Scarlet fever of the pharynx: causes, symptoms, diagnosis, treatment

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

At the end of the XVII century. T. Sydenham gave this disease the name of "scarlatina" and was the first to give his exact clinical description. In the XVIII and XIX century. The French doctors A.Trousseau and R.Vretonneau based on observations during epidemics that swept all European countries, developed a detailed clinical characterization of scarlet fever and all differential diagnostics from measles and diphtheria.

Epidemiology of scarlet fever. Scarlet fever is common in all countries of the world. The source of the causative agent of infection are patients with scarlet fever, streptococcal angina and nasopharyngitis (contagious throughout the disease), carriers of hemolytic streptococci in group A. Penicillin administration after 7-10 days leads to the release of streptococcus, and the patient becomes safe for others. In the event of complications, the timing of the infectious period is extended. A major epidemiological danger is presented by patients with unrecognized lungs and atypical forms of scarlet fever. The main route of transmission is airborne. Infection can occur only at a fairly close distance from the patient, for example, staying with him in one room (ward), since streptococci, despite their vitality under external conditions, quickly lose pathogenicity and contagiosity outside the body. It is also possible to get infected through common household items. The most common scarlet fever is observed in preschool and school-age children. The maximum incidence is noted in the autumn-winter period.

Immunity against scarlet fever is characterized by antitoxic and antimicrobial activity and is produced as a result of the disease, as well as in so-called household immunization caused by repeated streptococcal infections occurring in mild and often subclinical form. With insufficient intensity of immunity, there are repeated cases of scarlet fever, whose frequency at the end of the XX century. Has increased.

The cause of scarlet fever. The causative agents of scarlet fever are toxigenic beta-hemolytic streptococcus group A. Its constant presence in the throat of patients with scarlet fever was established in 1900 by Baginsky and Sommerfeld. I.G.Savchenke (1905) owns the discovery of streptococcal (erythropic, scarlet fever) toxin. In 1923, 1938 the spouses Dick (G.Dick and G.Dick) studied the patterns of the body's response to the introduction of scarlet 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 administration of scarlet fever exotoxin to persons who have had scarlet fever causes the development of symptoms characteristic of the first period of scarlet fever;
2. intradermal administration of toxin causes a local reaction in persons susceptible to scarlet fever;
3. in persons 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. The entrance gates for pathogens of infection in cases of scarlet fever are mucous membrane of the tonsils. On the lymphatic and blood vessels the pathogen enters the regional lymph nodes, causing their inflammation. The toxin of the pathogen, penetrating into the blood, in the first 2-4 days causes the development of severe toxic symptoms (fever, rash, headache, etc.). At the same time, there is an increase in the sensitivity of the organism to the protein component of the microorganism, which can manifest itself in 2-3 weeks of so-called allergic waves (urticaria rash, facial swelling, eosinophilia, etc.), which are especially pronounced in children sensitized by previous streptococcal diseases, and often occur in the early days of the disease.

Pathological anatomy. The site of the primary introduction of the scarlet pathogen, at the suggestion of K. Pirke, is called the primary scarlatinous affect, the site of primary localization of which is the palatine tonsils (according to MA Skvortsov, 1946, in 97% of cases). The process begins in the crypts of the tonsils, in which exudate and a cluster of streptococci are found. Then a zone of necrosis is formed in the surrounding crypt parenchyma, containing a large number of pathogens that penetrate into healthy tissue and cause further destruction of the amygdala. If the necrosis process stops, a reactive leukocyte shaft (myeloid metaplasia of the lymphadenoid tissue of the amygdala) forms on 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 lymph vessels and nodes. In the regional lymph nodes the same changes are observed as in the primary affect: necrosis, edema, fibrinous effusion, and myeloid metaplasia. Very rarely, the primary affect has the character of catarrhal inflammation, which masks the true disease, which dramatically increases its epidemiological danger. The rash, so characteristic of scarlet fever, histologically does not represent anything specific (foci of hyperemia, perivascular infiltrates and small inflammatory edema).

Symptoms of scarlet fever. 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 rise in body temperature to 39-40 ° C, nausea, vomiting, often chills and pain when swallowing. The general condition noticeably worsens already 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 the beginning of the second suugus. Usually the rash starts from the neck, spreads to the upper part of the chest, back and spreads rapidly throughout the body. It is more clearly manifested on the inner surfaces of the arms and hips, in the inguinal folds and lower abdomen. A more significant spread is noted in the places of natural folds of the skin, where often there are numerous petechiae forming dark-red strips that do not disappear when pressed (Pastia's symptom). For scarlet fever is characterized by the opposite phenomenon - the absence of a rash in the middle of the face, nose, lips and chin. Here, it is noted pathognomonic for scarlet fever, a triangle of Filatov (pallor of these formations in comparison with the brightly hyperplated rest of the face). Characteristically, the appearance of petechiae, especially in the folds and places of friction of the skin. The appearance of petechiae is due to the toxic fragility of the capillaries, which can be detected by pinching the skin or applying to the harness shoulder (the symptom of Konchalovsky-Rumpel-Leide).

In the blood of significant changes in the number of erythrocytes and hemoglobin is not observed. For the initial period of scarlet fever, leukocytosis (10-30) x10 ⁹ / l, neutrophilia (70-90%) with a marked shift in the leukocyte formula to the left, increased ESR (30-60 mm / h) are characteristic . At the onset of the disease, the amount of eosinophils decreases, then, as the sensitization to streptococcal protein develops (between the 6th and 9th days of the disease), it increases to 15% or more.

The rash usually lasts 3-7 days, then disappears without leaving pigmentation. Skin peeling usually begins at the second week of the disease, with a profuse rash earlier, sometimes even before the disappearance. The body temperature is reduced by a short lysis and is normalized by the 3rd-10th day of the disease. The tongue begins to clear from raids from the 2nd day of the disease and become, as noted above, bright red with enlarged papillae ("crimson" tongue) and retains its appearance for 10-12 days.

The characteristic and most constant symptom of scarlet fever is angina, the signs of which, unlike vulgar angina, grow very rapidly and are characterized by severe dysphagia and a sensation of a throat burn. Angina occurs at the very beginning of the disease in the invasion phase and manifests a bright hyperemia (erythematous angina) with clearly delineated boundaries. The tongue at the beginning of the disease is pale with hyperemia on the tip and along the edges; then within a week becomes completely red, getting a raspberry color. With scarlet fever of moderate severity, catarrhal sinus develops with superficial necrosis of the mucosa. Necrotic angina, observed with more severe forms of scarlet fever, develops not earlier than 2-4 days of the disease. The prevalence and depth of necrosis is determined by the severity of the process. In severe cases, which are very rare at the present time, they spread beyond the tonsils, on arches, soft palate, tongue and often, especially in young children, seize the nasopharynx. Rashes in scarlet fever are a coagulation necrosis of tissues and, in contrast to diphtheria, do not rise above the level of the mucous membrane. Angina lasts from 4 to 10 days (with necrosis). Increased regional lymph nodes remain longer.

Along with the typical scarlet fever of medium severity, there are also atypical forms - erased, hypertoxic and extra-bucolic scarlet fever. When the form is worn out, all symptoms of the disease are weak, the body temperature is normal or slightly elevated within 1-2 days, the general condition is not violated, in some cases rashes and language changes may be absent. However, the contagiousness with such little differentiated forms remains at a sufficiently high level and, since these kinds of scarlet fever remain practically unheeded, the danger of spreading the infection with them is the highest. Hypertoxic scarlet fever is characterized by a galloping increase in intoxication, reaching a critical level in the first day that can lead a patient to death (death on the threshold of the disease), when the main morphological manifestations have not yet developed sufficiently. Extrabulic scarlet fever occurs when a hemolytic streptococcus is infected with a wound or a burn in any part of the body. The incubation period is 1-2 days, regional lymphadenitis occurs near the site of infection, angina is absent or weakly expressed.

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

The diagnosis is based on epidemiological data (contact with a patient with scarlet fever), clinical and laboratory data, taking into account symptoms characteristic of scarlet fever (rash, raspberry tongue, tonsillitis, skin peeling). For scarlet fever are characterized by changes in blood: an increase in ESR, leukocytosis, neutrophilia with a shift in the leukocyte formula to the left, eosinophilia arising between the 4th and 9th days of the disease, in severe cases - vacuolization and granularity of neutrophils. In the urine often there are traces of protein and fresh red blood cells. Diagnostic difficulties arise with erased and extra-buccal forms of scarlet fever. In some cases, resort to bacteriological and immunological methods of diagnosis.

In differential diagnosis, it should be borne in mind that the appearance of "scarlet fever" rash is possible in the prodromal period of measles, chicken pox, and also with staphylococcal infection.

The prognosis in most cases with the timely detection of scarlet fever and proper treatment is favorable. With the hypertoxic form of scarlet fever and gangrenous-necrotic angina, the prognosis is cautious or even questionable.

Treatment of scarlet fever. Patients with mild forms of scarlet fever, not accompanied by complications, and if possible to isolate them at home, can not be hospitalized. In other cases, hospitalization in the infectious department is indicated. With a mild form of bed rest, 5-7 days, with heavy - up to 3 weeks. Locally, rinse the pharynx with solutions of sodium hydrogen carbonate, furacilin (1: 5000), a weak pink solution of potassium permanganate, sage broth, chamomile, etc. Intramuscularly inject penicillin from 500 000 to 1 000 000 units / day for 8 days or a single injection of bicillin -3 (5), or per os phenoxymethylpenicillin. In case of intolerance to penicillin drugs, erythromycin, oleandomy and other antibiotics active against streptococci are used. With kidney complications, sulfonamides try not to be prescribed. It is recommended the use of hyposensitizing, antihistamine, according to indications, detoxification therapy. In case of toxic myocarditis, polyarthritis or nephritis, consult the appropriate specialists.

The patient needs a full-fledged diet enriched with vitamins. With albuminuria - salt diet, abundant drinking of tea with lemon, juices made from fresh fruits.

On recovery, control tests of blood and urine are mandatory.

Prevention in children's institutions includes regular airing of premises, wet cleaning, disinfection of toys, treatment of utensils, boiling of milk before consumption, examination of entrants and personnel for the carriage of beta-hemolytic streptococcus. Isolation of the patient lasts at least 10 days, after which children who attend preschool institutions and the first 2 classes of the school are isolated from the collective for another 12 days. Adults who have undergone scarlet fever are not allowed to work in preschool institutions, first 2 classes of the school, surgical and maternity wards, in dairy kitchens, in children's hospitals and polyclinics within 12 days after the end of the isolation period. The focus is ongoing disinfection.

[1], [2], [3], [4], [5], [6], [7], [8],