Toxoplasmosis is an anthropozoonosis caused by the protozoan Toxoplasma gondii (T. gondii), an obligate intracellular parasite belonging to the phylum Apicomplexa, Sporozoea Class, Coccidia Sub-class, Eucoccidiida Order, Eimeriina Sub-order, Sarcocystidae Family and Toxoplasmatinae Sub-Family (Levine et al., 1988). It is a protozoan capable of infecting nucleated cells from a wide variety of mammals and birds as well as primary cell cultures of fish and insects (Mineo; Kasper, 1994). It presents a cosmopolitan geographic distribution, with high rates of infection in humans. It is estimated that one third of the world population has already been exposed to the T. gondii (Montoya, Liesenfeld, 2004). The first description of the species was carried out by Alfonso Splendore (1909 apud Cox, 2002) in Brazil in 1908, who reported the presence of the protozoan parasitizing laboratory rabbits. In that same year, the French parasitologists Charles Nicolle and Louis Hebert Manceaux (1908 apud Cox, 2002) isolated it in an African rodent (Ctenodactylus gondii), at the Pasteur Institute of Tunisia. Originally denominated Leishmania gondii, by its similarity with the protozoan of the genus Leishmania, the adequacy of its nomenclature only occurred in the following year. The life cycle of the T. gondii was only elucidated more than 50 years after the first report of its discovery (Evans, 1992). In the late 1960s, the analysis of cat fecal material made it possible to discover an evolutive type of protozoan, which was capable of inducing infection in other mammals and birds by its ingestion. Its coccidial cycle was elucidated in the 1970s, when the sexual stages of T. gondii were found in small intestine of cats (Frenkel et al. 1970; Dubey; Beattie, 1988). Although the protozoan T. gondii is considered the only valid species in its genus, three clonal genetic lineages were initially recognized. These are known as Type I, Type II and Type III, and they are predominant in Western Europe and the United States (Howe, Sibley, 1995; Howe et al., 1997). However, surveys on samples of this parasite from other regions of the world, such as South American localities, have revealed other genotypes, differing from the archetypes mentioned above (Soares et al., 2011; Clementino Andrade et al., 2013). When several markers were applied against Brazilian strains, a highly reticulated phylogenetic structure was identified, which suggests that recombination plays an important role in strain diversification in South America (Pena et al., 2008). Currently, it is known that its life cycle is divided between feline and non-feline infections, which are correlated with sexual and asexual replication, respectively (Black; Boothroyd, 2000). Definitive hosts are members of the family Felidae, for example domestic cats (Jackson; Hutchison, 1989; Dubey, 1986; 1993; Frenkel, 2000). Asexual stages of toxoplasma-like parasites were first observed at the turn of the century in tissues of non-felines, for example birds and mammals (Dubey; Beattie, 1988). They are probably all warm-blooded animals including most livestock, and humans. In intermediate hosts, T. gondii undergoes two phases of asexual development. In the first phase, tachyzoites (or endozoites) multiply rapidly by repeated endodyogeny in many different types of host cells. Tachyzoites of the last generation initiate the second phase of development which results in the formation of tissue cysts. Within the tissue cyst, bradyzoites (or cystozoites) multiply slowly by endodyogeny. Tissue cysts have a high affinity for neural and muscular tissues (Ferguson, Hutchison; 1987). They are located predominantly in the central nervous system (CNS), the eye as well as skeletal and cardiac muscles. Unsporulated oocysts are released into the intestinal lumen and passed into the environment with the faeces. Sporogony occurs outside the host and leads to the development of infectious oocysts which contain two sporocysts, each containing four sporozoites (Dubey; Beattie, 1988; Frenkel, 2000). Several studies have been carried out on the asexual stages of T. gondii, in particular on the tachyzoite, while much fewer studies have considered the sexual stages or their infectious product, i.e. the sporozoites within the oocyst. It is noteworthy that cats and wild felids are essential to the persistence of T. gondii in hosts such as grazing animals (e.g. sheep, deer and, more recently, chickens) because they serve as the sole source of the infectious oocysts that contaminate the environment. Environmental contamination by T. gondii oocysts is a concern from both public health and biodiversity perspectives. Surface run-off containing feline feces containing T. gondii oocysts enters in multiple ecosystems (Dubey, 1986; Jackson, Hutchison; 1989). Currently ingesting undercooked meat also provides an important avenue for T. gondii infection through the ingestion of viable tissue cysts (Dubey et al, 1998a). Undercooked pork is another common risk factor for T. gondii exposure; beef is not believed to be a major player, however, mammals and avians raw meat was found to be a risk factor in several epidemiological studies in developed and underdeveloped countries (Fayer et al., 2004). Even as other important risk factors in evidence are for infection include not washing kitchen knives after they have been used to cut raw meat, fruits, and vegetables, as well as infrequent hand washing (Jones et al, 2009). In general, the infection by the T. gondii has a higher prevalence in tropical or subtropical most climate zones, which favors the viability of oocysts in the environment (Tenter et al., 2000). The prevalence of reagents for anti-T. gondii antibodies increases with age and it varies depending on the cultural patterns of the population, its hygiene, food and urban and rural provenance (Amendoeira, 2003; Santos et al., 2012). The prevalence of the disease in children is relatively low, increasing with age and the time of exposure to risk factors throughout life (Kompalic-Cristo et al., 2005). In Brazil, the official statistics from the Ministry of Health indicate toxoplasmosis as responsible for 90 deaths annually. However, there is a lack of data on morbidity and mortality caused by this parasite, so this data is formed by sub-estimated numbers. Toxoplasma Gondii strain involved in the infection and host's immune status, the disease may cause severe illness in human beings and several other classes of animals (Dubey, Bettie, 1988; Cavalcante et al, 2006b). Over the last decades, toxoplasmosis has stimulated the interest of many researchers, mainly by public health relevance and by pervasive affected systems in the hosts, either as an opportunistic disease in immunocompromised patients and pregnant women, or as adaptative disease in immunocompetent animals where reproductive and neural systems is most affected (Tenter et al., 2000). Millions of people worldwide have a serological prevalence of between 15% and 85% in different regions of the planet (Kompalic-Cristo et al.; 2005). In the United States, the prevalence of seropositivity ranges from 10% to 30%, approximately 14% in the reproductive age. In Norway, for example, the positivity in serologic tests is only 10.9%. On the other hand, the prevalence is 28% in Denmark and it reaches 36.7% in Austria. In Malaysia, a recent study found a rate of prevalence of 49%, reaching rates of up to 70% in France, especially in Paris (Porto et al.; 2008). In Brazil, it is estimated that 70% of the population will manifest clinical signs of toxoplasmosis at some point in life. Surveys conducted in pregnant women have shown high seropositivity rates, ranging from 40% to 80% (Porto et al.; 2008). The frequency of seropositive pregnant women for IgG anti-Toxoplasma varies widely among regions, from 28.1% to 70.9% in the South, 70.7% to 98.8% in the Midwest, 50.1% to 90.0% in the Southeast and 66.4% to 72.7% in the Northern Region of the country. In the Northeast, information about the frequency of infections in pregnant women, capable of perinatal transmission, is scarce; in the Sergipe State there was a prevalence rate of 69% in a study performed with 9.550 pregnant women, in Salvador city (BA) the rate was of 69.3%, 71.5% in Ceará, 74.7% in Recife (PE), in João Pessoa (PB) it was observed a rate of 91% of prevalence in a study performed with 55 pregnant women, 86.2% in Alagoas, 66.38% in São Luis (MA) and in Natal (RN) Barbosa et al (2009) observed a rate of prevalence of 66% in a study comprising 190 pregnant women. In the North of Country, in Belém (PA), a rate of 73% was obtained in a study conducted with 531 pregnant women, a rate of 76.2% in Amapá and reaching levels above 70% in Amazonas city. In the Southeast, in the capital city of the state of São Paulo the prevalence rate of 67.7% was observed in a study comprising 481 pregnant women and, in Rio de Janeiro, 77.1%; 73.5% in EspÃrito Santo and 51.6% in Uberlândia (MG). In the South region, in the capital city of Rio Grande do Sul, a prevalence rate of 61.1% (Reis et al., 2006) was obtained by evaluating 10.468 pregnant women and the rate of 49.2% in Paraná. In the central region of the country, in Goiania, the prevalence rate has remained stable over the past 23 years. Nearly all species of animals are susceptible to infection by the protozoan, the seropositivity rates and clinical signs of toxoplasmosis in different hosts are varied (Dubey; Beattie, 1988).© 2013 by Nova Science Publishers, Inc. All rights reserved.