Toxoplasmosis in Pregnancy
from Clinician Reviews ®
Carol Soto, MS, ANP
Abstract and Introduction
Congenital toxoplasmosis, a disease that can be transmitted through the placenta, can cause mental retardation, blindness, seizures, or even death. While infected infants may be asymptomatic at birth, clinical manifestations can develop in the following months to years. In addition to aggressively fighting infection in pregnant women, medical practitioners should initiate primary, secondary, and tertiary measures to help prevent toxoplasmosis and minimize its potentially devastating effects.
Toxoplasmosis, caused by the protozoan parasite Toxoplasma gondii, ranks third in the United States for deaths caused by food-borne pathogens. Toxoplasmosis can be transmitted across the placenta in women who have the infection -- acquired either for the first time or recurring (especially in persons who are immunocompromised) -- during pregnancy.[1-3] Approximately one out of every 1,000 pregnant women becomes infected, resulting in anywhere from 400 to 4,000 cases of congenital toxoplasmosis each year in the United States.[1,4]
There is a less than 5% chance of transmission to the fetus if maternal infection occurs before the fifth week of pregnancy. As the pregnancy progresses, transmission rates increase to more than 80%.[2,4,5] Ironically, the risk of clinically severe congenital toxoplasmosis is greatest if disease transmission occurs during the first trimester. Mothers first exposed to Toxoplasma infection more than six months before becoming pregnant are not likely to pass the infection to their fetuses.
Many infants with congenital toxoplasmosis do not exhibit visible signs of infection at birth. However, serious clinical manifestations can emerge during childhood and advance through age 20 years. Infants with untreated congenital toxoplasmosis can develop mental retardation, seizures, and significant cognitive and motor deficits.[6-10] Newborns who do show symptoms often have neurologic anomalies (ie, hydrocephaly, microcephaly, or intracranial calcification).
The T gondii life cycle has three phases. During the active stage of infection, trophozoites invade and multiply in the blood and lymphatic cells of birds and mammals. Once the host develops immunity, the second stage begins. During this time, trophozoites evolve into bradyzoites that form cysts in the host's skeletal and heart muscles, brain, and eyes. In immunocompromised persons, dormant cysts can reactivate, causing recurrence of infection.
The third life cycle of T gondii, the sexual stage, occurs only in cats. Cats become infected by eating other infected mammals -- typically mice and rats -- or raw meat. Oocysts formed in the feline small intestine are excreted by the millions for one to three weeks after ingestion. Oocysts become infectious three days after excretion and can remain so for as long as one year in moist, shaded sand or soil. Birds and mammals become infected through contact with cat feces. Cockroaches, flies, and earthworms can carry oocysts deposited in soil onto fruits and vegetables.
Managing Human Infection
Humans can contract toxoplasmosis by ingesting cat excrement or inhaling aerosolized, decayed cat feces from the cat litter box or infected sand or soil. Toxoplasmosis can also be transmitted by eating raw or inadequately cooked pork, lamb, beef, and, occasionally, chicken.[1,5] Non-pasteurized dairy products and fruits and vegetables with oocysts on the surface may also be a source of infection.
Primary, secondary, and tertiary management strategies can help prevent, eradicate, or reduce maternal infection and lessen the effects in the newborn. For prevention -- the primary measure -- clinicians should consider establishing a toxoplasmosis prevention program for pregnant patients, with a focus on teaching certain practices known to reduce risk (see Table 1,[1,11]). Secondary measures involve T gondii screening and detection for both mother and fetus during pregnancy. The twofold challenge of treatment (ie, the tertiary measure) is to minimize disease progression during pregnancy and support any physical and developmental difficulties experienced by infants following birth.
Screening and Diagnosis
Ideally, Toxoplasma screening should begin before a woman plans to become pregnant as there is no vaccination available to protect humans against infection. If this is not possible, the health care provider should assess lifestyle factors and habits of the pregnant patient that may pose risk. This information could be valuable later in determining when T gondii infection occurred, since some patients harbor antibodies for six months to one year after the initial infection.[1,4]
A pregnant woman who presents with enlargement of the posterior cervical lymph nodes, malaise, fatigue, headaches, muscle aches, fever, chills, and sore throat, and who is seronegative for mononucleosis, should be tested for toxoplasmosis infection. However, in approximately 60% to 90% of cases, the patient may show no signs of disease.[1,4]
To confirm the diagnosis of a recent infection, both immunoglobulin M (IgM) and immunoglobulin G (IgG) assays should be performed immediately, then repeated in three weeks. A woman with a recent infection will show either conversion from a negative to a positive IgM titer (usually as much as a fourfold increase) or the presence of IgM antibodies and a slowly rising IgG titer. While commercial test kits for Toxoplasma-specific IgG and IgM antibodies are available, they may not be sufficiently specific.
Amniocentesis with a polymerase chain reaction assay for the detection of T gondii DNA in the amniotic fluid is an accurate and quick way to determine whether there has been transplacental transmission of Toxoplasma infection.[4,9] Ultrasonography may be performed to aid in the diagnosis, but it is useful only to determine the presence of intracranial calcifications or hepatomegaly -- symptoms that usually indicate late fetal infection.
In the newborn, an IgM-positive assay is usually diagnostic of congenital toxoplasmosis, although a Toxoplasma-specific immunoglobulin A assay may be more sensitive. Cranial CT scans, examination of the cerebral spinal fluid, and examination of the placenta through tissue inoculation will also aid in accurately diagnosing the infected newborn.
In immunocompetent persons other than pregnant women, toxoplasmosis treatment is generally not indicated unless symptoms (eg, swollen glands, muscle aches) are severe. Once it has been established that a pregnant woman has the infection, however, treatment should be initiated immediately.
Infection in the mother does not necessarily indicate that the fetus has been or will be infected. Research indicates that there may be a window of time in which to initiate treatment for a recent infection before the disease is transmitted to the fetus.
For acute infections in pregnant women, administering spiramycin from the first trimester until delivery has been shown to reduce the risk of fetal infection by 60%. Presently, this drug is not known to have a teratogenic effect.[4,5,12]
If fetal infection has been confirmed by radiographic and serologic testing, spiramycin should be prescribed along with pyrimethamine, sulfadiazine, and leucovorin calcium. This combination therapy should not be initiated until after 16 weeks of pregnancy because of pyrimethamine's teratogenic potential.[5,12] Leucovorin is given to counteract the bone marrow suppression caused by pyrimethamine use. It is also important to monitor the mother's complete blood cell count and platelet count once or twice weekly to screen for possible pyrimethamine toxicity.
If a newborn receives a diagnosis of congenital infection, treatment consists of sulfadiazine and pyrimethamine for at least one year. Leucovorin is administered for as long as pyrimethamine is given. Oral corticosteroids can be added to the regimen to reduce inflammation, especially for severe ocular toxoplasmosis.
Case management including a multidisciplinary team approach is most likely to help patients function at optimal levels. All infected children should receive appropriate treatment, as the prognosis for those who are treated pharmacologically (for at least one year) is much more positive than for children who are not treated.
Toxoplasmosis is a worldwide parasitic infection that can infect humans as well as animals. For any patient who is not pregnant, the disease can be treated successfully without any risk of long-term clinical sequelae. However, if an infected woman becomes pregnant, her fetus is at risk for acquiring the infection and developing severe congenital abnormalities. Medical practitioners who care for pregnant women can help improve outcomes by providing comprehensive case management.
Table 1. Strategies to Prevent Toxoplasma Infection in Pregnant Women
- Centers for Disease Control and Prevention. Preventing congenital toxoplasmosis. MMWR Morb Mortal Wkly Rep. 2000;49(RR02):57-75.
- Dunn D, Wallon M, Peyron F, et al. Mother to child transmission of toxoplasmosis: risk estimates for clinical counselling. Lancet. 1999;353:1829-1833.
- Centers for Disease Control and Prevention. Fact sheet: toxoplasmosis. Accessed May 21, 2002.
- Grant A. Varicella infection and toxoplasmosis in pregnancy. J Perinat Neonatal Nurs. 1996;10:17-29.
- Foulon W, Villena I, Stray-Pedersen B, et al. Treatment of toxoplasmosis during pregnancy: a multicenter study of impact on fetal transmission and children's sequelae at age 1 yr. Am J Obstet Gynecol. 1999;180:410-415.
- Holliman RE. Congenital toxoplasmosis: prevention, screening and treatment. J Hosp Infect. 1995;30:179-190.
- Heitman BB, Irizarry AF. Recognition and management of toxoplasmosis. Nurse Pract. 1997;22:75, 79-82, 85-86.
- Lebech M, Anderson O, Christensen NC, et al, for the Danish Congenital Toxoplasmosis Study Group. Feasibility of neonatal screening for Toxoplasma infection in the absence of prenatal treatment. Lancet. 1999;353:1834-1837.
- Foulon W, Pinon JM, Stray-Pedersen B, et al. Prenatal diagnosis of congenital toxoplasmosis: a multicenter evaluation of different diagnostic parameters. Am J Obstet Gynecol. 1999;181:843-847.
- Roizen N, Swisher CN, Stein MA, et al. Neurologic and developmental outcome in treated congenital toxoplasmosis. Pediatrics. 1995;95:11-20.
- Juckett G. Pets and parasites. Am Fam Physician. 1997;56:1763-1774, 1777-1778.
- Rosenblatt JE. Antiparasitic agents. Mayo Clin Proc. 1999;74:1161-1175.
- Guerina NG, Hsu HW, Meissner HC, et al, for the New England Regional Toxoplasma Working Group. Neonatal serologic screening and early treatment for congenital Toxoplasma gondii infection. N Engl J Med. 1994;330:1858-1863.
Clinician Reviews 12(6):51-56, 2002. © 2002 Clinicians Group, LLC. Used With Permission.
If you like this article, we'd be honored if you shared it using the button below.