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Scarlet fever
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Exam Tips
- Classic triad: fever + sore throat + diffuse blanching sandpaper rash; look for Pastia lines and strawberry tongue.
- On darker skin, texture and distribution of rash may be more useful than erythema intensity.
- Palms/soles are usually spared in scarlet fever, helping distinguish from staphylococcal TSS where palmoplantar involvement is common.
- Diagnosis is usually clinical; routine throat swab and blood tests are not needed in straightforward cases.
- ASO titres do not diagnose acute scarlet fever; they are retrospective tests for post-streptococcal complications.
- See figure: classic scarlet fever rash distribution and strawberry tongue in your paediatric infectious diseases chapter on GAS.
Definition
Scarlet fever (scarlatina) is a toxin-mediated illness caused by Group A beta-haemolytic Streptococcus (Streptococcus pyogenes), usually arising with streptococcal pharyngitis and a characteristic diffuse erythematous "sandpaper" rash. In UK practice it is a notifiable infection because of transmissibility and the risk of outbreaks in schools/nurseries, and because a small proportion progress to invasive Group A streptococcal disease.
Pathophysiology
Toxigenic strains of S. pyogenes infect the pharynx (or less commonly skin), then release streptococcal pyrogenic exotoxins (for example SpeA/SpeC) that act as superantigens. This drives widespread T-cell activation and cytokine release, producing fever, punctate erythema, Pastia lines, and mucosal changes such as strawberry tongue. Incubation is typically 2-3 days (range about 1-6 days), spread is mainly via respiratory droplets/direct contact, and untreated patients may remain infectious for 2-3 weeks. Later immune sequelae are due to host response rather than persistent local infection (molecular mimicry in acute rheumatic fever; immune-complex deposition in post-streptococcal glomerulonephritis).
Risk Factors
- Age 2-8 years (peak burden in young children)
- Close-contact settings (nurseries, schools, crowded households/institutions)
- Winter-spring seasonality in the UK (highest activity usually Dec-May)
- Recent or concurrent varicella (chickenpox) or influenza increases iGAS risk
- Immunosuppression/immunocompromise
- Comorbidity: diabetes, cardiovascular disease, skin breakdown, malignancy
- Pregnancy, postpartum period (within 28 days), and neonates
- Older age (especially >=75 years) for severe/invasive GAS outcomes
- Injecting drug use or alcohol dependence (for invasive disease risk)
Clinical Features
Symptoms
- Acute sore throat
- Fever (often >38.3 C)
- Headache, malaise/fatigue
- Nausea or vomiting
- Rash usually starts on chest/abdomen then generalizes within 24-48 hours
- Pruritus may occur; later desquamation at fingers/toes
Signs
- Blanching, finely punctate erythematous rash with sandpaper texture
- Pastia lines (deep red linear accentuation in flexures: neck/axilla/groin/elbows/knees)
- Strawberry tongue (initial white coat then red swollen papillae)
- Pharyngeal erythema/exudative tonsillitis and soft-palate petechiae
- Tender anterior cervical lymphadenopathy
- Flushed face with circumoral pallor
- Palms and soles usually spared early
Investigations
Clinical diagnosis (history + examination):Typical fever, sore throat, sandpaper rash, and strawberry tongue; diagnosis is usually clinical
Throat swab for GAS culture (before antibiotics when indicated):Growth of Group A Streptococcus; useful if diagnosis is uncertain, during suspected outbreak, true penicillin allergy (for susceptibility), or high-risk contact setting
Blood tests:Not routinely required in uncomplicated scarlet fever
ASO/anti-DNase B serology:Not useful acutely; rising titres after 1-3 weeks support prior GAS infection in suspected rheumatic fever or post-streptococcal glomerulonephritis
Management
Lifestyle Modifications
- Safety-net for red flags: toxicity, hypotension, severe pain out of proportion, rapidly progressive soft-tissue signs, breathing difficulty, reduced urine output, or persistent fever
- Oral hydration, rest, and soft diet for odynophagia
- Exclude from school/nursery until 24 hours after starting appropriate antibiotics
- Infection control: hand hygiene, respiratory etiquette, avoid sharing cups/utensils; clean high-touch surfaces
- Urgently assess for possible iGAS in high-risk groups or if clinical deterioration occurs
Pharmacological Treatment
First-line oral antibiotic (penicillin)
- Phenoxymethylpenicillin (penicillin V) for 10 days: 1-11 months 62.5 mg four times daily
- Phenoxymethylpenicillin (penicillin V) for 10 days: 1-5 years 125 mg four times daily
- Phenoxymethylpenicillin (penicillin V) for 10 days: 6-11 years 250 mg four times daily
- Phenoxymethylpenicillin (penicillin V) for 10 days: 12-17 years 500 mg four times daily
Use full 10-day course to reduce transmission and complications. Contraindicated in true penicillin hypersensitivity.
Alternative antibiotic in true penicillin allergy
- Clarithromycin for 5 days: 1 month-11 years 7.5 mg/kg twice daily (max 250 mg twice daily)
- Clarithromycin for 5 days: 12-17 years 250 mg twice daily
Check local resistance patterns and interactions. Macrolides can prolong QT interval and interact with CYP3A4 substrates; avoid in known macrolide hypersensitivity.
Symptomatic treatment
- Paracetamol: 15 mg/kg every 4-6 hours as needed (max 4 doses/24 h)
- Ibuprofen (>3 months): 5-10 mg/kg 3 times daily as needed (max 30 mg/kg/day)
Avoid aspirin in children (<16 years) due to Reye syndrome risk. Use NSAIDs cautiously in dehydration/renal impairment; avoid if contraindicated.
Complications
- Otitis media
- Acute sinusitis
- Peritonsillar abscess (quinsy) or retropharyngeal abscess
- Mastoiditis
- Cellulitis and necrotizing fasciitis (iGAS)
- Streptococcal toxic shock syndrome
- Sepsis, meningitis, streptococcal pneumonia, septic arthritis, endocarditis
- Acute rheumatic fever (carditis/arthritis sequelae)
- Acute post-streptococcal glomerulonephritis
Prognosis
Most children improve rapidly once treated, and the rash/systemic symptoms usually settle within about one week. Prognosis is generally excellent in uncomplicated disease, but delayed recognition of invasive GAS can be life-threatening, so early review of deterioration is essential. Recurrence after a confirmed episode is uncommon but possible.
Sources & References
🏥BMJ Best Practice(3)
✅NICE Guidelines(1)
- Scarlet fever[overview]
📖Textbook References(20)
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1843)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1476)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1519, 1520)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1527)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1518, 1519)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1518)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1519)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1572, 1573)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1476, 1477)[context]
- _OceanofPDF.com_Netters_Anatomy_-_8th_edition_-_Frank_H_Netter_MD.pdf(pp. 3114, 3115)[context]
- _OceanofPDF.com_Netters_Anatomy_-_8th_edition_-_Frank_H_Netter_MD.pdf(pp. 2602, 2603)[context]
- _OceanofPDF.com_Netters_Anatomy_-_8th_edition_-_Frank_H_Netter_MD.pdf(pp. 3115)[context]
- Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 445)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 156, 157)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 403)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 396, 397)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 403)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 396)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 395, 396)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 157)[context]