Scarlet Fever Clinical Presentation
- Author: Edward J Zabawski Jr, DO; Chief Editor: Dirk M Elston, MD more...
History
The cutaneous eruption of scarlet fever accompanies a streptococcal infection at another anatomic site, usually the tonsillopharynx. The illness generally has a 1- to 4-day incubation period. Its emergence tends to be abrupt, usually heralded by sudden onset of fever associated with sore throat,[9] headache, nausea, vomiting, abdominal pain, myalgias, and malaise. The characteristic rash appears 12-48 hours after onset of fever, first on the neck and then extending to the trunk and extremities.
In the untreated patient, fever peaks by the second day (temperature as high as 103-104°F) and gradually returns to normal in 5-7 days. Fever abates within 12-24 hours after initiation of antibiotic therapy.
A recent history of exposure to another individual with a “strep” infection may aid in the diagnosis.
Physical Examination
The patient usually appears moderately ill. Fever may be present. The patient may have tachycardia. Tender anterior cervical lymphadenopathy may be present.
The mucous membranes usually are bright red, and scattered petechiae and small red papular lesions on the soft palate are often present.
On day 1 or 2, the tongue is heavily coated with a white membrane through which edematous red papillae protrude (classic appearance of white strawberry tongue). By day 4 or 5, the white membrane sloughs off, revealing a shiny red tongue with prominent papillae (red strawberry tongue). Red, edematous, exudative tonsils (see the image below) are typically observed if the infection originates in this area.
The exudative pharyngitis typical of scarlet fever. Although the tongue is somewhat out of focus, the whitish coating observed early in scarlet fever is visible. Generally, the rash develops 12-48 hours after the onset of fever, first appearing as erythematous patches below the ears, chest, and axilla. Dissemination to the trunk and extremities occurs over 24 hours. Typically, the rash consists of scarlet macules over generalized erythema (boiled lobster appearance).
The characteristic exanthem consists of a fine erythematous punctate eruption that appears within 1-4 days after the onset of the illness. The eruption imparts a dry rough texture to the skin that is reported to resemble the feel of coarse sandpaper. The erythema blanches with pressure. The skin can be pruritic but usually is not painful.
The eruption first appears on the upper trunk and axillae and then becomes generalized, though it is usually more prominent in flexural areas (eg, axillae, popliteal fossae, and inguinal folds). It may also appear more intense at dependent sites and sites of pressure, such as the buttocks.
Capillary fragility is increased, and rupture may occur. Often, transverse areas of hyperpigmentation with linear arrays of petechiae in the axillary, antecubital, and inguinal areas (Pastia lines, or the Pastia sign) can be observed. These arrays may persist for 1-2 days after resolution of the generalized rash.
Another distinctive facial finding is a flushed face with circumoral pallor. In severe disease, small vesicular lesions termed miliary sudamina may appear on the abdomen, hands, and feet.
The cutaneous rash, shown below, lasts for 4-5 days, followed by fine desquamation, one of the most distinctive features of scarlet fever. The desquamation phase begins 7-10 days after resolution of the rash, with flakes peeling from the face. Peeling from the palms (see the image below) and around the fingers occurs about a week later and can last up to a month or longer. The extent and duration of this phase are directly related to the severity of the eruption.
Desquamation of the palms is a frequently observed self-limited manifestation of scarlet fever present in the healing period following resolution of the infection and acute eruption. Complications
Complications of scarlet fever may include the following:
- Cervical lymphadenitis
- Otitis media and/or mastoiditis
- Ethmoiditis
- Bronchopneumonia
- Intracranial venous sinus thrombosis
- Septicemia, meningitis, osteomyelitis, and septic arthritis
- Acute renal failure from poststreptococcal glomerulonephritis
- Hepatitis[10]
- Vasculitis[11]
- Uveitis
Of these, otitis media, pneumonia, septicemia, osteomyelitis, rheumatic fever, and acute glomerulonephritis are the most common. Appropriate evaluation and early intervention with antibiotics are essential to prevent these disorders.
Rare but lethal early toxin-mediated sequelae include myocarditis and toxic shocklike syndrome. A lethal form of streptococcal infection is capable of producing the toxic streptococcal syndrome.
Late complications of group A streptococcal infection include rheumatic fever and poststreptococcal glomerulonephritis. Risk of acute rheumatic fever following an untreated streptococcal infection has been estimated at 3% in epidemic situations and approximately 0.3% in endemic scenarios. If a nephritogenic strain of group A beta-hemolytic streptococci causes infection, the individual has a 10-15% chance of developing glomerulonephritis.
Weeks to months after the illness, transverse grooves (ie, Beau lines) may appear on the nail plates and hair loss (telogen effluvium) may occur.
Dong H, Xu G, Li S, Song Q, Liu S, Lin H, et al. Beta-haemolytic group A streptococci emm75 carrying altered pyrogenic exotoxin A linked to scarlet fever in adults. J Infect. Apr 2008;56(4):261-7. [Medline].
Yang SG, Dong HJ, Li FR, Xie SY, Cao HC, Xia SC, et al. Report and analysis of a scarlet fever outbreak among adults through food-borne transmission in China. J Infect. Nov 2007;55(5):419-24. [Medline].
Cunningham MW. Pathogenesis of group A streptococcal infections. Clin Microbiol Rev. Jul 2000;13(3):470-511. [Medline]. [Full Text].
Leslie DL, Kozma L, Martin A, Landeros A, Katsovich L, King RA, et al. Neuropsychiatric disorders associated with streptococcal infection: a case-control study among privately insured children. J Am Acad Child Adolesc Psychiatry. Oct 2008;47(10):1166-72. [Medline]. [Full Text].
Sandrini J, Beucher AB, Kouatchet A, Lavigne C. [Scarlet fever with multisystem organ failure and hypertrophic gastritis]. Rev Med Interne. May 2009;30(5):456-9. [Medline].
Gómez-Carrasco JA, Lassaletta A, Ruano D. [Acute hepatitis may form part of scarlet fever]. An Pediatr (Barc). Apr 2004;60(4):382-3. [Medline].
Güven A. Hepatitis and hematuria in scarlet fever. Indian J Pediatr. Nov 2002;69(11):985-6. [Medline].
Lau SK, Woo PC, Yuen KY. Toxic scarlet fever complicating cellulitis: early clinical diagnosis is crucial to prevent a fatal outcome. New Microbiol. Apr 2004;27(2):203-6. [Medline].
Finnish Medical Society Duodecim. Sore throat and tonsillitis. EBM Guidelines. Evidence-Based Medicine. Feb 2 2007Helsinki, Finland: Wiley Interscience. John Wiley & Sons;[Full Text].
Gidaris D, Zafeiriou D, Mavridis P, Gombakis N. Scarlet Fever and hepatitis: a case report. Hippokratia. Jul 2008;12(3):186-7. [Medline]. [Full Text].
Reddy UP, Albini TA, Banta JT, Davis JL. Post-streptococcal vasculitis. Ocul Immunol Inflamm. Jan-Feb 2008;16(1):35-6. [Medline].
Gaston DA, Zurowski SM. Arcanobacterium haemolyticum pharyngitis and exanthem. Three case reports and literature review. Arch Dermatol. Jan 1996;132(1):61-4. [Medline].
Sanz JC, Bascones Mde L, Martín F, Sáez-Nieto JA. [Recurrent scarlet fever due to recent reinfection caused by strains unrelated to Streptococcus pyogenes]. Enferm Infecc Microbiol Clin. Jun-Jul 2005;23(6):388-9. [Medline].
Gerber MA, Baltimore RS, Eaton CB, Gewitz M, Rowley AH, Shulman ST, et al. Prevention of rheumatic fever and diagnosis and treatment of acute Streptococcal pharyngitis: a scientific statement from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee of the Council on Cardiovascular Disease in the Young, the Interdisciplinary Council on Functional Genomics and Translational Biology, and the Interdisciplinary Council on Quality of Care and Outcomes Research: endorsed by the American Academy of Pediatrics. Circulation. Mar 24 2009;119(11):1541-51. [Medline].
Gerber MA, Shulman ST. Rapid diagnosis of pharyngitis caused by group A streptococci. Clin Microbiol Rev. Jul 2004;17(3):571-80, table of contents. [Medline]. [Full Text].
Bass JW. Antibiotic management of group A streptococcal pharyngotonsillitis. Pediatr Infect Dis J. Oct 1991;10(10 Suppl):S43-9. [Medline].
Derrick CW, Dillon HC. Erythromycin therapy for streptococcal pharyngitis. Am J Dis Child. Feb 1976;130(2):175-8. [Medline].
Stock I. [Streptococcus pyogenes--much more than the aetiological agent of scarlet fever]. Med Monatsschr Pharm. Nov 2009;32(11):408-16; quiz 417-8. [Medline].

