Scarlet Fever

oPatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

Synonyms: scarlatina, scarlatinella

This disease is notifiable in the UK.

Scarlet fever is an exotoxin-mediated disease arising from a specific bacterial infection by an erythrogenic toxin-producing strain of Streptococcus pyogenes (Group A beta-haemolytic streptococci or GpA BHS). In most cases scarlet fever evolves from a tonsillar or pharyngeal infection but the rash develops in less than 10% of so-called "strep throats". Scarlet fever can follow infection at other sites, including wounds, burns and postnatally (for example surgical scarlet fever and puerperal scarlet fever).

  • GpA BHS are normally found in the nasopharynx but can cause disease, for example, pharyngitis, skin infections and pneumonia.
  • Scarlet fever is associated with pharyngitis and only rarely with infection at other sites. Up to about 10% of GpA BHS sore throats will go on to cause scarlet fever.
  • GpA BHS secrete a variety of haemolysing enzymes and toxins including the erythrogenic toxins causing the characteristic rash of scarlet fever.
  • Person to person spread is mainly by respiratory droplets. The incubation is typically 2 to 4 days but ranges from 12 hours to 7 days.
  • Patients are contagious both during the acute illness and the initial subclinical stage. Advice on exclusion from school is variable (see Prevention below).

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  • In the 1800s there were serious epidemics of scarlet fever. The death rate from scarlet fever then was as high as 150/100,000. Complications, case mortality and incidence have fallen dramatically because of antibiotics, enhanced immunity and improved socio-economic conditions.[4] There are still sporadic outbreaks.[5]
  • There has been a marked reduction in the incidence of scarlet fever over the last 10 years, but an increase recently - there were 4176 notifications in England and Wales in 2009, compared with 2920 the year before.[6]
  • Infection usually affects children (peak between age 4 and 8 years). However it is unusual under age 2 years because of maternal antibodies to the exotoxin and lack of prior sensitisation.
  • The infection rate increases with overcrowding and close contact. School populations have a higher incidence.
  • Incidence decreases in adults as immunity develops.
  • Infection occurs throughout the year but pharyngitis occurs most often in school age children in spring and winter.
  • Geographically skin infections caused by streptococcal organisms are more common in warmer climates and in the warmer months.
  • Incubation is 2 to 4 days (range 12 hours to 7 days). Onset of the illness is usually sudden with fever. The rash follows 12-48 hours after the fever.
  • Often prodrome of sore throat, fever, headache, vomiting, abdominal pain, myalgia. Tachycardia accompanies the fever.
  • Scarlatiniform rash appears on second day of illness. The rash has the following characteristics:
    • Appears typically on the neck first and also chest and scapular regions. It then affects trunk and legs later.
    • Rash has a coarse texture like sandpaper. It is punctate on a diffuse erythematous base (that is pin-point dark red spots on a general reddening of the skin).
    • Circumoral pallor is evident. The area round mouth is unusually pale against surrounding flushed face. This effect is more prominent than in other fevers.
    • Rash lasts for several days but after a few days of becoming generalised it may appear more prominent in skin creases with confluent petechiae or lines (capillary fragility). This sign, seen particularly in axillae and groin, is Pastia's sign and the lines known as "Pastia's lines".
    • The skin may start to peel (desquamation) even during the febrile stage. This peeling which often produces flakes of skin on the face, continues for several weeks. It also affects tips of the fingers, toes, axilla, groin and ears. It is a valuable sign if patient has not been seen during febrile phase.
  • The throat may have some of the typical features described:[7]
    • There may be small haemorrhagic spots on palate.
    • The tonsils are often red and oedematous.
    • The tonsils may be covered with pale exudate.
    • Accompanying tender cervical lymphadenopathy is typical.
  • The tongue has a characteristic appearance which develops during the illness:[8]
    • Initially, during the first 2 days of the illness, patients may have a 'white strawberry tongue'. The tongue is covered by prominent red papillae seen through a white 'fur'.
    • After about 2 days the 'fur' is lost (desquamation). The tongue appears to look more raw and red, but still has prominent papillae. This is called the 'raspberry tongue' or 'red strawberry tongue'.
  • Throat swab and culture:
    • The most important proof of infection with 90% sensitivity for presence of GpA BHS. However less specific as there is 10-15% carrier rate in healthy subjects.
    • It is important to take throat swabs correctly avoiding lips, tongue and buccal mucosa.
    • Swab tonsils, posterior pharynx and any exudate under good illumination.

Other tests are not usually needed, but include:

  • Antigen detection kits:
    • Various kits are available for near patient testing. Rapid antigen tests (RATs) and 'strep tests' use latex agglutination. Enzyme-linked immunosorbent assays (ELISA) are more expensive.
    • These are promoted to allow quick diagnosis and hence more appropriate administration of antibiotics. However the cost and variable sensitivity and specificity are amongst some of the reasons that use is limited.
  • Streptococcal antibody tests:
    • Proves recent infection but of no value in acute infection.
    • Has a value in patients with complications such as acute glomerulonephritis.
  • Full blood count:
    • A polymorphonuclear lymphocytosis is typical.
    • During the second week an eosinophilia may develop.
  • The aims of treatment are to:
    • Shorten the illness.
    • Prevent suppurative complications (such as peritonsillar abscess formation, mastoiditis, cellulitis and ethmoiditis).
    • Reduce the risk of spread to others.
    • Prevent progression to other complications. Unfortunately, however, although early use of penicillin may reduce rheumatic fever it does not prevent post-streptococcal glomerulonephritis.
  • Medical treatment:
    • Antibiotics. Penicillin or erythromycin if penicillin-allergic are the treatments of choice given for a full 10 days.[10] There are no documented penicillin-resistant GpA BHS infections. A cephalosporin is an effective alternative to penicillin, but not if penicillin-allergic.
  • Referral and other treatment:
    • Recurrent infection would be an indication for ENT referral.
    • Difficulty swallowing may necessitate hospitalisation for intravenous fluids and antibiotics.
    • Management of complications may require hospitalisation.
  • Exclusion from School Advice is variable. HPA recommends children can return to school after 24 hours' antibiotics.[3]

Signs of complications developing may be indicated by a persistent fever, increased throat pain or swelling.

  • Local spread:
    • Cervical lymphadenopathy
    • Sinusitis
    • Mastoiditis
    • Peritonsillar abscess
  • Distant spread:
  • Rare, but feared, late complications include rheumatic fever (0.3%) or acute renal failure (post-streptococcal glomerulonephritis).[11][12]
  • Minor late sequelae:
    • Beau lines on nails
    • Telogen hair loss

Scarlet fever follows a benign course in the vast majority of cases. Any morbidity is likely to arise from suppurative complications most often in untreated patients.

Second in the historical order of classic exanthems identified:

  • Rubeola (measles).
  • Scarlet fever.
  • Rubella (German measles)
  • Dukes' disease (coxsackie virus or echovirus) - no longer considered as a separate entity.
  • Fifth disease, or erythema infectosum (parvovirus B19).
  • Exanthem subitum or roseola infantum (herpes virus, HH6).

A disease previously confused with measles, the credit for a definitive, distinctive name must go to Thomas Sydenham (1624-1689), the English Hippocrates, and the father of English medicine.

Further reading & references

  1. Balentine J; Scarlet Fever, eMedicine, March 2010; Emergency medicine perspective
  2. Dyne P, Bloomfield P; Scarlet Fever. eMedicine, July 2010; Paediatric perspective on Scarlet Fever.
  3. Scarlet Fever; Public Health England
  4. Radikas R, Connolly C; Young patients in a young nation: scarlet fever in early nineteenth century rural New England. Pediatr Nurs. 2007 Jan-Feb;33(1):53-5.
  5. Feeney KT, Dowse GK, Keil AD, et al; Epidemiological features and control of an outbreak of scarlet fever in a Perth primary school. Commun Dis Intell. 2005;29(4):386-90.
  6. Statutory Notifications of Infectious Diseases (NOIDs) - tables - England and Wales. Health Protection Agency
  7. Tewfik TL, Al Garni M; Tonsillopharyngitis: clinical highlights. J Otolaryngol. 2005 Jun;34 Suppl 1:S45-9.
  8. Mahajan VK, Sharma NL; Scarlet Fever. Indian Pediatr. 2005 Aug;42(8):829-30.
  9. Aber C, Alvarez Connelly E, Schachner LA; Fever and rash in a child: when to worry? Pediatr Ann. 2007 Jan;36(1):30-8.
  10. De Meyere M, Mervielde Y, Verschraegen G, et al; Effect of penicillin on the clinical course of streptococcal pharyngitis in general practice. Eur J Clin Pharmacol. 1992;43(6):581-5.
  11. Rodriguez-Iturbe B, Batsford S; Pathogenesis of poststreptococcal glomerulonephritis a century after Clemens von Pirquet. Kidney Int. 2007 Mar 7;.
  12. Mosquera J, Romero M, Viera N, et al; Could streptococcal erythrogenic toxin B induce inflammation prior to the development of immune complex deposits in poststreptococcal glomerulonephritis? Nephron Exp Nephrol. 2007;105(2):e41-4. Epub 2006 Nov 30.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Richard Draper
Current Version:
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Document ID:
2750 (v24)