Seroprevalence and risk factors of Toxoplasma gondii infection among pregnant women.

INTRODUCTION: Toxoplasma gondii is an obligate intracellular parasite affecting a broad range of warm-blooded animals, including humans. Infection acquired during pregnancy can be transmitted to the fetus and leading to serious problems such as spontaneous abortion, stillbirth, or severe mental and/or physical handicaps in the child. The purpose of this study was to investigate the seroprevalence of Toxoplasma infection and related risk factors in pregnant woman. METHODOLOGY: The study enrolled 1200 serum samples of pregnant women from February-November 2017. Then the samples were tested for the presence of anti-T. gondii antibodies (Ab) using enzyme-linked immunosorbent assay. RESULTS: Out of the 1200 samples, 381 (31.7%) and 41 (3.4%) subjects were positive for IgG and IgM Ab, respectively. Among the evaluated risk factors, the seroprevalence of Toxoplasma infection was not related to the occupation in a significant way. However significant relationship was observed with factors such as; contact with soil, cats, consumption of raw washed vegetables, and washed hands before meals. CONCLUSIONS: According to the results, more than two-thirds of pregnant women are susceptible to Toxoplasma infection, hence training health care programs should be provided to prevent infection.

Overview of Apoptosis, Autophagy, and Inflammatory Processes in Toxoplasma gondii Infected Cells.

Toxoplasma gondii (T. gondii) is an obligate intracellular parasite. During the parasitic invasion, T. gondii creates a parasitophorous vacuole, which enables the modulation of cell functions, allowing its replication and host infection. It has effective strategies to escape the immune response and reach privileged immune sites and remain inactive in a controlled environment in tissue cysts. This current review presents the factors that affect host cells and the parasite, as well as changes in the immune system during host cell infection. The secretory organelles of T. gondii (dense granules, micronemes, and rhoptries) are responsible for these processes. They are involved with proteins secreted by micronemes and rhoptries (MIC, AMA, and RONs) that mediate the recognition and entry into host cells. Effector proteins (ROP and GRA) that modify the STAT signal or GTPases in immune cells determine their toxicity. Interference byhost autonomous cells during parasitic infection, gene expression, and production of microbicidal molecules such as reactive oxygen species (ROS) and nitric oxide (NO), result in the regulation of cell death. The high level of complexity in host cell mechanisms prevents cell death in its various pathways. Many of these abilities play an important role in escaping host immune responses, particularly by manipulating the expression of genes involved in apoptosis, necrosis, autophagy, and inflammation. Here we present recent works that define the mechanisms by which T. gondii interacts with these processes in infected host cells.