conditions. Therefore, the aim of this study was to amplify Toxoplasma gondii DNA from routine samples of allogenic stem cell recipients using two real-time PCR assays on a LightCycler, and using conventional nested PCR. Conventional nested PCR revealed T. gondii DNA in 16 samples. Only 12 of the 16 samples yielded a positive result in both real-time PCRs. The accuracy of the conventional PCR results was demonstrated by direct sequencing. Amplification and detection of the amplicon was completed in only 1 h using the real-time PCR assays. Thus, real-time PCR substantially accelerates the detection of T. gondii DNA in the majority of positive specimens; however, conventional nested PCR is required for detection of T. gondii DNA in some samples.

Animals↗

PubMed2004

Phosphatidylcholine-specific phospholipase C but not gamma interferon regulate gene expression and secretion of CC Chemokine Ligand-2 (CCL-2) by human astrocytes during infection by Toxoplasma gondii.

We have used human astrocytoma-derived cells to investigate the cellular responses of central nervous system cells to Toxoplasma gondii infection. At 24 h post inoculation, the secretion of CCL-2 (or Monocyte Chemotactic Protein-1) was augmented six-fold over the control. This secretion was down-regulated by D609, a specific inhibitor of phosphatidylcholine-dependent phospholipase C (PC-PLC), but not modulated by gamma interferon (IFN-gamma). Ribonuclease protection assay analyses showed significant down-regulation of CCL-2 mRNA production during infection by Toxoplasma gondii when cells were treated by D609. The mRNA levels of the seven other chemokines studied were not modified by D609. CCL-2 seems to contribute to the cell recruitment during human cerebral reactivation of Toxoplasma gondii. Cellular production of this CC chemokine during toxoplasmosis may be regulated by a PC-PLC-dependent pathway.

Animals↗

PubMed1979

Some physicochemical characteristics of an immune lymphocyte product which inhibits the multiplication of toxoplasma within mouse macrophages.

In response to antigenic stimulation, the splenic lymphocytes from Toxoplasma-infected mice produce a factor which is called by the authors the Toxoplasma growth inhibitory factor (Toxo-GIF) and which inhibits the multiplication of Toxoplasma within nonimmune macrophages in vitro. In this study, partial characterization of murine Toxo-GIF was examined using Sephadex G-100 gel-filtration, isoelectric focusing, zonal electrophoresis and heat and enzymatic treatment. Peak activity of Toxo-GIF was found in a Sephadex G-100 fraction with a similar molecular size to that of the ovalbumin. The molecular weight of Toxo-GIF was calculated to be between 38,000 and 55,000. Toxo-GIF was stable to heating at 56 C for 30 min but lost its activity at 80 for 30 min or by exposure to pH values of 5 and 2. Exposure of Toxo-GIF to water-insoluble chymotrypsin or neuraminidase markedly decreased its ability to induce enhanced microbicidal activity of cultured macrophages, suggesting that Toxo-GIF was a glycoprotein. Furthermore, Toxo-GIF migrated in a region cathodal to mouse albumin on agar zone electrophoresis. Isoelectric focusing of active Sephadex fractions showed a well-defined peak of Toxo-GIF activity with an isoelectric point of pH 4.9 to 5.9.

Ammonium Sulfate↗

PubMed1987

Immune response to Toxoplasma gondii--alteration of antigen specificity of peripheral blood leukocyte proliferative responses in acute toxoplasmosis.

Ultrasonicated Toxoplasma gondii (RH strain) tachyzoite extract was chromatographed on Sephadex G-200, and one main peak (93,000 M.W.) and three small peaks (greater than 160,000 M.W., 110,000 M.W., and 20,000 M.W.) were eluted. Toxoplasma-specific proliferative T cell responses of peripheral blood leukocytes (PBL) from a patient with acute toxoplasmosis caused by accidental injection of tachyzoites of the protozoa were sequentially examined by using these fractioned antigens. As early as one week after the accidental injection of the protozoa, significant proliferative responses of PBL could be detected. The reaction of proliferative T cells was observed occurring mainly with Fr. II antigen. Then T cells began to respond to Fr. I and III in addition to Fr. II 3 weeks after the injection. Thus, expansion of antigen specificity in Toxoplasma-specific T cell responses was observed at the initial stage of acquired acute toxoplasmosis.

Acute Disease↗

PubMed1991

Role of L3T4+ and Lyt-2+ T cell subsets in protective immune responses of mice against infection with a low or high virulent strain of Toxoplasma gondii.

In order to elucidate the role of T cell subsets in protective immunity against infection with high virulent and low virulent strains of Toxoplasma gondii, monoclonal antibodies specific for T cell subsets were injected into mice before immunization or challenge infection. Treatment of mice with monoclonal antibody to either L3T4+ or Lyt-2+ T cells before they were immunized with Toxoplasma cell homogenate prepared from high virulent RH strain tachyzoites markedly reduced survival after mice were challenged with low virulent bradyzoites of the Beverley strain. Thus, induction of protective immunity against bradyzoites of the Beverley strain requires the presence of both L3T4+ and Lyt-2+ T cells. In contrast, mice injected with living bradyzoites of the low virulent Beverley strain after immunization with Toxoplasma cell homogenate acquired protective immunity against high virulent tachyzoites of the RH strain. Lyt-2+ T cells alone appear to be final effector cells for protection against the challenge with high virulent RH strain tachyzoites, since treatment of the bradyzoite-immune mice with anti-Lyt-2 antibody, but not anti-L3T4 antibody, before challenge significantly increased mortality.

Animals↗

PubMed1984

Chemiluminescence response of peritoneal exudate cells from mice infected with virulent and avirulent strains of Toxoplasma gondii.

The zymosan-triggered chemiluminescence response of peritoneal exudate cells from mice infected with relatively virulent or avirulent Toxoplasma gondii strains was examined at various intervals after infection. Toxoplasma infections increased the background chemiluminescence compared with controls, but higher values were attained earlier in virulent than avirulent infection. A phase of transient unresponsiveness to zymosan was observed with both types of toxoplasma strains. Chemiluminescence continued to decline even after the addition of zymosan on day 3 of infection with the virulent strain but only on day 10 with the avirulent strain. Generation of chemiluminescence was enhanced in mice which had been infected with either strain for 1 month.

Animals↗

PubMed2004

Toxoplasma gondii spreading in an urban area evaluated by seroprevalence in free-living cats and dogs.

Infection by the protozoan parasite, Toxoplasma gondii is widely prevalent in humans and animals throughout the world. Transmission takes place mainly by ingestion of raw or undercooked meat that contains parasite cysts or by ingestion of oocysts excreted in cat faeces, which can contaminate water and raw vegetables. The incidence of toxoplasmosis in urban areas can thus be also related to environmental contamination with oocysts. A direct measure of this environmental contamination by oocyst counting is unfeasible for technical reasons. An interesting alternative for measuring T. gondii urban spreading is the seroprevalence in free-living urban animals, used as sentinels, once they are exposed to similar risks of Toxoplasma infection-like humans. With this aim, we tested serum samples from stray cats and dogs for antibodies to T. gondii by indirect haemagglutination assay (IHA) and enzyme-linked immunosorbent assay (ELISA). Antibodies to T. gondii were found in 40% (40 of 100) of the cats, less than the 50.5% (101 of 200) found in dogs by ELISA (P < 0.05). Haemagglutination showed low resolution and concordance, precluding their use for diagnosis of T. gondii infection compared with ELISA. The prevalence of T. gondii was lower among stray cats probably due to their selective alimentary habits and lower water and food intake. Toxoplasma gondii seroprevalence in stray dogs and cats could be an indirect indicator of the parasite spreading in urban areas.

Animals↗

PubMed1989

Provision of a panel of anti-toxoplasma-negative blood donors.

Toxoplasma gondii has been reported to cause complications only in immunosuppressed patients receiving leucocyte transfusion, when severe acute toxoplasmosis has been reported with associated mortality. At the North London Blood Transfusion Centre (NLBTC) we have screened 392 plasmapheresis donors (using toxoreagent latex agglutination test manufactured by Eiken) to provide a panel of blood donors negative for antibody to toxoplasma for seronegative recipients. A toxoplasma-negative panel of donors would only be required for those rare instances when granulocyte concentrates are indicated for transfusion of seronegative recipients. The toxoreagent test classified the 392 blood donors as 36% positive, 23% weakly reactive and 41% negative; these negative sera were retested with toxoreagent and 17% of them reacted weakly but none were positive. The toxoreagent 'weakly-reactive' sera (all of which were Sabin-Feldman dye test negative) can probably best be accounted for by the exacting screening conditions under which we operated to ensure seronegativity in our special donor panel. 40% of the antibody-positive donors were female and 34% male. Seropositivity increased with age.

Adult↗

PubMed2004

Trans-genera reconstitution and complementation of an adhesion complex in Toxoplasma gondii.

Eimeria tenella and Toxoplasma gondii are obligate intracellular parasites belonging to the phylum Apicomplexa. In T. gondii, the microneme protein TgMIC2 contains two well-defined adhesive motifs and is thought to be a key participant in the attachment and invasion of host cells. However, several attempts by different laboratories to generate a knockout (KO) of TgMIC2 have failed, implying that TgMIC2 is an essential gene. As Eimeria and Toxoplasma utilize the same mechanisms of invasion and have highly conserved adhesive proteins, we hypothesized that the orthologous molecule in Eimeria, EtMIC1, could functionally substitute in Toxoplasma to allow a knockout of TgMIC2. TgMIC2 is partnered with a protein called TgM2AP, which corresponds to EtMIC2 in Eimeria. Because the activity of TgMIC2 is most likely tightly linked to its association with TgM2AP, it was thought that the activity of EtMIC1 might similarly require its partner EtMIC2. EtMIC1 and EtMIC2 were introduced into T. gondii, and the presence of EtMIC1 allowed the first knockout clone of TgMIC2 to be obtained. The TgMIC2 KO resulted in significantly decreased numbers of invaded parasites compared to the parental clone. In the absence of TgMIC2, TgM2AP was incorrectly processed and mistargeted to the parasitophorous vacuole instead of the micronemes. These findings indicate that the EtMIC1 can compensate for the essential requirement of TgMIC2, but it cannot fully functionally substitute for TgMIC2 in the invasion process or for supporting the correct maturation and targeting of TgM2AP.

Amino Acid Sequence↗

PubMed2005

Dissemination of Toxoplasma gondii to immunoprivileged organs and role of Toll/interleukin-1 receptor signalling for host resistance assessed by in vivo bioluminescence imaging.

Toxoplasma gondii infection can lead to life-threatening systemic disease in the immunocompromised individual and in the developing fetus. Despite intensive investigation in animal models of toxoplasmosis, the processes leading to systemic dissemination remain poorly characterized. In the present study, in vivo bioluminescence imaging (BLI) was applied to the Toxoplasma mouse model to study the dynamics of infection in real time. Photon emission analyses revealed rapid dissemination of parasites in the organism and dissemination to immunoprivileged organs (brain, eyes and testes). Spatio-temporal analysis by BLI in individual mice showed that the virulent RH strain (type I) and the non-virulent ME49/PTG strain (type II) disseminate widely, but the virulent RH strain (type I) exhibits a more dramatic expansion of parasite biomass. Assessment by BLI of the Toll/interleukin-1 receptor (TIR) signalling pathway in host resistance to T. gondii revealed that signal transduction to the adaptor protein MyD88 is probably mediated by Toll-like receptor(s) rather than by IL-1R or IL-18R signalling. However, TLR1(-/-), TLR2(-/-), TLR4(-/-), TLR6(-/-) and TLR9(-/-) animals did not exhibit increased susceptibility to infection. These results suggest that intricate mechanisms regulate TIR-mediated responses during Toxoplasma infection.

Adaptor Proteins, Signal Transducing↗

PubMed2005

Host cell lipids control cholesteryl ester synthesis and storage in intracellular Toxoplasma.

The intracellular protozoan Toxoplasma gondii lacks a de novo mechanism for cholesterol synthesis and therefore must scavenge this essential lipid from the host environment. In this study, we demonstrated that T. gondii diverts cholesterol from low-density lipoproteins for cholesteryl ester synthesis and storage in lipid bodies. We identified and characterized two isoforms of acyl-CoA:cholesterol acyltransferase (ACAT)-related enzymes, designated TgACAT1alpha and TgACAT1beta in T. gondii. Both proteins are coexpressed in the parasite, localized to the endoplasmic reticulum and participate in cholesteryl ester synthesis. In contrast to mammalian ACAT, TgACAT1alpha and TgACAT1beta preferentially incorporate palmitate into cholesteryl esters and present a broad sterol substrate affinity. Mammalian ACAT-deficient cells transfected with either TgACAT1alpha or TgACAT1beta are restored in their capability of cholesterol esterification. TgACAT1alpha produces steryl esters and forms lipid bodies after transformation in a Saccharomyces cerevisiae mutant strain lacking neutral lipids. In addition to their role as ACAT substrates, host fatty acids and low-density lipoproteins directly serve as Toxoplasma ACAT activators by stimulating cholesteryl ester synthesis and lipid droplet biogenesis. Free fatty acids significantly increase TgACAT1alpha mRNA levels. Selected cholesterol esterification inhibitors impair parasite growth by rapid disruption of plasma membrane. Altogether, these studies indicate that host lipids govern neutral lipid synthesis in Toxoplasma and that interference with mechanisms of host lipid storage is detrimental to parasite survival in mammalian cells.

Amino Acid Sequence↗

PubMed1983

Comparative effects of cotrimoxazole (trimethoprim-sulphamethoxazole), pyrimethamine-sulphadiazine and spiramycin during avirulent infection with Toxoplasma gondii (Beverley strain) in mice.

The antitoxoplasm effects of cotrimoxazole (Ctx), spiramycin (Spir) and pyrimethamine-sulphadiazine (Pmm-Sdz) were compared during both proliferative and chronic phases of infection of mice with the Beverley (Bev) strain of Toxoplasma gondii of low virulence. The therapeutic efficacy of the drugs was determined according to the following criteria: (i) specific antibody response; (ii) acquired resistance to lethal challenge with the virulent RH strain of Toxoplasma; and (iii) persistence of parasites in tissues (brain, liver, spleen) of treated mice. The results indicated that Ctx, like Pmm-Sdz, had a greater effect than Spir upon toxoplasma organisms during the proliferative phase of infection. In contrast, none of the three drugs tested was active against tissue cysts in chronically infected mice.

Animals↗

PubMedDate not supplied

Overcoating of Toxoplasma parasitophorous vacuoles with host cell vimentin type intermediate filaments.

The interaction between the Toxoplasma parasitophorous vacuole and vimentin-type intermediate filaments in Vero cells was investigated via immunofluorescence microscopy. A significant rearrangement of host cell vimentin around the Toxoplasma parasitophorous vacuoles occurs throughout the course of infection. Host cell vimentin associates with the parasitophorous vacuoles within an hour after invasion. This vimentin overcoating of the vacuole is initiated at the host cell nuclear surface. During parasite multiplication, vimentin retains a closely defined association with the cytosolic surface of the parasitophorous vacuole. In addition, the vimentin intermediate filaments originating from the host cell nuclear surface are progressively rearranged around the enlarging parasitophorous compartment. During infections, the order of vimentin cytoskeleton is normal throughout the cell and appears redefined only at the vicinity of the parasitophorous vacuole. Depolymerization of the intermediate filaments was achieved with the phosphatase inhibitors okadaic acid and calyculin A. Disruption of the intermediate filament networks resulted in displacement of the parasitophorous vacuoles from the host cell nuclear surface. The data indicate that host cell vimentin binds to the Toxoplasma parasitophorous vacuoles and that the host intermediate filament network serves to dock the parasite compartment to the host cell nuclear surface.

Animals↗