Scarlet fever is an acute infection with a predominant lesion of the oropharynx, severe intoxication and characteristic exanthema. The causative agent of scarlet fever is group A streptococcus, which is transmitted from the patient by contact or airborne droplets. The scarlet fever clinic includes general intoxication and fever, scarlet fever, regional lymphadenitis, crimson tongue, small-point rash followed by fine-scaly peeling on the skin. Diagnosis of scarlet fever is based on the presence of typical clinical symptoms.
A38 Scarlet Fever
Scarlet fever is caused by beta-hemolytic streptococcus group A, belonging to the genus of gram-positive, facultatively aerobic, ovoid bacteria Streptococcus. The reservoir and source of the causative agent of scarlet fever, as in the case of all streptococcal infections, is a person: a patient or a carrier. Scarlet fever patients pose the greatest danger in the first few days of the disease, the probability of transmission of infection completely disappears three weeks after the deployment of clinical symptoms. A significant percentage of the population (15-20%) refers to asymptomatic carriers of infection, sometimes people are the source of infection for months and years.
Streptococcus is transmitted by an aerosol mechanism (the patient secretes the pathogen when coughing, sneezing, talking) by airborne droplets or contact. If the pathogen gets into food products, it is possible to implement an alimentary transmission pathway. Infection is most likely when communicating closely with a sick person.
The natural susceptibility of a person to scarlet fever is quite high, the disease develops in persons infected with beta-hemolytic streptococcus (releasing erythrogenic toxin) in the absence of antitoxic immunity. The immunity formed after the infection is type-specific and does not prevent infection with another type of streptococcus. There is some seasonal dependence: the incidence increases in the autumn-winter period; as well as the connection with other respiratory streptococcal infections (angina, streptococcal pneumonia).
The entrance gate for the causative agent of scarlet fever is the mucous membrane of the pharynx, nasopharynx, sometimes (extremely rarely) of the genitals. It happens that bacteria enter the body through damage to the skin. In the area of the introduction of the pathogen, a local focus of infection with characteristic necrotic phenomena is formed. Microorganisms multiplying in the focus secrete toxins into the blood that contribute to the development of infectious intoxication. The presence of the toxin in the general bloodstream stimulates the expansion of small vessels in various organs and, in particular, the skin, which manifests itself in the form of a specific rash.
Antitoxic immunity is gradually formed, which contributes to the subsiding of signs of intoxication and the disappearance of the rash. Sometimes pathogens get into the blood directly, which leads to damage by microorganisms to other organs and tissues (lymph nodes, meninges, temporal bone tissues, hearing aid, etc.), causing purulent-necrotic inflammation.
Scarlet fever symptoms
The incubation period can last from a day to ten days. The disease begins acutely, there is a sharp increase in temperature, accompanied by signs of increasing intoxication: headache, muscle aches, weakness, tachycardia. High fever of the first days is often accompanied by increased mobility, euphoria, or vice versa: apathy, drowsiness and lethargy. Significant intoxication can provoke vomiting. Recently, the course of scarlet fever with moderate hyperthermia, which does not reach high numbers, has been increasingly noted.
When swallowing, soreness in the throat is noted, examination of the pharynx reveals pronounced hyperemia of the tonsils (much more intense than with angina), the arches of the tongue, the back wall of the pharynx, soft palate (the so-called “flaming pharynx”). At the same time, the hyperemia of the mucous membrane is clearly limited to the place of transition of the soft palate to the hard palate. Sometimes a clinical picture of follicular-lacunar angina develops: intensely hyperemic mucous membrane of the tonsils is covered with foci (often small, but sometimes large and deep) of plaque, mucopurulent, fibrinous or necrotic in nature.
At the same time, inflammation of the regional (anterolateral) lymph nodes develops: they increase somewhat in size, become dense to the touch and painful. The tongue, initially covered with a grayish-white coating, subsequently (on the 4th-5th day of the disease) acquires a rich scarlet-crimson color, papillary hypertrophy occurs. In severe cases, the lips are painted in the same color. As a rule, at this time, the symptoms of angina begin to subside. Attacks of a necrotic nature regress noticeably more slowly.
A characteristic small-point rash occurs on the first or second day of the disease. Against the background of general hyperemia, darker dots appear on the skin of the face and upper torso (and subsequently on the flexor surfaces of the arms, sides, inner thighs), thickening on the skin folds and in places of natural bends (elbow bend, groin, axillary fossa) and forming dark red stripes (symptom Pastia).
In some cases, there is a merging of the point elements of the rash into one large erythema. The rash on the face is characterized by localization on the cheeks, temples, forehead. There are no rashes in the nasolabial triangle, there is paleness of the skin (Filatov’s symptom). Rashes when pressed on them temporarily disappear. Due to the fragility of blood vessels, small hemorrhages may occur on the skin, in places subjected to friction or compression. Sometimes, in addition to scarlet fever, small papules, macules and vesicles are noted. In addition, there is a late manifestation of the rash (on the 3-4 day of the disease) or its absence.
As a rule, on 3-5 days from the onset of the disease, the patient’s condition improves, and the symptoms gradually subside, the rash pales and, by the end of the first or beginning of the second week, completely disappears, leaving a fine-scaled peeling on the skin (on the palms and feet – coarse-scaled). The severity of the rash and the rate of its disappearance vary depending on the severity of the disease. The intensity of peeling directly depends on the abundance and duration of the rash.
The extrabuccal form of scarlet fever occurs when the introduction of the pathogen occurred through damaged skin (in places of abrasions, wounds, surgical wounds). At the same time, a purulent-necrotic focus is formed in the area of damage, the rash spreads from the site of introduction, lesions in the pharynx are not observed.
In adults, there is sometimes an erased form of scarlet fever, characterized by minor intoxication, moderate catarrhal inflammation of the pharynx and a scanty, pale, short-term rash. In rare cases (also in adults), scarlet fever is extremely severe with the likelihood of developing toxic-septic shock: lightning-fast progression of intoxication, severe fever, development of cardiovascular insufficiency. Hemorrhages often appear on the skin. This form of scarlet fever is fraught with dangerous complications.
Purulent-inflammatory complications of scarlet fever (lymphadenitis, otitis media) and late complications associated with infectious-allergic mechanisms (carditis, arthritis, nephritis of autoimmune genesis) are most common.
The high degree of specificity of the clinical picture allows for a confident diagnosis during the survey and physical examination. Laboratory diagnostics: a general blood test – notes signs of bacterial infection: neutrophilic leukocytosis, a shift of the leukocyte formula to the left, an increase in ESR. As a specific express diagnosis, RKA is made, the pathogen is not isolated due to irrationality.
With the development of complications from the cardiovascular system, the patient needs to consult a cardiologist, conduct an ECG and ultrasound of the heart. If otitis occurs, an otolaryngologist examination and otoscopy are necessary. To assess the state of the urinary system, kidney ultrasound is performed.
Scarlet fever treatment
Treatment of scarlet fever is usually performed at home, patients with severe forms of the course are subject to hospitalization. Patients are prescribed bed rest for 7-10 days, a sparing diet (food of semi-liquid consistency) is recommended for the period of pronounced anginal symptoms, without forgetting about the balanced vitamin composition of the diet.
The drug of choice for the etiotropic treatment of scarlet fever is penicillin, which is prescribed for a course of 10 days. Macrolides and cephalosporins of the first generation (in particular: erythromycin and cefazolin) are used as reserve drugs. If there are contraindications to the use of the above drugs, it is possible to prescribe synthetic penicillins or lincosamides. In complex therapy, a combination of an antibiotic with an antitoxic serum is successfully used.
To sanitize the focus of infection, gargle is performed with a solution of furacilin in a dilution of 1:5000, infusions of medicinal herbs (chamomile, eucalyptus, calendula). In case of severe intoxication, glucose solutions or salts are infused, cardiac disorders are corrected with appropriate cardiological preparations (niketamide, ephedrine, camphor).
Modern medicine makes it possible to successfully suppress streptococcal infections, including scarlet fever, thanks to the use of antibiotics in the early stages of the disease. In the vast majority of cases, the disease has a favorable prognosis. Rare cases of severe course with the development of a toxic-septic form of the disease can cause complications. Currently, the disease, as a rule, proceeds favorably, although occasionally it is possible to meet with cases of toxic or septic scarlet fever, which are usually severe. Repeated disease occurs in 2-3% of cases.
General measures for the prevention of scarlet fever imply the timely identification of patients and carriers of infection, their proper isolation (at home or in a hospital), the implementation of quarantine measures (especially when detecting scarlet fever in kindergartens, schools, medical institutions). Patients are discharged from hospitals no earlier than on the 10th day after the onset of the disease, after which they are treated at home for another 12 days. Patients can return to the team no earlier than 22 days, subject to a negative bacteriological examination for the presence of the pathogen.
Children who have not previously had scarlet fever and have come into contact with patients are not allowed to kindergarten or school for 7 days after contact, adult contact persons are under supervision for 7 days, but without restrictions in work.