Toxoplasma Gondii

12 Key excerpts on "Toxoplasma Gondii"

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  Protozoa and Human Disease

  • Mark F Wiser(Author)
  • 2010(Publication Date)
  • Garland Science

    (Publisher)

  Toxoplasma Gondii is a coccidian parasite which infects humans as well as a wide variety of mammals and birds. It was first described in 1908 in an African hamster-like rodent called the gundi and the species name reflects this original host. Subsequently Toxoplasma was identified in numerous other animals and the first human case was reported in 1939. Despite the wide host range (essentially all warm-blooded vertebrates) only one species is recognized within the genus Toxoplasma . Toxoplasma exhibits a preda-tor–prey life cycle and felids are the only definitive host. Toxoplasmosis is found throughout the world (except extremely cold or dry climates) and tends to be more prevalent in tropical climates. It is estimated that approxi-mately one-third of the world’s population may be chronically infected with Toxoplasma based on serological evidence. The prevalence varies with location with the United States and the United Kingdom exhibiting prevalences ranging from 16 to 40%, whereas prevalences in continental Europe and Central and South America range from 50 to 80%. Despite the high incidence of infection, toxoplasmosis is often unrecognized because it most often causes a benign disease with few or no symptoms. Noted excep-tions are in the cases of congenital infection or immunocompromised individuals. Life Cycle and Transmission Toxoplasma has a complex life cycle consisting of intestinal and tissue phases (Figure 14.1). Although the organism was first discovered in 1908 as a tissue parasite of the gundi, its complete life cycle was not determined until 1970. The life cycle is described as being predator–prey transmission in that the predator acquires the infection by eating a prey infected with the tissue stage of the parasite.

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  Parasitic Infections in the Compromised Host

  • Peter D. Walzer, Robert M. Genta(Authors)
  • 2020(Publication Date)
  • CRC Press

    (Publisher)

  4Toxoplasma Gondii

  BENJAMIN J. LUFTState University of New York at Stony Brook, Stony Brook, New York

  I. Introduction

  Toxoplasma Gondii is an obligate intracellular protozoan that causes significant morbidity and mortality in both humans and animals. In 1908 the parasite was first described as the causative agent of a significant zoonosis (1 ,2 ), and in 1928 the organism was first isolated from a human (3 ). However, its life cycle was not established until 1969, when it was shown that T. gondii was a coccidian and the definitive host was found to be the cat (4 ).

  In 1937 Wolf and Cowen (5 ) and Sabin and Olitski (6 ) established Toxoplasma as a cause of neonatal encephalitis in humans, and it was subsequently found that the infection can be congenitally acquired (7 ). With the development in 1948 of a reliable serological test to detect anti-Toxoplasma antibody, the Sabin-Feldman dye test (8 ), the wide spectrum of clinical manifestations and ubiquitous nature of the infection throughout the world could first be fully appreciated. It is currently estimated that 3300 infants born in the United States are congenitally infected with T. gondii at an average lifetime cost per child of over $67,000 (9 ). Although Toxoplasma has long been recognized as a significant problem in the immunocompromised host (10 -13 ), with the advent of the acquired immune deficiency syndrome (AIDS), toxoplasmic encephalitis is being recognized in epidemic proportions. (14 ). Therefore, now more than ever, the need to control this disease is clearly evident for both humanitarian and economic reasons.

  The purpose of this chapter is to place the clinical manifestations of toxoplasma infection in the compromised host into perspective, with particular attention to the host-parasite immunological interaction. Knowledge of the host's ability to develop a protective response and of the parasite's capacity to suppress or evade these responses will give us insight into the pathogenesis of this disease as well as into the development of new rational therapeutic and diagnostic modalities.

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  Toxoplasma Gondii

  The Model Apicomplexan - Perspectives and Methods

  • Louis M. Weiss, Kami Kim(Authors)
  • 2020(Publication Date)
  • Academic Press

    (Publisher)

  Chapter 1

  The history and life cycle of Toxoplasma Gondii

  J.P. Dubey,    Animal Parasitic Diseases Laboratory, United States Department of Agriculture, Agricultural Research Service, Beltsville Agricultural Research Center, Beltsville, MD, United States

  Abstract

  Infections by the protozoan parasite Toxoplasma Gondii are widely prevalent in humans and other animals on all continents. There are many thousands of references to this parasite in the literature, and it is not possible to give equal treatment to all authors and discoveries. The objective of this chapter is, rather, to provide a history of the milestones in our acquisition of knowledge of the biology of this parasite.

  Keywords

  Toxoplasma Gondii ; history; cats; oocyst

  1.1 Introduction

  Infections by the protozoan parasite Toxoplasma Gondii are widely prevalent in humans and other animals on all continents. There are many thousands of references to this parasite in the literature, and it is not possible to give equal treatment to all authors and discoveries (Dubey, 2008 ). The objective of this chapter is, rather, to provide a history of the milestones in our acquisition of knowledge of the biology of this parasite.

  1.2 The etiological agent

  Nicolle and Manceaux (1908) found a protozoan in tissues of a hamster-like rodent, the gundi, Ctenodactylus gundi , which was being used for leishmaniasis research in the laboratory of Charles Nicolle at the Pasteur Institute in Tunis. They initially believed the parasite to be Leishmania but soon realized that they had discovered a new organism and named it T. gondii based on the morphology (mod. L. toxo =arc or bow, plasma =life) and the host (Nicolle and Manceaux, 1909 ). Thus its complete designation is T. gondii (Nicolle and Manceaux, 1908 , 1909 ). In retrospect the correct name for the parasite should have been T. gundii , as Nicolle and Manceaux (1908) had incorrectly identified the host as Ctenodactylus gondi . Splendore (1908 , see also English translation Splendore, 2009) discovered the same parasite in a rabbit in Brazil, also erroneously identifying it as Leishmania , but he did not name it. It is a remarkable coincidence that this disease was first recognized in laboratory animals and was first thought to be Leishmania

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  Zoonosis

  • Jacob Lorenzo-Morales(Author)
  • 2012(Publication Date)
  • IntechOpen

    (Publisher)

  Veterinary Parasitology, 164, 167–172. Zia-Ali, N.; Fazaeli, A.; Khoramizadeh, M.; Ajzenberg, D.; Darde, M. & Keshavarz-Valian, H. (2007). Isolation and molecular characterization of Toxoplasma Gondii strains from different hosts in Iran. Parasitology Research , 101, 111–115. 14 Major Role for CD8+T Cells in the Protection Against Toxoplasma Gondii Following Dendritic Cell Vaccination Isabelle Dimier-Poisson UMR ISP 1282 University-INRA, Parasite Immunology, Vaccinology and Anti-Infectious Biotherapies, University François Rabelais, Faculty of Pharmacy, Tours, France 1. Introduction Toxoplasma Gondii is an obligate intracellular protozoan that infects one-third of the world population. Asymptomatic in immunocompetent hosts, toxoplasmosis has severe consequences in immunosuppressed individuals and can even lead to death. 1,2 Congenital toxoplasmosis causes development of sequelae later in life, including chorioretinitis, hearing loss or mental retardation. 3 Toxoplasma Gondii is also recognized as being a major cause of abortion in farm animals, such as sheep and goats thus causing substantial reproductive and economic losses. 4 Additionally, these infected animals are a parasitic reservoir involved in human contamination. Recently it has been reported that Toxoplasma Gondii has some degree of causal relation to Schizophrenia 5 because of the positive relationships between the prevalence of Toxoplasma antibodies and the development of schizophrenia. A recent article reports that Toxoplasma infection in rodents blocks the aversion toward predator odors and develop an attraction suggesting an integrating effect of the parasite. 6 This study provides an example of the behavioral effects of Toxoplasma in models of psychiatric and emotional conditions. Once human beings or animals have been infected, no drug treatment available at present will eliminate the parasite. Nor is there any vaccine for human use to control the disease.

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  Biology of Foodborne Parasites

  • Lihua Xiao, Una Ryan, Yaoyu Feng, Lihua Xiao, Una Ryan, Yaoyu Feng(Authors)
  • 2015(Publication Date)
  • CRC Press

    (Publisher)

  209 12 Toxoplasma Gondii Dolores E. Hill and Jitender P. Dubey 12.1 Introduction Toxoplasma Gondii is a coccidian parasite with an unusually wide range of intermediate hosts. Felids serve as definitive hosts and produce the environmentally resistant oocyst stage. Toxoplasmosis is one of the most common parasitic infections of man, though its prevalence varies widely from place to place. It continues to be a significant public health problem in the United States, where 8%–22% of people are infected; a similar prevalence is seen in the United Kingdom. 1–5 In Central America, South America, and continental Europe, estimates of infection range from 30% to 90%. 2,6,7 Most infections in humans are asymptomatic, but at times, the parasite can produce devastating disease. Infection may be congenitally or postnatally acquired. In the United States, nationwide serological surveys demonstrated that seroprevalence in people remained stable at 23% from 1990 until 1998, 3 while recent surveys have demonstrated a significant decrease in seroprevalence to 10.8% over the last decade. 5 Similar decreases in seroprevalence have been observed in many European countries. 6 It is estimated that 1,075,242 persons are infected with T. gondii each year in the United States, and approximately 2,839 persons develop symptomatic ocular disease annually. 8 The cost of illness in the United States caused by Toxoplasma has been estimated to be nearly three billion dollars and an 11,000 quality-adjusted life year (QALY) loss annually. 9,10 Recent publications have linked suicide and schizo-phrenia to Toxoplasma infection. 11,12 T. gondii also infects food animals, including sheep, goats, pigs, chickens, and many game animal spe-cies. Infected animals harbor tissue cysts, and human consumers can be infected by ingestion of these cysts in raw or undercooked meat. Virtually all edible portions of an animal can harbor viable T.

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  Microbes, Viruses and Parasites in AIDS Process

  • Vladimir Zajac(Author)
  • 2011(Publication Date)
  • IntechOpen

    (Publisher)

  In contrast to other protozoans, T. gondii is a parasite that can parasitize all mammals. T. gondii has a large host range; this parasite can be found throughout the world. T. gondii is a common infection in humans; it becomes more important in the field of veterinary and medical infectious diseases. T. gondii is a potential organism causing a serious public health hazard due to infected meat-producing animals and a severe economic loss to the livestock owners. T. gondii can be transmitted (Figure 2) through one of the following routes (Tenter et al, 2000; Derouin et al, 2008). Fig. 1. The life cycle of T. gondii . Toxoplasmosis in HIV/AIDS Patients - A Living Legacy 309 In the definitive hosts, infection with T. gondii occurs following not only ingestion of tissue cysts in under-cooked meat but also after ingesting the rapidly-multiplying tachyzoite forms or the oocysts shed in feces. The cyst wall of T. gondii is dissolved by the proteolytic enzymes of both stomach and small intestine, releasing the slowly-multiplying bradyzoite form. The asexual cycle begins after the invasion of T. gondii into the epithelial cells of the small intestine. While, the sexual cycle is very specific and occurs only in the gut epithelial cells of feline species. The oocyst forms are produced by gamete fusion and are then shed in the feces of the definitive hosts. These oocysts are highly infective to other definitive and intermediate hosts once they are in contact with a susceptible environment (Frenkel, 1973). The oocysts of T. gondii are less infective and pathogenic in the definitive host (cat) as compared with intermediate hosts (mice, pigs, humans) (Dubey, 1998). In intermediate hosts, T. gondii undergoes two phases of asexual development. The infective stages (sporozoites or bradyzoites) transform into tachyzoites following Toxoplasma infection of the intestinal epithelial cells.

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  Toxoplasma Gondii

  The Model Apicomplexan - Perspectives and Methods

  • Louis M. Weiss(Author)
  • 2013(Publication Date)
  • Academic Press

    (Publisher)

  T. gondii DNA

  1.8 Treatment 1.9 Prevention and Control 1.9.1 Serologic Screening During Pregnancy 1.9.2 Hygiene Measures 1.9.3 Animal Production Practices 1.9.4 Vaccination Acknowledgements References

  Acknowledgements

  I would like to thank Drs. Georges Desmonts (now deceased), David Ferguson, Jack Frenkel, H.R. Gamble, Garry Holland, Jeff Jones, and Jack Remington for their helpful discussions in the preparation of this manuscript.

  1.1 Introduction

  Infections by the protozoan parasite Toxoplasma gondii are widely prevalent in humans and other animals on all continents. There are many thousands of references to this parasite in the literature and it is not possible to give equal treatment to all authors and discoveries (Dubey, 2008 ). The objective of this chapter is, rather, to provide a history of the milestones in our acquisition of knowledge of the biology of this parasite (Fig. 1.1 ).

  FIGURE 1.1 Life cycle of T. gondii .

  1.2 The Etiological Agent

  Nicolle and Manceaux (1908) found a protozoan in tissues of a hamster-like rodent, the gundi, Ctenodactylus gundi , which was being used for leishmaniasis research in the laboratory of Charles Nicolle at the Pasteur Institute in Tunis. They initially believed the parasite to be Leishmania , but soon realized that they had discovered a new organism and named it Toxoplasma Gondii based on the morphology (Modern Latin Toxo = arc or bow, plasma = life) and the host (Nicolle and Manceaux, 1909 ). Thus, its complete designation is Toxoplasma Gondii (Nicolle and Manceaux, 1908 ). In retrospect, the correct name for the parasite should have been Toxoplasma gundii ; Nicolle and Manceaux (1908) had incorrectly identified the host as Ctenodactylus gondi. Splendore (1908 , translated in 2009 into English ) discovered the same parasite in a rabbit in Brazil, also erroneously identifying it as Leishmania , but he did not name it. It is a remarkable coincidence that this disease was first recognized in laboratory animals and was first thought to be Leishmania

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  Human Emerging and Re-emerging Infections

  • Sunit Kumar Singh(Author)
  • 2015(Publication Date)
  • Wiley-Blackwell

    (Publisher)

  Chapter 16

  Pathogenesis of Toxoplasma Gondii in Humans

  Hong-Juan Peng1 , Feng Tan2 , and David S. Lindsay3

  1 Department of Pathogen Biology, School of Public Health and Tropical Medicine, Southern Medical University, Guangdong Province, P.R. China

  2 Department of Parasitology, Wenzhou Medical University, Zhejiang Province, P.R. China

  3 Center for Molecular Medicine and Infectious Diseases, Department of Biological Sciences and Pathobiology, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Tech, Blacksburg, VA, USA

  16.1 Pathogen epidemiology

  Toxoplasma Gondii is an intracellular protozoan in the Phylum Apicomplexa, Class Sporozoasida, Subclass Coccidiasina, Order Eucoccidiorida, Suborder Eimeriorina, and Family Sarcocystidae. There is only one species. It can infect and develop in almost all nucleated cells. The disease caused by the parasite is a zoonosis called toxoplasmosis. It can manifest itself as many clinical presentations including: (i) congenital toxoplasmosis (CT), causing mental retardation, hearing, and ocular problems in infected fetuses (Torgerson and Mastroiacovo, 2013), (ii) ocular toxoplasmosis (Bodaghi et al., 2012), (iii) transplantation-acquired infections, causing life-threatening infections in organ recipients (Derouin and Pelloux, 2008), (iv) reactivated encephalitis (toxoplasmic encephalitis) in highly immunosuppressed patients (Yan et al., 2013), and (v) non-specific, flu-like illness in immunocompetent individuals (Weiss and Dubey, 2009). Less well documented, is the association of chronic T. gondii infection with mental illness and behavioral alteration in patients (Webster et al., 2013).

  The prevalence rates of T. gondii infection among healthy people range from 7.5% to 80% worldwide. Prevalence is estimated to be 10–40% in the United States and the United Kingdom, 50–80% in Central and South America, and continental Europe, and about 7.5% among the Chinese population (Xiao et al., 2010). It is estimated that about one-third of the world's population is latently infected with T. gondii. The definitive hosts for T. gondii

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  Microbial Foodborne Diseases

  Mechanisms of Pathogenesis and Toxin Synthesis

  • Jeffrey W. Cary, John E. Linz, Deepak Bhatnagar(Authors)
  • 1999(Publication Date)
  • CRC Press

    (Publisher)

  PART IV PARASITIC PROTOZOA CHAPTER 13 Toxoplasma Gondii Strain Variation and Pathogenicity JUDITH E. SMITH NAOMI REBUCK 1. INTRODUCTION J Toxoplasma Gondii is one of the most common of all parasites. Its distribu-tion is global, ranging from Alaska to Australia, and it is estimated to infect about one third of the human population (Jackson and Hutchinson, 1989). The widespread distribution of the parasite may in part be due to its dual mechanisms of transmission, as infection may be either foodborne, due to ingestion of tissue cysts in uncooked meat, or environmental due to ingestion of oocysts excreted by cats. The spectrum of disease caused by the parasite is broad, but toxoplasmosis is mainly known as a cause of congenital disease and abortion both in humans and in livestock (Remington and Des-monts, 1990; Dubey and Beattie, 1988) and as a potentially lethal infection of AIDS patients (Luft and Remington, 1992). The cellular and molecular organization of Toxoplasma and host immune response to the parasite are well understood but parasite population biology has only recently been investigated (Sibley and Howe, 1996). The advent of molecular markers to analyze strain variation allows a reappraisal of several unresolved issues. Firstly, it is impor-tant to evaluate the extent to which parasite genotype influences the pathogene-sis of infection and, related to this, whether the molecular mechanism of virulence can be determined. Secondly, the markers enable closer investigation of parasite epidemiology and in particular, allow us to assess the relative importance of the two transmission routes. In this chapter we review current understanding of disease pathogenesis, giving a general overview of parasite biology, life cycle, epidemiology and immunoregulation before considering in detail the impact of molecular markers on analysis of population structure and disease epidemiology. 405

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  Zoonoses: Parasitic and Mycotic Diseases

  • Garg, Sudhi Ranjan(Authors)
  • 2021(Publication Date)
  • Daya Publishing House

    (Publisher)

  The genus Toxoplasma (from Greek words, toxo meaning bow and plasma meaning creature) was so named by Nicolle and Manceaux (1909) for its bow-like shape. The species designation originated from the name of the C. gundi from which this parasite was first isolated. Until 1970, only asexual stages of T. gondii were known. Sexual stages of the parasite resulting in oocyst formation in small intestine of cat (Dubey et al . 1970) and the complete life cycle were discovered in 1970 (Frenkel et al . 1970). The cats and wild felids are the definitive hosts while other non-feline warm blooded animals including humans are the intermediate hosts of T. gondii . The fact that man is an intermediate host makes it medically important. In immunocompetent hosts, most infections of T. gondii are asymptomatic resulting in a latent infection with tissue cysts. In immunocompromised patients, it can cause severe disease manifestations and even death (Singh 2003). The disease is transmitted mainly by ingestion of infective stage of the parasite. Other routes of transmission include organ transplant, blood transfusion, transplacental route and accidental inoculation of tachyzoites in the skin (Parija 1996). Pregnant women, children, cat owners, veterinarians, abattoir workers, cooks or butchers and immunologically impaired individuals are considered as high risk group. Geographical Distribution Toxoplasmosis is found worldwide from Alaska to Australia (Hill and Dubey 2002). The disease affects one-third of the total world population. In the United States and the United Kingdom, 16-40 per cent of the population is infected, whereas in Central and South America and Continental Europe, estimates of infection range from 50-80 per cent (Dubey and Beattie 1988). Toxoplasmosis is the third leading cause of death attributed to food-borne illness in the United States.

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  Schizophrenia Treatment

  The New Facets

  • Yu-Chih Shen(Author)
  • 2016(Publication Date)
  • IntechOpen

    (Publisher)

  Temporal and spatial distribution of Toxoplasma Gondii differentiation into bradyzoites and tissue cyst formation in vivo . Infect Immun. 2008; 76 (8):3491–3501. doi:10.1128/IAI.00254‐08 [72] Hermes G, Ajioka JW, Kelly KA, Mui E, Roberts F, Kasza K, Mayr T, Kirisits MJ, Wollmann R, Ferguson DJ, Roberts CW, Hwang JH, Trendler T, Kennan RP, Suzuki Y, Reardon C, Hickey WF, Chen L, McLeod R. Neurological and behavioral abnormalities, ventricular dilatation, altered cellular functions, inflammation, and neuronal injury in brains of mice due to common, persistent, parasitic infection. J Neuroinflamm. 2008; 5 :48. doi:10.1186/1742‐2094‐5‐48 [73] Vyas A, Kim SK, Giacomini N, Boothroyd JC, Sapolsky RM. Behavioral changes induced by Toxoplasma infection of rodents are highly specific to aversion of cat odors. Proc Natl Acad Sci U S A. 2007; 104 (15):6442–6447. doi:10.1073/pnas.0608310104 [74] Cotter DR, Pariante CM, Everall IP. Glial cell abnormalities in major psychiatric dis ‐ orders: the evidence and implications. Brain Res Bull. 2001; 55 (5):585–595. doi:10.1016/ S0361‐9230(01)00527‐5 [75] Shenton ME, Dickey CC, Frumin M, McCarley RW. A review of MRI findings in schizo ‐ phrenia. Schizophr Res. 2001; 49 (1–2):1–52. doi:10.1016/S0920‐9964(01)00163‐3 Toxoplasma Gondii and Schizophrenia: A Relationship That Is Not Ruled Out http://dx.doi.org/10.5772/66018 81 [76] Horacek J, Flegr J, Tintera J, Verebova K, Spaniel F, Novak T, Brunovsky M, Bubenikova‐ Valesova V, Holub D, Palenicek T, Höschl C. Latent toxoplasmosis reduces gray matter density in schizophrenia but not in controls: voxel‐based‐morphometry (VBM) study. World J Biol Psychiatry. 2012; 13 (7):501–509. doi:10.3109/15622975.2011.573809 [77] Conejero‐Goldberg C, Torrey EF, Yolken RH. Herpesviruses and Toxoplasma Gondii in orbital frontal cortex of psychiatric patients. Schizophr Res. 2003; 60 (1):65–69. doi:10.1016/ S0920‐9964(02)00160‐3 [78] Berdoy M, Webster JP, Macdonald DW.

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  Parasitic Infections and the Immune System

  • Felipe Kierzenbaum(Author)
  • 2013(Publication Date)
  • Academic Press

    (Publisher)

  T. gondii could be exploited to identify the loci contributing to virulence. Moreover, the use of PCR techniques should make it possible to examine parasite isolates from pregnant women and AIDS patients in efforts to establish whether there is any correlation between pathogenesis and infecting strains.

  References

  Adams, L.B., Hibbs, J.B., Taintor, R.R., Krahenbuhl, J.L. Microbiostatic effect of murine activated macrophages for Toxoplasma Gondii. Role for synthesis of inorganic nitrogen oxides from L-arginine. J. Immunol . 1990; 144:2725–2729.

  Alexander, J. (1992). Successful vaccination against congenital toxoplasmosis in the BALB/c mouse. In ’NATO Advanced Workshop on Toxoplasmosis,‘ June 28–July 2, 1992, Fontevraud, France.

  Ambroise-Thomas, P., Garin, J.P. Toxoplasmose. Encycl. Méd. Chir., Paris, Maladies Infectieuses, 8098A10 . 1984; 4:1–12.

  Anderson, S.E., Krahenbuhl, J.L., Remington, J.S. Longitudinal studies of lymphocyte response to Toxoplasma antigens in humans infected with Toxoplasma Gondii. J. Clin. Lab. Immunol . 1979; 2:293–297.

  Araujo, F.G. Depletion of L3T4+ (CD4+ ) T lymphocytes prevents development of resistance to Toxoplasma Gondii in mice. Infect. Immun . 1991; 59:1614–1619.

  Araujo, F.G., Remington, J.S. Partially purified antigen preparations of Toxoplasma Gondii protect against lethal infection in mice. Infect. Immun . 1984; 45:122–126.

  Araujo, F.G., Williams, D.M., Grumet, F.C., Remington, J.S. Strain-dependent differences in murine susceptibility to Toxoplasma. Infect. Immun . 1976; 13:1528–1530.

  Asai, T., O’Sullivan, W.J., Tatibana, M. A potent nucleoside triphosphate hydrolase from the parasitic protozoan Toxoplasma Gondii. J. Biol. Chem . 1983; 258:6816–6822.

  Barnert, G., Hassl, A., Aspöck, H. Isoenzyme studies on Toxoplasma Gondii isolates using isoelectric focusing. Zentralbl. Bakteriol. Hyg. Abt. 1, Orig. A

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