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Schizophr Bull. 2007 May; 33(3): 782–788.
Published online 2007 March 26. doi:  10.1093/schbul/sbm010
PMCID: PMC2526145

A Controlled Prospective Study of Toxoplasma gondii Infection in Individuals With Schizophrenia: Beyond Seroprevalence


Toxoplasma gondii (TG) infection has been reported to be more frequent in schizophrenia. The interaction of the lifelong persisting parasite with the host's immune system involves T-cell/interferon-gamma–induced degradation of tryptophan and provides a challenge to the host well beyond a possible role in the etiology of schizophrenia. The hypothesis we tested in this study was that TG infection may be more frequent (serofrequency) and/or more intense (serointensity) in patients with schizophrenia or major depression compared with psychiatrically healthy controls. In addition, these measures are associated with the clinical course. We did a cross-sectional, prospective investigation of individuals with schizophrenia (n = 277) and major depression (n = 465) admitted to our department (2002–2005) and of healthy controls (n = 214), with all groups adjusted for age and geographic home region. Serofrequency was comparable between the groups, but serointensity was significantly higher in the patients. In individuals with schizophrenia, serointensity was significantly positively associated with C-reactive protein levels and leukocyte counts, and first-episode patients yielded significantly higher serotiters. Immunomodulatory medication was associated with decreased serotiters. In addition, the route of infection appears to differ between patients and controls. Thus, our results support increased host responses to TG infection in the patients, as well as increased titers in first-episode patients with schizophrenia; this may relate to the shifted T-helper 1/2 status described in these patients. Therefore, we suggest that TG infection, particularly in individuals with schizophrenia, is an important environmental factor in the interaction between psychiatric vulnerability, genetic background, immunomodulation, and the neurotransmitter systems.

Keywords: infection, immunity, tryptophan, Toxoplasma gondii, psychosis, depression


Chronic infection with the intracellular parasite Toxoplasma gondii (TG) is more frequent in individuals with schizophrenia than in psychiatrically healthy controls, as indicated in several studies from different countries.1,2 Furthermore, first-episode patients might differ from patients with recurrent or chronic course by having more frequent TG infection and/or a more intense immune response.1,2 However, to date, the results are not equivocal,1,2 with subjects generally characterized as “psychiatric patients” being shown to be more frequently affected than healthy controls or nonpsychiatric patients.36 A study on well-characterized psychiatric patients with distinct diagnoses other than schizophrenia has not yet been published. Moreover, studies with relevant additional data, such as the interrelationship with psychiatric symptomatology and course of the disorder, are still lacking.

Briefly, TG infection in humans takes place when infectious microcysts, typically in affected undercooked and raw meat, are ingested or through contamination with infected cat faeces.7 Because the infection is ubiquitous, the probability of becoming infected increases with age, apart from any particular high-risk behavior, as described before.

When TG infects an organism, it invades various cells8 and persists intracellularly, including in neurons and glia.911 The host organism is not able to eradicate the infection.7 However, immunocompetent hosts control the chronic infection with a T-lymphocyte–driven defense.12 All immunologic mechanisms involved have not yet been unraveled, but it is known that interferon-gamma (IFN-γ) and the enzyme indoleamine 2,3-dioxygenase (IDO) play a role.1317 Activated T-helper cells secrete IFN-γ, which induces IDO. This enzyme degrades the tryptophan that is needed for the tachyzoitic phase of TG. Consequently, activated parasites die by tryptophan depletion.13 The tryptophan degradation products that accumulate via the kynurenine pathway18 may result in excess dopaminergic tone. Thus, the host defense system might produce a lack of serotonin and an accumulation of dopaminergic activity. Psychiatrically, this suggests depressive and psychotic syndromes.1922 Therefore, this parasitic chronic infection, which shifts between silent and microactivated states23 in conjunction with the host defense system, presents an attractive theoretical schema for increased serofrequencies of this infection in psychiatric patients with affective and psychotic syndromes.

We hypothesized that TG infection might be more frequent and/or more intense in patients with schizophrenia and in patients with major depression compared with age-adjusted psychiatrically healthy controls. We rated severity of the symptoms and the course of the disorder. In addition, we analyzed general inflammatory measures, took a careful medication history, and queried the subjects specifically about behaviors associated with a greater risk of TG infection.


All patients who were admitted to inpatient units of our department between 2002 and 2005 and who were diagnosed clinically with schizophrenia or major depression were analyzed for their serotiters to TG infection from blood drawn routinely at admission (including analysis of C-reactive protein [CRP] and leukocyte count). The patients were also rated by experienced psychiatrists (Wilms and Erdag) for the severity of their symptomatology using the German version of the Clinical Global Impression rating scale (CGI), item 1 (0–7)24; this was then collapsed to an arbitrary rating scale with 1 for none or mild (1 or 3 in CGI), 2 for moderate (4 in CGI), and 3 for severe symptoms (5 and 6 in CGI) because items 0, 2, and 7 of CGI had not been marked. In addition, the patients were asked to complete a short questionnaire on risky eating habits (now or ever consuming raw or undercooked meat at least several times) and close and risky cat contacts (now or ever cat ownership, cat in the same household, playing closely with cats, cleaning cat litters). When a patient was discharged, the same experienced psychiatrists analyzed the patient's records of the admission and all records, if any, of prior admissions. Diagnoses were assigned according to International classification of Diseases, 10th Revision (ICD-10)25 using ICD-10 checklists.26 The course of the disorder for schizophrenia and depression was rated by an arbitrary rating scale, with 0 for first episode, 1 for recurrent course, and 2 for chronic course. In addition, patients with schizophrenia were rated for first episode, second episode, recurrent episodes, and chronic course. Patients with acute or chronic infectious or inflammatory processes otherwise specified and with any major medical problems involving the immune system were excluded. Nonpsychiatrically affected controls were recruited from the same geographic region as the patients who are admitted to our department, which provides regional sectorized psychiatric care. The controls had blood drawn for TG serology, and they completed the questionnaires on risk behavior. They were screened for psychiatric disorders and major medical problems as well as for present or recent history of infection or inflammation. This study was approved by the local Ethics Committee of the Faculty of Medicine at the Christian-Albrechts-University, Kiel. All participants gave informed consent to take part in the study.

Psychotropic medication use was categorized for statistical analysis as follows: regular vs on-demand use, antipsychotic medication by potency,27 typical vs atypical, chemical structure, and all regular medication used by any patients by immunomodulatory potency according to human in vivo data (yes = amitriptylline,28 carbamazepine,29 clozapine,28 lithium,28,29 mirtazapine,30 and olanzapine28; no = haloperidol,28 paroxetin,28 and venlafaxin30; and unknown/possible immunomodulation = amisulpride, flupenthixol, levomepromazine, melperone, perazine, perphenazine, pipamperone, promethazine, quetiapine, risperidone, and ziprasidone, with respect to antipsychotics).

TG serology was done by microbiologists (Däubener and Stoltenberg) using the internationally established and widely used Toxo-Spot IF (bioMerieux, Lyon, France) according to the instruction of the supplier. Conventionally, for the detection of acute TG infections, the titers are defined as follows: <1:16 negative, no infection; 1:16–1:256 positive immune reaction suggestive of chronic infection; >1:256 positive, immune reaction suggestive of recent infection. However, we were interested in differentiating low and high titers in our subjects on the basis of microbiological and immunological expertise. Thus, we collated the individual serotiters as follows: <1:16 no contact with TG; 1:16–1:64 TG contact, low-titer response; and ≥1:128 TG contact, intense individual antibody reaction, high-titer response.

For statistical analysis, we used cross-tables and correlational analyses (SPSS for Windows 8.0). In order to test whether certain additional variables had an impact on our results, we tested these variables by cross-tables and correlational analyses with our variables of interest. If there were no significant results, we assumed that the additional variables did not have a significant effect on our results. The level of significance (2 tailed) was set at P ≤ .05. No adjustment of the error probabilities for multiple testing was performed, because of the explorative nature of the study.


Characteristics of the Patients and Controls

We included the following subjects in our study: 277 patients with schizophrenia (mean age 37.4 ± 12.0 years [range 18.7–92.1], of which 24% [n = 67] were older than 45 years); 465 with unipolar major depression (mean age 46.0 ± 15.5 years [range 18.2–92.3], of which 48% [n = 221] were older than 45 years); and 214 healthy controls (mean age 38.9 ± 13.3 years [range 18.4–72.7], of which 26% [n = 55] were older than 45 years). For statistical reasons, the larger the numbers per group, the more difficult the matching becomes for one variable between the groups. Therefore, it was not possible to age match all the groups in our study. However, in order to deal with microbiologically relevant age effects with respect to TG serology in the between-group analyses, we created subsets in each group (over 45 years of age, and 45 years of age and under) because 45 years of age was a turning point in TG serofrequency in our control group (figure 1). In the following sections, all results are reported separately for these 2 age groups.

Fig. 1.
Percentage of Toxoplasma gondii–Positive Subjects Among All Controls Depending on Age.

Gender and smoking habits did not significantly interfere with the data analyses to follow.

Data Analysis

With respect to serofrequency, the only significant difference between the diagnostic groups and controls was in the individuals older than 45 years of age for titers ≥128. As depicted in table 1, the frequency of TG infection (ie, titer <16 vs titer ≥16) did not differ significantly between the diagnostic groups and controls, whereas there was a significant group difference when the comparison was done by titer categories. There are significantly more individuals with serotiters ≥128 in both patient groups compared with the controls. Thus, the intensity of the antibody response, ie, serointensity, is higher in the patients than in the controls. The questionnaires on cat contact and eating habits show that patient groups and controls reported similar frequency of these risk behaviors (data not shown). However, when analyzing interrelationships between serofrequency and the items in the questionnaires, we found that serofrequency is significantly associated with the eating of raw meat in all patient groups, whereas in the controls there was an effect of close and risky cat contact (table 2).

Table 1.
Serofrequency and Serointensity Between Diagnostic Groups and Controls (age > 45 y)
Table 2.
Eating Habits in all Patients' Groups and Risky Cat Contact in the Healthy Controls

Further analyses of the schizophrenia group revealed a significant positive correlation between the titer categories and the number of leukocytes (rho = 0.130, P = .043 by Spearman correlation analysis). Moreover, high titers were significantly associated with high CRP values (table 3). With respect to the clinical course, first-episode patients were significantly more likely to have high antibody titers. Among the high–antibody titer patients, there are significantly more with first episode or chronic course vs recurrent course (table 4). These effects were not seen in seronegative or low–antibody titer patients. Whereas age did not interfere with these results, the use of antipsychotic medication with immunomodulatory or putative immunomodulatory effects did play a role. Using such medication was significantly correlated with lower antibody titers (rho = −0.118, P = .024 by Spearman correlation analysis). Other characteristics of the medication status did not have significant effects in our analysis.

Table 3.
CRP Values and Titer Categories in the Group “Schizophrenia”
Table 4.
Serointensity and Clinical Course in the Group “Schizophrenia”

Further analysis of the major depression group showed significant effects for medication only. As can be seen in table 5, TG seronegative patients were more likely to have had no antidepressants, whereas the medium antibody titer patients were most likely to have been medicated with antidepressants. In addition, medium antibody titer patients were more likely to have had tri/tetracyclic antidepressants (TCA), whereas seronegative individuals were evenly balanced in the use of TCAs vs selective serotonin reuptake inhibitors (SSRIs). The seropositive individuals had been administered TCAs significantly more often than SSRIs; monaminoxidase (MAO) inhibitors were not used. Immunomodulatory medication was more frequent in the medium antibody titer patients, as depicted in table 6. The use of antipsychotic and mood-stabilizing medication did not show any significant interrelationship with the TG antibody titer data.

Table 5.
Use of Antidepressants and Titer Category in the Group “Major Depression”
Table 6.
Use of Immunomodulatory Medication and Titer Category in the Group “Major Depression”


We have presented the first controlled, age-adjusted, prospective, large study of TG infection in psychiatric patients with schizophrenia and major depression diagnosed according to ICD-10 and all recruited in the same geographic region and during the same period. We found that serofrequency (titer <1:16 vs titer ≥1:16) did not differ between groups but that serointensity (<1:16 vs 1:16–1:64 vs ≥1:128) did differ between patients and controls, with higher serointensity in the patients. The analyses of interrelationships within each group between the TG antibody titers and further immunologic or psychopathologic parameters revealed significant results for the schizophrenia group only. High antibody titers were associated with higher inflammatory responses and with first-episode status.

The unique meta-analysis by Torrey and coworkers31 of all published studies included only well-described and methodologically sound studies and calculated an odds ratio of average 2.73. There was no systematic effect of the size of the groups and the results. The number of studies with control groups matched by any means to the patient groups is low, ie, 4 of 23, of which 3 dealt with first-episode patients only. For these 4 studies, the odds ratios range between 2.19 and 5.45. We cannot explain these discrepancies between different studies. However, we suggest for consideration the following issue: matching of the comparison groups is important with respect to age and geographic region of residence (particularly urban vs rural) for the likelihood of acquiring the infection.32 We matched for both of these criteria, whereas none of the previously published studies did so. From our experience, controlling for age is essential. Slight differences in mean age, particularly disequilibrium between the microbiologically relevant age blocks, may shift the results. If we had compared the groups without adjusting for age, seropositives would have been significantly more frequent in the oldest group of patients with major depression. Thus, we think that studies that do not carefully adjust for age between groups must be considered with caution. Furthermore, studies that report “increased antibody levels” in patients must be carefully evaluated because increased antibody levels are not identical to increased frequency of seropositives.33,34

Our study is the first that also systematically collected information on the putative routes of infection. Patients and controls did not differ with respect to the frequency of these risk factors, but they did differ with respect to the interrelationship between these risk factors and seropositivity: the eating of raw meat in the patients and risky cat contact in the controls were associated with higher seropositivity. Thus, if this association points to the infectious route, our patients might have eaten infected raw meat more often, and the controls might have been hygienically less careful in their contacts with infected cats. On the basis of our data, we cannot further analyze this issue. However, if there is particular risk behavior in psychiatric patients, it would be useful to know this and to specifically intervene.

We found that serotiters were significantly higher in the 2 patient groups compared with the controls in all individuals older than 45 years. Moreover, the patients with schizophrenia demonstrated significant interrelationships between the titer category (serointensity) and the course of the disorder as well as with inflammatory variables and the use of immunomodulatory medications. Our results are consistent with previous studies that found increased serotiters in first-episode patients with schizophrenia.33,34 As mentioned before, increased serotiters are not necessarily in the range of the microbiologically high titers suggestive of recent infection and, therefore, might rather support the more intense antibody response of the host.35 Consequently, the higher antibody titers in the first-episode patients, regardless of age, might be based on the special condition of the patients. This is further supported by the additional interrelationship between high antibody titers and increased CRP levels and numbers of leukocytes as markers of inflammatory activity. There is a vast literature on immunologic peculiarities in individuals with schizophrenia.1,3640 In the light of TG infection, these data are of special interest.1,36 As mentioned previously, one basic host defense strategy is through proinflammatory T-helper lymphocytes, ie, TH1 cells.12,13 It was described that individuals with schizophrenia with acute symptomatology display increased TH1-associated cytokine responses, returning to control levels during successful antipsychotic treatment.41 Therefore, an infection such as TG might recurrently induce a TH1 response that modulates the serotonin and dopamine neurotransmitter systems, leading to respective psychotic symptomatology. Antipsychotic treatment that reorganizes these neurotransmitter systems reduces the symptoms by modulating this common final pathway. Immunomodulating antipsychotics28,37,42 in addition might become involved in the host defense against this infection. We found that the use of immunomodulating antipsychotics was associated with lower TG titers. We suggest that the cytokine pattern of increased TH1 response in patients with acute symptoms might be caused by the proinflammatory response to infections such as TG. To our knowledge, there is no published study that investigated TG infection and TH1 immune variables simultaneously. Such a study will be necessary to determine whether TG infections in individuals with schizophrenia are associated with increased TH1 activation; it might also provide an explanation for the diverse findings in schizophrenia on the overactivation of TH1 or TH2 cytokines (for review of the TH2 hypothesis of schizophrenia see Schwarz39).

We found high TG titers in first-episode patients and an association between high titers and increased CRP and leukocyte values, as well as an association between the use of immunomodulating antipsychotics and low titers. One reason could be the use of immunomodulating antipsychotics from the first episode onward. On the other hand, because the high titers were seen in both first-episode and chronic-course patients, continuously high titers might favor a chronic course. Furthermore, a strong proinflammatory immune response to properly control TG microcysts could be counterproductive. One can speculate whether modulating this intense immune response might improve the clinical course in the patients with high titers and chronic course, as well as prevent the high-titer, first-episode patients from developing a chronic course.

Even if our data cannot answer all the questions and speculations presented, they represent the first detailed data on several important variables, and they support continued research on these questions. If TG infection is really able to induce a proinflammatory immune response that leads to dysregulated serotonin and dopamine neurotransmitter systems, to clinically relevant psychiatric symptoms, and perhaps even to the precipitation of schizophrenia in vulnerable subjects,43 then a specific and effective treatment of this infection, coupled with a better understanding of how this vulnerability is defined, will be mandatory.


We thank The Stanley Medical Research Institute for the generous support (grant # 01T-404). We appreciate the excellent technical support of Susanne Kell, Imke Petersen, Helga Dittmer, and Wilfried Schwippert. We thank Elfriede Fritzer, for her statistical expertise, and Dr Christine Miller for improving the use of English language in our article. Last but not least, we thank all our probands.


1. Torrey EF, Yolken RH. The schizophrenia-rheumatoid arthritis connection: infectious, immune, or both? Brain Behav Immun. 2001;15:401–410. [PubMed]
2. Torrey EF, Yolken RH. Toxoplasma gondii and schizophrenia. Emerg Infect Dis. 2003;9:1375–1380. [PMC free article] [PubMed]
3. Conejero-Goldberg C, Torrey EF, Yolken RH. Herpesviruses and Toxoplasma gondii in orbital frontal cortex of psychiatric patients. Schizophr Res. 2003;60:65–69. [PubMed]
4. Flegr J, Havlicek J. Changes in the personality profile of young women with latent toxoplasmosis. Folia Parasitol (Praha) 1999;46:22–28. [PubMed]
5. Smith MS, Mitchell J, Corey L, et al. Chronic fatigue in adolescents. Pediatrics. 1991;88:195–202. [PubMed]
6. Thomas HV, Thomas DR, Salmon RL, Lewis G, Smith AP. Toxoplasma and coxiella infection and psychiatric morbidity: a retrospective cohort analysis. BMC Psychiatry. 2004;4:32. [PMC free article] [PubMed]
7. Tenter AM, Heckeroth AR, Weiss LM. Toxoplasma gondii: from animals to humans. Int J Parasitol. 2000;30:1217–1258. [PMC free article] [PubMed]
8. Carruthers VB, Blackman MJ. A new release on life: emerging concepts in proteolysis and parasite invasion. Mol Microbiol. 2005;55:1617–1630. [PubMed]
9. Fischer HG, Nitzgen B, Reichmann G, Gross U, Hadding U. Host cells of Toxoplasma gondii encystation in infected primary culture from mouse brain. Parasitol Res. 1997;83:637–641. [PubMed]
10. Halonen SK, Lyman WD, Chiu FC. Growth and development of Toxoplasma gondii in human neurons and astrocytes. J Neuropathol Exp Neurol. 1996;55:1150–1156. [PubMed]
11. Luder CG, Giraldo-Velasquez M, Sendtner M, Gross U. Toxoplasma gondii in primary rat CNS cells: differential contribution of neurons, astrocytes, and microglial cells for the intracerebral development and stage differentiation. Exp Parasitol. 1999;93:23–32. [PubMed]
12. Filisetti D, Candolfi E. Immune response to Toxoplasma gondii. Ann Ist Super Sanita. 2004;40:71–80. [PubMed]
13. Daubener W, Hadding U. Cellular immune reactions directed against Toxoplasma gondii with special emphasis on the central nervous system. Med Microbiol Immunol (Berl) 1997;185:195–206. [PubMed]
14. Daubener W, Spors B, Hucke C, et al. Restriction of Toxoplasma gondii growth in human brain microvascular endothelial cells by activation of indoleamine 2,3-dioxygenase. Infect Immun. 2001;69:6527–6531. [PMC free article] [PubMed]
15. Fujigaki S, Saito K, Takemura M, et al. L-tryptophan-L-kynurenine pathway metabolism accelerated by Toxoplasma gondii infection is abolished in gamma interferon-gene-deficient mice: cross-regulation between inducible nitric oxide synthase and indoleamine-2,3-dioxygenase. Infect Immun. 2002;70:779–786. [PMC free article] [PubMed]
16. Fujigaki S, Takemura M, Hamakawa H, Seishima M, Saito K. The mechanism of interferon-gamma induced anti Toxoplasma gondii by 2,3-dioxygenase and/or inducible nitric oxide synthase vary among tissues. Adv Exp Med Biol. 2003;527:97–103. [PubMed]
17. Oberdorfer C, Adams O, MacKenzie CR, De Groot CJ, Daubener W. Role of IDO activation in anti-microbial defense in human native astrocytes. Adv Exp Med Biol. 2003;527:15–26. [PubMed]
18. Miller CL, Llenos IC, Dulay JR, Barillo MM, Yolken RH, Weis S. Expression of the kynurenine pathway enzyme tryptophan 2,3-dioxygenase is increased in the frontal cortex of individuals with schizophrenia. Neurobiol Dis. 2004;15:618–629. [PubMed]
19. Booij L, Van der Does AJ, Riedel WJ. Monoamine depletion in psychiatric and healthy populations: review. Mol Psychiatry. 2003;8:951–973. [PubMed]
20. Leyton M, Ghadirian AM, Young SN, et al. Depressive relapse following acute tryptophan depletion in patients with major depressive disorder. J Psychopharmacol. 2000;14:284–287. [PubMed]
21. Moreno FA, Heninger GR, McGahuey CA, Delgado PL. Tryptophan depletion and risk of depression relapse: a prospective study of tryptophan depletion as a potential predictor of depressive episodes. Biol Psychiatry. 2000;48:327–329. [PubMed]
22. Widner B, Laich A, Sperner-Unterweger B, Ledochowski M, Fuchs D. Neopterin production, tryptophan degradation, and mental depression—what is the link? Brain Behav Immun. 2002;16:590–595. [PubMed]
23. Hoff EF, Carruthers VB. Is Toxoplasma egress the first step in invasion? Trends Parasitol. 2002;18:251–255. [PubMed]
24. NIMH. Clinical Global Impression. Rockville, Md: Rev Ed Rockville; 1976.
25. WHO. ed. Tenth revision of the International Classification of Diseases, Chapter V (F): mental and behavioural disorders. Diagnostic criteria for research. 1993.
26. Hiller W, Zaudig M, Mombour W. Internationale Diagnosen Checklisten für ICD-10 und DSM-IV. Bern, Switzerland: Verlag Hans Huber; 1995.
27. Benkert O, Hippius H. Kompendium der Psychiatrischen Pharmakotherapie. Berlin, Germany: Springer Verlag; 2003.
28. Pollmacher T, Haack M, Schuld A, Kraus T, Hinze-Selch D. Effects of antipsychotic drugs on cytokine networks. J Psychiatr Res. 2000;34:369–382. [PubMed]
29. Himmerich H, Koethe D, Schuld A, Yassouridis A, Pollmacher T. Plasma levels of leptin and endogenous immune modulators during treatment with carbamazepine or lithium. Psychopharmacology (Berl) 2005;179:447–451. [PubMed]
30. Kraus T, Haack M, Schuld A, Hinze-Selch D, Koethe D, Pollmacher T. Body weight, the tumor necrosis factor system, and leptin production during treatment with mirtazapine or venlafaxine. Pharmacopsychiatry. 2002;35:220–225. [PubMed]
31. Torrey EF BJ, Lun ZR, Yolken RH. Antibodies to Toxoplasma gondii in patients with schizophrenia: a meta-analysis. Schizophr Bull. Nov. 2, 2006; doi:10.1093/schbul/sbl050. [PMC free article] [PubMed]
32. Mortensen PB, Norgaard-Pedersen B, Waltoft BL, et al. 2006. Toxoplasma gondii as a risk factor for early-onset schizophrenia: analysis of filter paper blood samples obtained at birth. Biol Psychiatry.doi:10.1016/j.biopsych.2006.05.024. [PubMed]
33. Leweke FM, Gerth CW, Koethe D, et al. Antibodies to infectious agents in individuals with recent onset schizophrenia. Eur Arch Psychiatry Clin Neurosci. 2004;254:4–8. [PubMed]
34. Yolken RH, Bachmann S, Ruslanova I, et al. Antibodies to Toxoplasma gondii in individuals with first-episode schizophrenia. Clin Infect Dis. 2001;32:842–844. [PubMed]
35. Montoya JG. Laboratory diagnosis of Toxoplasma gondii infection and toxoplasmosis. J Infect Dis. 2002;185(Suppl 1):S73–S82. [PubMed]
36. Hanson DR, Gottesman II. Theories of schizophrenia: a genetic-inflammatory-vascular synthesis. BMC Med Genet. 2005;6:7. [PMC free article] [PubMed]
37. Hinze-Selch D, Pollmacher T. In vitro cytokine secretion in individuals with schizophrenia: results, confounding factors, and implications for further research. Brain Behav Immun. 2001;15:282–318. [PubMed]
38. Rothermundt M, Arolt V, Bayer TA. Review of immunological and immunopathological findings in schizophrenia. Brain Behav Immun. 2001;15:319–339. [PubMed]
39. Schwarz MJ, Chiang S, Muller N, Ackenheil M. T-helper-1 and T-helper-2 responses in psychiatric disorders. Brain Behav Immun. 2001;15:340–370. [PubMed]
40. Sperner-Unterweger B, Whitworth A, Kemmler G, et al. T-cell subsets in schizophrenia: a comparison between drug-naive first episode patients and chronic schizophrenic patients. Schizophr Res. 1999;38:61–70. [PubMed]
41. Kim YK, Myint AM, Lee BH, et al. Th1, Th2 and Th3 cytokine alteration in schizophrenia. Prog Neuropsychopharmacol Biol Psychiatry. 2004;28:1129–1134. [PubMed]
42. Jones-Brando L, Torrey EF, Yolken R. Drugs used in the treatment of schizophrenia and bipolar disorder inhibit the replication of Toxoplasma gondii. Schizophr Res. 2003;62:237–244. [PubMed]
43. Bachmann S, Schroder J, Bottmer C, Torrey EF, Yolken RH. Psychopathology in first-episode schizophrenia and antibodies to Toxoplasma gondii. Psychopathology. 2005;38:87–90. [PubMed]

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