Category
JFL, Lower Atrium
Description
The parasite Toxoplasma gondii is a highly ubiquitous parasite that latently infects an estimated 33% percent of the global population. Toxoplasmosis is of obvious clinical significance due to the extremely high risks to the unborn who contract it congenitally. Less attention has been given to a more subtle aspect of latent infection, which is the behavioral alterations that are commonly experienced by those who contract the parasite. Infected individuals common display a variety of altered behaviors, such as increased aggression and risk-seeking behaviors, depression, higher tendency towards suicide and self-directed violence, a loss of fear response, and a greatly increased predisposition for schizophrenia. These behavioral changes often are associated with tragic consequences and should be treated as a major health concern. Many mechanisms have been proposed to explain these phenomena, and several will be described here, with an emphasis on neurotransmitter and endocrine dysregulation. It is likely that the most correct framework for understanding behavioral alteration in hosts of Toxoplasma is one that incorporates the interactions between several proposed mechanisms. Future research should be conducted that investigates a possible overarching mechanism which encompasses the many mechanisms described here.
Mechanisms of Behavioral Change in Hosts of Toxoplasma gondii: A Review
JFL, Lower Atrium
The parasite Toxoplasma gondii is a highly ubiquitous parasite that latently infects an estimated 33% percent of the global population. Toxoplasmosis is of obvious clinical significance due to the extremely high risks to the unborn who contract it congenitally. Less attention has been given to a more subtle aspect of latent infection, which is the behavioral alterations that are commonly experienced by those who contract the parasite. Infected individuals common display a variety of altered behaviors, such as increased aggression and risk-seeking behaviors, depression, higher tendency towards suicide and self-directed violence, a loss of fear response, and a greatly increased predisposition for schizophrenia. These behavioral changes often are associated with tragic consequences and should be treated as a major health concern. Many mechanisms have been proposed to explain these phenomena, and several will be described here, with an emphasis on neurotransmitter and endocrine dysregulation. It is likely that the most correct framework for understanding behavioral alteration in hosts of Toxoplasma is one that incorporates the interactions between several proposed mechanisms. Future research should be conducted that investigates a possible overarching mechanism which encompasses the many mechanisms described here.
Comments
Undergraduate