Toxoplasmosis Pranita Tamma Pediatrics in Review 2007;28;470 DOI: 10.1542/pir.

28-12-470

The online version of this article, along with updated information and services, is located on the World Wide Web at: http://pedsinreview.aappublications.org/content/28/12/470

Pediatrics in Review is the official journal of the American Academy of Pediatrics. A monthly publication, it has been published continuously since 1979. Pediatrics in Review is owned, published, and trademarked by the American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk Grove Village, Illinois, 60007. Copyright 2007 by the American Academy of Pediatrics. All rights reserved. Print ISSN: 0191-9601.

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in brief

In Brief
Toxoplasmosis
Pranita Tamma, MD Johns Hopkins University School of Medicine Baltimore, MD sults in the death of cells and acute inammatory reactions. In adolescents and adults, the severity of T gondii infection is correlated with the immune status of the infected person. Infections in immunocompetent hosts are asymptomatic or can result in lymphadenopathy, fever, and malaise. Such symptoms usually resolve within weeks to months without treatment. Infection in immunocompromised patients can be severe. Immunosuppression can result in reactivation of preexisting latent T gondii infections that most often involve the CNS. Women infected with T gondii prior to conception, with rare exception, do not transmit the infection to their fetuses because of protection of prior immunity. Unfortunately, this lack of transmission is not true for women infected during pregnancy. The risk of congenital disease is the lowest (10% to 25%) when acute maternal infection occurs during the rst trimester and the highest (60% to 90%) when maternal infection occurs during the third trimester. However, the severity of the disease is worse if infection is acquired in the rst trimester. Acute infections in pregnant women can cause serious health problems in the fetus if the parasites are transmitted. An estimated 400 to 4,000 cases of congenital toxoplasmosis occur in the United States per year. The spectrum of congenital toxoplasmosis includes mental retardation, seizures, blindness, and death. The classic triad of chorioretinitis, intracranial calcications, and hydrocephalus is present in fewer than 10% of infected infants. Most newborns infected with T gondii are asymptomatic at birth (70% to 90%). Any clinical manifestations are primarily nonspecic and include microcephaly, seizures, maculopapular rash, hepatosplenomegaly, jaundice, thrombocytopenia, and rarely, generalized lymphadenopathy. The manifestations of congenital toxoplasmosis may not become apparent until the second or third decade of life. Up to 80% of affected people have learning and visual disabilities later in life. Chorioretinitis can result in substantial retinal damage and loss of vision in up to 27% of congenitally infected adolescents and adults. Approximately 15% of women of child-bearing age in the United States have laboratory evidence of infection with T gondii, making about 85% susceptible to infection when pregnant. The most common method of diagnosis is based on antibody detection. In acute infection, concentrations of immunoglobulin M (IgM) antibodies generally rise within 1 to 2 weeks of infection and have been reported to persist for up to 18 months. IgG appears after IgM and persists at low concentrations for the remainder of a persons life. The sensitivity and specicity of antibody testing range from 93% to 100% and 77% to 99%, respectively. Because of the poor specicity and potential for false-positive results, positive IgM results should be conrmed by a Toxoplasma reference laboratory before treatment with potentially toxic drugs is considered. The Sabin Feldman dye test is considered the gold standard for diagnosis. This test is performed only in reference laboratories and detects either a change in antibody titers over a 3-week period or a signicantly high single antibody titer. For identication of T gondii intrauterine infection, polymerase chain reaction (PCR) testing

Author Disclosure Drs Tamma and Serwint did not disclose any nancial relationships relevant to this In Brief.

Congenital Toxoplasmosis: A Review. Jones J, Lopez A. Obstet Gynecol Surv. 2001;56:296 305 Toxoplasmosis: Beyond Animals to Humans. Sukthana Y. Trends Parasitol. 2006;22:137142 Preventing Congenital Toxoplasmosis. MMWR Morbid Mortal Wkly Rep. 2000;49(RR02):5775 Congenital Toxoplasmosis-Prenatal Aspects of Toxoplasma gondii Infection. Rorman E, Zamir CS. Reproduc Toxic. 2006;21:458 472

Toxoplasmosis is caused by infection with the protozoan Toxoplasma gondii. Domestic and feral cats are the denitive hosts of T gondii. During acute infections, cats excrete oocytes, which can remain infectious for about 1 year. Humans can become infected by eating raw or inadequately cooked meat containing oocytes. People also can ingest oocysts inadvertently that cats have passed in their feces. Such exposure may occur from contact with cat litter boxes, contamination with soil from gardening, or the eating of unwashed fruits or vegetables. The incubation period in adults ranges from 5 to 23 days. In the acute stage, T gondii invades many cell types, including muscle, heart, liver, spleen, lymph nodes, and the central nervous system (CNS). Cell invasion re470 Pediatrics in Review Vol.28 No.12 December 2007

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in brief

of amniotic uid can be used; this methodology has a sensitivity of 94% and specicity of 100%. T gondii PCR also can be used to detect the organism in cerebrospinal uid, with sensitivity ranging from 50% to 100% and specicity from 97% to 100%. Because congenital toxoplasmosis is so uncommon in the United States, The American College of Obstetricians and Gynecologists does not recommend routine screening. However, it seems prudent to screen pregnant women for acute toxoplasmosis if there are suspicious ultrasonographic ndings in the fetus, such as hydrocephalus, intracranial calcications, microcephaly, fetal growth restriction, ascites, or hepatosplenomegaly. In addition, human immunodeciency virus-infected pregnant women should be screened for toxoplasmosis. In the postnatal period, the diagnosis of congenital toxoplasmosis may be strongly suggested by the history and physical examination ndings. Ophthalmologic, auditory, and neurologic examinations as well as a lumbar puncture for T gondii PCR and a head computed tomography scan should be performed if the diagnosis is suspected. Treatment of toxoplasmosis in immunocompetent persons other than pregnant women generally is not indicated unless symptoms are severe or persistent. Spiramycin is used in many parts of the world for the prevention of placental infection. However, sys-

tematic reviews have found insufcient evidence to judge this therapy, and it is not currently approved by the United States Food and Drug Administration. If toxoplasmosis is diagnosed prenatally in the fetus, most experts recommend maternal treatment with pyrimethamine and sulfadiazine. Clindamycin is an alternative drug if there is intolerance to sulfa compounds. Leucovorin, which is folinic acid, must be taken with pyrimethamine to rescue human cells because T gondii cannot use exogenous folinic acid. Treatment of acute infection during pregnancy has been associated with a 50% reduction in fetal infection in some studies, although large controlled trials are lacking in this area. Pyrimethamine, sulfadiazine, and leucovorin also is the most widely accepted regimen for the treatment of overt toxoplasmosis in newborns. In one study, neurologic and developmental outcomes were signicantly better for treated children than for those who did not receive appropriate medications. Among treated infants, overall ocular prognosis usually is satisfactory, but late-onset retinal lesions can occur many years after birth. Much congenital toxoplasmosis can be prevented by educating pregnant women to avoid eating raw or undercooked meat, to avoid crosscontamination of other foods with raw or undercooked meat, and to wash fruits and vegetables thoroughly before eating. Pregnant women should wear

gloves when gardening and during any contact with soil or sand. They should avoid changing cat litter, if possible. Clinicians should begin educating women about the risks of toxoplasmosis at their rst prenatal visit. Comment: Dr Tammas suggestion that pregnant women be given appropriate education is essential. This responsibility must be shared by obstetricians and pediatricians. Pregnant women who own cats also should be counseled that cats have little risk of acquiring toxoplasmosis if they are not fed raw or undercooked meat and if they are solely indoor cats. If a pregnant woman does need to change the litter box, daily changes of litter while wearing gloves is recommended because the oocytes in the feces require several days to become infectious. Because toxoplasmosis is not a reportable disease, accurate estimates of congenital infectious rates are difcult; however, the most recent United States estimates range from 1 to 10 per 10,000 live births. Although national screening for toxoplasmosis takes place in high-risk countries such as France, where eating raw and undercooked meats is common, research in the United States is ongoing to determine the cost-effectiveness of national toxoplasmosis screening for newborns. Janet R. Serwint, MD Consulting Editor

Pediatrics in Review Vol.28 No.12 December 2007 471

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Toxoplasmosis Pranita Tamma Pediatrics in Review 2007;28;470 DOI: 10.1542/pir.28-12-470

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