Scarlatina

Scarlatina, or scarlet fever (from the Late Latin scarlatum — “bright red”) is an acute infectious disease representing one of the clinical forms of streptococcal infection. It is caused by Group A β-hemolytic streptococcus (GABHS), which produces the erythrogenic (scarlatinous) Dick toxin.

The disease presents with systemic intoxication, fever, acute tonsillitis, and a characteristic fine, punctate rash. It is not the acute phase of scarlet fever that poses the greatest risk, but rather severe autoimmune complications such as acute rheumatic fever and glomerulonephritis.

Aetiology and Pathophysiology

The source of infection is a person with scarlet fever, acute tonsillitis, or an asymptomatic carrier of GABHS. Transmission is primarily airborne. The most common portal of entry is the oropharyngeal mucosa; less commonly, the pathogen enters through damaged skin (“wound scarlatina”).

The pathogenesis of scarlet fever comprises three components:

1. Infectious: Local purulent inflammation at the site of pathogen entry, most often presenting as acute tonsillitis.
2. Toxic: The erythrogenic toxin released by streptococcus enters the bloodstream and triggers systemic responses — fever, intoxication, and the characteristic rash due to dilation of cutaneous capillaries.
3. Allergic: In response to streptococcal antigens, hypersensitivity develops that causes complications typically observed during weeks 2–3 of illness.

Post-infectious immunity is antitoxic in nature. This means that while a person may contract streptococcal tonsillitis again, the full clinical picture of scarlet fever (including the rash) usually occur only once in a lifetime.

Clinical Significance

The disease begins abruptly with a sudden fever, headache, malaise, and often vomiting. Diagnosis is based on a characteristic clinical triad: acute tonsillitis, intoxication, and rash.

Key clinical manifestations include:

• Acute tonsillitis: Systemic symptoms are accompanied by severe sore throat. Pharyngoscopy reveals marked mucosal hyperemia (“fiery pharynx”), and the tonsils may be covered with purulent exudate. Cervical lymph nodes are enlarged and tender.
• Rash: This sign appears on the first or second day of illness. The rash on a hyperemic skin is fine and bright pink; it feels like sandpaper (“shagreen skin”). It typically intensifies in natural skin folds (e.g., elbows, groin) as dark red lines — known as Pastia’s lines.
• Pale nasolabial triangle (Filatov’s sign): The bright facial rash contrasts with pallor in the nasolabial region. This is a pathognomonic sign of scarlet fever.
• “Strawberry Tongue”: In the early days, the tongue is coated with a thick white film. By days 2–4, the coating begins to clear from the center outward, revealing a bright crimson surface with swollen papillae.
• Desquamation: One to two weeks after the rash subsides, characteristic skin peeling begins: fine scaling on the trunk and large lamellar peeling on the palms and soles.

The cornerstone of treatment is antibiotic therapy with penicillins, aimed at eradicating the pathogen and, most importantly, preventing rheumatic complications.

Differential Diagnosis

Scarlatina must be differentiated from other exanthematous diseases: Measles: Distinguished by the absence of a catarrhal prodrome (cough, conjunctivitis) and the nature of the rash (measles presents with a maculopapular eruption). Rubella: Scarlet fever causes more pronounced intoxication, severe tonsillitis, and the pale nasolabial triangle. The differential diagnosis also includes pseudotuberculosis, enteroviral exanthems, and allergic dermatitis. Definitive diagnosis of scarlet fever is based on the combination of acute tonsillitis, fine punctate rash, and “strawberry tongue”.