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, see NOIDs article for more detail.

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 (GpA BHS). 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.[1] 
  • In most cases scarlet fever evolves from a tonsillar or pharyngeal infection but the rash is uncommonly seen in 'strep throats'.[2] 
  • GpA BHS secrete a variety of haemolysing enzymes and toxins including the erythrogenic toxins causing the characteristic rash of scarlet fever.[3] 
  • Person-to-person spread is mainly by respiratory droplets. The incubation is typically 2 to 5 days but ranges from 1 to 7 days.[4] 
  • 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.[5] There are still sporadic outbreaks.[6]
  • There had been a marked reduction in the incidence of scarlet fever over the last 10 years but it has increased recently -  3,548 notifications of scarlet fever have been made so far this season in England (weeks 37 2013 to 11 2014) compared to an average of 1,420 for this same period in the previous 10 years.[7] 
  • The age profile has remained unchanged. 87% being children are aged under 10 years with a median age of 4 years.[7] Scarlet fever is unusual under the age of 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.[8] 
  • 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 1 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 the 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 the trunk and legs later.
    • The 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 around the mouth is unusually pale against the surrounding flushed face. This effect is more prominent than in other fevers.
    • The 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 the axillae and groin, is Pastia's sign and the lines are 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 the tips of the fingers, the toes, axilla, groin and ears. It is a valuable sign if the patient has not been seen during the febrile phase.
  • The throat may have some of the typical features described:[10]
    • There may be small haemorrhagic spots on the 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:[11]
    • Initially, during the first two 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 two 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'.

The diagnosis is usually made clinically. However, investigations may be required in cases of diagnostic difficulty. These may include:

  • Throat swab and culture :
    • This has 90% sensitivity for presence of GpA BHS. However, it is less specific, as there is a 10-15% carrier rate in healthy subjects.
    • It is important to take throat swabs correctly, avoiding the lips, tongue and buccal mucosa.
    • Swab tonsils, posterior pharynx and any exudate under good illumination.
  • 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 (ELISAs) 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:
    • Prove recent infection but are of no value in acute infection.
    • Have a value in patients with complications such as acute glomerulonephritis.
  • FBC:
    • 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[9]

  • Antibiotics. Penicillin or azithromycin if penicillin-allergic are the treatments of choice given for a full 10 days. There are no documented penicillin-resistant GpA BHS infections. Amoxicillin can be used in children if compliance with penicillin is a problem.[12]
  • If there is high fever with marked systemic toxicity, the dose of antibiotic can be doubled or a second-line antibiotic (eg, a cephalosporin) used but in such circumstances specialist advice should be sought.
  • Rest and adequate fluids should be encouraged.
  • Ibuprofen or paracetamol should be offered to relieve symptoms.
  • Aspirin should be avoided in patients younger than 16 years.

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. Public Health England (PHE) recommends children can return to school after 24 hours of antibiotics.[12]

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

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 (Coxsackievirus or echovirus) - no longer considered as a separate entity.
  • Fifth disease, or erythema infectosum (parvovirus B19).
  • Exanthem subitum or roseola infantum (human herpesvirus 6 (HHV-6)).

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.[15] 

Further reading & references

  1. Smith A, Li A, Tolomeo O, et al; Mass antibiotic treatment for group A streptococcus outbreaks in two long-term care facilities. Emerg Infect Dis. 2003 Oct;9(10):1260-5.
  2. Choby BA; Diagnosis and treatment of streptococcal pharyngitis. Am Fam Physician. 2009 Mar 1;79(5):383-90.
  3. Todar K; Online Textbook of Bacteriology
  4. Scarlet Fever; Public Health England
  5. 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.
  6. 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.
  7. Group A streptococcal infections: update on seasonal activity, 2013/14; Health Protection Report, News Archives
  8. Wong S et al; Emerging Microbes and Infections, Nature.com, 2012
  9. Scarlet fever; NICE CKS, May 2010
  10. Tewfik TL, Al Garni M; Tonsillopharyngitis: clinical highlights. J Otolaryngol. 2005 Jun;34 Suppl 1:S45-9.
  11. Mahajan VK, Sharma NL; Scarlet Fever. Indian Pediatr. 2005 Aug;42(8):829-30.
  12. Interim guidelines for the public health management of scarlet fever outbreaks in schools, nurseries and other childcare settings; Public Health England, 2014
  13. Rodriguez-Iturbe B, Batsford S; Pathogenesis of poststreptococcal glomerulonephritis a century after Clemens von Pirquet. Kidney Int. 2007 Mar 7;.
  14. 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.
  15. Thomas Sydenham (1624-1689).; Thomas Sydenham (1624-1689). Can Med Assoc J. 1924 Oct;14(10):983-4.

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:
Peer Reviewer:
Dr Adrian Bonsall
Document ID:
2750 (v25)
Last Checked:
13/05/2014
Next Review:
12/05/2019