Scarlet fever

Also Known As: Scarlet fever, Strep Thoat

Scarlet fever is a disease caused by exotoxin released by Streptococcus pyogenes. Once a major cause of death, it is now effectively treated with antibiotics. The term scarlatina may be used interchangeably with scarlet fever, though it is most often used to indicate the less acute form of scarlet fever seen since the beginning of the twentieth century.

This disease is most common in 4–8 year olds with males and females being equally affected.[3] By the age of 10 years most children have acquired protective antibodies and scarlet fever at this age or older is rare.[4][dubious ]

It is usually spread by the aerosol route (inhalation) but may also be spread by skin contact or by fomites. Although not normally considered a food borne illness an outbreak due to chicken meat has been reported in China.[5]

Asymptomatic carriage may occur in 15–20% of school-age children.

The incubation period is 1–4 days.


The disease itself is caused by secretion of pyrogenic exotoxins by the infecting Streptococcus.[6][7] Exotoxin A (speA) is probably the best studied of these toxins. It is carried by the bacteriophage T12 which integrates in to the Streptococcal genome from where the toxin is transcribed. The phage itself integrates into a serine tRNA gene on the chromosome.[8]

The T12 virus itself has not been placed into a taxon by the International Committee on Taxonomy of Viruses. It has a double stranded DNA genome and on morphological grounds appears to be a member of the Siphoviridae.

The speA gene was cloned and sequenced in 1986.[9] It is 753 base pairs in length and encodes a 29.244 kiloDalton (kDa) protein. The protein contains a putative 30 amino acid signal peptide: removal of the signal sequence gives a predicted molecular weight of 25.787 (kDa) for the secreted protein. Both a promoter and a ribosome binding site (Shine-Dalgarno sequence) are present upstream of the gene. A transcriptional terminator is located 69 bases downstream from the translational termination codon. The carboxy terminal portion of the protein exhibits extensive homology with the carboxy terminus of Staphylococcus aureus enterotoxins B and C1.

Streptococcal phages other than T12 may also carry the speA gene.[10]

Symptoms and signs

Scarlet fever is characterized by:

  • the rash is fine, red and rough-textured
  • blanches upon pressure
  • appears 12–72 hours after the fever
  • generally starts on the chest, armpits and behind the ears. It may also involve the groin.
  • spares the face (although some circumoral pallor is characteristic)
  • is worse in the skin folds. These Pastia lines (where the rash runs together in the armpits and groin) appear and can persist after the rash is gone.
  • may spread to cover the uvula
  • begins to fade three to four days after onset and desquamation (peeling) begins. "This phase begins with flakes peeling from the face. Peeling from the palms and around the fingers occurs about a week later."[11] Peeling also occurs in axilla, groin and tips of the fingers and toes.[12]


Diagnosis of scarlet fever is clinical. The blood test shows marked leukocytosis with neutrophilia and conservated or increased eosinophils, high erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) (both indications of inflammation), and elevation of antistreptolysin O titer. Blood culture is rarely positive but the streptococci can usually be demonstrated in throat culture.

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