AT

Childhood Viral Exanthems & Paramyxoviruses

Microbiology · Virology · lean revision notes

Childhood Viral Exanthems & Paramyxoviruses

A rash plus fever in a child is a recurring NEET PG image-based and one-liner favourite. This note consolidates the "classic six" childhood exanthems with a sharp focus on measles, mumps and rubella (the paramyxovirus-heavy MMR triad) plus roseola (HHV-6), arming you with the eponyms, cut-offs and vaccine facts that examiners love.

Definition & the "Classic Six" exanthems

An exanthem is a widespread rash that erupts as a sign of systemic (usually viral) infection; the matching mucous-membrane eruption is an enanthem (e.g. Koplik spots, Forchheimer spots). Historically six classic childhood exanthems were numbered:

No. Disease Causative agent Family
First Measles (rubeola) Measles virus Paramyxoviridae (Morbillivirus)
Second Scarlet fever Streptococcus pyogenes (erythrogenic toxin) Bacterial (not viral)
Third Rubella (German/3-day measles) Rubella virus Matonaviridae (formerly Togaviridae)
Fourth "Filatov-Dukes" disease Disputed/obsolete entity
Fifth Erythema infectiosum Parvovirus B19 Parvoviridae
Sixth Roseola infantum (exanthem subitum) HHV-6 (and HHV-7) Herpesviridae

High-yield: Measles, mumps and rubella are the exam-darlings, but note the family trap — measles and mumps are paramyxoviruses (enveloped, ssRNA, negative-sense, helical), whereas rubella is NOT a paramyxovirus (it is a positive-sense RNA virus, now classified under Matonaviridae). Examiners frequently club rubella with measles to mislead you.

Paramyxoviridae snapshot

Paramyxoviruses are enveloped, non-segmented, negative-sense, single-stranded RNA viruses with helical nucleocapsids. Medically important members: Measles, Mumps, Parainfluenza, RSV, Nipah, Hendra. Two key surface glycoprotein patterns:

  • Measles (Morbillivirus): H (haemagglutinin, no neuraminidase) + F (fusion) protein. No neuraminidase.
  • Mumps & Parainfluenza (Rubulavirus/Respirovirus): HN (haemagglutinin-neuraminidase) + F protein.
  • RSV (Pneumovirus): only F protein, no haemagglutinin, no neuraminidase.

The F (fusion) protein mediates cell-to-cell fusion → multinucleated giant (syncytial) cells, the morphologic hallmark across this family.


Measles (Rubeola)

Pathophysiology

Measles virus enters via the respiratory tract, replicates in lymphoid tissue, and causes a primary then secondary viraemia. The receptor is CD150 (SLAM) on immune cells and nectin-4 on epithelium. It induces profound, transient immunosuppression ("immune amnesia") that predicts secondary bacterial infections.

Clinical features — the 3 C's

Cough, Coryza, Conjunctivitis (the "3 C's") + high fever in the prodrome. Then:

  1. Koplik spots → pathognomonic enanthem: tiny bluish-white/grey specks on an erythematous base on the buccal mucosa opposite the second molars, appearing 1–2 days before the rash.
  2. Rash → erythematous maculopapular, begins behind the ears/at the hairline → face → spreads cephalocaudally (head to trunk to limbs), becomes confluent, and clears with brownish staining and fine desquamation.

Disease flow: Exposure → incubation 10–14 days → prodrome (3 C's + fever + Koplik spots) rash on day 3–4 cephalocaudal spread resolution with desquamation.

Histology / cytology

Warthin-Finkeldey giant cells — multinucleated giant cells (reticuloendothelial syncytial cells with up to 50–100 nuclei) found in lymphoid tissue (tonsils, appendix, lymph nodes). These are the cytologic eponym of measles.

High-yield: Koplik spots = pathognomonic enanthem; Warthin-Finkeldey cells = pathognomonic histology; rash spreads cephalocaudally.

Complications

  • Otitis media — most common complication overall.
  • Pneumonia — most common cause of measles death; may be Hecht's giant cell pneumonia (in immunocompromised).
  • Acute post-measles encephalomyelitis (1 in 1000, days–weeks later, immune-mediated/ADEM-like).
  • Subacute sclerosing panencephalitis (SSPE) — a slow virus infection.

SSPE (very high yield)

A late, progressive, fatal degenerative CNS disease appearing ~7–10 years after measles (often after natural infection before age 2). Defective M (matrix) protein prevents viral budding → persistent intracellular virus.

Feature SSPE finding
EEG Periodic burst-suppression complexes (Radermecker complexes)
CSF Raised anti-measles antibody (oligoclonal IgG); high CSF:serum antibody ratio
Histology Intranuclear & intracytoplasmic inclusions (Dawson's inclusion bodies)
Clinical Myoclonic jerks, cognitive decline, dementia, death

High-yield: SSPE → defective M protein → high anti-measles antibody titres in CSF + periodic EEG complexes. Mnemonic: "M for Matrix, M for Measles, M for Myoclonus."

Diagnosis & management

  • Investigation of choice: Serology — measles-specific IgM (positive within 1–3 days of rash) or a 4-fold IgG rise. RT-PCR for RNA also used.
  • Management: Supportive. Vitamin A reduces morbidity and mortality (WHO recommends two doses on consecutive days). Vaccine: live attenuated (in MMR), given at 9 months (India schedule) and a second dose at 15–18 months.

Mumps

Pathophysiology & features

A paramyxovirus (Rubulavirus, HN + F proteins) transmitted by droplets. After respiratory replication and viraemia it shows tropism for glandular and neural tissue.

  • Parotitis — bilateral (or unilateral) painful swelling; classically the angle of the jaw is obscured and the ear lobe is pushed up and out. Eating sour food worsens pain (Stensen's duct orifice may be erythematous).
  • Orchitis — most common extra-salivary manifestation in post-pubertal males (15–30%); usually unilateral; sterility is rare despite the exam folklore.
  • Aseptic meningitis / meningoencephalitis — mumps is a leading viral cause of aseptic meningitis where vaccination is poor; CSF shows lymphocytic pleocytosis, and characteristically LOW CSF glucose may occur (a pitfall mimicking bacterial meningitis).
  • Pancreatitis, oophoritis, deafness (mumps is a cause of acquired unilateral sensorineural deafness), myocarditis.

High-yield: Mumps orchitis is usually unilateral and rarely causes sterility; mumps is a classic cause of aseptic meningitis with occasionally low CSF sugar.

Diagnosis & management

  • Investigation of choice: Serum mumps IgM; rising IgG; RT-PCR of saliva/CSF. Serum amylase is raised (from parotid and/or pancreas).
  • Management: Supportive. Live attenuated vaccine in MMR. Jeryl Lynn strain is the classic mumps vaccine strain.

Rubella (German measles / 3-day measles)

Virology & postnatal disease

Positive-sense ssRNA, enveloped virus, family Matonaviridae (reclassified out of Togaviridae). Mild self-limiting illness in children:

  • Tender post-auricular, suboccipital and posterior cervical lymphadenopathy — a near-signature.
  • Forchheimer spots — petechiae on the soft palate (enanthem; not specific, also seen in scarlet fever).
  • Pink maculopapular rash that, like measles, starts on the face and spreads down, but is milder, lasts ~3 days, and does not coalesce/desquamate.

Congenital Rubella Syndrome (CRS) — extremely high yield

Maternal infection in the first trimester is teratogenic (risk highest <12 weeks, ~80–90%). Classic Gregg's triad:

Component of Gregg triad Lesion
Eye Cataract (salt-and-pepper retinopathy), microphthalmia, glaucoma
Ear Sensorineural deafness (most common single defect overall)
Heart Patent ductus arteriosus (PDA) (and peripheral pulmonary artery stenosis)

Other features: "blueberry muffin" rash (dermal extramedullary haematopoiesis), hepatosplenomegaly, thrombocytopenia, microcephaly, intellectual disability, "celery-stalking" of long bones.

TORCH context flow: Maternal rubella in 1st trimester transplacental spread Gregg triad (cataract + SNHL + PDA) blueberry muffin baby; infants shed virus for months and are infectious.

High-yield: SNHL is the most common single defect in CRS; PDA is the most common cardiac lesion. The "blueberry muffin baby" appearance is shared with congenital CMV (and other congenital infections) — not unique to rubella.

Diagnosis & management

  • Investigation of choice (acquired): Rubella IgM serology.
  • Congenital: IgM in neonatal serum, or persistent/rising IgG beyond expected maternal decline; viral RNA from throat/urine.
  • Management: Supportive; no specific antiviral. Prevention via live attenuated MMR. Vaccine is contraindicated in pregnancy and pregnancy should be avoided for 4 weeks after vaccination (though no CRS case has ever been documented from the vaccine).

Roseola Infantum (Exanthem Subitum / Sixth Disease)

Caused by HHV-6 (chiefly variant B; HHV-7 causes a minority) — a Herpesvirus (dsDNA, enveloped), not a paramyxovirus.

  • Affects infants 6 months–2 years.
  • Classic course: 3–5 days of HIGH fever in a well-looking child → fever drops abruptly → THEN a rose-pink maculopapular rash erupts on the trunk (rash appears after defervescence — hence "subitum"=sudden).
  • Most common identifiable cause of febrile seizures in this age group.
  • Nagayama spots — papules on the soft palate/uvula (enanthem).
  • HHV-6 establishes latency; reactivation matters in transplant recipients.

High-yield: Roseola = fever first, rash later (rash appears when fever breaks). Leading viral cause of febrile convulsions in infants.


Comparison table: the three "measles-like" rashes

Feature Measles Rubella Roseola
Agent Measles virus (Paramyxo) Rubella virus (Matonaviridae) HHV-6 (Herpes)
Genome (−) ssRNA (+) ssRNA dsDNA
Prodrome Severe (3 C's, high fever) Mild High fever, child well
Pathognomonic sign Koplik spots Post-auricular nodes; Forchheimer spots Rash after fever; Nagayama spots
Rash spread Cephalocaudal, confluent, stains Cephalocaudal, mild, 3 days Trunk → periphery, after fever
Lymphadenopathy Generalised Post-auricular/suboccipital Mild
Key complication SSPE, pneumonia CRS in pregnancy Febrile seizures
Vaccine MMR (live) MMR (live) None

Erythema infectiosum (Parvovirus B19) — quick differential

Although not in the MMR group, B19 is a frequent distractor.

  • "Slapped-cheek" appearance then a lacy/reticular rash on limbs.
  • Binds the P antigen (globoside) receptor on erythroid precursorstransient aplastic crisis in chronic haemolysis (e.g. sickle cell, hereditary spherocytosis).
  • In pregnancy → hydrops fetalis; in immunocompromised → pure red cell aplasia.
  • Causes arthropathy in adults.

High-yield: Parvovirus B19 → slapped cheek, aplastic crisis in haemolytic anaemia, hydrops fetalis, single-stranded DNA, non-enveloped — the only DNA virus that is ssDNA.


Hand-foot-and-mouth & other vesicular mimics (differentials)

  • Hand-foot-mouth diseaseCoxsackievirus A16 / Enterovirus 71; oral ulcers + vesicles on palms/soles. EV71 causes more severe CNS disease.
  • Varicella (chickenpox) — VZV; centripetal, pruritic, vesicles in different stages simultaneously ("dew drop on rose petal"); contrast with smallpox (centrifugal, same-stage lesions).
  • Scarlet fever — sandpaper rash, strawberry tongue, perioral pallor, Pastia's lines; bacterial (GAS).

High-yield: Distinguish varicella (lesions in different stages, centripetal) from smallpox (same stage, centrifugal) — a perennial MCQ.


Diagnosis & investigation of choice — consolidated

  • Measles / Rubella / Mumps: Specific IgM serology is the practical investigation of choice for acute diagnosis; RT-PCR confirms and is used for outbreak genotyping.
  • SSPE: elevated CSF anti-measles antibody + periodic EEG complexes.
  • CRS: neonatal rubella IgM / persistent IgG / RNA from urine-throat.
  • Roseola: clinical; HHV-6 PCR if needed.

Management / prevention — consolidated

  • No specific antiviral for measles, mumps or rubella; care is supportive.
  • Vitamin A for measles (mortality benefit, esp. malnourished).
  • MMR is live attenuated → contraindicated in pregnancy and significant immunosuppression; can be given in HIV if not severely immunosuppressed.
  • India National Immunisation Schedule: Measles/MR at 9–12 months and 16–24 months (second dose); measles-rubella (MR) campaign targets rubella elimination.

High-yield: A live vaccine in pregnancy is a classic "wrong answer to choose" — MMR, varicella, OPV, BCG, yellow fever are all live and contraindicated in pregnancy.


Recently asked / exam angle

  • Image of buccal mucosa with white spots → Koplik spots → Measles (commonest image MCQ in this topic).
  • "Defective M protein, periodic EEG, high CSF antibody" → SSPE.
  • Most common single defect / commonest cardiac defect in CRS → SNHL / PDA.
  • "Rash appears after fever subsides in an infant" → Roseola/HHV-6, and HHV-6 as the commonest cause of febrile seizures.
  • Family identification: which is NOT a paramyxovirus among Measles/Mumps/RSV/Rubella → Rubella.
  • RSV has only the F protein (no H, no N) — frequently paired with bronchiolitis in paediatrics MCQs.
  • Warthin-Finkeldey giant cells asked as a stand-alone histology recall for measles.
  • Jeryl Lynn = mumps vaccine strain; Edmonston = measles vaccine lineage.
  • Blueberry muffin baby differential: congenital rubella vs congenital CMV.
  • Parvovirus B19 → transient aplastic crisis in a sickle-cell child.

Rapid revision

  1. Paramyxoviruses = enveloped, negative-sense ssRNA, helical; F protein → syncytia. Members: measles, mumps, parainfluenza, RSV, Nipah.
  2. Rubella is NOT a paramyxovirus — it is positive-sense RNA, family Matonaviridae.
  3. Measles 3 C's = Cough, Coryza, Conjunctivitis; Koplik spots are pathognomonic; rash spreads cephalocaudally.
  4. Warthin-Finkeldey cells = measles histology; measles receptor = CD150 (SLAM) + nectin-4.
  5. SSPE = defective M protein, 7–10 yrs later, high CSF anti-measles antibody, periodic EEG complexes, Dawson's inclusion bodies.
  6. Vitamin A reduces measles mortality; commonest measles complication = otitis media; commonest cause of death = pneumonia.
  7. Mumps = Rubulavirus (HN+F); orchitis (post-pubertal, usually unilateral, rarely sterile), aseptic meningitis (may have low CSF sugar); Jeryl Lynn vaccine strain.
  8. Rubella = post-auricular nodes, Forchheimer spots, 3-day mild rash.
  9. CRS Gregg triad = Cataract + SNHL + PDA; SNHL = commonest single defect; PDA = commonest cardiac lesion; blueberry muffin rash.
  10. Roseola (HHV-6, dsDNA herpesvirus) = high fever first, rash after defervescence; commonest cause of febrile seizures; Nagayama spots.
  11. Parvovirus B19 (ssDNA, non-enveloped) = slapped cheek, aplastic crisis, hydrops fetalis, P-antigen receptor.
  12. MMR is live attenuated → contraindicated in pregnancy and severe immunosuppression; India gives doses at 9 mo and 16–24 mo.