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Academic literature on the topic 'Metabolism in Toxoplasma Gondii'

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Published: 6 September 2023

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Journal articles on the topic "Metabolism in Toxoplasma Gondii"

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Krug, E. C., J. J. Marr, and R. L. Berens. "Purine Metabolism in Toxoplasma gondii." Journal of Biological Chemistry 264, no. 18 (June 1989): 10601–7. http://dx.doi.org/10.1016/s0021-9258(18)81663-5.

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Chang, Hernán R., and Jean-Claude Pechère. "Macrophage oxidative metabolism and intracellular Toxoplasma gondii." Microbial Pathogenesis 7, no. 1 (July 1989): 37–44. http://dx.doi.org/10.1016/0882-4010(89)90109-5.

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Chen, Min, Lijuan Zhou, Shengmin Li, Hiaxia Wei, Jiating Chen, Pei Yang, and Hongjuan Peng. "Toxoplasma gondii DNA methyltransferases regulate parasitic energy metabolism." Acta Tropica 229 (May 2022): 106329. http://dx.doi.org/10.1016/j.actatropica.2022.106329.

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Prandovszky, Emese, Elizabeth Gaskell, Heather Martin, J. P. Dubey, Joanne P. Webster, and Glenn A. McConkey. "The Neurotropic Parasite Toxoplasma Gondii Increases Dopamine Metabolism." PLoS ONE 6, no. 9 (September 21, 2011): e23866. http://dx.doi.org/10.1371/journal.pone.0023866.

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Sonda, Sabrina, Giusy Sala, Riccardo Ghidoni, Andrew Hemphill, and Jean Pieters. "Inhibitory Effect of Aureobasidin A on Toxoplasma gondii." Antimicrobial Agents and Chemotherapy 49, no. 5 (May 2005): 1794–801. http://dx.doi.org/10.1128/aac.49.5.1794-1801.2005.

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ABSTRACT The apicomplexan parasite Toxoplasma gondii is a leading opportunistic pathogen associated with AIDS and congenital birth defects. Due to the need for identifying new parasite-specific treatments, the possibility of targeting sphingolipid biosynthesis in the parasite was investigated. Aureobasidin A, an inhibitor of the enzyme synthesizing the sphingolipid inositol phosphorylceramide, which is present in fungi, plants, and some protozoa but absent in mammalian cells, was found to block in vitro T. gondii replication without affecting host cell metabolism. Aureobasidin A treatment did not induce tachyzoite to bradyzoite stage conversion in T. gondii but resulted in a loss of intracellular structures and vacuolization within the parasite. In addition, aureobasidin A inhibited sphingolipid synthesis in T. gondii. Sphingolipid biosynthetic pathways may therefore be considered targets for the development of anti-T. gondii agents.
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Mageed, Sarmad N., Fraser Cunningham, Alvin Wei Hung, Hernani Leonardo Silvestre, Shijun Wen, Tom L. Blundell, Chris Abell, and Glenn A. McConkey. "Pantothenic Acid Biosynthesis in the Parasite Toxoplasma gondii: a Target for Chemotherapy." Antimicrobial Agents and Chemotherapy 58, no. 11 (July 21, 2014): 6345–53. http://dx.doi.org/10.1128/aac.02640-14.

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ABSTRACTToxoplasma gondiiis a major food pathogen and neglected parasitic infection that causes eye disease, birth defects, and fetal abortion and plays a role as an opportunistic infection in AIDS. In this study, we investigated pantothenic acid (vitamin B5) biosynthesis inT. gondii. Genes encoding the full repertoire of enzymes for pantothenate synthesis and subsequent metabolism to coenzyme A were identified and are expressed inT. gondii. A panel of inhibitors developed to targetMycobacterium tuberculosispantothenate synthetase were tested and found to exhibit a range of values for inhibition ofT. gondiigrowth. Two inhibitors exhibited lower effective concentrations than the currently used toxoplasmosis drug pyrimethamine. The inhibition was specific for the pantothenate pathway, as the effect of the pantothenate synthetase inhibitors was abrogated by supplementation with pantothenate. Hence,T. gondiiencodes and expresses the enzymes for pantothenate synthesis, and this pathway is essential for parasite growth. These promising findings increase our understanding of growth and metabolism in this important parasite and highlight pantothenate synthetase as a new drug target.
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el Kouni, Mahmoud. "Adenosine Metabolism in Toxoplasma gondii: Potential Targets for Chemotherapy." Current Pharmaceutical Design 13, no. 6 (February 1, 2007): 581–97. http://dx.doi.org/10.2174/138161207780162836.

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Weilhammer, Dina R., Anthony T. Iavarone, Eric N. Villegas, George A. Brooks, Anthony P. Sinai, and William C. Sha. "Host metabolism regulates growth and differentiation of Toxoplasma gondii." International Journal for Parasitology 42, no. 10 (September 2012): 947–59. http://dx.doi.org/10.1016/j.ijpara.2012.07.011.

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Wu, Liang, Lipei Wu, Chenyu Tang, Jiajian Wang, Xiaoling Jin, Xugan Jiang, and Shengxia Chen. "Induction of FAS II Metabolic Disorders to Cause Delayed Death of Toxoplasma gondii." Journal of Nanoscience and Nanotechnology 18, no. 12 (December 1, 2018): 8155–59. http://dx.doi.org/10.1166/jnn.2018.16396.

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The exact mechanism of delayed death of Toxoplasma gondii is not known. FAS II synthesis in the apicoplast of T. gondii is essential for the survival of Toxoplasma gondii, while β-hydroxyacylacyl carrier protein dehydratase (FabZ) is indispensable for fatty acid synthesis. The present study investigated the relationship between the delayed death of T. gondii by inducing metabolic disorders due to suppression the expression of FabZ. A tetracycline-induced knockout vector inserted with T. gondii fabZ gene was constructed, and transfected into T. gondii TATi strain by electroporation. The stable mutants with tetracycline-induced knockout were selected, expression of FabZ was suppressed by using anhydrotetracycline (ATc), and FAS II deficient tachyzoites were prepared. The Western blot and qPCR results revealed that proliferation of FAS II deficient tachyzoites was not significantly different compared to the normal tachyzoites at 24 h and 48 h; however, after 72 h, the number of T. gondii tachyzoites in the ATc treated group was significantly (p < 0.05) less than that of non-treated group, indicating the delayed death of T. gondii caused by the loss of apicoplast and decrease in the expression of FabZ, which inhibited the FAS II metabolism. The results of this study can be used for prevention of toxoplasmosis by inducing delayed death of T. gondii.
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Li, Meiqi, Xiaoyu Sang, Xiaohan Zhang, Xiang Li, Ying Feng, Na Yang, and Tiantian Jiang. "A Metabolomic and Transcriptomic Study Revealed the Mechanisms of Lumefantrine Inhibition of Toxoplasma gondii." International Journal of Molecular Sciences 24, no. 5 (March 3, 2023): 4902. http://dx.doi.org/10.3390/ijms24054902.

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Toxoplasma gondii is an obligate protozoon that can infect all warm-blooded animals including humans. T. gondii afflicts one-third of the human population and is a detriment to the health of livestock and wildlife. Thus far, traditional drugs such as pyrimethamine and sulfadiazine used to treat T. gondii infection are inadequate as therapeutics due to relapse, long treatment period, and low efficacy in parasite clearance. Novel, efficacious drugs have not been available. Lumefantrine, as an antimalarial, is effective in killing T. gondii but has no known mechanism of action. We combined metabolomics with transcriptomics to investigate how lumefantrine inhibits T. gondii growth. We identified significant alternations in transcripts and metabolites and their associated functional pathways that are attributed to lumefantrine treatment. RH tachyzoites were used to infect Vero cells for three hours and subsequently treated with 900 ng/mL lumefantrine. Twenty-four hours post-drug treatment, we observed significant changes in transcripts associated with five DNA replication and repair pathways. Metabolomic data acquired through liquid chromatography-tandem mass spectrometry (LC-MS) showed that lumefantrine mainly affected sugar and amino acid metabolism, especially galactose and arginine. To investigate whether lumefantrine damages T. gondii DNA, we conducted a terminal transferase assay (TUNEL). TUNEL results showed that lumefantrine significantly induced apoptosis in a dose-dependent manner. Taken together, lumefantrine effectively inhibited T. gondii growth by damaging DNA, interfering with DNA replication and repair, and altering energy and amino acid metabolisms.
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Dissertations / Theses on the topic "Metabolism in Toxoplasma Gondii"

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Roohi, Aysha. "Toxoplasma gondii infection and the host cell metabolism." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648369.

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Ren, Bingjian. "Physiological importance of phospholipid biogenesis in Toxoplasma gondii." Doctoral thesis, Humboldt-Universität zu Berlin, 2019. http://dx.doi.org/10.18452/20721.

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Toxoplasma gondii ist ein obligater intrazellulärer Parasit, der bei Menschen und Nutztieren Toxoplasmose verursacht. Die Phospholipid-Biosynthese ist entscheidend für das erfolgreiche intrazelluläre Überleben und die Replikation des Parasiten, da sie eine wichtige Rolle bei der Biogenese von Membranorganellen, der Signal- transduktion und anderen zellulären Prozessen spielt. Hier untersuchten wir die physiologische Bedeutung von zwei Synthesewegen, die für PtdEtn und PtdIns verantwortlich sind. Wir zeigen das Vorhandensein einer neuartigen PtdIns-Synthase (PIS) in T. gondii, die als TgPIS bezeichnet wird und ein funktionelles Enzym mit einem katalytisch wichtigen CDP-Alkohol- Phosphotransferase-Motiv codiert, das sich ausschließlich im Golgi-Apparat befindet. Der Parasit importiert Myoinosit aus dem Milieu und verwendet es zusammen mit de novo synthetisiertem CDP- Diacylglycerin, um PtdIns zu produzieren. Eine durch Auxin induzierbare bedingte Unterdrückung von TgPIS schaltet den Lysezyklus des Parasiten aufgrund von Defekten in der Replikation, Motilität und Austritt in Säugetierzellen aus. Das Lipidom-Profiling der PIS-Mutante zeigt eine selektive Reduktion bestimmter PtdIns- und PtdThr-Spezies, wohingegen ausgewählte PtdGro-, PtdSer- und BMP-Spezies erhöht sind, was auf eine enge Interregulation und Homöostase von anionischen Phospholipiden zur Aufrechterhaltung der Membranintegrität hindeutet. Zusätzlich identifizierten wir eine Ethanolamin-Cytidyltransferase (TgECT), das geschwindigkeitsbestimmende Enzym des Kennedy-Signalwegs, das im Cytosol lokalisiert ist. Das Enzym ist eindeutig für den Lysezyklus essentiell, da seine genetische Ablation nicht durchführbar ist und der durch Auxin meditierte bedingte Abbau des Proteins das Parasitenwachstum in Plaqueassays stark beeinträchtigt. Die Lipidomanalyse der Mutante identifizierte eine wichtige Rolle bei der Biogenese ausgewählter Arten von PtdEtn, PtdSer und PtdThr. Darüber hinaus haben wir festgestellt, dass TgECT für die Erzeugung von Ethanolamin-Phosphor-Ceramid (EPC) erforderlich ist, einem seltenen Sphingolipid, das nur eine begrenzte Anzahl von Organismen enthalten.
Toxoplasma gondii is an obligate intracellular parasite that causes Toxoplasmosis in human and livestock. Phospholipid biosynthesis is crucial for the successful intracellular survival and replication of the parasites, as the phospholipids have important roles in the biogenesis of membrane organelles, signal transduction and other cellular processes. Here, we dissected the physiological importance of two pathways accounting for the synthesis of PtdEtn and PtdIns. We demonstrated the presence of a novel PtdIns synthase (PIS) in T.gondii termed TgPIS, expressing a functional enzyme with a catalytically vital CDP-alcohol phosphotransferase motif, which resides exclusively in the Golgi body. The parasite imports myo-inositol from milieu, and co-utilizes de novo-synthesized CDP-diacylglycerol to produce PtdIns. An auxin-inducible conditional repression of TgPIS abrogated the lytic cycle of the parasite in mammalian cells due to defects in the replication, motility and egress. Lipidomic profiling of the PIS mutant demonstrated selective reduction of certain PtdIns and PtdThr species, whereas selected PtdGro, PtdSer and BMP species were increased, which suggested a tight inter-regulation and homeostasis of anionic phospholipids to maintain the membrane integrity. In addition, we identified an ethanolamine cytidyltransferase (TgECT), the rate-limiting enzyme of Kennedy pathway, which is localized in the cytosol. The enzyme is clearly essential for the lytic cycle as its genetic ablation was not feasible, and auxin-meditated conditional knockdown severely impaired the parasite growth in plaque assays. Similarly, lipidomic analysis of the mutant identified an important role in the biogenesis of selected species of PtdEtn, PtdSer and PtdThr. Moreover, we discovered that TgECT is required for the generation of ethanolamine-phosphory ceramide (EPC), a rare sphingolipid present only a limited number of organisms.
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Nitzsche, Richard. "Genetic dissection of the central carbon metabolism in the intracellular parasite Toxoplasma gondii." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2017. http://dx.doi.org/10.18452/17744.

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Toxoplasma gondii ist ein weit verbreiteter einzelliger Parasit, der fast alle warmblütigen Organismen infizieren kann. Asexuelle Fortpflanzung des Parasiten in seiner Wirtszelle wird durch aufeinanderfolgende lytische Zyklen erreicht, was die Bereitstellung einer signifikanten Menge an Energie und Biomasse erforderlich macht. Diese Arbeit zeigt, dass Glukose und Glutamin die beiden wichtigsten physiologischen Nährstoffe für die Synthese von Makromolekülen (ATP, Nukleinsäure, Proteine und Lipide) in T. gondii sind. Die Verfügbarkeit einer der beiden Kohlenstoffquellen reicht aus, um das Überleben des Parasiten sicherzustellen. Der Parasit kann durch Erhöhen des Flusses von Glutamin-abstammendem Kohlenstoff durch den TCA-Zyklus und durch gleichzeitige Aktivierung der Gluconeogenese, eine stetige Biogenese von ATP und Biomasse zur Wirtszellinvasion und Replikation gewährleisten, bzw. der genetischen Deletion des Glukosetransporters entgegenwirken. Der Wachstumsdefekt in der Glykolyse-Mutante wird durch eine kompromittierte Synthese von Lipiden verursacht, die durch Glutamin nicht ausgeglichen werden kann. Die Zugabe von exogenem Acetat kann diesen Wachstumsdefekt allerdings kompensieren. In dieser Arbeit konnten darüber hinaus zwei unterschiedliche Phosphoenolpyruvat-Carboxykinase (PEPCK) Enzyme im Parasiten identifiziert werden, von denen eines im Mitochondrium lokalisiert ist (TgPEPCKmt), während das andere Protein nicht in Tachyzoiten (TgPEPCKnet) exprimiert wird. Parasiten mit intakter Glykolyse können die Deletion von TgPEPCKnet, als auch die genetische Deletion von TgPEPCKmt tolerieren, was ihre Redundanz für das Überleben der Tachyzoiten zeigt. TgPEPCKnet kann auch in der Glykolyse-defizienten Mutante deletiert werden, während TgPEPCKmt für das Überleben des Parasiten in dieser Mutante essentiell ist. Dies zeigte sich durch ein konditionelles Knockdown von TgPEPCKmt, das zu einer Inhibierung des Wachstums des Parasiten führte.
Toxoplasma gondii is a widespread protozoan parasite, infecting nearly all warm-blooded organisms. Asexual reproduction of the parasite within its host cells is achieved by consecutive lytic cycles, which necessitates biogenesis of significant energy and biomass. This work shows that glucose and glutamine are the two major physiologically important nutrients used for the synthesis of macromolecules (ATP, nucleic acid, proteins and lipids) in T. gondii, and either of them is sufficient to ensure the parasite survival. The parasite can counteract genetic ablation of its glucose transporter by increasing the flux of glutamine-derived carbon through the TCA cycle and by concurrently activating gluconeogenesis, which guarantee a continued biogenesis of ATP and biomass for host-cell invasion and parasite replication, respectively. Growth defect in the glycolysis-impaired mutant is caused by a compromised synthesis of lipids, which cannot be counterbalanced by glutamine, but can be restored by acetate. Consistently, supplementation of parasite cultures with exogenous acetate can amend the lytic cycle of the glucose transport mutant. Furthermore, this work revealed two discrete phosphoenolpyruvate carboxykinase (PEPCK) enzymes in the parasite, one of which resides in the mitochondrion (TgPEPCKmt), whereas the other protein is not expressed in tachyzoites (TgPEPCKnet). Parasites with an intact glycolysis can tolerate genetic deletions of TgPEPCKmt as well as of TgPEPCKnet, indicating their nonessential roles for the tachyzoite survival. TgPEPCKnet can also be ablated in glycolysis-deficient mutant, whereas TgPEPCKmt is refractory to deletion. In accord, the lytic cycle of a conditional mutant of TgPEPCKmt in the glycolysis-impaired strain was aborted upon induced repression of the mitochondrial isoform, demonstrating its essential role for the glucose-independent survival of tachyzoites.
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Sampels, Vera. "Plasticity of the phosphatidylcholine biogenesis in the obligate intracellular Parasite Toxoplasma gondii." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2012. http://dx.doi.org/10.18452/16491.

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Der obligat intrazelluläre Parasit Toxoplasma gondii ist der Erreger der Toxoplasmose, und dient zugleich als wichtiger Modellorganismus für weitere Human- und Tierpathogene, wie z.B. Plasmodium oder Eimeria. Die Vermehrung von T. gondii erfordert eine effiziente Biosynthese von Phospholipiden für die Herstellung neuer Membranen, was durch die de novo Synthese durch den Parasiten, und/oder den Import von Lipiden aus der umgebenden Wirtszelle gewährleistet werden kann. Während der Parasit zahlreiche Möglichkeiten für Synthese oder Import von PtdEtn und PtdSer verwendet, scheint die Biosynthese des abundantesten Membranlipids PtdCho auschließlich über den CDP-Cholin Weg zu erfolgen. Dieser erstreckt sich in T. gondii über 3 zelluläre Kompartimente, mit einer cytosolischen Cholin-Kinase (TgCK), einer im Zellkern lokalisierenden Cholin-Cytidylyltransferase (TgCCT) und einer Cholin-Phosphotransferase (TgCPT) im ER. Anders als die substrat-spezifische Ethanolamin-Kinase (TgEK), kann TgCK neben Cholin außerdem Ethanolamin phosphorylieren. TgCK zeigt eine geringe Affinität zu Cholin (Km ~0.77 mM), während eine verkürzte TgCK (TgCKS), welcher eine als Signalpeptid vorhergesagte N-terminale Sequenz (20 Aminosäuren) fehlt, eine etwa 3-fach höhere Aktivität aufweist (Km ~0.26 mM). Während jedoch die Wildtyp-TgCK cytosolische Cluster in Toxoplasma bildet, zeigt die verkürzte TgCK eine gleichmäßigere cytosolische Lokalisierung. Wir schlussfolgern daraus, dass der hydrophobe N-Terminus nicht notwendig ist für eine funktionale TgCK, sondern eine strukturelle Funktion bei der Protein-Lokalisierung hat. Eine konitionelle Mutante, in welcher der TgCK Promoter gegen den Tetracyclin-regulierbaren Promoter pTetO7Sag4 ausgetauscht wurde (Deltatgcki), zeigt erstaunlicherweise normales Wachstum und PtdCho Biosynthese. Die TgCK Aktivität und die daraus resultierende PtdCho Synthese sind nur zu ~30% regulierbar. Unsere Ergebnisse deuten auf die Verwendung eines alternativen Startcodons bzw. Promoters hin, welcher zur Expression einer verkürzten (~53-kDa) aber vermutlich aktiven Cholin Kinase führt, wodurch der Verlust der TgCK (~70-kDa) kompensiert wird. Der konditionelle Knockout von TgCCT, dem regulatorischen Enzym des CDP-Cholin Wegs, hatte einen 50%igen Wachstumsdefekt zur Folge. Diese Studie zeigt eine erstaunliche Flexibilität des Parasiten bezüglich seiner Membranzusammensetzung, und bestätigt zugleich die Annahme, dass PtdCho nicht von der Wirtszelle importiert werden kann. Diese Anpassungsfähigkeit stellt einen möglichen Faktor dar, der es T. gondii erlaubt sich in einem breiten Spektrum von Wirten zu vermehren.
Toxoplasma gondii is an obligate intracellular apicomplexan parasite that causes life-threatening disease in neonates and in immunocompromised people. Successful replication of Toxoplasma requires substantial membrane biogenesis, which must be satisfied irrespective of the host-cell milieu. Like in other eukaryotes, the two most abundant phospholipids in the T. gondii membrane are phosphatidylcholine (PtdCho) and phosphatidylethanolamine (PtdEtn). Bioinformatics and precursor labeling analyses confirm their synthesis via the CDP-choline and CDP-ethanolamine pathway, respectively. This work shows that the 3-step CDP-choline pathway, involving the activities of TgCK, TgCCT and TgCPT, localizes to the cytosol, nucleus and ER membrane, respectively. The initial reaction is catalyzed by a dual-specificity choline kinase (TgCK, ~70-kDa), capable of phosphorylating choline as well as ethanolamine. The purified full-length TgCK displayed a low affinity for choline (Km ~0.77 mM). TgCK harbors a unique N-terminal hydrophobic peptide that is required for the formation of enzyme oligomers in the parasite cytosol but not for activity. The displacement of the TgCK promoter in a conditional mutant of T. gondii (deltatgcki) attenuated the enzyme expression by ~80%. Unexpectedly, the ?tgcki mutant was not impaired in intracellular growth, and exhibited a normal PtdCho biogenesis. To recompense for the loss of full-length TgCK, the mutant appears to make use of an alternative promoter and/or start codon, resulting in the expression of a shorter but active TgCK isoform identified by the anti-TgCK antiserum, which correlated with its persistent choline kinase activity. Accordingly, the ?tgcki showed an expected incorporation of choline into PtdCho, and susceptibility to dimethylethanolamine (a choline analog). Interestingly, the conditional mutant displayed a regular growth in off state despite a 25% decline in PtdCho content, which suggests a compositional flexibility in T. gondii membranes and insignificant salvage of host-derived PtdCho. The two-step conditional mutagenesis of TgCCT, which caused a reduced growth rate to about 50%, further substantiated this finding. The enzymatic activity of TgCCT and its role in PtdCho synthesis remain to be proven, however. Taken together, the results demonstrate that the CDP-route is likely essential in T. gondii. The competitive inhibition of choline kinase to block the parasite replication appears a potential therapeutic application.The work also reveals a remarkably adaptable membrane biogenesis in T. gondii, which may underly the evolution of Toxoplasma as a promiscuous pathogen.
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Sundaram, Lalitha Sridevi. "Toxoplasma gondii-mediated host cell transcriptional changes lead to metabolic alterations akin to the Warburg effect." Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/267958.

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Toxoplasma gondii is an obligate intracellular parasite, that is able to infect any nucleated cell. An important global pathogen, T. gondii can cycle between primary and secondary hosts, thus enabling widespread penetrance. Within its intracellular niche – a membrane-bound parasitophorous vacuole – T. gondii is nevertheless able to subvert a variety of host cell processes to allow its continued survival and replication. This includes modulation of host signalling processes as well as the scavenging of nutrient macromolecules. In recent years, microRNAs have emerged as important regulators of cellular processes including inflammation, tumorigenesis and metabolism, as well as development. It has become increasingly clear that this species of non-coding RNA is of great importance in ‘fine tuning’ many cellular responses. I hypothesise in this work that host cell miRNAs may be yet another means by which T. gondii manipulates its host upon infection. Using high-throughput-sequencing, I examine host cell transcriptional responses to infection both at the mRNA and microRNA level, using two strains of T. gondii at a variety of Multiplicities of Infection over a time course of 43 hours. Through these transcriptional analyses I identify a number of dysregulated pathways common in tumorigenesis, and contemplate the hypothesis that T. gondii may be behaving as an ‘intracellular tumour’, subverting host cell metabolic processes to mimic a long-known feature of cancer metabolism – that of aerobic glycolysis (the Warburg effect) – in order to satisfy its own energetic and metabolic needs.
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Blume, Martin. "Characterization of the differential significance of sugar Import in the apicomplexan parasites Toxoplasma gondii and Plasmodium." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2011. http://dx.doi.org/10.18452/16396.

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Toxoplasma gondii und Plasmodium Spezies sind obligat intrazelluläre Parasiten, die Zucker zur Energiehomöostase als auch für die Synthese lebenswichtiger Makromoleküle verwenden. Die hier vorgestellten Daten zeigen, dass der Glukosetransporter von T. gondii, TgGT1, und die homologen Transporter von P. falciparum und P. berghei, PfHT1 und PbHT1, neben Glukose auch Mannose, Fructose und Galactose transportieren. Toxoplasma Tachyzoiten exprimieren neben TgGT1 noch einen weiteren putative Zuckertransporter (TgST2) an der Parasitenoberfläche. Beide Proteine sind nicht essentiell, wie durch ihre individuelle und gleichzeitige Gendeletion belegt wird. Die Deletion von TgGT1 bewirkt einen geringen Wachstumsdefekt. Die Mutante ?tggt1 zeigt keine Glukoseaufnahmeaktivität und folglich eine verminderte glukoseabhängige Motilität. In ?tggt1 Parasiten wird ein verstärkter Glutaminstoffwechsel nachgewiesen, der ausreichend ist dessen Motilität und Replikationsaktivität zu erhalten. Die ?tggt1 Mutante gewährt Einblick in die Anpassungsfähigkeit von T. gondii an unterschiedliche Wirtszellen. Im Gegensatz zu T. gondii benötigen erythrozytäre Plasmodien Glukose und der Transporter PfHT1 wird derzeit als drug-target eingestuft. Hier wird gezeigt, dass das PfHT1-Homolog, PbHT1, essentiell in Blutstadien des Nagerparasiten Plasmodium berghei ist, jedoch auch während des gesamten Lebenszyklus des Parasiten exprimiert wird. Ein PfHT1- und PbHT1-spezifischer Inhibitor (Compound 3361) kann die Entwicklung von P. berghei Leberstadien und Okineten stark hemmen. Um zukünftig PfHT1-Inhibitoren im Hochdurchsatzverfahren zu identifizieren und testen zu können, wurden auf Saccharomyces cerevisiae und P. berghei basierende Expressionssysteme für PfHT1 entwickelt. Abschließend stellt diese Arbeit die Unterschiedlichkeit des zentralen Kohlenstoffwechsels von Toxoplasma und Plasmodium Parasiten durch bisher unbekannter Aspekte heraus.
Toxoplasma gondii and Plasmodium species are obligate intracellular pathogens that utilize host sugars for energy homeostasis and macro molecular synthesis. Here, we report that the T. gondii glucose transporter, TgGT1, and of its homologs of P. falciparum and P. berghei (PfHT1 and PbHT1) transport glucose, mannose, galactose and fructose. Besides TgGT1, Toxoplasma harbours one additional surface localized putative sugar transporter (TgST2). Surprisingly both Proteins are nonessential and only the deletion of TgGT1 inflicts a mild defect in the parasite replication. The ?tggt1 mutant is unable to import glucose and consequently displays an attenuated glucose-dependent motility, which is completely rescued by glutamine. ?tggt1 performs increased glutamine metabolism that is sufficient to sustain motility and replication. The ?tggt1 strain provides a model for further investigating its adaptation to disparate host cells. In contrast to T. gondii, erythrocytic stages of Plasmodium species critically depend on glucose uptake, and the PfHT1 transporter is considered as a drug target against human malaria. Here, we report that PbHT1 (a PfHT1 homolog) is also essential for blood stage development in the rodent malaria parasite P. berghei. PbHT1 is expressed throughout the life cycle. Moreover, a PfHT1- and PbHT1-specific sugar analogue, compound 3361, can inhibit the hepatic development and ookinete formation in P. berghei. These results signify that PbHT1 and exogenous glucose are also required during the ex-erythrocytic stages of P. berghei. To permit a high-throughput screening of selective PfHT1 inhibitors and their subsequent in vivo assessment, we have established a PfHT1-expressing Saccharomyces cerevisiae mutant and generated a PfHT1-dependent ?pbht1 of P. berghei strain. This thesis underscores various previously unknown aspects of sugar metabolism in Toxoplasma and Plasmodium, and unravel their metabolic differences.
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Molan, Aus. "Involvement of Toxoplasma gondii and associated inflammatory markers in the pathogenesis of type 2 diabetes mellitus." Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2020. https://ro.ecu.edu.au/theses/2338.

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Type 2 diabetes mellitus (T2DM) continues to be a major challenge for public health authorities worldwide due to its growing prevalence rates. This chronic disorder is characterised by persistent hyperglycaemia with disturbances in fat, carbohydrate, and protein metabolism resulting from abnormalities in insulin secretion, action, or both. While potential causes such as obesity, physical inactivity, and dietary patterns have been proposed to explain the growing epidemic, there may also be additional unidentified novel risk factors, such as subclinical inflammation caused by infectious agents, that contribute to this rising prevalence. The intracellular protozoan parasite Toxoplasma gondii has been identified as an understudied pathogen of interest. Infecting approximately one third of the world’s population, T. gondii is considered one of the most successful human parasites. However, while more than 25,000 original research articles, several books, and book chapters have been published on this parasite, there are still many aspects of its biology, natural life cycle, and epidemiology of which we know relatively little about, including the prevalence rate in the general Australian human population. An emerging field of research is beginning to investigate the potential of this pathogen to cause low-grade inflammation that may subsequently increase the risk and development of various metabolic conditions, particularly T2DM. The main objectives of the present study were to: 1) determine seroprevalence of T. gondii infection in a representative Australian human population [Study One] ; 2) determine the seroprevalence of T. gondii in subjects with T2DM compared with control subjects [Study One]; 3) identify additional risk factors for T. gondii infection [Study One]; 4) examine cat ownership as an alternative risk factor for T2DM [Study Two]; 5) determine if T. gondii infection participates in the inflammatory process leading to the development of T2DM [Study Three]; and, 6) determine whether an inflammatory 11-biomarker panel could discriminate between controls, subjects with T. gondii infection, and T2DM patients, independently of other diagnostic indicators [Study Three]. Our group undertook the first set of case-control studies of their kind in Australia by utilising sera samples and survey data collected by the Busselton Population Medical Research Institute during the 2005-2007 Busselton Health Survey. The cohort comprised of 150 participants with T2DM and 150 age- and gender- matched control subjects. Commercial in-vitro diagnostic enzyme-linked immunosorbent assays were used to measure the IgG and IgM seroprevalence rates for study one and high-sensitivity multiplex methods were used to simultaneously measure the 11 biomarkers in study three. From the 300 subjects tested, 64% had T. gondii IgG antibodies detected and 7.7% had IgM antibodies detected. IgG seropositivity increased rapidly in all age groups remaining at over 70% in the 65–74, 75–84, and >84 age groups (p <0.05). No significant difference was observed in the T. gondii IgG seroprevalence rates between the T2DM group (62%) and the healthy control group (66%) (OR: 0.84; p = 0.471). Toxoplasma gondii IgM antibodies were detected in 5% of the T2DM patients and in 10% of the control subjects (OR: 0.51; p = 0.135). There were no significant differences between male and female IgG seroprevalence rates for both the T2DM and the control groups (OR: 0.88 and 0.80; p = 0.723 and p = 0.507, respectively). The IgG seropositivity rate increased significantly in T2DM patients aged 45 to 84 years in comparison to those aged 18 to 44 years (p <0.05). This trend was not observed in the healthy non-T2DM subjects. No risk factors were associated with T. gondii seropositivity in both T2DM patients and healthy controls. IL-β, IL-4, IL-6, and IL-12(p40) were not being produced or were below the levels of detection in the majority of subjects. Serum levels of leptin, IL-4, IL-10 and PAI-1 (total) were positively associated with age in the control T. gondii seronegative group. In contrast, decreasing levels of leptin, IL-10, and PAI-1 (total) was observed in the control seropositive and T2DM seronegative groups. Age was also positively associated with IFN-γ levels in control subjects and negatively associated in the T2DM group. Increased weight, BMI, waist circumference, glucose, insulin, triglycerides, white cell count, leptin, and PAI-1 (total) results were significantly associated with T2DM (p <0.05), while no significant associations with T. gondii infection were identified (p >0.05). Strong positive associations between IL-6 and IL-4; and IL-1RA and IL-β were observed in T. gondii seropositive subjects regardless of which group they belonged to. Likewise, IL-10 showed a strong positive correlation with IL-1RA only in seronegative subjects. High-density lipoprotein displayed significant correlation (p <0.01) with: IL-6 (r = 0.506); IL-4 (r = 0.492); IL-1β (r = 0.456); IL-1RA (r = 0.507); and, IFN-γ (r = 0.456) exclusively in seropositive subjects belonging to the T2DM group. We conclude that T. gondii infection in Western Australia is highly prevalent. Our results also showed that there is no serological evidence of an association between T. gondii infection and T2DM in the studied subjects. Although some biomarkers displayed strong association with T. gondii and/or T2DM, the differences were not significant enough in terms of discriminatory power hence the 11-biomarker panel selected for the present study is not suited for use in clinical practice independently of other diagnostic indicators. In addition, no evidence of an inflammatory association between T. gondii infection and T2DM was found. Further research is warranted to evaluate the potential of additional biomarkers as alternative and/or additional diagnostic targets to provide results with better clinical applicability. It is recommended that Australian health authorities should focus on raising awareness of toxoplasma infection and target T. gondii transmission control.
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Costa, Beatriz Guerreiro Basilio. "Estudo da modulação do metabolismo lipídico de células dendríticas humanas na infecção por Toxoplasma gondii." Instituto Oswaldo Cruz, 2012. https://www.arca.fiocruz.br/handle/icict/7036.

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Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil
A toxoplasmose é uma doença de alta prevalência no mundo, causada pelo Toxoplasma gondii, um parasita intracelular obrigatório. O T. gondii possui mecanismos de modulação do metabolismo do seu hospedeiro que garantem sua sobrevivência e a instalação da infecção crônica. Um dos tipos celulares mais permissivos à infecção e multiplicação do T. gondii são as células dendríticas (DC), paradoxalmente as células apresentadoras de antígeno mais eficazes, com capacidade de deflagrar uma resposta imune protetora eficaz e duradoura. Neste trabalho, estudamos a modulação do metabolismo lipídico de células dendríticas humanas na infecção por T. gondii. Mostramos que o parasita induziu a maturação da célula e um padrão misto de resposta inflamatória, com altas concentrações das citocinas pró-inflamatórias IL-6 e TNF- e da citocina antiinflamatória IL-10. Após 3 horas de infecção, verificamos que T. gondii induziu a expressão gênica de ciclooxigenase-2 (COX-2). De forma importante, observamos por qRT-PCR que a infecção com T. gondii regulou positivamente a expressão do gene do receptor nuclear (RN) regulado por lipídios PPAR, mas não do LXR. Já a expressão do mRNA das moléculas envolvidas no transporte e estoque de lipídios, FABP4 e ADRP, alvos do PPAR, e ABCA1, alvo do LXR, foram aumentadas pela infecção de 3 horas com o parasita. Utilizando duas técnicas distintas (BODIPY e coloração com ósmio) avaliamos a biogênese de corpúsculos lipídicos (CL) após infecção com o T. gondii e constatamos que essas organelas não foram induzidas após 3 horas de infecção. Entretanto, após 24 horas, 90% das DC apresentaram CL e o número de CL por DC foi estatisticamente maior. Observamos a presença de CL em DC não infectadas pelo parasita, mostrando que a indução da biogênese de CL é um fenômeno parácrino, não dependente da infecção celular. Avaliamos também a importância do PPAR na infecção por T. gondii, através do tratamento das DC com seu agonista ou antagonista. Após 3 horas, apenas os genes ADRP, FABP4 e ABCA1, alvos dos receptores nucleares, foram modulados. Por último, investigamos a influência do T. gondii na expressão das moléculas apresentadoras de antígenos lipídicos. Por citometria de fluxo, constatamos que não há alteração na expressão de membrana dessas moléculas. Contudo, por qRT-PCR, observamos que o T. gondii regula negativamente a expressão dos genes cd1d e cd1e. Em conclusão, mostramos que T. gondii foi capaz de regular positivamente o metabolismo lipídico das DC e negativamente as moléculas apresentadoras de lipídios CD1, sem a participação essencial de PPAR nesses processos.
Toxoplasmosis is a worldwide high prevalence disease caused by Toxoplasma gondii, an obligate intracellular parasite. T. gondii developed mechanisms for modulating the metabolism of its host, ensuring their survival and the chronic infection. Dendritic cells (DC) are one of the most permissive cell types to T. gondii infection and replication and are, paradoxically, considered the most effective antigen presenting cells, triggering an effective and long-lasting protective immune response. In this work, we studied the modulation of lipid metabolism in human dendritic cells infected with T. gondii. We showed that the parasite induced cell maturation, and a mixed pattern of inflammatory response with high levels of proinflammatory cytokines IL-6 and TNF-, and anti-inflammatory cytokine IL-10. After 3h of infection, we found that T. gondii induced increased gene expression of cyclooxygenase-2 (COX-2). Importantly, we observed by qRT-PCR that T. gondii infection upregulated the nuclear receptor (RN) PPAR gene expression, while the levels of LXR were unchanged. Furthermore, the mRNA expression of molecules involved in the transport and storage of lipids, FABP4 and ADRP, PPARtargets, and ABCA1, LXR target, were also increased at 3h of infection with the parasite. In parallel, using two different techniques, (BODIPY and osmium staining), we evaluated the biogenesis of lipid droplets (LD) after infection with T. gondii, and observed that these organelles were not induced after 3 hours of infection. However, after 24 hours, 90% of DC showed LD and the number of LD per DC was statistically enhanced. We observed the presence of LD in DC not infected with the parasite, showing that induction of biogenesis of LD is a paracrine phenomenon not dependent on cell infection. We also evaluated the role of PPAR in T. gondii infection by treating DC with its agonist or antagonist. After 3 hours of infection only the nuclear receptor target genes ADRP, FABP4 and ABCA1 were modulated. Finally, we investigated the influence of T. gondii in the expression of lipid antigens presenting molecules. By flow cytometry, we observed no variation in expression of these molecules in cell membrane. However, by qRT-PCR, we found that the T. gondii downregulated gene expression of cd1d and cd1e. In conclusion, we showed that T. gondii was able to upregulate the DC lipid metabolism, and downregulate CD1 lipid presentation. Apparently, the RN PPAR has no essential role in this process.
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Silva, Camila Luna da. "Estudo do metabolismo mitocondrial e da resposta anti-apoptótica de células endoteliais humanas durante a evolução da infecção por taquizoítos de Toxoplasma gondii." Universidade do Estado do Rio de Janeiro, 2013. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=8172.

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A toxoplasmose é uma zoonose amplamente distribuída que afeta mais de um terço da população mundial e de grande importância na saúde pública. A maioria das infecções em humanos por Toxoplasma gondii é assintomática. A toxoplasmose é amplamente investigada visto que se apresenta como uma doença grave em pessoas imunodeprimidas (portadores da síndrome da imunodeficiência adquirida (SIDA), não tratados, indivíduos transplantados, paciente em tratamento quimioterápico ou em uso de drogas supressoras e gestantes). A toxoplasmose congênita frequentemente pode levar ao aborto espontâneo ou até mesmo resultar na formação de crianças com algum grau de atraso no desenvolvimento mental e/ou físicos, deste modo, a transmissão congênita pode ser muito mais importante do que se pensava, pois os parasitos encontrados na circulação sanguinea são capazes de infectar as células endoteliais dos vasos e os tecidos circunjacentes, podendo resultar no encistamento do T. gondii. Atualmente a toxoplasmose vem sendo investigada devido a sua associação a inúmeras outras doenças, assim, estudos sobre a evolução da infecção por T. gondii em diferentes tipos de células hospedeiras se fazem necessários para uma abordagem terapêutica adequada. Ao invadir a célula hospedeira o parasito possui a capacidade de recrutar as mitocôndrias promovendo mudanças na organização mitocondrial ao longo da progressão da infecção, garantindo um ambiente favorável a sua multiplicação. Diante disso, investigamos se o parasito possui a capacidade de interferir no metabolismo mitocondrial e na resposta apoptótica da célula endotelial. O presente trabalho teve como objetivo analisar o metabolismo mitocondrial através da respirometria de alta-resolução e da resposta apoptótica através do western blotting das células endoteliais da veia umbilical humana (HUVEC) infectadas por 2, 6 e 20 horas por taquizoítos de T. gondii. A respirometria de alta-resolução revelou que o parasito interfere no metabolismo energético da célula hospedeira. A análise do conteúdo de proteínas da família Bcl-2 por western blotting revelou maior estímulo apoptótico no tempo inicial de infecção, quando comparado aos demais tempos. Os resultados dos conteúdos de caspase 3, proteína efetora da apoptose, não demonstrou diferença nos tempos iniciais de infecção Entretanto, em tempos mais tardios, o conteúdo de caspase 3 mostrou-se significativamente aumentado quando comparado às HUVEC não infectadas. A dinâmica de replicação do parasito foi observada através do monitoramento pelo sistema Time-Lapse Nikon BioStation IMQ em tempo real das células infectadas por T.gondii. Portanto, nossos resultados sugerem que o protozoário ao recrutar as mitocôndrias da célula hospedeira interfere no metabolismo mitocondrial e na modulação da apoptose para garantir um ambiente favorável a sua multiplicação.
Toxoplasmosis is a widespread zoonosis that affects more than a third of the world population and of great public health importance. Most human infections with Toxoplasma gondii are asymptomatic. Toxoplasmosis is widely investigated since it presents itself as a serious disease in immunocompromised persons (holders of acquired immunodeficiency syndrome (AIDS), untreated, transplant recipients, patients undergoing chemotherapy or suppressing drugs and pregnant). Congenital toxoplasmosis can often lead to miscarriage or even result in the formation of children with some degree of developmental delay mental and / or physical, thus congenital transmission may be much more important than previously thought, because the parasites found In the bloodstream are able to infect endothelial cells of blood vessels and surrounding tissues, which may result in encystment T. gondii. Currently toxoplasmosis has been investigated because of their association with other diseases, so, studies of the evolution of T.gondii infection in different types of host cells are necessary for an adequate therapeutic approach. To invade the host cell, the parasite has the ability to recruit mitochondria promoting changes in mitochondrial organization along the progression of infection, ensuring a favorable environment for their multiplication. Therefore, we investigated whether the parasite has the ability to interfere with mitochondrial metabolism and apoptotic response of endothelial cells. This study aimed to analyze the mitochondrial metabolism by high-resolution respirometry and apoptotic response by western blotting of endothelial cells of human umbilical vein (HUVEC) infected for 2, 6 and 20 hours per tachyzoites of T. gondii. The high-resolution respirometry revealed that the parasite interferes with the energy metabolism of the host cell. The analysis of the family protein content of Bcl-2 by western blotting revealed higher apoptotic stimulus at the initial time of infection, as compared to other times. The results of the contents of caspase 3 protein effector of apoptosis, showed no difference in the initial days of infection However, in more recent times, the content of caspase 3 was significantly increased when compared to non-infected HUVEC. The dynamics of parasite replication was observed by monitoring the system Time-Lapse Nikon BioStation IMQ in real time from infected cells by T. gondii. Therefore, our findings suggest that mitochondria in recruiting protozoan host cell interfere with mitochondrial metabolism and in the modulation of apoptosis to ensure a favorable environment for multiplication.
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HIRAMOTO, ROBERTO M. "Efeitos da radiacao ionizante sobre a estrutura, metabolismo e infecciosidade de um protozoario patogenico, Toxoplasma gondii (Nicolle and Manceaux, 1908)." reponame:Repositório Institucional do IPEN, 1998. http://repositorio.ipen.br:8080/xmlui/handle/123456789/10660.

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Instituto de Pesquisas Energeticas e Nucleares - IPEN/CNEN-SP
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Books on the topic "Metabolism in Toxoplasma Gondii"

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Gross, Uwe, ed. Toxoplasma gondii. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-51014-4.

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Tonkin, Christopher J., ed. Toxoplasma gondii. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-4939-9857-9.

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Pashley, T. V. Molecular genetic analysis of toxoplasma gondii. Manchester: UMIST, 1996.

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Toxoplasma gondii: The model apicomplexan : perspectives and methods. Amsterdam: Elsevier/Academic Press, 2007.

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1949-, Aosai Fumie, and Norose Kazumi 1952-, eds. Nihon ni okeru Tokisopurazuma-shō. Fukuoka-shi: Kyūshū Daigaku Shuppankai, 2007.

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Uggla, Arvid. Toxoplasma Gondii in farm animals: Some immunodiagnostic methods and their potential. Uppsala: Sveriges Lantbruksuniversitet, 1986.

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Flegr, Jaroslav. Pozor, Toxo!: Tajná učebnice praktické metodologie vědy. Praha: Academia, 2011.

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Lantbruksuniversitet, Sveriges, ed. Toxoplasma gondii infection in sheep: Studies on epidemiology, food hygiene and vaccination. Uppsala: Sveriges Lantbruksuniversitet, 1994.

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Strachan, Dina D. Construction of an epitope-tagged clone of GRA3 for electroporation into Toxoplasma Gondii. [New Haven, Conn: s.n.], 1994.

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Aegerter, Mary. Food safety during your pregnancy. [Pullman, Wash.]: Cooperative Extension, Washington State University, 2000.

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Book chapters on the topic "Metabolism in Toxoplasma Gondii"

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Cioffi, William G., Michael D. Connolly, Charles A. Adams, Mechem C. Crawford, Aaron Richman, William H. Shoff, Catherine T. Shoff, et al. "Toxoplasma gondii." In Encyclopedia of Intensive Care Medicine, 2244. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_3339.

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Coia, John, and Heather Cubie. "Toxoplasma gondii." In The Immunoassay Kit Directory, 918–70. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-009-0359-3_36.

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Stöcker, W. "Toxoplasma gondii." In Springer Reference Medizin, 2327–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_3074.

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Stöcker, W. "Toxoplasma gondii." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_3074-1.

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Ringelmann, R., and Beate Heym. "Toxoplasma gondii." In Parasiten des Menschen, 243–45. Heidelberg: Steinkopff, 1991. http://dx.doi.org/10.1007/978-3-642-85397-5_90.

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Mehlhorn, Heinz. "Toxoplasma gondii." In Encyclopedia of Parasitology, 2766–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_3207.

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Mehlhorn, Heinz. "Toxoplasma gondii." In Encyclopedia of Parasitology, 1–9. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_3207-2.

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Liesenfeld, Oliver. "Toxoplasma gondii." In Lexikon der Infektionskrankheiten des Menschen, 800–803. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-39026-8_1082.

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Kissinger, Jessica C., Michael J. Crawford, David S. Roos, and James W. Ajioka. "Toxoplasma gondii." In Pathogen Genomics, 255–79. Totowa, NJ: Humana Press, 2002. http://dx.doi.org/10.1007/978-1-59259-172-5_17.

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Jeoffreys, Neisha. "Toxoplasma gondii." In PCR for Clinical Microbiology, 389–92. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9039-3_68.

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Conference papers on the topic "Metabolism in Toxoplasma Gondii"

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Eassa, Souzan, Chhanda Bose, Pierre Alusta, Olga Tarasenko, and Olga Tarasenko. "DETECTION METHOD OF TOXOPLASMA GONDII TACHYZOITES." In BIOLOGY, NANOTECHNOLOGY, TOXICOLOGY, AND APPLICATIONS: Proceedings of the 5th BioNanoTox and Applications International Research Conference. AIP, 2011. http://dx.doi.org/10.1063/1.3587472.

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Pires, Sara M., Heidi Enemark, Thomas Rosendal, Anna Lundén, Pikka Jokelainen, and Lis Alban. "Toxoplasma gondii and the role of pork." In Safe Pork 2015: Epidemiology and control of hazards in pork production chain. Iowa State University, Digital Press, 2017. http://dx.doi.org/10.31274/safepork-180809-396.

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Fazli, Mojtaba S., Stephen A. Velia, Silvia N. J. Moreno, and Shannon Quinn. "Unsupervised discovery of toxoplasma gondii motility phenotypes." In 2018 IEEE 15th International Symposium on Biomedical Imaging (ISBI 2018). IEEE, 2018. http://dx.doi.org/10.1109/isbi.2018.8363735.

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Pyburn, David G., S. Patton, J. J. Zimmerman, James D. McKean, R. B. Evans, Annette M. O'Connor, K. L. Smedley, C. T. Faulkner, E. M. Zhou, and E. M. Zhou. "Risk Factors for Swine Infection with Toxoplasma gondii." In Fourth International Symposium on the Epidemiology and Control of Salmonella and Other Food Borne Pathogens in Pork. Iowa State University, Digital Press, 2003. http://dx.doi.org/10.31274/safepork-180809-228.

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Ludewig, M., K. de Buhr, and K. Fehlhaber. "Seroprevalence of Toxoplasma gondii in German swine herds." In First International Symposium on the Ecology of Salmonella in Pork Production. Iowa State University, Digital Press, 2007. http://dx.doi.org/10.31274/safepork-180809-43.

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Hammacher, Gabriela Koh, Saulo Bueno de Azeredo, Natália Gonçalves Rengel, Gean Scherer da Silva, and Fabiana Tonial. "Toxoplasma gondii NA GESTAÇÃO - DANOS NO DESENVOLVIMENTO FETAL." In I Congresso Brasileiro de Parasitologia Humana On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/704.

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Introdução: A toxoplasmose é uma parasitose provocada pelo Toxoplasma gondii, essa doença acomete aproximadamente um terço da população mundial. Apesar de sua alta incidência, o microrganismo possui baixa patogenicidade. No entanto, quando a primoinfecção ocorre na gestação ela pode resultar em graves consequências para o desenvolvimento do feto. Assim, é de suma importância o rastreio de toxoplasmose na gestação com intuito de diagnóstico e tratamento precoce, reduzindo os possíveis danos materno-fetais. Objetivo: Descrever as principais consequências fetais promovidas por infecção materna na gestação pelo Toxoplasma gondii evidenciadas na literatura. Material e métodos: Foi realizada uma revisão narrativa da literatura utilizando as bases de dados “PubMed” e “SciELO”, sendo usados para a busca a combinação dos seguintes descritores em inglês: “Toxoplasma gondii", "toxoplasmose", "gestação", "congênita”. Resultados: As consequências da toxoplasmose congênita dependem do grau de exposição do feto aos protozoários, da virulência da cepa infectante e do período gestacional. No primeiro trimestre de gestação a chance de contaminação materno-fetal fica em torno de 15%, pode ocorrer morte fetal e graves danos neurológicos. No terceiro trimestre de gestação a transmissão materno-fetal aumenta significativamente, é, em média, de 60%, e os danos fetais mais comuns são: retinocorodite, calcificação cerebral, hidrocefalia e retardo mental. As formas graves desse acometimento são divididas em generalizadas e neurológicas. Na forma generalizada pode ocorrer alterações liquóricas, linfadenopatia, trombocitopenia, hepatoesplenomegalia e icterícia. Em casos de doença neurológica pode ocorrer calcificações intracranianas, coriorretinite, hidrocefalia, convulsão e microcefalia. Conclusão: A primo-infecção por toxoplasmose no primeiro e no terceiro trimestres de gestação pode desencadear acometimentos graves ao feto, os quais justificam a necessidade de um consenso em relação ao rastreio, diagnóstico e tratamento da doença na gestação.
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Silva, Keyla Cristina Pereira Ponciano, and MELISSA DA SILVA PAES. "TOXOPLASMA GONDII EM ROEDORES SILVESTRES NO BRASIL: RESUMO." In I Congresso Brasileiro On-line de Clínica Médica Veterinária. Revista Multidisciplinar em Saúde, 2023. http://dx.doi.org/10.51161/convet/16222.

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Warid MAYA, Rana, Nesreen Ahmed NASSER, and Anas H. SADEK. "CORRELATION BETWEEN TOXOPLASMA GONDII (T. GONDII) AND VITAMIN D3 LEVELS IN IRAQI PREGNANT WOMEN." In VII. INTERNATIONAL SCIENTIFIC CONGRESSOF PURE,APPLIEDANDTECHNOLOGICAL SCIENCES. Rimar Academy, 2023. http://dx.doi.org/10.47832/minarcongress7-23.

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Abstract:
Background: Toxoplasmosis played a significant influence in causing abortions and congenital malformations in pregnant women . Vitamin D insufficiency contributed to bone fragility and osteoporosis, putting women at risk for fractures and abnormalities in their babies. nObjective: To evaluate the correlation in the middle of toxoplasmosis seropositivity and vitamin D defects in Iraqi pregnant women. nMethodology: A cross-sectional.study.was directed by examining.the.sera of 60 women, versus to 30 women negative toxoplasmosis (age ranged from 15 - 50 years). Results: the result showed that there is high significant changes between patient and control groups toxoplasmosis IGG P value (0.0001) and significant alterations between patient and control groups toxoplasmosis IGM p value (0.016)and (0.003) vitamin D and negative correlation between vitamin D with age, toxo IGM. Conclusions: there is high significant association between toxoplasmosis and vitamin D deficiency
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Boughattas, Sonia, Aarti Sharma, and Marawan Abu-Madi. "Seroprevalence of Toxoplasma Gondii Among Stray Cats in Qatar." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2016. http://dx.doi.org/10.5339/qfarc.2016.hbpp2667.

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Vesco, Gesualdo, F. Liga, A. Vella, G. Lo Cascio, and S. Villari. "Seroprevalence of Toxoplasma gondii in swine slaughtered in Sicily." In Seventh International Symposium on the Epidemiology and Control of Foodborne Pathogens in Pork. Iowa State University, Digital Press, 2007. http://dx.doi.org/10.31274/safepork-180809-102.

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Reports on the topic "Metabolism in Toxoplasma Gondii"

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Steinman, Richard A. The Dialogue of Metastasis-Uncovering Juxtacrine Genetic Cascades with a Toxoplasma Gondii Enzyme. Fort Belvoir, VA: Defense Technical Information Center, August 2008. http://dx.doi.org/10.21236/ada494955.

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