TORCH syndrome


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Related to TORCH syndrome: toxoplasmosis, CMV

TORCH syn·drome

a group of infections, seen in neonates, which have crossed the placental barrier with similar clinical manifestations, although symptoms may vary in degree and time of appearance: toxoplasmosis, other infections, rubella, cytomegalovirus infection, and herpes simplex.
See also: STORCH.

TORCH syn·drome

a group of infections, seen in neonates, which have crossed the placental barrier with similar clinical manifestations, although symptoms may vary in degree and time of appearance: toxoplasmosis, other infections, rubella, cytomegalovirus infection, and herpes simplex.
See also: STORCH.

TORCH syndrome

infection of the fetus or newborn by one of the TORCH agents. The outcomes of a pregnancy complicated by a TORCH agent may be abortion, stillbirth, intrauterine growth retardation, or premature delivery.
observations At delivery and during the first days after birth an infant infected with any one of the organisms may demonstrate various clinical manifestations, such as fever, lethargy, poor feeding, petechiae on the skin, purpura, pneumonia, hepatosplenomegaly, jaundice, hemolytic and other anemias, encephalitis, microcephaly, hydrocephalus, intracranial calcifications, hearing deficits, chorioretinitis, and microphthalmia. In addition, each of the agents is associated with several other abnormal clinical findings involving abnormal immune response, cataracts, glaucoma, vesicles, ulcers, and congenital cardiac defects.
interventions Before pregnancy, women may be tested for susceptibility to the rubella virus and inoculated against it if not immune. There are currently no vaccines that confer immunity to the other TORCH agents, but the mother may be serologically tested for antibody levels to them. During pregnancy toxoplasmosis is asymptomatic in about 90% of cases, making diagnosis unlikely. If infection is suspected, serial paired serological tests are performed. A high, rising titer indicates recent infection. Transplacental infection occurs in 35% of mothers infected during pregnancy. If the mother contracts infection in the first trimester, before the placenta is fully developed, the infant may not become infected. If the fetus contracts the infection, severe congenital manifestations of the syndrome usually occur. If the fetus is infected after the first trimester, the baby is usually born with asymptomatic or mild disease. The infection may be spread from the baby during the newborn period. SulfADIAZINE, pyrimethamine, and folic acid are sometimes given to treat the infection. Primary cytomegalovirus infection during pregnancy is usually asymptomatic. If the infection is suspected, serological testing may be performed to demonstrate primary infection because infants born to mothers infected for the first time during pregnancy are much more likely to develop severe congenital anomalies than if the infection is a reactivation of previous cytomegalovirus infection. There is no specific treatment. The child is considered to be infectious, but contagion among newborns from a congenitally infected infant has not been proven. Transplacental rubella virus infection in pregnancy during the first 8 weeks is likely to cause infection in 50% of fetuses and to result in demonstrable defects in 85% of those infected. The risk becomes less as gestation increases to 24 weeks, after which time infection has not been known to result in defects. Rubella is the only TORCH virus that is usually symptomatic, and therefore it is often recognized. Many mothers infected during the first trimester choose to abort the pregnancy. There is no treatment for the infection, but screening and immunization before pregnancy could prevent virtually all cases of congenital rubella. Herpesvirus infection in pregnancy is rarely transplacentally transmitted to the fetus. Primary infection during pregnancy sometimes results in spontaneous abortion or premature delivery. In the newborn the infection is usually systemic and life-threatening. The fetus is most apt to become infected by the virus shed from an active genital lesion during vaginal delivery or as the result of vaginal examination or the placement of an intrauterine catheter or a fetal scalp electrode during labor. If the mother has active genital herpesvirus lesions, intrapartal internal monitoring is contraindicated, vaginal examinations are often omitted, regional anesthetic techniques are avoided, and the infant is delivered by cesarean section. The TORCH infections caused by other agents are asymptomatic in pregnancy, revealing themselves by the syndrome after birth. The congenital effects are not amenable to change or to amelioration by any known treatment.