Scarlet Fever

Updated: Nov 06, 2020
Author: Bahman Sotoodian, MD; Chief Editor: William D James, MD 



Scarlet fever (known as scarlatina in older literature references) is a syndrome characterized by exudative pharyngitis (see the image below), fever, and bright-red exanthem. It is caused by streptococcal pyrogenic exotoxins (SPEs) types A, B, and C produced by group A beta-hemolytic streptococci (GABHS) found in secretions and discharge from the nose, ears, throat, and skin. Scarlet fever may follow streptococcal wound infections or burns, as well as upper respiratory tract infections. Food-borne outbreaks have been reported.[1, 2]  Reemergence of the condition is being recognized, perhaps because of newer virulence of the streptoccocal bacteria.[3, 4, 5, 6, 7, 8]

The exudative pharyngitis typical of scarlet fever 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.

See 15 Back-to-School Illnesses You Should Know, a Critical Images slideshow, to help identify conditions that may occur in young patients after they return to the classroom.

Ordinarily, scarlet fever evolves from a tonsillar/pharyngeal focus, although the rash develops in less than 10% of cases of “strep throat.” The site of bacterial replication tends to be inconspicuous compared to the possible dramatic effects of released toxins. Exotoxin-mediated streptococcal infections range from localized skin disorders to the widespread eruption of scarlet fever to the uncommon but highly lethal streptococcal toxic shock syndrome.


As the name “scarlet fever” implies, an erythematous eruption is associated with a febrile illness. The circulating toxin, produced by GABHS and often referred to as erythemogenic or erythrogenic toxin, causes the pathognomonic rash as a consequence of local production of inflammatory mediators and alteration of the cutaneous cytokine milieu. This results in a sparse inflammatory response and dilatation of blood vessels, leading to the characteristic scarlet color of the rash.[9]

Usually, the sites of GABHS replication in scarlet fever are the tonsils and pharynx. Clinically indistinguishable, scarlet fever may follow streptococcal infection of the skin and soft tissue, surgical wounds (ie, surgical scarlet fever), or the uterus (ie, puerperal scarlet fever).


Scarlet fever is a streptococcal disease. Streptococci are gram-positive cocci that grow in chains. They are classified by their ability to produce a zone of hemolysis on blood agar and by differences in carbohydrate cell wall components (A-H and K-T). They may be alpha-hemolytic (partial hemolysis), beta-hemolytic (complete hemolysis), or gamma-hemolytic (no hemolysis).

Group A streptococci are normal inhabitants of the nasopharynx. Group A streptococci can cause pharyngitis, skin infections (including erysipelas pyoderma and cellulitis), pneumonia, bacteremia, and lymphadenitis.

Most streptococci excrete hemolyzing enzymes and toxins. The erythrogenic toxins produced by GABHS are the cause of the rash of scarlet fever. The erythema-producing toxin was discovered by Dick and Dick in 1924. Scarlet fever is usually associated with pharyngitis; however, in rare cases, it follows streptococcal infections at other sites.

Although infections may occur year-round, the incidence of pharyngeal disease is highest in school-aged children during winter and spring and in a setting of crowding and close contact. Person-to-person spread by means of respiratory droplets is the most common mode of transmission. It can rarely be spread through contaminated food, as seen in an outbreak in China.[2]

The organism is able to survive extremes of temperature and humidity, which allows spread by fomites. Geographic distribution of skin infections tends to favor warmer or tropical climates and occurs mainly in summer or early fall in temperate climates.

The incubation period for scarlet fever ranges from 12 hours to 7 days. Patients are contagious during the acute illness and during the subclinical phase.


As many as 10% of the population contracts group A streptococcal pharyngitis. Of this group, as many as 10% then develop scarlet fever.

In the past century, the number of cases of scarlet fever has remained high, with marked decrease in case-mortality rates secondary to widespread use of antibiotics. Transmission usually occurs via airborne respiratory particles that can be spread from infected patients and asymptomatic carriers.

The infection rate increases in overcrowded situations (eg, schools, institutional settings) and it peaks during late fall, winter, and spring in temperate environments. Immunity, which is type specific, may be induced by a carrier state or overt infection. In adulthood, incidence decreases markedly as immunity develops to the most prevalent serotypes. Complications (eg, rheumatic fever) are more common in recent immigrants to the United States.

Scarlet fever predominantly occurs in children aged 5-15 years, although it can also occur in older children and adults. It is uncommon in children aged 3 years or younger.[10] By the time children are 10 years old, 80% have developed lifelong protective antibodies against streptococcal pyrogenic exotoxins, which prevent future disease manifestation. Scarlet fever is rare in children younger than 1 year because of the presence of maternal antiexotoxin antibodies and lack of prior sensitization.

Leslie et al suggest from a case-control study that antecedent streptococcal infection can increase the likelihood of children developing certain neuropsychiatric disorders, including Tourette syndrome, attention-deficit/hyperactivity disorder, and major depressive disorder.[11]

Males and females are affected equally. No racial or ethnic predilection is reported for group A streptococcal infection.


When the condition is identified in a timely fashion, the prognosis is excellent. Most patients recover fully after 4-5 days, with resolution of skin symptoms over several weeks. Attacks may recur.

In the preantibiotic era, infections due to GABHS were major causes of mortality and morbidity. Historically, scarlet fever resulted in death in 15-20% of those affected. However, scarlet fever is no longer associated with the deadly epidemics that made it so feared in the 1800s. Since the advent of antibiotic therapy, the mortality rate for scarlet fever has been less than 1%. However, school outbreaks still occur owing to significant close proximity of susceptible children in a limited and confined area, which can lasts for weeks.

Today, as a result not only of antibiotic therapy but also of enhanced immune status of the population and improved socioeconomic conditions, scarlet fever usually follows a benign course. Any undue morbidity and mortality are more likely to arise from suppurative complications (eg, peritonsillar abscess, sinusitis, bronchopneumonia, and meningitis) or problems associated with immune-mediated sequelae, rheumatic fever, or glomerulonephritis. Very rare complications, such as septic shock with multisystem organ failure, have been reported.[12]

Known complications, such as septicemia, vasculitis, hepatitis, or rheumatic fever, should be considered on a case-by-case basis as determined by the presence of clinical history and examination findings suggestive of those diseases.[13, 14] Localized soft tissue infections may suggest the presence of underlying osteomyelitis, but scarlet fever may occur from cellulitis alone.[15] When scarlet fever has been determined to be due to a soft tissue infection over or near bone, evaluation for bony involvement should be considered.

Patient Education

Patients must be instructed to complete the entire course of antibiotics, even if symptoms resolve. They should be advised to follow general good hygiene precautions, especially in households with other small children.

Patients should be warned that they will have generalized exfoliation over the next 2 weeks. In particular, they should be warned about signs of complications of streptococcal infection, such as persistent fever, increased throat or sinus pain, and generalized swelling.

For patient education resources, see the Children’s Health Center and the Ear, Nose, and Throat Conditions Center, as well as Strep Throat and Skin Rashes in Children.




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,[16] headache, chills, nausea, myalgias, and malaise. Young children may also present with vomiting, abdominal pain, and seizure. The characteristic rash appears 12-48 hours after the 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 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 exanthem develops 12-48 hours after the onset of fever, first appearing as erythematous patches below the ears and on the neck, chest, and axilla. 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. Dissemination to the trunk and extremities occurs over 24 hours. 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., Eventually scarlet macules are seen overlying the generalized erythema (“boiled-lobster” appearance).

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 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 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.


Complications of scarlet fever may include the following:

  • Cervical lymphadenitis

  • Otitis media and/or mastoiditis

  • Ethmoiditis

  • Peritonsillar abscess

  • Sinusitis

  • Bronchopneumonia

  • Meningitis

  • Brain abscess

  • Intracranial venous sinus thrombosis

  • Septicemia, meningitis, osteomyelitis, and septic arthritis

  • Acute renal failure from poststreptococcal glomerulonephritis

  • Hepatitis[17]

  • Vasculitis[18]

  • Uveitis

  • Myocarditis

  • Sepsis with abdominal wall abscess (rarely)[19]

  • Invasive group A streptococcal infections and streptococcal toxic shock syndrome (rarely)[20]

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.



Diagnostic Considerations

The overwhelming majority of cases of scarlet fever are caused by group A beta-hemolytic streptococci (GABHS). Other bacteria can cause a pharyngitis and similar rash, such as Staphylococcus aureus, Haemophilus influenzae, Arcanobacterium haemolyticum, and Clostridium species.[21] The differential diagnosis includes other causes of fever accompanied by erythematous eruptions. Recurrent cases of scarlet fever have been reported from reinfection with strains unrelated to Streptococcus pyogenes.[22]

The cutaneous eruption of fifth disease may be confused with that of scarlet fever, but the affected child is usually well and afebrile.

Rubella and rubeola may appear similar, but the presence of conjunctivitis, purulent rhinitis, and cough are helpful clues to the diagnosis of rubeola. In addition, the eruption of rubeola usually begins behind the ears and on the scalp and forehead, not on the torso. Rubella typically begins on the head and face.

Other viral exanthemata, such as those caused by Epstein-Barr virus (infectious mononucleosis), enterovirus, HIV infection, and Streptobacillus moniliformis infection (rat bite fever), may also have to be considered.

Other bacteria-associated syndromes with cutaneous eruptions (eg, toxic shock syndrome, secondary syphilis) may appear similar to scarlet fever, but the presence of vasomotor instability and ischemic necrosis of digits in the former and palmoplantar involvement with positive serology in the latter should suffice to differentiate them from scarlet fever.

Noninfectious diseases that should be considered include Kawasaki disease, acute lupus erythematosus, morbilliform drug eruption, and juvenile rheumatoid arthritis.

Other problems to be considered include the following:

  • Arcanobacterium haemolyticum

  • Atropine toxicity

  • Enteroviral infection and nonspecific viral infection

  • Fifth disease

  • Epstein-Barr virus (infectious mononucleosis)

  • HIV infection

  • Juvenile rheumatoid arthritis

  • Pediatric cellulitis

  • Plant allergic reactions

  • Roseola

  • S moniliformis infection (rat bite fever)

  • Severe sunburn

  • Viral exanthema

  • Guttate psoriasis: Streptococcal infection is known to precipitate guttate psoriasis and may also cause scarlet fever. The 2 are easily distinguished, as the flexural erythema with sandpaperlike texture and petechiae of scarlet fever are very different from the disseminated, round, erythematous lesions with silver scale of guttate psoriasis.

Differential Diagnoses



Approach Considerations

The diagnosis is mostly based on the clinical presentation. However, leukocytosis with left shift presentation and possibly eosinophilia a few weeks after convalescence on a standard blood test and urine tests are part of a complete medical workup. The following studies are indicated in scarlet fever:

  • Throat or nasal culture or rapid streptococcal test

  • Anti-deoxyribonuclease B, antistreptolysin-O titers (antibodies to streptococcal extracellular products), antihyaluronidase, and antifibrinolysin can be valuable in confirmation of the diagnosis

In most cases, no imaging studies are indicated.

Blood and Urine Studies

The complete blood cell (CBC) count commonly reveals a leukocytosis. The white blood cell (WBC) count in scarlet fever may increase to 12,000-16,000/μL, with a differential of up to 95% polymorphonuclear leukocytes. During the second week, eosinophilia, as high as 20%, can develop.

Urinalysis and liver function tests may reveal changes associated with complications of scarlet fever. Said tests are part of a complete medical workup. Hemolytic anemia can occur, and mild albuminuria and hematuria may be present early in the disease. 

Patients whose bacterial source may suggest another process (eg, a patient with a suppurative leg wound who may have osteomyelitis) should be evaluated accordingly.

Throat Culture

Throat culture remains the criterion standard for confirmation of group A streptococcal upper respiratory infection. American Heart Association guidelines for prevention and treatment of rheumatic fever state that group A streptococci virtually always are found on throat culture during acute infection.[23]

Throat cultures are approximately 90% sensitive for the presence of group A beta-hemolytic streptococci (GABHS) in the pharynx. However, because a 10-15% carriage rate exists among healthy individuals, the presence of GABHS is not proof of disease.

To maximize sensitivity, proper obtaining of specimens is crucial. Vigorously swab the posterior pharynx, tonsils, and any exudate with a cotton or Dacron swab under strong illumination, avoiding the lips, tongue, and buccal mucosa.

Direct antigen detection kits (ie, rapid antigen tests [RATs], strep screens) have been proposed to allow immediate diagnosis and prompt administration of antibiotics. Kits are latex agglutination or a costlier enzyme-linked immunosorbent assay (ELISA). Several studies of RAT kits report results of 95% specificity but only 70-90% sensitivity. Operator technique can also significantly influence the results of the test.[24]

Antideoxyribonuclease B and Antistreptolysin O Titers

Streptococcal antibody tests (eg, antideoxyribonuclease B [ADB] and antistreptolysin O [ASO] titers) are used to confirm previous group A streptococcal infection. The most commonly available streptococcal antibody test is the ASO test. An increase in ASO titers can sometimes be observed but is a late finding and usually of value only in retrospect.

Streptococcal antibody tests can provide confirmatory evidence of recent infection but have no value in acute infection and currently are not indicated in this setting. They may be of value in patients with suspected acute renal failure or acute glomerulonephritis.

Histologic Findings

The microscopic findings of the eruption of scarlet fever are nonspecific and have an appearance similar to that of other exanthematous eruptions. A sparse neutrophilic perivascular infiltrate is present, with a slight amount of spongiosis in the epidermis. Slight parakeratosis may be present, which probably correlates with the sandpaperlike texture of the skin. The spongiosis and parakeratosis are more noticeable during the desquamative stage. Engorged capillaries and lymphatic dilatation perifollicularly, as well as the presence of dermal hemorrhage and edema, are easily detected.



Approach Considerations

The goals in the treatment of scarlet fever are (1) to prevent acute rheumatic fever, (2) to reduce the spread of infection, (3) to prevent poststreptococcal glomerulonephritis and suppurative sequelae (eg, adenitis, mastoiditis, ethmoiditis, abscesses, cellulitis), and (4) to shorten the course of illness.

Antibiotic therapy is the treatment of choice for scarlet fever. Whether antibiotics prevent poststreptococcal glomerulonephritis is still debated in the literature.

Medical Care

Penicillin (or amoxicillin) remains the drug of choice (documented cases of penicillin-resistant group A streptococcal infections still do not exist). A first-generation cephalosporin may be an effective alternative, as long as the patient does not have any documented anaphylactic reactions to penicillin. If this is the case, clindamycin or erythromycin may be considered as an alternative.[25, 26]  However, some strains of group A streptococci may not be susceptible to macrolides.[27] Hence, in this situation, it is crucial to contact the microbiology laboratory with regard to the sensitivity of the organism to macrolide antibiotics. A 10- to 14-day course of treatment is usually recommended, and clinical improvement should be noted after 24-48 hours of antibiotic initiation.

Cultures should be obtained where organisms other than streptococcal bacteria are suspected. The desquamating rash that follows is self-limited, with only emollients necessary for care.

If odynophagia accompanying streptococcal pharyngitis is especially severe, hospitalization may be warranted for intravenous hydration and antibiotics.


At this time, a vaccine for group A streptococci does not exist.[28]  To minimize contagion, children with scarlet fever should not return to school or daycare until they have completed 24 hours of antibiotic therapy and are clinically improving. 

Hand hygiene and proper maintenance of environmental hygiene should be highly reinforced. 


If the diagnosis is unclear, consultation with a dermatologist is recommended. For serious complications, an infectious disease specialist should be consulted. Referral to an otolaryngologist for tonsillectomy may be recommended for patients with recurrent pharyngitis.

Long-Term Monitoring

Follow-up evaluation is recommended to ensure resolution of the primary infection. Some patients report pruritus associated with the desquamating rash. Oral antihistamines and emollients usually are sufficient to control the pruritus.



Medication Summary

Treatment is aimed at providing adequate antistreptococcal antibiotic levels for at least 10 days.

Treat patients who have scarlet fever with a standard 10-day course of oral penicillin VK or erythromycin. Patients can also be treated with a single intramuscular injection of penicillin G benzathine. These regimens may prevent acute renal failure if antibiotics are initiated within 1 week of the onset of acute pharyngitis. First-generation cephalosporins may also be used. Erythromycin should be considered in patients allergic to penicillin. Tetracyclines and sulfonamides should not be used.


Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Penicillin G benzathine (Bicillin LA)

Penicillin G interferes with synthesis of cell wall mucopeptides during active multiplication, which results in bactericidal activity.

Penicillin VK

Penicillin VK is the drug of choice. It inhibits biosynthesis of cell wall mucopeptides and is effective during active multiplication. Inadequate concentrations may produce only bacteriostatic effects.

Amoxicillin (Moxatag)

Amoxicillin is an alternative drug of choice. It interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.

Erythromycin (E.E.S., E-Mycin, Ery-Tab)

Erythromycin is the drug of choice in penicillin-allergic patients. It inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. It is used for treatment of infections caused by susceptible strains, including streptococci.

In children, age, weight, and severity of infection determine proper dosage. When twice-daily dosing is desired, half of the total daily dose may be taken every 12 hours. For more severe infections, double the dose.

Cephalexin (Keflex)

Cephalexin is an alternative drug of choice. It is a first-generation cephalosporin that arrests bacterial growth by inhibiting bacterial cell wall synthesis. It has bactericidal activity against rapidly growing organisms. Its primary activity is against skin flora; it is used for skin infections.


Questions & Answers


What is scarlet fever?

From what conditions does scarlet fever evolve?

What is the pathophysiology of rash in scarlet fever?

What are the common sites of GABHS replication in the pathogenesis of scarlet fever?

What causes scarlet fever?

How do group A streptococci cause scarlet fever?

What are risk factors for scarlet fever?

How does temperature affect transmission of scarlet fever?

What is the incubation period for scarlet fever?

What is the prevalence of scarlet fever?

How does the incidence of scarlet fever vary by age?

How does the incidence of scarlet fever vary between men and women or among races?

What is the prognosis of scarlet fever?

What was the impact of scarlet fever prior to the discovery of antibiotics?

What are possible complications of scarlet fever?

How are complications of scarlet fever diagnosed?

What information about scarlet fever should patients receive?


What are the signs and symptoms of scarlet fever?

If left untreated, how does scarlet fever progress?

What history can aid in the diagnosis of scarlet fever?

What are physical findings characteristic of scarlet fever?

How long does a cutaneous rash persist in scarlet fever?

What are possible complications of scarlet fever?

What are the most common complications of scarlet fever?

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What conditions should be included in the differential diagnoses of scarlet fever?

How are rubella and rubeola differentiated from scarlet fever?

What other viral and bacterial illnesses should be considered when diagnosing scarlet fever?

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What are the differential diagnoses for Scarlet Fever?


What is the role of lab tests in the diagnosis of scarlet fever?

What is the role of WBC count in the diagnosis of scarlet fever?

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What is the sensitivity of throat culture for diagnosing scarlet fever?

How can sensitivity be maximized in throat cultures for scarlet fever?

What is the role of direct antigen detection in the diagnosis of scarlet fever?

What is the role of streptococcal antibody testing in the diagnosis of scarlet fever?

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What are the goals of treatment of scarlet fever?

What is the treatment of choice for scarlet fever?

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When should cultures be obtained in the management of scarlet fever?

When is hospitalization indicated for scarlet fever?

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What is the standard treatment for scarlet fever?

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