Paediatrics chapters

Common neonatal skin rashes and TORCH infections

The harmless rashes and marks of the newborn and how to tell them from infection, followed by the congenital TORCHS infections (toxoplasmosis, syphilis, rubella, CMV, herpes and others): their typical features, diagnosis, treatment and prevention.

UHS PGET syllabus: Neonatology (10 MCQs), Common neonatal problems: common neonatal skin rashes; TORCHS infections and effectsUpdated November 2026
In 30 seconds
  • Most newborn rashes are harmless: erythema toxicum (red blotches with eosinophil-filled pustules, day 1-3), milia, Mongolian spots and cutis marmorata need only reassurance; blisters, purpura, sclerema or an ill baby suggest infection.
  • TORCH infections (toxoplasma, others such as syphilis, rubella, CMV, herpes) share IUGR, hepatosplenomegaly, jaundice, rash, low platelets, microcephaly and eye disease.
  • Clues: toxoplasma = hydrocephalus + chorioretinitis + diffuse calcification; rubella = cataract + PDA + deafness; CMV = microcephaly + periventricular calcification + deafness; herpes = vesicles, encephalitis; syphilis = snuffles, palm and sole rash, bone lesions.
On this page

Overview

Newborn skin is thin, less hairy and less well attached between layers than adult skin, so it reacts in its own ways. Most spots and marks seen in the first weeks are harmless and self-limiting; the doctor's job is to reassure the parents and to recognise the few rashes that mean infection.

TORCH infections are acquired before or during birth. They cause similar features, so the clue to the organism lies in a few characteristic signs.

Part 1: Common neonatal skin conditions

Harmless rashes and marks

ConditionAppearanceKey facts
Erythema toxicum neonatorumRed blotches with a small central papule or pustule, on the face, trunk and limbs; palms and soles sparedUp to 50% of term babies (fewer preterm); starts at 24-48 hours (can appear up to day 10); pustule smear shows eosinophils; clears in 5-7 days; no treatment
MiliaTiny pearly white or yellow spots on the nose, cheeks and chinBlocked glands; disappear in the first weeks
MiliariaFine clear vesicles (crystallina) or red papules (rubra) in skin folds and covered areasBlocked sweat ducts from overheating and overwrapping; cool the baby
Mongolian spotsFlat slate-grey to blue-black patches, mainly over the lumbosacral area and buttocksDermal melanocytes; Nelson notes dermal melanosis in 70-90% of Asian, African-American, Hispanic and Native American babies; usually fade by about 7 years (Akbar); record them so they are not mistaken for bruises
Cutis marmorataLacy, net-like bluish mottling when the baby is coldNormal vascular response; clears on rewarming; if it persists beyond 6 months, look for congenital hypothyroidism
Salmon patch (stork mark)Flat pink patches on the eyelids, forehead and napeCapillary marks; facial ones fade, nape ones may persist
Pustular melanosisSmall dry vesicles or pustules on a brown pigmented base, present at birthBenign (Nelson); commoner in dark-skinned babies; may mimic herpes or impetigo
Capillary (strawberry) haemangiomaRaised red lump; deeper cavernous ones look blueGrows after birth, then resolves by about 1-4 years (Nelson); large ones can cause heart failure or trap platelets
High-yield

Erythema toxicum looks alarming but the baby is well, and the pustule contains eosinophils, not neutrophils or bacteria.

Exam trap

Mongolian spots are not bruises and are not a sign of abuse; they are present from birth and do not change colour over days as bruises do.

Rashes and skin signs that suggest disease

ConditionFeaturesSignificance
ScleremaHard, cold, non-pitting skin, starting on the buttocks, cheeks and thighs and spreadingSign of severe illness: sepsis, pneumonia, severe gastroenteritis, hypothermia
Staphylococcal pustules and bullous impetigoPustules or blisters around the umbilicus, nappy area and folds; honey crustsS. aureus; topical or systemic antibiotics; check the cord
Staphylococcal scalded skin syndrome (SSSS)Starts with a crusted lesion (often umbilicus or nappy area), then tender red skin, large blisters and sheets of peeling; Nikolsky sign positiveExfoliative toxin of S. aureus splits the upper epidermis; spreads in nurseries; IV anti-staphylococcal antibiotic (cloxacillin); steroids contraindicated; heals in about 5-7 days without scars
Candida (thrush, nappy rash)White plaques in the mouth; bright red nappy rash with satellite spots involving skin foldsTopical antifungal (nystatin, clotrimazole)
Vesicles in clustersGrouped vesicles on a red base, skin, eyes or mouthNeonatal herpes until proven otherwise; urgent IV acyclovir
Petechiae and purpuraPinpoint or larger bleeds in the skinSepsis, TORCH, thrombocytopenia, DIC
"Blueberry muffin" rashBlue-purple papules (skin extramedullary haematopoiesis)Congenital rubella or CMV
Palm and sole rash with peelingCopper-red maculopapular rash, desquamationCongenital syphilis
OmphalitisRed, swollen umbilicus with pus and spreading rednessSystemic antibiotics; risk of sepsis and portal vein thrombosis
Memory hook

Nikolsky = "Nothing sticks": the top of the skin slides off with gentle rubbing in SSSS.

Part 2: TORCH(S) infections

What TORCH stands for

Toxoplasmosis, Others (syphilis, varicella, hepatitis B, HIV, parvovirus, TB), Rubella, Cytomegalovirus, Herpes simplex. The S in TORCHS stresses syphilis.

Shared features

  • IUGR / low birth weight (often symmetrical)
  • Hepatosplenomegaly, jaundice (often conjugated)
  • Thrombocytopenia, petechiae, purpura, anaemia
  • Rash (including blueberry muffin)
  • Microcephaly, seizures, intracranial calcification
  • Eye disease: chorioretinitis, cataract
  • Many are normal at birth but later develop deafness, intellectual disability and eye problems.

Diagnosis rests on IgM antibody in the baby (IgM does not cross the placenta), rising or persisting IgG over months (maternal IgG in an uninfected baby is usually gone by 4-9 months), culture and PCR.

Comparison table

InfectionHallmark featuresBrain imagingTreatment
ToxoplasmosisHydrocephalus, chorioretinitis, calcification (classic triad); seizures, hepatosplenomegalyDiffuse calcification scattered through the brainPyrimethamine + sulfadiazine + folinic acid; spiramycin in pregnancy
RubellaCataract, glaucoma, PDA, pulmonary artery stenosis, sensorineural deafness, blueberry muffin rash, metaphyseal lucenciesMicrocephalyNo specific treatment; follow-up; isolate
CMVMicrocephaly, chorioretinitis, sensorineural deafness, hepatosplenomegaly, petechiae, jaundice, pneumonitisPeriventricular calcificationValganciclovir (or ganciclovir) for CNS disease, organ involvement or hearing loss
Herpes simplexVesicles of skin, eyes and mouth; encephalitis; disseminated disease (liver, lungs, DIC)Haemorrhagic encephalitisIV acyclovir
SyphilisSnuffles, palm and sole rash, periostitis and osteochondritis, hepatosplenomegaly, jaundice; later Hutchinson teeth, saddle nose, bowed (sabre) shins-Penicillin
Memory hook

Calcification site: CMV is Central (periventricular); toxo is Total (scattered).

Toxoplasmosis

  • Toxoplasma gondii, a protozoan; infection comes from cat faeces (soil, litter) and undercooked meat or unpasteurised milk.
  • Mostly from a primary maternal infection in pregnancy. Infection later in pregnancy is transmitted more often, but infection earlier causes more severe fetal damage.
  • 70-90% of infected babies have no signs at birth but may later develop visual loss and learning problems.
  • Diagnosis: toxoplasma IgM (and IgA) in the baby, PCR of fluids, eye examination for chorioretinitis, CT for calcification, CSF (raised protein, mononuclear cells).
  • Treatment: pyrimethamine and sulfadiazine with folinic acid; steroids for active eye or CNS disease.
  • Prevention: avoid raw meat and contact with cat litter in pregnancy.

Rubella (congenital rubella syndrome)

  • Spread by respiratory droplets; maternal infection in the first trimester infects the fetus in more than 90% of cases. Previous immunity (infection or vaccine) protects the fetus.
  • Features: IUGR, microcephaly, cataract, glaucoma, microphthalmia, chorioretinitis ("salt and pepper" retinopathy), PDA and peripheral pulmonary artery stenosis, sensorineural deafness (the commonest late defect), blueberry muffin rash, hepatosplenomegaly, thrombocytopenia, metaphyseal lucencies on long-bone X-ray.
  • Diagnosis: rubella-specific IgM in the newborn, persisting IgG, virus from throat, urine or CSF.
  • Affected babies shed virus for up to a year; keep them away from non-immune pregnant women.
  • Prevention: rubella vaccine (MMR/MR) for girls and non-immune women; it is a live vaccine and must not be given in pregnancy.
Exam trap

A positive IgG in a newborn may simply be maternal antibody; congenital infection is shown by IgM in the baby or IgG that persists or rises over months.

High-yield

Congenital rubella classic triad: cataract, congenital heart disease (PDA) and sensorineural deafness.

Cytomegalovirus (CMV)

  • A DNA herpes virus; the commonest congenital (vertically transmitted) infection. It passes across the placenta, during birth and in breast milk.
  • Both primary and recurrent maternal infection can infect the fetus; symptomatic babies are usually born after a primary infection. Greatest risk to the brain is in the first 22 weeks of pregnancy.
  • Most infected babies are asymptomatic, but some develop progressive sensorineural deafness later; CMV is the leading infective cause of deafness in children.
  • Symptomatic disease: IUGR, microcephaly, periventricular calcification, chorioretinitis, hepatosplenomegaly, jaundice, petechiae, pneumonitis.
  • Diagnosis: virus in urine or saliva (culture or PCR) within the first 3 weeks of life (Nelson; later samples cannot separate congenital from acquired infection).
  • Treatment: valganciclovir for symptomatic CNS or organ disease; hearing follow-up for all.
  • Prevention: CMV-negative blood products for preterm babies; hand hygiene in pregnancy.
High-yield

CMV is the commonest congenital infection, and many infected babies look normal at birth but lose hearing later, so they need repeated hearing tests.

Neonatal herpes simplex

  • About three quarters are HSV-2; about 80% are caught during delivery from the mother's genital tract; some are intrauterine or postnatal.
  • Risk is much higher with a primary maternal infection (about 30-50%) than with a recurrent one (about 3-5%).
  • Three patterns:

1. Skin, eye and mouth disease (vesicles, keratoconjunctivitis) 2. CNS disease (encephalitis with seizures and lethargy) 3. Disseminated disease (sepsis-like, liver failure, pneumonitis, DIC; highest mortality)

  • Many babies have no skin lesions at first, so suspect HSV in any newborn with sepsis-like illness, seizures or raised liver enzymes.
  • Diagnosis: PCR of CSF, blood and vesicle fluid; Tzanck smear shows giant cells; CSF shows red and white cells.
  • Treatment: IV acyclovir at once.
  • Prevention: caesarean section for women with active genital lesions (especially primary infection) in labour.

Congenital syphilis

  • Early (under 2 years): snuffles (bloody nasal discharge), copper-red rash on palms and soles that peels, periostitis and osteochondritis (painful limbs, pseudoparalysis), hepatosplenomegaly, jaundice, condylomata lata, nephrotic syndrome.
  • Late (over 2 years): Hutchinson teeth (notched incisors), saddle nose, bowing of the shins (sabre shins), frontal bossing, mulberry molars, rhagades (scars at the mouth corners), Clutton joints, interstitial keratitis, eighth nerve deafness. Hutchinson triad = interstitial keratitis + eighth nerve deafness + Hutchinson teeth.
  • Diagnosis: treponemes in lesion scrapings; serology (non-treponemal and treponemal tests, IgM).
  • Treatment: penicillin. Prevention: screen and treat mothers in pregnancy.

Hepatitis B

  • Mainly caught at delivery from maternal blood; risk is highest when the mother has acute infection late in pregnancy (Akbar: 50-75% transmission) or is HBeAg positive.
  • Screen all pregnant women for HBsAg.
  • Babies of HBsAg-positive mothers: HBIG 0.5 mL IM plus hepatitis B vaccine 0.5 mL IM at a separate site, ideally within 12 hours of birth, then complete the vaccine course.
  • Breastfeeding is allowed.

Tuberculosis and the newborn

  • Congenital TB is rare; features are fever, failure to thrive, hepatosplenomegaly and respiratory distress.
  • Mother with active pulmonary TB: treat the mother; give the baby isoniazid prophylaxis until the mother has been sputum-culture negative for about 3 months, then do a Mantoux test: if negative, stop isoniazid and give BCG; if positive, give full treatment.
  • Breastfeeding continues.

Other "O" infections in brief

  • Varicella: maternal infection early in pregnancy causes limb hypoplasia, skin scarring and eye defects; around delivery it can cause severe neonatal chickenpox (give zoster immunoglobulin).
  • HIV: transmission reduced by maternal antiretroviral therapy and infant prophylaxis; follow the national programme.
  • Parvovirus B19: fetal anaemia and hydrops fetalis.
Exam focus

Expect: erythema toxicum with eosinophils in a well baby at 24-48 hours; Mongolian spots over the sacrum fading by school age; cutis marmorata persisting with hypothyroidism; sclerema as a sign of sepsis; SSSS with Nikolsky sign treated with cloxacillin and no steroids; the shared TORCH picture; toxoplasma triad with diffuse calcification; rubella cataract, PDA and deafness with first-trimester risk above 90%; CMV as the commonest congenital infection with periventricular calcification and deafness; HSV-2 caught during delivery treated with acyclovir and prevented by caesarean section; early and late signs of congenital syphilis; HBIG plus vaccine within 12 hours for babies of HBsAg-positive mothers; breastfeeding allowed with maternal hepatitis B and TB.

Quick revision

  • Erythema toxicum: well baby, day 1-3, eosinophils, gone in a week.
  • Milia: white spots on the nose; miliaria: sweat duct block from overheating.
  • Mongolian spots: lumbosacral, fade by about 7 years; not bruises.
  • Sclerema = severe illness; SSSS = Nikolsky positive, cloxacillin, no steroids.
  • TORCH common: IUGR, hepatosplenomegaly, jaundice, low platelets, microcephaly, eye disease.
  • Toxo: hydrocephalus + chorioretinitis + diffuse calcification; pyrimethamine + sulfadiazine.
  • Rubella: cataract + PDA + deafness; first trimester; live vaccine not in pregnancy.
  • CMV: commonest; microcephaly + periventricular calcification + deafness; valganciclovir.
  • HSV: HSV-2 at delivery; vesicles, encephalitis; IV acyclovir.
  • Syphilis: snuffles, palm/sole rash, periostitis; later Hutchinson teeth; penicillin.
  • Hep B: HBIG + vaccine within 12 h; breastfeed.

Written by The House Job from standard references (Basis of Paediatrics by Pervez Akbar; Nelson Essentials of Paediatrics).

FAQ

Is erythema toxicum a sign of infection?

No; it is a harmless rash of well babies, and a smear of the pustules shows eosinophils rather than bacteria.

How can CMV and toxoplasmosis be told apart on a brain scan?

CMV typically gives periventricular calcification with microcephaly, while toxoplasmosis gives scattered calcification with hydrocephalus.

What is the classic triad of congenital rubella?

Cataract, congenital heart disease (especially PDA) and sensorineural deafness.

Can a mother with hepatitis B breastfeed?

Yes, as long as the baby gets HBIG and hepatitis B vaccine at birth and completes the vaccine course.