Feature	Toxoplasma gondii	Rubella	Cytomegalovirus (CMV)	HIV	HSV-2	Syphilis	Streptococcus (GBS)
Pathogen Type	Parasite	Virus	Virus (Herpesvirus)	Virus (Retrovirus)	Virus (Herpesvirus)	Bacterium (Treponema pallidum)	Bacterium (Streptococcus agalactiae)
Classic Triad/Presentation	Chorioretinitis, hydrocephalus, intracranial calcifications	Cataracts, heart defects, sensorineural hearing loss	No classic triad, but periventricular calcifications, microcephaly, and SNHL are characteristic.	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)

Congenital rubella infection

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Clinical features

• Intrauterine rubella infection: miscarriage, preterm birth, fetal growth restriction (especially likely if infection occurs during the first trimester)
• Congenital rubella syndrome
  • Triad of congenital rubella syndrome
    • Cardiac defect: most common defect (e.g., patent ductus arteriosus, pulmonary artery stenosis)
    • Cataracts: Other eye manifestations may also occur later in life, including glaucoma and salt and pepper retinopathy (abnormal retinal pigmentation)
    • Cochlear defect: bilateral sensorineural hearing loss
  • Early features
    • Hepatosplenomegaly, jaundice
    • Hemolytic anemia, thrombocytopenia
    • Petechiae and purpura, i.e., blueberry muffin rash (due to extramedullary hematopoiesis in the skin)
  • Late features
    • CNS defects: microcephaly, intellectual disability, panencephalitis
    • Skeletal abnormalities

Mnemonic

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

• Prevention
  • Maternal preconception immunization with live attenuated rubella vaccine

Congenital syphilis

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Pathogen

Treponema pallidum

Transmission

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

Clinical features of congenital syphilis

• Perinatal
  • Intrauterine fetal demise
  • Prematurity, low birth weight
  • Focal necrosis of the umbilical cord
• Mucocutaneous
  • Snuffles: copious rhinorrhea, often purulent or serosanguineous
  • Desquamating, maculopapular rash involving palms/soles
  • Fissures near orifices (eg, anal, oral)
  • Jaundice
• Musculoskeletal
  • Long bone abnormalities (eg, periosteal thickening, metaphyseal erosion)
    • Bilateral and symmetric metaphyseal erosions and periosteal inflammation of long bones
    • Pathologic fractures
    • Swelling, pain, and limited movement of affected extremities
• Reticuloendothelial
  • Hepatomegaly ± splenomegaly
  • Lymphadenopathy
  • Anemia, thrombocytopenia, leukopenia/leukocytosis