Scarlet fever is an acute respiratory infectious disease caused by Streptococcus pyogenes (group A beta-hemolytic streptococcus). Its clinical manifestations include fever, pharyngitis, diffusely distributed scarlet-colored fine papular rash, and noticeable peeling of the skin after the rash subsides. In rare cases, post-infection complications such as rheumatic fever and acute glomerulonephritis may develop.
Pathogen
Streptococcus pyogenes is a group A streptococcus that belongs to the Streptococcus genus. It is Gram-positive, non-spore-forming, and non-flagellated, with beta-hemolytic properties. Most strains are facultative anaerobes. Its major antigens include polysaccharide antigens (C antigens), surface protein antigens, and nucleoprotein antigens (P antigens). Group A streptococcus produces a variety of virulence factors, including cell wall components, M proteins, peptidoglycans, as well as exotoxins, hemolysins, and extracellular invasive enzymes.
Streptococcus pyogenes demonstrates strong environmental survival capabilities. It can colonize the human oropharynx and survive for months in dry dust or for weeks in sputum or pus. However, it is less resistant to heat and desiccation, being inactivated at 56°C after 30 minutes of heating. It is sensitive to commonly used disinfectants.
Epidemiology
Infected individuals in the acute phase and carriers of the bacterium serve as the primary sources of transmission. The infection spreads mainly through nasopharyngeal secretions and droplets, or via close direct contact. Infectiousness is highest from 24 hours prior to symptom onset through the peak of the illness and may persist during the recovery period for 1–3 weeks.
Scarlet fever exhibits widespread susceptibility among humans and is most commonly seen in preschool- or school-aged children. Following infection, the host may develop long-lasting strain-specific antimicrobial and antitoxin immunity. However, because there is no cross-immunity between different strains of Streptococcus pyogenes or between different pyrogenic exotoxins, reinfections are possible.
Pathogenesis
After entering the host through the respiratory tract, Streptococcus pyogenes uses F protein and lipoteichoic acid to adhere to the surface of mucosal epithelial cells. It then invades tissues and induces inflammation. M proteins resist the bactericidal effects of phagocytic cells, while enzymes such as hyaluronidase and streptolysin enable the bacteria to spread via lymphatic vessels or interstitial spaces, leading to tissue necrosis. Pyrogenic exotoxins are absorbed locally and enter the bloodstream, resulting in inflammatory damage to cutaneous and mucosal blood vessels, which manifests as punctate erythematous rashes. Severe cases may present with hemorrhagic rashes and systemic toxemia.
Pyrogenic exotoxins also suppress the functions of the phagocytic system and T lymphocytes, triggering the Schwartzman reaction. Furthermore, the M protein of group A streptococcus shares cross-reactive antigens with cardiac muscle and glomerular basement membrane components. The specific antibodies produced in response can cause immune-mediated tissue damage or form antigen-antibody complexes that deposit in tissues, leading to disease.
Pathology
The main pathological changes include inflammatory lesions, toxic damage, and hypersensitivity-associated alterations.
Inflammatory Lesions
These are characterized by localized congestion, edema, and infiltration of inflammatory cells.
Infectious Changes
Diffuse congestion, edema, inflammatory cell infiltration, and epithelial hyperplasia are observed in the blood vessels of the skin and mucous membranes. Various degrees of congestion and fatty degeneration may affect organs such as the liver, spleen, and lymph nodes. Cardiomyocytes may display edema, degeneration, and necrosis. The kidneys may exhibit interstitial inflammatory changes.
Hypersensitivity-Associated Changes
In some cases, particularly 2–4 weeks after infection, non-suppurative lesions may arise in tissues such as the heart, kidneys, or synovial membranes due to hypersensitivity reactions.
Clinical Manifestations
Typical Form
The incubation period ranges from 1 to 7 days, typically lasting 2 to 4 days.
Prodromal Phase
The onset is often abrupt.
Systemic Symptoms
Symptoms include chills and fever, with mild cases presenting temperatures between 38–39°C, while severe cases exceed 39°C. These are accompanied by headache, general malaise, nausea, vomiting, and loss of appetite, all of which are signs of systemic toxicity.
Pharyngitis
Symptoms include sore throat that worsens upon swallowing, with marked congestion and edema of the oropharynx. Tonsils are inflamed and swollen, and may exhibit punctate or patchy purulent exudates, which are easily wiped away. Petechial mucosal rashes on the soft palate may appear, alongside submandibular and cervical lymphadenopathy with tenderness.
Exanthema Phase
Rash typically appears 2 days after the onset of fever, beginning behind the ears, on the neck, and the upper chest, and rapidly spreads across the body within one day.
Typical Rash
The rash consists of numerous fine scarlet-colored papules, widely and densely distributed against a diffusely erythematous background. It has a gooseflesh-like appearance, a fine sandpaper texture upon palpation, and may coalesce into patches. It is often pruritic. Upon pressing the skin, the redness temporarily dissipates within seconds, leaving a pale handprint known as "anemia skin scratches," a hallmark of scarlet fever. The rash typically peaks within 48 hours.
Other Features
These include:
- Circumoral Pallor: Facial erythema and flushing are present, but the area around the lips remains pale, creating a circumoral pallor.
- Pastia's Lines: In skin folds such as the neck, axillae, antecubital fossae, and groin, the rash appears denser and deeper red, with occasional petechiae forming linear patterns.
- Tongue Changes: Initially, the tongue is coated with a thick white fur, and the papillae appear swollen and red, referred to as a "strawberry tongue." After 2–3 days, the white coating sloughs off, leaving a smooth, bright red surface with protruding papillae, commonly called a "raspberry tongue."
- Miliary Sudamina: Rash-like lesions resembling small yellowish-white pustules, resistant to rupture, may appear on the abdomen, hands, and feet during the rash's peak.
Recovery Phase
After 3–5 days, the rash darkens and begins to fade in the same order as it appeared. Systemic symptoms and pharyngeal inflammation gradually resolve. The rash usually subsides within a week, followed shortly by desquamation. The extent of desquamation correlates with the density and severity of the initial rash. Peeling can appear as fine flakes in mild cases, or as sheet-like peeling on the palms and soles of the feet in severe cases, resembling gloves or socks. The desquamation phase generally lasts 1–2 weeks, but may be longer in severe cases.
Other Clinical Types
Mild Type
Fever is minimal or absent, pharyngitis is mild, and the rash is sparse, lighter in color, and resolves quickly. Peeling is absent or limited to slight flaking. The disease course may span only 2–3 days, and this type has become more common in recent years.
Infectious Type
Severe systemic symptoms are present, often with high fever exceeding 40°C, accompanied by altered consciousness, seizures, or even coma. The rash may be hemorrhagic and persist longer, while pharyngitis is often inconspicuous. Complications such as myocarditis, toxic hepatitis, and shock may occur. This form has become rare in recent years.
Septic Type
Severe purulent inflammation, necrosis, and ulceration of the pharynx are observed, potentially extending to adjacent tissues, causing complications such as purulent otitis media, sinusitis, cervical lymphadenitis, or cellulitis. There is also the risk of bloodstream invasion, resulting in sepsis and metastatic purulent foci. This form is now extremely rare.
Surgical or Obstetric Type
Infections arise from skin wounds or the genital tract, leading to localized purulent lesions. The rash appears initially near the site of the wound and then spreads to the rest of the body. Symptoms are mild, and pharyngitis is often absent.
Complications
Suppurative Complications
These are more commonly seen in young and immunocompromised children and result from direct invasion of adjacent tissues or spread via anatomical channels. Examples include otitis media, mastoiditis, lymphadenitis, peritonsillar abscess, retropharyngeal abscess, and cellulitis. In severe cases, hematogenous dissemination can lead to sepsis and metastatic abscesses, such as meningitis, pericarditis, or osteomyelitis. Rapid progression may result in toxic shock syndrome.
Non-Suppurative Complications
Rare occurrences of rheumatic fever develop approximately 3 weeks after infection in some older children. Manifestations include rheumatic myocarditis, endocarditis, pericarditis, and arthritis. Due to the early widespread use of antibiotics, rheumatic fever incidence has significantly decreased. Acute post-streptococcal glomerulonephritis may develop 2–3 weeks post-infection.
Laboratory Tests
Complete Blood Count
The total white blood cell count often ranges between (10–20) × 109/L or higher, with neutrophils comprising more than 80%. Severe cases may exhibit a shift to the left in the neutrophil count and the presence of toxic granules.
C-Reactive Protein (CRP)
Levels are frequently elevated, with marked increases in severe cases.
Bacterial Culture
Before initiating antimicrobial therapy, secretions or exudates from areas such as the pharyngeal tonsils or wounds can be collected for culture, enabling the isolation of Streptococcus pyogenes.
Specific Antigens
Detection of group A streptococcal aminopeptidase can be performed using the L-pyrrolidonyl-β-naphthylamide (PYR) test. A color change or fluorescence in the reaction product facilitates rapid diagnosis, while other hemolytic streptococci will yield negative results. Samples from throat swabs, urine, cerebrospinal fluid, or wound secretions can be used for testing.
Specific Antibodies
Several serum antibodies, including anti-streptolysin O (ASO), anti-streptodornase (ASD), anti-hyaluronidase, or anti-streptokinase antibodies, indicate recent streptococcal infection.
Diagnosis and Differential Diagnosis
The diagnosis is based on epidemiological data regarding local outbreaks, a history of close contact with an infected individual, and the presence of clinical features such as fever, characteristic rashes, pharyngitis, "strawberry tongue," and elevated white blood cell and neutrophil counts. Isolation of Streptococcus pyogenes from throat swabs or purulent secretions confirms the diagnosis.
Scarlet fever must be differentiated from common exanthematous diseases in children, such as measles, rubella, Staphylococcus aureus infections, drug-related rashes, and Kawasaki disease. This differentiation can be achieved through the evaluation of rash characteristics, the temporal relationship between fever and rash onset, systemic symptoms, and other clinical presentations.
Treatment
General Management
Rest and a liquid or semi-liquid diet are recommended for patients with significant throat pain. Maintaining oral hygiene by rinsing with warm saline may be helpful. Patients with persistent high fever may require physical cooling methods or antipyretics.
Pathogen-Directed Treatment
Streptococcus pyogenes remains highly sensitive to penicillin. Early treatment effectively eradicates the pathogen, shortens the disease course, and prevents complications, particularly rheumatic fever and acute glomerulonephritis.
Penicillin G (Preferred Choice)
The recommended dose is 100,000–200,000 U/kg/day, given via intravenous infusion every 4–6 hours for 10–14 days. For mild cases, oral amoxicillin can be administered at 50 mg/kg/day in two divided doses (maximum dose of 1 g/day) for 10–14 days.
Cephalosporins (For Penicillin Allergy)
Ceftriaxone 50–75 mg/kg/day is administered intravenously once daily for 10 days.
Cefalexin 40 mg/kg/day or cefadroxil 30 mg/kg/day, with a maximum dose of 1 g/day, is given orally in two divided doses. Alternatively, cefuroxime can be used at 20 mg/kg/day (maximum dose of 0.5 g/day) in two divided doses for 10 days.
Symptomatic Treatment
For patients with toxic or septic forms, high-dose penicillin can be supplemented with glucocorticoids. Severe cases may require close monitoring, correction of water and electrolyte imbalances, and intravenous immunoglobulin if necessary. Shock should be managed with appropriate anti-shock therapy.
Management of Complications
Necrotic tissue and abscesses may require surgical removal or drainage. Patients with rheumatic heart disease or rheumatic fever should receive long-term prophylactic antimicrobial therapy.
Prevention
Susceptible children who have had close contact with infected individuals should undergo medical observation for seven days. Carriers of the bacterium should receive anti-infective treatment until their cultures test negative. During outbreaks, children should avoid crowded public areas, and good ventilation in indoor spaces should be maintained. Improvements in environmental and personal hygiene, as well as avoidance of skin and soft tissue infections, are essential preventive measures.
Prognosis
Patients with typical, mild, or surgical forms of scarlet fever generally have a good prognosis.