Scarlet fever

Epidemiology

Pathogen
- Group A β‑hemolytic streptococci (Streptococcus pyogenes) produce erythrogenic exotoxin A, B, or C
  - These exotoxins cause the rash of scarlet fever via a delayed-type skin reaction.
Route of transmission: aerosol

Rash manifests 12–48 hours after fever onset.
Fine, erythematous, sandpaper‑like texture
Blanches with pressure, but nonblanching petechiae may also be present
Begins on neck or trunk and spreads rapidly across the body (except for the palms and soles)
Characteristic features include:
- Flushed cheeks with perioral pallor
- Strawberry tongue: bright red tongue color with papillary hyperplasia, which may initially be covered with a white coating
- Pastia lines
  - A characteristic sign of scarlet fever
  - Linear, petechial appearance
  - Most pronounced in the groin, underarm, and elbow creases (i.e., flexural areas)

Feature	Scarlet Fever	Acute Rheumatic Fever
Timing	Concurrent with active GAS infection	Delayed (2–4 weeks post-infection)
Pathophysiology	Toxin-mediated (SPEs)	Immune-mediated (molecular mimicry)
Rash	"Sandpaper" texture, diffuse, punctate	Erythema marginatum (serpiginous, clear centers)
Key Finding	Strawberry tongue, Pastia's lines	Migratory polyarthritis, carditis, chorea
Treatment Goal	Eradicate active infection, prevent ARF	Reduce inflammation, prevent recurrence with long-term prophylaxis

Initiate one of the recommended antibiotic regimens for acute GAS pharyngitis, e.g.:
- Oral penicillin V or amoxicillin
- Nonsevere penicillin reaction: oral cephalosporins (e.g., cephalexin)
- Severe penicillin reaction: oral macrolides (e.g., azithromycin) or clindamycin