by Michele Brown
Hey, all you pet lovers out there! This article is not to frighten you away from having a cat or two, but nowhere is the expression "an ounce of prevention is worth a pound of cure" more applicable than when one discusses toxoplasmosis in pregnancy. Below you'll find tips for pregnant women on how to reduce the chances of having their baby acquire congenital toxoplasmosis.
Why? Because toxoplasmosis is a devastating disease for the fetus and the newborn throughout the world. It often goes completely unrecognized but can be prevented with the proper precautions. Roughly 400 to 4,000 cases occur per year in the United States. Women are routinely tested in high risk countries like France, Austria, and Italy but the American College of Obstetrics and Gynecology does NOT routinely recommend screening in the United States.
Therefore, it is essential that all obstetricians take careful histories from their pregnant patients to determine if they are likely to have acquired this disease. If the patient clears the toxoplasmosis screening, the physician should further instruct specific rules the pregnant woman should follow to avoid getting infected.
Toxoplasmosis is caused by ingestion of cysts from the protozoan Toxoplasmosis gondii. The primary host of the parasite is cats which excrete the oocyte in the feces. Humans become infected by eating raw or undercooked meats containing the oocyte, ingesting oocytes from soil where unwashed fruits and vegetables have grown, or from contact with cat litter. The oocytes can remain infectious after being deposited for over 1 year. After ingestion of the oocytes, infection can occur between 4 and 21 days.
The protozoan after ingestion will invade muscle, heart, liver, spleen, lymph nodes, and the central nervous system. This can result in inflammation and cell death. Most normal adults with no immune problems go without symptoms and the disease is self limited. Occasionally one will have fever, swollen lymph nodes, and fatigue. If a woman is infected prior to pregnancy (greater than 6 months), transmission generally does not occur to the fetus except when her infection becomes reactivated due to a change in her immune status. (taking steroids, or she develops AIDS).
If a woman is pregnant and acquires the disease, the protozoan can travel through the placenta and infect the fetus resulting in mental retardation, seizures, malformations, blindness, deafness, and death. There is a classic triad of chorioretinitis (inflammation of the choroid and the retina of the eye), calcifications within the brain, and hydrocephalus (fluid accumulation within the brain) that occurs in less than 10% of cases.
Many infected newborns have no symptoms at birth (70–90%) and manifestations may not occur until the second or third decade of life where one can see learning and visual disabilities, retinal damage and loss of vision. Some infants do show signs of infection at birth with fever, enlargement of the liver and spleen, and rash. Other cases are suspected when ultrasound findings reveal the presence of structural abnormalities. Risk of the fetus acquiring the infection is lowest when maternal infection occurs first trimester and highest when infection occurs third trimester. However, infection tends to be worse if it occurs first trimester.
Infection is detected by a blood test that picks up antibodies to the protozoan (IgG and IgM). Using the results from these antibody tests, one can determine if an infection was never present, acquired before the pregnancy, or contracted during the pregnancy. Amniocentesis can also be performed to detect fetal infection. The earlier the blood test is obtained, the more helpful it will be in determining the timing of an infection. Treatment is with spiramycin early in the pregnancy or after 18 weeks with pyrimethamine-sulfadiazine and folinic acid since this crosses the placenta more readily. It is recommended that infected newborns should receive treatment, regardless of symptoms for up to a year since it is felt that treatment may improve the outcome.