Diphtheria — acute illness infectious nature, which poses a danger to human life. With diphtheria, inflammation of the upper respiratory tract develops, and an inflammatory process of the skin can also begin at the site where there are abrasions, inflammations and cuts.

However, diphtheria poses a danger to humans not by local lesions, but by general intoxication of the body and subsequent toxic damage to the nervous and cardiovascular systems. People have known about this disease since ancient times. The following names were attributed to diphtheria at different times: Syrian disease», « fatal throat ulcer», « croup», « malignant angina". As an independent nosological form a disease called "diphtheria" was isolated in the nineteenth century. Later it received its modern name.

The causative agent of diphtheria

The causative agent is a rod-shaped gram-positive bacterium Corynebacterium diphtheriae . It can be stored in the external environment for a long time, being in the dust and on the surface of objects. The source and reservoir of such an infection is a person who suffers from diphtheria, or who is a carrier of toxigenic strains. Most often, people with oropharyngeal diphtheria become sources of infection. The infection is transmitted by airborne droplets, but still in some cases it can also be transmitted through dirty hands or household items, linen, dishes, etc. The occurrence of diphtheria of the skin, genitals, eyes occurs due to the transfer of the pathogen through contaminated hands. Sometimes outbreaks of diphtheria are also recorded, which occur as a result of the multiplication of the pathogen in food. The infection enters human body mainly through the mucous membranes of the oropharynx, in more rare cases - through the mucous membrane of the larynx and nose. It is extremely rare that infection occurs through the conjunctiva, genitals, ears, and skin.

Features of diphtheria

Diphtheria is a disease that directly depends on the level of vaccination of the population. To date, periodic rises in the incidence are recorded, which occur with a poor level of vaccination. Currently, there is often a shift in the disease from childhood: adults suffer from diphtheria, especially those who, by virtue of their profession, have to intersect with a large number of people. With the deterioration of the epidemiological situation, the disease occurs in people in a more severe form and the number of deaths increases. However, in people who have previously received diphtheria vaccinations, the disease is mild and not accompanied by complications.

Symptoms of diphtheria

Duration with diphtheria is from two to ten days. There are several variants of diphtheria according to its clinical classification. The flow options for such forms are somewhat different. In most cases (approximately 90-95%), both children and adults develop oropharyngeal diphtheria . If this form of diphtheria develops, the symptoms are acute. The patient's body temperature rises, ranging from subfebrile to very high. It keeps for two or three days. There are signs of moderate intoxication organism. A person complains of headaches, a feeling of general malaise. His skin turns pale, his appetite decreases, periodically there is . When the patient's body temperature begins to subside, local manifestations of diphtheria, which are noted in the area of ​​​​the entrance gate of infection, may become more intense. In the oropharynx of the patient there is diffuse congestive hyperthermia, moderate swelling of the tonsils, arches and soft palate. A plaque appears on the tonsils, which is located in the form of a film or in separate islands. In the first hours of the development of the disease, fibrinous plaque looks like a jelly-like mass, later it looks like a cobweb-like film. But already on the second day of illness, the plaque becomes much denser, has a gray color and a pearly sheen. If you try to remove that plaque with a spatula, then the mucous membrane begins to bleed. At the same time, the next day, a new plaque will appear at the place where the film was removed from. In addition, in diphtheria, the symptoms are expressed by an increase and increased sensitivity . An asymmetric reaction or a unilateral process on the tonsils and an increase in regional lymph nodes is possible. Very rare currently registered catarrhal forms of localized oropharyngeal diphtheria . With this form of diphtheria, there are a minimum of symptoms. A person shows only slight discomfort in the process of swallowing, the mucous membrane of the oropharynx is small. In this case, diagnosis can be difficult. With the right approach to treatment, the disease is completely curable. Relatively rarely diagnosed common form of oropharyngeal diphtheria . If we compare it with a localized form, then the difference lies in the spread of plaque not only on the tonsils, but beyond them. With this form of the disease, a person also has a more pronounced and all the corresponding symptoms. At subtoxic form of diphtheria symptoms of intoxication of the body also occur. The patient complains about pain when swallowing, sometimes pain is also present in the neck. On the tonsils, painted in a purple-cyanotic color, a plaque is observed, which may slightly affect the uvula and palatine arches. There is also moderate swelling, soreness, and swollen lymph nodes. In addition, a feature of this form of diphtheria is the presence of local edema of the subcutaneous tissue over the regional lymph nodes. Common among adults toxic form of oropharyngeal diphtheria . It is characterized by a very rapid progression, a sharp rise in body temperature. With this form of diphtheria, pain may occur not only in the throat, but also in the abdomen, in the neck. In addition, some patients experience vomiting, agitation, delirium, delirium. A person's skin turns pale, there is a pronounced swelling of the oropharyngeal mucosa, diffuse hyperemia. The plaque spreads to the entire oropharynx, in the process of the development of the disease, the fibrin films coarsen. They don't last two weeks or more. If the patient has toxic diphtheria III degree , then swelling can appear on the face, on the back of the neck, on the back. There is a pronounced general toxic syndrome. If toxic diphtheria of the oropharynx is accompanied by a lesion of the larynx and nose, then such a disease is especially difficult to treat. The most serious form of diphtheria is hypertoxic form , which mainly develops in people suffering from alcoholism , , chronic hepatitis etc. In this case, the body temperature rises very quickly, there are sharp symptoms of intoxication of the body, tachycardia, a decrease in blood pressure, a weak pulse. Hemorrhages may occur in the skin and organs, fibrinous deposits are also saturated with blood. The patient develops very quickly, which can provoke a fatal outcome within one or two days after the onset of the disease. At diphtheria croup a manifestation of a localized form of the disease is possible, in which the larynx is affected, and a common one, when the trachea of ​​the larynx and bronchi are simultaneously affected. The manifestation of croup occurs in three successive stages − dysphonic , stenotic and asphyxia . For dysphonic stages characteristic rough cough, development. On the stenotic stage of the patient's voice, and the cough becomes silent. Gradually, the intensity of difficulty in breathing increases, manifested , tachycardia. AT asphyxia stage, the patient's breathing is clean, at first superficial, then rhythmic. The blood pressure drops, the pulse is thready, cyanosis increases. A person has convulsions, a violation of consciousness and, as a result, a lethal outcome occurs from asphyxia . In addition, there is diphtheria of the nose, eyes, genitals, ear. Such conditions in patients are recorded infrequently.

Diagnosis of diphtheria

When making a diagnosis, the specialist first of all pays attention to the presence of symptoms characteristic of diphtheria. If there is a membranous variant of the disease, then diphtheria is much easier to diagnose due to the presence of the fibrinous nature of the raids. At the same time, it is most difficult to diagnose the insular variant of oropharyngeal diphtheria, since the symptoms in this condition are similar to those coccal etiology . In the process of diagnosing toxic oropharyngeal diphtheria, it is important to differentiate the disease from necrotic sore throat , paratonsillar , . To make a diagnosis, laboratory research blood, as well as bacteriological studies. For this, the causative agent of the disease is isolated from the focus of the inflammatory process, after which its toxigenicity and type are determined.

Treatment of diphtheria

If the patient is diagnosed with diphtheria, then it is mandatory to immediately hospitalize him. Depending on how severe the form of the disease is, the duration of the process of inpatient treatment of the patient is determined. The main point in the treatment of diphtheria is the introduction to the patient antitoxic antidiphtheria serum . Its effect is to neutralize the toxin that circulates in the blood. Therefore, the action of such a serum is most effective if administered as early as possible. If there is a suspicion that the patient is developing a toxic form of the disease or diphtheria croup, then such serum should be administered immediately. A positive skin test result (called Shik auditions ) in a patient is a contraindication to the use of such serum in localized forms of diphtheria. In other cases, serum is administered, concurrently assigning antihistamines and glucocorticoids . This drug is administered intramuscularly and intravenously. Sometimes, in case of severe and prolonged intoxication, the drug may be re-administered. For detoxification treatment of diphtheria, crystalloid and colloid solutions are used intravenously. Sometimes, in especially severe cases, the introduction of glucocorticoids . The complex of treatment also includes vitamins that desensitize medicines. With toxic diphtheria II and III degrees, severe combined forms of the disease and hypertoxic diphtheria, plasmapheresis . In addition, in some forms of the disease (subtoxic, toxic), treatment is used . As auxiliary methods of treatment for diphtheria of the larynx, it is important to regularly ventilate the room where the patient lies, give him a warm drink, make steam inhalations, for which it is advisable to use soda, chamomile, eucalyptus. If there is a manifestation of hypoxia in patients with diphtheria, to eliminate this phenomenon, humidified oxygen is used through a nasal catheter, and the films are also removed with an electric suction. If the patient has a number of phenomena that indicate his serious condition, it is possible to use surgical intervention(carrying out tracheal intubation , tracheostomy ). It's over 40 per minute, tachycardia , hypercapnia , cyanosis , hypoxemia , respiratory acidosis . If a patient develops an infectious-toxic shock, his further treatment is carried out in the intensive care unit.

The doctors

Medications

Prevention of diphtheria

The main measure for the prevention of diphtheria is the coverage of the population with vaccination. It is also important to conduct regular epidemiological analysis, to predict the epidemic process of the disease in a particular area. To date, the main method of diphtheria control remains vaccination . Diphtheria vaccinations are children from the third month of life. Children will receive vaccinations against diphtheria three times, while the interval between vaccinations is 30-40 days. 9-12 months after vaccination, revaccination is carried out. Vaccinations against diphtheria are now also available for adults. First of all, vaccination is carried out for those who are included in the so-called high-risk groups. These are doctors, students, staff of schools and children's institutions, etc. When vaccinating adults, a vaccine is used, vaccinations are given every ten years until a person is 56 years old. Vaccinations against diphtheria are also given to those people who at one time had this disease. There are practically no contraindications for vaccination against diphtheria. At the same time, people who have not received vaccinations in due time and have been in contact with the patient must be immunized on an emergency basis. The effectiveness of diphtheria prevention depends directly on the vaccination coverage of the population, as well as on how high-quality the vaccine was used.

Complications of diphtheria

As complications of diphtheria, a number of serious conditions are distinguished: infectious-toxic shock , mono- and polyneuritis , myocarditis , toxic nephrosis , adrenal lesions . Such complications sometimes develop with localized diphtheria of the oropharynx, but most often they become a consequence of more severe forms diseases. Most often, complications occur with toxic diphtheria. The most common complication of toxic diphtheria is severe myocarditis .

Diet, nutrition for diphtheria

List of sources

• Diphtheria in children. Ed. V. V. Ivanova. - St. Petersburg: Polytechnic, 2000;
• Turyanov M. X. Diphtheria / M. X. Turyanov, N. M. Belyaeva, A. D. Tsaregorodtsev. - M., 1996;
• Pediatrics / ed. N. P. Shabalova. St. Petersburg: Spets-Lit, 2002;
• Chistyakova G.G. Diphtheria in adults: epidemiology and vaccine prophylaxis: Abstract of the thesis. dis. ... cand. honey. Sciences. - M., 2002.

Diphtheria is an acute infectious disease that poses a threat to human life.

With diphtheria, inflammation of the upper respiratory tract develops, and an inflammatory process of the skin can also begin at the site where there are abrasions, inflammations and cuts. However, diphtheria poses a danger to humans not by local lesions, but by general intoxication of the body and subsequent toxic damage to the nervous and cardiovascular systems.

People have known about this disease since ancient times. The following names were attributed to diphtheria at different times: "Syrian disease", "deadly ulcer of the pharynx", "croup", "malignant tonsillitis". As an independent nosological form, the disease with the name "diphtheria" was isolated in the nineteenth century. Later it received its modern name.

What it is?

Diphtheria is an acute infectious disease that is caused by a specific pathogen (infectious agent) and is characterized by damage to the upper respiratory tract, skin, cardiovascular and nervous systems. Much less often, diphtheria can affect other organs and tissues.

The disease is characterized by an extremely aggressive course (benign forms are rare), which, without timely and adequate treatment, can lead to irreversible damage to many organs, to the development of toxic shock, and even to the death of the patient.

The causative agent of diphtheria

The causative agent of the disease is a rod-shaped gram-positive bacterium Corynebacterium diphtheriae.

It can be stored in the external environment for a long time, being in the dust and on the surface of objects. The source and reservoir of such an infection is a person who suffers from diphtheria, or who is a carrier of toxigenic strains. Most often, people with oropharyngeal diphtheria become sources of infection. The infection is transmitted by airborne droplets, but still in some cases it can also be transmitted through dirty hands or household items, linen, dishes, etc.

The occurrence of diphtheria of the skin, genitals, eyes occurs due to the transfer of the pathogen through contaminated hands. Sometimes outbreaks of diphtheria are also recorded, which occur as a result of the multiplication of the pathogen in food. The infection enters the human body mainly through the mucous membranes of the oropharynx, in more rare cases - through the mucous membrane of the larynx and nose. It is extremely rare that infection occurs through the conjunctiva, genitals, ears, and skin.

How can you get infected?

The source of infection can be a sick person (one who has obvious signs of the disease) or an asymptomatic carrier (a patient in whose body there are Corynebacterium diphtheria, but there are no clinical manifestations of the disease). It is worth noting that during the outbreak of a diphtheria epidemic, the number of asymptomatic carriers among the population can reach 10%.

Asymptomatic carriage of diphtheria can be:

1. Transient - when a person releases corynebacteria into the environment for 1 to 7 days.
2. Short-term - when a person is contagious for 7 to 15 days.
3. Prolonged - a person is contagious for 15 to 30 days.
4. Prolonged - the patient is contagious for a month or more.

From a sick or asymptomatic carrier, the infection can be transmitted:

1. Airborne - in this case, corynebacteria pass from one person to another along with microparticles of exhaled air during a conversation, when coughing, when sneezing.
2. Contact-household way - this way of distribution is much less common and is characterized by the transmission of corynebacteria through household items contaminated by a sick person (dishes, bedding, toys, books, and so on).
3. Ingestion - Corynebacterium can be spread through milk and dairy products.

It should be noted that a sick person is contagious to others from the last day of the incubation period until the complete removal of corynebacteria from the body.

Can you get diphtheria again?

Relapses of diphtheria are possible. This disease leaves no permanent immunity behind.

After diphtheria in the blood, the titer of antibodies is high, which protect against re-infection. But gradually their level decreases. On average, recurrent diphtheria can occur after 10 years. However, the second time the disease is much easier. This is due to the fact that the body produces antitoxin faster and more efficiently.

Symptoms

Incubation period before the first symptoms of diphtheria in adults appear - from 2 to 10 days.

The course of the disease is subacute (that is, the main syndrome appears 2-3 days after the onset of the disease), however, with the development of the disease at a young and adult age, as well as with concomitant pathologies of the immune system, it may change.

diphtheria syndromes:

• syndrome of general infectious intoxication;
• tonsillitis (fibrinous) - leading;
• regional lymphadenitis (mandibular);
• hemorrhagic;
• edema of subcutaneous adipose tissue.

The onset of the disease is usually accompanied by a moderate rise in body temperature, general malaise, then clinical picture diverges according to the form of the disease.

1) Atypical form (characterized by a short fever for two days, mild discomfort and sore throat during swallowing, an increase in the maxillary lymph nodes up to 1 cm, slightly sensitive to light touch).

2) typical shape(quite noticeable heaviness in the head, drowsiness, lethargy, weakness, pallor of the skin, an increase in the maxillary lymph nodes from 2 cm or more, pain when swallowing):

• widespread(primarily common or developing from a localized one) - an increase in body temperature to febrile numbers (38-39 ° C), marked weakness, adynamia, pallor of the skin, dryness in the mouth, sore throat when swallowing of moderate intensity, painful lymph nodes up to 3 cm ;
• toxic (primarily toxic or occurring from a common one) - characterized by severe headache, apathy, lethargy, pale skin, dry oral mucosa, possible abdominal pain in children, vomiting, temperature 39-41 ° C, pain in the throat when swallowing, painful lymph nodes up to 4 cm, swelling of the subcutaneous fatty tissue around them, spreading in some cases to other parts of the body, difficulty in nasal breathing - nasal voice.

Degrees of edema of subcutaneous fatty tissue:

• subtoxic form (swelling of one-sided or parotid area);
• toxic I degree (up to the middle of the neck);
• toxic II degree (up to the collarbones);
• toxic III degree (edema passes to the chest).

In severe toxic forms of diphtheria, due to edema, the neck becomes visually short and thick, the skin resembles a gelatinous consistency (a symptom of "Roman consuls").

The pallor of the skin is proportional to the degree of intoxication. The plaques on the tonsils are asymmetrical.

• hypertoxic- acute onset, a pronounced syndrome of general infectious intoxication, obvious changes in the site of the entrance gate, hyperthermia from 40 ° C; acute cardiovascular failure, unstable blood pressure;
• hemorrhagic- impregnation of fibrinous deposits with blood, bleeding from the nasal passages, petechiae on the skin and mucous membranes (red or purple spots that form when capillaries are damaged).

If, in the absence of adequate treatment, body temperature returns to normal, then this cannot be unequivocally regarded as an improvement - this is often an extremely unfavorable sign.

There are rare diphtheria in vaccinated (similar to atypical diphtheria) and diphtheria in combination with streptococcal infection (no fundamental differences).

Diphtheria of other localizations

1. Ear diphtheria is a secondary pathology that develops when there is a focus of diphtheria infection in the body. The skin of the ear canal and the eardrum become inflamed, and a fibrinous coating appears on their surface.
2. Eye diphtheria is manifested by intoxication, unilateral or bilateral conjunctivitis, purulent yellowish-gray discharge. Often, fibrinous films appear on the surface of the hyperemic and edematous conjunctiva. The skin around the eyes becomes wet, the eyelids swell. Eye diphtheria occurs in one of three clinical forms - catarrhal, toxic or membranous.
3. In men with diphtheria, the genital organs are affected foreskin, and in women - the labia, vagina, perineum. Symptoms of the disease are swelling, hyperemia and cyanosis of the vulva, ulceration of the mucosa and off-white plaque.
4. In newborns, diphtheria infection can affect the umbilical wound.

Complications

Severe forms of diphtheria (toxic and hypertoxic) often lead to the development of complications associated with lesions:

1) Kidney (nephrotic syndrome) is not a dangerous condition, the presence of which can only be determined by urinalysis and blood biochemistry. With it, there are no additional symptoms that worsen the patient's condition. nephrotic syndrome completely disappears by the beginning of recovery;

2) Nerves - this is a typical complication in the toxic form of diphtheria. It can appear in two ways:

• complete / partial paralysis of the cranial nerves - it is difficult for a child to swallow solid food, he "chokes" on liquid food, double vision or eyelid droop;
• polyradiculoneuropathy - this condition is manifested by a decrease in sensitivity on the hands and feet (type of "gloves and socks"), partial paralysis on the arms and legs.

3) Symptoms of nerve damage, as a rule, completely disappear within 3 months;

• Heart disease (myocarditis) is a very dangerous condition, the severity of which depends on the time of the first signs of myocarditis. If problems with the heartbeat appear in the first week, AHF (acute heart failure) develops rapidly, which can lead to death. The onset of symptoms after the 2nd week has a favorable prognosis, as a complete recovery of the patient can be achieved.

Of the other complications, only anemia (anemia) can be noted in patients with hemorrhagic diphtheria.

Diagnostics

The first stage of diagnosis is the collection of anamnesis and examination of the patient. It is necessary to pay special attention to the condition of the cervical lymph nodes, as well as the presence of swelling of the neck. To do this, press on it with your finger for a few seconds, and then release it. If a hole appears in this place, which does not disappear immediately, then there is edema.

Investigations for which a person with suspected diphtheria is referred:

1. Donating blood for a general analysis. ESR and neutrophil levels increase significantly.
2. Urine for general analysis. This allows you to exclude kidney damage. The presence of a pathological process in the organs of the urinary system will be indicated by symptoms such as the appearance of protein in the urine, erythrocytes and renal cylinders.
3. Delivery of a smear from the nasopharynx. It is examined for the detection of bacteria in it. The results will be known after 5 days.
4. Conducting electrocardiography. This simple study allows you to evaluate the functions of the heart and detect deviations in its work in a timely manner.
5. Donating blood for biochemical analysis. Assessment of the functioning of the liver is carried out by the level of ALT, AST and bilirubin. Urea and creatinine provide information about the condition of the kidneys.

If required, the doctor will prescribe additional studies to the patient at his own discretion.

Dirty white film on the soft palate, a classic sign of diphtheria.

How to treat diphtheria?

Treatment of diphtheria is carried out only in the conditions of a specialized infectious diseases department, and the duration of bed rest and the period of the patient's stay in the hospital is determined by the severity of the clinical picture.

The main method of treating diphtheria is the introduction into the patient's body of antidiphtheria serum, which is able to neutralize the action of the toxin secreted by the pathogen. Parenteral (intravenous or intramuscular) administration of serum is carried out immediately (upon admission of the patient to the hospital) or no later than the 4th day of the disease. The dosage and frequency of administration depend on the severity of the symptoms of diphtheria and is determined individually. If necessary (the presence of an allergic reaction to serum components), the patient is prescribed antihistamines.

To detoxify the patient's body, various methods can be used:

• infusion therapy (polyionic solutions, Reopoliglyukin, glucose-potassium mixture with insulin, fresh frozen blood plasma, if necessary, glucocorticoids, ascorbic acid, B vitamins are added to the injected solutions);
• plasmapheresis;
• hemosorption.

With toxic and subtoxic forms of diphtheria, antibiotic therapy is prescribed. For this, patients may be recommended drugs of the penicillin group, erythromycin, tetracycline or cephalosporins.

Patients with respiratory diphtheria are recommended to frequently ventilate the ward and humidify the air, drink plenty of alkaline water, inhalation with anti-inflammatory drugs and alkaline mineral waters. With increasing respiratory failure the appointment of aminophylline, antihistamines and saluretics may be recommended. With the development of diphtheria croup and an increase in stenosis, intravenous administration of prednisolone is carried out, and with the progression of hypoxia, artificial ventilation of the lungs with humidified oxygen (through nasal catheters) is indicated.

Discharge of the patient from the hospital is allowed only after clinical recovery and the presence of a double negative bacteriological analysis from the pharynx and nose (the first analysis is carried out 3 days after antibiotics are discontinued, the second - 2 days after the first). Carriers of diphtheria after discharge from the hospital are subject to dispensary observation for 3 months. They are monitored by a local therapist or an infectious disease specialist from a polyclinic at the place of residence.

diet for diphtheria

It is recommended to add to the diet

It is recommended to exclude from the diet

soups on a weak meat or fish broth with mashed vegetables and cereals. yesterday's bread or dried. Well-baked pies with meat, cabbage, jam, no more than 2 times a week. meat - low-fat varieties, peeled from tendons. Preferably minced meat products, boiled or fried without a crust, sausages. porridge cereals on water or with the addition of milk. dairy products: cottage cheese, cheese, dairy products. Cream and sour cream are desirable to add to dishes. vegetables: boiled, stewed, baked in the form of cutlets, ripe tomatoes, finely chopped greens. confectionery: jam, marshmallow, marshmallow, caramel. butter and vegetable oil. boiled eggs (not hard boiled), in an omelet or fried without a crust. warm drink. Up to 2.5 liters of liquid.

milk soups, soups with peas or beans. fresh bread, pastry or puff pastry products. duck, goose, fatty meats, canned food, smoked meats. fatty, smoked, salted fish. cereals: legumes, barley, barley, corn. raw, pickled, salted vegetables. As well as garlic, mushrooms, radish, radish, sweet pepper. confectionery chocolate or with cream. cooking fat, lard.

When preparing food, it must be borne in mind that it is difficult for the patient to swallow. Dishes should be warm, semi-liquid consistency, preferably mashed.

Prevention

Specific prophylaxis of diphtheria:

1. The use of DTP vaccine from 3 months of age three times, with an interval of 1.5 months. And then in a year or 1.5 they carry out revaccination. When vaccinating and revaccinating, contraindications are observed: if there are contraindications to the use of DPT (whooping cough has been transferred, during primary vaccination - if for some reason it passes at the age of 4-6 years) - then ADS-anatoxin is used.
2. ADS-M is used for planned age-related revaccination (at 6 years, 17 years, and every 10 years for adults), for primary vaccination of the unvaccinated over 6 years old (2 vaccinations are given with an interval of 45 days, then revaccination after 9 months and after 5 years; then every 10 years). ADS-M is used for children with severe temperature reactions to ADS and DTP.

Diphtheria is a controlled infection. Active routine vaccination of the population plays an important role in the fight against diphtheria and is carried out according to the preventive vaccination schedule.

Nonspecific prophylaxis involves hospitalization of patients and carriers of diphtheria bacillus. Those who have recovered before being admitted to the team are examined once. In the outbreak, contact patients are monitored for 7-10 days with a daily clinical examination with a single bacteriological examination. Their immunization is carried out according to epidemic indications and after determining the intensity of immunity (using the serological method presented above).

Diphtheria - symptoms and treatment

What is diphtheria? We will analyze the causes of occurrence, diagnosis and treatment methods in the article of Dr. Alexandrov P.A., an infectious disease specialist with an experience of 12 years.

Definition of disease. Causes of the disease

Diphtheria(from the Latin diftera - film; pre-revolutionary - "disease of crying mothers", "disease of horror of mothers") - an acute infectious disease caused by toxigenic strains of diphtheria bacillus, which toxically affect the circulatory system, nervous tissue and adrenal glands, and also cause fibrinous inflammation in the area entrance gate (sites of infection). Clinically characterized by a syndrome of general infectious intoxication, maxillary lymphadenitis, tonsillitis, local inflammatory processes fibrinous.

Etiology

Kingdom - Bacteria

genus Corynebacterium

species - Corynebacterium diphteriae

These are gram-negative rods located at an angle V or W. At the ends there are club-shaped thickenings (from the Greek coryne - mace) due to volutin granules. There is a property of metachromasia - staining not in the color of the dye (according to Neisser - in dark blue, and bacterial cells - in light brown).

Contains lipopolysaccharide, proteins and lipids. The cell wall contains the cord factor, which is responsible for adhesion (sticking) to cells. Colonies mitis, intermedius, gravis are known. They remain viable in the external environment: under normal conditions, they remain alive in the air for up to 15 days, in milk and water they live up to 20 days, on the surfaces of things - up to 6 months. They lose their properties and die when boiled for 1 minute, in 10% hydrogen peroxide - in 3 minutes. Sensitive to disinfectants and antibiotics (penicillins, aminopenicillins, cephalosporins). They like nutrient media containing sugar (McLeod chocolate medium).

Highlights such pathogenic products as:

1) Exotoxin (toxin synthesis is determined by the tox+ gene, which is sometimes lost), which includes several components:

• necrotoxin (causes necrosis of the epithelium at the entrance gate, damages blood vessels; this leads to plasma exudation and the formation of fibrinoid films, since the thrombokinase enzyme is released from the cells, which converts fibrinogen into fibrin);
• true diphtheria toxin is an exotoxin (similar in action to cytochrome B, an enzyme of cellular respiration; it replaces cytochrome B in cells and blocks cellular respiration). It has two parts: A (an enzyme that causes a cytotoxic effect) and B (a receptor that promotes the penetration of A into the cell);
• hyaluronidase (breaks down hyaluronic acid, which is part of the connective tissue, which causes an increase in membrane permeability and the spread of the toxin outside the focus);
• hemolyzing factor;

2) Neuraminidase;

3) Cystinase (allows you to distinguish diphtheria bacteria from other types of corynebacteria and diphtheroids).

Epidemiology

Anthroponosis. Infection generator - a person who is ill various forms diphtheria, and a healthy carrier of toxigenic strains of diphtheria microbes. A possible source of infection for humans is domestic animals (horses, cows, sheep), in which the pathogen can be localized on the mucous membranes, cause ulcers on the udder, mastitis.

The most dangerous in terms of the spread of infection are people with diphtheria of the nose, throat and larynx.

Transmission mechanisms: airborne (aerosol), contact (through hands, objects), alimentary route (through milk).

A person who does not have natural resistance (resistance) to the pathogen and does not have the required level of antitoxic immunity (0.03 - 0.09 IU / ml - conditionally protected, 0.1 and above IU / ml - protected) is sick. After the disease, immunity lasts for about 10 years, then a re-disease is possible. The coverage of the population with preventive vaccinations affects the incidence. Seasonality is autumn-winter. When carrying out a full course of immunization against diphtheria in childhood and regular revaccination (once every 10 years), a stable intense immunity is developed and maintained, which protects against the disease.

Despite the successes of modern health care, the mortality rate from diphtheria at the global level (mainly underdeveloped countries) remains within 10%.

If you experience similar symptoms, consult your doctor. Do not self-medicate - it is dangerous for your health!

Symptoms of diphtheria

The incubation period is from 2 to 10 days.

The course of the disease is subacute (that is, the main syndrome appears 2-3 days after the onset of the disease), however, with the development of the disease at a young and adult age, as well as with concomitant pathologies of the immune system, it may change.

diphtheria syndromes:

• syndrome of general infectious intoxication;
• tonsillitis (fibrinous) - leading;
• regional lymphadenitis (mandibular);
• hemorrhagic;
• edema of subcutaneous adipose tissue.

The onset of the disease is usually accompanied by a moderate rise in body temperature, general malaise, then the clinical picture diverges according to the form of the disease.

Atypical form(characterized by a short fever for two days, mild discomfort and sore throat during swallowing, an increase in the maxillary lymph nodes up to 1 cm, slightly sensitive to a light touch);

typical shape(quite noticeable heaviness in the head, drowsiness, lethargy, weakness, pallor of the skin, an increase in the maxillary lymph nodes from 2 cm or more, pain when swallowing):

a) common(primarily common or developing from a localized one) - an increase in body temperature to febrile numbers (38-39 ° C), marked weakness, adynamia, pallor of the skin, dryness in the mouth, sore throat when swallowing of moderate intensity, painful lymph nodes up to 3 cm ;

b) toxic(primarily toxic or occurring from a common one) - characterized by severe headache, apathy, lethargy, pale skin, dry oral mucosa, possible abdominal pain in children, vomiting, temperature 39-41 ° C, pain in the throat when swallowing , painful lymph nodes up to 4 cm, swelling of the subcutaneous fatty tissue around them, spreading in some cases to other parts of the body, difficulty in nasal breathing - nasal voice.

Degrees of edema of subcutaneous fatty tissue:

• subtoxic form (swelling of one-sided or parotid area);
• toxic I degree (up to the middle of the neck);
• toxic II degree (up to the collarbones);
• toxic III degree (edema passes to the chest).

In severe toxic forms of diphtheria, due to edema, the neck becomes visually short and thick, the skin resembles a gelatinous consistency (a symptom of "Roman consuls").

The pallor of the skin is proportional to the degree of intoxication. The plaques on the tonsils are asymmetrical.

c) hypertoxic- acute onset, a pronounced syndrome of general infectious intoxication, obvious changes in the site of the entrance gate, hyperthermia from 40 ° C; acute cardiovascular insufficiency, unstable blood pressure joins;

d) hemorrhagic- impregnation of fibrinous deposits with blood, bleeding from the nasal passages, petechiae on the skin and mucous membranes (red or purple spots that form when capillaries are damaged).

If, in the absence of adequate treatment, body temperature returns to normal, then this cannot be unequivocally regarded as an improvement - this is often an extremely unfavorable sign.

There are rare diphtheria in vaccinated (similar to atypical diphtheria) and diphtheria in combination with streptococcal infection (no fundamental differences).

Other forms of diphtheria infection:

1. larynx (subfebrile condition - a slight increase in temperature; not pronounced syndrome of general infectious intoxication, first catarrhal period - Silent cough with sputum, with difficulty in both inhalation (stronger) and exhalation (less pronounced), changes in timbre or loss of voice; then stenotic period, accompanied by difficulty in breathing and retraction of labile places chest; further period of asphyxia- an excited state, accompanied by sweating, blue integuments and further replaced by respiratory depression, drowsiness, heart rhythm disturbances - can result in death);
2. nose (the temperature is normal or slightly elevated, there is no intoxication, first one nasal passage is affected with the manifestation of a serous-purulent or purulent discharge with hemorrhagic impregnation in it, then the second passage. Wetting and crusting occur on the wings of the nose, drying crusts may appear on the forehead, cheeks and chin area (possible swelling of the subcutaneous fatty tissue of the cheeks and neck in toxic forms);
3. eyes (expressed by edema and hyperemia of the conjunctiva of moderate intensity, grayish purulent discharge from the conjunctival sac of moderate severity. In the membranous form, there is a significant swelling of the eyelids and the formation of gray-white films that are difficult to remove on the conjunctiva);
4. wounds (long non-healing wounds with hyperemia of the edges, a dirty gray coating, infiltration of surrounding tissues).

Features for pharyngoscopy:

a) atypical (hyperemia and hypertrophy of the palatine tonsils);

b) typical (not pronounced redness with a bluish tint, membranous plaque, swelling of the tonsils. At the beginning of the disease, it is white, then gray or yellow-gray; removed with pressure, torn - after removal it leaves a bleeding wound. The film is dense, insoluble and quickly sinks in water, protrudes above the tissue.Little pain is characteristic, since there is anesthesia):

Diphtheria pathogenesis

Entrance gate - any area of ​​​​the integument (more often the mucous membrane of the oropharynx and larynx). Following the fixation of the bacterium, reproduction occurs at the site of introduction. Further, the production of exotoxin causes epithelial necrosis, tissue anesthesia, slowing of blood flow, and the formation of fibrinous films. Diphtheria microbes do not spread outside the focus, but the toxin spreads through the connective tissue and causes dysfunction of various organs:

Classification and stages of development of diphtheria

1. according to the clinical form:

a) atypical (catarrhal);

b) typical (with films):

• localized;
• common;
• toxic;

2. By severity:

• light;
• average;
• heavy.

3. By carrier:

• transient (once detected);
• short-term (up to 2 weeks);
• medium duration (15 days - 1 month);
• protracted (up to 6 months);
• chronic (more than 6 months).

4. By localization:

• pharynx (90% of occurrence);
• larynx (localized and widespread);
• nose, eyes, genitals, skin, wounds, combined.

5. With diphtheria of the pharynx:

a) atypical;

b) typical:

6. The nature of the inflammation:

signs	Localized form			Common the form
	catarrhal	island	membranous
symptoms infections	missing	minor weakness, mild headache	acute start, lethargy, moderate headache	acute start, strong headache pain, weakness, vomiting, pallor, dry mouth
temperature	37,3-37,5℃ 1-2 days	37,5-38℃	38,1-38,5℃	38,1-39℃
sore throat	minor	insignificant growing when swallowing	moderate, growing when swallowing	moderate, growing when swallowing
lymphadenitis (inflammation lymph nodes)	increase up to 1 cm feelings. on palpation	increase up to 1 cm or more feelings. on palpation	increase up to 2 cm painless	increase up to 3 cm painful
palatine tonsils	redness and hypertrophy	redness and hypertrophy, islets cobwebbed raids, easy filmed without bleeding	stagnant hyperemia, raids from pearl muddy shine, removed with pressure with bleeding	stagnant cyanotic hyperemia, edema tonsils, soft oropharyngeal tissue, filmy flying away abroad tonsils

Complications of diphtheria

• 1-2 weeks: infectious-toxic myocarditis (cardialgia, tachycardia, pallor, spreading of the borders of the heart, shortness of breath);
• 2 weeks: infectious-toxic polyneuropathy (III, VI, VII, IX, X);
• 4-6 weeks: paralysis and paresis (flaccid peripheral - paresis of the soft palate);
• infectious-toxic shock;
• infectious-toxic necrosis;
• acute adrenal insufficiency (pain in the epigastrium, sometimes vomiting, acrocyanosis, sweating, decreased blood pressure, anuria);
• acute respiratory failure (diphtheria of the larynx).

Diagnosis of diphtheria

Treatment of diphtheria

It is carried out in stationary conditions (mild forms can be unrecognized and treated at home).

The most effective start of therapy in the first three days of the disease. The regime in the hospital is boxing, bed (as there is a risk of developing heart paralysis). Terms for localized diphtheria - 10 days, for toxic - 30 days, for other forms - 15 days.

Diet No. 2 according to Pevzner at the height of the disease (mechanically and chemically sparing, full-fledged composition), then diet No. 15 (common table).

At the very first time, the introduction of antidiphtheria serum (i.m. or i.v.) after the test is indicated with medication:

• unburdened course - 15-150 thousand IU;
• at the risk of an unfavorable outcome - 150-500 thousand IU.

An integral part of the treatment is antibiotic therapy (penicillin, aminopenicillin, cephalosporin antibiotics).

Pathogenetic therapy includes detoxification, hormonal support if necessary.

The following groups of drugs can be used as symptomatic therapy:

• antipyretics at a temperature in adults over 39.5 ℃, in children over 38.5 ℃ (paracetamol, ibuprofen);
• anti-inflammatory and antimicrobials local action(tablets, lozenges, etc.);
• sedatives;
• antiallergic agents;
• antispasmodics.

Carriers are treated with antibiotics on a general basis.

Rules for discharge of patients:

• disappearance of the clinical picture of the disease;
• cessation of isolation of the pathogen (two negative cultures of mucus from the oropharynx and nose, performed no earlier than 14 days after normalization of the clinic with an interval of 2-3 days).

After discharge from the hospital, the final disinfection is carried out in the box.

Forecast. Prevention

The most important way to prevent severe forms of diphtheria infection worldwide is through vaccination. The primary course is carried out in childhood, then regular revaccinations are carried out in adulthood (every 10 years). Vaccination saves not from bacterial carriage, but from a toxin produced by the bacterium, which causes a severe clinical picture. In this light, it becomes clear the need to constantly maintain the protective level of antitoxic immunity, regularly revaccinate (in the Russian Federation - with the ADS-m vaccine).

General concepts of the transmission of diphtheria are necessary in order to prevent infection and competently build preventive (anti-epidemic) measures. Prevention of diphtheria involves specific(vaccination) and non-specific(sanitary and hygienic) measures that everyone needs to know.

Relevance of the issue

This infectious disease for many years was considered virtually eliminated. In works classical literature cases of death of artistic heroes are described, for example, Dr. Dymov, suffocating from diphtheria films. Throughout the 20th century, the incidence of diphtheria has steadily decreased - this became possible due to the introduction of mandatory vaccination.

The unconscious refusal to carry out routine vaccination in childhood, the lack of vaccinations already in adulthood, and many other points lead to the fact that diphtheria from a potentially controllable infection becomes an urgent problem again.

Compliance with even banal sanitary and hygienic rules that prevent the transmission of diphtheria infection can save more than one person.

Features of the causative agent of diphtheria

The causative agent of diphtheria infection is Corynebacterium diphtheriae. Currently, 3 of its variants are known - gravis, mitis and intermedius. Most experts believe that the disease caused by the gravis type is the most severe.

This stick does not have capsules and flagella, it has club-shaped thickenings at the ends, so it vaguely resembles dumbbells. The main danger that distinguishes the causative agent of diphtheria from other corynebacteria is the ability to produce exotoxin.

This toxic substance- one of the most powerful and dangerous not only for health, but also for the life of the patient. Toxin with a natural current spreads throughout the body, the most sensitive to its effects are the heart muscle, kidneys and adrenal glands, as well as the peripheral nervous system. Active substance exotoxin disrupts the structure of nerve fibers, which leads to disruption of their functions, the development of varying degrees of severity of paralysis and paresis.

Corynebacterium diphtheriae resistant to environmental factors. In the external environment (soil, water), the pathogen retains its activity for 2-3 weeks. On food (most often dairy) Corynebacterium diphtheriae can also persist for a long time.

The causative agent of diphtheria (any strain) quickly dies only under the influence of strong disinfectants. Boiling kills this microorganism only when exposed for a few minutes.

Epidemiology of diphtheria

Source of infection

The diphtheria infectious process belongs to the classical anthroponoses with an aerosol (aka drop-air) transmission mechanism. Anthroponosis is a variant of an infectious disease in which the source of infection (microbial agent) is only a living person.

In this case, there are several negative points. The causative agent of diphtheria can be isolated not only by a patient with a clinically manifest form of the disease, but also by the so-called healthy carrier. A person with symptoms of diphtheria is in an infectious diseases hospital, that is, isolated from other (healthy) persons.

A healthy carrier does not feel any discomfort and signs of ill health, therefore, leads a normal life, literally at every step infecting others.

Such a carrier is especially dangerous in children's groups, since children are most susceptible to this infectious disease. The duration of the release of the pathogen is calculated in days, sometimes it can last about 40-50 days. In the foci of diphtheria infection, the number of carriers is many times greater than the number of cases.

Given the stability of the pathogen, it is necessary to remember the presence of transmission factors.

Diphtheria is transmitted in the following cases, that is, by contact with certain transmission factors such as:

• tableware;
• toys;
• hygiene items;
• bed linen and towels;
• rarely - clothes, carpets, blankets.

Diphtheria is not transmitted through third parties, however, the presence of a healthy carriage and the resistance of the microbial agent to the action of environmental factors causes an almost constant circulation of the pathogen in the human population.

The incidence is highest in the cold season and in crowded conditions. The development of clinically manifest forms of the disease is facilitated by a variety of immunodeficiency states, as well as chronic inflammatory processes of the oropharynx and nasopharynx. Children of the first year of life are less susceptible to this infectious disease, since some protective antibody titer transmitted from the mother prevents the development of the disease.

How is diphtheria transmitted?

Modern medical sources indicate the following potentially realizable routes of infection with diphtheria:

• aerosol;
• contact household;
• air-dust

All variants of transmission routes involve certain life situations that are dangerous in terms of possible infection. In some cases, the probability of infection is low, in others, on the contrary, even a single contact is enough.

Diphtheria infection is not transmitted transmissibly and parenterally, that is, the patient's blood in this case does not pose any danger to others.

Aerosol transmission route

It is considered the leading and most dangerous in diphtheria infections. A patient with any form of diphtheria infection, namely with damage to the mucous membranes of the respiratory tract, sneezes and coughs intensively. With particles of secretion from its mucous membranes, the microbial agent enters the air and spreads with its natural current over a distance of several meters.

A person who does not wear a mask, in the process of talking with a sick person (or a carrier), receives a sufficiently large infectious dose Corynebacterium diphtheriae, which is quite enough for the development of a clinically manifest form of the disease.

Contact-household way of transmission

Relevant in a closed team or intra-family outbreak. If banal sanitary and hygienic measures are not carried out at the proper level - washing dishes with hot water and detergent, periodic wet cleaning, cleaning toys - the risk of infection increases as time passes.

This transmission route can also be realized in conditions when the carrier works, for example, in a children's team, is unaware of his own condition and infects others for a long time.

Air and dust

In fact, this transmission option is a violation of all known sanitary and hygienic norms and rules. If at least occasionally wet cleaning is carried out - in this case it is the current disinfection - then the diphtheria pathogen simply cannot be transmitted.

Features of immunity

After a disease, immunity is not developed to the pathogen Corynebacterium diphtheriae, but to its exotoxin. Thus, repeated cases of the disease that are caused by other variants of the pathogen are not excluded. An intense and universal immune response can only be achieved by following a preventive vaccination schedule.

The content of the article

Diphtheria- an acute infectious disease that is caused by toxigenic corynebacteria with an airborne transmission, characterized by diphtheritic or croupous inflammation with the formation of fibrinous films at the site of inoculation of the pathogen, and in some cases, toxic damage to the circulatory organs, nervous system, adrenal glands, kidneys.

Historical data on diphtheria

Epidemics of diphtheria have been known since the time of Hippocrates, and the first reliable description of the disease was made by Areteus in the 1st century BC. n. e. However, despite the prescription and ubiquity, as an independent nosological unit, the disease was isolated only in the twenties of the XIX century. French scientists P. Bretonneau, who gave her the name "diphtheria" (from the Greek. Diphthera - film), and A. Trousseau, who proposed the name "diphtheria".
The causative agent of diphtheria was discovered in 1883-1884 pp. E. Klebs and F. Loffler, the latter isolated a pure culture of bacteria. In 1884-1888 pp. E. Roux and A. Yersin obtained diphtheria bacillus exotoxin and studied its properties. The discovery in 1890 by the Russian scientist Orlovsky of an antitoxin in the blood of patients indicated the way to the creation of an antidiphtheria serum. it remedy, developed 1892-1894 pp. E. Roux in France, E. Behring in Germany and Ya. Yu. Bardakh in Russia, has significantly reduced mortality. N. F. Filatov and G. N. Gabrnchevsky were the first in Russia to use serum for treatment and convincingly proved its effectiveness. In 1912, V. Schick proposed a skin reaction to identify individuals susceptible to diphtheria. In 1923 p. G. Ramon proposed to carry out active immunization against diphtheria with toxoid (the toxin, under the influence of formalin and prolonged incubation in a thermostat, lost its toxic properties, but retained its antigenic properties).

Etiology of diphtheria

The causative agent of diphtheria, Corynebacterium diphtheriae, or Leffler's stick, belongs to the genus Corynebacterium. This is a motionless, gram-positive rod 1-8 microns long, 0.3-0.8 microns wide, does not form spores, often looks like a Roman numeral V. Corynebacterium has club-shaped thickenings at the ends - volutin grains (corune - mace). The causative agent of diphtheria - aerobe or facultative anaerobe - grows well on media containing blood or its serum, the optimum growth temperature is 36-37 ° C.
The main factor in the pathogenicity of the causative agent of diphtheria is exotoxin, which belongs to potent bacterial toxins and is second only to botulinum and tetanus.
The disease is caused only by toxigenic corynebacteria. The ability to toxin formation is a genetically fixed sign of the causative agent of diphtheria. Under the influence of bacterial viruses (phages) on their genome, non-toxigenic cultures turn into toxigenic ones. In addition to the toxin, diphtheria bacilli produce neuraminidase, hyaluronidase, necrotizing and diffuse factors. According to the nature of growth on telurite media and some biochemical properties, cultural and biological variants of the pathogen are distinguished - gravis, mitis, intermedins. The gravis type is the most toxigenic and virulent, but there is no definite correspondence between the type of Corinbacterium and the severity of the disease.
The causative agent is resistant to environmental factors. In a diphtheria film, droplets of saliva stuck to the walls of dishes, door handles, toys, it remains for 15 days, in water, milk - about 20 days. Tolerates drying well. At low temperatures, it is stored for 6 months without loss of pathogenic properties. Bacteria are sensitive to high temperatures (they die at 58 ° C), direct sunlight, disinfectants (chloramine, mercury dichloride - sublimate, carbolic acid, alcohol).

Epidemiology of diphtheria

The source of infection is patients with diphtheria (contagious from the last day of the incubation period until the 10-25th day of illness) and carriers of a toxigenic strain of the pathogen. Bacteriocarrier develops after an illness, as well as in healthy individuals. It is longer in those who suffer chronic diseases nasopharynx (pharyngitis, tonsillitis, adenoiditis, etc.). The infectiousness of patients is 15-20 times greater than that of bacteria carriers, but the latter, due to the large number and mass contacts, is the most frequent source of infection.
The main mechanism of infection is airborne. Due to the stability of the pathogen in the external environment, a contact route of transmission through objects, third parties is possible. In some cases, infection occurs through the alimentary route through infected products (milk, dairy products, etc.).
Susceptibility to diphtheria is low, the contagiousness index is 10-20%. Persons who do not have antitoxic immunity or its intensity is low (the content of antitoxin is lower than 0.03 AO in 1 ml of blood) get sick.
In connection with the vaccination of children, the age structure of the incidence has changed in the direction of its "growing up". In most cases, diphtheria affects adolescents and adults, which is explained by defects in immunoprophylaxis, unreasonable expansion of contraindications to prophylactic vaccinations, insufficient use of effective drugs diphtheria toxoid. Of certain importance is the absence of the so-called natural immunity of the population due to a decrease in 1960-1970 pp. circulation of the causative agent of diphtheria, as well as the preservation of the pathogenic properties of corynebacteria even when they spread among highly immune contingents.
Most cases of the disease occur in the autumn-winter period. By mass active immunization, there were periodic increases in the incidence (in 10-15 years). characteristic feature epidemic process Recently, there has been an increase in the incidence of diphtheria, adults are more likely to get sick in cities, and in rural areas, the incidence of children predominates. Antitoxic and antibacterial immunoglobulins play a major protective role in diphtheria immunity. In the absence of antibacterial antibodies in the blood serum, its protective properties are sharply reduced and a bacteriocarrier is formed.
Diphtheria occurs in all countries of the world. On all continents, unvaccinated children are more likely to get sick. Recently, there has been an increase in the incidence of diphtheria in Ukraine.
Diphtheria is a manageable infection. The main measure to ensure the protection of the population is the formation of its immunity. The disease disappears where vaccination with toxoid is carried out systematically and benignly.

Pathogenesis and pathomorphology of diphtheria

The entrance gates of infection are the mucous membranes of the palatine tonsils, nose, pharynx, larynx, genitals, conjunctiva, damaged skin, where the pathogen multiplies and produces a toxin. A high level of antitoxic immunity ensures the neutralization of the toxin in the body.
In this case, two options are possible:
a) diphtheria corynebacteria die and the body remains healthy,
b) due to the virulence factors inherent in the pathogen and the lack of local immunity, the microorganism survives, multiplies at the site of invasion and leads to the so-called healthy bacteriocarrier.
If there is no antitoxic immunity, the clinical picture of the disease develops. All clinical and morphological signs of the disease are associated with the action of the toxin. The toxin disrupts protein synthesis in cells, acting as a specific inhibitor of aminoacetyltransferase, an enzyme involved in the assembly of polypeptide chains from amino acids. Locally, exotoxin causes coagulative necrosis of the epithelium.
The toxin gradually penetrates deep into the tissues, enters the lymphatic and circulatory systems, causes local vascular paresis, and increases the permeability of the walls of small vessels in the lesion. Exudate rich in fibrinogen is formed in the intercellular space. With the participation of thrombokinase of necrotic tissue, fibrinogen is converted to fibrin, as a result of which a fibrinous plaque (film) is formed on the surface of the affected integument - a characteristic sign of diphtheria.
If the process develops on a mucous membrane covered with a single-layer cylindrical epithelium (larynx, trachea, bronchi), then only the epithelial layer undergoes coagulation necrosis, croupous inflammation develops, in which the film is formed loosely connected with the underlying tissue and can easily separate from it (sometimes in the form casts). When the process is localized on mucous membranes covered with stratified squamous epithelium (nose, pharynx, epiglottis, external genital organs), diphtheria inflammation develops when not only the epithelial cover, but also the connective tissue base of the mucous membrane is necrotic. Fibrinous plaque permeates the entire thickness of the mucous membrane, the film adheres tightly to it, the removal of plaque is accompanied by bleeding.
From the local focus, the toxin penetrates deep into the tissues through the lymphatic pathways, causing swelling of the mucous membranes, submucosal tissue, and regional lymph nodes. In toxic forms of the disease, exudate is formed in the intercellular and intermuscular spaces, which leads to swelling of the subcutaneous tissue.
Once in the blood, the toxin affects the circulatory and nervous system, adrenal glands, and kidneys. In the adrenal glands, foci of hemorrhages and destructive changes up to necrosis are detected. Strengthening the function of the adrenal glands in the first days of the disease is changed by their hypofunction to almost complete cessation of secretory function.
The circulatory organs are particularly affected. All forms of diphtheria are characterized by hemodynamic disorders of varying degrees, up to infectious-toxic shock. The deepest changes occur in the myocardium. They are characterized by degenerative rebirth muscle fibers up to complete myolysis and productive changes in the interstitial tissue. Deep violations of metabolic processes, in particular protein synthesis, lead to cell death with their replacement by connective tissue. Ganglion cells and nerve fibers of the intracardiac (intracardiac) nerve plexuses experience significant degenerative changes.
Diphtheria toxin is an acetylcholinesterase inhibitor. Its action on the nervous system leads to the accumulation of acetylcholine, which adversely affects the structures of the central and peripheral nervous system. Due to the increased activity of the parasympathetic nervous system, catastrophic disorders of the function of the circulatory organs and acute respiratory failure occur.
In the peripheral nerves and roots of the spinal nerves, multiple toxic parenchymal neuritis develops with a predominant involvement of the myelin and Schwann sheaths in the process, a non-sharp damage to the axons, which explains the reversibility of the process.
With toxic diphtheria, degenerative changes in the tubules of nephrons are observed with great stability, which are mainly due to the effect of toxins on the epithelium of the tubules. An important role in the pathogenesis of kidney damage is also played by the development of infectious-toxic shock (shock kidney), DIC in the acute period of the disease. In this case, the vessels of the renal glomeruli are predominantly affected. Perhaps the development of acute renal failure.
In the pathogenesis of diphtheria croup, in addition to mechanical causes (the formation of a fibrinous film), reflex spasm of the muscles of the larynx, swelling of its mucous membrane, especially under the vocal folds, is essential.
originality, clinical course toxic and hypertoxic forms of diphtheria due to non-specific sensitization of the body and the massive formation of toxin. Immunodeficiency and defective function play a role endocrine system.

diphtheria clinic

The classification of clinical forms is determined by the localization of the process and its severity. According to these signs, diphtheria of the pharynx (85-90% of cases), nose, larynx, trachea and bronchi, eyes, ears, external genital organs, skin (wounds) are distinguished. Combined forms are possible. According to the degree of intoxication, diphtheria is divided into non-toxic, subtoxic, toxic, hemorrhagic and hypertoxic, and according to the spread of plaque - into localized and widespread.

Diphtheria pharynx

The incubation period lasts from 2 to 10 days. The main signs of the inflammatory process are swelling of the mucous membranes, their unsharp hyperemia with a cyanotic tint (congestive). Fibrinous coating is dense, continuous, grayish-white in color, sometimes with a pearly tint, its surface is smooth, shiny. Characterized by an increase in plaque above the level of the mucous membrane (plus-tissue). Plaque is formed during the first 2-3 days: at first it looks like a translucent spider web, then it thickens (sometimes gelatinous), thickens, and when it is removed, bleeding of the mucous membrane (blood dew) is observed. Removed films do not dissolve in water and are not rubbed with a spatula. Characteristic features fibrinous plaques: dense consistency, formation of pectinate protrusions and folds, reappearance of the film in place of the removed one, tendency to spread on the surface of the mucosa. In recent years, hemorrhagic plaque saturation has been observed somewhat more often, some of its areas become dirty brown. There is a correspondence between the degree of local manifestations and intoxication. The more extensive the fibrinous plaque, the greater the intoxication.
The plaque disappears gradually - thinner and less from the edges, like ice that melts. It is also possible to reject it in the form of plates.
The catarrhal form of diphtheria of the pharynx is characterized by only slight edema and hyperemia with a cyanotic tint. Symptoms of intoxication are insignificant, there is no plaque on the tonsils. This form is recognized only by bacteriological examination.
The localized form is characterized by the formation of a typical fibrinous plaque that does not extend beyond the tonsils. Depending on its size, islet and membranous diphtheria are distinguished. With islet diphtheria, plaque has the form of islands of fibrinous layers, the size and shape of which varies from dotted and streaky to areas up to several millimeters in size, with membranous - plaque is larger in size, can cover the entire tonsil.
The onset of the disease, as a rule, is acute, the body temperature rises to 38-38.5 ° C, from the 2-3rd day it normalizes or decreases to subfebrile. Intoxication is moderate, there is a headache, malaise, loss of appetite, pallor of the skin. Pain in the throat when swallowing is weak, corresponds to the prevalence of the process on the tonsils. Characteristic is the formation of fibrinous plaque in the crypts and on the convex surface of the tonsils; Edema prevails over infiltration, which leads to a uniform increase in the tonsils, smoothing of their surface structure. Localization of the process, as a rule, is bilateral. Localized diphtheria of the pharynx refers to mild forms. In the case of timely administration of antidiphtheria serum, the patient's condition improves in a day, the plaque disappears on the 2nd-3rd day, and in the membranous form - on the 4th-5th day. Without specific treatment, the disease can progress and become widespread.
The common form is characterized by the spread of plaque beyond the tonsils to the palatine arches, uvula, and sometimes to the lateral and posterior walls of the pharynx.
The disease begins acutely, the body temperature rises to 38-39 ° C, after two or three days it decreases to normal or subfebrile, even in the case of progression of the pathological process on the mucous membrane. Symptoms of general intoxication are moderate: headache, weakness, anorexia, pallor of the skin. With a slight increase, regional pain becomes somewhat painful. The lymph nodes. Perhaps one-sided spread of plaque or the predominance of the process on the one hand. Compared to the localized form, plaque persists longer: with the timely administration of serum - within 3-6 days. If treatment is not carried out, it is possible to develop a more severe form (subtoxic, toxic) or spread the process to the larynx.
The toxic form of diphtheria of the pharynx is more often characterized by the rapid development of its inherent symptoms. Body temperature quickly reaches 39-40 ° C and is maintained for a longer period (3-5 days) than in localized and widespread diphtheria, but in the future it also decreases, despite the persistence of plaque. Symptoms of intoxication are significant: pallor of the skin, repeated vomiting, tachycardia, weakness. Sore throat when swallowing is more intense, but is not the main complaint of the patient. From the first hours there is a rapidly growing swelling of the tonsils, palatine arches, uvula, soft palate. Hyperemia of the mucous membrane is intense, with a cyanotic tinge. Sharply increased tonsils can close so that the posterior pharyngeal wall is not visible. Breathing through the mouth is difficult, the voice becomes nasal. A jelly-like (gelatinous) translucent film appears on the surface of the tonsils, against the background of which dense opalescent areas are revealed. Filmy raids quickly spread over the entire surface of the tonsils and beyond. There is a specific malty rotten smell from the mouth. Significantly increase and become dense, painful regional lymph nodes.
An important sign of toxic diphtheria is swelling of the subcutaneous tissue of the neck. It is always painless, of a doughy consistency, appears above the regional lymph nodes at the end of the first day of illness, sometimes on the second day, spreading down to the neck and chest. The skin in the edema area retains its usual staining. With jerky impacts, swollen tissues are shaken off, like jelly (jelly), which makes it possible to determine the boundaries of edema (a symptom of Nosov's jelly). Pressing in the edema area does not leave dimples. The prevalence of edema of the subcutaneous tissue corresponds to the degree of intoxication, therefore it is a criterion for the severity of toxic diphtheria: edema over the regional lymph nodes is regarded as a subtoxic form, up to the middle of the neck - toxic I degree, up to the collarbone - II degree, below the clavicle III degree.
Other variants of toxic diphtheria of the pharynx are rare and are particularly malignant. In patients with a hypertoxic (fulminant) form, in addition to a rapidly progressing local process, very severe intoxication is observed from the first hours (an increase in body temperature to 40-41 ° C, repeated vomiting, delirium, convulsions). Catastrophically accrue hemodynamic disorders (pallor of the skin, acrocyanosis, thready frequent pulse, deafness of heart tones, a sharp decrease in blood pressure). The patient dies in the first 2-5 days of illness with signs of infectious-toxic shock II-III degree.
The hemorrhagic form is characterized by a syndrome of toxic diphtheria II-III degree in combination with manifestations of disseminated intravascular coagulation. Its first sign is hemorrhages at the injection sites and bleeding of the mucous membranes of the nose and pharynx. Fibrinous films penetrate the blood, become brown, and subsequently black. There is bloody vomiting, bleeding gums, hemorrhages in the skin, hematuria. Death occurs on the 4-7th day with signs of progressive circulatory failure.
The gangrenous form develops against the background of hemorrhagic diphtheria. With it, gangrenous decay occurs in the throat under the influence of putrefactive bacteria.
A blood test revealed neutrophilic leukocytosis, thrombocytopenia, increased ESR.

Diphtheria of the larynx

With the localization of the process in the respiratory tract, diphtheria croup develops. Croup is an acute laryngitis or laryngotracheitis accompanied by stenosis of the larynx, manifested by a hoarse voice, barking cough and inspiratory dyspnea. On the mucous membrane of the epiglottis, scoop cartilage, vocal cords, subglottic space appears edema, hyperemia, fibrinous films are formed.
Laryngeal diphtheria is more common in children aged one to five years. Its main symptoms are: hoarse voice, rough barking cough, stenotic breathing. Gradual-onset and staged development of these three symptoms without a sharp violation of the general condition in the first days of the disease, against the background of subfebrile or normal body temperature, is characteristic. The first stage (catarrhal manifestations) is characterized by two main symptoms - dysphonia and a loud barking cough. Laryngoscopy reveals swelling of the epiglottis. This stage lasts 1-3 days and passes into the next stage - the stage of stenosis lasting from several hours to 2-3 days. At the same time, the voice and cough become silent (aphonia), the third sign of croup appears - stenosis. Noisy stenotic breathing gradually increases with increased and difficult inhalation, sharp retraction of the compliant parts of the chest (supraclavicular, subclavian, jugular fossa, intercostal spaces, epigastric region). The cause of retraction is negative pressure in the chest cavity due to insufficient air supply to the lungs and their incomplete expansion due to narrowing of the glottis. The latter is due to edema of the mucous membrane of the larynx, the presence of fibrinous films and spasm of the muscles of the larynx.
At the beginning of the stenotic stage, the lack of air is insignificant and the child remains calm, but oxygen starvation develops further, the patient becomes restless, rushes about, gets up, the auxiliary respiratory muscles (sternocleidomastoid, drabparts) noticeably tense, cyanosis appears, shallow breathing, paradoxical pulse - dropping out pulse wave at the height of inhalation (inspiratory asystole of Rauchfus). This is a consequence of a significant negative pressure in the chest during inspiration, which leads to aortic distension, prevents the heart from emptying during systole and the movement of blood into the peripheral vessels.
The appearance of a paradoxical pulse is a sign of the transition of the stenotic stage to the stage of asphyxia and one of the indications for primary intubation (tracheotomy). Respiratory failure increases, cyanosis of the nasolabial triangle increases. Breathing in the lungs is bad. Decompensation of the activity of the circulatory organs develops: tachycardia, dilatation of the heart, signs of stagnation in the pulmonary circulation. If intubation or tracheostomy is not done at this time, asphyxia develops. The lips, the tip of the nose, the nail bed and the mucous membrane of the mouth become cyanotic, the face turns pale, the skin is covered with sweat. The respiratory center is depressed, the patient's strength is exhausted, he lies calmly in bed, shortness of breath decreases, involvement of the compliant areas of the chest disappears. Despite the apparent decrease in the signs of stenosis, the child develops general cyanosis, muscle hypotension, hypothermia, dilated pupils, and no reaction to injections. Pulse is fast, thready, blood pressure is low. Consciousness is clouded or fainting, convulsions due to cerebral edema are possible. Breath sounds are barely audible in the lungs. The appearance of bradycardia precedes cardiac arrest. In most cases of laryngeal diphtheria, general intoxication is moderate. Disorders of the function of the circulatory organs are caused by hypoxia. Death comes from asphyxia.
The above development of symptoms occurs only with delayed treatment or its absence. The introduction of serum in the catarrhal or initial stage of stenosis prevents the progression of the croup.
Already after 12-18 hours, the signs of stenosis gradually decrease, the cough becomes softer, becomes wet, then stops. At this time, a sudden development of asphyxia is possible due to obstruction of the airways by torn films. Voice long time remains silent or hoarse and normalizes 4-6 days after the disappearance of the stenosis.
Features of laryngeal diphtheria in adults are the possible absence of a characteristic cough and signs of stenosis, when the only symptom1 may be hoarseness. In such cases, it helps to establish the diagnosis of laryngoscopy. Failure to take these features into account can lead to an unfavorable course of the disease, when the process (film formation) spreads to the trachea, bronchi (descending croup), and the diagnosis is established late.

Nasal diphtheria

Nasal diphtheria is observed more importantly in children early age. Symptoms of general intoxication are almost not expressed, body temperature is subfebrile or normal. At first, the lesion may be unilateral. Due to mucosal edema, the nasal passage narrows, slight serous-bloody or serous-purulent discharges appear, irritating the upper lip and skin near the nasal openings. Erosions, ulcers covered with bloody scabs (catarrhal-ulcerative form), films (membraneous form) appear on the nasal septum. Films can spread to the mucous membrane of the paranasal sinuses. Sometimes on the upper lip, cheeks, chin, the skin becomes macerated, ulcers and crusts are found with a dense infiltrated base, which is a manifestation of skin diphtheria caused by infection from the primary focus.
diphtheria eye characterized by the presence of a fibrinous film on the hyperemic conjunctiva of the eyelids and their significant edema, serous, purulent or purulent-bloody (serous-bloody) discharge. First, one eye is affected. Inflammatory process upper eyelid more distinct than the lower one (Bogdanov's symptom). Perhaps this is due to the lysozyme of the lacrimal fluid, which has a bactericidal effect on the bacterial flora of the conjunctiva of the eyelids, especially the lower one. Allocate croupous diphtheritic and catarrhal forms of diphtheria of the eyes.
The croupous form is characterized by films on the conjunctiva of the eyelids, easily removed, slight soreness and the absence of photophobia. The cornea is not affected, there is no intoxication.
With the diphtheritic form, the edema of the eyelids is expressive and firmer, the films adhere tightly to the underlying tissues, often spreading to the eyeball and cornea. Serous-bloody discharge from the eyes further becomes abundant, purulent. Vision is almost always reduced, up to its complete loss due to panophthalmitis. General disorders in this form are manifested by low body temperature, adynamia, pallor.
The catarrhal form is clinically difficult to distinguish from other types of conjunctivitis and is diagnosed only on the basis of the results of a bacteriological study, epidemiological data and the effectiveness of serotherapy.
Diphtheria of the external genitalia characterized by severe swelling of the labia majora and minor, hyperemia with a cyanotic tinge, the presence of films and (or) ulcers on the mucous membrane, covered with a dirty gray coating. Inguinal lymph nodes are enlarged, painful. There are localized, widespread and toxic forms. With a common form, the process covers the skin of the external genital organs, the perineum around the back. The toxic form is characterized by swelling of the genital organs (I degree), subcutaneous tissue of the inguinal regions and thighs (II degree).
Skin diphtheria (wounds) develops when the integumentary epithelium is damaged. It is characterized by hyperemia, hemorrhagic spots, pustules, crusts, fibrinous films, swelling of the skin. Distinguish membranous, ulcerative membranous and toxic forms. A variety (very liquid) of diphtheria of the skin is the defeat of the umbilical wound in newborns.
diphtheria eye, genital organs and skin often develops secondarily, in combination with diphtheria of the pharynx or nose. Diphtheria of the middle ear and oral mucosa belongs to very rare forms.
Features of the modern trend. In recent years, the course of diphtheria is characterized by some features that are not inherent in the classical picture of the disease: an acute onset, a significant increase in body temperature (up to hyperthermia), especially in the early days; strong, the prolonged sore throat; the density of edema of the subcutaneous tissue in toxic diphtheria of the pharynx; hemorrhagic syndrome of varying degrees - from hemorrhagic impregnation of raids to nosebleeds and hemorrhages in the subcutaneous tissue with a toxic form; the appearance of complications from the nervous system in the long term (4-5 weeks of illness). Predominantly older children are affected school age and adults. In most cases, diphtheria of the pharynx is observed, which has a severe course with the development of toxic forms. Toxic diphtheria more often than before, begins acutely. The prevalence of the local process in toxic diphtheria of the pharynx II-III degree has decreased. This is also manifested in the increase in the predominantly unilateral process in the pharynx, which is accompanied by asymmetric swelling of the mucous membrane, which may be the cause of the erroneous diagnosis of paratonsillar abscess.
In the vast majority of those vaccinated, diphtheria is characterized by a mild, sometimes abortive course. The localized form of diphtheria of a pharynx is more often observed. Quite rarely, toxic forms develop. In children with incomplete vaccination, full-fledged immunity is not formed, on the contrary, hypersensitivity to diphtheria toxin occurs. When infected, such children develop toxic diphtheria with a rapid course, even more severe than in unvaccinated.
The carriage of the causative agent of diphtheria can be short-term (2 weeks), medium-term (1 month), protracted and recurrent. Longer carriage is observed in persons with chronic inflammatory processes of the nasopharynx. In many carriers, in addition to minimal local changes, ECG changes are detected, which makes it possible to think that carriage in diphtheria is the most mild form infectious process.

Complications of diphtheria

The most typical are complications from the circulatory organs (myocarditis), peripheral nervous system (polyneuritis) and kidneys (nephrosonephritis), which is taken into account in retrospective diagnosis. They are associated with specific intoxication, occur, as a rule, with toxic forms, in the case of delayed treatment with antidiphtheria serum.
Myocarditis- often a formidable complication. In patients with toxic diphtheria II-III degree, it develops in 80-100% of cases and becomes almost the only cause of death. As a rule, the development of myocarditis begins from the 6-8th day of illness. Death is possible in the 2nd or 3rd week. The patient develops weakness, severe weakness, pallor, dizziness, palpitations. The pulse is frequent, soft, arrhythmic, tachycardia can reach 200 in 1 min. With the defeat of the sinus node, on the contrary, there is a sharp bradycardia (up to 50-30 per minute). Significantly and rapidly expand the boundaries of the heart, appears systolic murmur over the apex, deafness of heart tones. Many patients have various cardiac arrhythmias (pendulum-like rhythm, extrasystole, gallop rhythm). Arterial pressure decreases. The liver enlarges and thickens. An unfavorable prognostic sign, indicating an irreversible decompensation of the activity of the heart, is Botkin's "fatal" triad: vomiting, abdominal pain and gallop rhythm (embryocardia, or pendulum heart rhythm). Vomiting is associated with cerebral hypoxia, abdominal pain is due to stretching of the liver capsule with its rapid increase, heart rhythm disturbances are caused by damage to the conduction system of the heart. The ECG shows signs of myocardial damage, blockade of the atrioventricular bundle, or complete atrioventricular blockade. In this state, most often in full consciousness, the patient dies from heart paralysis. Mild and moderate forms of myocarditis develop less rapidly and are not accompanied by acute heart failure. Changes on the ECG reflect damage to the contractile myocardium without being drawn into the process of the conduction system of the heart. On the 25-30th day of the disease, recovery occurs.
A complication of the nervous system is multiple toxic parenchymal neuritis (polyneuritis). The nerves located near the localization of the primary diphtheria process, as well as the two upper cervical sympathetic nodes and the autonomous nodes of the heart, are more severely affected. The frequency of polyneuritis in patients with diphtheria has recently increased to 25%. More often this complication develops in adults. According to clinical signs, the polyneuropathic syndrome in diphtheria is mixed, there are sensory, motor and vegetative disorders. Symptoms of damage to the autonomic system (acrocyanosis, hyperhidrosis, increased sensitivity of the extremities to cold) appear during the entire period of the disease. Peripheral paralysis usually develops on the 2nd-3rd week, and in recent years - on the 4th-5th and later. Paralysis is characterized by all signs of peripheral: hypotension and muscle atrophy, the disappearance of tendon reflexes. More often, not complete paralysis is observed, but paresis, which is sometimes not diagnosed in time.
Characteristic sequence of development of a neurological syndrome.
First, bulbar disorders appear in patients in the form of paralysis or paresis of the soft pidnebinnia Gm of the muscles of the pharynx due to damage to the glossopharyngeal and vagus nerves. Clinically, this is manifested by a nasal voice, difficulty in swallowing, tickling while eating, pouring liquid food through the nose, drooping of the soft palate and its immobility during phonation, and a decrease or absence of the pharyngeal reflex.
In the case of accommodation paralysis (damage n. ciliares), patients do not distinguish objects at close range, but distant objects see well, when reading the letters merge in them.
Relatively rarely, strabismus (n. abducens), eyelid prolapse (n. oculomotorius), facial asymmetry (n. facialis) may appear. Damage to the cranial nerves is especially characteristic of early paralysis, which develops between the third and eleventh days of illness.
Subsequently, a picture of polyneuritis with a lesion of the distal extremities joins. Movement disorders in lower limbs precede and may be more pronounced than in the upper ones. Tendon and periosteal reflexes sharply decrease (extinguish), strong pain sensations disappear. Later it turns out to be a polyneuritic type of sensitivity disorder - a syndrome of gloves and socks. Musculo-articular sensitivity is often suppressed. Very rarely, paralysis develops according to the type of Landry's descending paralysis with dysfunction of the respiratory muscles and a significant boulevard syndrome. In some cases, Guillain-Barré-type polyradiculoneuritis develops on the 4-5th week with protein-cell dissociation in the cerebrospinal fluid. muscles. In the occurrence of late polyneuritis and polyradiculoneuritis, the leading factor is autoimmune (autoallergic) reactions. One of the causes of autoimmune reactions is the breakdown of myelin with the formation of substances with high antigenic properties.
In most cases, the prognosis of diphtheria polyneuritis is favorable. After a few weeks, the function of wandering and oculomotor nerves is being restored. Paresis of the arms and legs undergo reverse development for a long time - from 2-3 to 4-6 months. Residual manifestations of limb paresis can be stored for a year or more. The early period of polyneuropathies is very dangerous, because due to damage to the cardiac branches of the vagus nerve, sudden cardiac arrest or severe aspiration pneumonia associated with swallowing disorders is possible. The prognosis worsens dramatically in patients with phrenic nerve paresis. With the development of complications from the nervous system, mortality is 8-15%.
Nephrosis develops in the acute period of the disease, characterized by proteinuria up to 16-32 g/l, leukocyturia, cylindruria. The more severe the diphtheria, the clearer the changes in the urine. Clinical manifestations of nephrosis are insignificant. However, views on kidney damage in diphtheria exclusively by the type of nephrosis with a benign course require correction. According to our data, recently there have been cases when patients with toxic diphtheria develop acute renal failure with oligoanuria, hyperazotemia, which was not only the cause of death, but also the only difficulty.
In addition to those specific to diphtheria, there are also complications caused by secondary bacterial flora, such as pneumonia, which often accompanies diphtheria croup.

Diphtheria prognosis

The consequences of diphtheria depend on the severity of the disease, the age of the patients, the timeliness of serotherapy and the usefulness of the treatment. For localized pharyngeal diphtheria without serotherapy possible complications(myocarditis, paralysis). With toxic diphtheria, lethality depends directly on the timeliness of serum administration. The cause of deaths in pharyngeal diphtheria is primarily myocarditis, then - paralysis of the respiratory muscles, and in the hypertoxic form - infectious toxic shock. Mortality in children is higher than in adults.

diphtheria diagnosis

Supporting symptoms clinical diagnostics diphtheria of the pharynx is: dense, continuous, as a rule, with a smooth shiny surface and a tendency to spread, a gray-white fibrinous coating, after which the mucous membrane bleeds (“blood dew”) and again forms (first cobweb-like) plaque; swelling, mild hyperemia with a cyanotic tinge of the mucous membrane; moderate fever, an increase in regional lymph nodes, sore throat when swallowing, with a toxic form - swelling of the cervical subcutaneous tissue of varying prevalence, sweetish-putrefactive odor from the mouth; with diphtheria of the larynx - gradual (within 3-6 days) and in stages against the background of normal or subfebrile body temperature with an almost undisturbed general condition, the development of croup symptoms: hoarse voice and barking cough, and subsequently stenotic breathing and aphonia, characteristic changes with laryngoscopy.

Specific diagnosis of diphtheria

The most likely confirmation of the diagnosis of diphtheria is the results of a bacteriological study. The material for this is obtained from the tonsils and nose. If there is plaque, the material is taken from its edges, slightly spherical film with a swab. With liquid localization of the process, in addition to smears from the affected areas, mucus from the tonsils and nose must be examined. Swabs from the tonsils are done on an empty stomach or 2 hours after eating, without touching the tongue and teeth with a swab. The material must be delivered to the laboratory no later than 3 hours after receipt, where it is inoculated on the surface of a dense medium (blood-telurite is most often used) in Petri dishes. A preliminary answer about the presence of bacteria suspicious of diphtheria can be obtained after 24-48 hours, and the final answer, the determination of toxigenicity (gravis or mitis) and biochemical variant isolated corynebacteria - only after 48-96 hours. The toxigenicity of bacteria is determined in vitro by the Ouchterlony agar precipitation method. Direct bacterioscopy of smears stained with aniline dyes is also performed. The result of microscopy is obtained after 30 minutes and is regarded only as preliminary. With an appropriate clinic, the absence of bacteriological confirmation does not negate the diagnosis of diphtheria.
For serological diagnostics, RIGA is used, carried out with the patient's blood serum and corynebacteria antigen. An increase in antibody titer in paired sera obtained before the 7th day of illness (before the administration of therapeutic serum) and after 1-2 weeks is regarded as positive result. This is a retrospective method. A negative result does not negate the diagnosis of diphtheria. At the onset of the disease, antitoxin is not detected or its amount does not exceed 0.5 AO / ml.
Recently, an accelerated method for indicating a toxin has been introduced - the antibody neutralization reaction (NAT) for commercial diphtheria antigen (anatoxin diphtheria diagnosticum).
A preliminary response to the detection of diphtheria toxin in the RHA orients the doctor to the early appointment of serum and the timely implementation of anti-epidemic measures in the focus of infection.

Differential diagnosis of diphtheria

Localized pharyngeal diphtheria should be differentiated from lacunar, follicular, mycotic and necrotic tonsillitis, infectious mononucleosis, angina Simanovsky-Plaut-Vincent, herpetic (aphthous) stomatitis, burns of the mucous membrane of the pharynx.
Lacunar and follicular angina is recognized by an acute onset, high body temperature, severe pain in the throat, bright hyperemia of the palatine tonsils, arches, tongue, yellow-white purulent plaque, which is easily removed. In patients with follicular angina, yellowish purulent follicles (small subepithelial abscesses) appear under the mucous membrane. Regional lymph nodes with angina are significantly enlarged and sharply painful.
Mycotic angina is characterized by plump, cheese-like white layers of various sizes that rise above the surface of the palatine tonsils. They are easily removed and completely rubbed between glass slides. The same layers appear on the mucous membrane of the oral cavity (tongue, cheeks).
The difference between necrotic tonsillitis is the presence of dirty gray layers on the tonsils, which are easily removed (it turns out to be minus tissue), bright hyperemia of the surrounding mucous membrane, and a significant reaction of regional lymph nodes.
Angina Simanovsky-Plaut-Vincent, - as a rule, unilateral lesion of the tonsils, necrosis does not rise above their surface (minus-tissue), on the 3rd-4th day of illness, a crater-shaped ulcer is observed at the site of necrosis, covered with a dirty yellow-green coating. Putrid smell from the mouth. In smears obtained from the surface of the ulcer, during direct bacterioscopy, symbiotic saprophytic microorganisms - spirochetes and fusiform rods - are shown.
Herpetic (aphthous) stomatitis, along with the defeat of the tonsils, is accompanied by gingivitis, stomatitis, individual yellowish superficial ulcers on the tongue, mucous membrane of the cheeks, gums, palate, salivation, severe soreness in the mouth during meals, fever.
With burns (thermal and chemical) of the oral mucosa, there is pain when swallowing, the mucous membrane is matte, fibrinous-necrotic layers are thin, yellowish in color, with a halo of hyperemia around. common cause a burn is the lubrication of the mucous membrane with an alcohol solution of brilliant green, a concentrated solution of potassium permanganate, etc.
A common and toxic form of diphtheria pharynx is differentiated with paratonsilitis, infectious mononucleosis, viral mumps, blood diseases.
Infectious mononucleosis is usually accompanied by an increase in all groups of lymph nodes, hepatolienal syndrome, the presence of lymphocytosis, monocytosis, atypical mononuclear cells and heterophilic antibodies in the blood. An increase in the posterior cervical lymph nodes often precedes the appearance of layers on the tonsils, which sometimes pass to the arches. The raids are loose, of various thicknesses, yellowish or yellowish-white in color, easily removed.
Viral mumps disease differs from diphtheria in the absence of plaque, painful chewing, Moores symptom, swelling and soreness of the parotid salivary glands, which fill the space between the mastoid process and the angle mandible, an increase in the submandibular salivary glands, as well as data from an epidemiological history.
Paratonsilitis - acute inflammation paratonsillar tissue, characterized by edema and infiltration, bright hyperemia of the supramygdalic area, anterior or posterior arch on one side. The tonsil is displaced to the midline, the corresponding anterior palatine arch is smoothed, the uvula is displaced in the opposite direction. Very sharp pain when swallowed with irradiation to the ear, increased salivation. Significantly limited mouth opening, nasal voice. The submandibular lymph nodes on the side of the lesion are enlarged and sharply painful. Unlike diphtheria, the patient's face is hyperemic, he is agitated, suffers from a sharp pain in the throat. Often, changes can be detected on the tonsil, as with lacunar or follicular tonsillitis. Misdiagnosis of paratonsillar abscess in patients with toxic diphtheria of the pharynx and an incision in the mucous membrane of the palatine arch, as a rule, lead to a deterioration in the patient's condition, increased intoxication, spread of plaque, increased swelling of the subcutaneous tissue of the neck, and further development of complications.
In blood diseases, along with necrotic tonsillitis, there is a sharp pallor of the skin, splenomegaly, lymphadenitis, hemorrhagic syndrome. Blood tests play a decisive role in diagnosis. Diphtheria of the larynx should be differentiated from stenosing laryngotracheitis with parainfluenza and other acute respiratory viral infections, as well as with aspiration of a foreign body.
Stenosing laryngotracheitis of viral etiology, unlike diphtheria croup, occurs suddenly, often at night, often repeatedly, against the background of catarrhal manifestations, high body temperature and symptoms of intoxication. Difficulty stenotic breathing, rough barking cough appears. Although the voice becomes hoarse, voiced notes remain at the height of the cry. All the main manifestations of croup occur simultaneously. Stenosis of the larynx in SARS can be quickly eliminated with the appropriate treatment. Laryngoscopy reveals varying degrees of swelling of the mucous membrane under the vocal cords.
When a foreign body is aspirated, an asthma attack occurs suddenly, during the day, while eating or playing against the background full health. Immediately after aspiration, short-term apnea with cyanosis occurs, followed by a spasmodic debilitating cough and stenotic breathing. The voice does not change, the body temperature is normal. To clarify the diagnosis, direct laryngoscopy or x-ray examination is performed.
Catarrhal form of diphtheria of the nose differentiate from foreign body, in which purulent-sanitary discharge from the nose has an unpleasant odor. Rhinoscopy allows you to clarify the diagnosis.
diphtheria eye must be differentiated from acute adenoviral conjunctivitis with fever and catarrhal symptoms from the upper respiratory tract. In contrast to diphtheria, in this disease, the swelling of the eyelids is mild, they are easily everted. The discharge is serous or seropurulent, not sanious, the plaque is loose, easily removed, the conjunctiva is bright red.

Treatment of diphtheria

Hospitalization of patients is mandatory. With toxic diphtheria, patients are transported only lying down. Strict bed rest is necessary for 20-25 days, after which, in the absence of complications, the patient is allowed to sit down and gradually expand the motor regimen. In mild forms (localized diphtheria of the pharynx, diphtheria of the nose), the duration of bed rest is reduced to 5-7 days. In the acute period of the disease, liquid or semi-liquid complete food is needed. Treatment should be specific and pathogenetic.
Specific treatment is carried out with highly purified horse hyperimmune serum "Diaferm". To prevent an anaphylactic reaction, serum is administered according to the Bezredka method. First, 0.1 ml diluted 1:100 serum is injected intradermally into the flexor surface of the forearm. If after 20-30 minutes no changes are detected at the injection site or a papule with a diameter of not more than 0.9 cm is formed, the reaction is considered negative and 0.1 ml of undiluted serum is injected subcutaneously, and if there is no reaction, after 30 minutes the entire prescribed dose is intramuscularly intramuscularly.
In case of toxic diphtheria of the II-III degree and the hypertoxic form of serotherapy, it is necessary to carry out, under the protection hormonal drugs and sometimes anesthesia. In the case of a positive intradermal test or in the presence of an anaphylactic reaction to subcutaneous administration, further serum is administered only according to unconditional indications. First, serum in a dilution of 1: 100 is injected into the subcutaneous tissue of the shoulder in doses of 0.5; 2.5 ml sequentially at intervals of 20 min. If there is no response to the previous dose, 0.1 ml of undiluted serum is injected subcutaneously. If there is no reaction, after 30 minutes, the entire prescribed dose is administered subcutaneously. In exceptional cases, serum is administered under anesthesia.
Antitoxic serum neutralizes only the toxin that circulates in the blood, and does not affect the fixed in the tissues. Therefore, specific treatment should be carried out as early as possible (optimally on the 1-3rd day of illness).
Serum doses for the first administration and course of treatment are determined by the form of diphtheria.
In case of late (after the 2nd day of illness) initiation of treatment in patients with a common or toxic form, the first dose of serum should be increased by 1/3-1/2 compared to that given in the table.
The frequency of administration of serum is also determined by the form of the disease. With localized diphtheria of the pharynx, nose, liquid localization of the process and early serotherapy, one can confine oneself to a single administration of serum. With a delay in the "melting" of the plaque, it is administered again in a day. If diphtheria of the pharynx is widespread, the serum is administered within 2-3 days (with a toxic form - every 12 hours), and then - according to indications. The first dose is 1/3-1/2 course; in the first two days the patient should receive 3/4 of the course dose.
With diphtheria croup, the initial dose of serum is determined by its stages: stages - 15-20 thousand AO, stage II - 30-40 thousand AO, stage III - 40 thousand AO; 24 hours later, this dose is repeated, and on subsequent days, if necessary, a half dose of orphan is administered.
Usually the course of serotherapy lasts no more than 3-4 days. Indications for the abolition of serotherapy is the disappearance or a significant decrease in plaque, swelling of the pharynx and subcutaneous tissue of the neck, with croup, the complete disappearance or decrease in stenotic breathing. If toxic diphtheria is suspected, serum is administered immediately; for a localized form - some waiting is possible until the results of bacterioscopy, ENT examination, etc. are obtained, but subject to constant monitoring in the hospital; for diphtheria croup - the introduction of serum is mandatory if this diagnosis is not removed after intensive retraction and antispastic therapy for 1 - 1.5 hours.
To enhance the effect of the serum, it is recommended intramuscular injection once a day 25% solution of magnesium sulfate immediately after the start of serotherapy.
Pathogenetic treatment is aimed at detoxification, restoration of hemodynamics and elimination of adrenal insufficiency. Detoxification therapy involves the introduction of a 10% glucose solution with insulin, protein preparations (10% albumin - 10 ml / kg) and colloidal solutions (rheopolyglucin - 10 ml / kg) in a ratio of 1:1:1. The liquid is injected at the rate of 20-30 ml / kg of mass. Detoxification therapy is combined with the appointment of diuretics (lasix, mannitol) under the control of blood pressure and diuresis.
To improve tissue metabolism, cocarboxylase (50-100 mg), 5% ascorbic acid solution (3-5 ml), 1% nicotinic acid solution (1-2 ml), 1% ATP solution (0.3-1 ml) are prescribed. A nicotinic acid also weakens the effect of diphtheria toxin, and ascorbic stimulates immunogenesis and the function of the adrenal cortex.
Patients with common and toxic forms of diphtheria of the pharynx, diphtheria of the larynx for the purpose of substitution, anti-inflammatory and hyposensitizing treatment for 5-8 days are prescribed prednisolone (2-C mg / kg) or hydrocortisone (5-10 mg / kg per day). In the first 2-3 days, glycocorticosteroids are administered intravenously, then orally. In hypertoxic and hemorrhagic form, the daily dose of prednisolone is increased to 5-20 mg/kg, respectively, the degree of shock.
If diphtheria occurs in a toxic form, a 0.1% solution of strychnine nitrate (0.5-1.5 ml subcutaneously) is prescribed from the first day, depending on age, for 2-3 weeks or more. Strychnine increases the tone of the central nervous system, stimulates the respiratory and vasomotor centers, tones the skeletal muscles and myocardium, and stimulates redox processes in the myocardium. Cordiamin, corazole are used, which increase the tone of the circulatory organs. In cases of DIC, for disaggregation, in addition to rheopolyglucin, antihistamines are prescribed, vasodilators, trental, xanthinol. To obtain an anticoagulant effect, heparin is administered (150-300-400 units / kg per day). Since reopoliglyukin enhances the effect of heparin, with their simultaneous administration, the dose of the latter is reduced by 30-50%. The introduction of protease inhibitors - trasilol, contrical, Gordox, anthagosan, pantrypin and aminocaproic acid is recommended.
Antibacterial therapy is prescribed to influence diphtheria corynebacterium and secondary flora. It is advisable to use benzylpenicillin, tetracyclines, cephalosporins, erythromycin.
Treatment of patients with diphtheria of the larynx. Along with specific treatment, pathogenetic treatment is carried out. The excitement and anxiety of the child increase the stenosis, so it is important to provide her with a long medication sleep. For this purpose, a 20% solution of sodium oxcbutyrate (50-100 mg / kg), a 0.25% solution of droperidol (0.1-0.15 ml / kg, but not more than 1.5 ml for a child under 2 years old), sibazon (seduxen) and others. Oxygen therapy is provided. In case of stenosis of the larynx without respiratory failure, Retraction therapy gives a good effect - a warm bath (37.5-38.5 ° C) for 5-10 minutes, warm soda drink, mustard plasters, etc. To reduce swelling of the mucous membrane, apply hyposensitizing drugs (diphenhydramine, pipolfen, tavegil, etc.), locally prescribed decongestants and anti-inflammatory drugs in aerosols (in the form of inhalations).
Complex treatment also involves the appointment of glycocorticosteroids, in particular prednisolone (2-3 mg / kg per day), which, in addition to anti-inflammatory action, help reduce laryngeal edema, reduce capillary wall permeability and exudation. Half of the daily dose is first administered intravenously or intramuscularly, the rest is given orally. According to the indications, detoxification therapy is carried out. Early administration of antibiotics is essential a wide range actions. If a conservative treatment ineffective, surgical intervention is indicated.
Indicators for primary intubation (tracheotomy) is a triad of symptoms (according to G. Ivashentsov):
a) paradoxical pulse (Rauhfus inspiratory asystole),
b) Baye's symptom - constant tension of the sternocleidomastoid muscle during inspiration,
c) persistent cyanosis of the lips and face. In the case of localized croup, prolonged nasotracheal intubation with plastic tubes is possible; with widespread descending croup, a tracheostomy is necessary, followed by drainage of the trachea and bronchi.
Treatment for complications. With myocarditis, the optimal duration of the bed rest period ranges from 3-4 weeks. Patients are fed in small portions 5-6 times a day. Assign strychnine (long course); the introduction of a 20% glucose solution with cocarboxylase, ascorbic acid; ATP within 2 weeks; calcium pangamate (50-150 mg per day); agents that affect tissue metabolism - anabolic agents (methandrostenolone orally for 1-1.5 months, potassium orotate 10-20 mg / kg per day for 2-3 weeks). In severe and moderate myocarditis, oral and parenteral prednisolone is recommended (at a daily dose of 2 mg/kg for children, 40-60 mg for adults). The introduction of cardiac glycosides is allowed only with manifestations of heart failure without conduction disturbances. The appointment of strophanthin or corglicon requires careful monitoring of the clinic and ECG data. Anticoagulants are used to prevent thromboembolic complications. indirect action(dicoumarin, neodicoumarin, or pelentan). The doses of these drugs are selected in such a way as to reduce the prothrombin index and keep it at the level of 40--50%.
Patients with diphtheria polyneuritis are prescribed strychnine, B vitamins, and glycocorticosteroids. In the recovery period, oksazil is used orally for 15-20 days, massage, therapeutic exercises (carefully), diathermy, galvanization, quartz. If the patient has difficulty swallowing and breathing, it is necessary to aspirate mucus from the respiratory tract using an electric suction. If there are signs of damage to the respiratory muscles, broad-spectrum antibiotics are prescribed in maximum doses for the prevention of pneumonia. According to the indications of the patient, they are transferred to apparatus breathing in the conditions of the intensive care unit. Based on the action of diphtheria toxin as an inhibitor of acetylcholinesterase, prozerin is prescribed for neurological complications after extinction acute manifestations illness.
Treatment of carriers of toxigenic corynebacterium diphtheria. With repeated isolation of bacteria, erythromycin, tetracycline antibiotics, and rifampicin are recommended in age-related doses. After a seven-day course, sanitation usually occurs. The focus is on chronic diseases nasopharynx. Treatment begins with general strengthening (methyluracil, pentoxyl, aloe, vitamins) and hyposensitizing agents, supplementing physiotherapy (UHF, UV irradiation, ultrasound). If there are indications, tonsils and adenoids are removed. Sometimes, after the operation, the carrier state quickly stops.
The length of stay in the hospital is determined by the severity of diphtheria and the nature of complications. If there are no complications, patients with a localized form can be discharged on the 12th-14th day of illness, a common one - on the 20th-25th (Bed rest - 14 days). Patients with subtoxic and toxic grade I forms should be on bed rest for 25-30 days; they are discharged on the 30-40th day of illness. With toxic diphtheria II-III degree and severe course of the disease, bed rest lasts 4-6 weeks or more. A prerequisite for discharge of a patient with any form of diphtheria is a negative result of two control cultures obtained with an interval of 2 days and not earlier than 3 days after the end of the course. antibiotic therapy.

Prevention of diphtheria

Active immunization plays a leading role in the fight against diphtheria. For this purpose, adsorbed pertussis-diphtheria-tetanus (DTP) vaccine and adsorbed diphtheria-tetanus toxoid (ADS) toxoid, diphtheria-tetanus toxoid with a reduced content of both antigens (ADS-M), diphtheria toxoid with a reduced content of antigen (AD-M) are used. .
Recently, a preventive vaccination scheme has been introduced, which is designed to protect almost the entire population. Preventive immunization with DTP vaccine is carried out from the age of three months three times with an interval of 45 days (0.5 ml intramuscularly). The first revaccination is carried out in 1.5-2 years once (0.5 ml), and subsequent revaccinations - once with ADS-anatoxin (0.5 ml) at 6, 11 and 14-15 years. Due to the fact that diphtheria has "matured", the active immunization scheme involves revaccination of adults every subsequent ten years (26, 36, 46 and 56 years) with ADS-M-toxoid (0.5 ml) once.
ADS-anatoxin is used in children with contraindications to the introduction of the DTP vaccine or in those who have recovered from whooping cough. ADS-Manatoxin is used in cases of contraindications to the above drugs, as well as for the purpose of age-related revaccination of children, adolescents and adults. Vaccination with ADS-M-anatoxin consists of two injections of 0.5 ml with an interval of 45 days. AD-M-anatoxin is used for vaccination of persons who have a negative result in RPHA with diphtheria diagnosticum and a positive one with tetanus.
The epidemiological effectiveness of vaccination depends not only on the quality of drugs. Vaccination coverage of 95% of the population susceptible to this infection guarantees maximum success; The means of preventing the spread of diphtheria is the early detection, isolation and treatment of patients and carriers of toxigenic corynebacteria. After isolation, the final disinfection is carried out. Surveillance of the focus of infection is carried out within 7 days with the obligatory bacteriological research mucus from the nose of all persons who had contact with patients. Individuals within 10 recent years did not vaccinate, carry out immunization with AD-M-or ADS-M-anatoxin; in the rest, at the age of 3-6 years, the degree of tension of antitoxic immunity is urgently determined.
All non-immune individuals (with a TPHA titer less than 0.03 IU / ml) are immediately vaccinated.
For the complete identification of patients with diphtheria, especially with erased forms, active supervision of patients with tonsillitis is carried out (at least 3 days from the onset of the disease) with a mandatory bacteriological examination for corynebacterium diphtheria. Hanging toxigenic diphtheria bacilli in a patient with tonsillitis is a direct basis for establishing a diagnosis of diphtheria in him. The occurrence of characteristic complications (myocarditis, nephrosis, paresis of the soft palate, polyradiculoneuritis) in patients with angina is the basis for a retrospective diagnosis of diphtheria.