There are three clinical forms of the disease, including ocular, congenital and cerebral ones. Toxoplasma gondii is potentially responsible for significant morbidity and mortality in the congenitally infected fetus (especially in the first trimester of pregnancy) because it can cause a serious disease course and even miscarriage. In a congenital disease course, hepatitis and pneumonia may be followed by central nervous system involvement resulting in hydrocephalus, retinochoroiditis and cerebral calcifications
[10]. In immunocompetent humans, the disease is said to be latent (clinically asymptomatic), but the disease course can be severe in immunocompromised or immunosuppressed patients
[10][13]. In an oligosymptomatic course, the disease may produce mild, flu-like illness. In less than 10% of cases, it causes mononucleosis-like syndrome with headache, malaise, fever, cervical lymphadenopathy and fatigue
[13]. Some tachyzoites can evade the immune response or drugs used in the treatment and transform into bradyzoites inside quiescent cysts, long-term forms of the parasite. Additionally, Toxoplasma can use immune cells to migrate and infiltrate the brain. Recent investigations indicate that toxoplasmosis may increase the risk of brain cancer
[13][20]. In the brain, Toxoplasma prefers neurons because these cells do not react to inflammatory cytokines. Thus, a strong anti-parasitic immune response is not induced
[13]. As a result, central nervous system (CNS) toxoplasmosis, or toxoplasmic encephalitis (TE), which is the most severe (even fatal) course of the disease, may develop in immunocompromised individuals. Encephalitis is the predominant clinical manifestation of toxoplasmosis in acquired immune deficiency syndrome (AIDS) patients and is believed to be due to the reactivation of latent infections
[15]. Clinically, the most common manifestations of TE are neurological abnormalities and brain abscesses accompanied by fever
[13]. Interestingly, Toxoplasma can change the behavior of hosts, including humans. Infected rodents experience less fear of feline odors, which makes them more likely to be eaten by the parasite definite host
[21]. The possible relationship of Toxoplasma infection with mental illness in humans has focused the attention of many researchers
[22]. There have been numerous studies on T. gondii infection and its impact on human behavior and mental diseases
[23]. Nonetheless, the effect of the parasite on human behavior is still less certain than in rodents
[24]. The influence of T. gondii on the increased probability of developing psychiatric disorders, including schizophrenia, bipolar disorder and obsessive-compulsive disorder, has been confirmed
[21]. However, no parasite genes or effector proteins responsible for parasitic behavioral changes have been identified
[21]. Postulated mechanisms linking toxoplasmosis and behavior include generalized inflammation, alteration in endocrine signaling and changes in neurotransmitter pathways
[24]. The main weakness of the studies conducted so far is that they rely on the correlation between T. gondii seropositivity and behavioral or cognitive outcomes but do not assess directly the causal role of the infection in a given pattern of behavior
[23]. Taking into account study limitations and the results of meta-analyses, it could be suggested that the effect of the parasite on human behavior or disease might be rather mild. It is likely that the influence of T. gondii on human behavior and mental health may be dependent on a number of factors, including the parasite strain type, route and duration of infection, host genotype, and others
[23]. Undoubtedly, more research is needed in this area.