Toxoplasma gondii is the most prevalent parasite of humans, infecting 30% to 50% of the world population. In the USA, the prevalence of toxoplasmosis is 11%, with more than 40 million people infected. While house cats and other felids serve as definitive hosts, almost any warm-blooded animal can carry the parasite; cats acquire Toxoplasma by consuming infected prey. Toxoplasma has evolved strategies to enhance its transmission to its feline definitive hosts: it preferentially migrates to and forms cysts in the brain, eyes, and muscle, where it induces a range of cognitive, motor, and physiological changes. For example, infected rodents display impaired motor performance and coordination, as well as changes in testosterone, vasopressin, and dopamine synthesis. These changes result in behavior shifts: Toxoplasma- infected rodents are more likely to frequent open spaces, are less responsive to normally aversive stimuli, and even become attracted to the smell of cat urine. This Toxoplasma- driven manipulation of host behavior is adaptive for the parasite because it increases the odds of infected prey being consumed by cats. The realization that Toxoplasma actively manipulates the neurophysiology of rodents has raised concerns that it may have similar effects on infected humans. Although chronically infected humans are typically considered asymptomatic from a clinical perspective, they are more likely to engage in risky activities (e.g., starting their own business, enlisting in the military, increased rates of traffic accidents), exhibit altered behaviors (e.g., rule following and novelty seeking, suspicion of others, decreased altruism, antisocial attitudes), and tend to respond calmly or passively to imminent danger. Infected humans also display impaired psychomotor performance including increased reaction time and decreased concentration. Toxoplasma alters synthesis of neurotransmitters such as dopamine and serotonin, and has sex-dependent effects on testosterone (i.e., increases in infected males, decreases in infected females). Infected humans experience higher risk of traffic and work-related accidents and may be more susceptible to some forms of mental illness, including schizophrenia. Considering the wide range of endocrine, psychomotor, and behavioral effects noted above, it seems likely that infection by Toxoplasma might negatively affect athletic performance, whether via decreased reaction times and increased passivity, or by changing an athlete’s ability to respond to stress or navigate team dynamics. Conversely, increased risk taking and increases in the tendency to respond calmly to danger may have beneficial effects for athletes in some sports. Unfortunately, there is a complete lack of research on Toxoplasma seropositivity rates in athletes, or on the parasite’s effect on athletic training and performance. In our poster, we discuss possible approaches to address this significant knowledge gap.