eMedicine Specialties > Emergency Medicine > Pediatric

Pediatrics, Scarlet Fever

Pamela L Dyne, MD, Professor of Clinical Medicine/Emergency Medicine, David Geffen School of Medicine at UCLA; Attending Physician, Department of Emergency Medicine, Olive View-UCLA Medical Center
Peter Bloomfield, MD, MPH, Resident Physician, UCLA Medical Center/Olive View-UCLA Medical Center Emergency Medicine Residency Program

Updated: Aug 12, 2009

Introduction

Background

Scarlet fever is a syndrome characterized by exudative pharyngitis, fever, and scarlatiniform rash. It is caused by an infection with a pyogenic exotoxin-producing group A beta-hemolytic streptococci.

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.

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.

Pathophysiology

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).

Streptococci may be alpha-hemolytic (partial hemolysis), beta-hemolytic (complete hemolysis), or gamma-hemolytic (no hemolysis). Most streptococci excrete hemolyzing enzymes and toxins. Erythrogenic toxins cause the rash of scarlet fever. The erythema-producing toxin was discovered by Dick and Dick in 1924.

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. Scarlet fever is usually associated with pharyngitis; however, in rare cases, it follows streptococcal infections at other sites.

Infections occur year-round, but the incidence of pharyngeal disease is highest in school-aged children (5-15 y) 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 a recent outbreak in China.¹

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.

Frequency

United States

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

Mortality/Morbidity

In the preantibiotic era, infections due to group A beta-hemolytic streptococci were major causes of mortality and morbidity. Now with antibiotics, enhanced immune status of the population and improved socioeconomic conditions, the incidence and rate of complications of these infections has decreased.

Sex

No predilection is observed.

Age

Scarlet fever predominantly occurs in children aged 5-15 years.

Clinical

History

• Scarlet fever is characterized by the following findings:
  • Sore throat²
  • Headache
  • Vomiting
  • Abdominal pain
  • Fever
• The rash appears 1-2 days after onset of illness, first on the neck and then extending to the trunk and extremities.

Physical

• The patient usually appears moderately ill.
• Fever may be present.
• The patient may have tachycardia.
• Tonsils are edematous, erythematous, and covered with a yellow, gray, or white exudate.
• Petechiae is noted on the soft palate.
• Tender anterior cervical lymphadenopathy may be present.
• Flushed face with perioral pallor is observed.
• Scarlatiniform rash is noted.
  • Exanthem texture is usually of coarse sandpaper, and the erythema blanches with pressure.
  • The skin can be pruritic but usually is not painful.
  • A few days following generalization of the rash, it becomes more intense along skin folds and produces lines of confluent petechiae known as the Pastia sign. These lines are caused by increased capillary fragility.
  • The rash begins to fade 3-4 days after onset, and the desquamation phase begins. This phase begins 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.
• Appearance of the tongue consists of the following:
  • During the first 2 days of the disease, the tongue has a white coat through which the red and edematous papillae project. This is referred to as a white strawberry tongue.
  • After 2 days, the tongue also desquamates, resulting in a red tongue with prominent papillae called the red strawberry tongue.

Causes

• Scarlet fever results from an erythrogenic toxin produced by group A streptococci.

Differential Diagnoses

Other Problems to Be Considered

Erythema toxicum
Enteroviral infection and nonspecific viral infection
Pediatric cellulitis
Severe sunburn
Arcanobacterium haemolyticum
Drug hypersensitivity
Viral exanthema
Plant allergic reactions

Workup

Laboratory Studies

The following studies are indicated in scarlet fever:

• Throat culture or rapid streptococcal test
• Anti-deoxyribonuclease B and antistreptolysin-O titers (antibodies to streptococcal extracellular products)
  • This test can provide confirmatory evidence of recent infection but have no value in acute infection.
  • This test may be of value in patients with suspected acute renal failure or acute glomerulonephritis.

Treatment

Emergency Department Care

• Treatment of streptococcal infections is primarily directed at preventing acute renal failure from poststreptococcal glomerulonephritis and suppurative sequelae (eg, adenitis, mastoiditis, ethmoiditis, abscesses, cellulitis).
• Whether antibiotics prevent poststreptococcal glomerulonephritis is still debated in the literature.

Consultations

• Referral to an otolaryngologist for tonsillectomy may be recommended for patients with recurrent pharyngitis.

Medication

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.

Antibiotics

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

Penicillin (Bicillin L-A, Beepen-VK, Pen-Vee K)

Inhibits biosynthesis of cell-wall mucopeptide. Bactericidal against sensitive organisms when adequate concentrations reached and most effective during stage of active multiplication. Inadequate concentrations may produce only bacteriostatic effects. If patients have supportive complications, increased doses may be required. May be administered PO as penicillin VK (Beepen-VK, Pen-Vee K) or IM as penicillin G benzathine (Bicillin L-A).

Dosing

Adult

Penicillin VK: 250-500 mg PO qid for 10 d
Penicillin G benzathine: 1.5 million U IM once

Pediatric

Penicillin VK:
<12 years: 25-50 mg/kg/d PO divided qid; not to exceed 3 g/d
>12 years: Administer as in adults
Penicillin G benzathine:
<12 years: 25,000-50,000 U/kg IM once; not to exceed 1.2 million U/dose
>12 years: Administer as in adults

Interactions

Probenecid may increase effectiveness by decreasing clearance; tetracyclines are bacteriostatic, decreasing effectiveness of penicillins when administered concurrently

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in renal impairment

Erythromycin (E.E.S.)

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal infections. Appropriate therapy for patients allergic to penicillin.

Dosing

Adult

250 mg PO qid for 10 d

Pediatric

30-50 mg/kg/d PO divided qid for 10 d

Interactions

Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin, increases risk of rhabdomyolysis

Contraindications

Documented hypersensitivity; hepatic impairment

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in liver disease; estolate formulation may cause cholestatic jaundice; GI adverse effects are common (give doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur

Follow-up

Deterrence/Prevention

• Children with scarlet fever should not return to school or day care until they have completed 24 hours of antibiotic therapy.

Complications

• Suppurative complications
  • Cervical adenitis
  • Otitis media and/or mastoiditis
  • Ethmoiditis
  • Sinusitis
  • Peritonsillar abscess
  • Pneumonia
  • Septicemia, meningitis, osteomyelitis, and septic arthritis
• Rheumatic fever
• Acute renal failure from poststreptococcal glomerulonephritis
• Hepatitis: A recent case report described a 6-year-old boy with hepatitis as a complication of scarlet fever.³

Prognosis

• The prognosis is excellent; most patients fully recover.
• Attacks may recur.

Patient Education

• Patients must complete the entire course of antibiotics, even if symptoms resolve.
• Warn patients that they will have generalized exfoliation over the next 2 weeks.
• Emphasize warning signs for complications of streptococcal infection such as persistent fever, increased throat or sinus pain, and generalized swelling.
• For excellent patient education resources, visit eMedicine's Children's Health Center and Ear, Nose, and Throat Center. Also, see eMedicine's patient education articles Strep Throat and Skin Rashes in Children.

Miscellaneous

Medicolegal Pitfalls

• Missing or not recognizing the diagnosis entirely, diagnosing a viral etiology, and failing to initiate antibiotics are the most common pitfalls.
• Other pitfalls include failure to obtain a history of penicillin allergy and administration of long-acting penicillin given intramuscularly (IM).

Multimedia

Media file 1: 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.

Media file 2: 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.

References

1. Yang SG, Dong HJ, Li FR, Xie SY, Cao HC, Xia SC. 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].

2. [Guideline] Finnish Medical Society Duodecim. Sore throat and tonsillitis. EBM Guidelines. Evidence-Based Medicine. Feb 2 2007;Helsinki, Finland: Wiley Interscience. John Wiley & Sons:[Full Text].

3. Gidaris D, Zafeiriou D, Mavridis P, Gombakis N. Scarlet Fever and hepatitis: a case report. Hippokratia. Jul 2008;12(3):186-7. [Medline].

4. Chiesa C, Pacifico L, Nanni F, Orefici G. Recurrent attacks of scarlet fever. Arch Pediatr Adolesc Med. Jun 1994;148(6):656-60. [Medline].

5. Davis H, Karasic R. Pediatric infectious disease. In: Atlas of Pediatric Physical Diagnosis. 3^rd ed. 1997:355-7.

6. Fisher RG, Boyce TG. Rash syndromes. In: Moffet's Pediatric Infectious Diseases: A Problem-Oriented Approach. Lippincott Williams & Wilkins; 2005:374-6.

7. Gerber MA. Diagnosis and treatment of pharyngitis in children. Pediatr Clin North Am. Jun 2005;52(3):729-47, vi. [Medline].

8. Gerber MA. Group A streptococcus. In: Nelson Textbook of Pediatrics. Philadelphia, Pa: WB Saunders Co; 2004:870-4.

9. Hamour A, Bonnington A, Wilkins EG. Severe community acquired pneumonia associated with a desquamating rash due to group A beta-haemolytic streptococcus. J Infect. Jul 1994;29(1):77-81. [Medline].

10. Kaplan EL, Gerber MA. Group A, group C and group G beta-hemolytic streptococcal infections. In: Textbook of Pediatric Infectious Diseases. Philadelphia: PA: Saunders; 2004:1142-56.

11. Kleiegman RM, Feigin RD. Streptococcal infections. In: Nelson Textbook of Pediatrics. 14^th ed. Philadelphia, Pa: WB Saunders Co; 1992:698-703.

Keywords

scarlatina, scarlatinella, scarlatiniform rash, group A streptococcal pharyngitis, strep throat, group A streptococci, group A beta-hemolytic streptococci, group A streptococcal toxin, strep throat, erythrogenic toxins, pharyngitis, petechiae on soft palate, flushed face with perioral pallor, anterior cervical lymphadenopathy, erythematous exanthem, Pastia sign, white strawberry tongue, red strawberry tongue, treatment, diagnosis

Contributor Information and Disclosures

Author

Pamela L Dyne, MD, Professor of Clinical Medicine/Emergency Medicine, David Geffen School of Medicine at UCLA; Attending Physician, Department of Emergency Medicine, Olive View-UCLA Medical Center
Pamela L Dyne, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Peter Bloomfield, MD, MPH, Resident Physician, UCLA Medical Center/Olive View-UCLA Medical Center Emergency Medicine Residency Program
Disclosure: Nothing to disclose.

Medical Editor

Garry Wilkes, MBBS, FACEM, Director of Emergency Medicine, Bunbury Hospital, Western Australia; Medical Director, St John Ambulance, WA Ambulance Service; Adjunct Associate Professor, Edith Cowan University; Clinical Associate Professor, Rural Clinical School, University of Western Australia, Australia.
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Grace M Young, MD, Associate Professor, Department of Pediatrics, University of Maryland Medical Center
Grace M Young, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Emergency Physicians
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Richard G Bachur, MD, Associate Professor of Pediatrics, Harvard Medical School; Associate Chief and Fellowship Director, Attending Physician, Division of Emergency Medicine, Children's Hospital of Boston
Richard G Bachur, MD is a member of the following medical societies: American Academy of Pediatrics, Society for Academic Emergency Medicine, and Society for Pediatric Research
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Kelli N McCartan, MD, to the development and writing of this article.

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