Congenital TORCH infections

ToRCHHeS

Feature	Toxoplasma gondii	Rubella	Cytomegalovirus (CMV)	HIV	HSV-2	Syphilis	GBS
Pathogen Type	Parasite	Virus	Virus (Herpesvirus)	Virus (Retrovirus)	Virus (Herpesvirus)	Bacterium (Treponema pallidum)	Bacterium (Streptococcus agalactiae)
Classic Triad/Presentation	Chorioretinitis, hydrocephalus, diffuse intracranial calcifications c	Cataracts, heart defects, sensorineural hearing loss	No classic triad, but periventricular calcifications, microcephaly, and SNHL are characteristic. c	No classic triad; failure to thrive, recurrent infections, and developmental delay are common	No classic triad; skin/mucous membrane lesions, encephalitis, or disseminated infection characterize.	Early: “Snuffles,” rash, bone lesions, lymphadenopathy and hepatosplenomegaly; Late: Hutchinson teeth, interstitial keratitis, saddle nose, saber shins	Early-onset: Respiratory distress, sepsis, pneumonia, meningitis (within first week, usually <24 hrs); Late-onset: Bacteremia, meningitis (after first week)
Other Key Differentiators	Often asymptomatic at birth, later chorioretinitis. Linked to cat feces/undercooked meat.	”Blueberry muffin” rash, often mild maternal illness. Preventable by MMR vaccine.	Most common congenital viral infection. Hearing loss can be late-onset.	Opportunistic infections are a hallmark. ART is crucial for prevention.	Vesicular lesions (but not always present). Often acquired during birth.	Multisystem; early/late manifestations differ. Penicillin is treatment.	Leading cause of neonatal sepsis/meningitis. Maternal colonization is key risk factor. Intrapartum antibiotics prevent early-onset disease.
Transmission	Transplacental, ingestion	Transplacental, respiratory	Transplacental, body fluids	Transplacental, birth, breastfeeding	Primarily during birth	Transplacental, birth	Vertical transmission during birth (primarily), ascending infection, rarely nosocomial/community-acquired (late-onset)

Tip

All TORCH infections can cause blueberry muffin rash, except GBS.

Congenital rubella infection

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Clinical features

• Classic Triad: c2
  1. Sensorineural hearing loss (SNHL): Most common finding overall.
  2. Cataracts: Often bilateral, presents with leukocoria (white pupillary reflex). May also show microphthalmia, glaucoma, or “salt-and-pepper” retinopathy.
  3. Cardiac defects: Patent ductus arteriosus (PDA) (continuous machine-like murmur) or peripheral pulmonary artery stenosis.
• Neonatal Systemic Signs:
  • “Blueberry muffin” rash: Dermal extramedullary hematopoiesis (purpuric macules/papules).
  • Intrauterine growth restriction (IUGR) & low birth weight.
  • Microcephaly, anterior fontanelle fullness.
  • Hepatosplenomegaly, jaundice, thrombocytopenia.
  • Radiolucent bone lesions: “Celery stalk” appearance in long bones.

Mnemonic

CCC-Triad of congenital rubella syndrome: Cataracts, Cochlear defects, Cardiac abnormality

• Prevention
  • Maternal preconception immunization with live attenuated rubella vaccine

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Congenital syphilis

Pathogen

Treponema pallidum

Transmission

• Fetus: transplacental transmission from infected mother
• Neonate: perinatal transmission during birth

Clinical features

• Early Presentation (< 2 years of age):
  • “Snuffles”: Copious, persistent mucopurulent or bloody rhinitis.
  • Maculopapular rash: Desquamating or vesiculobullous rash involving palms and soles. c
  • Bone changes: Periostitis, Wimberger sign (metaphyseal erosion of medial proximal tibia), pseudoparalysis of Parrot (refusal to move painful limb).
  • Systemic: HSM, jaundice, generalized lymphadenopathy, hydrops fetalis, IUGR.
• Late Presentation (> 2 years of age):
  • Hutchinson Triad:
    1. Hutchinson teeth (notched, peg-shaped central incisors).
    2. Interstitial keratitis (can lead to blindness).
    3. Sensorineural hearing loss (CN VIII deficit).
  • Facial/Skeletal: Saddle nose, saber shins (anterior tibial bowing), frontal bossing, Mulberry molars, Clutton joints (painless bilateral knee effusions).