Biological Sciences
Toxoplasmosis
Toxoplasmosis is a parasitic infection caused by the Toxoplasma gondii parasite. It can be transmitted through the ingestion of contaminated food or water, or through contact with infected cat feces. While most healthy individuals may not experience severe symptoms, it can pose serious risks to pregnant women and individuals with weakened immune systems.
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11 Key excerpts on "Toxoplasmosis"
eBook - PDF- 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.
eBook - PDF- 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.
eBook - PDF- 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.
eBook - PDF- 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.
eBook - PDFMicrobial 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
eBook - ePubToxoplasma Gondii
The Model Apicomplexan - Perspectives and Methods
- Louis M. Weiss, Kami Kim(Authors)
- 2020(Publication Date)
- Academic Press(Publisher)
Congenital Toxoplasmosis – a study of 103 cases . Am J Dis Child. 1953;86:487.152. Ferguson DJ, Graham DI, Hutchison WM.Pathological changes in the brains of mice infected with Toxoplasma gondii : a histological, immunocytochemical and ultrastructural study. Int J Exp Pathol. 1991;72(4):463–474.153. Ferguson DJ, Bowker C, Jeffery KJ, Chamberlain P, Squier W. Congenital Toxoplasmosis: continued parasite proliferation in the foetal brain despite maternal immunological control in other tissues . Clin Infect Dis. 2013;56(2):204–208.154. Fernàndez-Sabé N, Cervera C, Fariñas MC, et al. Risk factors, clinical features, and outcomes of Toxoplasmosis in solid-organ transplant recipients: a matched case-control study . Clin Infect Dis. 2012;54(3):355–361.155. Ferrandiz J, Mercier C, Wallon M, Picot S, Cesbron-Delauw MF, Peyron F.Limited value of assays using detection of immunoglobulin G antibodies to the two recombinant dense granule antigens, GRA1 and GRA6 Nt of Toxoplasma gondii , for distinguishing between acute and chronic infections in pregnant women. Clin Diagn Lab Immunol. 2004;11:1016–1021.156. Fischer HG, Stachelhaus S, Sahm M, Meyer HM, Reichmann G.GRA7, an excretory 29 kDa T. gondii dense granule antigen released by infected host cells. Mol Biochem Parasitol. 1998;91:251–262.157. Flament-Durand J, Coers C, Waelbroeck C, van Geertruyden J, Tousaint C. Toxoplasmic encephalitis and myositis during treatment with immunodepressive drugs . Acta Clin Belg. 1967;22:44–54.158. Flegr J. Effects of toxoplasma on human behavior . Schizophr Bull. 2007;33(3):757–760 https://doi.org/10.1093/schbul/sbl074 .159. Flegr J. Influence of latent Toxoplasma infection on human personality, physiology and morphology: pros and cons of the Toxoplasma-human model in studying the manipulation hypothesis . J Exp Biol. 2013;216(Pt 1):127–133.160. Flegr J, Havlícek J, Kodym P, Malý M, Smahel Z. Increased risk of traffic accidents in subjects with latent Toxoplasmosis: a retrospective case-control study
- Vladimir Zajac(Author)
- 2011(Publication Date)
- IntechOpen(Publisher)
The course of Toxoplasmosis in HIV/AIDS patients should be able to provide us with a better understanding of the clinical scenario and future management of this so-called “enigmatic parasite” of the tropics. 2. Pathogenesis - from source to host defense mechanism 2.1 Morphology T. gondii is a coccidian, that is ubiquitous and an obligate intracellular parasite with a complex life cycle and felids are the definitive hosts. There are three infectious stages of T. gondii in the environment. Tachyzoites (or endozoites), crescent to oval in shape, are seen in an active infection. They can be transmitted through the placenta from mother to fetus, by blood transfusion, or by organ transplantation. Tissue cysts, containing thousands of bradyzoites, the terminal life cycle stage, are transmitted by eating infected meat or organs, and may persist life-long in an intermediate host. In this stage, they are associated with Microbes, Viruses and Parasites in AIDS Process 308 latent infections, but reactivation occurs in persons who lose their immunity. Bradyzoites (or cystozoites) are less susceptible to chemotherapy and the presence of this infective stage in host tissues is of clinical significance, particularly in immunosuppressed individuals. The oocyst stage, is excreted in the cat’s feces, and this most tolerant form of T. gondii , is ubiquitous in nature, is highly resistant to disinfectants and environmental influences, as well as playing a key role in transmission through the fecal-oral route. 2.1.1 Life cycle and transmission The life cycle of T. gondii was described in 1970, before it was determined that members of the family Felidae, including domestic cats, were the definitive hosts and warm-blooded animals including most livestock and humans serve as intermediate hosts (Figure 1). 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.
eBook - ePubToxoplasma Gondii
The Model Apicomplexan - Perspectives and Methods
- Louis M. Weiss(Author)
- 2013(Publication Date)
- Academic Press(Publisher)
Chapter 1The 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, USAAbstract
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.OutlineKeywords
tachyzoite; bradyzoite; sporozoite; sexual cycle; transmission; Toxoplasmosis; diagnosis1.1 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 Test1.7.4 Detection of T. gondii DNA1.8 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 ReferencesAcknowledgements
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.
eBook - PDF- Is?n Akyar, Isın Akyar, Isın Akyar(Authors)
- 2017(Publication Date)
- IntechOpen(Publisher)
Section 3 Diagnosis of Toxoplasmosis Chapter 6 The Laboratory Diagnosis in Toxoplasma Infection María de la Luz Galván Ramírez, Laura Verónica Sánchez Orozco and Cynthia Guadalupe Temores Ramírez Additional information is available at the end of the chapter http://dx.doi.org/10.5772/67999 Abstract The diagnosis of Toxoplasmosis is of great importance due to the damage caused by this parasite in immunosuppressed people or in pregnant women, the diagnosis of an active Toxoplasmosis represents a sign to initiate a pharmacological treatment immediately. The diagnosis of Toxoplasma can be performed with direct methods through intraperitoneal inoculation of serum or cerebrospinal fluid, in susceptible mice evaluating the survival and detection of tachyzoites of biological samples. Indirect methods detecting the IgM and IgG isotypes against Toxoplasma have been the tools mostly used and had leaded to discrimi-nate between an active and acute, from a chronic Toxoplasmosis. Molecular methods actually Toxoplasma -DNA identification by molecular biology tests like the polymerase chain reac -tion (PCR) allow the direct detection of the parasite. Polymerase chain reaction-restriction fragment length polymorphisms (PCR-RFLPs) have been used to identify three strain lin-ages (type I, II and III). Recently, a high-resolution melting method was described to deter-mine the genotype of the infection by Toxoplasma gondii directly from biological samples. Keywords: Toxoplasma infection, diagnosis, Toxoplasmosis, methods 1. Introduction The diagnosis of Toxoplasmosis represents a very important decision to whether to initiate or not an anti-parasitic treatment. The immunological methods that detect the IgM and IgG isotypes against Toxoplasma have been the tools mostly used and had leaded to discriminate between acute and chronic Toxoplasmosis.
No longer available |Learn more- (Author)
- 2014(Publication Date)
- Library Press(Publisher)
________________________ WORLD TECHNOLOGIES ________________________ Chapter- 4 Parasitic Disease A parasitic disease is an infectious disease caused or transmitted by a parasite. Many parasites do not cause diseases. Parasitic diseases can affect practically all living organi-sms, including plants and mammals. The study of parasitic diseases is called parasi-tology. Some parasites like Toxoplasma gondii can cause disease directly, but other organisms can cause disease by the toxins that they produce. Terminology Although organisms such as bacteria function as parasites, the usage of the term parasitic disease is usually more restricted. The three main types of organisms causing these conditions are protozoa (causing protozoan infection), helminths (helminthiasis), and ectoparasites. Protozoa and helminths are usually endoparasites (usually living inside the body of the host), while ectoparasites usually live on the surface of the host. Occa-sionally the definition of parasitic disease is restricted to diseases due to endoparasites. Causes Mammals can get parasites from contaminated food or water, bug bites, or sexual contact. Ingestion of contaminated water can produce Giardia infections. Parasites normally enter the body through the skin or mouth. Close contact with pets can lead to parasite infestation as dogs and cats are host to many parasites. Approximately 240 diseases may be spread from animals to humans through parasites. Other risks that can lead people to get parasites are walking barefeet, inadequate disposal of faeces, lack of hygiene, close contact with someone who carries specific parasites, eating undercooked or exotic foods. Parasite infections are even worse when people have a high carbohydrate diet, low in protein, and high in alkaline. Sugar should be avoided when candidiasis (yeast infection) is suspected. ________________________ WORLD TECHNOLOGIES ________________________ Symptoms Symptoms of parasites may not always be obvious.
eBook - ePub- Felipe Kierzenbaum(Author)
- 2013(Publication Date)
- Academic Press(Publisher)
Van de Ven, 1992 ). In contrast, sheep congenital Toxoplasmosis, which is of considerable economic importance, cannot be considered as a relevant experimental model since the ovine placenta is structurally very different from human, rodent, and primate placentas.The mechanisms by which T. gondii acute infection affects the host immune system are not yet fully understood. In human acute Toxoplasmosis, the T-cell dysfunction is characterized by impaired T-cell proliferation as well as IFN-γ and IL-2 production in response to stimulation with T. gondii or parasite-unrelated antigens, but not with mitogens. Abnormalities in cell populations, mostly an increase in the CD8+ T-cell subset, as well as T-cell dysfunction are more pronounced in symptomatic patients than in asymptomatic ones. The mechanisms responsible for the increased in vivo selection of CD8+ T cells remain to be disclosed. Further studies are also needed to determine whether the CD8+ T cells act as suppressor cells (responsible for pathology) or as cytotoxic cells which could play a role in further healing. In mice, the immunological disorders that accompany T. gondii acute infection differ to some extent from those observed in humans. If CD8+ T-cell subsets are also increased, the more striking increase affects spleen and lymph node macrophages. T-cell functions such as proliferation and IFN-γ production are markedly depressed, in response not only to T. gondii antigens but also to mitogens. Moreover, a marked decrease in antibody production to both T -dependent and T -independent antigens is observed. This suppressive effect on T and B memory cells is mediated by suppressive plastic-adherent cells, and not by CD8+ T cells. The mechanisms implicated in the in vivo induction of these “suppressor” macrophages and in their action on the lymphocyte stimulation involved in primary antibody responses deserve further study. Here again, and because of differences in immunologic dysfunction developing in humans and mice with acute T. gondii
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