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The Lifecycle, Etiology, Risk Factors, and Prevalence of Toxoplasma gondii

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The Lifecycle, Etiology, Risk Factors, and Prevalence of Toxoplasma gondii

Toxoplasma gondii is a protozoan parasite that causes congenital toxoplasmosis (Carneiro et al, 2013, p. 901), as well as other serious clinical presentations in immune-compromised humans. The parasite is also linked to behavioral diseases in human beings. Toxoplasma gondii genotypes are linked to these particular clinical presentations. T. gondii is an essential pathogen of human beings, particularly in AIDS patients as well as the developing fetus (Adomako-Ankomah et al, 2016, p. 284). Nevertheless, the population structure of Toxoplasma gondii is characterized by contrasting geographic patterns of strain diversity at peculiar spatial scales (Galal et al, 2019). Regarding the diversity pattern, the strains differ between the Americans and Europeans. A substantial diversity of strains has been found in South America. The most common ancestor of T. gondii populations emerged 1.5 million years ago (Galal et al, 2019).

A complementary hypothesis that could explain the high genetic diversity of T. gondii strains in South America would be a more frequent incidence of sexual reproduction between different strains of T. gondii. Moreover, early researches that applied multilocus isoenzyme analyses to study the isolates of the mostly European origin indicated little diversity. Other analyses consisting of a larger set of isolates from North American as well as European sources showed the existence of a striking clonal population structure, with acutely virulent strains comprising a single clonal type (Sibley et al, 2009, p. 2753). Exhaustive studies with a larger group of strains collected from human diseases as well as chronic animal diseases, particularly from North America and Europe, reveal that isolates fall into one of three distinct clonal genotypes called types I, II and III (Halonen & Weiss, 2013, p. 2; Xiao & Yolken, 2016, p. 2). Although, studies +suggest a fourth clonal lineage that is common in wildlife in North America.

The life cycle of Toxoplasma gondii Parasite

  1. gondii consists of four major forms, for instance, oocysts which are always shed in the feces of the definitive host; tachyzoites, these are the organisms that are found in the tissues and which rapidly multiplies; bradyzoites, which are the slowly multiplying organisms found in the tissues; and tissue cysts, these are walled structures that contain bradyzoites (Sibley et al, 2009, p. 2749; Karakavuk, et al, 2018). In all species, T. gondii undergoes an asexual reproductive cycle. When the parasite is taken into the body through various ways, for example, through ingestion, the wall of the tissue cyst or oocyst is dissolved during digestion. The bradyzoites or the tachyzoites are released. The organisms multiply as tachyzoites after penetrating the lamina propria of the small intestines. Within the few hours of infection, the tachyzoites disseminate to the extra-intestinal tissues through the lymph and the blood.

Furthermore, the parasites have the capability of penetrating any cell in the host and multiply. More importantly, the cell of the host ruptures to release the tachyzoites that enter the new cells. Tachyzoites disappear as the host slowly undergoes resistance development. As such, bradyzoites are formed within the tissue cysts. Particularly, the tissue cysts are found in the skeletal muscles, myocardium as well as the central nervous system (CNS). Generally, they do not result in the host reaction; therefore, they showcase continuous persistence for many years. Several types of research indicate that the bradyzoites continue the process of replication. T. gondii undergoes a complex life cycle involving sexual replication in members of the cat family as well as asexual propagation in warm-blooded hosts (Xiao & Yolken, 2016, p. 2). Nevertheless, the tissue cysts occasionally rupture hence releasing the parasites. As a result, the parasites that are released are readily controlled by the immune response in the immunocompetent individuals, if the body of the host becomes immunosuppressed, the parasites multiply and spread. Therefore, toxoplasmosis is often a reactivated rather than a new infection in AIDS patients.

According to Sibley et al (2009), they posit that sexual development only occurs within enterocytes of the cat gut, yielding diploid oocysts, that undergoes meiosis after shedding. Having a clue regarding the adaptations of these stages for various steps in the life cycle gives a framework for considering the peculiar population structure of T. gondii.

Besides, another feature of North America and European clonal lineages of T. gondii is the presence of a biallelic polymorphism at each locus. As such, the biallelic is evident from the studies and is further underscored by sequencing genes from a variety of isolates.

Etiology and Risk Factors of Toxoplasma gondii

According to Halonen & Weiss (2013, p. 3; Rouatbi et al, 2019, p. 9; Jones et al, 2009, p. 879), the most important risk factors is eating of unwashed raw vegetables or fruits and ingestion of water that is contaminated with the oocysts. However, the research shows that oocysts induced infections in individuals are severe than tissue cyst acquired infections. Furthermore, the water-borne infections were seen as being rare, the widespread infection of marine mammals in the USA and also, the outbreaks that are linked to contamination of municipal water reservoir in Canada by wild felids leads to the realization that toxoplasmosis can a water-borne infection. T. gondii is caused by individuals consuming contaminated meat that is raw or not thoroughly cooked (Rouatbi et al, 2019, p. 9; Jones et al, 2009, p. 879). In a smaller percentage, the parasite may be transmitted through blood transfusion as well as an organ transplant. In this case, the oocysts are transferred on the organ or in the blood from a person carrying it. The parasites take long to die hence they can get new attachments on the person being given blood through transfusion or organ transplant.

Nevertheless, the parasite can be found in feces. Regarding this, it can be found on products that are unwashed and are contaminated with manure. Moreover, in the US, the cat feces carry the parasite. Albeit, Toxoplasma gondii is found on warm-blooded animals, the cats are the most known hosts. Through the process of excretion, the eggs exit the body of the feline (Rouatbi et al, 2019, p. 2). Even though the cats are the main hosts, they do not openly show the symptoms of the T. gondii parasite. The women who are pregnant possess an increased risk of passing the parasite to the unborn baby. More importantly, the parasite is not infectious until one to five days after it is shed.

Global Prevalence of Toxoplasma gondii

According to the study carried out by Montazeri et al (2020, p. 5), it is indicated that the countries with the highest number of reports in domestic cats are Brazil, China, the USA, Japan, and Iran respectively. Nevertheless, Brazil has the highest reports in wild felids. Therefore, America as a continent is the most exposed region to the T. gondii parasite compared to other parts of the world. Despite this, the parasite is usually prevalent in moist, warm as well as low altitude regions. As such, it is associated with longer viability of Toxoplasma gondii sporulated oocysts in warm and humid areas.

In the United States, it is estimated that 11 % of the population who are 6 years and above have been infected with the Toxoplasma parasite causing disease. Moreover, in various places in the world, it has been indicated that more than 60 % of the population has been infected with this parasite. Changes in temperature have a significant effect on the prevalence of toxoplasma gondii. For instance, Molan et al, (2019, p. 912; Nissapatorn, Lau & Fong, 2013), discovered a positive relationship between average annual temperatures in unique areas in Sweden as well as the incidence of Toxoplasma gondii in pregnant women. Additionally, rainfall creates a humid environment that eventually increases oocyst survival in addition to increasing the availability of food to support intermediate hosts.

Genotypes and virulence of T. gondii

The strains of T. gondii are always highly diverse albeit only a few lineages are widely spread. The parasite’s different genotypes indicate greater diversity in pathogenicity as well as drug sensitivity (Flegr, et al, 2014, p. 2). In Europe, Africa, and North America, the three clonal lineages of Toxoplasma gondii are more dominant, for instance, type I, type II, and Type III. Recent studies support the concept that many atypical genotypes differ in pathogenicity as well s transmissibility from typical genotypes (Xiao & Yolken, 2016, p. 3). Nevertheless, most atypical genotypes differ in prevalence, virulence, migratory capacity within the host, as well as the capabilities of converting to the phase of bradyzoite cyst. Unique cytokinin responses are induced by the different strains of T. gondii, therefore, triggers the development of clinical as well as biochemical disturbances in the host. Besides, in Northern America, the parasite serotype II causes congenital toxoplasmosis whereas, the parasite’s prematurity and severity at birth are associated with the coccidian II serotype (Flegr, et al, 2014, p. 2). The serotype is always associated with lower socioeconomic status, rural residence as well as Hisparic ethnicity. A bigger margin of the genotypes is found in South America and Africa compared to North America and Europe. Therefore, it is evident that in these continents the parasite’s sexual replication occurs frequently compared to other parts of the world.

Strain Diversity of the Parasite

The clinical manifestations in individuals have been reported in Rio Grande do Norte. Besides, it has been reported in Minas Gerais and Sao Paulo amongst the patients living with AIDS as well as in newborns (Ferreira et al, 2011, p. 191; da Silva, Langoni & Megid, 2017, p. 180). However, this suggests a high genetic diversity that involves atypical genotypes. Some factors influence the occurrence of toxoplasmosis caused by the T. gondii parasite. For example, the stage of T. gondii, the genotype of T. gondii, the genotype of the host as well as factors that affect the immune status of the host (Wendte, Gibson, & Grigg, 2011. p. 3). Nevertheless, in T. gondii, the virulent alleles at multiple locations in the genome always determine the pathogenicity (Adomako-Ankomah et al, 2016, p. 296). Generally, the geographical origins of the hosts always influence the presence of different T. gondii strains. However, the type I genotype containing virulent strains, or atypical alleles are viewed to more pathogenic and more likely to cause severe diseases in individuals. According to Da Silva & Langoni (2016), polymorphism is contributed by the adaptations of the parasite to different regions as well as different hosts (da Silva, Langoni & Megid, 2017, p. 580). Regarding this, Central America and South America showcases a wide genetic diversity of T. gondii strains compared to that in Europe and North America.

Statistically, while humans are affected by T. gondii at a rate of over 1 % (Wilking et al, 2016) annually, they are inaccessible as prey for domestic cats (Muller, & Howard, 2016, p. 20), as are other species of birds or mammals. Nevertheless, the parasite in Germany is highly prevalent and that eating habits seem to be of high epidemiological relevance (Halonen & Weiss 2013, p. 3; Rouatbi et al, 2019, p. 9). During pregnancies, a high number of seroconversions pose risks for unborn babies.

Conclusion

  1. gondii affects all human beings’ genders. Albeit, pregnant women are the most affected hosts thus spreading the parasites to the unborn children which eventually can cause diseases. Therefore, humans and animal generations should focus on the correlation between the genome as well as the corresponding unusual clinical manifestations. Consequently, this will help individuals to understand the interaction between the host genomes and environmental variables, with the polymorphs introduced to the population of the parasite, hence, changing the clinical patterns of the infections caused by the parasite

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