Congenital TORCH infections

• A handful of infections acquired during pregnancy or around delivery can cross to the fetus and produce overlapping patterns of brain, eye, ear, liver and skin disease; together they are grouped as congenital TORCH infections.
• The group started as toxoplasmosis, "other" infections (classically syphilis), rubella, cytomegalovirus and herpes simplex, and is now used more loosely to include varicella, parvovirus B19 and Zika virus.
• Each has a different maternal illness and different timing of danger: rubella is worst in early pregnancy, varicella embryopathy follows first-trimester infection, parvovirus threatens the fetus mainly in the first half of pregnancy, and herpes simplex is most often caught by the baby during birth.
• Cytomegalovirus is now the leading infectious cause of congenital sensorineural hearing loss in high-income countries, and congenital rubella syndrome still disables about 32,000 infants each year worldwide, almost all in countries without rubella vaccination. ^[1]
• There is no single "TORCH screen." Each infection is diagnosed with its own serology, polymerase chain reaction (PCR) test and imaging, and treated differently; many have no cure, which is why prevention before pregnancy matters.
• This page compares all eight infections in one table and gives the diagnostic and treatment steps that do exist, with the doses and cut-offs taken from current guidelines.

By the end of this page you should be able to:

1. Define the TORCH group and list the eight infections it covers in this page.
2. Recognize the recurring neonatal clues (chorioretinitis, intracranial calcification, hearing loss, cataracts, microcephaly, hepatosplenomegaly, blueberry muffin rash) and match each to the likely agents.
3. Choose the right maternal and neonatal tests for each infection and state when a test can and cannot separate past from recent infection.
4. State which infections have a specific treatment and give the guideline doses and durations for them.
5. Describe how each infection is prevented, including which vaccines are used before rather than during pregnancy.
6. Plan the follow-up of an infant born to a mother with a suspected or confirmed congenital infection.

Congenital TORCH infections are the infections that reach the baby before birth (transplacentally), during delivery (intrapartum) or, less often, shortly afterwards. The baby can be apparently normal at birth and still carry an infection that declares itself months later as hearing loss, visual impairment or developmental delay. A second problem is that the mothers are often well or have only a mild viral illness, so the diagnosis is made retrospectively from the baby's findings.

Maternal TORCH-related infection remains a major cause of adverse pregnancy outcome despite advances in prenatal care, with vertical transmission possible transplacentally, intrapartum or through breast milk and able to produce miscarriage, stillbirth, preterm birth, fetal growth restriction, malformation, hearing loss and long-term neurological impairment. ^[1] The group is not fixed. The original acronym (toxoplasmosis, "other", rubella, cytomegalovirus and herpes simplex) still appears in textbooks, but modern practice expands "other" to include syphilis, and adds varicella, parvovirus B19 and Zika virus. ^[10]

• TORCH (or TORCHES) groups infections that can be carried across the placenta or acquired during birth and that produce overlapping neonatal disease. The letters are toxoplasmosis; other (classically syphilis and sometimes hepatitis B); rubella; cytomegalovirus (CMV); and herpes simplex (HSV).
• Expanded TORCH adds varicella-zoster virus, parvovirus B19, Zika virus and, in some centres, human immunodeficiency virus (HIV). Hepatitis B is covered with vaccines and immunoglobulin at birth and is not a TORCH disease in the usual sense of antenatal diagnosis.
• Congenital infection is an infection acquired before birth or, for HSV, usually during passage through the birth canal. It is different from an infection the baby acquires after birth on the ward or at home.
• Maternal infection is not the same as fetal infection. Transmission rates and fetal damage vary by agent and by gestational age, and a positive maternal serological test does not by itself mean the baby is infected.
• Classification for clinical purposes splits these infections into those with a specific treatment (toxoplasmosis, syphilis, HSV, CMV in selected infants) and those managed supportively and with surgery (rubella, parvovirus, varicella, Zika).

• Rubella and congenital rubella syndrome (CRS). When a woman is infected with rubella in early pregnancy, up to 90% of babies may have CRS, and about one third of infants born with CRS die before their first birthday. About 32,000 children were estimated to be born with CRS in 2019, almost always in countries without rubella vaccination programmes. ^[9][10]
• Cytomegalovirus. About 1 in 200 babies is born with congenital CMV infection, and about 1 in 5 babies with congenital CMV has birth defects or other long-term health problems; CMV is the most common infectious cause of birth defects in the United States. ^[4]
• Syphilis. In the United States, 1,870 cases of congenital syphilis were reported in 2019 (48.5 cases per 100,000 live births), a value that mirrors sharp rises in syphilis among women of reproductive age and underscores why routine antenatal screening is repeated. ^[2]
• Varicella. Most women of childbearing age are already immune. Congenital varicella syndrome is rare and follows maternal chickenpox in the first 20 weeks of pregnancy; neonatal varicella, acquired from 5 days before to 2 days after delivery, carried a historical mortality of about 30% and falls to about 7% with modern neonatal care and varicella-zoster immune globulin. ^[6]
• Parvovirus B19. Parvovirus B19 is ubiquitous; most adults are already immune by the childbearing years. Infection during the first half of pregnancy can lead to fetal anaemia, hydrops fetalis, miscarriage or, less often, fetal death. ^[7]
• Zika virus. Zika is geographically restricted to parts of the Americas, Africa and Asia and causes outbreaks; congenital Zika syndrome appeared most prominently during the 2015 to 2016 outbreak in the Americas. Infection does not affect future pregnancies. ^[8]
• Toxoplasmosis. Maternal toxoplasmosis is a preventable cause of congenital disease, with environmental and dietary exposure continuing in many regions, including areas where screening is not routine. ^[1][3]

• Transplacental spread is the main route (transmission through the placenta) and can occur at every stage of pregnancy for CMV and toxoplasmosis.
• Near-term or peripartum exposure carries the greatest danger for herpes simplex: prevention of neonatal herpes depends on preventing acquisition of genital herpes late in pregnancy and on avoiding exposure of the baby to herpetic lesions or viral shedding during delivery. ^[5]
• Varicella embryopathy follows maternal chickenpox, usually in the first 20 weeks, and neonatal varicella follows maternal rash from 5 days before to 2 days after delivery. ^[6]
• Parvovirus B19 threatens the fetus mainly in the first half of pregnancy. ^[7]
• Zika virus crosses the placenta at any stage and its effect on the fetus is not limited to microcephaly; some infants look well at birth. ^[8]
• Rubella is worst in the first 12 weeks of pregnancy. ^[9]
• Common maternal risk factors include non-immune status, lack of pre-conception vaccination (rubella, varicella), untreated sexually transmitted infection (syphilis, HSV), contact with young children (CMV, parvovirus), travel to Zika-affected areas, contact with cat faeces or undercooked meat (toxoplasma), and late or absent antenatal care. ^[2][3][6]

These infections share a path: maternal viraemia or parasitaemia, placental infection, fetal infection, and then organ-specific damage that depends on gestational age and on the tropism of the organism. Three patterns dominate.

1. Early first-trimester infection disrupts organ formation, so rubella damages the developing eye, ear, heart and brain, while early varicella produces limb hypoplasia and skin scarring.
2. Infection later in pregnancy produces encephalitis, retinitis, hepatitis and haematological upset in an already formed fetus: CMV, toxoplasmosis and syphilis fit this pattern. Transplacental transmission of toxoplasma becomes more frequent as pregnancy advances, even though severity is greatest with early infection, which is why suspicion and follow-up matter at every gestation.
3. Intrapartum exposure, for HSV in particular, causes disseminated, central nervous system (CNS) or skin, eye and mouth (SEM) disease after birth.

The fetus with any of these infections can be anaemic (from bone-marrow suppression or haemolysis), hepatosplenomegalic and jaundiced (extramedullary haematopoiesis and liver involvement), petechial and thrombocytopenic, or microcephalic with intracranial calcification. That shared picture is what the old acronym described, but the agent responsible is usually identifiable from the pattern.

• Toxoplasmosis: most often asymptomatic in a healthy adult; occasionally a mild febrile illness with lymphadenopathy. Many adults are already infected and IgG-positive, so interpreting serology needs reference-laboratory support. ^[3]
• Rubella: usually a mild febrile rash illness in adults; infection during pregnancy, especially early, endangers the fetus. ^[9]
• Cytomegalovirus: usually asymptomatic or a mononucleosis-like illness in immunocompetent adults; there is no proven treatment to prevent or treat fetal infection. ^[4][1]
• Herpes simplex: primary genital infection presents with painful vesicles and ulcers, dysuria and systemic symptoms; recurrent disease is milder; most women with genital HSV are asymptomatic. ^[5]
• Syphilis: primary chancre, secondary rash or condyloma lata, then latent disease; often clinically silent; sexual risk factors and previous infection status must be reviewed. ^[2]
• Varicella: fever and malaise followed by an itchy, vesicular rash in crops; pneumonia is a risk in pregnancy. ^[6]
• Parvovirus B19: the classic "slapped-cheek" rash of fifth disease, sometimes with a lacy reticular rash and arthropathy; infection is often subclinical. ^[7]
• Zika virus: often asymptomatic; otherwise fever, maculopapular rash, arthralgia and non-purulent conjunctivitis, usually mild and short-lived. ^[8]

The recurring neonatal clues are chorioretinitis, intracranial calcification, hearing loss, cataracts, microcephaly, hepatosplenomegaly and the "blueberry muffin" rash. None is pathognomonic; the combination and the agent determine the diagnosis.

• Chorioretinitis is characteristic of toxoplasmosis and CMV, also described in rubella, varicella and syphilis.
• Intracranial calcification is typical of CMV (periventricular) and toxoplasmosis (more diffuse), and is part of the cerebral damage of Zika and severe rubella; intracranial imaging is therefore routine.
• Hearing loss, usually sensorineural, is the signature of congenital CMV and of CRS; it may be progressive and can present after an infant passes a newborn screen.
• Cataracts are the hallmark ocular lesion of congenital rubella, with glaucoma also described; toxoplasma and varicella can scar the retina.
• Microcephaly occurs in Zika, CMV, toxoplasmosis and severe rubella, and can develop after birth.
• Hepatosplenomegaly with conjugated jaundice and transaminitis occurs in syphilis, toxoplasmosis, CMV, rubella and parvovirus-related hydrops.
• Blueberry muffin rash (dermal extramedullary haematopoiesis, purple papules) is reported in congenital CMV, rubella and, occasionally, toxoplasmosis and parvovirus infection.
• Other useful clues: petechiae and purpura with thrombocytopenia; non-immune hydrops (parvovirus B19, severe CMV or syphilis); rash and snuffles (syphilis); limb hypoplasia or skin scarring (varicella); contractures, rigid tone and feeding difficulty (Zika).

A newborn with chorioretinitis, calcification, hepatosplenomegaly or a rash does not automatically have a TORCH infection. The differential includes the following.

• Non-infectious causes. Metabolic disease, chromosomal disorders, intracranial haemorrhage, periventricular leukomalacia, congenital hypothyroidism, and storage disorders can all produce hepatosplenomegaly, calcification or microcephaly.
• Other congenital infections. HIV, hepatitis B, enteroviruses, parvovirus-related phenotypes, lymphocytic choriomeningitis virus, and congenital tuberculosis or malaria mimic TORCH disease in endemic areas.
• Isolated prematurity. Anaemia of prematurity, rickets, and intraventricular haemorrhage can be confused with congenital infection.
• Drug and asphyxia injury. Neonatal abstinence, severe birth asphyxia and anticonvulsants can produce overlapping neurological findings.
• Maternal autoimmune disease. Neonatal lupus can produce rash, hepatobiliary disease and thrombocytopenia.
• Skin lesions. Blueberry muffin rash must be separated from dermal erythropoiesis of other causes; the organism is identified by PCR and serology, not by the rash.

• Serology. IgG documents past infection or immunity; IgM suggests recent infection but is not specific; IgG avidity separates recent from past infection when collected early. For toxoplasmosis and CMV, send equivocal results to a reference laboratory rather than acting on a single commercial IgM. ^[3][4]
• Syphilis screening. Screen every pregnant woman at the first prenatal visit; repeat at 28 weeks and at delivery for women in high-prevalence areas, women with HIV, and those with increased risk. A quantitative RPR or VDRL at delivery is needed for comparison with the baby's titre. ^[2]
• Rubella immunity. Test IgG before conception or in early pregnancy; women who are non-immune are vaccinated after delivery. ^[9]
• Varicella immunity. Establish evidence of immunity; vaccinate non-immune women before pregnancy and, if needed, after delivery. ^[6]
• CMV screening is not recommended for pregnant women generally, because available tests cannot predict whether the fetus will be infected or harmed. ^[4]
• Toxoplasmosis screening is not routine everywhere; ask about symptoms, exposure and, when suspicious, send serology to the Jack S. Remington Laboratory for Specialty Diagnostics. ^[3]
• Parvovirus B19. Test IgG and IgM after exposure or compatible symptoms in pregnancy. ^[7]
• Zika. Test on the basis of symptoms plus travel or sexual exposure, or when fetal ultrasound suggests congenital Zika syndrome. Routine screening of asymptomatic pregnant travellers is no longer recommended in current CDC guidance. ^[8]

• Ultrasound. Look for microcephaly, ventriculomegaly, intracranial calcifications, hepatosplenomegaly, hydrops, growth restriction, placental thickening and extremity abnormalities. A normal ultrasound does not exclude infection.
• Amniocentesis. PCR of amniotic fluid for Toxoplasma gondii is often performed at 18 weeks when fetal infection is suspected; amniotic fluid PCR is used in selected cases of suspected Zika. ^[3][8]
• Fetal assessment for parvovirus. Middle cerebral artery Doppler and follow-up scans assess fetal anaemia; specialist fetal medicine is required for any intervention. ^[7]

• Syphilis. All babies born to mothers with reactive nontreponemal and treponemal tests have a quantitative nontreponemal test on neonatal serum (not cord blood). A full evaluation includes CSF VDRL, cell count and protein, CBC and platelets, long-bone radiographs, and other tests as clinically indicated; HIV testing should be arranged for any baby at risk for congenital syphilis. ^[2]
• CMV. CMV PCR or NAAT on urine, and preferably saliva, within 2-3 weeks of birth; blood is not the best sample. ^[4]
• HSV. PCR from vesicles, CSF and blood, plus surface cultures when suspected. Do not wait for results before starting empiric acyclovir in a sick neonate with herpetic skin lesions. ^[5]
• Toxoplasmosis. IgM and IgA, PCR, Sabin-Feldman dye test, brain imaging, ophthalmology; a full newborn examination. ^[3]
• Rubella. Rubella IgM and RT-PCR from nasopharyngeal and urine specimens; the virus can be shed for months. ^[9]
• Zika. Evaluate every infant with possible congenital Zika infection with head imaging, hearing and eye assessment; laboratory confirmation depends on the timing of testing after exposure or symptoms and on maternal and infant findings. ^[8]
• Varicella. Vesicle PCR if a rash is present; document maternal varicella history and immunity; give VariZIG if indicated and do not delay. ^[6]
• Parvovirus. FBC, reticulocyte count and bilirubin; echocardiogram if hydrops; infection is usually diagnosed clinically and serologically in the mother. ^[7]

• Congenital infection is identified by demonstrating the organism or its nucleic acid in the baby early in life, or by a specific IgM/IgA response, or by culture or PCR positivity.
• CMV: urine or saliva PCR within the first 2-3 weeks of life. Testing after this window cannot distinguish congenital from postnatally acquired infection. ^[4]
• Syphilis: diagnosis requires a constellation of maternal status, adequacy of treatment, clinical evidence in the baby and a neonatal nontreponemal titre at least fourfold that of the mother at delivery. ^[2]
• HSV: disease is classified as SEM, CNS or disseminated, on clinical and CSF findings. ^[5]
• Rubella: laboratory confirmation in the infant (IgM and/or RT-PCR) plus compatible clinical findings; the CDC surveillance definition also counts infants born to mothers exposed during pregnancy. ^[9]
• Toxoplasmosis: diagnosis is biochemical and molecular; results from a reference laboratory usually take precedence over a single IgM screen. ^[3]
• Varicella: congenital varicella syndrome is a clinical diagnosis backed by maternal history of chickenpox in the first 20 weeks; neonatal varicella is diagnosed by vesicle PCR and a maternal rash around delivery. ^[6]
• Zika: congenital Zika syndrome is a clinical pattern (brain abnormalities, eye abnormalities, joint contractures, hypertonia, hyper-reflexia) supported by laboratory evidence of maternal or infant infection; brain imaging is required. ^[8]
• Parvovirus B19: diagnosis rests on maternal serology plus evidence of fetal red-cell aplasia or anaemia/hydrops; it is a diagnosis of probability in most cases. ^[7]

• Start treatment on suspicion for HSV. A neonate with vesicles, seizures, hepatitis or disseminated disease should receive intravenous acyclovir while awaiting PCR. ^[5]
• Syphilis. Complete a full evaluation for every baby at risk, and give penicillin according to the CDC scenario. Do not let the baby leave hospital without documented maternal serological status. ^[2]
• CMV. Treatment is reserved for babies with signs of congenital CMV at birth and is considered case by case; the decision needs paediatric infectious diseases input. ^[4]
• Non-immune hydrops from any cause needs urgent neonatology, obstetrics and transfusion-medicine input; parvovirus-related severe anaemia may warrant intrauterine transfusion under a fetal-medicine team, although intrauterine transfusion is a high-risk specialist procedure with limited evidence in parvovirus-related hydrops. ^[7]

Toxoplasmosis. Management varies by centre. In general, spiramycin is used for acute maternal infection acquired and diagnosed before 18 weeks of gestation, when fetal infection is not documented or suspected; pyrimethamine, sulfadiazine and leucovorin (folinic acid) are used when infection is acquired at or after 18 weeks, or whenever fetal infection is proven or suspected, with amniotic-fluid PCR at about 18 weeks. Pyrimethamine is avoided in the first trimester and sulfonamides after 32 weeks of pregnancy. A congenitally infected baby is treated with pyrimethamine, sulfadiazine and leucovorin for 12 months: pyrimethamine 2 mg/kg by mouth daily in two divided doses for the first 2 days, then 1 mg/kg daily every day from day 3 to 2 months (or to 6 months if symptomatic), then 1 mg/kg three times weekly; sulfadiazine 100 mg/kg daily by mouth divided twice daily; and leucovorin 10 mg three times weekly. These doses come from the Remington and University of Chicago recommendations cited by CDC and should be prescribed and monitored by a specialist, with blood-count monitoring because of bone-marrow suppression. ^[3]

Rubella. There is no antiviral. Management is surgical correction of heart disease, cataract surgery, hearing amplification and rehabilitative support, with counselling that there is no cure. A mother who is non-immune is vaccinated with MMR after delivery. ^[9]

CMV. Valganciclovir 16 mg/kg per dose by mouth twice daily for 6 months improves hearing and developmental outcomes in infants with moderately-to-severely symptomatic congenital CMV, starting in the first month of life; a 6-week course is suggested for infants whose only manifestation is sensorineural hearing loss. Intravenous ganciclovir is used when oral therapy is not tolerated or in severe disease, with specialist dosing. Oral valganciclovir has only been studied in symptomatic disease and its benefit in infants with hearing loss alone is limited. Regular hearing and vision checks are needed for all children with congenital CMV, even those who look well, because hearing loss can be delayed. ^[4]

HSV. Parenteral acyclovir is the standard: 20 mg/kg (equivalent to 60 mg/kg per day in three divided doses) intravenously every 8 hours, for 14 days for SEM disease and 21 days for CNS or disseminated disease, followed by oral suppressive acyclovir for 6 months in many infants; a 21-day repeat dose is used if CSF remains positive. Treatment before laboratory confirmation is encouraged when NHSV is suspected; the interval may need lengthening in premature infants. ^[5]

Syphilis. Maternal syphilis is treated with the stage-appropriate penicillin G regimen from current STI guidelines, ideally at least 30 days before delivery. For the neonate, aqueous crystalline penicillin G (100,000-150,000 units/kg/day IV) or procaine penicillin G (50,000 units/kg/day IM for 10 days) is used when infection is confirmed or possible; a single dose of benzathine penicillin G (50,000 units/kg IM) is used when congenital syphilis is less likely; and infants 1 month or older with congenital syphilis receive aqueous penicillin G 200,000-300,000 units/kg/day IV for 10 days. If congenital syphilis is unlikely, no treatment may be required, but the baby is followed serologically. Penicillin-allergic neonates should be desensitised and given penicillin; there is insufficient evidence for ceftriaxone. In a penicillin shortage, aqueous or procaine penicillin is preferred; ceftriaxone is a fallback with specialist advice. ^[2]

Varicella. Mothers and babies without immunity who are exposed receive VariZIG as soon as possible and within 10 days (ideally within 96 hours). Neonates whose mothers had chickenpox from 5 days before to 2 days after delivery are a priority group. Established neonatal varicella is treated with acyclovir and supportive care. Uncomplicated maternal varicella in pregnancy needs specialist obstetric review; there is no routine antiviral in the guidance reviewed. ^[6]

Parvovirus B19. There is no specific antiviral. Most maternal infections need only reassurance and follow-up, with referral to fetal medicine if exposure occurs in the first half of pregnancy or if ultrasound shows anaemia or hydrops; intrauterine transfusion is considered only in severe cases by a specialist team. ^[7]

Zika virus. Management is supportive. Infants with congenital Zika syndrome need multidisciplinary care (neurology, ophthalmology, audiology, physiotherapy, feeding support) and long-term follow-up; microcephaly can develop after birth, so a single normal head circumference at delivery does not exclude disease. ^[8]

• Referral to fetal-medicine, paediatric infectious-diseases, cardiology, ophthalmology, audiology and neurodevelopmental teams as the pattern indicates.
• Parent counselling, which must be realistic: many outcomes are not modifiable after infection, and prognosis is uncertain in mild cases.
• Isolation precautions for rubella and CMV (urine and respiratory), because prolonged shedding complicates ward logistics.

• Syphilis. Nontreponemal titres every 2-3 months until non-reactive; by 3 months the titre of an untreated, uninfected infant should fall and by 6 months it should be non-reactive; treated babies with persistent titres at 6-12 months need re-evaluation. Retesting at 3 months catches incubating infection even when the birth test was negative. ^[2]
• CMV. Newborn hearing screen, repeat if needed and then audiology; vision testing; early intervention referral. ^[4]
• HSV. Oral suppressive acyclovir, follow-up CSF if indicated, and neurodevelopmental review. ^[5]
• Rubella. Cardiac, ophthalmological and audiological review at 3, 6 and 12 months; test for thyroid dysfunction. ^[9]
• Zika. Neurology, eye and hearing follow-up into childhood. ^[8]
• Parvovirus. Neonatal FBC and, if indicated, cardiac surveillance. ^[7]

• Permanent sensorineural hearing loss (CMV, rubella, Zika), often progressive.
• Visual loss from chorioretinitis, scar, cataract or glaucoma (toxoplasmosis, rubella, varicella, CMV, Zika).
• Structural brain injury: microcephaly, hydrocephalus, calcification, white-matter injury (toxoplasmosis, CMV, Zika, severe rubella).
• Epilepsy and severe developmental delay (Zika, CMV, toxoplasmosis, HSV).
• Congenital heart disease, especially patent ductus arteriosus and pulmonary stenosis (rubella).
• Liver disease, conjugated jaundice and portal hypertension (syphilis, toxoplasmosis, CMV).
• Haematological complications: anaemia, thrombocytopenia, extramedullary haematopoiesis, non-immune hydrops (parvovirus, syphilis, CMV, toxoplasmosis).
• Endocrine disease: thyroid dysfunction and diabetes mellitus in CRS.
• Long-term behavioural and learning problems even in babies who are apparently well at birth.
• Neonatal death, especially with disseminated HSV, severe varicella and overwhelming syphilis, and with hydrops from parvovirus.

• Babies with asymptomatic congenital CMV usually do well, although 1 in 5 may develop hearing or other long-term problems; babies with signs at birth need treatment and close follow-up. ^[4]
• Congenital syphilis is curable if detected, but untreated disease causes permanent organ damage or neonatal death. ^[2]
• Neonatal herpes remains serious despite acyclovir, so prevention and early treatment matter. ^[5]
• Neonatal varicella mortality has fallen from about 30% historically to about 7% with VariZIG and modern care, but it is still a high-risk condition. ^[6]
• CRS has no cure and carries lifelong disability; heart, vision and hearing problems dominate. ^[9]
• The prognosis in mild or borderline cases, especially CMV and toxoplasmosis, is genuinely uncertain and should be presented as such; false reassurance and false doom are both harmful.
• Most adults who acquire infection during pregnancy themselves recover fully; the burden is on the fetus.

• Rubella. A single dose of rubella-containing vaccine provides lifelong protection. Vaccinate girls and women before conception; the vaccine is contraindicated in pregnancy, and non-pregnant women should avoid conception for 4 weeks after vaccination. ^[9][10]
• Varicella. Varicella vaccination for non-immune individuals before pregnancy; the vaccine is contraindicated in pregnancy, with avoidance of conception for 1 month after. Non-immune women are vaccinated postpartum. In 2015, the WHO Region of the Americas became the first in the world to be declared free of endemic rubella and congenital rubella syndrome. ^[9][10]
• Syphilis. Antenatal screening at first visit, with repetition at 28 weeks and delivery in high-prevalence areas; treat the mother at least 30 days before delivery; treat partners; re-screen for reinfection. ^[2]
• Toxoplasmosis. Primary prevention: cook meat thoroughly, wash fruit and vegetables, peel or cook produce, wear gloves when handling soil or cat litter, and avoid feeding cats raw meat. Pyrimethamine is avoided in the first trimester. ^[3]
• CMV. Hand hygiene after nappy changes, wiping children's noses and handling toys; no licensed vaccine; antenatal screening is not recommended. ^[4]
• HSV. Counsel women with genital herpes about suppressive therapy (acyclovir 400 mg three times daily or valacyclovir 500 mg twice daily late in pregnancy), safe sex near term, and delivery mode. ^[5]
• Parvovirus B19. Hand washing and hygiene in daycare and household settings; no vaccine. Non-immune pregnant women can be counselled about outbreaks but need not stop working where hygiene is good. ^[7]
• Zika. Avoid travel to areas with active transmission during pregnancy; strict mosquito protection; condoms or abstinence are recommended after a male partner returns from an area with transmission, because Zika can remain in semen. Zika infection does not affect future pregnancies. ^[8]
• Global perspective. Where vaccination and screening are unavailable, the single most cost-effective measure against CRS remains rubella immunisation of children and of women of childbearing age, and against congenital syphilis, antenatal RPR testing and treatment with penicillin.

• Premature or low-birth-weight infants. They are vulnerable to infection and may not mount an IgM response; the dosing interval of intravenous acyclovir and of ganciclovir-based regimens may need adjusting according to renal function and post-menstrual age. ^[5][4]
• Immunocompromised women or babies, for example mothers with HIV, need the same screening for syphilis, but management of CMV and HSV is more complex and usually needs specialist care.
• HIV-positive mothers. Congenital syphilis is managed the same regardless of HIV status, but all babies at risk for congenital syphilis should be evaluated and tested for HIV. ^[2]
• Transplant and immunosuppressed mothers have reactivation risk for CMV and toxoplasmosis and often need drug-specific prophylaxis and fetal surveillance beyond this page.
• Women from countries without rubella vaccination are at the highest risk of CRS; travel-related cases still occur in rubella-eliminated regions.
• Low birth weight and "missed" mild cases. Many congenital infections are not detected at birth, so hearing and neurodevelopmental surveillance is needed for any baby with maternal risk factors.

• Syphilis. Antenatal RPR or rapid treponemal point-of-care testing and a single intramuscular dose of benzathine penicillin G in pregnancy are effective and affordable; the biggest barriers are late booking and stock-outs.
• Rubella and varicella. Vaccination before conception is the lever; where rubella vaccine is not in the schedule, susceptible women continue to face the risk of CRS.
• Toxoplasmosis. Counselling on meat and soil handling, plus access to reference serology, is cheaper than treatment; management of maternal infection is limited by drug availability (pyrimethamine, sulfadiazine) and monitoring.
• CMV. No antenatal screening and no maternal antiviral is recommended even in well-resourced settings, so hygiene counselling is the intervention. Hearing screening, where available, is the practical route to early CMV detection.
• HSV. Oral acyclovir and caesarean section for active disease may be unavailable; triage should focus on any active genital lesions at labour.
• Zika. Mosquito control, sexual counselling and basic developmental follow-up are the realistically available measures.
• Parvovirus. Awareness and serial ultrasound where available; fetal transfusion is rarely an option outside specialised centres.
• In all these settings, the mother-infant pair should not be separated because of suspicion alone, and treatment should not be started without a defensible diagnostic aim.

• TORCH is an acronym (toxoplasmosis, other infections including syphilis, rubella, CMV, HSV) that has expanded to include varicella, parvovirus B19 and Zika virus.
• These infections share neonatal patterns (chorioretinitis, intracranial calcification, hearing loss, cataracts, microcephaly, hepatosplenomegaly, blueberry muffin rash), but each requires different tests and treatment.
• Cytomegalovirus is the leading infectious cause of congenital sensorineural hearing loss; congenital rubella syndrome still affects tens of thousands of infants each year in unvaccinated regions.
• Rubella is most dangerous in the first 12 weeks; varicella syndrome follows first-trimester maternal chickenpox; parvovirus threatens the fetus mainly in the first half of pregnancy; HSV is most often acquired at birth.
• There is no single "TORCH test"; maternal serology, fetal imaging, pathogen-specific PCR and neonatal examination must be combined.
• Treatable or partly treatable infections: syphilis (penicillin), toxoplasmosis (spiramycin; pyrimethamine-sulfadiazine-leucovorin), HSV (acyclovir), CMV (valganciclovir for selected symptomatic infants).
• Infections without specific antiviral therapy: rubella, varicella, parvovirus, Zika; management is supportive, surgical and rehabilitative.
• Specific doses: valganciclovir 16 mg/kg per dose twice daily for 6 months (symptomatic CMV) and 6 weeks for isolated hearing loss; acyclovir 20 mg/kg IV every 8 hours (14 days SEM, 21 days CNS/disseminated); penicillin-based regimens for congenital syphilis as above.
• Prevention rests on pre-conception vaccination (MMR, varicella), hygiene (toxoplasmosis, CMV, parvovirus), antenatal screening (syphilis) and mosquito and sexual precautions (Zika).
• Prognosis is uncertain in mild and borderline cases and should be communicated as such.

• Congenital cytomegalovirus
• Congenital syphilis
• Congenital toxoplasmosis
• Congenital rubella syndrome
• Neonatal herpes simplex
• Varicella in pregnancy
• Parvovirus B19 and fifth disease
• Zika virus and pregnancy