eMedicine Specialties > Dermatology > Bacterial Infections

Scarlet Fever

Edward J Zabawski Jr, DO, RPh, Dermatologist, Spencer Dermatology Group

Updated: Apr 28, 2009

Introduction

Background

Scarlet fever is an infection caused by toxin-producing 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, but food-borne outbreaks have been reported.^{[1,2 ]}

Pathophysiology

As the name scarlet fever implies, an erythematous eruption is associated with a febrile illness. The circulating toxin, often referred to as erythemogenic toxin, causes the 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.^{[3 ]}

Mortality/Morbidity

Historically, scarlet fever resulted in death in 15-20% of those affected. Since the advent of antibiotic therapy, the mortality rate for scarlet fever is less than 1%. Although uncommon, case reports describe patients, including adults, who are severely affected.^{[4 ]}Morbidity and mortality associated with scarlet fever is usually minimal. 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.^{[5,6 ]}Localized soft tissue infections may suggest the presence of underlying osteomyelitis, but scarlet fever may occur from cellulitis alone.^{[7 ]}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.

Race

No racial or ethnic predilection is reported for group A streptococcal infection.

Age

The infection usually occurs in children, with peak age incidence from 1-10 years. However, it can occur in older children and adults.

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.^{[8 ]}

Clinical

History

The cutaneous eruption of scarlet fever accompanies a streptococcal infection at another anatomic site, usually the tonsillopharynx. Abrupt onset of fever, headache, vomiting, malaise, chills, and sore throat occurs. Rash appears 1-4 days after the onset.

Physical

The mucous membranes usually are bright red, and scattered petechiae and small red papular lesions on the soft palate are often present.

• During the first days of infection, 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, as shown 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.

    
    
• The characteristic exanthem consists of a fine erythematous punctate eruption that appears within 1-4 days following the onset of the illness. It first appears on the upper trunk and axillae and then becomes generalized, although it is usually more prominent in flexural areas, such as the axillae, popliteal fossae, and inguinal folds. It may also appear more intense at dependent sites and sites of pressure, such as the buttocks.
• Capillary fragility is increased, and often, transverse areas of hyperpigmentation with petechiae in the axillary, antecubital, and inguinal areas (Pastia lines) can be observed.
• The face is usually flushed, and circumoral pallor is observed.
• The eruption imparts a dry rough texture to the skin that is reported to resemble the feel of sandpaper.
• The cutaneous rash, shown below, lasts for 4-5 days, followed by fine desquamation, the extent and duration of which is directly related to the severity of the eruption.
  • 
    

    

    Desquamation of the palms is a frequently observed self-limited manifestation of scarlet fever present in the healing period following resolution of the infection and acute eruption.

    
    

Causes

The overwhelming majority of cases of scarlet fever are caused by beta hemolytic Lancefield group A streptococcus (GABHS). Other bacteria can cause a pharyngitis and similar rash, such as Staphylococcus aureus, Haemophilus influenzae, Arcanobacterium haemolyticum, and Clostridium species.^{[9 ]}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.^{[10 ]}

• 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, hepatitis B infection, HIV, and Streptobacillus moniliformis infection (rat bite fever) may also need 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 allow for distinction.
• Noninfectious diseases that should be considered include Kawasaki disease, acute lupus erythematosus, morbilliform drug eruption, and juvenile rheumatoid arthritis.

Differential Diagnoses

Drug Eruptions
Lupus Erythematosus, Acute
Measles, Rubeola
Rubella
Toxic Shock Syndrome

Other Problems to Be Considered

Fifth disease
Rubeola
Epstein-Barr virus (infectious mononucleosis)
Enterovirus
Hepatitis B infection
Human immunodeficiency virus
S moniliformis infection (rat bite fever)
Toxic shock syndrome
Secondary syphilis
Juvenile rheumatoid arthritis
Atropine toxicity

Workup

Laboratory Studies

• Cultures of the infected oropharynx or other infected areas should be obtained.
• CBC count commonly reveals a leukocytosis. Urinalysis and liver function tests may reveal changes associated with complications of scarlet fever. Said tests are part of a complete medical workup.
• An increase in antistreptolysin O titers can be observed but is a late finding and usually of value only in retrospect.
• Patients whose bacterial source may suggest another process (eg, a patient with a suppurative leg wound who may have osteomyelitis) should be evaluated accordingly.

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 perivascular infiltrate usually consisting of lymphocytes primarily with a slight amount of spongiosis in the epidermis is present. Slight parakeratosis may be present, which probably correlates with the sandpaperlike texture of the skin.

Treatment

Medical Care

Antibiotic therapy is the treatment of choice for scarlet fever. 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.

Consultations

If the diagnosis is unclear, consultation with a dermatologist is recommended.

Medication

DOC is benzathine penicillin G administered IM or penicillin VK administered PO for 10 days. First-generation cephalosporins may also be used. Erythromycin should be considered in patients allergic to penicillin.

Antibiotics

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

Penicillin G benzathine (Bicillin LA)

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

Dosing

Adult

1.2 million U IM administered as single injection

Pediatric

<27 kg: 300,000-600,000 U IM
>27 kg: 900,000-1.2 million U IM

Interactions

Probenecid can increase penicillin effectiveness by decreasing clearance; coadministration with tetracyclines can decrease effectiveness of penicillin

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 impaired renal function

Penicillin VK (Veetids, Beepen-VK)

DOC; inhibits biosynthesis of cell wall mucopeptides and is effective during active multiplication. Inadequate concentrations may produce only bacteriostatic effects.

Dosing

Adult

500 mg PO qid for 10 d

Pediatric

25-50 mg/kg/d PO divided bid/qid for 10 d

Interactions

Probenecid can increase effects of penicillin by decreasing clearance; coadministration of tetracyclines can decrease effects of penicillin

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 impaired renal function

Amoxicillin (Amoxil, Polymox, Trimox)

Alternate DOC; interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.

Dosing

Adult

250-500 mg PO tid for 10 d

Pediatric

40 mg/kg/d PO divided tid for 10 d

Interactions

Reduces efficacy of PO contraceptives

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

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

Precautions

Adjust dose in renal impairment

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

DOC in penicillin-allergic patients. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
In children, age, weight, and severity of infection determine proper dosage. When bid dosing is desired, half-total daily dose may be taken q12h. For more severe infections, double the dose.

Dosing

Adult

250-500 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; cisapride, cyclosporine, or warfarin administration, use alternate drug

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; adverse GI effects are common (administer doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occurs

Cephalexin (Keflex, Biocef)

Alternate DOC; first-generation cephalosporin arrests bacterial growth by inhibiting bacterial cell wall synthesis. Bactericidal activity against rapidly growing organisms. Primary activity against skin flora; used for skin infections.

Dosing

Adult

250-500 mg PO qid for 10 d

Pediatric

25-50 mg/kg/d PO divided qid for 10 d

Interactions

Coadministration with aminoglycosides increase nephrotoxic potential

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

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

Precautions

Adjust dose in renal impairment; causes an allergic reaction in approximately 10% of penicillin-allergic patients

Follow-up

Further Outpatient Care

• 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.

Complications

• A number of serious complications may develop as a consequence of streptococcal infection. 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.

Prognosis

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

Patient Education

• Completion of the prescribed antibiotic regimen is essential. Follow general good hygiene precautions, especially in households with other small children.
• 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.

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. Dong H, Xu G, Li S, et al. Beta-haemolytic group A streptococci emm75 carrying altered pyrogenic exotoxin A linked to scarlet fever in adults. J Infect. Apr 2008;56(4):261-7. [Medline].

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. Nov 2007;55(5):419-24. [Medline].

3. Cunningham MW. Pathogenesis of group A streptococcal infections. Clin Microbiol Rev. Jul 2000;13(3):470-511. [Medline].

4. Sandrini J, Beucher AB, Kouatchet A, Lavigne C. [Scarlet fever with multisystem organ failure and hypertrophic gastritis.]. Rev Med Interne. May 2009;30(5):456-9. [Medline].

5. Gomez-Carrasco JA, Lassaletta A, Ruano D. [Acute hepatitis may form part of scarlet fever]. An Pediatr (Barc). Apr 2004;60(4):382-3. [Medline].

6. Guven A. Hepatitis and hematuria in scarlet fever. Indian J Pediatr. Nov 2002;69(11):985-6. [Medline].

7. Lau SK, Woo PC, Yuen KY. Toxic scarlet fever complicating cellulitis: early clinical diagnosis is crucial to prevent a fatal outcome. New Microbiol. Apr 2004;27(2):203-6. [Medline].

8. Leslie DL, Kozma L, Martin A, et al. Neuropsychiatric Disorders Associated With Streptococcal Infection: A Case-Control Study Among Privately Insured Children. J Am Acad Child Adolesc Psychiatry. Aug 21 2008;[Medline].

9. Gaston DA, Zurowski SM. Arcanobacterium haemolyticum pharyngitis and exanthem. Three case reports and literature review. Arch Dermatol. Jan 1996;132(1):61-4. [Medline].

10. Sanz JC, Bascones Mde L, Martin F, Saez-Nieto JA. [Recurrent scarlet fever due to recent reinfection caused by strains unrelated to Streptococcus pyogenes.]. Enferm Infecc Microbiol Clin. Jun-Jul 2005;23(6):388-9. [Medline].

11. Swartz MN, Weinberg AN. Infections due to Gram-Positive Bacteria. In: Dermatology in General Medicine. Vol 2. 4^th ed. New York, NY: McGraw-Hill; 1993:2318-20.

Keywords

scarlet fever, scarlatina, group A beta hemolytic streptococci, GABHS, septicemia, rheumatic fever, erythematous eruption, rash, upper respiratory infections, streptococcal wound infections, osteomyelitis, white strawberry tongue, red strawberry tongue, fine erythematous punctate eruption, Pastia lines, beta hemolytic Lancefield Group A streptococcus

Contributor Information and Disclosures

Author

Edward J Zabawski Jr, DO, RPh, Dermatologist, Spencer Dermatology Group
Disclosure: Nothing to disclose.

Medical Editor

Craig A Elmets, MD, Director of Dermatology, Departments of Dermatology, Pathology, and Environmental Health Sciences; Professor, The Kirklin Clinic, University of Alabama at Birmingham
Craig A Elmets, MD is a member of the following medical societies: American Academy of Dermatology, American Association of Immunologists, American College of Physicians, American Federation for Medical Research, and Society for Investigative Dermatology
Disclosure: Palomar Medical Technologies Stock None; Amgen Consulting fee Review panel membership; Astellas Consulting fee Review panel membership; Massachusetts Medical Society Salary Employment; Abbott Laboratories Grant/research funds Independent contractor

Pharmacy Editor

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Lester F Libow, MD, Dermatopathologist, South Texas Dermatopathology Laboratory
Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Texas Medical Association
Disclosure: Nothing to disclose.

CME Editor

Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds Investigator; Genentech Grant/research funds investigator; Centocor Consulting fee Consulting; Abbott Grant/research funds investigator; Abbott Consulting fee Consulting; Novartis  investigator; Pfizer Grant/research funds investigator; Celgene Consulting fee DMC Chair; NIAMS and NHLBI Grant/research funds investigator

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

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