Infection and tumors provoke substantial changes accompanied with the disbalance of many neuroendocrine factors which in their summarizing effects influence the life span of animals. Our previous results showed enhanced mortality after one injection of morphine in association with Friend leukaemia virus infection. The aim of this study was to examine the effects of some other opioids (pethidine and pentazocine) and an acetylcholine esterase inhibitor neostigmine on the survival of animals under two conditions: (1) Friend leukaemia virus infection which mostly depressed immune functions, and (2) Toxoplasma gondii infection which in general enhanced the immune status. In contrast to our previous observation with morphine, the mortality induced by single doses of pethidine (150 mg/kg) or pentazocine (50-75 mg/kg) was unchanged during the Friend leukaemia virus infection. A single injection of neostigmine (0.42 or 0.56 mg/kg) was significantly more lethal in DBA-2 mice infected with Friend leukaemia virus. Neostigmine in doses of 0.33 and 0.4 mg/kg caused death in 46 % and 57 %, respectively, of animals infected with Toxoplasma gondii which was significantly higher in comparison with only 8 % and 12.5 % in control groups. Pethidine (150 mg/kg) killed 70 % of Toxoplasma gondii infected animals and even 90 % of non-infected mice. Thus, the Friend leukaemia virus and Toxoplasma gondii infections increased toxicity only of some drugs which may, at least partly, be associated with altered immune status during infection and involvement of the cholinergic system.
We assessed IgG antibody to Toxoplasma gondii in 300 inpatients with schizophrenia (SG), 150 outpatients with anxiety and depressive disorders (PCG), and 150 healthy blood donors (HCG). Seropositivity rates were 60.7% for SG, 36.7% for PCG, and 45.3% for HCG (p<0.001). The seropositivity rate for anti-Toxoplasma IgG antibodies in SG was significantly higher that in PCG (X2=23.11, OR=2.66, p=0.001) and HCG (X2=9.52, OR=1.86, p=0.002). Among SG, 85% of those who reported close cat contact had IgG antibodies to T. gondii. Close cat contacts were reported by 59% of SG, 6% of PCG, and 9% of HCG (p<0.001). There was a nonsignificant positive association between toxoplasmosis and schizophrenia for people with a contact with a cat (OR=2.221, p=0.127, CI95=0.796-6.192), and significant negative association between toxoplasmosis and schizophrenia for people without contact with a cat (OR=0.532, p=0.009, CI95=0.332-0.854). Close cat contact (OR=2.679, p<0.001), 51-65-year age group (OR=1.703, p<0.001) and education [illiterate+primary (OR=6.146, p<0.001) and high school (OR=1.974, p=0.023)] were detected as independent risk factors in multivariate logistic regression. The effect of toxoplasmosis on risk of schizophrenia disappeared in the complex model analyzed with multivariate logistic regression. In conclusion, our data suggest that the toxoplasmosis has no direct effect on the risk of schizophrenia in Turkey but is just an indication of previous contacts with a cat.
A convincing body of evidence now exists, from both human and animal studies, and encompassing epidemiological to experimental, to indicate that the common protozoan Toxoplasma gondii can cause specific behavioural changes in its host. Such behavioural alterations are likely to be the product of strong selective pressures for the parasite to enhance transmission from its intermediate host reservoir, primarily rodent, to its feline definitive host, wherein sexual reproduction can occur and the parasite's life cycle completed. Here we consider what the available data to date may reveal about the potential mechanisms involved, the future research that needs to be performed, and the subsequent implications for animal and human health.
Background - There is growing interest in the role of microbial agents in the causation of psychiatric disorders. The neurotropic protozoan parasite Toxoplasma gondii is one of the main candidates and has been associated with various psychiatric conditions, including schizophrenia. Methods - A narrative review of the literature from the main medical databases (Medline, PubMed, PsycINFO), Google Scholar and Google using combinations of applicable terms. Results - T. gondii affects the brain in both the acute and the latent stages of infection causing apparent brain pathologies in infected rodents and both immuno-compromised and immuno-competent humans. In immuno-competent individuals, behavioural disorders are primarily related to the latent stages of the illness. Behavioural/mental disorders that include schizophrenia, mood disorders, personality changes and cognitive impairments may be related to infection with T. gondii. Evidence for a behavioural effect of T. gondii comes from observational reports in animal models and controlled behavioural analysis in humans. Indirect clues of infection also come from raised seroprevalence or serotitres of antitoxoplasma antibodies among those with mental disorders. The pathophysiologic mechanism through which T. gondii may exert its effect is not clear, but direct impact on the brain and changes in neuroimmunomodulation, neurotransmission and some gene-environment interactions are postulated. Conclusion - There is evidence supporting a potential role of T. gondii infection in the onset of some behavioural disorders. Confirmation of such a role would prove a significant breakthrough in the search for the aetiology, treatment and prevention of behavioural disorders, such as schizophrenia. However, the associations remain preliminary.
Toxoplasmosis is caused by intracellular protozoan parasite, Toxoplasma gondii (Nicolle et Manceaux, 1908). Cats and other felids are the definitive hosts. It could be transmitted to man and animals by consumption of infected undercooked meat and contaminated food items including drinking water. Results of toxoplasmosis epidemiological surveys in animals and humans in South-West, North-West, North-East and North-Central Zones of Nigeria have been reported with greater impact on the health of pregnant women and HIV-infected individuals. Meanwhile, studies in states within the South-South and South-East Zones are relatively scanty or non-existent. Overall, the seroprevalence of human toxoplasmosis in Nigeria is estimated at 32% with the following reports for North-West (32%), North-East (22%), North-Central (24%) and South-West (37%). Information on the genetic diversity of isolates of T. gondii in humans and animals including the role of the environment in transmission and maintenance of the disease are highly needed., John Asekhaen Ohiolei, Clement Isaac., and Obsahuje bibliografii
In this study, a loop-mediated isothermal amplification (LAMP) assay was established to detect Toxoplasma gondii DNA in mice infected with T. gondii PRU strain. This LAMP assay was based on the sequence of highly repetitive B1 gene. The detection limit of T. gondii LAMP assay was 1 pg of T. gondii DNA, which was evaluated using 10-fold serially diluted DNA of cultured parasites. The LAMP assay was also highly specific for T. gondii and able to detect T. gondii DNA in urine of mice treated with dexamethasone at 90 day post infection (p.i.), although this assay could not detect the DNA in mice urine 2-6 days p.i. These results demonstrated that LAMP is effective for evaluation of therapy effectiveness for T. gondii infection. The established LAMP assay may represent a useful and practical tool for the routine diagnosis and therapeutic evaluation of human toxoplasmosis.