Disease onset and intoxication
Scarlet fever always begins acutely and suddenly. Pathogenic components of the microbial cell wall and released exotoxins (the so-called "cytokine storm") trigger pronounced general intoxication syndrome.
Key manifestations at disease onset:
- Rapid body temperature spike up to 38.6–39.5 °C.
- Pronounced general weakness and headache.
- Significant decrease in appetite or complete anorexia.
- Sore throat, worsening upon swallowing.
- Vomiting is frequently observed in children during the first hours of illness.
Toxemia triggers generalized dilation of small blood vessels, setting the stage for typical cutaneous signs.
Characteristics of the exanthema (rash)
The rash is the hallmark of scarlet fever. It appears very rapidly, within hours of fever onset (rarely on days 2–3) and quickly spreads to the face, neck, trunk, and extremities.
Features of a typical scarlet fever rash:
- Elements: punctate (roseolar) rash overlying confluent skin erythema.
- Localization: densest concentration of elements is noted on the lateral trunk, lower abdomen, and flexor surfaces of the extremities.
- Pastia's sign: intensive clustering of the rash in natural skin folds (axillae, groin, elbow and popliteal creases). This sign may persist up to days 10–12 and is critically important for differential diagnosis.
- "Palm sign": pressing a palm against the affected skin area causes the rash to momentarily disappear.
The skin is dry, patients are often bothered by pruritus, so scratch marks (excoriations) may be found upon examination. Positive endothelial signs are also elicited. Note that additional rash types exist (miliaria with tiny vesicles, papular with "goosebumps" / sandpaper texture, hemorrhagic), while atypical forms may lack a rash entirely.
Oropharyngeal and lymph node involvement
Changes in the fauces are an obligatory and constant symptom of typical scarlet fever. The inflammatory process presents as tonsillitis (catarrhal or purulent), lasting about 4–5 days.
A specific sign is the so-called "fiery red throat". There is bright, intense hyperesthesia and erythema of the palatine tonsils, pillars, and uvula with a sharp border that never extends to the hard palate mucosa. Necrotic areas frequently form at sites of primary pathogen attachment.
Concurrently, regional lymphadenitis develops. Primarily anterior cervical lymph nodes are involved. Palpation reveals them to be enlarged, firm, and tender. In severe (septic) cases, inflammation may extend beyond the capsule, developing into perilymphadenitis.
Dynamics of skin manifestations: desquamation stage
The rash persists on the skin for 3 to 7 days. As antitoxic immunity develops, toxins are neutralized, and the exanthema fades without leaving pigmentation. It is followed by desquamation, which exhibits a strict sequence:
- First, areas with the most delicate skin are affected (earlobes, neck, scrotum) — here desquamation is fine and branny (furfuraceous).
- Next, the process spreads to the trunk and proximal extremities.
- Finally, the palms and soles begin to peel. Due to the thick epidermal layer on the palms and soles, desquamation here is sheet-like (skin peels off in large flakes).
Note: in infants, the desquamation process is significantly more pronounced than in older children.
Changes in the autonomic nervous and cardiovascular systems
Toxic effects disrupt neurohumoral regulation mechanisms. In the acute (peak) period, sympathetic nervous system tone predominates.
Cardiovascular manifestations include pronounced tachycardia (up to 130–140 beats per minute) and moderate blood pressure elevation. Cardiac borders and heart sound clarity remain unchanged. White dermographism is noted on the skin — delayed during the first days (appearing only after 1–2 minutes).
During convalescence (from day 4–5 or the second week), sympathicotonia is replaced by parasympathicotonia. Clinically, this manifests as bradycardia, blood pressure dropping to normal or subnormal levels, and frequent sinus respiratory arrhythmia. White dermographism during this period is elicited rapidly and persists for a long time.
Briefly: answers to topical questions
How does the appearance of the tongue change day by day in scarlet fever?
The appearance of the tongue in scarlet fever undergoes characteristic sequential changes, forming a pathognomonic sign.
- Disease onset — the tongue is heavily coated with grayish or gray-yellow plaque.
- Days 2–3 — the tongue surface begins actively clearing from the edges and tip.
- Subsequent days — the tongue becomes completely clean, bright red with prominent hypertrophied papillae (forming the "strawberry tongue" sign).
The tongue remains in this cleaned, brightly hyperemic state for 1–2 weeks.
What atypical forms of scarlet fever exist?
Several atypical forms of scarlet fever are distinguished:
- Mild (abortive / erased) form — clinical manifestations are mild and short-lived.
- Hypertoxic form — characterized by catastrophically escalating intoxication; fatal outcome from infectious-toxic shock is possible within the first day of illness.
- Extrapharyngeal (extrabuccal) form — includes burn, wound, and puerperal variants. Characterized by a shortened incubation period of 1–2 days, rash onset starting at the portal of entry, regional lymphadenitis near the portal of entry, while tonsillitis is absent or mild.
Which infectious diseases require differential diagnosis for scarlet fever?
Differential diagnosis of scarlet fever must be performed against infectious diseases accompanied by exanthema and oropharyngeal involvement. First to be ruled out:
- Measles
- Rubella
- Yersiniosis
- Infectious mononucleosis
- Pharyngeal diphtheria (throat swab required to differentiate plaques)
Alongside infectious pathologies, differential evaluation must also consider non-infectious allergic (drug-induced) dermatitis, which can present with similar cutaneous manifestations.
What late infectious-allergic complications are characteristic of scarlet fever?
Late complications of scarlet fever are infectious-allergic (autoimmune) in nature and develop predominantly in weeks 2–4 from illness onset. Major systemic manifestations include:
- Glomerulonephritis — renal filtration barrier damage.
- Myocarditis — heart muscle damage.
- Synovitis and polyarthritis — multiple joint inflammation.
- Arteritis.
The development of these complications is linked to hypersensitivity allergic reactions and antibody cross-reactivity (molecular mimicry) targeting streptococcal antigens.
Three main skin signs in scarlet fever — the "P-F-L" rule: • P — Pastia's sign (lines of confluent rash in skin folds); • F — Filatov's sign (pale perioral contrast); • L — Palm sign (rash disappears when pressing with the palm).
Class and exam questions
How to distinguish scarlet fever pharyngeal hyperemia from a common ARVI?
In scarlet fever, hyperemia has a clear boundary: it is very bright on the tonsils, uvula, and soft palate, but abruptly terminates and does not extend to the hard palate mucosa.
Why do palms peel in scarlet fever?
Exotoxins cause the epidermis to become infiltrated with exudate and keratinized. Since the epidermis is thick on the palms and soles and cellular adhesion is strong, the dead skin peels off in large sheets.
What else to study on this topic
- The role of superantigens (exotoxins) and the mechanism of the "cytokine storm".
- Pathogenesis of late autoimmune complications (glomerulonephritis, rheumatic heart disease) due to molecular mimicry.
- Features of atypical forms of scarlet fever (extrapharyngeal, mild/abortive, hypertoxic).
- Pathomorphological changes in internal organs during severe toxico-septic course.
- Characteristics of antitoxic and antimicrobial type-specific immunity following the infection.
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