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Scarlet Fever

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]

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 (eg, bullous impetigo)
to the widespread eruption of scarlet fever to the uncommon but highly lethal streptococcal
toxic shock syndrome.

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, [12] 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
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
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 1-10 years, though it can also occur in
older children and adults. 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. [7]
Males and females are affected equally. No racial or ethnic predilection is reported for group
A streptococcal infection.

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
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 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. [6]
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

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 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, 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 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.

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. [17] 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. [18]
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 moniliformisinfection (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.

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. [19]
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. [20]

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.

Differential Diagnoses
 Abortion Complications
 Drug Eruptions
 Erythema Infectiosum
 Exfoliative Dermatitis
 Epstein-Barr Virus (EBV) Infectious Mononucleosis (Mono)
 Kawasaki Disease
 Measles
 Pediatric Erythema Toxicum
 Pediatric Pharyngitis
 Pediatric Pneumonia
 Pediatric Rubella
 Pityriasis Rosea
 Recurrent toxin-mediated perineal erythema
 Staphylococcal Scalded Skin Syndrome (SSSS)
 Toxic Shock Syndrome
 Viral exanthem

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. [21, 22] However, some strains of group A streptococci may not be
susceptible to macrolides. 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. [23] 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

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

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
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)
 View full drug information
Penicillin G interferes with synthesis of cell wall mucopeptides during active multiplication,
which results in bactericidal activity.
Dosing Form & Strengths
injectable suspension
 600,000 units/1mL syringe
 1.2 million units/2mL syringe
 2.4 million units/4mL syringe

Group A Streptococcal Infections

<27 kg: 600,000 unit IM x1 (AHA guidelines 2009)
27 kg or greater: 1.2 million units IM x1 (AHA guidelines 2009)
Rheumatic Fever, Prophylaxis
<27 kg: 600,000 units IM q4Weeks; high-risk patients q3Weeks (AHA guidelines 2009)
27 kg or greater: 1.2 million units IM q4Weeks; high-risk patients q3Weeks (AHA guidelines
Congenital (<2 years old): 50,000 units/kg IM x 1 dose
Early: 50,000 units/kg IM x 1 dose; not to exceed 2.4 million units/dose
>1 year duration: 50,000 units/kg qWeek x3 weeks; not to exceed 2.5 million units/dose
Renal Impairment
Not defined in children; see adult recommendations

Penicillin VK
 View full drug information
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.
Dosage Forms & Strengths
oral solution
 125mg/5mL
 250mg/5mL
 250mg
 500mg

Pneumococcal Systemic Infections

<12 years
 50-75 mg/kg/day PO q6-8hr
 Not to exceed 3 g/day
>12 years
 250-500 mg PO q6-8hr until the patient is afebrile for at least 2 days

Pneumococcal Infection Prophylaxis

<5 years: 125 mg PO q12hr
>5 years: 250 mg PO q12hr
Streptococcal Pharyngitis
Children: 250 mg PO q8-12hr for 10 days
Adolescents: 250 mg PO q6hr or 500 mg PO q12hr for 10 days
Rheumatic Fever
Primary prevention
<5 years: 125 mg q12hr PO for 10 days
>5 years: 250 mg q12hr PO for 10 days
Recurrent Rheumatic Fever
Children: 125-250 mg PO q12hr on a continuing basis
Take on empty stomach

Amoxicillin (Moxatag)
 View full drug information
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.
Dosage Forms & Strengths
oral solution
 125mg/5mL
 200mg/5mL
 250mg/5mL
 400mg/5mL
 250mg
 500mg
 500mg
 875mg
tablet, chewable
 125mg
 250mg
tablet, extended release (Moxatag)
 775mg

Ear, Nose, & Throat Infections

Mild to moderate infections
 <3 months: ≤30 mg/kg/day PO divided q12hr for 48-72 hours; for ≥10 days for S
pyogenes infections
 >3 months and <40 kg: 25 mg/kg/day PO divided q12hr or 20 mg/kg/day PO divided
 >40 kg: 500 mg PO q12hr or 250 mg PO q8hr for 10-14 days
Severe infections
 <3 months: ≤30 mg/kg/day PO divided q12hr for 48-72 hours; for ≥10 days for S
pyogenes infections
 >3 months and <40 kg: 45 mg/kg/day PO divided q12hr or 40 mg/kg/day PO divided
 >40 kg: 875 mg PO q12hr or 500 mg PO q8hr for 10-14 days
Tonsillitis/Streptococcal pharyngitis
 50 mg/kg PO qDay for 10 days, not to exceed 1 g/day, OR 25 mg/kg PO BID for 10
days, not to exceed 500 mg/dose
 >12 years: 775 mg (Moxatag) PO qDay for 10 days, taken within 1 hour after meal
(swallow tablet whole; do not crush or chew)
Acute Otitis Media
>3 months and <40kg: 80-90 mg/kg/day PO divided q8-12hr
>40 kg: 500 mg PO q12hr or 250 mg PO q8hr for 10-14 days
Lower Respiratory Tract Infections
Mild, moderate, or severe infections
 <3 months: ≤30 mg/kg/day PO divided q12hr for 48-72 hours; for ≥10 days for S
pyogenes infections
 >3 months and <40 kg: 45 mg/kg/day PO divided q12hr or 40 mg/kg/day PO divided
 >40kg: 875 mg PO q12hr or 500 mg PO q8hr for 10-14 days
Pneumonia, community-acquired (Off-label)
 Since M. pneumoniae is the primary pathogen that causes pneumonia in patients 5-15
years old, a macrolide antibiotic may be a fist choice treatment
 <3 months: Safety and efficacy not established
 ≥3 months:
 Immediate release
o Empiric treatment: 90 mg/kg/day PO divided q12 hr for 10 days; not to exceed
4,000 mg/day
o Group A Streptococcus: 50-75 mg/kg/day PO divided q12hr for 10 days; not to
exceed 4,000 mg/day
o H. influenza: 75-100 mg/kg/day PO divided q8hr for 10 days; not to exceed 4,000
o S. pneumoniae (mild infection or step-down therapy or when MICs to penicillin
≤2.0 mcg/mL): 90 mg/kg/day PO divided q12hr or 45 mg/kg/day divided q8hr for
10 days; not to exceed 4,000 mg/day

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

 View full drug information
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.

Dosing Form & Strengths

 400mg
oral suspension
 200mg/5mL
 400mg/5mL

General Dosing Recommendations

 <1.2 kg: 20 mg/kg/day PO divided q12hr
 1.2 kg or more, 0-7 days old: 20 mg/kg/day PO divided q12hr
 ≥1.2 kg or more, 7 days or older: 30 mg/kg/day PO divided q8hr
 Chlamydial conjunctivitis and pneumonia: 50 mg/kg/day PO divided q6hr for 14days
 Mild-to-moderate infections: 30-50 mg/kg/day PO divided q6-12hr
 Severe infection: 60-100 mg/kg/day PO divided q6-12hr

Cephalexin (Keflex)
 View full drug information
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

Dosage Forms & Strengths

 250mg
 500mg
oral suspension
 125mg/5mL
 250mg/5mL
 125mg
 250mg

Uncomplicated Cystitis
<15 years: 25-50 mg/kg/day PO divided q6-8hr for 10 days; not to exceed 4 g/day
>15 years: 250 mg PO q6hr; dosage range, 1-4 g/day in divided doses
Genitourinary Tract Infections
25-50 mg/kg/day PO divided q6-8hr for 10 days; not to exceed 4 g/day
Beta-Hemolytic Streptococcal Infections
25-50 mg/kg/day PO divided q6-8hr for 10 days; not to exceed 4 g/day
Bone Infections
25-50 mg/kg/day PO divided q6-8hr for 10 days; not to exceed 4 g/day
Otitis Media
75-100 mg/kg/day PO divided q6hr for 10 days; not to exceed 4 g/day
Skin/Skin Structure Infections
25-50 mg/kg/day PO divided q6-8hr for 10 days; not to exceed 4 g/day
Respiratory Tract Infections
25-50 mg/kg/day PO divided q6-8hr for 10 days; not to exceed 4 g/day
Streptococcal Pharyngitis
25-50 mg/kg PO q12hr for 10 days; not to exceed 500 mg q12hr
Cellulitis and Mastitis
Adolescents: 500 mg PO q6hr; dosage range, 1-4 g/day in divided doses

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 [13]
 Vasculitis [14]
 Uveitis
 Myocarditis
 Sepsis with abdominal wall abscess (rarely) [15]
 Invasive group A streptococcal infections and streptococcal toxic shock syndrome
(rarely) [16]
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
Weeks to months after the illness, transverse grooves (ie, Beau lines) may appear on the nail
plates and hair loss (telogen effluvium) may occur.

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. [8]
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. [9, 10]Localized soft tissue infections may
suggest the presence of underlying osteomyelitis, but scarlet fever may occur from cellulitis
alone. [11] 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 Center, as well as Strep Throat and Skin Rashes in Children.

1. 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. 2008 Apr. 56(4):261-7. [Medline].
2. 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. 2007 Nov. 55(5):419-24. [Medline].
3. Brinker A. Scarlet Fever. N Engl J Med. 2017 May 18. 376 (20):1972. [Medline].
4. Andrey DO, Posfay-Barbe KM. Re-emergence of scarlet fever: old players
return?. Expert Rev Anti Infect Ther. 2016 Aug. 14 (8):687-9. [Medline].
5. Park DW, Kim SH, Park JW, Kim MJ, Cho SJ, Park HJ, et al. Incidence and
Characteristics of Scarlet Fever, South Korea, 2008-2015. Emerg Infect Dis. 2017
Apr. 23 (4):658-661. [Medline].
6. Cunningham MW. Pathogenesis of group A streptococcal infections. Clin Microbiol
Rev. 2000 Jul. 13(3):470-511. [Medline]. [Full Text].
7. 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. 2008
Oct. 47(10):1166-72. [Medline]. [Full Text].
8. Sandrini J, Beucher AB, Kouatchet A, Lavigne C. [Scarlet fever with multisystem
organ failure and hypertrophic gastritis]. Rev Med Interne. 2009 May. 30(5):456-
9. [Medline].
9. Gómez-Carrasco JA, Lassaletta A, Ruano D. [Acute hepatitis may form part of scarlet
fever]. An Pediatr (Barc). 2004 Apr. 60(4):382-3. [Medline].
10. Güven A. Hepatitis and hematuria in scarlet fever. Indian J Pediatr. 2002 Nov.
69(11):985-6. [Medline].
11. Lau SK, Woo PC, Yuen KY. Toxic scarlet fever complicating cellulitis: early clinical
diagnosis is crucial to prevent a fatal outcome. New Microbiol. 2004 Apr. 27(2):203-
6. [Medline].
12. Finnish Medical Society Duodecim. Sore throat and tonsillitis. EBM Guidelines.
Evidence-Based Medicine. Feb 2 2007Helsinki, Finland: Wiley Interscience. John
Wiley & Sons. [Full Text].
13. Gidaris D, Zafeiriou D, Mavridis P, Gombakis N. Scarlet Fever and hepatitis: a case
report. Hippokratia. 2008 Jul. 12(3):186-7. [Medline]. [Full Text].
14. Reddy UP, Albini TA, Banta JT, Davis JL. Post-streptococcal vasculitis. Ocul
Immunol Inflamm. 2008 Jan-Feb. 16(1):35-6. [Medline].
15. Wilson PF, Wannemuehler TJ, Matt BH. Invasive group A Streptococcus resulting in
sepsis and abdominal wall abscess after adenotonsillectomy. Laryngoscope. 2015
May. 125 (5):1230-2. [Medline].
16. Warnier H, Depuis Z, Nyamugabo K, Desprechins B, Seghaye MC. [An rare
complication of scarlet fever : invasive group A streptococcal infection with
streptococcal toxic shock syndrome]. Rev Med Liege. 2017 Mar. 72 (3):132-
137. [Medline].
17. Gaston DA, Zurowski SM. Arcanobacterium haemolyticum pharyngitis and
exanthem. Three case reports and literature review. Arch Dermatol. 1996 Jan.
132(1):61-4. [Medline].
18. 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. 2005 Jun-Jul. 23(6):388-9. [Medline].
19. 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. 2009 Mar 24. 119(11):1541-51. [Medline].
20. Gerber MA, Shulman ST. Rapid diagnosis of pharyngitis caused by group A
streptococci. Clin Microbiol Rev. 2004 Jul. 17(3):571-80, table of
contents. [Medline]. [Full Text].
21. Bass JW. Antibiotic management of group A streptococcal
pharyngotonsillitis. Pediatr Infect Dis J. 1991 Oct. 10(10 Suppl):S43-9. [Medline].
22. Derrick CW, Dillon HC. Erythromycin therapy for streptococcal pharyngitis. Am J
Dis Child. 1976 Feb. 130(2):175-8. [Medline].
23. Stock I. [Streptococcus pyogenes--much more than the aetiological agent of scarlet
fever]. Med Monatsschr Pharm. 2009 Nov. 32(11):408-16; quiz 417-8. [Medline].