TORCH infections

General rules

• Transmission to the fetus generally rises with gestation (placenta larger and thinner), while severity falls: first-trimester infection damages organs as they form.
• IgM does not cross the placenta, so specific IgM in the baby means fetal infection; IgG in the newborn may be maternal and clears by 12–18 months.
• IgG avidity: low avidity means primary infection within about 3–4 months; high avidity means older infection (IgM can persist for a year).
• Primary maternal infection is far more dangerous than reactivation. CMV is the commonest congenital infection and a leading infective cause of learning disability and deafness.

The classic patterns

Rubella

• Mother has fever, fine rash and postauricular and suboccipital nodes.
• Risk depends on timing: under 12 weeks up to 80–90% of fetuses are affected; heart defects need infection in the first 8–10 weeks, while the heart forms. At 13–16 weeks the main risk is deafness (the cochlea stays vulnerable longest); after 20 weeks defects are rare.
• Deafness is the commonest single feature; PDA is the most characteristic cardiac defect.
• Confirm with rubella IgM plus low-avidity IgG. Confirmed primary infection in the first trimester (positive maternal IgM) is the classic indication to discuss termination. Infected infants shed virus for up to a year.
• Prevention: vaccinate non-immune girls and women before pregnancy with live MMR; avoid conception for 1 month. Accidental vaccination in pregnancy is not a reason for termination.

Cytomegalovirus

• Herpesvirus, latent in monocytes; spread by urine and saliva of young children, sex, transfusion and transplantation. Leucocyte-depleted blood is CMV-safe.
• Primary infection transmits in 30–40%, recurrent infection in about 1%. The virus destroys dividing germinal matrix cells, giving periventricular calcification and microcephaly.
• Diagnose congenital CMV by urine or saliva PCR within 21 days of birth. Most look normal at birth but need hearing follow-up.

Toxoplasma gondii

• A protozoan parasite whose definitive host is the cat; humans swallow oocysts from cat faeces or soil, or cysts in undercooked meat.
• Late infection transmits more often but is milder; early infection is severe.
• Spiramycin is started as soon as maternal infection is confirmed. It concentrates in the placenta and reduces placental transfer of the parasite; it does not treat a fetus that is already infected.
• Fetal infection is shown by amniotic fluid PCR after 18 weeks and at least 4 weeks after maternal infection. If positive, switch to pyrimethamine and sulfadiazine with folinic acid, which bypasses the dihydrofolate reductase block in human marrow.

Herpes simplex

• HSV-2 (and increasingly HSV-1) causes painful vesicles and shallow genital ulcers; latent in sacral ganglia. Oral HSV-1 is latent in the trigeminal ganglion.
• Neonatal risk is highest with primary infection in late pregnancy (25–50%, no maternal IgG yet) and under 3% with recurrence; caesarean section is advised for primary lesions near term.
• Neonatal encephalitis appears at days 10–28, often without skin vesicles: fever, lethargy, focal seizures, CSF lymphocytes with red cells. Confirm with CSF HSV PCR and give intravenous aciclovir.
• A nursing mother with a cold sore takes aciclovir, covers lesions and washes hands; breastfeeding continues unless a lesion is on the breast. Herpes keratitis (dendritic ulcer) is treated with topical aciclovir, never steroids alone.

Varicella-zoster

• After chickenpox the virus stays latent in sensory (dorsal root and cranial nerve) ganglia, reactivating as shingles.
• Non-immune woman exposed: check varicella IgG; give VZIG or aciclovir. Live vaccine is contraindicated in pregnancy.
• Maternal rash from 5 days before to 2 days after delivery: the baby receives virus but no protective maternal IgG, which takes about a week to form and cross. Severe neonatal varicella follows, so give VZIG to the baby. A rash 3 weeks before birth gives time for IgG to pass.
• Fetal infection after 20 weeks can be silent; the virus becomes latent and reactivates as shingles in infancy, without postnatal chickenpox.

Syphilis

• *Treponema pallidum*: a thin, motile spirochaete that cannot be cultured or Gram-stained. It crosses the placenta at any stage; transmission is highest in primary and secondary syphilis (60–100%).
• Primary chancre is painless with painless rubbery nodes; diagnose by dark-ground microscopy of chancre fluid. VDRL/RPR is non-treponemal, non-specific and falls with cure; TPHA/FTA-ABS is treponemal, the best confirmatory test, and stays positive for life.
• Congenital syphilis: infant IgM (IgM FTA-ABS or ELISA) proves infection, since IgM does not cross. Snuffles and moist skin lesions contain live treponemes, so staff wear gloves until 24 hours of penicillin. Bone lesions are osteochondritis and periostitis: irregular metaphyses and periosteal reaction cause painful pseudoparalysis, which can be mistaken for nerve injury or abuse.
• Benzathine penicillin treats mother and fetus; erythromycin crosses the placenta poorly, so the baby must be treated after birth.
• Jarisch–Herxheimer reaction: within hours of the first dose, cytokines (TNF, IL-6, IL-8) released as treponemes are killed cause fever, rigors, myalgia, contractions and reduced fetal movements. It is not penicillin allergy.

Parvovirus B19

• Slapped cheek (fifth disease). The virus infects erythroid progenitors via P antigen, halting red cell production for about a week.
• The mother's red cells live about 120 days, so her Hb barely falls. Fetal red cells survive a much shorter time (45–70 days) in a rapidly expanding red cell mass, so the fetus becomes severely anaemic, with high-output failure and hydrops. Check MCA Doppler; intrauterine transfusion if needed. Adults get aplastic crisis only when red cell survival is already short (sickle cell, spherocytosis).

Listeria monocytogenes

• Gram-positive rod with tumbling motility at room temperature. It multiplies at 4 °C, so refrigeration enriches it in soft cheese, pâté and stored cold meats.
• Reaches the placenta by the blood (internalin binds E-cadherin), causing villitis with microabscesses, brown-stained liquor, preterm labour, stillbirth and neonatal sepsis. A mild flu-like maternal illness can hide serious fetal infection.
• Resistant to cephalosporins: treat with ampicillin (or amoxicillin).

Remember Calcification near the ventricles is CMV; calcification scattered everywhere with hydrocephalus is toxoplasma.

Exam trap Rubella after the first trimester is not harmless: deafness can still follow infection up to about 16 weeks.

Exam trap IgG in a newborn does not prove infection; look for specific IgM or a rising titre.

How FCPS asks about this

• Commonest congenital infection: cytomegalovirus.
• Most characteristic cardiac defect in congenital rubella: patent ductus arteriosus; deafness is the commonest feature.
• Purpose of spiramycin in maternal toxoplasmosis: reduce placental transfer.
• Neonatal herpes encephalitis without vesicles: confirm with CSF HSV PCR.
• Best test for primary syphilis: dark-ground microscopy; best confirmatory serology is FTA-ABS.
• Fever and contractions hours after benzathine penicillin: Jarisch–Herxheimer reaction from cytokine release.
• Why refrigerated food spreads Listeria: it grows at 4 °C.