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There is a lack of studies using Toxoplasma gondii strains isolated from human patients. Here, we present a pathological study of three strains obtained from human cases of congenital toxoplasmosis in Brazil using inbred mice after oral infection with 10 tissue cysts. Multiplex-nested PCR-RFLP of eleven loci revealed atypical genotypes commonly found in Brazil: toxodb #8 for TgCTBr5 and TgCTBr16 strains and toxodb #11 for the TgCTBr9 strain. BALB/c and C57BL/6 mice were evaluated for survival and histological changes during the acute phase of the disease. All mice inoculated with the non-virulent TgCTBR5 strain survived after 30 days, although irreversible tissue damage was found. In contrast, no mice were resistant to infection with the highly virulent TgCTBR9 strain. The TgCTBr16 strain resulted in 80% survival in mice. However, this strain presented low infectivity, especially by the oral route of infection. Despite being identified with the same genotype, TgCTBr5 and TgCTBr16 strains showed biological differences. Histopathologic analysis revealed liver and lungs to be the most affected organs, and the pattern of tissue injury was similar to that found in mice inoculated perorally with strains belonging to clonal genotypes. However, there was a variation in the intensity of ileum lesions according to T. gondii strain and mouse lineage. C57BL/6 mice showed higher susceptibility than BALB/c for histological lesions. Taken together, these results revealed that the pathogenesis of T. gondii strains belonging to atypical genotypes can induce similar tissue damage to those from clonal genotypes, although intrinsic aspects of the strains seem critical to the induction of ileitis in the infected host., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Congenital toxoplasmosis is caused by Toxoplasma gondii. The incidence of death due to congenital toxoplasmosis in Japan from 1974 to 2007 was calculated using the autopsy database of the Japanese Society of Pathology and vital statistics from the Ministry of Health, Labour and Welfare. Two neonatal deaths due to congenital toxoplasmosis were reported during that time. As there were 161,195 neonatal deaths during this period and 32,465 autopsies were performed, the yearly neonatal death from congenital toxoplasmosis was calculated as 2 × 161,195/32,465/34 = 0.29 and the autopsy rate as 32,465/161,195 = 0.2014 (20.14%). The calculated number of annual deaths in infants was 0.82 and in children aged 1-4 years it was 2.09; thus, although few, deaths from congenital toxoplasmosis do still occur in neonates, infants, and young children. Therefore, obstetricians and pediatricians should be aware of the potential for congenital toxoplasmosis, and pregnant women should make every effort to avoid T. gondii infection., (© 2014 Japan Pediatric Society.)

Congenital toxoplasmosis can cause fetal damage in humans and domestic animals. This study was focused on the effects of Toxoplasma gondii (Prugniaud strain) infection at different stages of pregnancy on the offspring of mice. Results showed that newborn mice from all infected groups were significantly lower in weight than those from the control group but significant difference was not found among these groups at day 60 after birth. The survival rate of the offspring from the group of mice infected at the earlier stage of pregnancy was significantly lower than those of infected and control groups. The positive offspring (with cysts found in their brain tissues) born from the mice infected at the earlier and intermediate stages of pregnancy showed a shorter latency and greater number of errors in the step-through passive avoidance test than those born from the mice infected at the late stage of pregnancy, the control group and the negative offspring from the infected groups. The number of cysts in the brain tissue was significantly higher in the offspring born from the groups of mice infected at the earlier and intermediate stages of pregnancy than those from the group of mice infected at the late stage of pregnancy. In addition, our results indicated that a high congenital transmission rate (90%) occurred in this NIH mouse model. In conclusion, the earlier and intermediate maternal infection of T. gondii can result in severe congenital toxoplasmosis, exhibiting conditions such as stillbirth or non-viability, and learning or memory capability damage in this mouse model. These results not only provide useful data for better understanding the effects of T. gondii infection on the offspring of mice infected at different stages of pregnancy but also for better consideration of the effect of this infection on other mammalian hosts including humans., (Copyright © 2010 Elsevier Inc. All rights reserved.)

Background: The effectiveness of prenatal treatment to prevent serious neurological sequelae (SNSD) of congenital toxoplasmosis is not known., Methods and Findings: Congenital toxoplasmosis was prospectively identified by universal prenatal or neonatal screening in 14 European centres and children were followed for a median of 4 years. We evaluated determinants of postnatal death or SNSD defined by one or more of functional neurological abnormalities, severe bilateral visual impairment, or pregnancy termination for confirmed congenital toxoplasmosis. Two-thirds of the cohort received prenatal treatment (189/293; 65%). 23/293 (8%) fetuses developed SNSD of which nine were pregnancy terminations. Prenatal treatment reduced the risk of SNSD. The odds ratio for prenatal treatment, adjusted for gestational age at maternal seroconversion, was 0.24 (95% Bayesian credible intervals 0.07-0.71). This effect was robust to most sensitivity analyses. The number of infected fetuses needed to be treated to prevent one case of SNSD was three (95% Bayesian credible intervals 2-15) after maternal seroconversion at 10 weeks, and 18 (9-75) at 30 weeks of gestation. Pyrimethamine-sulphonamide treatment did not reduce SNSD compared with spiramycin alone (adjusted odds ratio 0.78, 0.21-2.95). The proportion of live-born infants with intracranial lesions detected postnatally who developed SNSD was 31.0% (17.0%-38.1%)., Conclusion: The finding that prenatal treatment reduced the risk of SNSD in infected fetuses should be interpreted with caution because of the low number of SNSD cases and uncertainty about the timing of maternal seroconversion. As these are observational data, policy decisions about screening require further evidence from a randomized trial of prenatal screening and from cost-effectiveness analyses that take into account the incidence and prevalence of maternal infection. Please see later in the article for the Editors' Summary.

Although the outcomes of toxoplasmosis have been well documented, an integrated estimate of the impact of this infection on the health status of the population is not available. "Disability-adjusted life years" are the sum of years of life lost and years lived with disability, weighted for the severity of the illness. The estimated disease burden of congenital toxoplasmosis in The Netherlands is 620 (range, 220-1900) disability-adjusted life years per year, which is similar to that for salmonellosis and is mainly caused by fetal loss and chorioretinitis. However, there is considerable uncertainty in this estimate. Scenario analysis indicates that the true burden may be underestimated. In other countries, the disease burden is expected to vary with the incidence of congenital infection, but it may also depend on the health care system. In countries that actively screen for toxoplasmosis, such as France, there may be a lower burden of morbidity but a higher burden of mortality.

Fatal cases of toxoplasmosis seen at the Hospital Infantil de México between 1943 and 1973, together with postmortem studies are reviewed. There were five postmortem studies where it was possible to identify toxoplasma in histologic lesions. Clinical manifestations were grouped in pictures; thus, the infectious picture, the intracranial hypertensive, the neurological and the meningeal pictures were made up. In all five cases of this small group, toxoplasma was identified within and without parasitized cells and was found specially abundant in the central nervous system. Considering the early initiation of neurological manifestations and the intensity of encephalic lesions, it may be assumed that all five cases of prenatal toxoplasmosis. The reason why an infection so usually light in the mother is able to cause a disease so severe in the fetus seems to have an explanation on the fact that toxoplasma increases in virulence when reaching the product as second-step infection. In all five cases, the intensity of the lesions agrees with the severeness of the clinical picture and with the early manifestations following birth. The parasite was identified in the brain in all cases and in some of them, in the liver and lungs.