eMedicine Specialties > Emergency Medicine > Infectious Diseases

Scarlet Fever

Jerry Balentine, DO, Professor of Emergency Medicine, New York College of Osteopathic Medicine; Executive Vice President, Chief Medical Officer, Attending Physician in Department of Emergency Medicine, St. Barnabas Hospital
Daniel P Lombardi, DO, Clinical Assistant Professor, New York College of Osteopathic Medicine; Clinical Preceptor, Albert Einstein College of Medicine of Yeshiva University; Attending Physician and Interim Program Director, Department of Emergency Medicine, Saint Barnabas Hospital

Updated: May 7, 2009

Introduction

Background

Scarlet fever (known as scarlatina in older literature references) is an exotoxin-mediated disease arising from group A beta-hemolytic streptococcal infection. Ordinarily, scarlet fever evolves from a tonsillar/pharyngeal focus, although the rash develops in fewer 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 systemic rash of scarlet fever to the uncommon but highly lethal streptococcal toxic shock syndrome.

Pathophysiology

Usually, the sites of group A beta-hemolytic streptococcal 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).

Group A beta-hemolytic streptococci secrete a number of toxins, enzymes, and erythrogenic toxins. Release of erythrogenic toxin causes the pathognomonic rash of scarlet fever. Local lesions reveal a characteristic inflammatory reaction, specifically hyperemia, edema, and polymorphonuclear cell infiltration.

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.

Frequency

United States

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). 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.

Mortality/Morbidity

Scarlet fever is no longer associated with the deadly epidemics that made it so feared in the 1800s.

• Today, scarlet fever infection usually follows a benign course, and any undue morbidity and mortality are more likely to arise from suppurative complications, such as peritonsillar abscess, sinusitis, bronchopneumonia, and meningitis, or problems associated with immune-mediated sequelae, rheumatic fever, or 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. A lethal form of streptococcal infection is capable of producing the toxic streptococcal syndrome.

Sex

• Males and females are affected equally.

Age

• Peak incidence of scarlet fever occurs in children aged 4-8 years.
• By the time children are 10-years-old, 80% have developed lifelong protective antibodies against streptococcal pyrogenic exotoxins.
• Scarlet fever is rare in children younger than 2 years because of the presence of maternal antiexotoxin antibodies and lack of prior sensitization.

Clinical

History

• Scarlet fever generally has a 1- to 4-day incubation period.
• Emergence of the illness tends to be abrupt, usually heralded by sudden onset of fever associated with sore throat, headache, nausea, vomiting, abdominal pain, myalgias, and malaise.
• The characteristic rash appears 12-48 hours after onset of fever.
• 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.
• Recent history of exposure to another individual with a "strep" infection may aid in the diagnosis.

Physical

• Exudative tonsillitis preceding scarlet fever often is accompanied by erythematous oral mucous membranes, along with petechiae and punctate red macules on the hard and soft palate and uvula (ie, Forchheimer spots).
• On day 1 or 2, a white coating covers the dorsum of the tongue with reddened papillae projecting through, giving rise to the white strawberry tongue.

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.

• By day 4 or 5, the white coating disappears, revealing the representative raspberry tongue.
• 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).
  • As the skin lesions evolve and become more diffuse, they turn punctate and resemble a sunburn with goose pimples.
  • Numerous punctate lesions the size of pinheads give the skin a rough sandpaperlike texture.
  • Lesions tend to be accentuated in the skin folds, particularly in the region of the neck, axilla, antecubital fossae, and inguinal and popliteal creases.
  • Rupture of fragile capillaries at these sites displays linear arrays of petechiae (ie, Pastia lines) that may persist for 1-2 days after resolution of the generalized rash.
• Another distinctive facial finding is circumoral pallor.
• In severe disease, small vesicular lesions termed miliary sudamina may appear on the abdomen, hands, and feet.
• Mitigation of the exanthem occurs in approximately 1 week.
  • Desquamation, one of the most distinctive features of scarlet fever, begins 7-10 days after resolution of the rash and may continue up to 6 weeks.

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.

• Peeling of the skin is most prominent in the axilla, groin, and tips of the fingers and toes.
• Extent and duration of desquamation is directly proportional to initial intensity of the rash.

Causes

Infection of group A beta-hemolytic streptococci causes scarlet fever.

Differential Diagnoses

Abortion, Septic
Mononucleosis
Pediatrics, Kawasaki Disease
Roseola
Staphylococcal Scalded Skin Syndrome

Other Problems to Be Considered

Drug-induced syndromes

Workup

Laboratory Studies

• 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 is found on throat culture during acute infection.¹
  • Throat cultures are approximately 90% sensitive for the presence of group A beta-hemolytic streptococci in the pharynx. However, because a 10-15% carriage rate exists among healthy individuals, the presence of group A beta-hemolytic streptococci 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.²
• Streptococcal antibody tests are used to confirm previous group A streptococcal infection.
  • The most commonly available streptococcal antibody test is the antistreptolysin O test.
  • Currently, streptococcal antibody tests are not indicated during acute illness.
• Complete blood count
  • White blood cell (WBC) count in scarlet fever may increase to 12,000-16,000 per mm³, with a differential of up to 95% polymorphonuclear lymphocytes.
  • During the second week, eosinophilia, as high as 20%, can develop.

Imaging Studies

In most cases, no imaging studies are indicated.

Treatment

Emergency Department Care

• The goals when treating scarlet fever are to (1) prevent acute rheumatic fever, (2) reduce the spread of infection, (3) prevent suppurative complications, and (4) shorten the course of illness.
• Penicillin remains the drug of choice (documented cases of penicillin-resistant group A streptococci 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, erythromycin can be considered as an alternative.^3,4

Consultations

Consult infectious disease specialists for serious complications.

Referral to an ENT specialist may be warranted for recurrent pharyngitis.

Medication

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

The mainstay of treatment includes penicillin and erythromycin.

Tetracyclines and sulfonamides should not be used.

Antibiotics

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

Penicillin VK (Veetids, Beepen-VK)

Inhibits biosynthesis of cell wall peptidoglycan and is effective during the stage of active multiplication. Inadequate concentrations may produce only bacteriostatic effects.

Dosing

Adult

250 mg PO tid/qid for 10 d

Pediatric

<12 years: 25-50 mg/kg/d PO divided tid/qid; not to exceed 3 g/d
>12 years: Administer as in adults

Interactions

Probenecid can increase penicillin effectiveness by decreasing its clearance; concurrent administration of tetracyclines can decrease penicillin effectiveness

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Caution with impaired renal function

Penicillin G benzathine (Bicillin L-A)

Interferes with synthesis of cell wall peptidoglycan during active multiplication, resulting in bactericidal activity against susceptible bacteria.

Dosing

Adult

1.2 million U IM

Pediatric

<27 kg: 600,000 U IM
>27 kg: Administer as in adults

Interactions

Probenecid can increase penicillin effectiveness by decreasing its clearance; concurrent administration of tetracyclines can decrease penicillin effectiveness

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Caution with impaired renal function

Erythromycin (EES, E-Mycin, Ery-Tab)

Treatment of infections caused by susceptible strains, including streptococci.

Dosing

Adult

250 mg erythromycin stearate/base (or 400 mg ethylsuccinate) q6h 1 h PO ac or 500 mg PO q12h
Alternatively: 333 mg PO q8h; increase up to 4 g/d, depending on severity of infection
Bid dosing: 500 mg PO q12h (recommended dose); bid dosing not recommended with doses >1 g/d

Pediatric

30-50 mg/kg/d (15-25 mg/lb/d) PO in divided doses for 10 d (age, weight, and severity of infection determine proper dosage)
If bid dosing desired, one half of total daily dose may be taken q12h; not to exceed 1 g/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 - Usually safe but benefits must outweigh the risks.

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

Further Inpatient Care

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

Further Outpatient Care

• To minimize contagion, a minimum of 24 hours of antibiotic therapy is indicated before a child should return to school.

Complications

• Cervical lymphadenitis
• Otitis media
• Peritonsillar abscess
• Sinusitis
• Bronchopneumonia
• Meningitis
• Brain abscess
• Intracranial venous sinus thrombosis
• Septicemia
• Hepatitis⁵
• Vasculitis⁶
• Uveitis
• Rare but lethal early toxin-mediated sequelae include myocarditis and toxic shocklike syndrome. Late complications of group A streptococcal infection include rheumatic fever and poststreptococcal 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.

Patient Education

• 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

• Failure to recognize and treat streptococcal infection in a timely manner is a pitfall. Treatment should be started as soon as possible to reduce the occurrence of rheumatic fever.

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

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2. 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].

3. Bass JW. Antibiotic management of group A streptococcal pharyngotonsillitis. Pediatr Infect Dis J. Oct 1991;10(10 Suppl):S43-9. [Medline].

4. Derrick CW, Dillon HC. Erythromycin therapy for streptococcal pharyngitis. Am J Dis Child. Feb 1976;130(2):175-8. [Medline].

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

6. Reddy UP, Albini TA, Banta JT, Davis JL. Post-streptococcal vasculitis. Ocul Immunol Inflamm. Jan-Feb 2008;16(1):35-6. [Medline].

7. 2006 Report of the Committee on Infectious Diseases. Summaries of Infectious Diseases. In: Pickering LK, Baker CJ, Long SS, McMillan JA, eds. Red Book. 27^th ed. American Academy of Pediatrics; 2006:610-618.

8. Bialecki C, Feder HM Jr, Grant-Kels JM. The six classic childhood exanthems: a review and update. J Am Acad Dermatol. Nov 1989;21(5 Pt 1):891-903. [Medline].

9. Burns JC, Kushner HI, Bastian JF, et al. Kawasaki disease: A brief history. Pediatrics. Aug 2000;106(2):E27. [Medline].

10. Dajani A, Taubert K, Ferrieri P, Peter G, Shulman S. Treatment of acute streptococcal pharyngitis and prevention of rheumatic fever: a statement for health professionals. Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of the Council on Cardiovascular Disease in the Young, the American Heart Association. Pediatrics. Oct 1995;96(4 Pt 1):758-64. [Medline].

11. Danjani AS, Bisno AL, Chung KJ, et al. Prevention of rheumatic fever. A statement for health professionals by the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of the Council on Cardiovascular Disease in the Young, the American Heart Association. Circulation. Oct 1988;78(4):1082-6. [Medline].

12. Del Castillo LD, Macaset T, Olsen J. Group A streptococcal pharyngitis and scarlatiniform rash in an 8-week-old infant. Am J Emerg Med. Mar 2000;18(2):233-4. [Medline].

13. Duncan SR, Scott S, Duncan CJ. Modelling the dynamics of scarlet fever epidemics in the 19th century. Eur J Epidemiol. 2000;16(7):619-26. [Medline].

14. Facklam RR. Specificity study of kits for detection of group A streptococci directly from throat swabs. J Clin Microbiol. Mar 1987;25(3):504-8. [Medline].

15. Hoebe CJ, Wagenvoort JH, Schellekens JF. [An outbreak of scarlet fever, impetigo and pharyngitis caused by the same Streptococcus pyogenes type T4M4 in a primary school]. Ned Tijdschr Geneeskd. Nov 4 2000;144(45):2148-52. [Medline].

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18. Katz AR, Morens DM. Severe streptococcal infections in historical perspective. Clin Infect Dis. Jan 1992;14(1):298-307. [Medline].

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Keywords

scarlet fever, scarlatina, group A beta-hemolytic streptococci, group A streptococci, strep throat, bullous impetigo, streptococcal toxic shock syndrome, toxic streptococcal syndrome, surgical scarlet fever, puerperal scarlet fever, rheumatic fever, peritonsillar abscess, sinusitis, bronchopneumonia, meningitis, glomerulonephritis, hepatitis, vasculitis, uveitis, Forchheimer spots, white strawberry tongue, raspberry tongue, Pastialines

Contributor Information and Disclosures

Author

Jerry Balentine, DO, Professor of Emergency Medicine, New York College of Osteopathic Medicine; Executive Vice President, Chief Medical Officer, Attending Physician in Department of Emergency Medicine, St. Barnabas Hospital
Jerry Balentine, DO is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American College of Physician Executives, American Osteopathic Association, and New York Academy of Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Daniel P Lombardi, DO, Clinical Assistant Professor, New York College of Osteopathic Medicine; Clinical Preceptor, Albert Einstein College of Medicine of Yeshiva University; Attending Physician and Interim Program Director, Department of Emergency Medicine, Saint Barnabas Hospital
Daniel P Lombardi, DO is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, and American Osteopathic Association
Disclosure: Nothing to disclose.

Medical Editor

Joseph A Salomone, III, MD, Associate Professor, Department of Emergency Medicine, Truman Medical Center, University of Missouri at Kansas City School of Medicine
Joseph A Salomone, III, MD is a member of the following medical societies: American Academy of Emergency Medicine, Society for Academic Emergency Medicine, and Southern Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Eric L Weiss, MD, DTM&H, Director of Stanford Travel Medicine, Medical Director of Stanford Lifeflight, Assistant Professor, Departments of Emergency Medicine and Infectious Diseases, Stanford University School of Medicine
Eric L Weiss, MD, DTM&H is a member of the following medical societies: American College of Emergency Physicians, American College of Occupational and Environmental Medicine, American Medical Association, American Society of Tropical Medicine and Hygiene, Physicians for Social Responsibility, Southeastern Surgical Congress, Southern Association for Oncology, Southern Clinical Neurological Society, and Wilderness Medical Society
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

Robert E O'Connor, MD, MPH, Professor and Chair, Department of Emergency Medicine, University of Virginia Health System
Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Heart Association, American Medical Association, Medical Society of Delaware, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Diana Kessler, DO, to the development and writing of this article.

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