Toxoplasmosis is caused by Toxoplasma gondii (T. gondii), an obligate intracellular protozoan parasite which belongs to the phylum Apicomplexa. T. gondii was first simultaneously identified in 1908 by Splendore and Nicolle & Manceux infecting rabbits and rodents, respectively. However, it was not until 1937 that Wolf and Cowen reported a human infection with T. gondii of a three days old baby suffering from encephalomyelitis. This first report not only demonstrated that T. gondii could be a human pathogen but also represents the first report of a congenital infection with this protozoon. Since these first reports, there has been growing interest in the biology and epidemiology of T. gondii, especially pertaining to the two most clinically relevant infection situations: congenital infections and those occurring in immunosuppressed individuals. T. gondii stands as one of the most prevalent zoonotic parasites globally, chronically infecting 25–50 % of the worldwide population. However, worldwide seroprevalence varies largely, with rates ranging between 0.5 % and 87 % whereby Africa, South America and Oceania display the highest average seroprevalence rates.1, 2, 3

T. gondii presents two main hosts in its life cycle. Definitive hosts include all felines, whereby the parasite can sexually differentiate and genetically recombine. Cats shed oocyst onto the environment, which upon contact with oxygen rapidly become infectious, both to humans and to other intermediate hosts (that houses the non-sexual stages of the parasite). Upon accidental ingestion of infective oocysts, sporozoites contained within oocysts emerge in the intestine, passing through the epithelial membrane and disseminate generating a widespread acute infection. Acute infection is systemic, with the rapidly dividing life form of T. gondii, the tachyzoite, colonizing virtually any nucleated cell within the host. The acute period of the disease is paucisymptomatic in immunocompetent humans and often goes unnoticed as it resembles a mild cold, characterized by myalgia, mild lymphadenopathy and fatigue.4 Following this period, tachyzoites are mostly cleared out and the latent slow dividing bradyzoite stage persists as tissue cysts in immune privileged sites such as the central nervous system and skeletal muscles.5 Consumption of undercooked meat of other chronically infected intermediate hosts containing tissue cysts constitutes one of the main routes for horizontal human infection.6 Humans may also acquire the infection by the ingestion of contaminated vegetables or water, or by contact with cat feces.7 Also, a primary infection of pregnant women may infect the fetus by transplacental transmission.8

Tissue cysts can persist for the life of an immunocompetent individual without causing clinical symptoms. However, it is well established that chronic infections are of concern due to their potential for reactivation upon immunosuppression. Reactivation of brain cysts can lead to toxoplasmic encephalitis. Ocular reactivation is also frequently documented in immunocompetent individuals whereby persistent cyst reactivation in the eye can lead to increasing retinal damage which may eventually lead to sight loss. Both intermediate and definitive female hosts can also transmit T. gondii to their progeny. In fact, T. gondii constitutes one of the few pathogens with a documented ability to cross the placental barrier in humans, belonging to the infamous TORCH pathogens group (where T stands for “T. gondii”). Primary prevention measures to pregnant women include avoiding eating or handling raw or undercooked meat, washing hands thoroughly after gardening, avoid handling contaminated soil or water or come in contact with cat feces.9 Educational strategies for pregnant women reduce the risk of acquiring the infection.10

In most cases, a prior toxoplasmosis infection protects subsequent pregnancies from transplacental transmission. However, the consequences for fetal infection vary according to the gestational period, the fetal age, the inoculum, and the genetic background of both the host and the parasite.11,12 In general, the earlier the gestational period, the lower the probability of transmission, but if it occurs, the probability of pregnancy loss or severe fetal neurological or ocular damage is very high. On the other side, the higher the gestational age, the increasing vascularity makes the placental barrier more and more permeable, increasing the probability of transmission to the fetus, but clinical manifestations in the fetus tend to be less severe.8,13,14 Specifically, the probability of transmission starting at week 13 of gestational age was estimated at 15 %, increasing to 44 % at week 26 and 71 % at week 36.15

Should infection occur, provided the detection occurs before week 18th of gestation, a regime of spiramycin reduces the likelihood of fetal transmission. Cohort studies have shown that a large percentage of treated pregnancies will result in fetal protection. Considering this, it becomes mandatory to both timely diagnose a primo infection during pregnancy and to predict the approximate time of infection. T. gondii detection can be safely carried out during pregnancy using serological survey type tests.16,17