Toxoplasma gondii is a very common parasite and yet, unlike other common parasites, the disease it causes – toxoplasmosis – is nearly not as famous (or infamous). But with recent links to other illnesses such as schizophrenia, depression and autism, that might be about to change.
T. gondii is found throughout the world and the Center For Disease Control found that more than 40 million people in the United States may be infected with the parasite. While the definitive host – the species where the sexual reproduction stage of the organism’s life cycle takes place – might be felids such as cats, it has the potential to infect any warm-blooded animal. Humans, while exposed to the pathogen in large numbers are not affected by it as much because our immune system is more than capable of dealing with it.
Toxoplasmosis is the illness that arises when the immune system is incapable of dealing with the parasite. Usually, it affects people with compromised immune systems – such as those with HIV – and infants born to mothers who are infected with Toxoplasma during or just before pregnancy.
The concept of infectious agents being implicated in mental health disorders like schizophrenia goes back to 1896 when it was first proposed.
T. gondii, in mice, have been shown to impair learning and memory and produce behavioural changes in mice and in rats. It was discovered that T. gondii reduces the natural aversion of a rat to the odour of a cat. This allowed cats to catch and eat their prey more easily, in the process allowing T. gondii to complete its life cycle – proving to be an example of evolutionarily-driven manipulation of host behaviour by the parasite.
T. gondii is of special interest in mental health problems because of its known affinity for brain tissue and its capacity for long-term infection starting in early life.
The effect of T. gondii infection on any given person may differ, depending on factors such as individual genetic predisposition, the state of the immune system, the dose, the virulence of the infecting strain, the timing (e.g., infections in the first trimester of pregnancy differ from those in the third trimester; prenatal and postnatal infections differ; etc.), and the part of the brain affected.
Numerous studies indicate that, although the symptoms of schizophrenia and others generally do not manifest until late adolescence or early adulthood, the disease process has its origins in earlier stages of brain development. The ability of Toxoplasma organisms to infect the perinatal brain is thus consistent with this aspect of schizophrenia pathogenesis. Evidence also exists of patients infected with T. gondii exhibiting more aggressive behaviour than others.
There are many theories as to the exact way in which T. gondii affects the brain – with not much proof for any of them. In studies on mice, they seem to have an inflammatory effect on specific cell types within the brain with glial cells – mainly astrocytes – being particularly affected.
Infectious aetiology for chronic mental health problems have long been proposed and while links have been established between pathogen and disease, the exact mechanism by which it works is the subject of much research and debate and will be for years to come.