Diphtheria symptoms in adults without fever. Diphtheria - symptoms, causes, treatment and prevention of diphtheria

Diphtheria is an acute infectious disease caused by the bacterium Corynebacterium diphtheriae. The disease is characterized by symptoms such as the development of an inflammatory process at the site of introduction of the pathogen and toxic damage to the nervous and cardiovascular systems. Previously, this disease was more often observed in children, but in recent years there has been a steady increase in the number of cases among the adult population. Diphtheria most often affects people aged 19-40 years (sometimes patients aged 50-60 years are also identified). That is why the prevention of diphtheria among both children and adults comes to the forefront in terms of importance. We will tell you about the treatment of this disease and everything you need to know about it in this article.

Classification of diphtheria

Based on the localization of diphtheria corynobacteria introduced into the body, infectious disease specialists distinguish the following forms of diphtheria:

• diphtheria of the upper respiratory tract;
• diphtheria croup;
• nasal diphtheria;
• diphtheria of the eyes;
• diphtheria of rare localization (wounds and genitals).

Depending on the severity of the course, this infectious disease can be of the following types:

• non-toxic: this clinical picture is more typical for vaccinated people, the disease occurs without serious symptoms of intoxication;
• subtoxic: intoxication is moderate;
• toxic: accompanied by severe intoxication and the development of swelling of the soft tissues of the neck;
• hemorrhagic: accompanied by bleeding of varying intensity (from the nose, mucous membranes of the mouth and other organs) and severe symptoms of intoxication, ending in death after 4-6 days;
• hypertoxic: the symptoms of the disease increase at lightning speed and are characterized by a severe course, death occurs after 2-3 days.

Diphtheria can be:

• uncomplicated;
• complicated.

Causes and routes of transmission

The causative agent of diphtheria is Corynobacterium (diphtheria bacillus), which during reproduction produces a particularly toxic diphtheria exotoxin. The infection can enter the human body through the mucous membranes of the respiratory organs or through the skin and ears.

The source of this pathogenic agent is a sick person or a bacteria carrier. Most often, diphtheria bacilli are spread by airborne droplets, but there is also a possibility of infection through infected objects (dishes, towels, door handles) and food (milk or meat).

The development of diphtheria can be promoted by:

• ARVI and;
• chronic diseases of the upper respiratory tract;

After suffering from diphtheria, temporary immunity is formed in the human body, and an already ill person can become infected with the diphtheria bacillus again. Vaccinations against this disease provide little protection against infection, but vaccinated people experience diphtheria in a much milder form.

After the introduction of diphtheria corynobacteria, a focus of inflammation appears at the site of its penetration. The affected tissues become inflamed, swell, and at the site of the pathological process, fibrinous films of light gray color are formed, which are tightly adhered to the wound surface or mucous membranes.

As the pathogen multiplies, a toxin is formed, which spreads through the blood and lymph throughout the body and causes damage to other organs. Most often it affects the nervous system and adrenal glands.

The degree of severity of local changes at the site of introduction of diphtheria corynobacteria may indicate the severity of the disease (i.e., the degree of general intoxication of the body). The most common entry point for infection is the mucous membranes of the oropharynx. The incubation period for diphtheria ranges from 2 to 7 days.

Symptoms

Characteristic signs of the disease are sore throat with difficulty swallowing and intoxication.

Symptoms of diphtheria can be divided into two groups: intoxication and inflammation at the site of infection.

Inflammation of the mucous membranes of the pharynx and tonsils is accompanied by:

• redness;
• difficulty swallowing;
• sore throat;
• hoarseness of voice;
• soreness;
• coughing.

Already on the second day of infection, smooth and shiny fibrinous films of gray-white color with clearly defined edges appear at the site of introduction of the diphtheria pathogen. They are difficult to remove, and after they are separated, the tissue begins to bleed. After a short period of time, new films appear in their place.

In severe cases of diphtheria, swelling of the inflamed tissues spreads to the neck (up to the collarbones).

Reproduction of the pathogen, which releases diphtheria toxin, causes symptoms of intoxication of the body:

• general malaise;
• temperature rise to 38-40 °C;
• severe weakness;
• headache;
• drowsiness;
• pallor;
• tachycardia;
• inflammation of regional lymph nodes.

It is intoxication of the body that can provoke the development of complications and death.

Diphtheria of other organs occurs with the same symptoms of intoxication, and local manifestations of the inflammatory process depend on the site of introduction of the pathogen.

Diphtheria croup

With this form of the disease the following may be affected:

• pharynx and larynx;
• trachea and bronchi (most often diagnosed in adults).

With diphtheria croup the following symptoms are observed:

• pallor;
• intense and barking cough;
• hoarseness;
• difficulty breathing;
• cyanosis.

Nasal diphtheria

This type of infectious disease occurs against the background of moderate intoxication of the body. The patient experiences difficulty in nasal breathing and complains of nasal discharge of a purulent or sanguineous nature. On the mucous membrane of the nasal cavity, areas of redness, swelling, ulcers, erosions and diphtheria films are found. This form of the disease may accompany diphtheria of the upper respiratory tract or eyes.

Diphtheria eye

This type of infectious disease can occur in:

• catarrhal form: the patient’s conjunctiva becomes inflamed and slight ichorous discharge appears from the eyes, signs of intoxication are not observed, and the body temperature remains normal or rises slightly;
• membranous form: a fibrin film forms in the lesion, the conjunctival tissue swells, purulent-serous contents are released, the temperature is subfebrile, and signs of intoxication are moderate;
• toxic form: begins rapidly, is accompanied by an intense increase in intoxication and regional lymphadenitis, the eyelids swell, and the swelling can spread to nearby tissues, the eyelids become inflamed, and inflammation of the conjunctiva may be accompanied by inflammation of other parts of the eye.

Rare diphtheria

This form of diphtheria is quite rare and affects the genital area or wound surfaces on the skin.

When the genitals become infected, the inflammation spreads to the foreskin (in men) or the labia and vagina (in women). In some cases, it can spread to the anus and perineum. The affected areas of the skin become hyperemic and swollen, bloody discharge appears, and attempts to urinate are accompanied by pain.

With diphtheria of the skin, the causative agent of infection is introduced into the wound surface, cracks, abrasions, diaper rash or areas of the skin. In the foci of infection, a dirty gray film appears, from under which serous-purulent discharge oozes. Symptoms of intoxication with this form of diphtheria are mild, but local symptoms regress over a long period of time (the wound can heal within a month or more).

Complications

Diphtheria toxin, released when the pathogen multiplies, can lead to the development of severe complications, which determine the danger of diphtheria. With a localized form of the disease, the course of the disease can be complicated in 10-15% of cases, and with a more severe infection (subtoxic or toxic), the likelihood of possible complications steadily increases and can reach 50-100%.

Complications of diphtheria:

• infectious-toxic shock;
• DIC syndrome;
• poly- or mononeuritis;
• toxic nephrosis;
• adrenal gland damage;
• multiple organ failure;
• respiratory failure;
• cardiovascular failure;
• otitis;
• paratonsillar abscess, etc.

The time at which the complications described above appear depends on the type of diphtheria and its severity. For example, toxic myocarditis can develop at 2-3 weeks of the disease, and neuritis and polyradiculoneuropathy - against the background of the disease or 1-3 months after complete recovery.

Diagnostics

Diagnosis of diphtheria, in most cases, is based on an epidemiological history (contact with a patient, the appearance of foci of the disease in the area of ​​residence) and examination of the patient. The patient may be prescribed the following laboratory diagnostic methods:

• general blood analysis;
• bacteriological smear from the source of infection;
• blood test to determine the titer of antitoxic antibodies;
• serological blood tests (ELISA, RPHA) to detect antibodies to the causative agent of diphtheria.

Therapeutic treatment

Treatment of diphtheria is carried out only in 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 anti-diphtheria serum, which can neutralize the effect 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 diphtheria symptoms and are determined individually. If necessary (if there is an allergic reaction to serum components), the patient is prescribed antihistamines.

Various methods can be used to detoxify the patient’s body:

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

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

Patients with diphtheria of the respiratory organs are recommended to frequently ventilate the room and humidify the air, drink plenty of alkaline fluids, and inhale with anti-inflammatory drugs and alkaline mineral waters. With increasing respiratory failure, the use of aminophylline, antihistamines and saluretics may be recommended. With the development of diphtheria croup and increasing 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 permitted only after clinical recovery and the presence of a double negative bacteriological analysis from the throat and nose (the first analysis is carried out 3 days after discontinuation of antibiotics, 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 local clinic.

Surgery

Surgical treatment of diphtheria is indicated in difficult cases:

• for diphtheria croup: using special surgical instruments, diphtheria films are removed that the patient cannot cough up on his own (the manipulation is performed under general anesthesia);
• with a sharp progression of respiratory failure: tracheal intubation or tracheostomy is performed, followed by artificial ventilation of the lungs.

Today, there are no outbreaks of epidemics of this disease, but it continues to excite many people. It is important to be aware of this issue in order to sound the alarm at the very first cases of detection of a characteristic plaque or affected mucous membranes. Consider what diphtheria is - the symptoms and differences in the signs of the disease in an adult and a child.

What is diphtheria

Basically, the disease is characterized by inflammation of the upper respiratory tract, damage to the skin and other sensitive areas of the body. When diphtheria is observed, few can accurately identify its symptoms. The nature of the disease is infectious, but this disease is dangerous not so much with local manifestations as with consequences for the nervous and cardiovascular systems. The cause of their defeat is poisoning with a toxin produced by the pathogens of diphtheria - Corynebacterium diphteriae. These bacteria are transmitted by airborne droplets.

Kinds

Diphtheria is distinguished depending on the location of the acute infection. The respiratory tract, eyes, skin, ears and genitals may be affected. By the nature of the course, the disease is typical or membranous, catarrhal, toxic, hypertoxic, hemorrhagic. There are several stages indicating the severity of the disease:

• mild (localized) form;
• average (common);
• severe stage (toxic diphtheria).

Clinical manifestations of diphtheria

It is difficult to diagnose the disease yourself. Diphtheria - its local symptoms may be similar to manifestations of a sore throat, and not a dangerous infectious inflammation. The disease is determined by conducting tests of the mucous membrane. The pathogen enters vulnerable areas of the skin, where it begins to multiply and creates pockets of inflammation. Locally, necrosis of the epithelium occurs, and hyperemia appears.

Exotoxin or diphtheria toxin, produced by diphtheria bacteria, spreads through the blood and lymphatic pathways, contributing to general intoxication of the body. In the presence of autoimmune processes, complications aimed at the nervous system may develop more quickly. After recovery, signs of diphtheria disappear in the body and antibodies appear, but they do not always reduce the risk of becoming infected again.

In adults

In recent years, cases of such infectious diseases among the adult population have become more frequent. Several organs can be affected at the same time. The most common form is a disease of the pharyngeal mucosa, which is why it is often confused with sore throat. The patient experiences fever, chills and severe sore throat. Swelling of the tonsils occurs, and on their surface you can notice a filmy coating, which is absent in healthy people. It persists even after the temperature returns to normal.

If a person abuses alcohol, he or she increases the risk of developing toxic and hypertoxic forms. They provoke the spread of edema throughout the body and cause convulsions. These processes occur rapidly. After a few hours, the patient’s blood pressure drops and toxic shock occurs. These events are often fatal. Symptoms of diphtheria in adults are often more severe than in children.

In children

In order to minimize the severity of symptoms when children become infected, they are given vaccinations to prevent diphtheria. The extent of symptoms will depend on whether pre-immunization has been given. Children without vaccinations are at risk of dangerous complications and death. In newborns, the localization of inflammatory processes is observed in the umbilical wound. At the age of breastfeeding, the affected area may be the nose, after a year - the lining of the larynx and the lining of the oropharynx.

Symptoms of oropharyngeal diphtheria

This is the most common manifestation of the disease (95% of cases). The incubation period ranges from 2 to 10 days. When the mucous membrane of the oropharynx is affected by diphtheria, the symptoms are similar to those of a sore throat. A characteristic sign is the appearance of a dirty-white coating on the tonsils. The severity of how the symptoms appear depends on the form of diphtheria, so at the first suspicion it is important to see a doctor for tests.

With a common form

If the form is common, then diphtheria - its local symptoms are important to notice at an early stage, because it affects not only the tonsils, but also neighboring tissues. There is a risk of the following manifestations of intoxication:

• the diphtheria film on the tonsils, tongue and pharynx is difficult to remove with a spatula, and blood comes out at the place of removal;
• body temperature rises to 38-39°C;
• headache, pain when swallowing occurs;
• lack of appetite, general malaise.

Toxic

This form of the disease occurs in children who have not undergone the vaccination procedure. It is characterized by an acute onset, when the temperature rises sharply to 40 degrees. The patient refuses to eat and suffers from vomiting. Pallor of the skin is noticeable, and spasm of the masticatory muscles occurs. Swelling of the oropharynx and neck develops. The coating on fabrics turns from translucent to dense, with clear edges. The most dangerous of all the symptoms are seizures.

Hypertoxic

At risk of developing a hypertoxic form are patients with an unfavorable premorbid background (for example, diabetes, alcoholism, chronic hepatitis). With the onset of this stage, a rapid increase in temperature occurs. All signs of intoxication are observed. The dysfunction of the cardiovascular system progresses. There is tachycardia, pressure drops, subcutaneous hemorrhages form. With such characteristic clinical pictures, a lethal outcome can occur in 1-2 days.

Diphtheria croup

Presentation of croupous diphtheria or diphtheria croup has recently been observed among adult patients. The disease has three stages that develop sequentially:

• dysphoric – characteristic signs are barking cough, hoarseness;
• stenotic - loss of voice, silent cough, but noisy breathing, tachycardia, pale skin;
• asphyxia - superficial frequent breathing, cyanosis increases, pressure drops, consciousness is disturbed, convulsions occur. The last stage is the most dangerous, since the supply of oxygen to the body is disrupted and a person can die from asphyxia.

Symptoms of localized diphtheria

Almost any manifestation of the disease has a similar clinical picture. If a person is suspected of having diphtheria, it is important to discuss local symptoms with a doctor as soon as possible. This will prevent its development in the early stages. The toxin released by bacteria in the affected areas spreads throughout the body, but in the localized form, foci of infection are immediately noticeable. It can be:

• nose and nasopharynx;
• the mucous membranes of the eye are affected;
• genital tissue;
• skin, wounds and breaks in the epithelial cover.

Diphtheria eye

The incubation period is 2-10 days. Children aged 2-10 years are most often susceptible to eye diphtheria. This is a rare form of the disease that occurs against the background of diphtheria of the pharynx, nasopharynx and other areas. A characteristic symptom is hyperemia of the skin of the eyelids, the appearance of transparent bubbles, which, when bursting, form a scab in their place. Gradually it develops into a painless ulcer. There are diphtheria, croupous and catarrhal forms. In some cases, scars can lead to deformation of the eyelids.

Nose

Let's look at the following: nasal diphtheria - symptoms and features. The manifestation can be isolated or against its background the larynx and trachea may be affected. Sometimes the attacks spread to the descending paths. Most often, newborns and children under 2 years of age suffer from this form. As in the cases described above, the patient experiences fever, weakness and apathy. Nasal congestion, bloody discharge, and dermatitis of the affected areas of the skin occur. Inflammation of the mucous membrane occurs, it becomes covered with ulcers and fibrinous plaque.

Genital organs and skin

The affected areas can be the genitals and skin areas. If diphtheria is diagnosed in such cases, what local symptoms will it have? This form is also complex in nature and occurs against the background of a disease of the pharynx. In rare cases, an isolated manifestation is observed. The patient feels pain when urinating, mild itching in the intimate area. Redness and swelling of the mucous membrane and adjacent tissues are noticeable. Due to the proliferation of bacteria, cell necrosis occurs, and plaque and ulcers appear in their place. There is an enlargement of the lymph nodes in the groin area.

Wound surfaces

If there are deep wounds on the surface of the skin, an infectious agent can enter there. As the body fights the infection, the temperature rises, the wound swells, and becomes more painful. A white-yellow coating appears, which after a few days develops into a dense film. The patient also has a sparkle in his eyes and reddening of his cheeks.

Symptoms of specific complications

When a patient is diagnosed with diphtheria, its external symptoms may worry doctors less than the symptoms of intoxication or the occurrence of complications. After all, with proper treatment, it is possible to cope with external manifestations at an early stage. Due to toxic damage to the entire body through the blood and lymphatic channels, recovery may be accompanied by complications that are specific in nature and affect all body systems:

• cardiovascular – the functioning of the adrenal glands and heart muscle is disrupted, toxic myocarditis develops;
• nervous - the sympathetic and autonomic ganglia, the vagus and glossopharyngeal nerves, and in rare cases, the nerve endings in the arms and legs can be damaged, which often leads to paralysis;
• excretory – toxic nephrosis is a common complication, especially in those who did not receive anti-diphtheria serum in a timely manner;
• circulatory - 75% of patients may suffer from leukemia, monocytosis was recorded in 31%, and ESR levels increased in 66%. Anemia or thrombocytopenia may occur.

Video

In ancient times, diphtheria was said to be a suffocating disease. In some sources it is described under the name “deadly pharyngeal ulcer” due to the specific filmy coating in the throat and the large number of deaths. But with the advent and active introduction of vaccines against diphtheria, this infectious disease has become rare, and the number of deaths from it has practically not been observed.

What is diphtheria and how is it treated? How dangerous is this disease even today and what preventive measures will protect you from contracting it? Let's find out.

What kind of disease is diphtheria?

What group of infectious diseases does diphtheria belong to? This is a bacterial acute infectious process or disease that affects the upper respiratory tract. The causative agents of diphtheria are Corynebacterium diphtheriae or Loeffler's bacillus.

How does infection occur?

There are three main types of bacteria that cause throat infections. The most dangerous of them and most often leads to an acute infectious disease is Corinebacterium diphtheriae gravis, which releases an exotoxin in the human body.

The source of infection is a sick person or a bacteria carrier. From the moment of active manifestation of diphtheria until complete recovery, a person releases bacteria into the environment, therefore, if a sick person is in the house, he must be isolated. Bacteria carriers pose a serious threat, as they can release pathogenic microorganisms into the environment for a long time.

The causative agent of the disease is resistant to many factors, but quickly dies when exposed to moisture and light or disinfectant solutions. Boiling clothing that has been in contact with a person with diphtheria kills Leffler's bacillus within seconds.

How is diphtheria transmitted? The disease is transmitted by airborne droplets from a sick person to a healthy person or through objects during contact with contaminated material. In the latter case, the hot climate and the lack of regular, thorough cleaning of the room play a big role. There is another route of transmission of infection - food through contaminated products. This often happens if the food was prepared by a bacteria carrier or a person suffering from an acute infectious process.

Diphtheria is not a viral disease; only bacteria lead to its development.

Classification of diphtheria

Depending on the location of the infection, several forms of diphtheria are distinguished.

1. Localized, when manifestations are limited only to the site of introduction of the bacterium.
2. Common. In this case, the plaque extends beyond the tonsils.
3. Toxic diphtheria. One of the most dangerous forms of the disease. It is characterized by a rapid course and swelling of many tissues.
4. Diphtheria of other localizations. This diagnosis is made if the entry points of infection were the nose, skin, and genitals.

Another type of classification is based on the type of complications accompanying diphtheria:

• damage to the heart and blood vessels;
• the appearance of paralysis;
• nephrotic syndrome.

Nonspecific complications are the addition of a secondary infection in the form of pneumonia, bronchitis or inflammation of other organs.

Diphtheria symptoms

The incubation period of diphtheria can range from two to 10 days, with an average of 5 days. This is exactly the time in the development of the disease when there are no pronounced clinical manifestations, but the bacteria have already entered the human body and began to affect internal organs. From the last day of the incubation period, a person becomes infectious to others.

The classic course of the disease is localized diphtheria of the pharynx. It is characterized by the following symptoms.

1. Weakness, general malaise, lethargy, decreased appetite.
2. Headaches and minor difficulties when swallowing food appear.
3. Body temperature rises to 38–39 °C. Its peculiarity with this disease is that it goes away on its own after just three days, regardless of the presence of other signs of the disease.
4. A symptom of diphtheria in an adult during the development of the disease is the formation of plaque in the tonsil area. It comes in several varieties in the form of a grayish smooth shiny film; there may be small islands of white or grayish color. The plaque is tightly fused to the surrounding tissues, it is difficult to remove it, since drops of blood appear at this place. The plaque appears again some time after an attempt to get rid of it.
5. The catarrhal form of diphtheria is characterized by redness and enlargement of the tonsils.

Another important type of diphtheria is the toxic form of the disease. Its course has its own characteristics.

Complications

Complications of toxic diphtheria most often develop on days 6–10 of the disease.

Complications may be the following.

1. Inflammation of the heart muscle or myocarditis. Sick people are weak and complain of abdominal pain and periodic vomiting. The pulse quickens, the heart rhythm is disturbed, and blood pressure decreases.
2. Peripheral paralysis. They develop in the second or fourth week of the disease. This is often paralysis of the soft palate and impaired accommodation (the ability to see objects at different distances). A sick person complains of difficulty swallowing and visual disturbances.
3. Nephrotic syndrome, when there are pronounced changes in urine analysis, but the basic functions of the liver are preserved.
4. In severe cases, death occurs due to shock or asphyxia.

Treatment

Due to the high likelihood of complications, treatment of diphtheria should be carried out only in a hospital setting. Treatment with traditional methods is ineffective!

Treatment of diphtheria in children and adults involves the administration of antitoxic diphtheria horse serum (EDS). The dosage depends on the course of the disease.

Additionally, depending on the indications, antibiotics are prescribed (but they are not always effective), more often with the development of a secondary infection. Antiseptics are used for gargling, detoxification therapy for toxic forms. If croup develops - blockage of the respiratory tract, then sedatives are prescribed, and
In severe cases, hormonal drugs are used.

The outcome of treatment depends on timely and early consultation with doctors.

Prevention of diphtheria

The main prevention of diphtheria is the identification of bacteria carriers and timely scheduled vaccinations. They are administered in childhood in complex vaccines - (for diphtheria, whooping cough and tetanus). Immunization is carried out for all children unless it is contraindicated.

At what age is the diphtheria vaccine given? The first vaccine is administered three months after the birth of the child, then at 4.5 and 6 months. At 18 months, the first revaccination is carried out, the next one should be carried out at 6 years, and the third at 14. The vaccination calendar has undergone some changes in recent decades. Therefore, in some cases, the last revaccination during adolescence could be carried out at 15 or 16 years of age.

When are adults vaccinated against diphtheria? All previously unvaccinated adults or those who do not have data on vaccinations (they are considered unvaccinated in this case) are administered ADS-M toxoid twice. This is 0.5 ml of a drug with a reduced content of antigens, which is administered intramuscularly or deep subcutaneously. The interval between administration of the drug is 1.5 months, reductions are not allowed. If it was not possible to administer the drug within the prescribed time frame, vaccination is carried out as soon as possible. Diphtheria revaccination for adults in this case is carried out once every 9–12 months. Then vaccination is carried out every 10 years, planning in advance. If previously the maximum age for revaccination was 66 years, there are currently no such restrictions.

When and where are adults vaccinated against diphtheria? Vaccination is carried out in the clinic to which the person is assigned if he is completely healthy.

What vaccines are there for diphtheria?

1. Children under 6 years of age are given DTP.
2. ADS - adsorbed diphtheria-tetanus toxoid.
3. AD-M - diphtheria toxoid with reduced antigen content.

Each of these vaccines is administered according to strict indications.

Diphtheria is a dangerous disease that is feared even in our time. It is difficult to predict its consequences, especially if the diagnosis was not made in a timely manner. To get rid of the infection forever, you need to carry out prevention.

The content of the article

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

Historical data of diphtheria

Epidemics of diphtheria have been known since the time of Hippocrates, and the first reliable description of the disease was made by Aretaeus in the 1st century. n. e. However, despite its long history and widespread distribution, the disease was identified as an independent nosological unit only in the twenties of the 19th century. French scientists P. Bretonneau, who gave it 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 of antitoxin in the blood of patients in 1890 by Russian scientist Orlovsky pointed the way to the creation of anti-diphtheria serum. This is a remedy developed 1892-1894 pp. E. Roux in France, E. Behring in Germany and J. Yu. Bardach in Russia, allowed to significantly reduce mortality. N.F. Filatov and G.N. Gabrnchevsky were the first in Russia to use the serum for treatment and convincingly proved its effectiveness. In 1912, W. Schick proposed a skin reaction to identify individuals susceptible to diphtheria. In 1923 p. G. Ramon proposed active immunization against diphtheria with toxoid (the toxin, under the influence of formaldehyde 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 Loeffler's bacillus, belongs to the genus Corynebacterium. This is a stationary, gram-positive rod 1-8 µm long, 0.3-0.8 µm wide, does not form spores, often has the appearance of a Roman numeral V. Corynebacterium has club-shaped thickenings at the ends - grains of volutin (corune - club). The causative agent of diphtheria - an aerobe or facultative anaerobe - grows well on media containing blood or its serum, the optimal growth temperature is 36-37 ° C.
The main pathogenicity factor of the causative agent of diphtheria is exotoxin, which is a potent bacterial toxin and is second only to botulinum and tetanus.
The disease is caused only by toxigenic corynebacteria. The ability to produce toxins is a genetically fixed feature of the causative agent of diphtheria. Under the influence of bacterial viruses (phages) on their genome, nontoxigenic cultures turn into toxigenic ones. In addition to the toxin, diphtheria bacilli produce neuraminidase, hyaluronidase, necrotizing and diffuse factors. Based on 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 Corynbacterium and the severity of the disease.
The pathogen is resistant to environmental factors. In diphtheria film, droplets of saliva adhering to the walls of dishes, to door handles, toys, it persists for 15 days, in water, milk - about 20 days. Tolerates drying well. At low temperatures it persists for 6 months without loss of pathogenic properties. Bacteria are sensitive to high temperature (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 from chronic diseases of the 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 morbidity has changed towards “growing up”. In most cases, adolescents and adults suffer from diphtheria, which is explained by defects in immunoprophylaxis, unjustified expansion of contraindications to preventive vaccinations, and the use of insufficiently effective diphtheria toxoid preparations. Of particular importance is the absence of the so-called natural immunity of the population due to the 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 high-immune populations.
Most cases of the disease occur in the autumn-winter period. Before mass active immunization, periodic increases in morbidity were observed (every 10-15 years). A characteristic feature of the epidemic process in recent years is the increase in the incidence of diphtheria; in cities, adults are more likely to get sick; in rural areas, the incidence of children is predominant. After suffering from diphtheria, immunity of varying strength and duration is formed, and individuals may get sick again. Antitoxic and antibacterial immunoglobulins play a major protective role in anti-diphtheria immunity. In the absence of antibacterial antibodies in the blood serum, its protective properties are sharply reduced and bacterial carriage is formed.
Diphtheria occurs in all countries of the world. On all continents, unvaccinated children are more likely to get sick. In Ukraine, there has recently been an increase in the incidence of diphtheria.
Diphtheria is a controlled 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 entry points for infection are the mucous membranes of the tonsils, nose, pharynx, larynx, genitals, conjunctiva, damaged skin, where the pathogen multiplies and produces a toxin. A high level of antitoxic immunity ensures neutralization of the toxin in the body.
In this case, two options are possible:
a) corynebacteria diphtheria 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 carriage of bacteria.
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 composition of polypeptide chains from amino acids. Locally, the exotoxin causes coagulative necrosis of the epithelium.
The toxin gradually penetrates deep into the tissues, enters the lymphatic and circulatory systems, leading to local vascular paresis and increased permeability of the walls of small vessels in the lesion. An exudate rich in fibrinogen is formed in the intercellular space. With the participation of thrombokinase of necrotic tissue, fibrinogen is converted into fibrin, as a result of which a fibrinous plaque (film) is formed on the surface of the affected tissue, a characteristic sign of diphtheria.
If the process develops on the mucous membrane covered with a single-layer cylindrical epithelium (larynx, trachea, bronchi), then only the epithelial layer is subject to coagulation necrosis, lobar inflammation develops, in which the formed film is loosely connected to 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 genitalia), diphtheritic inflammation develops when not only the epithelial cover, but also the connective tissue base of the mucous membrane becomes necrotic. Fibrinous plaque penetrates the entire thickness of the mucous membrane, the film adheres tightly to it, and removal of the plaque is accompanied by bleeding.
From the local focus, the toxin penetrates deep into the tissues through the lymphatic system, causing swelling of the mucous membranes, submucosal tissue, and regional lymph nodes. In toxic forms of the disease, exudate forms in the intercellular and intermuscular spaces, which leads to swelling of the subcutaneous tissue.
Once in the blood, the toxin affects the circulatory system and nervous system, adrenal glands, and kidneys. Foci of hemorrhage and destructive changes up to necrosis are detected in the adrenal glands. Strengthening the function of the adrenal glands in the first days of the disease is altered by their hypofunction to the almost complete cessation of secretory function.
The circulatory organs are especially intensively affected. All forms of diphtheria are characterized by hemodynamic disorders of varying degrees, up to infectious-toxic shock. The most profound changes occur in the myocardium. They are characterized by degenerative degeneration of muscle fibers up to complete myolysis and productive changes in interstitial tissue. Profound disturbances in metabolic processes, in particular protein synthesis, lead to cell death with their replacement by connective tissue. Ganglion cells and nerve fibers of the intracardiac (intracardial) nerve plexuses experience significant degenerative changes.
Diphtheria toxin is an acetylcholinesterase inhibitor. Its effect on the nervous system leads to the accumulation of acetylcholine, which has a harmful effect on the structures of the central and peripheral nervous system. Due to increased activity of the parasympathetic nervous system, catastrophic disorders of the circulatory system and acute respiratory failure occur.
In peripheral nerves and spinal nerve roots, multiple toxic parenchymal neuritis develops with predominant involvement of the myelin and Schwann sheaths in the process, mild damage to axons, which explains the reversibility of the process.
In toxic diphtheria, degenerative changes in the nephron tubules are observed with great stability, which are mainly caused by the effects of toxins on the tubular epithelium. The development of infectious-toxic shock (shock kidney), DIC syndrome in the acute period of the disease also plays an important role in the pathogenesis of kidney damage. In this case, the vessels of the renal glomeruli are predominantly affected. The development of acute renal failure is possible.
In the pathogenesis of diphtheria croup, in addition to mechanical causes (formation of a fibrinous film), reflex spasm of the muscles of the larynx and swelling of its mucous membrane, especially under the vocal folds, are of significant importance.
The originality of the clinical course of toxic and hypertoxic forms of diphtheria is explained by nonspecific sensitization of the body and massive formation of toxin. Immunodeficiency and inadequate function of the endocrine system play a certain role.

Diphtheria Clinic

The classification of clinical forms is determined by the localization of the process and its severity. Based on these signs, diphtheria is distinguished in the pharynx (85-90% of cases), nose, larynx, trachea and bronchi, eyes, ears, external genitalia, skin (wounds). Combined forms are possible. According to the degree of intoxication, diphtheria is divided into non-toxic, subtoxic, toxic, hemorrhagic and hypertoxic, and based on 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 mild hyperemia with a cyanotic tint (stagnant). Fibrinous plaque is dense, continuous, grayish-white in color, sometimes with a pearlescent tint, its surface is smooth and shiny. An increase in plaque above the level of the mucous membrane (plus tissue) is characteristic. The plaque forms during the first 2-3 days: at first it looks like a translucent cobweb-like mesh, 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 cannot be rubbed with a spatula. Characteristic signs of fibrinous plaques: dense consistency, the formation of comb-shaped protrusions and folds, reappearance of the film in the place where it was removed, a tendency to spread on the surface of the mucosa. In recent years, hemorrhagic saturation of plaque has been observed somewhat more often, and 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 more significant the intoxication.
The plaque disappears gradually - thinner and smaller from the edges, like ice that melts. It is also possible for it to be rejected in the form of plates.
The catarrhal form of diphtheria of the pharynx is characterized by only slight swelling and hyperemia with a cyanotic tint. Symptoms of intoxication are minor, there is no plaque on the tonsils. This form is recognized only during 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, a distinction is made between islet and membranous diphtheria. With islet diphtheria, the plaque looks like islands of fibrinous deposits, the size and shape of which varies from dotted and streak-like to areas up to several millimeters in size; with membranous diphtheria, the plaque is larger in size and can cover the entire tonsil.
The onset of the disease is usually acute, body temperature rises to 38-38.5 ° C, and from the 2-3rd day it normalizes or decreases to low-grade fever. Intoxication is moderate, headache, malaise, loss of appetite, pale skin are noted. Pain in the throat when swallowing is mild, consistent with the prevalence of the process in the tonsils. The formation of fibrinous plaque in the crypts and on the convex surface of the tonsils is characteristic; Edema prevails over infiltration, which leads to a uniform enlargement of the tonsils and smoothness of their surface structure. Localization of the process is usually bilateral. Localized diphtheria of the pharynx is a mild form. In the case of timely administration of anti-diphtheria serum, the patient’s condition improves within a day, the plaque disappears on the 2-3rd day, and in the case of a filmy form - on the 4-5th day. Without specific treatment, the disease may 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, body temperature rises to 38-39 ° C, after two or three days it decreases to normal or subfebrile, even if the pathological process on the mucous membrane progresses. Symptoms of general intoxication are moderate: headache, weakness, anorexia, pale skin. With a slight increase, regional lymph nodes become somewhat painful. Possible unilateral spread of plaque or the predominance of the process on one side. Compared to the localized form, plaque lasts longer: with timely administration of serum - for 3-6 days. If treatment is not carried out, a more severe form may develop (subtoxic, toxic) or the process may spread to the larynx.
The toxic form of diphtheria of the pharynx is often characterized by the rapid development of its inherent symptoms. Body temperature quickly reaches 39-40 ° C and lasts for a longer period (3-5 days) than with localized and widespread diphtheria, but later it also decreases, despite the persistence of plaque. Symptoms of intoxication are significant: pale skin, repeated vomiting, tachycardia, adynamia. Sore throat when swallowing is more intense, but is not the main complaint of the patient. From the first hours, rapidly increasing swelling of the tonsils, palatine arches, uvula, and soft palate is noted. The hyperemia of the mucous membrane is intense, with a cyanotic tint. Sharply enlarged tonsils can close so that the back wall of the pharynx is not visible. Breathing through the mouth is difficult, and the voice takes on a nasal tone. A jelly-like (gelatinous) translucent film appears on the surface of the tonsils, against which dense opalescent areas are revealed. Filmy plaque quickly spreads over the entire surface of the tonsils and beyond. A specific licorice-rotten odor appears from the mouth. Regional lymph nodes enlarge significantly and become dense and painful.
An important sign of toxic diphtheria is swelling of the subcutaneous tissue of the neck. It is always painless, doughy in consistency, appears above the regional lymph nodes at the end of the first day of the disease, sometimes on the second day, spreading down to the neck and chest. The skin in the area of ​​edema retains its normal coloration. With a jerky impact, the swollen tissues are shaken off, like jelly (jelly), which makes it possible to determine the boundaries of the edema (Nosov’s jelly symptom). Pressing on the area of ​​edema does not leave any pits. The prevalence of swelling of the subcutaneous tissue corresponds to the degree of intoxication, therefore it is a criterion for the severity of toxic diphtheria: swelling above 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 the hypertoxic (fulminant) form, in addition to a rapidly progressing local process, very severe intoxication is observed from the first hours (increase in body temperature to 40-41 ° C, repeated vomiting, delirium, convulsions). Hemodynamic disorders increase catastrophically (pallor of the skin, acrocyanosis, threadlike rapid pulse, dullness of heart sounds, sharp decrease in blood pressure). The patient dies in the first 2-5 days of illness with signs of infectious-toxic shock of II-III degree.
The hemorrhagic form is characterized by toxic diphtheria syndrome of 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. Bloody vomiting, bleeding gums, hemorrhages in the skin, and hematuria are observed. 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 pharynx under the influence of putrefactive bacteria.
A blood test reveals neutrophilic leukocytosis, thrombocytopenia, and increased ESR.

Diphtheria of the larynx

With the localization of the process in the respiratory tract, diphtheria croup develops. Croup is acute laryngitis or laryngotracheitis, accompanied by laryngeal stenosis, manifested by a hoarse voice, barking cough and inspiratory shortness of breath. On the mucous membrane of the epiglottis, scooped cartilages, vocal cords, and subglottic space, swelling, hyperemia appears, and fibrinous films are formed.
Laryngeal diphtheria is most often observed in children aged one to five years. Its main symptoms are: hoarse voice, rough barking cough, stenotic breathing. Characteristic is the gradual onset and staged development of these three symptoms without a sharp disturbance in the general condition in the first days of the disease, against the background of low-grade or normal body temperature. 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), and a third sign of croup appears - stenosis. Noisy stenotic breathing gradually increases with increased frequency and difficulty in inhaling, a sharp retraction of the pliable parts of the chest (supraclavicular, subclavian, jugular fossa, intercostal spaces, epigastric area). 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 caused by swelling of the laryngeal mucosa, the presence of fibrinous films and spasm of the laryngeal muscles.
At the beginning of the stenotic stage, the lack of air is insignificant and the child remains calm, but then oxygen starvation develops, the patient becomes restless, rushes about, stands up, the auxiliary respiratory muscles (sternocleidomastial, drabin parts) noticeably tense, cyanosis appears, shallow breathing, paradoxical pulsation. loss of the pulse wave at the height of inspiration (Rauchfuss inspiratory asystole). This is a consequence of significant negative pressure in the chest during inspiration, which leads to stretching of the aorta, preventing the heart from emptying during systole and the movement of blood into the peripheral vessels.
The appearance of 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 poor. 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 performed at this time, asphyxia develops. The lips, tip of the nose, nail bed and oral mucosa become cyanotic, the face turns pale, and the skin becomes covered with sweat. The respiratory center is depressed, the patient's strength is depleted, he lies quietly in bed, shortness of breath decreases, and the involvement of the pliable areas of the chest disappears. Despite the apparent decrease in signs of stenosis, the child develops general cyanosis, muscle hypotonia, hypothermia, dilated pupils, and there is no reaction to injections. The pulse is frequent, thread-like, blood pressure is low. Consciousness is clouded or fainting, convulsions are possible due to cerebral edema. Breath sounds in the lungs are barely audible. The appearance of bradycardia precedes cardiac arrest. In most cases of laryngeal diphtheria, general intoxication is moderate. Disorders of the function of the circulatory system are caused by hypoxia. Death comes from asphyxia.
The above development of symptoms occurs only with delayed treatment or its absence. Administration of serum in the catarrhal or initial stages of stenosis prevents the progression of croup.
After 12-18 hours, the signs of stenosis gradually decrease, the cough becomes softer, becomes moist, and then stops. At this time, a sudden development of asphyxia is possible due to obstruction of the respiratory tract by rejected films. The voice remains silent or hoarse for a long time and returns to normal 4-6 days after the stenosis disappears.
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, laryngoscopy helps establish the diagnosis. Failure to take these features into account can lead to an unfavorable course of the disease, when the process (formation of films) spreads to the trachea, bronchi (descending croup), and the diagnosis is made late.

Nasal diphtheria

Nasal diphtheria is observed especially in young children. Symptoms of general intoxication are almost not expressed, body temperature is subfebrile or normal. At first the lesion may be one-sided. Due to swelling of the mucous membrane, the nasal passage narrows, minor serous-bloody or serous-purulent discharge appears, irritating the upper lip and skin near the nasal openings. Erosion, ulcers covered with bloody scabs (catarrhal-ulcerative form), films (membranous form) appear on the nasal septum. Films can spread to the mucous membrane of the paranasal sinuses. Sometimes on the upper lip, cheeks, and chin the skin becomes macerated, ulcers and crusts with a dense infiltrated base are found, 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 significant swelling, serous, purulent or purulent-bloody (serous-bloody) discharge. One eye is affected first. The inflammatory process of the upper eyelid is more distinct than the lower eyelid (Bogdanov's symptom). This may be due to lysozyme in the tear fluid, which has a bactericidal effect on the bacterial flora of the conjunctiva of the eyelids, especially the lower one. There are lobar diphtheria and catarrhal forms of diphtheria of the eyes.
The croupous form is characterized by films on the conjunctiva of the eyelids, easily removed, slight pain and lack of photophobia. The cornea is not affected, there is no intoxication.
In the diphtheritic form, the swelling of the eyelids is pronounced and harder, the films adhere tightly to the underlying tissues, often spreading to the eyeball and cornea. Serous-bloody discharge from the eyes subsequently becomes profuse and purulent. Vision almost always decreases, up to its complete loss due to panophthalmitis. General disturbances in this form are manifested by low body temperature, adynamia, and pallor.
The catarrhal form is clinically difficult to distinguish from other types of conjunctivitis; it is diagnosed only on the basis of the results of bacteriological examination, epidemiological data and the effectiveness of serotherapy.
Diphtheria of the external genitalia characterized by pronounced swelling of the labia majora and minora, hyperemia with a cyanotic tint, the presence of films and (or) ulcers on the mucous membrane, covered with a dirty gray coating. The inguinal lymph nodes are enlarged and painful. There are localized, widespread and toxic forms. In the most common form, the process covers the skin of the external genitalia, the perineum around the back. The toxic form is characterized by swelling of the genital organs (I degree), subcutaneous tissue of the groin and thighs (II degree).
Skin diphtheria (wounds) develops when the surface epithelium is damaged. Characterized by hyperemia, hemorrhagic spots, pustules, crusts, fibrinous films, swelling of the skin. There are membranous, ulcerative-membranous and toxic forms. A type of (very liquid) diphtheria of the skin is the lesion of the umbilical wound in newborns.
Diphtheria eye, genitals and skin often develops secondarily, in combination with diphtheria of the pharynx or nose. Very rare forms include diphtheria of the middle ear and oral mucosa.
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: acute onset, a significant increase in body temperature (to hyperthermia), especially in the first days; severe, 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 plaque to nosebleeds and hemorrhages in the subcutaneous tissue in the toxic form; the appearance of complications from the nervous system in the long term (4-5 weeks of illness). Mostly children of high school age and adults are affected. In most cases, diphtheria of the pharynx is observed, which has a severe course with the development of toxic forms. Toxic diphtheria begins acutely more often than before. The prevalence of the local process in toxic diphtheria of the throat II-III degrees has decreased. This is also manifested in an increase in the prevalence of a predominantly unilateral process in the pharynx, which is accompanied by asymmetric swelling of the mucous membrane, which may be the reason for the erroneous diagnosis of peritonsillar abscess.
In the vast majority of those vaccinated, diphtheria is characterized by a mild, sometimes abortive course. A localized form of diphtheria of the pharynx is more often observed. Toxic forms develop very rarely. 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 bacteria carriers, in addition to minimal local changes, ECG changes are detected, allowing us to think that carriage of diphtheria is the mildest form of the infectious process.

Complications of diphtheria

The most typical are complications from the circulatory system (myocarditis), the peripheral nervous system (polyneuritis) and the kidneys (nephrosonephritis), which are taken into account in retrospective diagnosis. They are associated with specific intoxication and occur, as a rule, with toxic forms, in case of delayed treatment with anti-diphtheria serum.
Myocarditis- often a dangerous complication. In patients with toxic diphtheria of 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 on the 6-8th day of illness. Death is possible in 2-3 weeks. The patient develops weakness, severe weakness, pallor, dizziness, and palpitations. The pulse is frequent, soft, arrhythmic, tachycardia can reach 200 per minute. When the sinus node is damaged, on the contrary, there is a sharp bradycardia (up to 50-30 per minute). The boundaries of the heart expand significantly and quickly, systolic murmur appears above the apex, and deafness of heart sounds appears. Many patients experience various heart rhythm disturbances (pendulum-like rhythm, extrasystole, gallop rhythm). Blood pressure decreases. The liver enlarges and thickens. An unfavorable prognostic sign indicating irreversible decompensation of the heart is Botkin’s “fatal” triad: vomiting, abdominal pain and gallop rhythm (embryocardia, or pendular heart rhythm). Vomiting is associated with brain hypoxia, abdominal pain is caused by stretching of the liver capsule with its rapid enlargement, cardiac arrhythmias are caused by damage to the conduction system of the heart. The ECG shows signs of myocardial damage, blockade of the anterior sac bundle or complete anterior sac block. In this state, most often, in full consciousness, the patient dies from cardiac paralysis. Mild and moderate forms of myocarditis develop less rapidly and are not accompanied by acute heart failure. Changes in the ECG reflect damage to the contractile myocardium without being drawn into the conduction system of the heart. On the 25-30th day of illness, 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, patients develop bulbar disorders 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 the lower extremities precede and may be more pronounced than in the upper extremities. Tendon and periosteal reflexes sharply decrease (extinct), and severe pain disappears. Later it turns out to be a polyneuritic type of sensitivity disorder - glove and toe syndrome. Musculo-articular sensitivity is often suppressed. Very rarely, paralysis develops like Landry's descending paralysis with dysfunction of the respiratory muscles and significant boulevard syndrome. In some cases, at the 4-5th week, polyradiculoneuritis of the Guillain-Barré type develops with protein-cell dissociation in the cerebrospinal fluid. The appearance of early polyneuritis, bulbar and oculomotor disorders is caused by the direct influence of the toxin, and degenerative changes begin with the terminal branches of the nerves in muscles. The leading factor in the occurrence of late polyneuritis and polyradiculoneuritis 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 the vagus and oculomotor nerves is restored. Paresis of the arms and legs undergoes reverse development for a long time - from 2-3 to 4-6 months. Residual manifestations of limb paresis can persist for a year or more. The early period of polyneuropathy is very dangerous, so 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 sharply in patients with phrenic nerve palsy. With the development of complications from the nervous system, the mortality rate 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 more pronounced the changes in the urine. Clinical manifestations of nephrosis are insignificant. However, views on kidney damage in diphtheria solely based on the type of nephrosis with a benign course require correction. According to our data, recently there have been cases where 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, complications caused by secondary bacterial flora are also observed, for example 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 completeness of treatment. With localized diphtheria of the pharynx without serotherapy, complications are possible (myocarditis, paralysis). In toxic diphtheria, mortality depends directly on the timeliness of serum administration. The cause of death in pharynx 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

The main symptoms of the clinical diagnosis of diphtheria of the pharynx are: a dense, continuous, usually with a smooth shiny surface and a tendency to spread, gray-white fibrinous plaque, after removal of which the mucous membrane bleeds (“blood dew”) and forms on it again (at first arachnoid) plaque; swelling, mild hyperemia with a cyanotic tint of the mucous membrane; moderate fever, enlarged regional lymph nodes, sore throat when swallowing, in the toxic form - swelling of the cervical subcutaneous tissue of varying prevalence, sweetish-putrid odor from the mouth; for diphtheria of the larynx - gradual (over 3-6 days) and in stages against the background of normal or subfebrile body temperature with an almost undisturbed general condition, the development of symptoms of croup: Hoarse voice and barking cough, and subsequently stenotic breathing and aphonia, characteristic changes during laryngoscopy .

Specific diagnosis of diphtheria

The most likely confirmation of the diagnosis of diphtheria is the results of bacteriological examination. The material for this is obtained from the tonsils and nose. If there is plaque, the material is taken from its edges, slightly forming a spherical film with a swab. In case of liquid localization of the process, in addition to smears from the affected areas, mucus from the tonsils and nose must be examined. Smears from the tonsils are made on an empty stomach or 2 hours after meals, without touching the tongue and teeth with the 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 suspected of diphtheria can be obtained after 24-48 hours, and a final answer, determining the toxigenicity (gravis or mitis) and biochemical variant of the isolated corynebacteria, can be obtained 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 microscopy result 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 diagnosis, 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 a 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 the toxin of the causative agent of diphtheria 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 diphtheria of the throat should be differentiated from lacunar, follicular, mycotic and necrotic tonsillitis, infectious mononucleosis, Simanovsky-Plaut-Vincent's tonsillitis, herpetic (aphthous) stomatitis, burns of the mucous membrane of the pharynx.
Lacunar and follicular tonsillitis is recognized by its acute onset, high body temperature, severe sore throat, bright hyperemia of the palatine tonsils, arches, uvula, and a yellow-white purulent coating that 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 the disease, a crater-shaped ulcer is observed at the site of necrosis, covered with a dirty yellow-green coating. Putrid odor 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, separate yellowish superficial ulcers on the tongue, mucous membrane of the cheeks, gums, palate, salivation, severe soreness in the mouth during meals, and 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, with a halo of hyperemia around. A common cause of a burn is lubrication of the mucous membrane with an alcohol solution of brilliant green, a concentrated solution of potassium permanganate, etc.
Common and toxic forms of diphtheria pharynx is differentiated with paratonsilitis, infectious mononucleosis, viral mumps, blood diseases.
Infectious mononucleosis is usually accompanied by enlargement of all groups of lymph nodes, hepatolienal syndrome, the presence of lymphocytosis, monocytosis, atypical mononuclear cells and heterophilic antibodies in the blood. Enlargement of the posterior cervical lymph nodes often precedes the appearance of layers on the tonsils, which sometimes extend to the arches. The deposits are loose, of varying thickness, yellowish or yellowish-white in color, and can be easily removed.
Viral mumps disease differs from diphtheria by the absence of plaque, painful chewing, Moores' sign, swelling and tenderness of the parotid salivary glands, which fill the space between the mastoid process and the angle of the mandible, enlargement of the submandibular salivary glands, as well as epidemiological history.
Paratonsilitis is an acute inflammation of the paratonsillar tissue, characterized by swelling and infiltration, pronounced hyperemia of the supramygdaloid area, anterior or posterior arch on one side. The tonsil is shifted to the midline, the corresponding anterior palatine arch is smoothed, the uvula is shifted to the opposite side. There is a very sharp pain when swallowing, radiating to the ear, and increased salivation. The opening of the mouth is significantly limited, the voice is nasal. The submandibular lymph nodes on the affected side are enlarged and sharply painful. Unlike diphtheria, the patient's face is hyperemic, he is excited, and suffers from a sharp pain in the throat. Often changes can be found in the tonsil, as in lacunar or follicular tonsillitis. Erroneous diagnosis 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, the spread of plaque, increased swelling of the subcutaneous tissue of the neck, and the development of further complications.
In case of blood diseases, along with necrotizing tonsillitis, severe pallor of the skin, splenomegaly, lymphadenitis, and hemorrhagic syndrome are observed. A blood test plays 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 foreign body aspiration.
Stenotic laryngotracheitis of viral etiology, in contrast to 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, and a rough barking cough appear. Although the voice becomes hoarse, the ringing notes remain at the height of the scream. All major manifestations of croup occur simultaneously. Laryngeal stenosis during ARVI can be quickly eliminated with appropriate treatment. Laryngoscopy reveals varying degrees of swelling of the mucous membrane under the vocal cords.
With aspiration of a foreign body, an attack of suffocation occurs suddenly, during the day, while eating or playing against the background of complete health. Immediately after aspiration, short-term apnea with cyanosis occurs, followed by a spastic 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 nasal diphtheria differentiated from a foreign body, in which purulent nasal discharge 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 of the upper respiratory tract. Unlike diphtheria, in this disease the swelling of the eyelids is mild, they are easily turned out. The discharge is serous or serous-purulent, and not sanguineous, 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 the motor regime is gradually expanded. 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 nutritious food is needed. Treatment must be specific and pathogenetic.
Specific treatment is carried out with highly purified equine hyperimmune serum “Diaferm”. To prevent an anaphylactic reaction, the serum is administered according to the Bezredki method. First, 0.1 ml of serum diluted 1:100 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 no more than 0.9 cm is formed, the reaction is considered negative and 0.1 ml of undiluted serum is administered subcutaneously, and if there is no reaction, after 30 minutes the entire prescribed dose is administered intramuscularly.
In case of toxic diphtheria of II-III degree and hypertoxic form, serotherapy is mandatory, under the protection of hormonal drugs, and sometimes under anesthesia. In the case of a positive intradermal test or in the presence of an anaphylactic reaction to subcutaneous administration, the serum is then administered only for absolute indications. First, the serum, diluted 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, administer 0.1 ml of undiluted serum 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 one fixed in the tissues. Therefore, specific treatment should be carried out as early as possible (optimally on the 1st-3rd day of illness).
Serum doses for the first administration and course of treatment are determined by the form of diphtheria.
If treatment is started late (after the 2nd day of illness) 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. For localized diphtheria of the pharynx, nose, liquid localization of the process and early serotherapy, you can limit yourself to a single injection of serum. With a delay in the "melting" of the plaque, it is administered again in a day. If diphtheria of the pharynx is common, the serum is administered for 2-3 days (in the case of 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.
For diphtheria croup, the initial dose of serum is determined by its stages: stage - 15-20 thousand AO, stage II - 30-40 thousand AO, stage III - 40 thousand AO; After 24 hours, this dose is repeated, and in the following days, if necessary, a half dose of the orphan is administered.
Typically, the course of serotherapy lasts no more than 3-4 days. Indications for discontinuation of serotherapy are the disappearance or significant reduction of plaque, swelling of the pharynx and subcutaneous tissue of the neck, and in croup - complete disappearance or reduction of stenotic breathing. If toxic diphtheria is suspected, serum is administered immediately; for a localized form - some waiting may be possible until the results of bacterioscopy, ENT examination, etc. are obtained, but subject to constant monitoring in the hospital; for diphtheria croup - administration of serum is mandatory if this diagnosis is not removed after intensive traction and antispastic therapy for 1 - 1.5 hours.
To enhance the effect of the serum, intramuscular injection of a 25% solution of magnesium sulfate is recommended once a day immediately after the start of serotherapy.
Pathogenetic treatment is aimed at detoxification, restoration of hemodynamics and elimination of adrenal insufficiency. Detoxification therapy involves the administration of a 10% glucose solution with insulin, protein preparations (10% albumin - 10 ml/kg) and colloidal solutions (reopolyglucin - 10 ml/kg) in a ratio of 1:1:1. Liquid is administered at the rate of 20-30 ml/kg body weight. Detoxification therapy is combined with the prescription 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. Nicotinic acid also weakens the effect of diphtheria toxin, and ascorbic acid stimulates immunogenesis and the function of the adrenal cortex.
Patients with common and toxic forms of pharynx diphtheria and laryngeal diphtheria are prescribed prednisolone (2-C mg/kg) or hydrocortisone (5-10 mg/kg per day) for 5-8 days for replacement, anti-inflammatory and hyposensitizing treatment. In the first 2-3 days, glycocorticosteroids are administered intravenously, then orally. In the hypertoxic and hemorrhagic form, the daily dose of prednisolone is increased to 5-20 mg/kg according to the degree of shock.
If diphtheria occurs in a toxic form, from the first day a 0.1% solution of strychnine nitrate (0.5-1.5 ml subcutaneously) is prescribed, 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 skeletal muscles and myocardium, and stimulates redox processes in the myocardium. Cordiamine and corazol are used, which increase the tone of the circulatory system. In cases of DIC, for disaggregation, in addition to rheopolyglucin, antihistamines, vasodilators, trental, and xanthinol are prescribed. To obtain an anticoagulant effect, heparin is administered (150-300-400 units/kg per day). Since rheopolyglucin enhances the effect of heparin, when administered simultaneously, the dose of the latter is reduced by 30-50%. It is recommended to administer protease inhibitors - trasylol, contrical, gordox, antagosan, pantrypin and aminocaproic acid.
Antibacterial therapy is prescribed to influence Corynebacterium diphtheria and secondary flora. It is advisable to use benzylpenicillin, tetracyclines, cephalosporins, erythromycin.
Treatment of patients with laryngeal diphtheria. Along with specific treatment, pathogenetic treatment is carried out. The child's agitation and anxiety increase the stenosis, so it is important to provide her with long-term medicated sleep. For this purpose, a 20% solution of sodium oxtbutyrate (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 of age), sibazon is prescribed (seduxen) and others. Oxygen therapy is provided. In case of laryngeal stenosis without respiratory failure, a good effect is achieved by traction therapy - a warm bath (37.5-38.5 ° C) for 5-10 minutes, warm soda drinks, mustard plasters, etc. To reduce swelling of the mucous membrane, use hyposensitizing drugs (diphenhydramine, pipolfen, tavegil, etc.), decongestants and anti-inflammatory drugs in aerosols (in the form of inhalations) are prescribed locally.
Complex treatment also involves the appointment of glycocorticosteroids, in particular prednisolone (2-3 mg/kg per day), which, in addition to the anti-inflammatory effect, help reduce laryngeal edema, reduce the permeability of the capillary wall and exudation. Half of the daily dose is first administered intravenously or intramuscularly, the rest is given orally. According to indications, detoxification therapy is carried out. Early prescription of broad-spectrum antibiotics is mandatory. If conservative treatment is ineffective, surgery is indicated.
Indicators for primary intubation (tracheotomy) are a triad of symptoms (according to G. Ivashentsov):
a) paradoxical pulse (inspiratory asystole of Rauchfuss),
b) Bayeux's symptom - constant tension of the sternocleidomastial muscle during inspiration,
c) persistent cyanosis of the lips and face. In the case of localized croup, long-term nasotracheal intubation with plastic tubes is possible; in case of widespread descending croup, tracheostomy is necessary, followed by drainage of the trachea and bronchi.
Treatment for complications. For myocarditis, the optimal duration of bed rest ranges from 3-4 weeks. Patients are fed small portions 5-6 times a day. Strychnine is prescribed (long course); administration of a 20% glucose solution with cocarboxylase, ascorbic acid; ATP for 2 weeks; calcium pangamate (50-150 mg per day); agents affecting tissue metabolism - anabolic agents (methandrostenolone orally for 1-1.5 months, potassium orotate 10-20 mg/kg per day for 2-3 weeks). For severe and moderate myocarditis, prednisolone orally and parenterally is recommended (daily dose 2 mg/kg for children, 40-60 mg for adults). The administration of cardiac glycosides is allowed only in cases of manifestations of heart failure without conduction disturbances. The prescription of strophanthin or corglycon requires careful monitoring of the clinic and ECG data. To prevent thromboembolic complications, indirect anticoagulants (dicoumarin, neodicoumarin, or pelentan) are used. The doses of these drugs are selected in such a way as to reduce the prothrombin index and keep it at 40-50%.
Patients with diphtheria polyneuritis are prescribed strychnine, B vitamins, and glycocorticosteroids. In the recovery period, oxazil 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 suck out the 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 to prevent pneumonia. According to indications, the patient is transferred to mechanical breathing in the intensive care unit. Based on the action of diphtheria toxin as an acetylcholinesterase inhibitor, proserin for neurological complications is prescribed after the acute manifestations of the disease have subsided.
Treatment of carriers of toxigenic corynebacteria diphtheria. When bacteria are repeatedly isolated, erythromycin, tetracycline antibiotics, and rifampicin are recommended in age-specific doses. After a seven-day course, sanitation usually occurs. The main focus is on chronic diseases of the nasopharynx. Treatment begins with general restoratives (methyluracil, pentoxyl, aloe, vitamins) and hyposensitizing agents, supplemented by physiotherapy (UHF, UV irradiation, ultrasound). If indicated, tonsils and adenoids are removed. Sometimes, after surgery, the carrier state quickly stops.
The length of hospital stay 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 12-14th day of the disease, widespread - on the 20-25th (Bed rest - 14 days). Patients with subtoxic and toxic I degree forms must be on bed rest for 25-30 days; they are discharged on the 30-40th day of illness. In case of toxic diphtheria of 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 at an interval of 2 days and no earlier than 3 days after the end of the course of antibacterial therapy.

Prevention of diphtheria

Active immunization plays a leading role in the fight against diphtheria. For this purpose, adsorbed diphtheria-tetanus-pertussis (DPT) vaccine and adsorbed diphtheria-tetanus (DT) toxoid, diphtheria-tetanus toxoid with reduced content of both antigens (ADS-M), diphtheria toxoid with reduced antigen content (AD-M) are used. .
Recently, a preventive vaccination scheme has been introduced, which is designed to provide protection to 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 after 1.5-2 years once (0.5 ml), and subsequent revaccinations are carried out once with ADS toxoid (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.
DTP toxoid is used in children with contraindications to the administration of DPT vaccine or in those who have had 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 toxoid consists of two injections of 0.5 ml with an interval of 45 days. AD-M toxoid is used for vaccination of persons who have a negative result in the RPGA with diphtheria diagnosticum and a positive result with tetanus.
The epidemiological effectiveness of vaccination depends not only on the quality of the 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, final disinfection is carried out. Surveillance of the source of infection is carried out for 7 days with mandatory bacteriological examination of nasal mucus from all persons who had contact with patients. Persons who have not been vaccinated within the last 10 years are immunized with AD-M or ADS-M toxoid; for 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 titer in RPHA less than 0.03 IU / ml) are immediately vaccinated.
To fully identify patients with diphtheria, especially those with erased forms, active surveillance of patients with tonsillitis is carried out (at least 3 days from the onset of the disease) with mandatory bacteriological testing for Corynebacterium diphtheria. The presence of toxigenic diphtheria bacilli in a patient with tonsillitis is a direct basis for diphtheria diagnosis. The occurrence of characteristic complications (myocarditis, nephrosis, paresis of the soft palate, polyradiculoneuritis) in patients who have had tonsillitis is the basis for a retrospective diagnosis of diphtheria.

Children began to be vaccinated against diphtheria, but before that, mortality from this infectious disease was quite high. Now children are more protected, but none of those vaccinated are safe from infection. You will learn about the symptoms, treatment and prevention of diphtheria in children by reading this article.

What it is?

Diphtheria is a bacterial infection caused by Bacillus Loeffler. These bacteria of the genus Corynebacterium do not pose a particular danger in and of themselves. A poisonous exotoxin is dangerous for humans, which is produced by microbes in the course of their life and reproduction. It blocks protein synthesis, practically depriving the cells of the body of the opportunity to perform their natural functions.

The microbe is transmitted by airborne droplets - from person to person. The more pronounced the patient's symptoms of diphtheria, the more bacteria he spreads around him. Sometimes infection occurs through food and water. In countries with a hot climate, Loeffler's bacillus can also be spread through household contact.

A child can become infected not only from a sick person, but also from a healthy person who is a carrier of diphtheria bacillus. Most often, the causative agent of the disease affects the organs that are the first to meet it on the way: the oropharynx, larynx, less often the nose, genitals, and skin.

Today, the prevalence of the disease is not too high, since all children are compulsorily vaccinated with DTP, ATP. The letter "D" in these abbreviations stands for the diphtheria component of the vaccine. Due to this, the number of infections over the past 50 years has been significantly reduced, but the disease cannot be completely eradicated.

The reasons are that there are parents who refuse mandatory vaccination of their child, and their sick children spread the diphtheria bacillus to others. Even a vaccinated child can become infected, but his disease will be milder and it is unlikely that it will reach the point of severe intoxication.

Signs

The incubation period, during which the rod only “examines” in the body without causing any changes, ranges from 2 to 10 days. In children with stronger immunity, the incubation period lasts longer; children with weakened immune defenses can show the first signs of an infectious disease as early as 2-3 days.

These signs may remind parents of a sore throat. The baby's temperature rises (up to 38.0-39.0 degrees), headache, and fever appear. The skin looks pale, sometimes somewhat bluish. From the first day of illness, the child’s behavior changes greatly - he becomes lethargic, apathetic, and drowsy. Painful sensations appear in the throat, and it becomes difficult for the child to swallow.

When examining the throat, enlarged palatine tonsils are clearly visible, the mucous membranes of the oropharynx look swollen and reddened. They are increased in size. The palatine tonsils (and sometimes the tissues bordering them) are covered with a coating that resembles a thin film. It most often has a gray or gray-white color. The film is very difficult to remove - if you try to remove it with a spatula, bleeding marks remain.

A symptom that may indicate diphtheria is swelling of the neck. Her parents will notice without difficulty. Against the background of soft tissue swelling, you can also palpate enlarged lymph nodes.

The most severe form of diphtheria is toxic. With it, all the above symptoms are more pronounced - the temperature rises to 40.0 degrees, the child may complain of severe pain not only in the throat, but also in the abdomen. The deposits on the tonsils and arches are very dense, serous, and continuous. The intoxication is severe.

Swelling of the neck is pronounced, the lymph nodes are greatly enlarged and painful. It is difficult for the baby to breathe through his nose due to hyperemia of the tonsils, and sometimes ichor comes out of the nose.

Hypertoxic diphtheria has the most severe manifestations. With it, the child is often unconscious or delirious, and has convulsions. All symptoms (fever, fever, swelling of the larynx and tonsils) develop rapidly. If proper medical care is not provided in time, coma occurs within two to three days. Death is possible due to developing failure of the cardiovascular system.

However, not all forms of diphtheria are so dangerous. Some (for example, nasal diphtheria) occur with almost no symptoms and do not threaten the child’s life.

Danger

A rather dangerous complication of diphtheria is the development of diphtheria croup. In this case, stenosis of the respiratory organs occurs. Due to swelling, the larynx narrows, the trachea and bronchi swell. At best, this leads to a change in the voice, hoarseness, and difficulty breathing. At worst, it leads to suffocation.

The most dangerous complication of diphtheria is the development of myocarditis (inflammation of the heart muscle). Irregular heart rhythm and impaired pulmonary respiration can lead to the development of respiratory as well as cardiovascular failure after 2-3 days. This condition is also deadly for the child.

Due to the action of a strong toxin, kidney failure can develop, as well as neurological disorders such as neuritis and regional paralysis. Paralysis is most often temporary and disappears without a trace after some time after recovery. In the vast majority of cases, paralysis of the cranial nerves, vocal cords, soft palate, neck muscles and upper limbs is recorded.

Some of the paralytic changes occur after the acute stage (on the 5th day), and some appear after diphtheria - 2-3 weeks after the apparent recovery.

The most common complication of diphtheria is acute pneumonia (pneumonia). As a rule, it occurs after the acute period of diphtheria is left behind (after 5-6 days from the onset of the disease).

The main danger lies in late diagnosis. Even experienced doctors cannot always recognize diphtheria in the first day or two. Namely, this time is important in order to introduce the child with antidiphtheria serum, which is an antitoxin, a substance that suppresses the toxic effects of exotoxin. Most often, in case of a fatal outcome, it is precisely the fact of untimely diagnosis that is revealed, as a result, the failure to provide proper assistance.

To prevent such situations, all doctors have clear instructions in case of detection of dubious symptoms, which may even indirectly indicate that the child has diphtheria.

Varieties

A lot in the choice of treatment tactics and in the prognosis for recovery depends on what kind of diphtheria and to what extent the baby was struck. If the disease is localized, then it is easier to tolerate than a diffuse (common) form. The smaller the source of infection, the easier it is to deal with it.

The most common form that occurs in children (about 90% of all cases of diphtheria) is oropharyngeal diphtheria. It happens:

• localized(with minor “islands” of plaque);
• spilled(with the spread of inflammation and plaque beyond the pharynx and oropharynx);
• subtoxic(with signs of intoxication);
• toxic(with a rapid course, swelling of the neck and severe intoxication);
• hypertoxic(with extremely severe manifestations, with loss of consciousness, critically large and extensive raids and swelling of the entire respiratory system);
• hemorrhagic(with all the signs of hypertoxic diphtheria and general systemic infection with diphtheria bacillus in the bloodstream).

With the development of diphtheria croup, the child’s condition worsens, and at the same time, the croup itself is divided into:

• diphtheria of the larynx - localized form;
• diphtheria of the larynx and trachea - diffuse form;
• descending diphtheria - the infection quickly moves from top to bottom - from the larynx to the bronchi, affecting the trachea along the way.

Nasal diphtheria is considered the mildest type of the disease, since it is always localized. With it, nasal breathing is disrupted, mucus mixed with pus and sometimes blood comes out of the nose. In some cases, nasal diphtheria is concomitant and accompanies pharynx diphtheria.

Diphtheria of the organs of vision manifests itself as ordinary bacterial conjunctivitis, which, by the way, is quite often mistaken for damage to the mucous membrane of the eyes by Loeffler's bacillus. Usually the disease is unilateral and is not accompanied by fever or intoxication. However, with toxic diphtheria of the eyes, a more violent course is possible, in which the inflammatory process spreads to both eyes and the temperature rises slightly.

Skin diphtheria can develop only where the skin is damaged - there are wounds, abrasions, scratches and ulcers. It is in these places that the diphtheria bacillus will begin to reproduce. The affected area swells, becomes inflamed, and a thick gray diphtheria plaque develops on it quite quickly.

It can persist for quite a long time, and the general condition of the child will be quite satisfactory.

Genital diphtheria in childhood is rare. In boys, foci of inflammation with typical serous plaques appear on the penis in the area of ​​the head; in girls, inflammation develops in the vagina and is manifested by bloody and serous purulent discharge.

Diagnostics

Existing laboratory tests help to quickly and promptly recognize diphtheria in a child. A swab from the child's throat must be taken for diphtheria bacillus. Moreover, it is recommended to do this in all cases when a dense grayish coating is noticeable on the tonsils. If the doctor does not neglect the instructions, he will be able to diagnose the disease in time and administer the antitoxin to the baby.

The smear is not very pleasant, but quite painless. The doctor runs a clean spatula over the filmy plaque and places the scraping into a sterile container. Then the sample is sent to a laboratory, where specialists can determine which microbe caused the disease.

After establishing the presence of corynebacteria, and this usually happens 20-24 hours after laboratory technicians receive the material, additional tests are taken to determine how toxic the microbe is. At the same time, specific treatment with anti-diphtheria serum is started.

Additional tests include a blood test for antibodies and a general blood test. It should be noted that every child who has been vaccinated with DTP has antibodies to the diphtheria bacillus. A diagnosis cannot be made based on this test alone.

With diphtheria, the number of antibodies rapidly increases, and during the recovery stage it decreases. Therefore, it is important to monitor the dynamics.

A general blood test for diphtheria in the acute stage shows a significant increase in the number of leukocytes, high ESR levels (the erythrocyte sedimentation rate during acute inflammation increases significantly).

Treatment

Diphtheria should be treated exclusively in a hospital - according to clinical recommendations. In a hospital setting, the child will be under round-the-clock supervision of doctors who will be able to respond in a timely manner to complications if they arise. Children are hospitalized not only with a confirmed diagnosis, but also with suspected diphtheria, since delay in dealing with this disease can have very disastrous consequences.

In other words, if a called doctor finds a thick gray coating in the child’s throat and a number of other symptoms, then he is obliged to immediately send the child to an infectious diseases hospital, where he will be prescribed all the necessary examinations (smear, blood tests).

Although Loeffler's bacillus is a bacterium, it is practically not destroyed by antibiotics. Not a single modern antibacterial drug has the desired effect on the causative agent of diphtheria, and therefore antimicrobial agents are not prescribed.

Treatment is based on the administration of a special antitoxin - PDS (anti-diphtheria serum). It stops the effect of the toxin on the body, and the child’s own immunity gradually copes with the stick as such.

Humanity owes the appearance of this serum to horses, since the drug is obtained by hypersensitizing these graceful animals with diphtheria bacillus. Antibodies from horse blood, which are contained in the serum, help the human immune system to mobilize as much as possible and begin the fight against the causative agent of the disease.

If a severe form of diphtheria is suspected, doctors in the hospital will not wait for test results and will immediately administer the serum to the baby. PDS is done both intramuscularly and intravenously - the choice of administration method is determined by the severity of the child’s condition.

PDS horse serum can cause severe allergies in a child, like any foreign protein. It is for this reason that the drug is prohibited for free circulation and is used only in hospitals, where a child who develops a rapid reaction to PDS can be provided with timely assistance.

During the entire treatment, you will need to gargle with special antiseptics that have a pronounced antibacterial effect. Most often, Octenisept spray or solution is recommended. If laboratory tests show the addition of a secondary bacterial infection, then antibiotics can be prescribed for a short course - for 5-7 days. Most often, drugs of the penicillin group are prescribed - “Ampicillin” or “Amoxiclav”.

To reduce the negative impact of exotoxin on the child’s body, droppers with detoxifying drugs are prescribed - saline, glucose, potassium supplements, vitamins, especially vitamin C. If it is very difficult for a child to swallow, Prednisolone is prescribed. To save a child’s life, in severe toxic forms, plasmapheresis procedures (donor plasma transfusion) are performed.

After the acute stage, when the main danger has passed, but the likelihood of complications remains, the child is prescribed a special diet, which is based on gentle and soft food. Such food does not irritate the affected throat. These are porridges, soups, purees, jelly.

Everything spicy is excluded, as well as salty, sweet, sour, spices, hot drinks, soda, chocolate and citrus fruits.

Prevention

A person can get diphtheria several times in his life. After the first illness, acquired immunity usually lasts for 8-10 years. But then the risks of getting infected again are high, although repeated infections are much milder and easier.

Specific prevention is vaccination. The DTP and ADS vaccines contain anti-diphtheria toxoid. In accordance with the national vaccination calendar, they are given 4 times: 2-3 months after birth, the next two vaccinations are carried out with an interval of 1-2 months (from the previous vaccination), and the fourth vaccine is administered a year after the third vaccination. The child is revaccinated at 6 years and 14 years old, and then vaccinated every 10 years.

Early detection of the disease prevents its widespread spread, which is why if you suspect a sore throat, peritonsillar abscess or infectious mononucleosis (diseases similar in symptoms to diphtheria), it is important to immediately conduct laboratory tests.

In a group where a child with diphtheria is identified, a seven-day quarantine is declared, and all children are required to take throat swabs for diphtheria bacillus. If in such a group there is a child who, for some reason, has not been vaccinated with DPT or ADS, he must be given anti-diphtheria serum.

Much depends on parents in preventing this disease. If they have taught the child hygiene, constantly strengthen his immunity, make sure that the baby grows healthy, and do not refuse preventive vaccinations, then we can assume that they are maximally protecting the child from a dangerous disease, the course of which is unpredictable. Otherwise, the consequences can be very sad.

See the following video for all about the rules of vaccination against diphtheria.