SCARLET .

Scarlet fever is an acute infectious disease, which characterized by symptoms of the general intoxication, angina and on the skin. The disease is known for a long time, but was described in group of other , accompanying with a rash. In 1554y. Sycilian doctor Ingrassias described this disease under the name of rossania, delimiting it from the . The more complete description of clinical manifestation of illness under the name of scarlet fever –the purple fever- was made by the English doctor Sidengham. Etiology. The causative agent of scarlet fever, according to the most researchers, is beta-haemolytic of the group A. Beta-haemolytic streptococci account for the majority of streptococcal diseases, although not all beta-haemolitic sreptococci are pathogenic. Classification of streptococci. 1. Haemolysis pattern. The first system for classification was based on the type of haemolysis the organism exhibited on blood agar (are distinguished alpha-, beta- and gamma- haemolytic streptococci). 2. Lancefield system. Determination of the antigenecity of a streptococcal cell wall carbohydrate called the C substance . 3. Determinants of pathogenecity. Pathogenic streptococci tend to produce a hyaluronic acid capsule and a surface called an M protein. A. . (1) M protein is the major virulence factor of group -haemolytic streptococci. a) The M-protein has antiphagocytic and anticomplement properties. It is also cytotoxic for neutrophils (in the presence of serum). b) The M-protein is strongly immunogenic and against type-specific M-protein are protective. However, because there are more than 80 antigenic types, development of a general is non feasible. (2) Protein F (fibronectin-binding protein) is an adhesion factor that, together with protein M, enables group A streptococci to bind to pharyngeal epithelial cells. (3) Protein G binds IgG through the Fc region (which is the wrong orientation for opsonization) and may hinder binding, thus preventing effective phagocytosis. B. Hyaluronic capsule. The capsule is not immunogenic (probably because bacterial hyaluronic acid is similar, if not identical, to human hyaluronic acid), but has antiphagocytic properties. C. C substance and cytoplasmic membrane antigens are believed to play a pathogenic role in the nonsuppurative sequelae of streptococcal infections. D. Exotoxins. (1) Erythrogenic toxins are only produced by lysogenized strains. These toxins act directly on the hypothalamus to exert their pyrogenic properties and they cause the rash characteristic of scarlet fever. (2) Exotoxin A, which is closely related to and perhaps to TSST-1, is a responsible for the systemic manifestations of group A streptococcus . (3) Exotoxin B, a cysteine protease, is responsible for tissue destruction in patients with . (4) Cardiohepatic toxin causes heart and liver failure. E. Haemolysins. (1) Streptolysin O. This oxygen-labile protein is responsible for the area of complete haemolysis seen around group A streptococcus colonies. It is also believed to be toxic to leukocytes. Streptolysin O is strongly immunogenic; the titration of antistreptolysin O antibodies is used diagnostically as an indicator of prior or recent streptococcal infection.

1 (2) Streptolysin S is oxygen-stable and nonimmunogenic. However, like streptolysin O, streptolysin S is haemolytic and cytotoxic. F.Spreading factors are enzymes that help streptococci to invade tissues by dissolving clots and destroying connective tissues. Proteins in this group include hyaluronidase, proteinases, streptokinase, and nucleases (e.g., streptodornase, a deoxyribonuclease). Most of those enzymes are immunogenic and the quantification of antibodies formed against then is used diagnostically to determine whether a patient has been infected in the recent past with group A streptococcus. Streptococci survive at low temperatures for a long time, are resistant to drying,die up to 56`c for 30 minute.In and sputum,on the subjects surrounding the patient they survive for months. Streptococci of A group are sensitive to ,especially to . The decisive role in occurrence of scarlet fever belongs to a level of antitoxic immunity of the child. It is considered that scarlet fever develops after infection with the -haemolytic streptococcus of the group A in the absence of antitoxic immunity. When persons immune to the toxin but having no antimicrobial immunity are infected, they develop angina, pharyngitis, asymptom infection and other signs of streptococcal infection. Epidemiology. Humans are the only reservoir of infection. The source of infection in scarlet fever are the patients with explicit or blurred form of illness and also the patients with any other form of streptococcal infection and carriers. The patient is infective from the first hours of the disease. The causative agent is expelled into the environment with the secretion of the mucous membrane of the fauces and nasopharynx; it may also be contained in the discharge of various open purulent foci (otitis, , purulent lymphadenitis, etc.). The patient is contagious during the whole period of the disease, which is connected with streptococcus discharge. The most important forms in the epidemiology of scarlet fever are the so-called formes frustes with an incomplete or weakly expressed symptom complex. These forms often escape diagnosis; the patients are not isolated and therefore serve as sources of infection. Forms that follow the course of common «vulgar» catarrhal or lacunar angina are of particular importance. The epidemiological significance of scarlatinal angina is great, because of the considerable difficulty in diagnosing its true nature. Epidemiological observations have demonstrated that healthy carriers serve as sources of infection, and that is supported by the fact of growing immunity among healthy children during an epidemic, i.e. the existence of latent immunization. Healthy carriers harbour the infective micro-organisms for only a short time; a healthy scarlatina carrier is supposed to be much less contagious than a patient or convalescent. A convalescent discharged with complications or catarrh of the fauces and nasopharynx is a great source of danger. In scarlet fever the causative agent is discharged from the patient's or carrier's organism mainly in secretion from the fauces and nasopharynx. Owing to this the aerial-droplet mechanism is the main way the infection is spread. Unlike such aerial-droplet infections as measles and , the possibility of aerial infection in scarlet fever would seem to exist only at relatively short distances from the patient. Infection can also occur through infected articles, or through an intermediary. The last depends on the known stability of the causative agent, i.e. on its ability to remain viable for some time. A particularly important role is played by objects of the environment that can become infected by the causative agent from the mucous membranes of the mouth and throat. Transmission of scarlet fever infection through objects, however, is of secondary significance in its epidemiology. Finally, the infection can be conveyed by yet another route, via infected food, chiefly through milk and dairy products (ice-cream, cream, etc.). This mode of infection, although very rare, may cause considerable sudden epidemic outbreaks. In degree of infectivity scarlet fever occupies a middle position among children's infectious diseases; its susceptibility index is 0,4 or 40, which means that an average of 40 out of 100 persons coming into contact with scarlet fever patients become infected. Susceptibility to

2 scarlet fever varies considerably with age. Children between two and six or seven years of age are mostly affected; the disease is rare among adolescents over 15 and in adults. The fall in the scarlet fever incidence with age is usually explained by specific immunity acquired through infection (in marked clinical or very mild atypical form) and carrier state (latent immunization). The well known, almost absolute immunity of babies under three months to scarlet fever cannot be explained by specific immunity acquired through mother's placenta. Even being in a constant and close contact with the nursing mother with scarlatina, infants of this age do not develop scarlet fever, thus showing complete insusceptibility to this disease, which is probably the result of the specific reactivity of the neonates. In scarlet fever, as in other aerial-droplet infections, a clear dependence on season is noted, rising regularly during the autumn and winter months (September-January), and falling in the summer. As in other aerial-droplet infections a periodicity of illness in scarlet fever is also noted, apart from the seasonal variations: epidemic upsurges are repeated every four to six years. Variations in the susceptibility of the population underlie this periodicity. The scarlet fever is distributed unevenly. The incidence of scarlet fever also depends on the climate; it is almost never encountered in the tropics and subtropics, but the causes of this have not been much studied. The high resistance to scarlet fever in the inhabitants of hot countries is possibly associated with abundant solar radiation and the great amounts of vitamins in their food. Social and home factors play a much greater role in raising the incidence of scarlet fever: housing conditions, migration, forms of contact between people, living conditions, general and hygienic level, etc. Pathogenesis. Development of disease with a characteristic clinical picture, peculiar to scarlet fever, is connected with toxic, septic and allergic influence of streptococcus. According to A.Koltypin, three principal components can be schematically distinguished in the pathogenesis of scarlet fever: toxic, infectious (septic) and allergic. They are closely interrelated, their distinction is, of course, rather artificial, and they are manifested in a different degree. In some cases toxic phenomena, and in others septic, predominate, in some cases there may be allergic waves and in others none. The portal of entry of streptococcus are mucous membranes of tonsils, fauces, less often the wound and burn surfaces. Getting on a mucous membrane or damaged skin, streptococcus causes the inflammatory changes on the place of introduction. The causative agent by the lymphatic ways and superficial vessels penetrates in regional lymph nodes. The toxic substances of -haemolytic streptococcus occur in blood, which influence on the cardiovascular, nervous and endocrine system. There are three distinct streptococcal pyrogenic exotoxins (SPEs): A,B and C, of which A and C are structurally similar. These toxins are responsible for the rash of scarlet fever (erythrogenic toxins) and stimulate macrophages to produce tumour necrosis factor, with all the resulting metabolic and immunological consequences. Toxic syndrome is characterized by symptoms of general intoxication, exhibiting by increase of body temperature, rash, headache, vomiting and by sympathetic mood of vessel changes. In the heaviest cases there are possible the haemodynamic disturbances with haemorrhage in the adrenal cortex, oedema of brain, dystrophic changes in myocard, lesions of the vegetative nervous system up to the picture of sympathicoparesis. The average duration of initial toxaemia is four days; as its protective reaction develops the organism loses its sensitivity to the toxin. The action of the streptococcus itself is thought to condition the development of the infectious (septic) component of scarlet fever, which is expressed in an inflammatory-necrotic process at the portal of entry, a septic condition, and complications of a septic order (purulent lymphadenitis, purulent otitis, sinusitis, septic metastases, etc.). The septic symptoms usually appear between the third and fifth day, often as the signs of toxaemia begin to subside. They may recur with new force (usually as a result of re-infection) in

3 the late stage of the disease (between the 15th and 25th days); recurrent angina, purulent complications and so on, develop. At the same time other late non-septic complications are encountered (diffuse , synovitis, secondary angina, and secondary non- purulent lymphadenitis). All these manifestations of the so-called second stage of scarlet fever develop on a background of allergic reconstruction of the organism. As already mentioned, given preliminary sensitization of the organism, signs of begin to develop from the very onset of the disease. Allergy can arise from the first days of disease, but it is the most expressed on 2-th and 3- rd weeks from the beginning of scarlet fever. Clinically allergic syndrome is displayed by various eruption on the skin, acute lymphadenitis, glomerulonephritis, myocarditis, synovitis. In result of transferred scarlet fever is developed the steadfast antitoxic immunity, common to the whole A group of haemolytic streptococci. It is kept lifelong. Antimicrobial immunity is less firm and type specific, i.e. it is formed only to that serotype of streptococcus, which caused the disease. In the children of the first six months of life there is a transplacentar antitoxic immunity, received it from the mother, earlier sick with scarlet fever. Therefore the children of this age practically are not fall ill with scarlet fever. Antitoxic immunity to the - haemolytic streptococcus is also created in result of “silent” immunization after other forms of transferred streptococcal infections. The peculiarity is that in the absence of antitoxic immunity in blood of child, any his type can cause the scarlet fever. At the same time, after contamination with -haemolytic streptococcus, presence of antitoxic immunity protects the child from scarlet fever, but thus there is other clinical forms of streptococcal infection (angina, , etc.). The early application of penicillin for treatment of scarlet fever patients promotes to fast disappearance of streptococcus from the organism and, thus obstacles in formation intense antitoxic immunity, in this connection there is probably repeated cases of scarlet fever. Classification. The clinical picture of scarlet fever varies considerably in severity and in the character of its symptoms.Scarlet fever is classified by Koltypin. The disease is divided by the type, severity and current. Depending on type, scarlet fever is defined as typical and atypical forms. To typical forms are concerned these forms which proceed with all characteristic for scarlet fever clinical symptoms: intoxication, angina and distinctive rash. Apart from the typical forms there are various atypical forms with deviations from their clinical picture. Hypertoxic form, so-called formes frustes (abortive form) and extrapharyngeal (extrabuccal) scarlet fever should be classed among the atypical forms. In extrabuccal forms of scarlet fever the poprtal of entry of infection is not the fauces, but damaged skin or mucose in various regions. The following variants can be distinguished according to the portal of entry and the mechanism of infection: a) burn, b) wound, or traumatic, c) surgical, d) puerperal, e) complicating various exposed purulent foci on the skin. The clinical picture and epidemiology of extrabuccal scarlet fever have the following features:a) absence of inflammatory changes in the fauces and accordingly, in the cervical lymph nodes; b) the presence of regional lymphadenitis in conformity with the portal of entry, c) rash making its appearance first near the portal of entry, d) relatively low contagiosity, since the infection is not transmitted by the aerial-droplet route. In the hypertoxic or fulminant form the symptoms of severe toxaemia progress with extreme rapidity. This form is usually fatal. A number authors distinguish the following forms of scarlet fever, according to the severity of its course: mild, moderately severe, and severe. Depending on the predominance of toxic or septic phenomena, the severe form is distinguished as toxic or septic. If both component are present, the scarlet fever is defined as mixed or toxicoseptic. In recent years severe toxic or severe septic forms are very seldom encountered. The parameters of severity of disease are determined by expression of toxic symptoms and local inflammatory changes in oropharynx.

4 Clinical features. The of scarlet fever averages from two to seven days. It may be curtailed to a day or even a few hours, or may be protracted to twelve days. Its onset is acute, almost sudden, and is manifested in a rapid rise of temperature attended with malaise,weakness, and tachycardia. General symptoms of toxaemia. In mild cases of scarlet fever toxaemia is expressed only as a temperature reaction, with a certain disturbance of the patient’s general condition and loss of appetite; sometimes there may be vomiting and increased tonus of the sympathetic nervous system. In severe cases these symptoms become more pronounced and may be accompanied with marked involvment of the central nervous system and severe cardiovascular disturbances. Height of the fever reaction is an index of the degree of toxaemia. The rise of temperature is usually abrupt, and may become high (39-400C) within the first few hours. Onset is also sometimes signaled by chilliness, and occasionally by shivering. The temperature has a tendency at first to rise, then fluctuates irregularly between the third and sixth days, and gradually falls to normal by the fifth to tenth day. But given complications high temperature may persist for a long time and its intensity and duration depend on their character. Vomiting is a frequent symptom of scarlet-fever toxaemia; it is the result of the action of toxin on the emetic centre. Repeated persistent vomiting is characteristic of severe toxaemia; diarrhoea is also not uncommon. Lesions of the central nervous system are characteristic, and are always present in severe toxic cases of scarlet fever.Persons with different types of the nervous system display a different reaction to the scarlatinal toxin: in some children the symptoms are mainly irritation, excitation, insomnia, delirium, and convulsions; other patients are adynamic, apathetic, and sleepy to the point of stupor. There are quite regular symptoms of affection of the vegetative nervous system, which have been studied in great detail by A.Koltypin and his school. The changes from the vascular system in the beginning of disease are characterized by prevalence tonus of the sympathetic nervous system (sympathicus phase): tachycardia (a pulse rate of 120 to 140 per minute), elevation of arterial pressure (110-140 mm Hg), white dermographism with a prolonged latent period (9-10 seconds) and a short apparent one (1-1,5 minutes). For healthy person the latent period is equalled 7-8 seconds and apparent one – 2,5-3 minutes. In severe toxaemia there may be a syndrome of paresis or paralysis of the sympathetic nervous system, with adynamia, marked , cyanosis, an absence of white dermographism, a very sluggish vasomotor reaction, low arterial pressure, thready pulse, and a weak or no reaction of the pupil to light. The sequelae on the fourth or fifth day are decreased tone of the sympathetic and increased tone of the parasympathetic nervous system (vagus phase), expressed in bradycardia, reduction of arterial pressure, pronounced white dermographism with a shortened latent period (5-7 seconds) and a prolonged apparent one (5-8 minutes). In this period of illness the heart dilates, heart sounds are diminished and muffled, and there is a systolic murmur at the apex. Electrocardiography usually indicates bradycardia and arrhythmia. These changes are accepted to treat as an «infectious heart». In their basis lay the extracardial influences and only in rare cases there is a lesions of heart. The disturbances from the cardiovascular system are usually kept during 2-4 weeks, then without leaving a trace disappear. The dynamic equilibrium of the vegetative nervous system is restored at the phase of convalescence. The rash is a most distinctive symptom of scarlet fever. Appearing first on the skin of the neck and the upper part of the body, it spreads rapidly over the whole body, face, and limbs. At first glance it seems that the whole skin is erythematous, but on closer examination the rash proves to consist of a dense mass of small points, bright pink or red in colour, more intense in the centre than on the periphery. The elements of the rash are distributed on a hyperaemic background. In some places (the lower part of the abdomen, groins, buttocks, and internal aspect of the extremities) they are particularly numerous, and in fusing create a picture of complete . Digital pressure produces a transient, rapidly disappearing, blanching. This vivid

5 vascular reaction of the skin is a favourable prognostic sign; in severe attacks of scarlet fever it is sluggish; hyperaemia is restored very slowly due to reduced tonus of the cutaneous vessels. The skin feels dry, and in some cases smooth, since the rash is not elevated above the surface of the skin; but at the height of the disease it usually feels rough as the elements become maculopapular. This is mainly noted on the extensor aspects of the limbs. The appearance of the patient's face is characteristic: the forehead and temples are covered with a minutely punctate pink rash; the cheeks are flushed, but the skin of the nose, lips and chin is pale. This pallor around the mouth and nose, described by N.Filatov, distinctly delimited by the nasolabial folds, is a typical sign of scarlet fever. In the flexures of joints, where rash is especially abundant, the folds of the skin are distinguished by a dark red, sometimes even slightly cyanotic, colour, which later takes on a brownish tinge. Thorough examination of the skin here (at the elbow and knee, in the armpits, and the anterior and posterior axillary folds) reveals minute petechiae, which are sometimes, especially when the rash is bright, quite profuse. When the rash is pale and its elements sparse, only individual petechiae are noted. Although of no prognostic significance, this sign is of some diagnostic value. The rash is almost always accompanied with itching, especially when it is abundant, and fresh scratches are therefore often seen on the patient's skin. Very rare cases of haemorrhagic rash have been described, characterized by numerous and extensive haemorrhages into the skin and mucous membranes. They are a sign of a very grave form of the disease. In mild attacks the rash fades in the course of two to four days, but persists in severe cases for six to eight days. In very mild cases it may disappear in a day, and even in a few hours. The rash fades gradually, losing its brightness and taking on a brownish tinge; after its disappearance the skin remains slightly pigmented, as if dirty. Pigmented striae also persist in the flexures of joints for several days. usually begins after, but sometimes before, the rash subsides. Scarlatinal desquamation is the result of a condition known as parakeratosis – imperfect formation of horn cells of the epidermis impregnated with exudate. It begins at the end of the first week, or the beginning of the second, and the brighter the rash, the greater the desquamation. Following a pale, sparse rash, desquamation is usually delayed and not pronounced; and not infrequently it does not occur at all (especially in children under two years of age). The peeling begins first on the neck, chest, ears, and pubis, and then spreads over the whole trunk and to the limbs. On the wrists and feet peeling begins from the back and sides or from the fingertrips, where separation begins as a fissure parallel to the free edge of the nail. The face and neck shed a fine powder; larger flakes peel from the trunk. The most typical form of desquamation is on the limbs, which occurs later; here the skin peels in large strips, the epidermis separating in large layers, especially coming off the palms and soles. The period of desquamation averages between two and three weeks, but can last as long as five or six weeks, depending on its intensity. Not uncommonly there is a repeated desquamation. Angina is a constant symptom of scarlet fever, absent only in the extrapharyngeal form. Typical is angina with an intense bright redness of the whole fauces and the soft palate, which is quite sharply delineated along the margin of the hard palate. During the first days a punctate enantema, or punctate haemorrhages, may be seen on the mucous membrane of the soft palate rather than overall redness. The changes in oropharynx are so brightly expressed, that they and till nowadays are designated, on expression of Filatov, as an «fire in fauces» or «flaming angina». The tonsils are enlarged and loose, and may be covered with films, which are usually of the same character as in common lacunar angina. In the lacunae there are easily detachable yellowish-white or greyish-white films that disappear quite quickly toward the end of the initial period.

6 Very typical of scarlet fever is the necrosis that develops usually on the third or fourth day. Necrotic angina is a typical constant symptom of the septic form of scarlet fever. It is characterized by the appearance on the tonsils, without association with the lacunae, of dirty- white patches of necrosis that tend to spread over their whole surface and, in severe cases, to the palatine arches, uvula, soft palate, and walls of the pharynx. At first necrotic angina is accompanied with marked pain on swallowing; later, even when necrosis persists for a long time, the pain eases considerably. Clearance of the fauces from necrosis proceeds slowly, and the more extensive and deeper the lesions, the slower is the process. The condition can last as long as two or three weeks; in connection with that fever of an irregular type usually persists for a long time. The incidence of necrotic angina varies depending on the severity of the scarlet fever and the incidence of its septic form. Angina is usually accompanied in scarlet fever with another quite constant symptom, that of cervical lymphadenitis. The superior cervical lymph glands, which enlarge from the very first day, become hard and tender on palpation. Lymphadenitis with marked inflammatory phenomena is classed as a complications. The tongue coated with white fur at the onset of the disease begins to clear on the second or third day; towards the fourth or fifth day it clears completely and takes on a characteristic appearance known as «strawberry tongue»: the tongue is bright red in colour with a crismon tinge, with swollen papillae protruding through the white fur and resembling raspberry. This symptom is the result of desquamative catarrh of the mucosa, and persists up to the ninth or tenth day, after which the tongue resumes its normal appearance. In mild attacks the picture of «strawberry tongue» is sometimes not very distinct or entirely absent. In the severe septic form, with extensive necrosis, it remains coated for a long time. Blood changes have certain characteristic features. Leucocytosis up to 10-109/l-30-109/l (from 10 000 to 30 000) and above, depending on the form, is found in the very first days. Neutrophil count rises to 60-70 per cent, and in severe cases even to 90 per cent; neutrophils display a nuclear shift to the left, to young forms and even to myelocytes. The degree of leucocytosis and neutrophilosis, and the extent of the nuclear shift, are in direct proportion to the severity of the disease, and are highest in severe septic forms. Eosinophil count, which begins to increase from the third day, sometimes rises to 15 or 20 per cent. It reaches a maximum at the end of the first week. An increase in neutrophil and subsequently eosinophil counts is typical of scarlet fever and aids diagnosis. The ESR is accelerated (20-50 mm an hour by Panchenkov's method), and the acceleration is especially marked in septic forms and when there are complications. Complications. Complications are very frequent and varied in scarlet fever, and are distinguished as early and late according to when they occur. Early complications develop in the initial period of the disease, and are the result of the toxaemia in streptococcal infection. Late complications are generally encountered during the third or fourth week, and are apparently allergic in origin; streptococci play an important role in most of them. The most common complications in young children are purulent processes like otitis, lymphadenitis, and so on. Nephritis and synovitis of allergic origin, on the contrary, are quite rare.In older children complications are less frequent but are more varied; they quite often develop nephritis, myocarditis, and synovitis. The incidence of complications, particularly of early ones, also depends on the severity of form of the disease and is greatest in severe septic and toxicoseptic scarlet fever. Cervical lymphadenitis. The cervical lymph nodes are always inflamed in scarlet fever and their moderate swelling is an almost constant symptom of the disease. When the inflammatory phenomena are sharply pronounced cervical lymphadenitis is classed as a .

7 Adenophlegmon or hard phlegmon develops almost exclusively in severe septic and toxicoseptic forms of scarlet fever, and is accompanied with infiltration of the cellular tissue around the lymph nodes, and of the skin, and muscles. Peritonsillar (quinsy) is the commonest complication of tonsillar sepsis. Otitis and . Inflammation of the middle ear, now usually catarrhal, develops in either the initial or the second, allergic stage of the disease. The infection can spread from the tympanic membrane to the mastoid process with resulting mastoiditis; but like otitis, mastoiditis may be of haematogenic origin. Inflammation of paranasal sinuses or sinusitis is a complication mainly occuring early in the septic form of scarlet fever.In later years these complications have become very rare. The introduction of penicillin therapy has considerably shortened the course of this complications. Septicopyaemia. When purulent complications develop (purulent lymphadenitis, adenophlegmon, purulent otitis, mastoiditis, sinusitis) there is a danger of general septicaemia or septicopyaemia. Synovitis. Serous aseptic inflammation of the joints is a rare complications of scarlet fever, which usually occurs, when it does, during the first or second week. Cardiac complications. Septic myocarditis may occur in severe forms of scarlet fever., but septic is rare. Endocarditis with a subsequent vitium cordis is mostly associated with rheumatism. Diffuse glomerulonephritis. A characteristic complication of scarlet fever is diffuse glomerulonephritis, arising during the second stage of the disease (mostly during the third or fourth week). The incidence of nephritis in scarlet fever used to be significant in the past (10 to 12 per cent), but now it is rare. Diagnosis. Recognition of scarlet fever should be based mainly on thorough clinical examination and observation of the patient in the light of the epidemiological data. Mild streptococcal is difficult to recognize clinically. However, a neutrophilia in the peripheral blood is a predictor of bacterial rather than viral etiology (with a sensitivity of 75%), and allows an early decision for antibiotictreatment to be made.Bacteriological techniques are of relative significance at present. Detection of a streptococcus, even of a serologically identified strain, does not confirm a diagnosis of scarlet fever, since this micro-organism may be found in the nasopharynx of patients without scarlet fever Laboratory identification of . 1.Chains of Gram-positive cocci growing on blood agar, plus beta-haemolysis, plus Lancefield group A antigen. 2.Rapid antigen detection in throat swabs. 3.Antibody detection: high or rising titres of antistreptolysin O, antihyaluronidase and /or antiDNAse. Among the auxiliary methods recommended for diagnosis of scarlet fever, the blanching test must be mentioned. The phenomenon is elicited as follows: 0,1 ml of serum obtained from a scarlet-fever convalescent or the same amount of therapeutic is injected intradermally to a patient with a rash suspected of being scarlatinal. The reaction is usually read in 12 to 20 hours; a positive result is indicated by the presence of a pale area (subsidence of the rash) around the point of injection. The Dick test, used dynamically, can also be of some assistance in retrospective diagnosis of scarlet fever. A change from positive to negative reaction in repeated tests favours a diagnosis of scarlet fever. But it should be remembered that in modern scarlatina the Dick test is often negative during the very first days of the disease. These auxiliary diagnostic methods are not almost used now.

Treatment. The hospitalization of scarlet-fever patients is carried out by clinical-epidemiological indications. The patients with the mild and moderately severe form of scarlet fever are treated in home

8 conditions. The hospitalization is necessary in the severe form of scarlet fever and when in home it is impossible to isolate the patient and to create necessary conditions for his treatment. The scarlatina department should preferably be occupied by patients who were delivered to the hospital within two or three days. If the number of patients is not great, patients delivered to the hospital within two or three days should be placed in one ward. Patients placed in the ward should be kept there until full recovery and should not be allowed to associate with patients of other wards. Food should be fluid or semifluid, mainly carbohydrates with an adequate vitamin content, vitamin C in particular. Antibacterial therapy. The treatment of choice is penicillin. Early and mild cases may respond to oral therapy with ampicillin, but established and severe infections can require inpatient treatment with intravenous benzylpenicillin. Suitable alternative drugs are and . Treatment of streptococcal . 1.Early and mild cases: oral ampicillin 250-500 mg 6 hourly for 10 days, or erythromycin in the same dosage and schedule. 2.Severe cases: benzylpenicillin 1,2-2,4 g 4-6 hourly. Penicillin and other antibiotics that are now used to treat scarlatina are mainly responsible for the mild course of this disease. Phenoxymethyl penicillin in tablets is especially effective in home treatment. The dose should be doubled as compared with parenteral one. Prolonged-action preparations (e.g. bicillin) should be preferred. Bicillin is given in a single dose of 20 000 U/kg intramuscularly. Antibiotics of prolonged action are especially convenient for home treatment. Corticosteroids (in combination with antibiotics) are recommended to treat grave toxic and toxico-septic forms of scarlatina. Prednisolone should be given in a dose of 1-1.2mg/kg daily; the dose should be gradually decreased in 2-3 days. The treatment should continue for 5-7 days. Disintoxication therapy is also necessary: intravenous infusion of colloidal solutions (polyglukin, neocompensan), 20 per cent glucose solution with strophanthin and vitamins, plasma substitutes and other measures. These methods should be used in various combinations depending on each particular case. Treatment of complications carry out on general rules depending on their character. In the purulent complications (otitis, lymphadenitis, sinusitis, etc.) antibiotics are prescribed. Symptomatic therapy are recommended: local thermal procedures (warm compresses, Sollux lamp irradiation, paraffin therapy), mercury-quartz lamp irradiation, UHF therapy. Surgical intervention is seldom necessary. It must be prompt, particularly in purulent-necrotic otitis, as with delay there is great danger of intracranial complications. Prevention. The specific preventive maintenance of scarlet fever does not elaborate. Immunization by the combined vaccine is not carried out owing to complexity, reactogenecity and insufficient efficacy. A scarlet-fever patient must be isolated whatever the severity of the disease. That also applies to patients with sore throat suggestive of scarlet fever. The isolation continues for at least ten days from the day of the onset of the disease, provided all signs of the acute period subside. Recovering children and adults who attend preschool children's institutions (and schoolchildren of the first two years) may be admitted to these institutions in 12 days after suspension of the isolation. These rules hold also for angina patients revealed in the scarlatina focus. Gamma-globulin has been used for prophylaxis of scarlet-fever contacts among children (3 to 5 ml). Rational and prompt application of the whole complex of antiepidemic measures outlined above can lead to successful control of scarlet fever.

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