REVIEW Toxoplasma, testosterone, and behavior manipulation: the role of parasite strain, host variations, and intensity of infection Amir ABDOLI (✉) 1,2 1 Department of Parasitology, Faculty of Medical Sciences, Kashan University of Medical Sciences, Kashan, Iran 2 Department of Parasitology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran © Higher Education Press and Springer-Verlag Berlin Heidelberg 2014 Abstract Toxoplasma gondii is an intracellular parasite involved in the etiology of various behavioral and hormonal alterations in humans and rodents. Various mechanisms, including induction changes of testosterone production, have been proposed in the etiology of behavioral alterations during T. gondii infection. However, controversy remains about the effects of T. gondii infection on testosterone production; in some studies, increased levels of testosterone were reported, whereas other studies reported decreased levels. This is a significant point, because testosterone has been shown to play important roles in various processes, from reproduction to fear and behavior. This contradiction seems to indicate that different factors—primarily parasite strains and host variations—have diverse effects on the intensity of T. gondii infection, which consequently has diverse effects on testosterone production and behavioral alterations. This paper reviews the role of parasite strains, host variations, and intensity of T. gondii infection on behavioral alterations and testosterone production, as well as the role of testosterone in the etiology of these alterations during toxoplasmosis. Keywords Toxoplasma gondii, testosterone, behavior manipulation, parasite strain, host variations, intensity of infection, neurologic and psychiatric disorders Introduction Toxoplasmosis is one of the most common zoonotic diseases worldwide. It is estimated that up to a third of the world’s human population is latently infected by T. gondii. Felines, including the domestic cat, are the only definitive host, and various warm-blooded animals and humans are intermediate hosts. Transmission of T. gondii occurs via the oral route and congenital transmission (Tenter et al., 2000; Montoya and Liesenfeld, 2004). Moreover, sexual transmission of T. gondii was observed in animal models of toxoplasmosis (Liu et al., 2006; Arantes et al., 2009; de Moraes et al., 2010; Dass et al., 2011; Lopes et al., 2013; Wanderley et al., 2013). Although, approximately 25% to 30% of the world’s human population is infected by T. gondii, the most common form of infection is latent (asymptomatic) (reviewed by Robert-Gangneux and Dardé, 2012). However, latent toxoplasmosis can induce various hormonal and behavioral alterations in humans and rodents and may be involved in the etiology of different neurologic and psychiatric disorders (Dalimi and Abdoli, 2012; Flegr, 2013a, 2013b; Webster et al., 2013; McConkey et al., 2013; Abdoli et al., 2014). Various mechanisms have been proposed in the etiology of behavioral alterations and neuropsychiatric disorders during T. gondii infection, including hormonal manipulation (increased testosterone [Flegr et al., 2008a, 2008b, 2013a; Lim et al., 2013]), neurotransmitter alteration (particularly increased dopamine [Stibbs, 1985; Skallová et al., 2006; Gaskell et al., 2009; Prandovszky et al., 2011] and decreased serotonin [due to reduction of tryptophan] (Flegr, 2013b)), hippocampus and amygdala abnormalities [Vyas et al., 2007; Hermes et al., 2008; Mitra et al., 2013], decreased tryptophan, and increased kynurenic acid (Schwarcz and Hunter, 2007). In the subject of Toxoplasma and testosterone, Lim et al. (2013) published a remarkable article showing the relation- ship of latent T. gondii infection, testosterone, and behavioral alterations in experimentally infected male rats. The results of this study showed that concentrations of testicular testoster- one, mRNA expression of luteinizing hormone receptor Received August 25, 2013; accepted December 10, 2013 Correspondence: Amir ABDOLI E-mail: a.abdoli@modares.ac.ir, a.abdoli25@gmail.com Front. Biol. 2014, 9(2): 151–160 DOI 10.1007/s11515-014-1291-5