Toxoplasmosis is an infection caused by the microscopic parasite Toxoplasma gondii. While infection in a healthy adult often results in no symptoms or a mild, self-limiting illness, acquiring the parasite during pregnancy is a concern for the developing fetus. The primary worry is congenital infection, where the parasite crosses the placenta, potentially leading to serious health issues for the child. Understanding the risks and pathways of infection allows expectant parents to take informed, protective steps.
Assessing the Risk of Maternal Infection
The probability of acquiring an acute T. gondii infection during pregnancy is generally low in industrialized nations, estimated at approximately 0.5% in Europe and 1.1% globally. A pregnant person is only at risk of transmitting the infection to the fetus if they experience a primary, or first-time, infection while pregnant. Serological testing determines immune status: seronegative individuals are susceptible, while seropositive individuals have prior immunity that protects the fetus. In the United States, seroprevalence is around 9.1% among women of childbearing age, meaning most remain susceptible.
The timing of the primary maternal infection dictates both the risk of transmission and the severity of the fetal outcome. The risk of the parasite crossing the placenta is lowest in the first trimester, with transmission rates typically between 10% and 15%. However, if transmission does occur early in gestation, the resulting congenital disease is often the most severe, with the highest risk of fetal loss or significant long-term damage.
Conversely, the probability of transmission increases significantly as the pregnancy progresses, reaching 30% in the second trimester and rising to 60% or more in the third trimester. Although the parasite is more likely to be transmitted later in the pregnancy, the severity of the resulting congenital infection is generally lower. Infants infected in the third trimester are often asymptomatic at birth, though they remain at risk for developing complications years later.
Primary Sources of Transmission
Humans acquire the T. gondii parasite through three main routes. The most common source of infection in some regions, including the United States, is the consumption of raw or undercooked meat. This tissue, particularly pork, lamb, or venison, can contain dormant cysts of the parasite, known as bradyzoites.
Another significant route is the ingestion of food or water contaminated with oocysts, the environmentally resistant form of the parasite. Cats are the only definitive hosts where the parasite reproduces sexually, and they shed millions of unsporulated oocysts in their feces for a short period. These oocysts then contaminate the soil, sand, and water sources.
The oocysts become infectious, or sporulate, after being shed into the environment, typically taking between one and five days depending on temperature and humidity. This explains why exposure to contaminated environmental sources, such as gardening in soil where cats have defecated or consuming unwashed produce grown in that soil, is a mechanism of transmission. Direct contact with a cat’s litter box is a less frequent cause of human infection than contaminated food but remains a potential source of exposure.
Essential Prevention Strategies
Controlling exposure relies on adopting specific food safety protocols. All meat, including poultry, should be cooked to the minimum internal temperature to ensure the tissue cysts are destroyed. Ground meats should reach 160°F (71°C), and whole cuts of meat should reach 145°F (63°C) followed by a three-minute rest.
When preparing food, it is important to avoid cross-contamination by thoroughly washing cutting boards, utensils, and countertops that have come into contact with raw meat, poultry, or unwashed produce. Fruits and vegetables should be washed or peeled before consumption to remove any surface contamination from oocysts. Untreated drinking water and unpasteurized milk should be avoided entirely.
Managing environmental exposure, particularly to soil and cat feces, is also necessary. When gardening, working with soil, or handling sand from a sandbox, wearing gloves is recommended, followed by thorough hand washing with soap and water. Since oocysts only become infectious after 24 to 48 hours in the environment, the litter box should be cleaned daily.
Ideally, a non-pregnant member of the household should handle the daily litter box cleaning to eliminate the risk of exposure. If the pregnant person must clean the box, wearing gloves and washing hands immediately afterward offers protection. Keeping cats indoors and feeding them only commercial cat food, rather than raw meat, also helps prevent them from acquiring and shedding the parasite.
Diagnosis and Potential Fetal Outcomes
Diagnosis of maternal infection typically begins with blood tests measuring two types of antibodies: Immunoglobulin G (IgG) and Immunoglobulin M (IgM). IgG indicates past exposure and immunity, while IgM suggests a recent or acute infection. If results are equivocal or show a positive IgM, a subsequent test, such as an IgG avidity test, may be used to estimate the approximate time of infection.
If an acute maternal infection is confirmed, further testing is offered to determine if the parasite has been transmitted to the fetus. The standard method for this is an amniocentesis, which involves testing the amniotic fluid for the parasite’s DNA using a Polymerase Chain Reaction (PCR) test. This procedure is generally performed after 18 weeks of gestation and at least four weeks after the estimated time of maternal infection.
Congenital toxoplasmosis can result in a wide range of outcomes for the infant, with many showing no immediate symptoms at birth. However, a small percentage of infected infants may present with the classic triad of symptoms: hydrocephalus (fluid in the brain), chorioretinitis (inflammation of the retina), and intracranial calcifications.
Treatment is initiated to reduce the risk of transmission to the fetus or lessen the severity of the disease if the fetus is already infected. The antibiotic spiramycin is often used during pregnancy when maternal infection is confirmed but fetal infection is not, as it concentrates in the placenta to prevent transmission. If fetal infection is confirmed or the maternal infection occurred later in pregnancy, a combination therapy of pyrimethamine and sulfadiazine, along with folinic acid to mitigate side effects, is typically used.