Toxoplasmosis is an infection that pregnant females can get from a microscopic parasite. This parasite is called Toxoplasma gondii. The protozoan parasite Toxoplasma gondii, an obligate intracellular eukaryotic pathogen of the phylum Apicomplexa may cause toxoplasmosis in many warm-blooded animals, including humans. Trans-placental passage of the parasite causes congenital toxoplasmosis. Transmission frequency and severity of disease vary with gestation time: during the first weeks, vertical transmission is of low rate, although if it occurs, it causes major damage to the embryo. The transmission frequency increases to near 80% by the end of pregnancy, but the proportion of ill new borns is low. The changes in endocrine phenomena occurring during pregnancy, as well as the size and maturity of the placenta and of the embryonic/fetal immune response certainly affect the ability to be protected from invasion or to fight infection. The size of the inoculum is also relevant for congenital infection risk and disease severity. Besides, the genetic background of the mother and the product is likely to influence outcome. Recent investigations have shown surprising phenomena; that is, molecules and cells that protect the mother might favor vertical transmission. Few direct data are available, but indirect evidence points to several candidate polymorphic host immune response genes that may influence fetal infection or clinical outcome of the product.

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Toxoplasma gondii (T. gondii) is considered as one of the most successful parasites in the world. This success is first illustrated by its worldwide distribution, from arctic to hot desert areas, including isolated islands and in cities. T. gondii is also among the most prevalent parasites in the global human population, with around one third of the population being infected. Finally, it is able to infect, or be present in, the highest number of host species: any warm-blooded animal may act as an intermediate host, and oocysts may be transported by invertebrates such as filtrating mussels and oysters. Beyond this ubiquitous distribution lies a fascinating transmission pattern: simply saying that T. gondii has a complex life cycle does not encompass all transmission routes and modes that can be used by the parasite to pass from definitive hosts (DHs), where sexual reproduction occurs, to intermediate hosts (IHs). The “classicalâ€Â complex life cycle uses felids (domestic and wild-living cats) as DHs and their prey as IHs. Felids are infected by eating infected prey and host the sexual multiplication of the parasite. They excrete millions of oocysts that sporulate in the environment. Sporulated oocysts may survive during several years and may disperse through water movements, soil movements and micro fauna. Ingesting a single sporulated oocyst may be sufficient to infect an IH and begin the asexual reproduction phase. This classical life cycle thus relies on a prey-predator relationship and on environmental contamination, like other parasites, e.g., Echinococcus multilocularis. However, beside this classical cycle, T. gondii shows specific abilities that allow it to use “complementaryâ€Â transmission routes. During the phase of asexual multiplication, tachyzoites may disseminate to virtually any organ within the IH, in particular to muscles, brain, placenta, udder and gonads. Asexual forms are then infectious to new hosts, thus direct infection among IH is possible by several routes which epidemiological importance has to be discussed: vertical transmission through the placenta, pseudo-vertical transmission through the milk, and sexual transmission through the sperm. In humans, T. gondii may also be transmitted during blood or organ transplant. Finally, the infectivity of asexual forms towards new IHs entails the ability for the parasite to be transmitted among IHs by carnivory. This transmission route is estimated to cause the majority of cases in humans, although people may also get contaminated by ingesting oocysts after a contact with contaminated soil, water, vegetables or cat litter. All the possible transmission routes among IH make the parasite able to maintain its life cycle, at least during a few generations, in the absence of DH and without environmental stage. Moreover, at a high dose, oocysts from the environment may also be infectious for DHs, thus the parasite may bypass the IH and use a DHs-environment cycle. The infectivity of oocysts towards cats is relatively low thus the importance of this cycle may be questioned. However, taken together, these observations suggest that T. gondii may theoretically have two distinct life cycles, one among IHs and the other one between DHs and environment. Moreover, in IHs, the infection of the brain results in several specific clinical manifestations, modifications of host behaviour and life history that influence transmission. As a result of its presence in the brain of IHs, T. gondii manipulates host behaviour in two ways, by specifically increasing attractiveness of cat odours to rodent IHs, thus favouring transmission from IH to DH, and by increasing the sexual attractiveness of infected males, which favours sexual transmission. These numerous capacities of transmission clearly allow T. gondii to be distributed worldwide. However, this does not mean that the risk of toxoplasmosis is identical everywhere. On the contrary, a highly structured pattern of infection can be demonstrated, for example by comparing the level of infection of different human populations.
Signs and Symptoms
Many patients have developed this disease but have had similar symptoms to those of flu or mononucleosis. These symptoms include body aches, swollen lymph nodes, headaches, fever, fatigue and occasionally sore throats. When a female develops this disease prior to or during pregnancy there is about 30% chances that the infection can be passed unto the baby. The baby is at risk of contracting the disease mostly if a female becomes infected in the third trimester and least on the first trimester. Yet if the infection occurs in the early stages of pregnancy, the outcomes are more serious. Many pregnancies can result in stillbirth or miscarriage, and children who survive are born with seizures, enlarged liver or spleen, jaundice, anaemia, bruises and eye infections. A small number of babies that are born with the disease show signs of the disease at birth. Most of those infected develop signs and symptoms until they are on their teens or later. Also babies can develop serious problems such as hydrocephalus, intracranial calcifications, intellectual disabilities, motor and developmental delays, and hearing loss.
Diagnostic Tests:
When acute T. Gondii infection is suspected in pregnant women, toxoplasmosis is diagnosed on the basis of antibody detection. IgG and IgM antibody levels rise generally one to two weeks of infection. However when using the antibody detection it does not distinguish between whether the infection is recent or it was acquired in the distant past. When a woman is found to be infected, the second step is to determine if the baby or fetus is infected. PCR testing of amniotic fluid is used to diagnose congenital toxoplasmosis. Babies can be tested using amniocentesis or ultrasound scan.
Treatment:
Once diagnosed with Toxoplamosis a treatment with spiramycin (rovamycine) is initiated. If the fetus is confirmed through amniocentesis, the woman can switch to pyrimethamine (daraprim) and sulfadiazine after the first trimester. When women take pyrimethamine, accompanied with it is folinic acid (leucovorin). It protects the bone marrow from the suppressive effects of pyrimethamine. The drug is used to lessen the severity of the disease, but it does not undo previous damage done.
Prevention:
In order to prevent contracting this disease, pregnant woman should eat fully cooked meat. They should keep kitchen utensils sanitized by washing it with hot soapy water after having contact with raw meat; also they should wear gloves when gardening or touching soil, avoid changing cat litter pans, and be informed about prevention of toxoplasmosis.