Scarlatina of the pharynx: causes, symptoms, diagnosis, treatment

Scarlet fever is an acute infectious disease characterized by a cyclical course, general intoxication, sore throat, small-spotted rash and a tendency to purulent-septic complications.

At the end of the 17th century, T. Sydenham gave this disease the name "scarlatina" and was the first to provide its precise clinical description. In the 18th and 19th centuries, French doctors A. Trousseau and P. Bretonneau, based on observations during epidemics that swept through all European countries, developed a detailed clinical description of scarlet fever and its differential diagnosis from measles and diphtheria.

Epidemiology of scarlet fever of the throat. Scarlet fever is common in all countries of the world. The source of the infectious agent are patients with scarlet fever, streptococcal tonsillitis and nasopharyngitis (infectious throughout the disease), carriers of hemolytic streptococci of group A. The use of penicillin after 7-10 days leads to liberation from streptococcus, and the patient becomes safe for others. If complications occur, the infectious period is extended. Patients with unrecognized mild and atypical forms of scarlet fever pose a great epidemiological danger. The main route of transmission of infection is airborne. Infection can occur only at a fairly close distance from the patient, for example, staying with him in the same room (ward), since streptococci, despite their viability in external conditions, quickly lose pathogenicity and contagiousness outside the body. Infection is also possible through household items shared with the patient. Scarlet fever is most often observed in preschool and school-age children. The maximum incidence is observed in the autumn-winter period.

Immunity against scarlet fever is characterized by antitoxic and antimicrobial action and is developed as a result of the disease, as well as during so-called household immunization, caused by repeated streptococcal infections, occurring in a mild and often subclinical form. With insufficient immunity, repeated cases of scarlet fever occur, the frequency of which increased at the end of the 20th century.

The cause of scarlet fever of the pharynx. The causative agent of scarlet fever is the toxigenic beta-hemolytic streptococcus of group A. Its constant presence in the pharynx of patients with scarlet fever was established in 1900 by Baginsky and Sommerfeld. I.G.Savchenko (1905) discovered streptococcal (erythrotropic, scarlet fever) toxin. In 1923, 1938, the Dick spouses (G.Dick and G.Dick) studied the patterns of the body's response to the introduction of scarlet fever toxin, on the basis of which they developed the so-called Dick reaction, which played a significant role in the diagnosis of scarlet fever. The essence of the results obtained by these authors is as follows:

1. the introduction of scarlet fever exotoxin to individuals who have not had scarlet fever causes the development of symptoms characteristic of the first period of scarlet fever;
2. Intradermal administration of the toxin causes a local reaction in individuals susceptible to scarlet fever;
3. In individuals who are immune to scarlet fever, this reaction is negative, since the toxin is neutralized by a specific antitoxin present in the blood.

Pathogenesis of scarlet fever of the pharynx. The entry point for pathogens in cases of scarlet fever angina is the mucous membrane of the tonsils. Through the lymphatic and blood vessels, the pathogen enters the regional lymph nodes, causing their inflammation. The pathogen's toxin, penetrating the blood, causes the development of pronounced toxic symptoms (fever, rash, headache, etc.) in the first 2-4 days. At the same time, the body's sensitivity to the protein component of the microorganism increases, which can manifest itself after 2-3 weeks as so-called allergic waves (urticaria, facial swelling, eosinophilia, etc.), which are especially pronounced in children sensitized by previous streptococcal diseases and often occur in the first days of the disease.

Pathological anatomy. The site of primary penetration of the scarlet fever pathogen, according to K. Pirquet, is called the primary scarlet fever affect, the site of primary localization of which is the palatine tonsils (according to M.A. Skvortsov, 1946, in 97% of cases). The process begins in the crypts of the tonsils, in which exudate and accumulation of streptococci are found. Then, in the parenchyma surrounding the crypts, a necrotic zone is formed, containing a large number of pathogens that penetrate into healthy tissue and cause further destruction of the tonsil. If the necrosis process stops, a reactive leukocyte shaft (myeloid metaplasia of the lymphadenoid tissue of the tonsil) is formed at its border, preventing further spread of the infection. In the first days of the disease, reactive edema and fibrinous effusion develop in the tissues surrounding the primary affect, as well as the introduction of bacteria into the blood and lymphatic vessels and nodes. The same changes as in the primary affect are observed in the regional lymph nodes: necrosis, edema, fibrinous effusion and myeloid metaplasia. Very rarely, the primary affect has the character of catarrhal inflammation, which masks the true disease, which sharply increases its epidemiological danger. The rash, so characteristic of scarlet fever, is not histologically specific (foci of hyperemia, perivascular infiltrates and slight inflammatory edema).

Symptoms of scarlet fever of the throat. The incubation period ranges from 1-12 (usually 2-7) days. In typical cases of moderate severity, the disease most often begins with a rapid increase in body temperature to 39-40 ° C, nausea, vomiting, often chills and pain when swallowing. The general condition noticeably worsens in the first hours of the disease. The skin in the first 10-12 hours is clean, but dry and hot. The rash on it appears at the end of the first or beginning of the second day. Usually the rash begins from the neck, spreads to the upper chest, back and quickly spreads throughout the body. It is more clearly manifested on the inner surfaces of the arms and thighs, in the groin folds and lower abdomen. A more significant spread is noted in places of natural folds of the skin, where numerous petechiae are often observed, forming dark red stripes that do not disappear when pressed (Pastia's symptom). Scarlet fever is also characterized by the opposite phenomenon - the absence of a rash in the middle of the face, nose, lips and chin. Here, a pathognomonic sign for scarlet fever is noted - Filatov's triangle (the pallor of these formations compared to the brightly hyperemic rest of the face). The appearance of petechiae is also characteristic, especially in folds and places of friction of the skin. The appearance of petechiae is caused by toxic fragility of capillaries, which can be detected by pinching the skin or applying a tourniquet to the shoulder (Konchalovsky-Rumpel-Leede symptom).

In the blood, no significant changes in the number of erythrocytes and hemoglobin are observed. The initial period of scarlet fever is characterized by leukocytosis (10-30) x 10 ⁹ /l, neutrophilia (70-90%) with a pronounced shift in the leukocyte formula to the left, increased ESR (30-60 mm/h). At the onset of the disease, the number of eosinophils decreases, then, as sensitization to streptococcal protein develops (between the 6th and 9th days of illness), it increases to 15% and higher.

The rash usually lasts 3-7 days, then disappears, leaving no pigmentation. Peeling of the skin usually begins on the 2nd week of the disease, earlier in case of abundant rash, sometimes even before its disappearance. Body temperature decreases with a short lysis and normalizes by the 3rd-10th day of the disease. The tongue begins to clear from plaque from the 2nd day of the disease and becomes, as noted above, bright red with enlarged papillae ("raspberry" tongue) and retains its appearance for 10-12 days.

The characteristic and most constant symptom of scarlet fever is tonsillitis, the symptoms of which, unlike vulgar tonsillitis, increase very quickly and are characterized by pronounced dysphagia and a burning sensation in the pharynx. Tonsillitis occurs at the very beginning of the disease in the invasion phase and is manifested by bright hyperemia (erythematous tonsillitis) with clearly defined boundaries. At the beginning of the disease, the tongue is pale with hyperemia at the tip and along the edges; then within a week it becomes completely red, acquiring a crimson color. With moderate scarlet fever, catarrhal tonsillitis with superficial necrosis of the mucous membrane develops. Necrotic tonsillitis, observed in more severe forms of scarlet fever, develops no earlier than the 2nd-4th day of the disease. The prevalence and depth of necrosis are determined by the severity of the process. In severe cases, which are extremely rare at present, they spread beyond the tonsils, to the arches, soft palate, uvula and often, especially in small children, to the nasopharynx. Scarlet fever plaques represent coagulation tissue necrosis and, unlike diphtheria plaques, do not rise above the level of the mucous membrane. Tonsillitis lasts from 4 to 10 days (with necrosis). The enlargement of regional lymph nodes persists for a longer period.

Along with typical moderate scarlet fever, there are also atypical forms - latent, hypertoxic and extrabuccal scarlet fever. In the latent form, all symptoms of the disease are weakly expressed, the body temperature is normal or slightly elevated for 1-2 days, the general condition is not disturbed, in some cases, rash and changes in the tongue may be absent. However, contagiousness in such poorly differentiated forms remains at a fairly high level and, since such types of scarlet fever remain virtually unnoticed, the risk of spreading the infection is highest. Hypertoxic scarlet fever is characterized by a galloping increase in intoxication, reaching a critical level in the first day, which can lead to the patient's death (death on the threshold of the disease), when the main morphological manifestations have not yet received sufficient development. Extrabuccal scarlet fever occurs when a wound or burn on any part of the body is infected with hemolytic streptococcus. The incubation period is 1-2 days, regional lymphadenitis occurs near the site of infection, sore throat is absent or mild.

Complications of scarlet fever can occur at any severity of the disease. They are divided into early and late. Early complications that occur in the initial period of scarlet fever include pronounced lymphadenitis, sometimes with suppuration of the lymph nodes, otitis accompanied by pronounced destruction of the structures of the middle ear, mastoiditis, rhinosinusitis, synovitis of small joints, etc. Late complications usually occur in the 3rd to 5th week from the onset of the disease and are manifested by allergic myocarditis, diffuse glomerulonephritis, serous polyarthritis and purulent complications. In the 3rd to 4th week of the disease, relapses of scarlet fever are possible, caused by repeated infection (group A 3-hemolytic streptococcus of another serotype.

The diagnosis is based on epidemiological data (contact with a patient with scarlet fever), clinical and laboratory examination data, and consideration of symptoms characteristic of scarlet fever (rash, "raspberry" tongue, sore throat, peeling skin). Scarlet fever is characterized by changes in the blood: increased ESR, leukocytosis, neutrophilia with a shift in the leukocyte formula to the left, eosinophilia occurring between the 4th and 9th days of illness, and in severe cases - vacuolization and granularity of neutrophils. Traces of protein and fresh erythrocytes often appear in the urine. Diagnostic difficulties arise with latent and extrabuccal forms of scarlet fever. In some cases, bacteriological and immunological diagnostic methods are used.

In differential diagnostics, it is necessary to take into account that the appearance of a “scarlet fever” rash is possible in the prodromal period of measles, chickenpox, and also with staphylococcal infection.

The prognosis in most cases is favorable if scarlet fever is detected in time and treated correctly. In the hypertoxic form of scarlet fever and gangrenous-necrotic tonsillitis, the prognosis is cautious or even questionable.

Treatment of scarlet fever of the pharynx. Patients with mild forms of scarlet fever, not accompanied by complications, and if possible to isolate them at home, may not be hospitalized. In other cases, hospitalization in the infectious diseases department is indicated. In mild cases, bed rest is 5-7 days, in severe cases - up to 3 weeks. Locally, gargling with solutions of sodium bicarbonate, furacilin (1:5000), weak pink solution of potassium permanganate, decoctions of sage, chamomile, etc. are prescribed. Penicillin is administered intramuscularly from 500,000 to 1,000,000 U / day for 8 days or a single administration of bicillin-3 (5), or per os phenoxymethylpenicillin. In case of intolerance to penicillin drugs, erythromycin, oleandomycin and other antibiotics active against streptococci are used. In case of renal complications, sulfonamides are avoided. It is recommended to use hyposensitizing, antihistamine, and, if indicated, detoxification therapy. In case of toxic myocarditis, polyarthritis or nephritis - consultations with relevant specialists.

The patient needs a complete diet, enriched with vitamins. In case of albuminuria - a salt diet, drinking plenty of tea with lemon, juices made from fresh fruits.

After recovery, follow-up blood and urine tests are mandatory.

Prevention in children's institutions includes regular ventilation of premises, wet cleaning, disinfection of toys, treatment of dishes, boiling milk before use, examination of applicants and personnel for carriage of beta-hemolytic streptococcus. Isolation of the patient continues for at least 10 days, after which children attending preschool institutions and the first 2 grades of school are isolated from the group for another 12 days. Adults who have had scarlet fever are not allowed to work in preschool institutions, the first 2 grades of school, surgical and maternity wards, milk kitchens, children's hospitals and clinics for 12 days after the end of the isolation period. Routine disinfection is carried out in the outbreak area.

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