Epidemiology and significance of the problem
Streptococcal infections cause a colossal burden on healthcare: the economic damage from them is approximately 10 times higher than that from viral hepatitis. Over 700 million cases of streptococcus-related infections (ranging from pharyngitis to skin lesions) are registered worldwide every year, with more than 18 million people suffering from severe forms.
In the Russian Federation, the incidence of scarlet fever remains stably high, accounting for at least 40–50 cases per 100,000 population. The infection is transmitted primarily via airborne droplets. In modern realities, the disease course has changed: up to 90% of all cases present in a mild form.
Etiology and pathogenicity factors
The genus Streptococcus includes 240 species, of which 49 are of medical importance. The main culprit of scarlet fever is Streptococcus pyogenes (GAS). These are Gram-positive spherical or oval bacteria that form chains on nutrient media.
The pathogenicity of the causative agent is determined by a whole arsenal of structures and toxins:
- Capsule: consists of hyaluronic acid. Its main danger is that it is identical to the hyaluronic acid of human connective tissue, which allows the bacterium to disguise itself from the immune system.
- Cell wall elements: M-protein (which defines over 100 serotypes), F-protein, A-polysaccharide, peptidoglycan, lipoteichoic acid, and T-protein.
- Secreted factors: exotoxins types A, B, and C (formerly known as Dick toxin), as well as streptolysins O and S.
Classification of diseases caused by GAS
Group A Streptococcus is capable of causing a wide range of pathologies, which are divided into several groups:
- Primary forms: scarlet fever, erysipelas, pharyngitis, impetigo, ecthyma.
- Secondary (with an autoimmune mechanism): acute rheumatic fever, glomerulonephritis, vasculitis, rheumatic heart disease.
- Secondary (without an autoimmune component): peritonsillar and metatonsillar abscesses, soft tissue necroses.
- Rare forms: toxic shock syndrome, sepsis, necrotizing fasciitis, primary peritonitis.
Clinical presentation
The disease always begins acutely. Four main syndromes dominate the clinical presentation:
- Intoxication syndrome: sharp rise in temperature (often up to 39°C and above), headache, possible vomiting. Antipyretics often provide only a short-term effect with profuse sweating, after which the fever returns.
- Tonsillitis: severe throat pain upon swallowing appears within the first hours. Objectively, bright hyperemia of the oropharyngeal mucosa (faucial pillars, uvula, posterior pharyngeal wall), tonsillar hypertrophy with patchy white plaques that are easily removed with a tongue depressor are observed. The tongue is coated with a grayish-white coating.
- Exanthem syndrome (rash): appears by the evening of the first day of the disease. Initially localized on the neck and chest, it then rapidly spreads throughout the body. The rash is finely punctate, abundant, and located on a hyperemic skin background. Characteristic features include white dermographism and the condensation of rash elements into dark red lines in natural skin folds (elbow, inguinal). Meanwhile, the nasolabial triangle remains pale and free of rash.
- Lymphadenopathy: enlargement, induration, and tenderness upon palpation of the anterior cervical lymph nodes.
Diagnosis and management tactics
The diagnosis of scarlet fever is established primarily based on the characteristic clinical presentation and a thorough collection of the epidemiological history (contact with patients having tonsillitis or acute respiratory infections during the incubation period, staying in childcare facilities).
Bacteriological examination (throat swab culture) does not possess high diagnostic significance in routine practice. A complete blood count reveals classic signs of bacterial inflammation: leukocytosis, neutrophilia with a left shift, and an accelerated ESR.
The disease requires differential diagnosis with measles, rubella, yersiniosis, infectious mononucleosis, and drug allergy. Most patients are treated on an outpatient basis. Hospitalization is indicated when isolation is impossible (e.g., living in a dormitory), as well as when dynamic monitoring is required to rule out complications and administer comprehensive antibacterial and pathogenetic therapy.
Briefly: answers to topical questions
Which antibiotic groups are the drugs of choice for etiotropic therapy of scarlet fever?
The drugs of choice for etiotropic antibacterial therapy of scarlet fever are penicillins / beta-lactam antibiotics; for mild uncomplicated courses for oral administration, macrolides or beta-lactam antibiotics are indicated in sources.
Sources also indicate:
- Penicillin — drug of choice; for moderate severity forms, penicillin-series antibiotics are the drugs of choice.
- Macrolides — erythromycin, azithromycin.
- First-generation cephalosporins — alternative drugs, e.g., cefazolin.
- Semi-synthetic penicillins and lincosamides — used when there are contraindications to the aforementioned drugs.
The duration of etiotropic antibacterial therapy is 10 days.
Which toxin is directly responsible for the development of the finely punctate rash (exanthem) in scarlet fever?
Erythrogenic (pyrogenic) exotoxin is responsible for the development of the specific finely punctate rash in scarlet fever.
The historical name of this substance is Dick toxin, or scarlatinal toxin. It is produced by beta-hemolytic Streptococcus pyogenes (types A, B, and C) and represents a heat-stable fraction of exotoxin. Toxin synthesis is directly related to the process of lysogeny (the presence of temperate bacteriophage genes). Entering the bloodstream (toxinemia), this toxin exerts a necrotic effect on the vascular endothelium and causes their generalized dilation. Clinically, such damage manifests as bright skin hyperemia and the formation of a characteristic exanthem.
How does the appearance of the tongue change in a scarlet fever patient by days 3-5 of the disease?
By days 3–5 of the disease, a patient with scarlet fever develops the specific pathognomonic sign of a "strawberry tongue".
In the first days of the disease, the tongue is usually densely coated with a grayish or gray-yellow coating. However, starting from days 2–3, staged clearing of its surface occurs, beginning from the edges and tip. As a result, the tongue becomes completely free of coating and acquires a characteristic bright red (raspberry) color. Against this hyperemic mucous membrane, hypertrophied papillae are clearly exposed and prominent. This specific enanthem usually persists for 1–2 weeks.
What late (weeks 2–3) complications are characteristic of a past episode of scarlet fever?
In weeks 2–4 from the onset of the disease, the development of late immunopathological, allergic complications is characteristic of scarlet fever. They are associated with molecular mimicry and cross-reactivity of streptococcal antigens with body tissues.
Late non-suppurative complications include:
- Acute glomerulonephritis.
- Myocarditis.
- Endocarditis.
- Synovitis / arthritis.
- Arteritis.
Sources also indicate that rheumatic fever can be considered a delayed consequence of streptococcal sensitization.
For quick memorization of the key manifestations of scarlet fever, use the acronym ITLE: Intoxication, Tonsillitis, Lymphadenopathy, Exanthem.
Class and exam questions
Is it mandatory to perform a throat swab to confirm scarlet fever?
No, the bacteriological method of isolating the causative agent from the oropharyngeal mucosa does not have high diagnostic significance. The diagnosis is established based on clinical and epidemiological data.
How to distinguish the rash of scarlet fever from other exanthems?
Scarlet fever is characterized by a finely punctate rash on a hyperemic background, condensation of elements in natural skin folds, and a pale nasolabial triangle (Filatov's sign).
In which cases is hospitalization necessary for a patient with scarlet fever?
Hospitalization is mandatory for epidemiological indications (if the patient lives in a dormitory and cannot be isolated) as well as clinical indications—in severe cases or when there is a risk of complications.
What else to study on this topic
- Pathogenesis of streptococcal infection and port of entry
- Mechanisms of development of secondary autoimmune complications (rheumatic fever, glomerulonephritis)
- Criteria for assessing the severity of the disease course
- Principles of etiotropic, pathogenetic, and symptomatic therapy of scarlet fever
- Rules for discharge and follow-up observation of convalescents
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