Scarlet Fever

How to Cite This Chapter: Loeb M, Leszczyszyn-Pynka M. Scarlet Fever. McMaster Textbook of Internal Medicine. Kraków: Medycyna Praktyczna. https://empendium.com/mcmtextbook/chapter/B31.II.18.76. Accessed July 23, 2024.
Last Updated: December 2, 2021
Last Reviewed: December 2, 2021
Chapter Information

Etiology and PathogenesisTop

Scarlet fever, also known as scarlatina, presents as diffuse erythematous rash occurring in the setting of streptococcal infection, usually pharyngitis.

1. Etiologic agent: Group A beta-hemolytic streptococci (GABHS), primarily Streptococcus pyogenes, integrated with a bacteriophage producing the specific type of erythrogenic toxin.

2. Pathogenesis: The site of bacterial entry is the oral cavity for classic scarlet fever, and damaged skin, for surgical scarlet fever. Clinical manifestations (fever, rash, vomiting) are caused by pyrogenic exotoxins produced by some streptococcal strains. Skin involvement is due to erythrogenic toxin (types A, B, and C). The streptococcal superantigen that causes the streptococcal toxic shock syndrome is also a pyrogenic toxin.

3. Reservoir and transmission, risk factors, incubation and contagious period: see Pharyngitis (Tonsillitis). The risk of infection following household contact with an infected person in susceptible individuals (with no immunity to erythrogenic toxin–producing streptococci) is estimated at 25%. The disease is most common in children, while adults are rarely affected. Schools and preschool facilities are the primary sites of transmission. In temperate climate infections are more frequent in autumn and winter.

Clinical Features And Natural HistoryTop

The disease onset is acute, with fever, vomiting, sore throat, and rash beginning on the second day of illness.

1. Manifestations of pharyngitis: see Pharyngitis (Tonsillitis). Absent in surgical scarlet fever.

2. Scarlet fever rash: Finely punctate rash (the finest rash is of infectious etiology) on the face (absent in the perioral region, between nasolabial folds [the Filatov triangle]), trunk, and extremities. Scarlet fever rash resembles skin pricked with a dandy brush. Applying pressure to the rash causes it to blanch for a while, revealing yellowish skin underneath. Petechiae in a linear pattern, caused by the rupture of fragile small vessels damaged by the toxin, are seen in the elbows, around the armpits and groin, and in skinfolds. The skin has a rough feel. Pronounced, confluent lesions give the skin a "boiled lobster" appearance. In week 2 or 3 of illness, characteristic desquamation is observed (bran-like flakes on the face and trunk; larger flakes on the palms and soles), initially on the face and subsequently on the trunk and extremities. The desquamation phase may persist for several weeks.

3. Symptoms of damage to other organs: Inflammation of other organs (eg, myocarditis) may develop in severe cases (see Pharyngitis (Tonsillitis)).

DiagnosisTop

Diagnostic Tests

1. Identification of the etiologic agent: Throat and tonsil swab culture or a rapid GABHS antigen detection test.

2. Other tests:

1) Complete blood count: Leukocytosis and neutrophilia (in up to 95% of cases); often with the presence of immature neutrophils; possible eosinophilia (in up to 20% of cases) in the recovery phase (from week 2).

2) Urinalysis and antistreptolysin O (ASO) titers.

3) Other tests (for visceral organ complications).

Differential Diagnosis

Other diseases with fever and rash (with or without pharyngitis and/or tonsillitis):

1) Infectious: Rubella, measles, infectious mononucleosis, secondary syphilis, acute HIV infection, toxic shock syndrome, staphylococcal scalded skin syndrome, sepsis with coagulopathy.

2) Noninfectious: Kawasaki disease, drug-induced rash.

TreatmentTop

As in pharyngitis (tonsillitis).

ComplicationsTop

As in pharyngitis (tonsillitis).

PrognosisTop

Mortality in untreated scarlet fever is 15% to 20%. The prognosis in uncomplicated disease is good.

PreventionTop

Specific Prevention

Vaccination: None available. An attack of scarlet fever confers immunity against the specific toxin type.

Nonspecific Prevention

Patient isolation for 24 hours from the initiation of appropriate antibiotic treatment.

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