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Download the presentation on the topic of scarlet fever prevention. Presentation, report infectious disease - scarlet fever

Acute infectious disease - SCARLATINA The work was carried out by 3rd year student Filippova I.N.

Scarlet fever Scarlet fever is an acute infectious disease manifested by a pinpoint rash, fever, general intoxication, and sore throat. The causative agent of the disease is group A streptococcus. Infection occurs from patients through airborne droplets (when coughing, sneezing, talking), as well as through household items (dishes, toys, underwear). Patients are especially dangerous as sources of infection in the first days of illness.

Incubation period The incubation period usually lasts 2-7 days, it can be shortened to several hours and extended to 12 days. Typical scarlet fever begins acutely with a rise in body temperature. Malaise, loss of appetite, sore throat when swallowing, headache, tachycardia are noted, and vomiting is often observed. A few hours after the onset of the disease, a pink, dotted skin rash appears in the area of the cheeks, torso and limbs. The skin of the nasolabial triangle remains pale and free of rash. The rash is more intense in the natural folds of the skin, on the sides of the body, and in the lower abdomen. Sometimes, in addition to pinpoint elements, there may be rashes in the form of small (1-2 mm in diameter) bubbles filled with clear or cloudy liquid.

Symptoms The first symptoms of scarlet fever are signs of acute intoxication of the body: a sharp increase in temperature (39-40? C), refusal to eat, drowsiness, pain throughout the body, weakness, irritability. A local reaction to the proliferation of microbes in the area of the tonsils (tonsils) and pharynx manifests itself in the form of redness of the tonsils and pain when swallowing. Young children may vomit or have diarrhea. These symptoms of scarlet fever, however, do not yet allow us to identify scarlet fever, since exactly the same symptoms can occur with many other “cold” diseases. However, symptoms characteristic of scarlet fever appear quite quickly: a pink rash all over the body

Treatment Treatment is usually carried out at home. Inpatient treatment is necessary in severe cases and in the presence of complications. Until the temperature drops, patients should remain in bed. In the acute period of the disease, you need plenty of warm drinks (tea with lemon, fruit juices), liquid or semi-liquid food with some restriction of proteins. Penicillin antibiotics (amoxicillin, retarpen, amoxicillin, amoxiclav) are prescribed for 5-7 days. Additionally, vitamin therapy is prescribed (B vitamins, vitamin C). In severe cases, a glucose solution or hemodez is prescribed intravenously to reduce intoxication.

After suffering from the disease, the body develops immunity, and the person no longer suffers from it throughout his life. Most often the disease occurs in children.

THANK YOU FOR YOUR ATTENTION!

An acute infectious disease characterized by fever, intoxication, sore throat and profuse pinpoint rash. The causative agent of scarlet fever is group A streptococcus, which can also cause kidney damage (glomerulunophritis), sore throat, chronic tonsillitis, rheumatism and other diseases. Scarlet fever occurs if at the time of infection there is no immunity to streptococcus The source of infection is a patient with scarlet fever, tonsillitis or a “healthy” carrier of streptococci

The infection is transmitted by airborne droplets (by sneezing, kissing, etc.). In addition, you can become infected with scarlet fever through food, shared utensils, clothing, or simply by holding a door handle that was previously opened by a completely healthy-looking carrier of the infection.

How does it manifest? Scarlet fever begins acutely: with a sharp rise in temperature to 39º C. The child complains of headache, nausea, severe malaise, and severe pain when swallowing. At the end of the first and beginning of the second day, a small, itchy rash appears, which covers almost the entire body within a few hours. An important sign of scarlet fever is thickening of the rash in the form of dark red stripes on the skin folds in places of natural folds in the groin folds, armpits, and elbows. The skin feels very dry and feels like sandpaper.

If you look into the patient’s mouth, you can see bright red inflamed mucous membrane, purulent deposits on the tonsils and a crimson tongue with sharply enlarged papillae. Doctors characterize this condition of the throat with the expression “flaming throat.” On the face, the rash is located on the cheeks, to a lesser extent on the forehead and temples, while the nasolabial triangle remains pale and free of rash elements (a characteristic sign of scarlet fever)

After 3-5 days, the skin turns pale and severe peeling begins, especially pronounced on the child’s palms: the skin is removed from them like gloves. Lymphadenitis (damage to the lymph nodes) Purulent otitis (ear inflammation) Allergic kidney disease - glomerulonephritis Arthritis, synovitis - joint inflammation Allergic myocarditis - heart damage Pneumonia (pneumonia) Complications

The diagnosis is made on the basis of contact with a patient with scarlet fever, tonsillitis, in the presence of a characteristic rash and throat lesions. Treatment is usually carried out at home. Children with severe and complicated forms of scarlet fever are hospitalized. Bed rest must be observed for 7-10 days. To suppress the growth of streptococcus, antibiotics are used for a 10-day course. In addition, gargling with a solution of furacillin, infusions of chamomile, calendula, and eucalyptus is prescribed. Antiallergic drugs and vitamins will also be used. The diagnosis is made on the basis of data on contact with a patient with scarlet fever, tonsillitis, in the presence of a characteristic rash and throat lesions. Treatment is usually carried out at home. Children with severe and complicated forms of scarlet fever are hospitalized. Bed rest must be observed for 7-10 days. To suppress the growth of streptococcus, antibiotics are used for a 10-day course. In addition, gargling with a solution of furacillin, infusions of chamomile, calendula, and eucalyptus is prescribed. Antiallergic drugs and vitamins are also used

Lecture 26 Diphtheria Scarlet fever Measles http://prezentacija.biz/ 1 Diphtheria is an acute infectious disease characterized by toxic damage mainly to the cardiovascular and nervous systems and a local inflammatory process with the formation of fibrinous plaque. Refers to airborne anthroponoses. 2 The causative agent is Loeffler's bacillus, which produces a neurotropic exotoxin. The predominant localization of inflammation is the pharynx, larynx, nasopharynx, less commonly the bronchi, nose, and external genitalia in girls. 3 Clinically, there are two main forms - diphtheria of the pharynx and diphtheria of the larynx. With diphtheria of the pharynx, local changes are observed in the tonsils - sore throat. Typically fibrinous inflammation of the tonsils with the transition of fibrinous films to the arches and soft palate. The films are tightly bound to the mucous membrane and do not come off for a long time, which contributes to intoxication. The lymph nodes of the neck are enlarged due to necrosis and edema, which can spread to the entire neck and chest. 4 “Bull neck” with toxic diphtheria of the pharynx 5 Fibrinous films on the tonsils of the pharynx. 6 Toxic diphtheria of the throat. 7 Diphtheria tracheobronchitis 8 105 – croupous tracheitis 9 790 – diphtheritic amygdalitis 10 112 – diphtheritic amygdalitis 11 Exotoxin affects the myocardium, the nerves passing behind the tonsils, especially the vagus, in which neuritis develops with a break in the axial cylinders. Parenchymal, often fatty degeneration and parenchymal myocarditis occur in the myocardium. This can lead to death in the second week of illness from early cardiac paralysis. In such cases, myogenic dilatation of the ventricular cavities, dull, flabby myocardium, and often tiger heart are noted. 12 Myogenic dilatation of the heart muscle 13 67 - fatty degeneration of the myocardium “tiger 14 heart” A28 - fatty degeneration of the myocardium “tiger 15 heart” 102 – diphtheritic myocarditis 16 After 1.5-2 months, when local changes in the pharynx disappear, late cardiac paralysis may occur from damage to the vagus. At the same time, the heart appears unchanged at autopsy. 17 The third target of the toxin, in addition to the myocardium and vagus, is the adrenal gland, where a hematoma occurs, threatening death from collapse. 18 With diphtheria of the larynx, intoxication is less pronounced, since mucus collects under the fibrinous film, interfering with the absorption of the toxin. The main danger of this form is true croup - fibrinous inflammation of the larynx caused by diphtheria bacillus. 19 In the absence of any of these components, croup is not considered true, despite clinical manifestations such as suffocation and hoarseness. Such phenomena can occur with laryngeal edema (false croup). 20 Death in diphtheria is caused by acute insufficiency of the pituitary-adrenal system, toxic myocarditis, and asphyxia as a result of laryngeal stenosis. 21 Scarlet fever is an acute streptococcal disease; characterized by fever, general intoxication, sore throat, punctate exanthema, tachycardia. Refers to airborne anthroponoses. 22 Scarlet fever is a childhood infection. The causative agent is group A streptococcus, which causes tissue necrosis typical of scarlet fever. 23 227 – pharynx and esophagus with toxic scarlet fever 24 Pathogenesis. In the pathogenesis of scarlet fever, the pathogen itself, its toxins and allergens (infectious, toxic and allergic components of pathogenesis) are important. Streptococci secrete a pyrogenic exotoxin, which causes the fever and rash of scarlet fever. 25 Towards the end of the first and second days, a characteristic exanthema appears. Against the background of hyperemic skin, a bright, pinpoint rash appears, which thickens in the area of natural folds of the skin (armpits, inguinal folds, inner thighs). 26 The face shows bright hyperemia of the cheeks and a pale nasolabial triangle. Along the edges of the blush, individual small-pointed elements of the rash can be distinguished. In the folds of the skin (especially in the elbow bends) there are small hemorrhages, which, merging, form a peculiar rich color of the folds (Pastia's symptom). 27 Pale nasolabial triangle and rash on the torso 28 Pinpoint rash on the torso 29 Rash on the thigh 30 Pastia's symptom 31 Subsequently, after 3-5 days (in mild forms earlier), the rash turns pale, and in the second week of the disease lamellar peeling appears, the most pronounced on the toes and hands. 32 Peeling on the hand 33 The tongue is coated at the root, but very quickly clears of plaque and takes on the characteristic appearance of a “raspberry” tongue - clean, purple in color, with enlarged papillae; the pharynx is brightly hyperemic; the zone of hyperemia is sharply demarcated from the pale hard palate. 34 White strawberry tongue (first 1-2 days of illness). 35 Red strawberry tongue (in a few days). 36 The tonsils are enlarged, sometimes they show necrotic changes, covered with fibrinous films. Regional nodes are enlarged and painful. Possible enlargement of the liver and spleen. 37 Based on clinical manifestations, scarlet fever is classified into mild, moderate, severe and extrabuccal scarlet fever. Currently, light and erased forms predominate. Severe forms are observed very rarely. 38 Extrabuccal scarlet fever (wound, burn, postpartum) is characterized by a short incubation period, a bright rash that begins around the gate of infection and is expressed most intensely here; there is no sore throat. Patients with extrabuccal scarlet fever are less contagious. 39 There are two periods of scarlet fever - the first with the phenomena of intoxication and degeneration of parenchymal organs and hyperplasia of the immune organs, in particular, with severe hyperplasia of the spleen, and locally - with necrotizing tonsillitis and exanthema. 40 The second period begins at 3-4 weeks. It is caused by the production of antibodies and bacteremia. The sore throat recurs, but is expressed moderately, in a catarrhal form. Allergic arthritis occurs, but the main thing is glomerulonephritis (!), which represents the main danger of the modern course of scarlet fever. 41 The main complications of scarlet fever are glomerulonephritis, necrotizing otitis media, after which hearing loss develops, otogenic brain abscesses, rheumatism, and myocarditis. 42 Measles is an acute viral disease characterized by fever, intoxication, a peculiar enanthema and maculopapular exanthema, damage to the conjunctiva and upper respiratory tract. Refers to airborne anthroponoses. 43 During the prodromal period of the disease, measles enanthema appears in the form of small red spots located on the mucous membrane of the soft and hard palate, Belsky-Filatov-Koplik spots, pathognomaniac for measles. These spots, most often localized on the mucous membrane of the cheeks, are small whitish, slightly raised spots, surrounded by a narrow reddish border. In appearance they resemble semolina or bran. With the appearance of exanthema they disappear. 44 Koplik spots 45 Ulcerative lesions of the oral mucosa in the area of the exit of the salivary gland duct at the level of the small lower molars (Koplik spots) are caused by necrosis, neutrophilic exudate and neovascularization. 46 Measles exanthema is characterized by stages of rash: on the first day, elements of the rash appear on the face and neck; on the second - on the torso, arms and thighs, on the third day the rash covers the legs and feet, and the face begins to turn pale. The rash consists of small papules of about 2 mm, surrounded by an irregularly shaped spot. 47 The mottled, red-brown measles rash on the face, trunk, and proximal extensor muscles is observed due to skin vasodilation, edema, and moderate, nonspecific mononuclear perivascular infiltration. 48 Measles exanthema consists of large spots and papules 49 Koplik spots usually disappear with the appearance of the rash, but sometimes they persist 50 Measles exanthema on the face (1st day) 51 Large spots on the trunk (2nd day) 52 Confluent spots on the trunk ( 3rd day)53 Severe bronchitis due to measles occurs only as complications when a secondary infection occurs. Unlike influenza, it is characterized by damage to small bronchi and bronchioles with necrosis of the epithelium, accompanied by panbronchitis, as well as peribronchitis, i.e. inflammation of the adjacent alveoli. 54 Multinucleated giant cells (called Warthin-Finkeldey cells) that have eosinophilic inclusions in the nucleus and cytoplasm. These are pathognomaniac cells for measles and are found in lymph nodes, lungs and sputum. 55 Measles pneumonia giant mononuclear cells 56 Giant cell in measles pneumonia 57 Measles bronchopneumonia 58 Complications of measles - pneumonia, otitis, mastoiditis. Damage to the central nervous system (encephalitis, meningoencephalitis). Acute necrotizing laryngitis (measles croup), stomatitis, noma. 59 Measles encephalitis 60 Noma 61 Thank you for your attention 62

Childhood infections

Slide 2: Scarlatina

– an acute infectious disease caused by group A streptococcus, transmitted by airborne droplets, characterized by fever, intoxication syndrome, acute tonsillitis with regional lymphadenitis, pinpoint rash, and a tendency to complications of a septic and allergic nature.

Slide 3: Etiology

The causative agent of scarlet fever is group A streptococcus, which is capable of producing erythrogenic exotoxin. The causative agent of scarlet fever is no different from streptococcus, which causes erysipelas, sore throat and other forms of streptococcal infection. However, scarlet fever occurs only when infection occurs with highly toxigenic strains of GAS in the absence of antitoxic and antimicrobial immunity in the child.

Slide 4: Epidemiology

The source of infection is patients with scarlet fever and other forms of streptococcal infection, as well as carriers of GAS. A significant role in the spread of infection belongs to children with mild and atypical forms of streptococcal diseases. The patient becomes dangerous from the onset of the disease, the duration of the infectious period varies from several days to weeks (and even months) depending on the quality of the antibacterial treatment, the condition of the nasopharynx, and the possibility of re-infection with new strains of GAS. Early use of penicillin contributes to the rapid release of the macroorganism from streptococcus: with a smooth course, after 7-10 days from the onset of the disease, the child practically does not pose an epidemic danger. Transmission mechanism: drip.

Slide 5

The main route of transmission is airborne droplets. A contact-household route of infection through objects and things previously used by the patient is possible. Transmission of infection through food has been proven, mainly through milk, dairy products, and creams. The intensity of spread of the pathogen increases sharply when coughing and sneezing, which explains the appearance of scarlet fever foci in children's institutions during the period of rising incidence of ARVI. The spread of SGA is facilitated by overcrowding of children, dusty air, as well as prolonged presence of the source of infection in the team. Contagiousness index – 40%.

Slide 6

The incidence is high everywhere, and is typical in children's groups. Age structure. The maximum incidence of scarlet fever is observed in the age group from 3 to 8 years. Children attending children's institutions suffer from scarlet fever 2-4 times more often than unorganized children. Seasonality is clearly revealed - an increase in incidence in the autumn-winter period of the year. Periodicity: characterized by periodic rises and falls in incidence with an interval of 5-7 years. Antitoxic immunity after scarlet fever is persistent; repeated cases of the disease are due to the lack of strong immunity in some of those who have recovered from the disease.

Slide 7: Pathogenesis

The entrance gates are the mucous membranes of the palatine tonsils, sometimes damaged skin (wound or burn surface), mucous membranes of the genital tract (in postpartum women). In the macroorganism, streptococcus spreads by lymphogenous and hematogenous routes, through canals (intracanalicular) and by contact to nearby tissues. Clinical manifestations of the disease are caused by the septic, toxic and allergic effects of the pathogen (three syndromes of the pathogenesis of streptococcal infection).

Slide 8

Septic (or infectious) syndrome of pathogenesis is characterized by inflammatory or necrotic changes at the site of introduction of streptococcus. The inflammation initially has a catarrhal character, but has a tendency to quickly turn into purulent, purulent-necrotic.

Slide 9

Toxic syndrome is caused mainly by an exotoxin, which, when released into the blood, causes fever and symptoms of intoxication: impaired condition and well-being, pinpoint rash, changes in the pharynx and tongue, reaction of regional lymph nodes (in the first 2-3 days of illness), changes in the cardiovascular systems. The most pronounced manifestations of toxic syndrome are observed in toxic forms of scarlet fever. A decrease in the tone of the sympathetic nervous system, inhibition of the release of corticosteroid hormones against the background of severe damage to the central nervous system can lead to a sharp decrease in blood pressure and death from infectious-toxic shock.

Slide 10

The allergic syndrome develops from the first days of scarlet fever, but reaches its greatest severity in the 2-3rd week. illness and persists for a long time. Allergization is mainly specific and is caused by protein substances of streptococcus. It, as a rule, is not accompanied by visible clinical manifestations, but leads to an increase in the permeability of the walls of blood vessels, a decrease in the phagocytic activity of leukocytes and other changes. In this regard, there is a danger of developing complications of an infectious-allergic nature (glomerulonephritis, myocarditis, synovitis, rheumatism), which usually develop in the 2-3rd week. diseases resulting from secondary infection with other streptococcal serotypes.

Slide 11

In the pathogenesis of scarlet fever, a change in phases of autonomic nervous activity occurs: at the beginning of the disease, there is an increase in the tone of the sympathetic part of the autonomic nervous system (“sympathetic phase”), which is later replaced by a predominance of the tone of the parasympathetic part of the nervous system (“vagal phase”).

Slide 12: Classification of scarlet fever

By type: 1. Typical; 2. Atypical (extratonsillar): - burn; - wounded; - postpartum; - postoperative

Slide 13

By severity: 1. Light form. 2. Moderate form. 3. Severe form: - toxic; - septic; - toxic-septic Severity criteria: - severity of intoxication syndrome; - severity of local changes.

Slide 14

Slide 15: Clinical picture

4 periods: incubation initial rash convalescence

Slide 16

The incubation period ranges from several hours to 7 days, most often 2-4 days. The initial period covers the period of time from the onset of the first symptoms of the disease to the appearance of the rash; its duration ranges from several hours to 1-2 days. Scarlet fever usually begins acutely. Characterized by intoxication, fever, acute tonsillitis with regional lymphadenitis. Intoxication syndrome is manifested by a violation of the general condition, headache, often nausea and vomiting, and tachycardia. Body temperature rises to 38°C and above. Acute tonsillitis syndrome is characterized by sore throat (especially when swallowing), limited hyperemia of the mucous membrane of the pharynx and palatine tonsils, sometimes pinpoint enanthema on the soft palate, reaction of the anterior superior cervical (tonsillar) lymph nodes (enlargement, moderate hardening and sensitivity to palpation). Tonsillitis is most often catarrhal in nature, but can be lacunar or follicular. Necrotizing tonsillitis is currently rare and is a complication.

Slide 17

Rash period. Against the background of the maximum severity of the initial period syndromes (intoxication, tonsillitis), a pinpoint rash appears. Exanthema syndrome develops early, usually in the first 2 days of the disease. In terms of morphology, the rash is pinpoint-like, consisting of small roseola 1-2 mm in size, located close to each other. The color of the rash on the first day is bright, sometimes bright red, and by the 3-4th day it fades to faint pink. The rash is often quite abundant, less often - scanty, localized mainly on the flexor surfaces of the limbs, the front and side surfaces of the neck, the sides of the chest, on the abdomen, lumbar region, inner and back surfaces of the thighs and legs, in places of natural folds - axillary, elbow, groin , popliteal In these areas, the rash is more abundant, brighter, located on the hyperemic background of the skin and persists for a longer time. As a result of mechanical trauma to the vessels of the skin, small petechiae often appear, located in isolation or forming hemorrhagic stripes (Pastia's lines), which remain for some time after the disappearance of the rash and serve as one of the additional signs in the diagnosis of scarlet fever in the later stages. The skin of patients is dry, rough (due to hypertrophy of hair follicles).

Slide 18

The period of convalescence begins from the 2nd week. disease and lasts 10-14 days. It is characterized by the presence of peeling skin and a “papillary” tongue in some patients. Typical of scarlet fever is large-plate peeling, especially on the fingers and toes. Small pityriasis-like peeling on the skin of the neck, torso, and earlobes is possible. During the period of convalescence, increased sensitivity to streptococcal superinfection and the associated risk of developing infectious-allergic and septic complications remain.

Slide 19: Based on severity, there are mild, moderate and severe forms of scarlet fever

The mild form in modern conditions is the most common and is characterized by a mild intoxication syndrome, moderate changes in the pharynx in the form of catarrhal tonsillitis. The children's condition remains satisfactory, body temperature does not exceed 37.5-38.5°C. There are no complaints, sometimes there is a short-term headache, malaise, sore throat when swallowing, and possible single vomiting. The pinpoint rash is faint and not abundant, subsides by the 3-4th day of illness; changes in the pharynx last 4-5 days. The moderate form is accompanied by significant intoxication and pronounced changes at the site of the entrance gate. Children complain of weakness, headache, loss of appetite, and pain when swallowing. Body temperature rises to 38.6-39.5° C. vomiting is usually repeated. In the pharynx, phenomena of tonsillitis are observed with bright, delimited hyperemia, often with purulent effusion in the lacunae or suppurated follicles. On the mucous membranes of the soft palate, punctate enanthema is sometimes observed. The rash is bright, abundant, against a hyperemic background of the skin; changes in the cardiovascular system are revealed: tachycardia, muffled heart sounds, increased blood pressure. A severe form of scarlet fever can occur with pronounced symptoms of intoxication (toxic form) or septic lesions (septic form). With a combination of pronounced initial symptoms of toxicosis and septic manifestations, the form of scarlet fever is regarded as toxic-septic.

Slide 20

The toxic form of scarlet fever is characterized by pronounced symptoms of intoxication, repeated vomiting, headache, agitation, delirium, loss of consciousness, and convulsions are noted. Body temperature rises to 40°C and above. The appearance of the patient's face is characteristic: bright red cheeks with a pronounced pale nasolabial triangle, bright dry lips, injection of scleral vessels. The throat is bright, flaming; hyperemia reaching the border of the soft and hard palate, punctate enanthema of a hemorrhagic nature. The rash on the body is bright, on a hyperemic background of the skin, often with hemorrhages. Symptoms of damage to the cardiovascular system are detected already at the onset of the disease - pronounced tachycardia, muffled heart sounds, and increased blood pressure are noted. As toxicosis increases, sometimes even in the first day, infectious-toxic shock (ITS) may develop: cyanosis, coldness of the extremities, rapid thread-like pulse, muffled heart sounds, and a sharp drop in blood pressure appear. oliguria. In the absence of adequate therapy, death occurs within the first day from the onset of the disease. The septic form of scarlet fever is accompanied by the development of severe inflammatory purulent and purulent-necrotic processes emanating from the primary lesion. The patient's condition is progressively worsening. Body temperature increases, the inflammatory process in the pharynx acquires a necrotic character, with foci of necrosis appearing not only on the palatine tonsils, but also on the arches, at the base of the uvula. Purulent lymphadenitis of the tonsillar lymph nodes develops with the involvement of surrounding tissue (adenophlegmon) in the pathological process, purulent otitis, ethmoiditis, and mastoiditis. In the absence of etiotropic therapy, the disease rapidly progresses, severe septic condition and death develop.

Slide 21: Supportive diagnostic signs of scarlet fever:

Contact with a patient with scarlet fever or another form of streptococcal infection is an acute onset of the disease; - fever corresponding to the severity of the disease; - intoxication syndrome - acute tonsillitis syndrome with regional lymphadenitis - bright, delimited hyperemia in the pharynx (“flaming pharynx”); - pale nasolabial triangle against the background of hyperemia of the cheeks (Filatov’s symptom); - early appearance of pinpoint rash; - dynamics of language changes (“raspberry tongue”); - large-plate peeling of the skin of the fingers and toes.

Slide 22: Laboratory diagnostics

a bacteriological method that makes it possible to detect SGA in material from any lesion; an express method based on the coagglutination reaction and allowing to detect the GAS antigen in the test material (mucus from the throat and nose, wound discharge, etc.) within 30 minutes; hematological method (presence of leukocytosis, neutrophilia, increased ESR in the blood during the acute period of the disease)

Slide 23: Differential diagnosis

with diseases accompanied by a rash: rubella, measles, chickenpox, staphylococcal infection with scarlet-like syndrome, meningococcemia, allergic rashes, prickly heat, hemorrhagic vasculitis, pseudotuberculosis, enterovirus infection.

Slide 24: Treatment

patients with scarlet fever complex, etiopathogenetic; It is carried out both in a hospital and at home. Hospitalization is carried out according to clinical (severe and moderate forms), age (children under 3 years of age) and epidemiological (patients from closed groups living in dormitories, communal apartments, etc.) indications. Bed rest during the entire acute period of the disease. The diet must be appropriate for the child's age and contain the necessary nutritional ingredients.

Slide 25

Antibacterial therapy is necessary for all patients with scarlet fever, regardless of the severity of the disease. The most effective and safe is penicillin therapy. For any severity of scarlet fever in children of different ages, benzylpenicillin sodium salt (i.m., i.v.) is used at a dose of 100-150 thousand units/kg/day (for mild and moderate forms) and up to 500-800 thousand units/kg /day or more (for severe cases). The mode of administration is 4 times a day, the course is from 7 to 10-14 days. For mild forms of scarlet fever, antibiotics (phenoxymethylpenicillin, smallpox, amoxicillin, amoxiclav, augmentin) are prescribed orally. If penicillin therapy is not possible, macrolides (erythromycin, roxithromycin, azithromycin, etc.), cephalosporins of the first and second generation (cephalexin, cefuroxime, etc.) are used. Pathogenetic and symptomatic therapy. In severe toxic forms of scarlet fever, detoxification therapy is carried out - 10% glucose solution, 10% albumin solution, hemodez, rheopolyglucin are administered intravenously. Desensitizing agents are prescribed only if indicated - for children with allergic rashes, allergic dermatitis in the acute stage.

Slide 26: Clinical observation

Children who have had scarlet fever are subject to medical examination: within 1 month. (after mild and moderate forms), 3 months. (after severe forms of the disease). Clinical examination of convalescents is carried out once every 2 weeks; laboratory examination, including a clinical blood test, a general urine test, determination of GAS in material from the throat and nose - at 2 and 4 weeks. clinical examination (after severe forms, additionally at the end of the observation period). Consultations with an infectious disease specialist, otolaryngologist, rheumatologist and other specialists are carried out according to indications.

Slide 27: Prevention

The main preventive measures are early detection and isolation of sources of infection. Isolation of patients with scarlet fever is carried out in a hospital or at home. Children are discharged from the hospital no earlier than on the 10th day from the onset of the disease if the result of a bacteriological test for group A streptococcus is negative. Convalescents of scarlet fever are not allowed into preschool institutions and the first 2 grades of school for 12 days. The same isolation periods (22 days) are recommended for patients with tonsillitis from scarlet fever. Impact on the route of transmission: carry out ongoing (daily) and final (on the day of registration of recovery) disinfection by parents and staff. Contact preschoolers and schoolchildren in grades 1-2 are subject to quarantine for 7 days from the moment of isolation of the patient with scarlet fever with the implementation of the entire range of anti-epidemic measures.

Slide 28: Chicken pox

Slide 29: Chicken pox (Varicella)

An acute infectious disease caused by a virus from the Herpesviridae family, transmitted by airborne droplets, characterized by fever, moderate intoxication and a widespread vesicular rash.

Slide 30: Etiology

The causative agent of chickenpox, the Varicella zoster virus, belongs to the Herpesviridae family, subfamily of type 3 α-viruses, and contains DNA. The size of the virion reaches 150-200 nm in diameter. The virus infects cell nuclei with the formation of eosinophilic intranuclear inclusions and can cause the formation of giant multinucleated cells. The pathogen is unstable in the external environment, inactivated at +50-52° C for 30 minutes, sensitive to ultraviolet radiation, and tolerates low temperatures and repeated freezing and thawing.

Slide 31: Epidemiology

The source of infection is a person suffering from chickenpox and herpes zoster. The patient is contagious from the last 2 days of the incubation period until the 5th day after the appearance of the last vesicle.

Slide 32

Transmission mechanisms: drip, contact. Routes of transmission: airborne; rarely – contact-household, vertical. The pathogen can be transported over long distances by air flow (to adjacent rooms, from one floor of a building to another).

Slide 33

Susceptibility to chickenpox is very high. Contagiousness index – 100%. The incidence is extremely high. Mostly children of preschool age are affected. Seasonality: incidence increases in the autumn-winter period,

Slide 34

Periodicity. There are no pronounced periodic rises and falls in incidence. Immunity after illness is persistent. Repeated cases of chickenpox are very rare. However, the virus persists in the body for life and, with a decrease in the protective forces of the macroorganism, causes the development of herpes zoster. Lethal outcomes are possible in patients with generalized, hemorrhagic, gangrenous, bullous forms of the disease and with the development of bacterial complications.

Slide 35: Pathogenesis

The entrance gates are the mucous membranes of the upper respiratory tract. This is probably where the replication and primary accumulation of the virus occurs. From where it enters the blood through the lymphatic pathways and spreads throughout the body. The chickenpox virus has a tropism for the cells of the spinous layer of the skin and the epithelium of the mucous membranes, fixes in them, causes dystrophic changes with the formation of characteristic vesicles (vesicles) filled with serous contents. Typical rashes are also observed on the mucous membranes of the oral cavity, upper respiratory tract, and rarely, the urinary tract and gastrointestinal tract. In patients with generalized forms of infection, internal organs are affected - the liver, lungs, meninges, brain matter, in which small foci of necrosis are detected with hemorrhages along the periphery. In addition, the virus has a tropism for nervous tissue and causes damage to the intervertebral spinal ganglia, ganglia of the facial and trigeminal nerves, where it remains latent for a long time. If the immunological reactivity of the macroorganism decreases, the infection is reactivated: the virus reaches the skin along sensory nerves and causes the development of clinical manifestations in the form of herpes zoster.

Slide 36: Classification of chickenpox

By type: 1. Typical. 2. Atypical: - rudimentary; - pustular; - bullous; - hemorrhagic; - gangrenous; - generalized (visceral).

Slide 37

By form: Light to medium-heavy form. Severe form. Criteria of severity: - severity of intoxication syndrome - severity of local changes.

Slide 38

With the flow (by character); 1. Smooth. 2. Unsmooth: - with complications; - - with a layer of secondary infection - with exacerbation of chronic diseases

Slide 39: Clinical picture

The incubation period lasts from 11 to 21 days (usually 14-17 days). The prodromal period lasts from several hours to 1-2 days (usually absent). Characterized by a mild intoxication syndrome, low-grade body temperature, rarely – exanthema syndrome: punctate

Slide 40

The rash period lasts 2-5 days. The disease usually begins acutely, with an increase in body temperature to 37.5-38.5 ° C, moderate manifestations of intoxication (headache, irritability), as well as the development of a characteristic macular-vesicular rash on the skin, mucous membranes, cheeks, tongue, palate . The first bubbles, as a rule, appear on the body, scalp, and face. Unlike smallpox, the face is affected less and later than the trunk and limbs. A rash on the palms and soles is rare, mainly in severe forms. The evolution of the development of rash elements (spot - papule - vesicle - crust) occurs quickly: a spot turns into a vesicle within a few hours, a vesicle into a crust within 1-2 days. Chickenpox elements (size 0.2-0.5 cm in diameter) have a round or oval shape, are located on a non-infiltrated base, surrounded by a rim of hyperemia; the wall of the vesicles is tense, the contents are transparent. Unlike smallpox, the vesicles are single-chambered and collapse when punctured. From the 2nd day of the rash period, the surface of the vesicle becomes sluggish, wrinkled, and its center begins to sink. In the following days, hemorrhagic crusts form, which gradually (over 4-7 days) dry out and fall off; in their place, light pigmentation may remain, in some cases - single scars (“the hallmark of chickenpox”).

Slide 41: Based on severity, there are mild, moderate and severe forms of chickenpox

Mild form - body temperature rises to 37.5-38.5 ° C for 2-3 days, symptoms of intoxication are absent or mildly expressed. The rashes are not abundant, last 2-3 days, disappear without a trace. Moderate form - body temperature rises to 38.6-39.5 ° C for 3-5 days, symptoms of intoxication are moderate. The rashes are abundant, including on the mucous membranes, last 5-7 days, after their disappearance short-term pigmentation may remain. Severe form - body temperature above 39.6 ° C for 7-10 days, possible development of convulsive syndrome and meningoencephalic reactions. The rashes are abundant, large, “frozen” in one stage of development, and are observed both on the skin (including on the palms and soles) and on the mucous membranes (including the upper respiratory tract and genitourinary tract). The duration of the rash is 7-8 days; after the rash disappears, along with pigmentation, superficial scars may remain.

Slide 42: Complications

Specific: acute stenosing laryngotracheitis and laryngotracheobronchitis, encephalitis, keratitis, hemorrhagic nephritis, carditis, Reye's syndrome. Nonspecific complications: abscesses, phlegmons, lymphadenitis, otitis, pneumonia, sepsis.

Slide 43: Supportive diagnostic signs of chickenpox:

Contact with a patient with chickenpox or herpes zoster - intoxication syndrome - incorrect type of temperature curve; - vesicular rash on the skin and mucous membranes; - false polymorphism of the rash.

Slide 44: Laboratory diagnostics

Express methods: microscopic - identification of Aragao bodies (clumps of virus) in smears of vesicular fluid stained with silver according to Morozov using conventional or electron microscopy; immunofluorescent - detection of virus antigens in fingerprint smears from the contents of vesicles. Serological method - using RSK. An increase in the titer of specific antibodies by 4 times or more is diagnostic. The virological method is the isolation of the virus on human embryonic cell cultures. Hematological method - a blood test reveals leukopenia, lymphocytosis, and normal ESR.

Slide 45: Differential diagnosis

Impetigo differs from chickenpox by the predominant localization of the rash on the face and hands; the vesicles are not tense, their contents quickly become serous-purulent and dry out to form a loose straw-yellow crust. The bullous form of streptoderma can begin with the appearance of small blisters. They are of a regular round shape, quickly increase in size and become flat and tense. Their wall is easily torn, and erosions with fragments of bubbles along the edges are formed. Strophulus is characterized by the appearance of red itchy papules, the development of dense waxy nodules located symmetrically on the limbs, buttocks, and lumbar region. Elements of the rash are usually absent on the face and scalp. Body temperature remains normal. The mucous membranes of the oral cavity are not affected. Generalized forms of herpes simplex usually occur in children of the first year of life and occur with symptoms of neurotoxicosis. Lymphadenopathy may be present. hepatosplenomegaly, damage to internal organs. With herpangina, smallpox, herpes simplex, insect bites.

Slide 46: Treatment

Conducted at home. Children with severe, complicated forms of the disease, as well as for epidemic indications, are subject to hospitalization in Meltzer boxes. Bed rest for the acute period. Age-appropriate diet, mechanically gentle, rich in vitamins. Much attention should be paid to caring for a sick child: strictly monitor the cleanliness of bed and underwear, clothes, hands, and toys. Locally: vesicles on the skin should be lubricated with a 1% alcohol solution of brilliant green or a 2-5% solution of potassium permanganate; rashes on the mucous membranes are treated with aqueous solutions of aniline dyes. It is recommended to rinse the mouth after eating.

Slide 47: Causal therapy

used only for severe forms. Acyclovir (Zovirax), specific varicella zoster immunoglobulin (at the rate of 0.2 ml/kg), as well as interferon preparations and its inducers are used. If purulent complications develop, antibiotics are prescribed.

Slide 48: Clinical observation

are carried out for children who have suffered complicated forms of chickenpox (encephalitis, etc.).

Slide 49: Prevention

The patient is isolated at home (or in a Meltzer box) until the 5th day from the moment the last element of the vesicular rash appears. Children under 7 years of age who have not had chickenpox (herpes zoster) are separated from 9 to 21 days from the moment of contact with the patient. Contacts are monitored daily with thermometry, examination of the skin and mucous membranes. Healthy children who have not had chickenpox can be vaccinated with varicella zoster vaccine in the first 72 hours after exposure. Disinfection is not carried out; ventilation of the room and wet cleaning are sufficient. For the purpose of active specific prevention, a live attenuated varicella-zoster vaccine (Varilrix) is used. Passive specific prevention (administration of specific varicella-zoster immunoglobulin) is indicated for contact children at risk (with blood diseases, various immunodeficiency conditions), as well as contact pregnant women who have not had chickenpox (herpes zoster).

Slide 50: Rubella

Slide 51: Rubella (Rubeola) is a viral disease that occurs in the form of acquired and congenital infection

Acquired rubella is an acute infectious disease caused by the rubella virus, transmitted by airborne droplets, characterized by a small-spotted rash, enlarged peripheral lymph nodes, mainly occipital and posterior cervical, moderate intoxication and minor catarrhal symptoms. Congenital rubella is a chronic infection with transplacental transmission, leading to fetal death, early miscarriage or severe developmental defects.

Slide 52: Etiology

Rubella virus belongs to the toxonomic group of togaviruses (family Toga viridae, genus Rubivirus). Virions are spherical in shape with a diameter of 60-70 nm and contain RNA. The virus is unstable in the environment, resistant to antibiotics, tolerates low temperatures well, and dies immediately when exposed to ultraviolet irradiation. In terms of antigenic properties, all strains of the rubella virus represent a single serotype.

Slide 53: Epidemiology

The source of infection is patients with a typical form of acquired rubella, as well as persons with atypical forms (erased, asymptomatic, etc.); children with congenital rubella and virus carriers. A patient with acquired rubella becomes contagious 7 days before the development of the first clinical signs of the disease and can continue to shed the virus for 21 days after the appearance of the rash (a patient with rubella is especially contagious during the first 5 days after the onset of the rash). In children with congenital rubella, the virus is excreted for a long time - 1.5-2 years after birth (with sputum, urine, feces).

Slide 54

Transmission mechanisms: droplets (acquired), blood-contact (congenital). Routes of transmission: airborne droplets, household contact (for acquired rubella), transplacental (for congenital rubella). Children are highly susceptible to rubella. Children of the first 6 months. are immune to rubella if they have innate immunity. However, newborns and children in the first months of life can get rubella in the absence of specific antibodies.

Slide 55

Age structure. Children aged 2 to 9 years are most often affected by rubella. Seasonality. Rubella diseases are observed at any time of the year, with an increase in the cold season. Periodicity. Rubella is often recorded in the form of epidemic outbreaks with an interval of 3-5 years to 6-9 years. Immunity after rubella is persistent, lifelong, and is developed after exposure to both manifest and asymptomatic forms.

Slide 56: Pathogenesis

In acquired rubella, the portal of entry is the mucous membranes of the upper respiratory tract. The virus multiplies in the lymph nodes. Later, already in the incubation period, viremia occurs. The virus spreads through the bloodstream to various organs and tissues; during the rash period, skin damage is noted (the rubella virus spreads in the skin of patients regardless of the presence of exanthema). Isolation of the virus from the mucus of the nasopharynx, feces and urine indicates the generalized nature of the changes during rubella infection. From the moment the rash appears, viremia ends and virus-neutralizing antibodies appear in the blood.

Slide 57

With congenital rubella, the virus enters the embryo transplacentally, infects the epithelium of the chorionic villi and the endothelium of the blood vessels of the placenta, which subsequently leads to chronic ischemia of the tissues and organs of the fetus. The virus causes disturbances in the mitotic activity of cells, chromosomal changes leading to the death of the fetus or the formation of severe developmental defects in the child. The cytodestructive effect of the virus is sharply expressed in the lens of the eye and the cochlear labyrinth of the inner ear, resulting in cataracts and deafness. The rubella virus primarily affects organs and systems that are in the process of formation, in the so-called critical period of intrauterine development. The critical periods are: for the brain - 3-11 weeks, for the eyes and heart - 4-7 weeks, for the hearing organ - 7-12 weeks. The frequency of congenital deformities depends on the timing of pregnancy: infection with the rubella virus at the 3-4th week. pregnancy causes fetal damage in 60% of cases, 9-12 weeks. – 15%, 13-16th week. – 7%, in patients with congenital rubella, despite the presence of specific anti-rubella antibodies in the blood, the pathogen can remain in the body for a long time (2 years or more). This fact confirms the position of congenital rubella as a chronic infection.

Slide 58: Classification of rubella

A. Acquired. By type: 1. Typical. 2. Atypical; - with isolated exanthema syndrome; - with isolated lymphadenopathy syndrome; - erased; - asymptomatic.

Slide 59

By severity: 1. Light form. 2. Moderate form. 3. Severe form. Severity criteria; - severity of intoxication syndrome; - severity of local changes.

Slide 60

By flow (character): 1. Smooth. 2. Unsmooth: - with complications; - with a layer of secondary infection; - with exacerbation of chronic diseases.

Slide 61

B. Congenital. 1. “Minor” rubella syndrome (damage to the organs of vision, hearing, and heart). 2. “Major” rubella syndrome (damage to various organs and systems).

Slide 62: Clinical picture of acquired rubella

The typical form is characterized by the presence of all classical syndromes (zanthema, lymphadenopathy, catarrhal), a cyclical course with alternating periods - incubation, prodromal, rash and convalescence. The incubation period ranges from 11 to 21 days (usually 16-20 days). The prodromal period is variable, lasting from several hours to 1-2 days, U

Slide 63

The period of rash is characterized by the appearance of exanthema syndrome against the background of clinical manifestations observed in the prodromal period; lasts 2-3 days. The rash appears simultaneously and covers the face, chest, abdomen, back, and limbs within 24 hours. It is localized mainly on the extensor surfaces of the arms, the lateral surfaces of the legs, on the back, lower back, buttocks against an unchanged skin background. At the same time, the rash can be quite abundant on the flexural surfaces, while the places of natural folds, as a rule, remain free from rashes. All patients have a rash on the face. The rash is finely spotted, with smooth outlines, quite abundant, pale pink, without a tendency to merge individual elements. Disappears without a trace, without pigmentation and peeling of the skin. There is no staged progression of the rash.

Slide 64

Polyadenitis is a constant sign of rubella. Damage to the posterior cervical and occipital lymph nodes is typical; enlargement of the parotid, anterior cervical, popliteal, axillary nodes is possible; enlargement of the lymph nodes is usually moderate, sometimes accompanied by slight pain. Fever is observed intermittently and is mildly expressed. Body temperature is normal or subfebrile (in some cases it rises to 39° C), persists for 1-3 days. Catarrhal inflammation of the mucous membranes of the upper respiratory tract is usually moderate or mild and manifests itself as rhinitis, pharyngitis; Conjunctivitis may occur. Clinically, a dry cough, slight mucous discharge from the nose, swelling of the eyelids, lacrimation, and photophobia are observed. The convalescence period for rubella is usually favorable.

Slide 65: Clinical picture of congenital rubella

“Minor” rubella syndrome (Gregg's triad) includes deafness, cataracts, and heart defects. 2. “Grand” (extended) congenital rubella syndrome is manifested by deep brain damage (anencephaly, microcephaly, hydrocephalus), malformations of the heart and blood vessels (patent ductus arteriosus, pulmonary stenosis, ventricular septal defect, atrial septal defect, tetralogy of Fallot, coarctation aorta, transposition of the great vessels); eye damage (glaucoma, cataracts, microphthalmia, retinopathy); malformations of the skeleton (tubular bones in the metaphysis) and skull (non-fusion of the hard palate); defects of the genitourinary organs and digestive system; damage to the organ of hearing (deafness); hepatosplenomegaly. reactive hepatitis, thrombocytopenic purpura, interstitial pneumonia, myocarditis.

Slide 66: Supportive diagnostic signs of acquired rubella:

Contact with a person with rubella; - small spotted rash; - lymphadenopathy syndrome with a predominant increase in the occipital and posterior cervical lymph nodes; - body temperature is normal or moderately elevated; - moderate catarrhal syndrome.

Slide 67: Laboratory diagnostics

METHODS Virological Serological Hematological

Slide 68: Treatment

For patients with rubella, bed rest is recommended for the acute period, then semi-bed rest for another 3-5 days. Etiotropic therapy is carried out with recombinant interferons (viferon, intron A, roferon A, etc.) according to indications (all cases of congenital rubella with signs of an active infection; acquired rubella, occurring with damage to the central nervous system). For mild and moderate forms, symptomatic treatment is prescribed. For rubella arthritis, delagil (chloroquine), nonsteroidal anti-inflammatory drugs (brufen, indomethacin), and antihistamines (claritin, suprastin, fenkarol) are used.

Slide 69: Clinical observation

Children who have had rubella encephalitis are examined for at least 2 years by a neurologist and a pediatric infectious disease specialist.

Slide 70: Prevention

Patients with acquired rubella are isolated until complete recovery, but not less than 5 days from the onset of the disease. It is recommended to isolate the first sick person in a child care facility for up to 10 days from the onset of the rash. In some cases (if there are pregnant women in the family or team), it is advisable to extend the separation period to 3 weeks. The impact on the transmission mechanism of rubella consists of ventilation and wet cleaning of the room or ward where the patient is located. Contact children under the age of 10 who have not had rubella are not allowed to be sent to closed children's institutions (sanatoriums, orphanages, etc.) within 21 days from the moment of separation from the patient.

Slide 71: Specific prevention

They use the live attenuated vaccine "Rudivax", as well as the combined vaccine against measles, mumps, rubella - "MM R", "Priorix". Pregnant women cannot be vaccinated: pregnancy is undesirable for 3 months. after immunization against rubella (the possibility of post-vaccination damage to the fetus cannot be ruled out). Administration of the rubella vaccine is accompanied by the production of specific antibodies in 95% of immunized individuals. In case of contact of a pregnant woman with a patient with rubella, the question of maintaining pregnancy should be decided taking into account the results of a 2-fold serological examination (with the obligatory determination of the quantitative content of specific immunoglobulins of classes M and G). If a pregnant woman has a stable titer of specific antibodies, contact should be considered not dangerous.

Slide 72: MEASLES

Slide 73: Measles (Morbilli)

– an acute infectious disease caused by the measles virus, transmitted by airborne droplets, characterized by catarrhal syndrome, damage to the mucous membranes of the oral cavity, intoxication syndrome, and the presence of a maculopapular rash with transition to pigmentation.

Slide 74: Etiology

The causative agent of measles Pollinosa morbillarum belongs to the paramyxoviruses (family Paramyxoviridae, genus Morbillivirus), contains RNA, has an irregular spherical shape with a virion diameter of 120-250 nm. The measles virus strains are antigenically identical and have complement-fixing, hemagglutinating, hemolyzing properties and symplast-forming activity.

The source of infection is only a person with measles, including those carrying atypical forms. The patient is contagious from the last days of the incubation period (2 days), during the entire catarrhal period (3-4 days) and the period of rash (3-4 days). From the 5th day of the appearance of the rash, a person with measles becomes non-contagious.

Slide 78: Transmission mechanism

– drip

Slide 79: Path of transmission

– airborne. The virus enters the environment when coughing, sneezing, talking and, spreading over significant distances with air currents, can penetrate into neighboring rooms; through corridors and staircases through the ventilation system, even to other floors of the building. Transmission of infection through objects and third parties of the virus is practically absent due to low resistance in the external environment. Intrauterine infection (transplacental transmission) cannot be ruled out if a woman becomes ill at the end of pregnancy.

Slide 80: Contagiousness index

Slide 81: Pathogenesis

The entrance gates are the mucous membranes of the upper respiratory tract and conjunctiva. The virus is adsorbed on the mucosal epithelium, then penetrates the submucosa and regional lymph nodes, where its primary reproduction occurs. From the 3rd day of the incubation period, the virus enters the blood, causing the first wave of viremia. In the middle of the incubation period, there is already a high concentration of the virus in the lymph nodes, spleen, liver, tonsils, follicles, and myeloid tissue of the bone marrow, which increases even more towards the end of incubation. Subsequently, a new and more significant increase in viremia is noted, which clinically corresponds to the catarrhal period of measles. The virus has pronounced epitheliotropy and causes catarrhal inflammation of the pharynx, nasopharynx, larynx, trachea, bronchi, bronchioles. The digestive tract is also affected - the mucous membrane of the oral cavity, small and large intestines. Pathological changes in the mucous membranes of the lips. gums, cheeks are manifested by Belsky-Filatov-Koplik spots, pathognomonic for measles, which represent areas of epithelial micronecrosis with subsequent desquamation; cannot be removed with a tampon or spatula. One of the characteristic properties of the pathological process in measles is its penetration into the depths of tissues. Patients with measles develop a specific allergic restructuring of the body that persists for a long time. The role of the measles virus in the development of slow infections that occur with degenerative changes in the central nervous system (chronic encephalitis, subacute sclerosing panencephalitis) has been established. Of great importance in the pathogenesis of measles is the developing anergy (secondary immunodeficiency) - a decrease in local and general immunity, as a result of which favorable conditions are created for the activation of both pathogenic and opportunistic microflora and the frequent development of complications, mainly of the respiratory system. It is known that measles leads to exacerbation of chronic diseases.

Slide 86: Based on severity, there are mild, moderate and severe forms of measles

Mild form – the patient’s condition is satisfactory, body temperature is subfebrile or increased to 38.5°C. The rash is faint, not abundant, maculopapular in nature, with a weak tendency to merge and pale pigmentation. Moderate form - intoxication syndrome is pronounced, the patient’s well-being is significantly disturbed, vomiting and loss of appetite are noted; body temperature rises to 38.6-39.5 ° C; The rash is abundant, bright, large maculopapular, prone to fusion. Severe form - intoxication syndrome is significantly expressed: convulsions, loss of consciousness, repeated vomiting; body temperature over 39.5° C; hemorrhagic syndrome is noted.

Slide 92: Laboratory diagnostics

virological serological hematological

Slide 93: Differential diagnosis

In the catarrhal period - with ARVI (adenovirus, influenza, parainfluenza, etc.), in some cases whooping cough and parawhooping cough, thrush. During the period of rash - with rubella, scarlet fever. zenterovirus infection, meningococcemia, allergic rashes, pseudotuberculosis, Stevens-Johnson syndrome and Lyell's syndrome.

Slide 94: Treatment

at home. Children with severe forms of the disease, complications, and concomitant diseases are subject to hospitalization; young children from socially vulnerable families, closed child care institutions. Bed rest is prescribed during the entire period of fever and for the first 2 days. The diet is prescribed taking into account the age of the child, the form and period of the disease. During the acute period, dairy and plant foods should be given, mechanically and chemically gentle, with a sufficient content of vitamins

Slide 95: Drug therapy

depending on the severity of the symptoms of the disease, as well as the presence and nature of complications. As etiotropic therapy, we can recommend RNase (irrigation of the mucous membranes of the oral cavity, instillation into the nose and eyes, in severe cases - intramuscularly), recombinant interferons (Viferon, Reaferon, Realdiron, Interlock).

Slide 96: Clinical observation

Children who have had measles encephalitis (meningoencephalitis). observed for at least 2 years (neurologist, pediatric infectious disease specialist).

Slide 97: Prevention

A patient with measles is isolated until the 5th day from the onset of the rash. Quarantine for 17 days from the moment of contact - for contacts who have not been vaccinated and have not had measles. The quarantine period is extended to 21 days for children who were administered immunoglobulin, plasma, or blood during the incubation period. During the first 7 days from the moment of contact, the child can be allowed to visit a child care facility, since the infectious disease begins from the last two days of the incubation period, the minimum period of which is 9 days. Schoolchildren older than second grade are not subject to quarantine.

Last presentation slide: Scarlet fever: Specific prevention

National vaccination calendar for 12 months and 6 years Vaccine Live measles vaccine L-16 Live measles vaccine “Ruvax” Trivalent vaccine “MM R” Trivalent vaccine “Priorix”

"Necrotizing tonsillitis (tonsillitis) with scarlet fever." WITH the mucous membrane of the pharynx (pharynx) is hyperemic (red), covered with mucus. The tonsils are slightly enlarged. There are numerous foci of necrosis of a grayish color, in some places, at the site of rejection of necrotic masses, ulceration. Foci of necrosis spread to the mucous membrane of the pharynx.

SCARLET FEVER

COMPLICATIONS:

1. Septic - retropharyngeal abscess, phlegmon of the neck

Arthritis

- purulent osteomyelitis of the temporal bone

- brain abscess, meningitis

Sepsis

2. infectious-allergic

- glomerulonephritis

- myocarditis, endocarditis

Synovitis

Vasculitis

MENINGOCOCCAL INFECTION

Meningococcal infection – an acute infectious disease that occurs in the form of nasopharyngitis, meningococcemia and purulent meningitis, less often with damage to other organs and systems.

Pathogen - Neisseria meningitidis

Source of infection – sick or carrier of bacteria

Transmission mechanism– airborne

Entrance gate – mucous membrane of the nasopharynx

1. Menigococcal nasopharyngitis– catarrhal inflammation of the mucous membrane and hyperplasia of the lymphoid apparatus of the posterior pharyngeal wall.

2. Meningococcemia(meningococcal sepsis)

- hemorrhagic rash with foci of necrosis in the center

- fibrin thrombi in the vessels of the dermis

Bilateral massive adrenal hemorrhage (Waterhouse-Friderickson syndrome)

Hemorrhagic rash

Waterhouse-Frederickson syndrome

Hyperemia

epiglottis

Hemorrhages in both adrenal glands

3. Meningococcal meningitis – diffuse purulent inflammation of the soft meninges

The most common and characteristic symptoms of meningitis

promotion

fever, headaches, neck muscle tension, photophobia, drowsiness, joint pain, forced position due to muscle tension.

Complications of meningitis:

Cerebral edema, hydrocephalus

Dilatation Dilatation of the fourth brain plumbing ventricle with pus on the ependyma

Dilatation of the third and both lateral ventricles of the brain

I.V.Davydovsky

During the Second World War, he headed the pathoanatomical service of the rear evacuation hospitals of the People's Commissariat of Health of the USSR.

The results of the study of combat trauma and its complications - a two-volume book “Human Gunshot Wound” (1952-54).

Sepsis - a special form of generalization of infection with loss of dependence of the general reaction of the body on the local focus, which was the source of generalization.