Cytomegalovirus is a herpesvirus. It is one of the most common and benign infections seen in young children, but can cause serious problems to the congenitally infected newborn. Women who work in day care centers and nurseries are at increased risk of acquiring the infection. It is important for these high risk individuals to practice good hygiene such as hand washing after exposure with saliva or urine.
Around 10% of infected newborns are symptomatic at birth. These symptoms include microcephaly, intellectual impairment, sensorineural hearing loss, hepatosplenomegaly, thrombocytopenia, jaundice, low birth weight, pneumonitis, and congenital heart disease. (1) Around 90% of newborns have asymptomatic CMV in the newborn period. Long term risks for these infants include neurological problems such as hearing loss, mental retardation, speech and language delay, and microcephaly. (1) It is important to note that most newborns who acquire these abnormalities are born to mothers who contracted the disease during pregnancy. Children of mothers with recurrent disease are less likely to be affected. (1)
Physicians can be made aware of the possibility of CMV in the fetus through maternal ultrasound. The test can show oligohydramnios, fetal ascites, microcephaly, hydrocephalus, or intracranial calcifications among others. (2) Currently, the only drug used for congenital CMV is ganciclovir. (3) It has mostly been known to work against the progression of the sensorineural hearing loss. (3)
There is no evidence that suggests that termination of pregnancy should be offered to mothers with CMV infections. (4)
A CMV vaccine is currently being studied and CMV-IVIG is currently available for the prophylaxis of high risk patients such as organ transplant recipients.
Parvovirus is a DNA virus that affects humans. It is most commonly seen among school aged children. Although adults can be affected, the illness is usually benign in older patients. However, pregnant women should know that fetal parvovirus can lead to aplastic anemia, spontaneous abortion, nonimmune hydrops, and ultimately fetal death. Symptoms include a low grade fever, flu-like symptoms, and a bright red rash over the cheeks.
In an article published in the Journal of Infectious Diseases in Obstetrics and Gynecology, they studied 25 women who had parvovirus infection during their pregnancy. Of the 25 fetuses, 3 developed hydrops fetalis and 4 had fetal death. The results indicated that parvovirus can cause more fetal morbidity/mortality than previously expected. (5)
Serologic Testing- If labwork indicates recent infection, weekly ultrasounds are required.
If ultrasound indicates hydrops or moderate to severe anemia, then intrauterine transfusion is indicated.
If ultrasound shows no evidence of hydrops or anemia, then continue surveillance through week 12 after being exposed.
Varicella –Zoster virus is a herpesvirus responsible for causing varicella (chickenpox) and herpes zoster (shingles). Although it is a rare disease in the pregnant woman due to the fact that most women of reproductive age are immune, it can have serious consequences on the mother and fetus. (6) Severe complications of the disease are also more commonly seen in adults than in young children. These complications include encephalitis and pneumonia with pneumonia being a risk factor for mortality in the mother. (7)
In a non-immune susceptible person, the chances of acquiring the disease is between 60-90%. The incubation period is between 10-20 days with an average of 14 days after exposure. A person is infectious 48 hours after the rash appears and continues to be infectious until the vesicles crust over. Symptoms include fever and a maculopapular rash which becomes vesicular. (7)
The infection can be transmitted to the fetus through the placenta and can result in congenital and neonatal chickenpox depending on when the mother becomes infected. Congenital varicella syndrome is associated with abnormalities of the central nervous system which in most cases is associated with mental retardation. (8) The risk of congenital varicella syndrome occurs during the first 20 weeks of pregnancy. If the mother develops the disease 5 days before delivery up to 2 days post-partum, the infant is at risk of neonatal varicella-zoster infection. Neonatal varicella has a high mortality rate for the neonate. (7)
The treatment of choice is acyclovir. Although it does not cause complete resolution of the illness, it has been shown to reduce the number of lesions. Also, if varicella is complicated by pneumonia in the pregnant woman, intravenous acyclovir can reduce both morbidity as well as mortality. The immune globulin (VZIG) should be given to infants born to women who acquire the disease 5 days before to 48 hours after delivery. If the infant were to develop the disease within the first 2 weeks of life, IV acyclovir is recommended. (7)
Toxoplasmosis is an infection caused by the parasite Toxoplasma gondii. There are different ways of contracting the disease, for example, eating undercooked meat of infected animals, by contact with the feces of infected cats, or through contact with infected soil or insects in the soil. (7) Symptoms include cervical lymphadenopathy, fever, night sweats, myalgias , and hepatosplenomegaly. (7) The infection can get into the blood causing a parasitemia that can get into the placenta and cause fetal infection. Although the disease seems to be self-limited in healthy adults, it can severely compromise the infants of affected mothers. Infection early in pregnancy carries the highest risk of neurological impairment. Infection in later pregnancy, if detected early and treated, has a good prognosis for the child. Follow-up [eye exams, hearing testing, growth monitoring, and psychomotor evaluations] for at least ten years after birth may improve the outcome of children affected by intrauterine toxoplasmosis infection. (9) Some of the clinical signs of infection in infants include hearing loss, chorioretinitis, mental retardation, rash, hepatosplenomegaly, ascites, fever, ventriculomegaly, and seizures. (7)
The primary way to diagnose this illness is through specific fetal serum antibody (IgM or IgG) to Toxoplasma gondii. Ultrasound can also be used to look for findings such as intracranial calcifications, microcephaly, hepatoslenomegaly, ventriculomegaly, and IUGR. (7) Fetal blood samples for antibodies are usually obtained at 20 weeks gestation, but PCR testing can be done earlier. (10) While the fetal tests are being done, the infected mother should be treated with Spiramycin. (11) If the infection is identified in the infant, the appropriate treatment includes pyrimethamine and sulfadiazine alternating on a monthly basis with spiramycin for one year. This treatment has been known to reduce the number of intracranial calcifications and therefore improve the neurologic development of the infant. (7)
Studies indicate that pregnancy doesn’t need to be interrupted if repeated ultrasounds show normal findings. (12, 13)
REFERENCES:
1. Bhatia P, Narang A, Minz RW. Neonatal cytomegalovirus infection: diagnostic modalities available for early disease detection. Indian J Pediatr. Jan;77(1):77-79.
2. Nelson CT, Demmler GJ. Cytomegalovirus infection in the pregnant mother, fetus, and newborn infant. Clin Perinatol. Mar 1997;24(1):151-160.
3. Schleiss MR. Congenital Cytomegalovirus Infection: Update on Management Strategies. Curr Treat Options Neurol. May 2008;10(3):186-192.
4. Griffiths PD, Baboonian C. A prospective study of primary cytomegalovirus infection during pregnancy: final report. Br J Obstet Gynaecol. Apr 1984;91(4):307-315.
5. Beigi RH, Wiesenfeld HC, Landers DV, Simhan HN. High rate of severe fetal outcomes associated with maternal parvovirus b19 infection in pregnancy. Infect Dis Obstet Gynecol. 2008;2008:524601.
6. Connan L, Ayoubi J, Icart J, Halasz A, Thene M, Berrebi A. Intra-uterine fetal death following maternal varicella infection. Eur J Obstet Gynecol Reprod Biol. Sep 1996;68(1-2):205-207.
7. ACOG practice bulletin. Perinatal viral and parasitic infections. Number 20, September 2000. (Replaces educational bulletin number 177, February 1993). American College of Obstetrics and Gynecologists. Int J Gynaecol Obstet. Jan 2002;76(1):95-107.
8. Daley AJ, Thorpe S, Garland SM. Varicella and the pregnant woman: prevention and management. Aust N Z J Obstet Gynaecol. Feb 2008;48(1):26-33.
9. Berrebi A, Assouline C, Bessieres M-H, et al. Long-term outcome of children with congenital toxoplasmosis. Am J Obstet Gynecol. 2010; 203:552.e1-6.
10. Wallon M, Franck J, Thulliez P, et al. Accuracy of real-time polymerase chain reaction for Toxoplasma gondii in amniotic fluid. Obstet Gynecol. Apr;115(4):727-733.
11. Daffos F, Forestier F, Capella-Pavlovsky M, et al. Prenatal management of 746 pregnancies at risk for congenital toxoplasmosis. N Engl J Med. Feb 4 1988;318(5):271-275.
12. Berrebi A, Bardou M, Bessieres MH, et al. Outcome for children infected with congenital toxoplasmosis in the first trimester and with normal ultrasound findings: a study of 36 cases. Eur J Obstet Gynecol Reprod Biol. Nov 2007;135(1):53-57.
13. Berrebi A, Kobuch WE, Bessieres MH, et al. Termination of pregnancy for maternal toxoplasmosis. Lancet. Jul 2 1994;344(8914):36-39.


