Toxoplasma Gondii Life Cycle

11 Key excerpts on "Toxoplasma Gondii Life Cycle"

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  Toxoplasma Gondii

  The Model Apicomplexan - Perspectives and Methods

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

    (Publisher)

  Chapter 1

  The History and Life Cycle of Toxoplasma gondii

  Jitender P. Dubey,    Animal Parasitic Diseases Laboratory, Beltsville Agricultural Research Center, Agricultural Research Service, United States Department of Agriculture, Beltsville, Maryland, USA

  Abstract

  Toxoplasma gondii has a complex life cycle with multiple forms. Intermediate hosts such as humans are infected by sporozoites in oocysts or bradyzoites in pseudocysts whereas the sexual stages occur in the intestine of the definitive host, feline species. The parasite is unusual in that it does not need to pass through sexual stages or its definitive host for transmission to other species. This chapter summarizes the history of the discovery of the parasite, identification of the definitive host and transmission stages of the parasite, as well as other important discoveries in the basic biology and life cycle of T. gondii . This chapter also provides photomicrographs of the life cycle stages of this organism.

  Keywords

  tachyzoite; bradyzoite; sporozoite; sexual cycle; transmission; toxoplasmosis; diagnosis

  Outline

  1.1 Introduction 1.2 The Etiological Agent 1.3 Parasite Morphology and Life Cycle 1.3.1 Tachyzoites 1.3.2 Bradyzoite and Tissue Cysts 1.3.3 Enteroepithelial Asexual and Sexual Stages 1.4 Transmission 1.4.1 Congenital 1.4.2 Carnivorism 1.4.3 Faecal–Oral 1.5 Toxoplasmosis in Humans 1.5.1 Congenital Toxoplasmosis 1.5.2 Acquired Toxoplasmosis 1.5.2.1 Children 1.5.2.2 Toxoplasmosis in Adults 1.6 Toxoplasmosis in Other Animals 1.7 Diagnosis 1.7.1 Sabin–Feldman Dye Test 1.7.2 Detection of IgM Antibodies 1.7.3 Direct Agglutination Test

  1.7.4 Detection of 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.

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  Parasitic Infections and the Immune System

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

    (Publisher)

  6

  Toxoplasmosis

  Françoise Darcy and Ferrucio Santoro

  Publisher Summary

  This chapter discusses toxoplasmosis, which is an infection of worldwide distribution affecting almost all warm-blooded animal species. In intermediate hosts, such as birds and mammals, including humans, T. gondii undergoes asexual multiplication with two parasite stages: (1) the tachyzoite, which is the intracellular proliferative form present during the acute phase of infection, and (2) the bradyzoite, which is the slowly dividing encysted form characteristic of the chronic phase of toxoplasmosis. Bradyzoites persist for the lifetime of the host. In humans, T. gondii is generally acquired by the oral route, after ingestion of raw or undercooked meat containing parasite cysts, vegetables, or water contaminated by oocysts from infected cat feces. Another way of transmission is the transplacental passage of parasites from infected mothers to fetuses. When orally ingested, the bradyzoites or sporozoites enter enteroepithelial cells where they give rise to tachyzoites within a few hours. The tachyzoites are capable of infecting all cell types and quickly divide by endodyogeny. This chapter discusses the distinctions that have been made between toxoplasmosis acquired by the oral route and congenital toxoplasmosis, in which fetal infection is parenteral via the umbilical vein from the placenta.

  I Toxoplasma gondii Life Cycle

  Toxoplasmosis is an infection of worldwide distribution affecting almost all warm-blooded animal species (reviewed by Dubey and Beattie, 1988 ). Toxoplasma gondii, the causative agent, is an intracellular coccidian parasite discovered in 1908 simultaneously at the Tunis Pasteur Institute in the wild rodent Ctenodactylus gondi (Nicolle and Manceaux, 1908 ) and in Brazil in a laboratory rabbit (Splendore, 1908 ). Although T. gondii is an important pathogen for humans, it was not until 1923 that it was isolated at autopsy from the retina of a child (Janku, 1923 ). The high incidence of human toxoplasmosis could be established only after the development of a reliable test (Sabin and Feldman, 1948

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  Toxoplasma Gondii

  The Model Apicomplexan. Perspectives and Methods

  • Louis M. Weiss, Kami Kim(Authors)
  • 2011(Publication Date)
  • Academic Press

    (Publisher)

  1

  The History and Life Cycle of Toxoplasma gondii

  J.P. Dubey

  Publisher Summary

  Infections by the protozoan parasite Toxoplasma gondii are widely prevalent in humans and other animals on all continents. This chapter provides a history of the milestones in the acquisition of knowledge of the biology of this parasite. Toxoplasmosis in sheep deserves special attention because of its economic impact. The identification of T. gondii abortion in ewes is considered a landmark discovery in veterinary medicine; prior to that, protozoa were not recognized as a cause of epidemic abortion in livestock. The ability to identify T. gondii infections based on a simple serological test opened the door for extensive epidemiological studies on the incidence of infection. It became clear that T. gondii infections are widely prevalent in humans in many countries. It also demonstrated that the so-called tetrad of clinical signs considered indicative of clinical congenital toxoplasmosis occurred in other diseases and assisted in the differential diagnosis. Vaccination of sheep with a live cystless strain of T. gondii reduces neonatal mortality in lambs, and the vaccine is available commercially.

  1.1. Introduction

  1.2. The etiological agent

  1.3. Parasite morphology and life cycle

  1.4. Transmission

  1.5. Toxoplasmosis in humans

  1.6. Toxoplasmosis in other animals

  1.7. Diagnosis

  1.8. Treatment

  1.9. Prevention and control

  Acknowledgements References

  1.1 INTRODUCTION

  Infections by the protozoan parasite Toxoplasma gondii

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  Protozoans in Macrophages

  • Eric Denkers, Ricardo T. Gazzinelli(Authors)
  • 2007(Publication Date)
  • CRC Press

    (Publisher)

  T. gondii has a complex life cycle consisting of haploid replicating stages that infect a variety of intermediate hosts and meiosis following infection of felines, which are the only known definite host.12 Transmission of T. gondii occurs by one of two routes: ingestion of oocysts that are shed in the feces from infected cats or ingestion of tissue cysts contained within undercooked meat. Direct infectivity of tissue cysts (containing bradyzoites) to other intermediate host is a unique feature in the life cycle of T. gondii , as all related parasites have a strictly obligatory two-host cycle. Following oral ingestion, sporozoites (contained within oocysts) or bradyzoites (contained within tissue cysts) emerge and penetrate epithelial cells of the small intestine. Herein they may develop, or may pass across the intestinal barrier to reach deeper tissues. When infec­ tion commences in the cat gut, haploid replication (schizogony) is followed by differentiation into gametocytes, which ultimately fuse to form a zygote and develop into an oocyst. When infection occurs in all other hosts, the parasite undergoes conversion to fast growing, lytic form called the tachyzoite, which is responsible for dissemination throughout the host. Replication of tachyzoites is ultimately curtailed by the innate and adaptive immune systems (dealt with elsewhere in this volume). Throughout these different developmental phases and within differ­ ent tissues, T. gondii remains an obligate intracellular parasite. Actin-Based M otility and Cell Invasion Apicomplexan parasites are equipped with a unique form of motility termed gliding.13 Motility is strictly substrate dependent and occurs in the absence of cilia, flagella, or crawling behaviors exhibited by amoeboid cells. Instead, forward propulsion relies on a continuous conveyor belt of adhesive proteins attached the substrate.

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  Protozoa and Human Disease

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

    (Publisher)

  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. Within the prey host the parasite undergoes Disease(s) Toxoplasmosis Etiological agent(s) Toxoplasma gondii Major organ(s) affected Brain, eyes Transmission mode or vector Ingestion of food or water contaminated with oocysts from cat feces, ingestion of raw or undercooked meat containing tissue cysts, congenitally Geographical distribution Worldwide Morbidity and mortality Causes a benign disease in immunocompetent persons and only results in serious disease if obtained congenitally or if immunocompromised Diagnosis Serology Treatment Antifolates Control and prevention Avoid ingestion of contaminated food or water or raw meat Toxoplasma gondii and Tissue Cyst Forming Coccidia 14 152 CHAPTER 14: TOXOPLASMA GONDII AND TISSUE CYST FORMING COCCIDIA an intestinal phase resulting in the excretion of the form infective for the predator. The intestinal phase of Toxoplasma only occurs in felids and is nearly identical to that of Isospora (Chapter 13). Cats acquire the infection by eating animals infected with the tissue stage of the parasite. This stage is often referred to as the tissue cyst and contains hundreds to thousands of bradyzoites. The bradyzoites invade intestinal epithelial cells and undergo an asexual replication called merogony that ends in the production of merozoites. The resulting merozoites are released from the infected cell and invade other intestinal epithelial cells and can then either undergo additional rounds of merogony or undergo gametogony . Similarly to other apicomplexa (Chapter 11), gametogony results in the production of macro- and microgametes.

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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)

  However, it results in the formation of a vacuole that appears larger than normal and devoid of an IPM network. The parasite does not divide in this vacuole but undergoes stage conversion to become a tachyzoite. At around 20 hrs post-infection the parasite escapes to form and divide within a typical tachyzoite vacuole (Speer et al., 1995; Tilley et al., 1997). 2.2. LIFE CYCLE Parasitic protozoa typically have complex life cycles, which involve a highly coordinated series of developmental changes which produce phenotypically Toxoplasma gondii Strain Variation and Pathogenicity 409 distinct stages. In apicomplexan parasites there is an obligate cycle with alternating phases of sexual and asexual reproduction. The simplest form of the cycle is seen in directly transmitted parasites such as Eimeria where several rounds of asexual amplification are followed by the generation of gametes that fuse to form the transmission stage, the oocyst (Figure 13.2a). More commonly, parasites alternate between two hosts: for example, malaria para-sites have a sexual cycle in the mosquito and two distinct cycles of asexual division (exoerythrocytic and erythrocytic) in the mammalian host (Figure 13.2b). Toxoplasma follows the general life cycle pattern, with a sexual cycle in the cat and an asexual cycle in a variety of intermediate hosts (Figure 13.2c), but there are two important exceptions. Firstly, the parasite does not take a one-way route around the life cycle as interconversion can occur between two stages, the tachyzoite and the bradyzoite. Secondly, the parasite can be transmitted directly via the asexual bradyzoite stage and is not obliged to use the sexual cycle. The asexual cycle begins with ingestion of oocysts or tissue cysts, which release infective sporozoites and bradyzoites, respectively. Sporozoites pene-trate gut enterocytes and pass the lamina propria prior to undergoing endody-ogeny and transforming into tachyzoites (Dubey et al., 1997b).

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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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  Protozoa and Human Disease

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

    (Publisher)

  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 exceptions 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. Within the prey host the parasite undergoes an intestinal phase resulting in the excretion of the form infective for the predator. The intestinal phase of Toxoplasma only occurs in felids and is nearly identical to that of Isospora (Chapter 13 ). Cats acquire the infection by eating animals infected with the tissue stage of the parasite. This stage is often referred to as the tissue cyst and contains hundreds to thousands of bradyzoites. The bradyzoites invade intestinal epithelial cells and undergo an asexual replication called merogony that ends in the production of merozoites. The resulting merozoites are released from the infected cell and invade other intestinal epithelial cells and can then either undergo additional rounds of merogony or undergo gametogony. Similarly to other apicomplexa (Chapter 11 ), gametogony results in the production of macro and microgametes. Thus, the cat is considered the definitive host

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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)

  There are three infectious stages of T. gondii : the tachyzoites (in groups) (Figure 12.3a), the bradyzoites (in tissue cysts) (Figure 12.3b and c), and the sporozoites (in oocysts) FIGURE 12.1 Life cycle of T. gondii. 211 Toxoplasma gondii (a) (b) FIGURE 12.2 Tachyzoites of T. gondii . Bar = 10 µ m. (a) Individual (small arrows), binucleate (large arrow), and divided (arrowhead) tachyzoites. Impression smear of lung. Compare size with red blood cells and leukocytes. Giemsa stain. (b) Tachyzoites in a group (large arrow) and in pairs (small arrows) in section of a mesenteric lymph node. Note organisms are located in PVs, and some are dividing (arrowhead). Hematoxylin and eosin (H & E) stain. (a) (b) (c) (d) (e) (f) (g) FIGURE 12.3 Stages of T. gondii . Scale bar in a–d = 20 µ m and in e–g = 10 µ m. (a) Tachyzoites in impression smear of a lung. Note crescent-shaped individual tachyzoites (arrows) and dividing tachyzoites (arrowheads) compared with the size of host red blood cells and leukocytes. Giemsa stain. (b) Tissue cysts in section of muscle. The tissue cyst wall is very thin (arrow) and encloses many tiny bradyzoites (arrowheads). H & E stain. (c) Tissue cyst separated from host tissue by homogenization of infected brain. Note tissue cyst wall (arrow) and hundreds of bradyzoites (arrowheads). Unstained. (d) Schizont (arrow) with several merozoites (arrowheads) separating from the main mass. Impression smear of infected cat intestine. Giemsa stain. (e) A male gamete with two flagella (arrows). Impression smear of infected cat intestine. Giemsa stain. (f) Unsporulated oocyst in fecal float of cat feces. Unstained. Note double-layered oocyst wall (arrow) enclosing a central undivided mass. (g) Sporulated oocyst with a thin oocyst wall (large arrow), two sporocysts (arrowheads). Each sporocyst has four sporozoites (small arrow), which are not in complete focus. Unstained.

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  Parasitic Infections in the Compromised Host

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

    (Publisher)

  Similarly, toxoplasmic encephalitis was noted with very high frequency in Africans with AIDS (56). Toxoplasmic encephalitis occurred in 5% of homosexual patients with AIDS or generalized lymphadenopathy seen at the University of California at San Francisco (57) and in 2.6% of homosexual patients in New York with AIDS (52). In the review of the clinical experience of neurological disease in AIDS patients at New York Hospital Memorial Sloan-Kettering Cancer Center (58 -60), Toxoplasma accounted for 38% of known central nervous system infections and 36% of focal intracerebral lesions. It has been estimated that toxoplasmic encephalitis may eventually afflict 10-15% of AIDS patients (60). These studies emphasize the pervasiveness and importance of toxoplasma infection as a significant cause of morbidity and mortality in AIDS patients. III. Life Cycle There are two cycles in the development of Toxoplasma that can be linked into a life cycle (17) (Fig. 1). In the cat, which is the definitive host for Toxoplasma, the organism undergoes the complete life cycle, including both an enteroepithelial cycle and an extraintestinal cycle. The enteroepithelial cycle of development is similar to that of other coccidians. In other mammalian and avian hosts, which are incidental hosts, the organism only has an extraintestinal phase of Figure 1 Life cycle of Toxoplasma gondii. development. The enteroepithelial cycle results in the productions of oocysts, whereas in the extraintestinal cycle the tachyzoite form and tissue cysts are found. A. Oocysts Ovoid in shape and 10-12 μm in diameter, oocysts have been found only in members of the cat family. After the cat ingests either tissue cysts or oocysts, T. gondii is released and invades the epithelial cells of the small intestine, where it undergoes an enteroepithelial cycle (17, 61). The organism undergoes sequential stages of development and multiplication, finally resulting in the formation of oocysts

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  Human Emerging and Re-emerging Infections

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

    (Publisher)

  Principles and Practice of Infectious Disease. 5th ed. Philadelphia, PA: Churchill Livingstone. pp. 2858–2888.
• Morampudi, V., Braun, M.Y., and D'Souza, S. 2011. Modulation of early β-defensin-2 production as a mechanism developed by type I Toxoplasma gondii to evade human intestinal immunity. Infect. Immun., 79, 2043–2050.
• Naot, Y., Barnett, E.V., and Remington, J.S. 1981. Method for avoiding false-positive results occurring in immunoglobulin M enzyme-linked immunosorbent assays due to presence of both rheumatoid factor and antinuclear antibodies. J. Clin. Microbiol., 14, 73–78.
• Pearce, B.D., Kruszon-Moran, D., and Jones, J.L. 2012. The relationship between Toxoplasma gondii infection and mood disorders in the third national health and nutrition survey. Biol. Psych., 72, 290–295.
• Pedersen, M.G., Mortensen, P.B., Norgaard-Pedersen, B., and Postolache, T.T. 2012. Toxoplasma gondii infection and self-directed violence in mothers. Arch. Gen. Psychiatry, 69, 1123–1130.
• Peng, H-J., Chen, X-J., and Lindsay, D.S. 2011. Review: Competent, Compromise and concomitance: Reaction of the host cell to Toxoplasma gondii infection and development. J. Parasitol., 97, 620–628.
• Remington, J.S., McLeod, R., and Desmonts, G. 1995. Toxoplasmosis. In: Remington, J.S., and Klein, J.O., editors. Infectious Disease of the Fetus and Newborn Infant. Philadelphia, PA: W.B. Saunders Company. pp. 140–267.
• Remington, J.S., McLeod, R., Thuilliez, P., and Desmonts, G. 2006. Toxoplasmosis. In: Remington, J.S., Klein, J.O., Wilson, C.B., and Baker, C., editors. Infectious Diseases of the Fetus and Newborn Infant, 6th ed. Philadelphia, PA: Elsevier Saunders. pp. 947–1091.
• Sibley, L.D. 2011. Invasion and intercellular survival by protozoan parasites. Immunol. Rev., 240, 72–91.
• Sibley, L.D., and Boothroyd, J.C. 1992. Virulent strains of Toxoplasma gondii comprise a single clonal lineage. Nature, 359, 82–85.
• Stepick-Biek, P., Thulliez, P., Araujo, F.G., and Remington, J.S. 1990. IgA antibodies for diagnosis of acute congenital and acquired toxoplasmosis. J. Infect. Dis.