476 Tropical Biomedicine 27(3): 476–482 (2010) Serological survey of Toxoplasma gondii in schizophrenia patients referred to Psychiatric Hospital, Sari City, Iran Ahmad Daryani, Mehdi Sharif * , Sayed Hamzeh Hosseini, Sayed Ahmad Karimi and Shirzad Gholami Department of Parasitology and Mycology, School of Medicine, Mazandaran University of Medical Sciences, PC 48168-95475, Sari, Iran. * Corresponding author email: msharifmahdi@yahoo.com Received 13 June 2010; received in revised form 4 July 2010; accepted 8 July 2010 Abstract. Schizophrenia is a severe neuropsychiatric disorder of unknown etiology. As there is little information about the association between Toxoplasma gondii infection and schizophrenia in Iran, we investigated the seroprevalence of T. gondii in these patients and compared with that obtained in control individuals in Sari City, Iran, 2009. Eighty schizophrenia patients and 99 healthy people were examined for the presence of IgG and IgM antibodies to T. gondii by enzyme linked immunosorbent assay (ELISA). Overall prevalence rates of anti-T. gondii antibodies (IgG/IgM) in case and control groups were 72.5% and 61.6%, respectively (P>0.05). IgG antibodies indicating chronic form of toxoplasmosis were found in 28 (35%) and 25 (25.3%) of case and control groups, respectively ( P>0.05). IgM antibodies (acute form) were also seen in 9 (11.2%) and 11 (11.1%) of case and control individuals, respectively (P>0.05). The highest 10 th percentile of IgG titers in schizophrenia individuals (18.8%) was significantly higher than control group (6.1%, P=0.02). As prevalence rate of T. gondii antibodies in patients with schizophrenia was high, it seems that designing a cohort study will determine the causative relationship between Toxoplasma infection and schizophrenia. INTRODUCTION Toxoplasma gondii is a protozoan parasite found worldwide (Alvarado-Esquivel et al., 2006) that infects all kinds of mammals, including cats, livestock, and human beings. In its life cycle, cats and other felids are the definitive hosts and the other warm- blooded vertebrates are intermediate hosts. Humans may become infected with T. gondii by eating food or drinking water contaminated with oocysts shed by cats or by ingesting undercooked or raw meat containing tissue cysts from sheep, goats, or other animals that have acquire infection from cats (Dubey, 2004; Dawson, 2005). The importance of these modes of transmission may vary in different populations (Tenter et al., 2000). Depending on eating habits and exposure to cats, up to 80% of the population may be infected with this protozoan (Tenter et al., 2000). Human response to T. gondii is related to immune status of the infected person, strain of T. gondii and course of infection (Suzuki, 2002). Toxoplasma gondii invades any type of nucleated cells (Carruthers & Blackman, 2005) and persists intracellularly in brain cells including glia and neurons (Halonen et al ., 1996; Fischer et al ., 1997; Luder et al ., 1999). Immunocompetent hosts can contain the infection with host defense involving activated T-lymphocytes. Although all immunologic mechanisms involved are not known, it is shown that interferon-gamma (IFN-γ) and the enzyme indoleamine 2,3- dioxygenase (IDO) play an important role (Daubener & Hadding, 1997; Fujigaki et al., 2003; Oberdorfer et al., 2003). Secretion of