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Fetal Infections - Parvo, CMV and Toxo

Oct 2008 – by M. Socol, MD

Parvovirus

Parvovirus B19 is a single stranded DNA virus which causes erythema infectiosum, also known as fifth disease. Clinical manifestations include flu-like signs and symptoms, low-grade fever, malaise, arthralgia, and a classic "slapped cheek" rash. Maternal infection most often is contracted from an affected child. Infection is confirmed with acute and convalescent serology documenting the presence of IgM antibody or a four-fold rise in IgG antibody.

Fetal infection can result in profound anemia and fetal hydrops, presumably secondary to aplastic crisis, but other proposed etiologies include myocarditis and hepatitis. Parvovirus is the likely cause of a substantial portion of non-immunologic hydrops cases which were previously thought to be idiopathic. Hydrops can develop eight to ten weeks after the primary infection. Therefore, a reasonable plan for fetal surveillance is weekly middle cerebral artery peak systolic velocity waveform measurements for ten to twelve weeks. If fetal hydrops should develop, fetal intravascular intrauterine transfusion is most often curative. A concern about long-term neurologic abnormalities has been raised, but most newborns are free of neurologic sequelae.

Cytomegalovirus

Cytomegalovirus is a double stranded DNA virus. Transmission requires close personal contact, and the most common vehicle is a child who contracted the infection in day care. Other modes of horizontal transmission include sexual contact and blood transfusion. Clinical findings may include malaise, fever and lymphadenopathy, but most infections are asymptomatic. Suspicion of infection arises from a conversion in serology. However, serology for CMV tends to be poorly reproducible. Consequently, the focus in the United States has been on prevention, with serologic screening primarily directed to immunocompromised patients or those with definite exposure.

It is estimated that thirty to fifty percent of primary maternal infections result in vertical transmission. Fetal infection occurs more commonly if the exposure occurs in the third trimester, but fetal sequelae are greatest with first trimester infection. These sequelae include fetal growth restriction, intracranial calcifications, microcephaly, chorioretinitis, and hearing loss. The most reliable means of documenting fetal infection is PCR of amniotic fluid. There is no in utero fetal therapy available. Approximately ten percent of newborns will exhibit signs of congenital infection and ninety percent of these will develop long-term symptomatology. In the normal appearing cohort of newborns, ten percent will demonstrate sequelae in childhood. Reactivated maternal infection can occur but this is much less likely to be transmitted to the fetus.

Toxoplasmosis

Toxoplasma gondii is a protozoan which can lead to human infection through infected uncooked meat or food contaminated by cat feces. Most infections are asymptomatic but immunocompromised hosts (eg. HIV positive individuals) can manifest such problems as central nervous system infection, myocarditis, or pneumonitis. The diagnosis is made by serology but this is not well standardized. As a result, a positive conversion requires confirmation in a reference laboratory.

Congenital infection is most likely to occur following maternal infection in the third trimester. Most infected fetuses are asymptomatic at birth, but fetal growth restriction, microcephaly, periventricular calcifications, ventriculomegaly, chorioretinitis, and hepatosplenomegaly can be observed. The diagnosis of congenital infection is confirmed by ultrasound and PCR of amniotic fluid. Treatment may include pyrimethamine, sulfonamides, and spiramycin. Efforts in the United States are primarily directed toward prevention of infection rather than routine screening. Careful hand washing, washing of fruits and vegetables, and the avoidance of uncooked meat or cat litter are all advised.

Reference: Maternal-Fetal Medicine, Principles and Practice. Editors: Creasy, R.K. and Resnik, R. 5th Edition, Saunders, 2004.