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]
View Image
The exudative pharyngitis typical of scarlet fever. Although the tongue is somewhat out of focus, the whitish coating observed early in scarlet fever ....
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.
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.
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.
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.
View Image
The exudative pharyngitis typical of scarlet fever. Although the tongue is somewhat out of focus, the whitish coating observed early in scarlet fever ....
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.
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
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 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.
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.
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.
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. 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.[27] 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.
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.
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.
Clinical Context:
Penicillin G interferes with synthesis of cell wall mucopeptides during active multiplication, which results in bactericidal activity.
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
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.
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?What are rare complications in scarlet fever?What are late complications in scarlet fever?Which symptoms may occur weeks to months after of scarlet fever?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?What noninfectious diseases should be considered when diagnosing scarlet fever?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?What is the role of urinalysis and liver function tests in the evaluation of scarlet fever?What is the role of throat culture in the diagnosis of scarlet fever?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?Which microscopic findings are characteristic of scarlet fever?What are the goals of treatment of scarlet fever?What is the treatment of choice for scarlet fever?Which drugs are used in the treatment of scarlet fever?When should cultures be obtained in the management of scarlet fever?When is hospitalization indicated for scarlet fever?How can contagion be minimized in scarlet fever?When are specialists consultations indicated for the treatment for scarlet fever?What monitoring is needed following treatment for scarlet fever?What is the standard treatment for scarlet fever?Which medications in the drug class Antibiotics are used in the treatment of Scarlet Fever?
Bahman Sotoodian, MD, Resident Physician, Department of Dermatology, University of Alberta Faculty of Medicine and Dentistry, Canada
Disclosure: Nothing to disclose.
Coauthor(s)
Jaggi Rao, MD, FRCPC, Clinical Professor of Medicine, Division of Dermatology and Cutaneous Sciences, Director of Dermatology Residency Program, University of Alberta Faculty of Medicine and Dentistry, Canada
Disclosure: Nothing to disclose.
Chief Editor
William D James, MD, Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine
Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier; WebMD.
Additional Contributors
Edward J Zabawski, Jr, DO, Medical and Surgical Dermatology
Disclosure: Nothing to disclose.
Acknowledgements
Jerry Balentine, DO Professor and Chair of Emergency Medicine, New York Institute of Technology College of Osteopathic Medicine; Executive Vice President, 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.
Peter Bloomfield, MD, MPH Clinical Instructor, Department of Emergency Medicine, Olive View-UCLA Medical Center
Disclosure: Nothing to disclose.
Pamela L Dyne, MD Professor of Clinical Medicine/Emergency Medicine, University of California, Los Angeles, David Geffen School of Medicine; 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.
Craig A Elmets, MD Professor and Chair, Department of Dermatology, Director, UAB Skin Diseases Research Center, University of Alabama at Birmingham School of Medicine
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
Daniel P Lombardi, DO Clinical Assistant Professor, New York College of Osteopathic Medicine; Attending Physician, Associate Department Director and Program Director, Department of Emergency Medicine, St 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.
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.
Joseph A Salomone III, MD Associate Professor and Attending Staff, Truman Medical Centers, University of Missouri-Kansas City School of Medicine; EMS Medical Director, Kansas City, Missouri
Joseph A Salomone III, MD is a member of the following medical societies: American Academy of Emergency Medicine, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Reference Salary Employment
Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster 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.
Eric L Weiss, MD, DTM&H Medical Director, Office of Service Continuity and Disaster Planning, Fellowship Director, Stanford University Medical Center Disaster Medicine Fellowship, Chairman, SUMC and LPCH Bioterrorism and Emergency Preparedness Task Force, Clinical Associate Progressor, Department of Surgery (Emergency Medicine), Stanford University Medical Center
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.
Garry Wilkes, MBBS, FACEM Director of Emergency Medicine, Calvary Hospital, Canberra, ACT; Adjunct Associate Professor, Edith Cowan University, Western Australia
Disclosure: Nothing to disclose.
Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Nothing to disclose.
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
Centers for Disease Control and Prevention. Scarlet Fever. Available at https://www.cdc.gov/groupastrep/diseases-hcp/scarlet-fever.html. November 1, 2018; Accessed: June 21, 2019.
Finnish Medical Society Duodecim. Sore throat and tonsillitis. EBM Guidelines. Evidence-Based Medicine. Feb 2 2007Helsinki, Finland: Wiley Interscience. John Wiley & Sons.
Scarlet Fever: All You Need to Know. Centers for disease control and prevention. Available at https://www.cdc.gov/groupastrep/diseases-public/scarlet-fever.html. Accessed: November 1, 2018.
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 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 exudative pharyngitis typical of scarlet fever. Although the tongue is somewhat out of focus, the whitish coating observed early in scarlet fever is visible.
){kind=link}