The apicomplexan parasite Toxoplasma gondii is remarkable in several aspects, since it is a protozoan that infects most nucleated cells in many warm-blooded animals, worldwide. Although the cellular immune response against T. gondii is critical for infection control, antibodies may either enhance or block protective mechanisms, and even mediate immunological damage, directly or indirectly. Since cytokines regulate the class/subclass switch, antibodies may also be the biomarkers of protective or pathological cellular immune events. There is a scientific and clinical interest in the presence of natural and autoreactive antibodies, as well as in the 'chronic' immunoglobulin M (IgM) response and the post-treatment 'rebound'. Another interesting aspect is compartmentalization; certain immunoglobulins may uniquely be found in specific host fluids. Local synthesis has been demonstrated, but antibodies may also traverse several cell layers, like the blood-brain and haemato-ocular barriers, and the placenta. In some instances, Fc receptors (FcRs) facilitate transport and may even have a concentrator effect, which can be related to resistance or pathology. These aspects of the humoral response against T. gondii are reviewed in the present paper.

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Toxoplasmosis is a parasitic zoonosis distributed worldwide, caused by the ingestion of contaminated water/food with the parasite Toxoplasma gondii . If a pregnant woman is infected with this parasite, it may be transmitted to the fetus and produce ocular, neurological, or systemic damage with variable severity. The strength and profile of mother's immune response have been suggested as important factors involved in vertical transmission rate and severity of clinical outcome in the congenitally infected fetus. The aim of this work was to evaluate a possible relation between the mother's immune response during pregnancy and congenital transmission to the fetus. We obtained peripheral blood from T. gondii infected pregnant woman and tested it for anti T. gondii (IgG1, IgG2, IgG3, IgG4, and IgA) in serum. Peripheral blood mononuclear cells (PBMCs) were isolated to analyze the in vitro effect of soluble T. gondii antigens on proliferation and production of cytokines. We found that IgG2-4 and IgA antibodies and lymphocytes proliferation, especially CD4 + , CD8 + , and CD19 + were positive in a higher proportion of cases in transmitter than in non-transmitter women. Furthermore, IgG2-3 and IgA anti- Toxoplasma antibody levels were higher in those mothers who transmitted the infection than in those who did not. Interestingly, a higher proportion of positive cases to IFN-γ and negatives to the immunoregulatory cytokine TGF-β, were related to T. gondii vertical transmission. Our descriptive results are consistent with the paradoxical previous observations in murine models of congenital toxoplasmosis, which suggest that an increased immune response that protects the mothers from a disseminated or severe disease, and should protect the fetus from infection, is positively related to parasite transmission.

Global warming has had serious implications on dispersion of infectious diseases like toxoplasmosis. Since the frequency of Toxoplasma gondii largely depends on climatic conditions, we studied its prevalence by means of 3599 samples of the National Health Survey 2000 (NHS-2000) and 2916 of the National Health and Nutrition Survey 2006 (NHNS-2006) serum banks, obtained from 1-98 year old subjects of both genders and all states of Mexico. Anti-T.gondii IgG antibodies were determined by ELISA and confirmed by western blot. Crude, epidemiologically weighted and diagnosis-performance-adjusted prevalence values were calculated. Seroprevalence changes were compared between both surveys and among regions (north, center and coast). Also, correlations between changes in temperature or humidity and those in prevalence were measured. National crude prevalence was 60.1% and 62.6% for NHS-2000 and NHNS-2006, respectively. Weighted and adjusted values were 62.5% and 40.0% for NHS-2000, and 63.7 and 43.1% for NHNS-2006. Coastal states and children presented the largest increases between surveys, while the center of the country showed a decrease. An apparently higher prevalence of T. gondii infection was observed in both surveys compared to that performed in 1987, while a geographical re-distribution was found from 2000 to 2006, with a positive correlation between temperature and frequency deltas in 21 states where prevalence increased.

Objective: To detect immunoglobulin M (IgM) anti-Toxoplasma gondii antibodies and determine immunoglobulin G (IgG) titer and avidity in filter paper-embedded blood (FPEB) samples of pregnant women.Study Design: A total of 100 FPEB samples of pregnant women (30 positive and 70 negative) were analyzed for anti-T. gondii-specific IgM antibodies. Eleven and nine pairs of serum and FPEB samples were used to standardize IgG titration and avidity, respectively. Then, the correlation of avidity results was determined with 23 serum/FPEB pairs from IgG-positive cases.Result: IgM detection in FPEB was 92% sensitive and 100% specific. The titration of IgG antibodies in FPEB correlated with that of serum (r X0.9). Significant difference in avidity between the acute and the undetermined/chronic cases was observed in both samples. As expected, no correlation was found between IgM levels and avidity. Conclusion:The FPEB is useful to infer infection phase, and thus to speed clinical decisions in congenital toxoplasmosis management.

Gómez-Chávez et al. The Immune Response in Human Congenital Toxoplasmosis to children who developed mild clinical complications. Our results suggest that a distinctive, not regulated, proinflammatory immune response might favor T. gondii vertical transmission and the development of severe clinical manifestations in congenitally infected newborns.

A 7-year-old Mexican boy with end-stage cirrhosis underwent liver transplantation and was maintained with cyclosporine and prednisolone. No specific data about Toxoplasma gondii or cytomegalovirus (CMV) infections in the cadaver donor were available. The recipient was seronegative for Toxoplasma, but CMV-IgG positive before transplantation. Ganciclovir was administered for prophylaxis during 3 months, but 5 months later he presented with icterus and increased transaminases. Acute transplant rejection was ruled out by biopsy. A seroconversion for T. gondii IgM and IgG and a small increase in CMV-IgM antibodies were observed, although the CMV-polymerase chain reaction (PCR) was negative. Ganciclovir was re-started, and the patient improved, but 6 months later he relapsed, and chorioretinitis lesions compatible both with T. gondii and CMV infections appeared. Pyrimethamine, sulfadiazine, folinic acid, and ganciclovir were administered. The boy showed favorable clinical improvement and remained stable for 12 months. Then, new retinal CMV lesions appeared in both eyes and the PCR for CMV became positive; therefore, the patient received a new regimen of ganciclovir, and clinically improved. From these data we concluded that the child presented a reactivation of CMV and a primary infection with T. gondii after transplantation.

Toxoplasma gondii disseminates and causes congenital infection by invasion of the endothelial cells. The aim of this study was to analyze the ability of two strains to invade two endothelial cell types. Tachyzoites of the RH and ME49 strains were expanded in Balb/c and C57BL6-RAG2-/- mice, respectively. Tachyzoites were harvested from 72 h Vero cell cultures and incubated for 30 min to 4 h at 10:1 parasite/cell ratio in 24-well plates, containing monolayers of either HMEC-1 line or human umbilical cells (HUVECs). The number of infected cells and parasitic vacuoles per infected cell were counted in Wright stained slides. A slow increase in the proportion of infected cells occurred but varied according to cell type-parasite strain combination: ME49 tachyzoites invaded up to 63% HMEC-1 cells, while RH parasites infected up to 19% HUVECs. ME49 and RH tachyzoites invaded 49 and 46% HUVECs and HMEC-1 cells, respectively. Reinvasion and formation of new parasitophorous vacuoles of infected cells was more frequent than invasion of noninfected cells. The results support that the factors influencing invasion, and thus dissemination and vertical transmission, are parasite type, host cell type/subtype, and activation state. Interestingly, T. gondii virulence does not seem to relay on its invasion efficiency, but probably on replication speed.