Toxic diphtheria treatment. Diphtheria of other localizations. Signs and symptoms of diphtheria pharynx in toxic form

Diphtheria is an acute infection, the causative agents of which are Loeffler's bacilli. Depending on the location of the pathogenic focus, several types of diphtheria are distinguished: diphtheria of the pharynx, larynx and nose. Forms of rare localization include the eyes, mucous membranes of the mouth and skin.

The causative agents of the disease are pathogenic immobile rods, which are located at an angle to each other and, when viewed under a microscope, resemble the Roman numeral V. The pathogen is resistant to external environment and is capable of exhibiting great variability depending on the conditions in which it finds itself.

Leffler's wand

Leffler's stick tolerates temperatures down to 0 °C and remains viable for a long time when dry. The causative agent of diphtheria is covered with a film or mucus, so even when dried it can remain viable and toxic for up to several months. If bacteria are in a sprayed state in the air, then even in sunlight they remain viable for several hours, and in the dark - up to 2 days.

The only thing that kills Loeffler's wand, – disinfectant solutions. When multiplying, the diphtheria bacterium releases an exotoxin, which is very dangerous for humans. The source of infection is a sick person or a bacteria carrier.

Infection

Infection occurs on the last day of the incubation period. After the pathogen ceases to be excreted from the patient’s body, it ceases to pose a danger to others.

As a rule, the process of cleansing the body of the pathogen lasts on average about 1 month, but depending on the severity of the disease it can be longer or shorter.

Diphtheria is transmitted by airborne droplets. The pathogen is transmitted to a person by talking, sneezing, or coughing. However, there is also a non-contact route of transmission of the disease, since the pathogen persists for a long time on household items, and in some products the rod can even multiply.

The disease begins with the formation of a local inflammatory focus in the place where the pathogen has penetrated. Diphtheria bacteria secrete a toxin that spreads throughout the body lymphogenously, resulting in general intoxication. The most common sites of localization of the pathogenic focus are the larynx, pharynx and ear. The nose and even mucous membranes, eyes and skin are often affected.

Inflammatory process

The inflammatory process at the site of infection is fibrinous in nature. This is manifested by cell necrosis, fibrinogen coagulation and the formation of a fibrinous film. Fibrinous inflammation can be lobar and diphtheric. In the first case, superficial damage to the mucous membrane occurs (in this case, the affected film is easily separated from the lower tissues). During the diphtheria process, deep-lying tissues are also affected (in this case, the film is tightly connected to them).

The tissues surrounding the location of the pathogenic focus become swollen, and the inflammatory process spreads widely, capturing the fiber.

Forms

Severe forms of the disease are characterized by hemorrhages in various parts of the body. The disease is especially dangerous because, as a result of severe intoxication of the body, damage occurs to the central nervous system the patient, as well as the kidneys and adrenal glands. The cardiovascular system also suffers. One of the common complications of diphtheria is myocarditis, in which the heart muscle greatly increases in size and becomes flabby.

As a result of the formation of wall thrombi, cerebral embolism and the development of central paralysis can occur. Death from diphtheria in most cases occurs due to cardiovascular failure and myocarditis.

Recovery occurs due to the accumulation of antitoxin in the body. The film is gradually rejected, and superficial ulcerations heal.

The most common form of diphtheria is pharyngeal diphtheria. It can be toxic and non-toxic. In toxic forms of pharynx diphtheria, swelling is observed in the area of ​​regional lymph nodes. Non-toxic forms can be localized and widespread. More common is a localized form, characterized by the concentration of the pathological process in the tonsil area.

The prognosis for this form of the disease is favorable; with timely and correct therapy, the disease proceeds without complications.

Depending on the severity of local changes, diphtheria can be tonsillar, island and catarrhal. At the onset of the disease, patients' temperature rises slightly (up to 38°). In this case, the patient has difficulty swallowing. On examination, the tonsils are moderately red and covered with plaque. In the first days of the disease, this plaque looks like a thin film, but after some time its edges take on distinct outlines, and the plaque itself protrudes above the surface of the tonsils.

In the tonsillar form of the disease, plaque resembles plaques or islands. The patient feels pain when swallowing, the lymph nodes are inflamed and painful. With the catarrhal form there are no pronounced symptoms of intoxication, so the diagnosis can only be established using laboratory research methods.

For localized forms of diphtheria, the patient is advised to administer anti-diphtheria serum. As a rule, in such cases, after 2-3 days the patient’s condition improves significantly. If left untreated, the disease takes on a toxic form.

The toxic form of diphtheria in most cases develops as a result of untimely or improper treatment. The disease begins acutely: a high temperature immediately rises, the patient complains of severe headache, weakness, abdominal pain and vomiting. Fibrinous plaque affects not only the tonsils, but also the soft and hard palate. As a result of damage to the nasopharynx, the patient's breathing is difficult, and hemorrhage may occur.

In the subtoxic form, the swelling is not significant and is localized mainly on one side, covering the area around the regional lymph nodes. It should be taken into account that the more pronounced the swelling, the more enlarged the lymph nodes are. In severe forms of the disease, the nodes are large, dense and painful.

The most dangerous forms of diphtheria

Most dangerous forms diphtheria – fulminant and hemorrhagic, which are hypertoxic. In the first case, swelling of the pharynx occurs quickly; in a few hours, intoxication of the body begins to appear. In the second case, the plaque is brown in color due to the accumulation of blood in it.

In the fulminant form of the disease, the patient experiences clouding of reason, blood pressure drops, and heart function slows down. Progressive intoxication leads to death a few days after the onset of the disease. In most cases, the cause of death is vascular insufficiency.

Diphtheria of the larynx is also called croup. Primary croup is localized in the larynx, secondary - in the nose or pharynx. Characteristic signs of laryngeal diphtheria are severe cough, voice changes and stenosis. The disease goes through 3 stages - catarrhal, stenotic and asphyxial.

During the catarrhal stage, the patient's body temperature rises, at the same time coughing and hoarseness are observed. After 2 days, the stenotic stage begins, in which a dense fibrinous film causes spasm of the laryngeal muscles. This process is accompanied by swelling of the mucous membrane, resulting in the development of stenosis.

Stenosis usually develops gradually and goes through 4 stages. At the first stage, the patient experiences noisy breathing, at the second stage the voice disappears. When inhaling, the intercostal spaces and subclavian fossae are retracted. At the third stage, symptoms of oxygen deficiency appear, resulting in hypoxia of the cerebral cortex. At the fourth stage, poisoning of the cerebral cortex with carbon dioxide occurs. After some time, death occurs.

Nasal diphtheria is usually observed in infants. This form of the disease does not cause high fever. It becomes difficult for the child to breathe, and thin bloody discharge appears from the nose. A fibrinous film appears on the nasal mucosa.

Diphtheria of the eyes can be lobar or diphtheric. In the first case, a fibrinous film covers the conjunctiva. In this case, the patient’s eyelids are swollen, bloody discharge from the eyes is observed, and the palpebral fissures are narrowed. The fibrinous film is easily removed from the conjunctiva. In the diphtheric form, the film fuses with the underlying tissues. In this case, the patient’s temperature rises significantly and pronounced swelling of the eyelids is observed. The plaque is covered with blood and is difficult to remove from the conjunctiva. This is the most severe form of the disease, the complication of which is complete blindness.

Diphtheria of the ear is characterized by damage to the epithelium of the ear canal and eardrum. A fibrinous film forms in these areas. With diphtheria of the skin, diaper rash or eczema, covered with diphtheria films, occurs. As a result of the disease, various toxemia and toxic complications often develop.

The most dangerous complication of diphtheria is adrenal insufficiency, which develops as a result of extensive damage to the adrenal cortex. In most cases, the complication appears on the third day of the disease. When palpated, the patient's pulse is rapid and thread-like, and blood pressure is low. This complication almost always ends in collapse and death.

However, with timely use of serum and corticosteroids medicines the patient can be brought out of this state. Another complication of diphtheria is toxic nephrosis. Nephrosis is not life-threatening, and symptoms disappear as you recover.

A dangerous complication of diphtheria is myocarditis, which manifests itself at the beginning of the second week of the disease. The patient's general health deteriorates, weakness appears, and he looks pale. The patient is restless and complains of abdominal pain and nausea. Upon auscultation, expansion of the borders of the heart is observed, the liver enlarges, and the pulse is disturbed. All of these phenomena indicate a severe pathological process that can lead to death.

The process of recovery of a patient after myocarditis is long, as a rule, it lasts 2-3 months. In addition to myocarditis, symptoms of early paralysis may occur against the background of diphtheria. In most cases, there is paralysis of the soft palate with the disappearance of its mobility.

The patient often experiences difficulty eating and has difficulty swallowing. Paralysis is a prerequisite for the further occurrence of polyneuritis. Polyradiculoneuritis is detected a month after the onset of the disease. Patients show a decrease tendon reflexes. Particularly dangerous are paralysis, leading to disruption of the functions of many systems and organs. If pneumonia is added to the pathological process, death is possible.

Treatment

Anti-diphtheria serum is used in the treatment of diphtheria. Moreover, the earlier the serum is administered, the more favorable the prognosis. For mild forms of diphtheria, a single injection of serum is sufficient, and in case of intoxication, the drug must be administered over several days.

For toxic forms of diphtheria, intravenous drip infusions of protein preparations - albumin or plasma - are indicated. In addition, the patient is administered neocompensan and hemodez with a 10% glucose solution, and cocarboxylase and prednisolone are also prescribed.

During treatment, the patient needs vitamin therapy. The patient must maintain strict bed rest during the entire treatment period. With diphtheria croup, the patient should be provided with rest and a supply of fresh air. During the treatment period, sedatives are indicated: phenobarbital, aminazine, bromides. However, it is necessary to carefully ensure that the patient does not fall into deep sleep.

To weaken laryngeal stenosis, gluco-corticosteroids are used. Films and mucus from the respiratory tract are removed using an electric suction. To prevent complications of croup with pneumonia, the patient is prescribed antibiotics. In severe cases of stenosis, a tracheotomy is performed.

Bacteria carriers undergo treatment for 1 week. They are shown erythromycin, tetracycline and ascorbic acid.

– an acute infectious disease of a bacterial nature, characterized by the development of fibrinous inflammation in the area of ​​introduction of the pathogen (mainly the upper respiratory tract and the mucous membrane of the oropharynx are affected). Diphtheria is transmitted by airborne droplets and airborne dust. The infection can affect the oropharynx, larynx, trachea and bronchi, eyes, nose, skin and genitals. Diagnosis of diphtheria is based on the results of a bacteriological examination of a smear from the affected mucous membrane or skin, examination data and laryngoscopy. If myocarditis and neurological complications occur, consultation with a cardiologist and neurologist is required.

ICD-10

A36

General information

– an acute infectious disease of a bacterial nature, characterized by the development of fibrinous inflammation in the area of ​​introduction of the pathogen (mainly the upper respiratory tract and the mucous membrane of the oropharynx are affected).

Causes of diphtheria

Diphtheria is caused by Corynebacterium diphtheriae, a gram-positive, non-motile bacterium that has the appearance of a rod, at the ends of which there are grains of volutin, giving it the appearance of a club. The diphtheria bacillus is represented by two main biovars and several intermediate variants. The pathogenicity of the microorganism lies in the release of a potent exotoxin, second only to tetanus and botulinum in toxicity. Strains of bacteria that do not produce diphtheria toxin do not cause disease.

The pathogen is resistant to environmental influences and can survive on objects or in dust for up to two months. It tolerates low temperatures well and dies when heated to 60 °C after 10 minutes. Ultraviolet irradiation and chemical disinfectants (Lysol, chlorine-containing agents, etc.) have a detrimental effect on the diphtheria bacillus.

The reservoir and source of diphtheria is a sick person or carrier who secretes pathogenic strains of diphtheria bacillus. In the vast majority of cases, infection occurs from sick people; erased and atypical clinical forms of the disease are of greatest epidemiological significance. Isolation of the pathogen during the period of convalescence can last 15-20 days, sometimes extending to three months.

Diphtheria is transmitted via the aerosol mechanism mainly by airborne droplets or airborne dust. In some cases, it is possible to implement a contact-household route of infection (using contaminated household items, dishes, transmission through dirty hands). The pathogen is capable of multiplying in food products (milk, confectionery), facilitating the transmission of infection through nutritional routes.

People have a high natural susceptibility to infection; after suffering from the disease, an antitoxic immunity is formed, which does not prevent the carriage of the pathogen and does not protect against re-infection, but contributes to an easier course and the absence of complications if it occurs. Children of the first year of life are protected by antibodies to diphtheria toxin transmitted transplacentally from the mother.

Classification

Diphtheria varies depending on the location of the lesion and clinical course to the following forms:

• diphtheria of the oropharynx (localized, widespread, subtoxic, toxic and hypertoxic);
• diphtheria croup (localized croup of the larynx, widespread croup when the larynx and trachea are affected, and descending croup when it spreads to the bronchi);
• diphtheria of the nose, genitals, eyes, skin;
• combined damage to various organs.

Localized diphtheria of the oropharynx can occur in the catarrhal, island and membranous form. Toxic diphtheria is divided into first, second and third degrees of severity.

Diphtheria symptoms

Diphtheria of the oropharynx develops in the vast majority of cases of infection diphtheria bacillus. 70-75% of cases are represented by a localized form. The onset of the disease is acute, the body temperature rises to febrile levels (less often, low-grade fever persists), symptoms of moderate intoxication appear (headache, general weakness, loss of appetite, pale skin, increased pulse rate), sore throat. The fever lasts 2-3 days, by the second day the plaque on the tonsils, previously fibrinous, becomes denser, smoother, and acquires a pearlescent sheen. Plaques are difficult to remove, leaving areas of bleeding mucosa after removal, and the next day the cleaned area is again covered with a film of fibrin.

Localized diphtheria of the oropharynx manifests itself in the form of characteristic fibrinous plaques in a third of adults; in other cases, the plaques are loose and easily removable, leaving no bleeding behind. Typical diphtheria plaques become like this after 5-7 days from the onset of the disease. Inflammation of the oropharynx is usually accompanied by moderate enlargement and sensitivity to palpation of regional lymph nodes. Inflammation of the tonsils and regional lymphadenitis can be either unilateral or bilateral. Lymph nodes are affected asymmetrically.

Localized diphtheria rarely occurs in the catarrhal form. In this case, low-grade fever is noted, or the temperature remains within normal limits, intoxication is mild, and upon examination of the oropharynx, hyperemia of the mucous membrane and some swelling of the tonsils are noticeable. Pain when swallowing is moderate. This is the mildest form of diphtheria. Localized diphtheria usually ends in recovery, but in some cases (without proper treatment) it can progress to more widespread forms and contribute to the development of complications. Typically, the fever goes away on days 2-3, and plaque on the tonsils – on days 6-8.

Common diphtheria of the oropharynx is observed quite rarely, no more than 3-11% of cases. With this form, plaque is detected not only on the tonsils, but also spreads to the surrounding mucous membrane of the oropharynx. In this case, general intoxication syndrome, lymphadenopathy and fever are more intense than with localized diphtheria. The subtoxic form of oropharyngeal diphtheria is characterized by intense pain when swallowing in the throat and neck area. When examining the tonsils, they have a pronounced purple color with a cyanotic tint, covered with plaque, which is also noted on the uvula and palatine arches. This form is characterized by swelling of the subcutaneous tissue above compacted, painful regional lymph nodes. Lymphadenitis is often unilateral.

Currently, the toxic form of oropharyngeal diphtheria is quite common, often (in 20% of cases) developing in adults. The onset is usually violent, with a rapid increase in body temperature to high values, an increase in intense toxicosis, cyanosis of the lips, tachycardia, and arterial hypotension. There is severe pain in the throat and neck, and sometimes in the stomach. Intoxication contributes to disruption of central nervous activity, possibly causing nausea and vomiting, mood disorders (euphoria, excitement), consciousness, perception (hallucinations, delirium).

Toxic diphtheria of II and III degrees can contribute to intense swelling of the oropharynx, interfering with breathing. Plaques appear quite quickly and spread along the walls of the oropharynx. The films thicken and become coarser, and plaques persist for two or more weeks. Early lymphadenitis is noted, the nodes are painful and dense. Usually the process involves one side. Toxic diphtheria is characterized by painless swelling of the neck. The first degree is characterized by swelling limited to the middle of the neck, in the second degree it reaches the collarbones and in the third it spreads further to the chest, face, back surface neck and back. Patients note an unpleasant putrid odor from the mouth and a change in the timbre of the voice (nasality).

The hypertoxic form is the most severe and usually develops in people suffering from severe chronic diseases (alcoholism, AIDS, diabetes, cirrhosis, etc.). Fever with tremendous chills reaches critical levels, tachycardia, low pulse, drop in blood pressure, severe pallor in combination with acrocyanosis. With this form of diphtheria, it can develop hemorrhagic syndrome, progress infectious-toxic shock with adrenal insufficiency. Without proper medical care, death can occur within the first or second day of the disease.

Diphtheria croup

With localized diphtheria croup, the process is limited to the mucous membrane of the larynx, with a widespread form, the trachea is involved, and with descending croup, the bronchi. Croup often accompanies oropharyngeal diphtheria. Increasingly recently, this form of infection has been observed in adults. The disease is usually not accompanied by significant general infectious symptoms. There are three successive stages of croup: dysphonic, stenotic and asphyxia.

The dysphonic stage is characterized by the appearance of a rough “barking” cough and progressive hoarseness of the voice. The duration of this stage ranges from 1-3 days in children to a week in adults. Then aphonia occurs, the cough becomes silent - the vocal cords become stenotic. This condition can last from several hours to three days. Patients are usually restless; upon examination, pale skin and noisy breathing are noted. Due to the obstruction of air passage, retraction of the intercostal spaces may occur during inhalation.

The stenotic stage turns into asphyxia - difficulty breathing progresses, becomes frequent, arrhythmic until it stops completely as a result of obstruction of the respiratory tract. Prolonged hypoxia disrupts brain function and leads to death from suffocation.

Nasal diphtheria

Manifests itself in the form of difficulty breathing through the nose. With the catarrhal variant of the course - discharge from the nose of a serous-purulent (sometimes hemorrhagic) nature. Body temperature, as a rule, is normal (sometimes low-grade fever), intoxication is not pronounced. Upon examination, the nasal mucosa is ulcerated, fibrinous deposits are noted, which in the filmy version are removed like shreds. The skin around the nostrils is irritated, maceration and crusts may occur. Most often, nasal diphtheria accompanies oropharyngeal diphtheria.

Diphtheria eye

The catarrhal variant manifests itself in the form of conjunctivitis (mostly unilateral) with moderate serous discharge. General condition is usually satisfactory, there is no fever. The membranous variant is characterized by the formation of fibrinous plaque on the inflamed conjunctiva, swelling of the eyelids and discharge of a serous-purulent nature. Local manifestations are accompanied by low-grade fever and mild intoxication. The infection may spread to the other eye.

The toxic form is characterized by an acute onset, rapid development of general intoxication symptoms and fever, accompanied by severe swelling of the eyelids, purulent hemorrhagic discharge from the eye, maceration and irritation of the surrounding skin. Inflammation spreads to the second eye and surrounding tissues.

Diphtheria of the ear, genital organs (anal-genital), skin

These forms of infection are quite rare and, as a rule, are associated with the peculiarities of the method of infection. Most often combined with diphtheria of the oropharynx or nose. They are characterized by edema and hyperemia of the affected tissues, regional lymphadenitis and fibrinous diphtheria plaques. In men, genital diphtheria usually develops on the foreskin and around the glans, in women - in the vagina, but can easily spread and affect the labia minora and majora, perineum and anus. Diphtheria of the female genital organs is accompanied by hemorrhagic discharge. When inflammation spreads to the urethral area, urination causes pain.

Diphtheria of the skin develops in places where the integrity of the skin is damaged (wounds, abrasions, ulcerations, bacterial and fungal infections) if they are exposed to a pathogen. It appears as a gray coating on an area of ​​hyperemic, swollen skin. The general condition is usually satisfactory, but local manifestations can persist for a long time and slowly regress. In some cases, asymptomatic carriage of the diphtheria bacillus is recorded, which is more often characteristic of persons with chronic inflammation of the nasal cavity and pharynx.

Determining the increase in the titer of antitoxic antibodies is of auxiliary importance and is carried out using RNGA. Diphtheria toxin is detected using PCR. Diphtheria croup is diagnosed by examining the larynx using a laryngoscope (swelling, hyperemia and fibrinous films are noted in the larynx, in the glottis, and trachea). If neurological complications develop, a patient with diphtheria needs to consult a neurologist. If signs of diphtheria myocarditis appear, a consultation with a cardiologist, ECG, and ultrasound of the heart are prescribed.

Treatment of diphtheria

Patients with diphtheria are hospitalized in infectious diseases departments, etiological treatment consists of administering anti-diphtheria antitoxic serum according to the modified Bezredki method. In severe cases it is possible intravenous administration serum.

The complex of therapeutic measures is supplemented with drugs according to indications; for toxic forms, detoxification therapy is prescribed using glucose, cocarboxylase, vitamin C, and, if necessary, prednisolone, in some cases -. If there is a threat of asphyxia, intubation is performed, in cases of obstruction of the upper respiratory tract - tracheostomy. If there is a threat of developing a secondary infection, antibiotic therapy is prescribed.

Prognosis and prevention

The prognosis for localized forms of mild and moderate diphtheria, as well as with timely administration of antitoxic serum, is favorable. The prognosis can be aggravated by the severe course of the toxic form, the development of complications, and late onset. therapeutic measures. Currently, due to the development of means of helping patients and mass immunization of the population, the mortality rate from diphtheria is no more than 5%.

Specific prevention is carried out as planned for the entire population. Vaccination of children begins at three months of age, revaccination is carried out at 9-12 months, 6-7, 11-12 and 16-17 years. Vaccinations are carried out with a complex vaccine against diphtheria and tetanus or against whooping cough, diphtheria and tetanus. If necessary, adults are vaccinated. Patients are discharged after recovery and a double negative bacteriological examination.

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 (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 (infectious from the last day of the incubation period until the 10-25th day of illness) and bacteria carriers of a toxigenic strain of the pathogen. Bacterial carriage develops after an illness, as well as in healthy individuals. It lasts 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 their large numbers and mass contacts, are the most common source of infection.
The main mechanism of infection is airborne. Due to the stability of the pathogen in the external environment, contact transmission through objects and third parties is possible. In some cases, infection occurs through the nutritional 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 whose intensity is low (the antitoxin content is lower than 0.03 AO in 1 ml of blood) become ill.
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 wall permeability small vessels at the site of 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, resulting in the formation of fibrinous plaque(film) is 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 to varying degrees, up to infectious-toxic shock. The most profound changes occur in the myocardium. They are characterized by degenerative degeneration muscle fibers up to complete myolysis and productive changes in interstitial tissue. Deep violations metabolic processes, in particular protein synthesis, lead to cell death with their replacement by connective tissue. Ganglion cells and nerve fibers 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.
At 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), essential has a reflex spasm of the muscles of the larynx, swelling of its mucous membrane, especially under the vocal folds.
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 last years Somewhat more often, hemorrhagic saturation of the plaque is observed, some of its parts 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 back wall 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 clavicle - 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 (skin pallor, 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

When the process is localized 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: hoarse voice, rude 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 pliable parts 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 (sternoclavicular-mamillary, 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 occurs 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 bacterial flora 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 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 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 vaccinated people, 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 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 children.
Carriage of the causative agent of diphtheria can be short-term (2 weeks), medium-long (1 month), prolonged and recurrent. Longer carriage is observed in persons with chronic inflammatory processes 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 serious 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 from 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 autonomic 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. By clinical signs polyneuropathic syndrome in diphtheria is mixed, sensory, motor and autonomic disorders are noted. Symptoms of the lesion autonomic system(acrocyanosis, hyperhidrosis, increased sensitivity of the extremities to cold) appear throughout the entire period of the disease. Peripheral paralysis usually develop in the 2-3rd week, and in recent years - in the 4th-5th and later. Paralysis is characterized by all the peripheral signs: hypotonia and muscle atrophy, 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 pharyngeal muscles of the pharynx due to damage to the glossopharyngeal and vagus nerves. Clinically, this is manifested by a nasal voice, difficulty swallowing, soreness while eating, pouring liquid food through the nose, drooping of the soft palate and its immobility during phonation, decreased or absent pharyngeal reflex.
In the case of paralysis of accommodation (damage to the n. ciliares), patients poorly distinguish objects at a close distance, but they see distant objects well, and when reading, the letters in them merge.
Relatively rarely, strabismus (n. abducens), drooping eyelid (n. oculomotorius), and 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 damage to the distal extremities appears. Movement disorders in lower limbs precede and may be more pronounced than in the upper ones. 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 it is possible sudden stop heart disease or severe aspiration pneumonia associated with swallowing disorders. 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. The mortality rate is higher in children than in adults.

Diphtheria diagnosis

Reference symptoms clinical diagnostics diphtheria of the pharynx is: 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 a plaque (at first cobweb-like) forms on it again; 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 almost no disturbance general condition development of croup symptoms: 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 the final answer, determining the toxigenicity (gravis or mitis) and the 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 diagnostics RIGA is used, carried out with the patient’s blood serum and corynebacteria antigen. The increase in antibody titer in paired sera obtained before the 7th day of illness (before the administration of therapeutic serum) and after 1-2 weeks is regarded as positive result. This is a retrospective method. A negative result does not negate the diagnosis of diphtheria. At the onset of the disease, the antitoxin is not detected or its amount does not exceed 0.5 AO / ml.
Recently, an accelerated method of toxin indication has been introduced - the antibody neutralization reaction (ANTR) using a commercial diphtheria antigen (diphtheria toxoid diagnosticum).
A preliminary response to the identification of the toxin of the causative agent of diphtheria in the RNA guides the doctor towards early prescription of serum and timely implementation of anti-epidemic measures at the source of infection.

Differential diagnosis of diphtheria

Localized diphtheria of the throat should be differentiated from lacunar, follicular, mycotic and necrotizing tonsillitis, infectious mononucleosis, Simanovsky-Plaut-Vincent 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 pain in the throat, bright hyperemia of the palatine tonsils, arches, uvula, yellow-white purulent coating, which is easily removed. In patients with follicular angina, yellowish lesions appear under the mucous membrane purulent follicles(small subepithelial abscesses). Regional lymph nodes with angina are significantly enlarged and sharply painful.
Mycotic tonsillitis is characterized by plump, cheese-like white deposits of varying 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 oral mucosa (tongue, cheeks).
The difference between necrotic tonsillitis is the presence of crusty, 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 the regional lymph nodes.
Angina Simanovsky-Plaut-Vincent, - as a rule, unilateral damage to the tonsils, necrosis does not rise above their surface (minus tissue), on the 3-4th day of illness, at the site of necrosis, a crater-shaped ulcer is observed, covered with a dirty yellowish-green coating. Putrid odor from the mouth. In smears obtained from the surface of the ulcer, during direct bacterioscopy, symbiotic saprophytic microorganisms - spirochetes and spindle-shaped rods - appear.
Herpetic (aphthous) stomatitis, along with damage to the tonsils, is accompanied by gingivitis, stomatitis, individual yellowish superficial ulcers on the tongue, mucous membrane of the cheeks, gums, palate, salivation, severe pain in the mouth while eating, and fever.
In case of burns (thermal and chemical) of the oral mucosa, pain is felt when swallowing, the mucous membrane is damaged, the fibrinous-necrotic layers are thin, yellowish, with a rim of hyperemia around. A common cause of burns 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 from paratonsillitis, infectious mononucleosis, viral mumps, and blood diseases.
Infectious mononucleosis is usually accompanied by enlargement of all groups of lymph nodes, hepatolienal syndrome, the presence of lymphocytosis, monocytosis in the blood, atypical mononuclear cells and heterophilic antibodies. Enlargement of the posterior cervical lymph nodes often precedes the appearance of layers on the tonsils, which sometimes extend to the arches. The plaques are loose, various thicknesses, yellowish or yellowish-white in color, easily removable.
Viral mumps disease differs from diphtheria by the absence of plaque, painful chewing, Moore's sign, swelling and tenderness of the parotid salivary glands, which fill the space between the mastoid process and the angle of the mandible, an increase in the submandibular salivary glands, as well as epidemiological history data.
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. It is noted very sharp pain when swallowing with irradiation into the ear, 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.
Stenosing laryngotracheitis viral etiology, unlike diphtheria croup, occurs suddenly, often at night, often repeatedly, against the background of catarrhal manifestations, high body temperature and symptoms of intoxication. Difficulty, stenotic breathing, 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 in the background full 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 anaphylactic reaction The serum is administered using the Bezredka 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 II-III degree and hypertoxic form, serotherapy is mandatory, under protection hormonal drugs, and sometimes - anesthesia. In the case of a positive intradermal test or in the presence of an anaphylactic reaction to subcutaneous administration, 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 minutes. If there is no response to the previous dose, administer 0.1 ml of undiluted serum subcutaneously. If there is no reaction, the entire prescribed dose is administered subcutaneously after 30 minutes. In exceptional cases, the 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 serum administration 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. If the “melting” of plaque is delayed, it is reintroduced every other 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 of the 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 - it is possible to wait some time 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. A 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. With 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, xanthinol. 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 carry out pathogenetic. 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 good effect gives Extraction 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, hyposensitizing drugs are used (diphenhydramine, pipolfen, tavegil and 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 ineffective, surgical intervention 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, oral and parenteral prednisolone is recommended (in 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 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 for the prevention of 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 inhibitor of acetylcholinesterase, proserin for neurological complications is prescribed after extinction acute manifestations diseases.
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.

Toxic diphtheria is a dangerous infectious disease various forms, included in the vaccination calendar since the times of the USSR. They try to prevent the disease in advance, because it is not only difficult, but also causes irreversible consequences in the form of serious disruptions to the functioning of organs and the nervous system.

Description of the disease

Toxic diphtheria is one of the forms of ordinary diphtheria related to acute infections bacterial nature and accompanied by fibrinous damage to the organ into which the pathogen has penetrated. Usually these are the upper respiratory tract and pharynx, but sometimes the eyes and even the genitals are covered with a specific film.

The French doctor F. Bretanno began to describe diphtheria in 1826. Then the infection got its name from the Greek word diphthero - skin. At that time, with toxic diphtheria, it was the skin that was affected, because people did not particularly care about hygiene, and outer layer the dermis was often too sensitive to infections.

Pathogen

The causative agent of diphtheria was discovered later than the disease itself. It was only in 1883 that E. Klebs discovered the bacterium in cultures, and the antitoxic diphtheria serum was obtained 11 years later. Almost immediately, the drug began to be used in Russia, where diphtheria had already spread by that time.

Curious! In 1912 they began to conduct skin tests with diphtheria toxin to determine the susceptibility of people to diphtheria.

The causative agent of diphtheria (Clostridum diphteriae) is a rod no more than 3 microns long. It is not straight, like the intestinal one, but has a slight bend. Its ends are slightly enlarged, because they contain special inclusions - nutritious grains. According to the degree of virulence, there are three types of diphtheria bacteria: gravis (the most dangerous, causing severe forms of diphtheria), mitis (mild forms of disease), intermedius (moderate).

Diphtheria bacteria live in different liquids body: in saliva, in nasopharyngeal mucus, in vaginal secretions. In the external environment, they can remain viable for up to 2-3 weeks.

Routes of infection

The danger of diphtheria is also due to the fact that the disease is easily transmitted by airborne droplets. For this reason, in 1990-1999, more than 150 thousand people fell ill in the countries of the USSR, of whom almost 5 thousand died. The outbreak was caused by people ignoring the booster vaccination program, where adults should have been vaccinated against diphtheria again but did not.

They become infected from a sick person by sneezing, coughing and even normal conversation. A person's susceptibility to diphtheria bacteria is very high, and if he has not been vaccinated at the time, the risk of contracting the disease is almost 100%. Children from 2 to 11 years old are especially easily infected. Sometimes the infection enters the body through the conjunctiva of the eye (i.e., bacteria settle on the mucous membrane of the sclera). In this case, they talk about diphtheria conjunctivitis.

By the way! It is easiest to get diphtheria in the fall and winter, when a person’s immunity is reduced and conditions for the spread of various infections through the air are most favorable.

You can also become infected with diphtheria through common objects, incl. clothes, toys, dishes. Food products also fall into this category, because bacteria not only settle on them, but also multiply very actively. Dairy products, whipped cream, and butter creams are considered especially dangerous.

Symptoms

Symptoms of diphtheria depend on the form of its manifestation. But there are always general signs, indicating the presence of infection in the body. These are headache, high temperature, pale skin, increased heart rate. Local lymph nodes also enlarge (depending on the affected organ). The remaining symptoms are specific and inherent in a particular form of diphtheria.

Oropharynx lesion

The most common case, because bacteria enter the body through airborne droplets and settle on the mucous membrane of the nose and throat. Diphtheria of the oropharynx can be judged by the fibrinous whitish coating on the tonsils. Gradually it moves to the throat and the root of the tongue.

Diphtheria plaque is not an outer covering, but a modification of the mucous membrane, so it is very difficult to remove. After removing the whitish film, an erosive layer with bleeding areas remains. And the next day the raid returns. It smells bad and makes it difficult to swallow and sometimes even breathe normally.

The toxic form of oropharyngeal diphtheria is more severe. Common symptoms include blue lips, rapid heartbeat, and neck pain. Intoxication is painful for the patient and leaves him powerless; he may fall into a state of delirium and often vomit. Sometimes toxic diphtheria leads to lymphadenitis and swelling of the pharynx and neck. The patient breathes heavily, wheezes and nasally when speaking.

Important! People with chronic diseases (AIDS, diabetes, cirrhosis of the liver) develop hypertoxic diphtheria, which can be fatal within 2-3 days after infection.

Diphtheria croup

The larynx and trachea are affected. Less often - bronchi. Sometimes diphtheria croup develops against the background of toxic diphtheria of the oropharynx. It is characterized by a barking cough, hoarseness of voice, and restlessness of the patient associated with the fear of suffocation. The patient breathes heavily and frequently, drawing in his stomach as he exhales. Fibrinous films are also present in the throat.

This form of diphtheria can progress to severe asphyxia, when brain cells begin to die due to lack of oxygen. If not accepted emergency measures, a person may die or suffer serious complications.

This form affects people with chronic diseases of the nasopharynx (sinusitis, rhinitis, nasopharyngitis, etc.). Serous-purulent mucus is discharged from the nose, sometimes mixed with blood, which indicates erosion of the mucous membrane. The high temperature does not last long, and signs of intoxication also quickly subside. Due to frequent nose blowing and fibrin secretion, the skin under the nostrils becomes irritated and inflamed.

Diphtheria conjunctivitis

Damage to diphtheria infection of one or both eyes, on the conjunctiva of which fibrinous plaque also forms. At the same time, the eyelids swell, the eyes constantly water, and purulent discharge comes out of them. In the morning, a person may find it difficult to open their eyes because the pus has clumped together.

Rare forms of diphtheria

Infection of the genital organs is accompanied by the formation of plaque at the entrance to the vagina or on the head of the penis. Urination is painful, and some blood may come out along with the urine. Less commonly, diphtheria spreads to anus. The inguinal lymph nodes are enlarged.

Diphtheria of the skin develops in places where it is affected (scratches, wounds). The plaque has a grayish color and a putrid odor. Rarely does the bacterium infect the ears, but if this happens, the symptoms are the same: purulent discharge from the ear, pain, hearing problems due to serous plugs.

Diagnostics

Diphtheria is most easily recognized during mass outbreaks of the disease, but there have not been any in Russia since 1999. Today, when this infection is rare, a doctor may not detect diphtheria during an examination and medical history. In addition, many young doctors have never seen a diphtheria patient, so the diagnosis must be confirmed by laboratory tests.

The bacteria Clostridum diphteriae can be detected in the patient's blood and in a smear of his plaque. Bacterial seeding is done immediately, because microbes do not live in the external environment for more than 2 hours. It is possible to carry out specific analysis: the film removed from the patient’s throat is lubricated with a solution of sodium tellurite. And if it turns black, it is diphtheria.

Differential diagnosis of diphtheria is necessary to distinguish it from streptococcal tonsillitis, peritonsillar abscess and infectious mononucleosis. All of these diseases have similar symptoms but require different treatment approaches.

Treatment

Even though diphtheria is a bacterial disease, antibiotics are not suitable for treatment. It is necessary to use a special anti-diphtheria serum obtained from the blood plasma of horses. It neutralizes the effect of diphtheria toxin. The dosage is calculated based on the patient’s age and the form of diphtheria.

The patient also undergoes classical symptomatic treatment to restore strength and return to the previous functionality of all organs and systems.

• Additionally, penicillin injections are given.
• Glucose drips are placed.
• Vitamins C and PP (in the form of pills or solutions for droppers).
• Injections of cortisone or prednisolone to reduce inflammation of the mucous membranes.
• Cardiovascular drugs (according to indications);
• Gargle three times a day, for example, with calendula infusion or other remedy prescribed by your doctor.
• Maintaining bed rest balanced diet, sufficient amount of liquid.

Immunity after diphtheria is fragile: you can easily get sick again. In addition, a recovered person remains a carrier of the bacteria for some time, so you should wear a mask and not have contact with unvaccinated people.

Prevention

The only one effective method prevention of diphtheria - vaccination. Primary vaccination is carried out at 3 months. Revaccination should be done every 10 years. The vaccine is a modified bacterial toxin in minute quantities. Its entry into the body provokes the production of antibodies, which in the future will protect a person from a real infection.

Recently, some mothers deliberately refuse vaccination, ignoring the vaccination calendar. And this does not exclude the possibility that in the future the country will face a repeat epidemic of diphtheria, which will be transmitted through children who are not vaccinated today. In this case, only one method of prevention will be effective - do not leave the house to avoid a collision with a carrier of the bacteria.

Diphtheria is an acute infectious disease that is life-threatening. It occurs in the form of acute inflammation of the upper respiratory tract, mainly the pharynx (approximately 90% of cases), nose, skin in places where it is damaged, eyes or genitals.

The main threat, however, is not inflammation, but poisoning with a toxin produced by the bacteria that causes the disease, which primarily affects the cardiovascular and nervous systems.

The causative agent of diphtheria and routes of infection

The causative agent of diphtheria is Corynebacterium diphteriae– gram-positive bacteria in the form of rods with characteristic flask-shaped thickenings at the ends, which in smears are arranged in pairs, at an angle in the form of a Roman numeral V relative to each other. During their life processes, diphtheria bacilli secrete diphtheria toxin, neuraminidase enzyme and other biochemically active compounds.

The synthesis of diphtheria toxin by microbial cells is controlled by a special tox gene. Bacteria can lose it in the process of life, losing along with it their ability to produce a toxin (toxigenicity). Conversely, initially non-toxigenic strains can acquire pathogenic properties; fortunately, this happens extremely rarely.

The disease is transmitted by airborne droplets from patients with diphtheria or from healthy carriers of the infection, much less often - through household items.

Risk group

Children aged 3–7 years are most susceptible to diphtheria infection, but in recent years the incidence has increased in adolescents and adults.
The source of infection is sick people or healthy carriers of toxigenic bacteria. Those suffering from diphtheria of the pharynx, nose and larynx are the most contagious, as they actively excrete pathogens with exhaled air. Patients with diphtheria of the eyes and skin can spread the infection through contact (hands, household objects). Healthy carriers of bacteria are much less infectious, but their lack of any external signs their condition does not allow us to control the spread of infection by them, because they can only be detected by chance during mass dispensary examinations. As a result, most cases of diphtheria infection are caused by contact with healthy carriers of the diphtheria bacillus.

The incubation period (the time from the moment of infection to the appearance of the first signs of the disease) is 2–10 days.

Diphtheria toxin

The toxin produced by the diphtheria bacillus consists of several components. One of them, the enzyme hyaluronidase, destroys hyaluronic acid in capillaries and increases their permeability, which leads to the release of blood vessels and saturation of surrounding tissues with blood plasma with the deposition of fibrinogen protein. The second component, necrotoxin, destroys epithelial cells and releases the enzyme thrombokinase from them. Thrombokinase promotes the conversion of fibrinogen into fibrin and the formation of a fibrin film on the surface of tissues. When diphtheria toxin acts on the palatine tonsils, which are covered with several layers of epithelial cells, a fibrin film is formed that penetrates deep into the epithelium of the tonsils and is tightly fused to it.

The third (main) component, the toxin itself, is capable of blocking the processes of cellular respiration and the synthesis of protein molecules. The most sensitive to its action are capillaries, myocardial cells and nerve cells. As a result, myocardial dystrophy and infectious-toxic myocarditis develop, damage to capillaries leads to infectious-toxic shock, damage to Schwann cells (auxiliary cells of nerve tissue) leads to demyelination of nerve fibers (destruction of the electrically insulating layer of myelin with disruption of the conduction of nerve impulses along nerve fibers). In addition, diphtheria toxin causes general intoxication of the body.

Symptoms and course

Diphtheria pharynx usually begins with a slight increase in temperature, slight pain when swallowing, redness and swelling of the tonsils, the formation of a specific filmy coating on them, and enlargement of the anterior upper cervical lymph nodes. The color of the films is usually white in the first 2–3 days of the disease, but then becomes gray or yellowish-gray. After about a week, the disease either ends with recovery (a mild form, as a rule, in those vaccinated against diphtheria), or turns into a more severe toxic form caused by the systemic action of diphtheria toxin.

The toxic form of diphtheria is always very difficult. It is characterized by very high body temperature (39.5-41.0°C), severe headaches, drowsiness, and apathy. The skin becomes pale, the mouth becomes dry, and children may experience repeated vomiting and abdominal pain. Swelling of the tonsils becomes pronounced, can lead to complete closure of the entrance to the pharynx, spreads to the soft and hard palate, often also to the nasopharynx, breathing becomes difficult, the voice often becomes nasal. The plaque spreads to all tissues of the oropharynx. Classic sign The toxic form of diphtheria of the pharynx is swelling of the subcutaneous tissue in the neck and sometimes the chest, as a result of which the skin acquires a gelatinous consistency. The anterior upper cervical lymph nodes are significantly enlarged and painful.

Nasal diphtheria proceeds against the background of normal or slightly elevated temperature body, there is no intoxication. Serous-purulent or bloody-purulent discharge is visible from the nasal passages. Weeping areas and then dry crusts appear on the wings of the nose, cheeks, forehead and chin. Filmy deposits are visible inside the nose. Pathological process may also affect the paranasal sinuses. In the toxic form, swelling of the subcutaneous tissue of the cheeks and neck is observed.

Diphtheria eyes proceeds as a banal conjunctivitis and is characterized by moderate hyperemia and swelling of the conjunctiva of the eyelid, a small amount of serous-purulent discharge from the conjunctival sac (catarrhal form). The membranous form is manifested by pronounced swelling of the eyelids and the presence of greyish-white films on their conjunctiva that are difficult to remove. The toxic form is also accompanied by swelling of the tissue around the orbit.

Skin diphtheria leads to prolonged non-healing of any skin damage, hyperemia, a dirty gray coating is present on the skin, and dense infiltration of the surrounding skin is noted.

Diagnostics

Diphtheria is diagnosed based on examination of the patient and test results. Upon examination, the diagnosis of diphtheria is indicated by the following signs: the presence of characteristic films, as well as difficulty breathing and a whistling noise when inhaling, not characteristic of a sore throat, a barking cough. The diagnosis of diphtheria based on characteristic clinical signs in a mild form of the disease is more difficult to make.

Analyzes:

A general blood test shows signs of an acute inflammatory process.

Examination of a smear under a microscope (bacterioscopy) - identification of bacteria with a characteristic appearance Corynebacterium diphteriae.

Bacteriological research is the inoculation of biological material on a special nutrient medium and the cultivation of colonies of microorganisms.

Determination of the level (titer) of antitoxic antibodies (a high titer of 0.05 IU/ml and above allows diphtheria to be excluded).

Serological study - determination of specific antibodies in blood serum using the methods of RPGA, ELISA, etc.

Diphtheria of the pharynx must be differentiated from acute tonsillitis(follicular and lacunar forms), Simanovsky-Vincent angina ( fungal infection), syphilitic tonsillitis, pseudofilm tonsillitis with infectious mononucleosis, paratonsillar abscess, mumps, leukemia. In children, the diagnosis of false croup should be avoided.

Treatment

All patients with diphtheria, regardless of the severity of the condition, must be hospitalized in an infectious diseases hospital.

Treatment is as follows:

Diet – fortified, high-calorie, thoroughly cooked food.

Etiotropic therapy (that is, aimed at eliminating the cause of the disease) - administration of anti-diphtheria serum (ADS), the dose and number of times of administration depend on the severity and form of the disease. In mild forms, PDS is administered intramuscularly once at a dose of 20–40 thousand IU; in moderate forms, 50–80 thousand IU is administered once or, if necessary, again in the same dose after 24 hours. When treating a severe form of the disease, the total dose increases to 90–120 thousand IU or even 150 thousand IU (infectious-toxic shock, disseminated intravascular coagulation syndrome). In this case, 2/3 of the dose is administered immediately, and during the first day of hospitalization, 3/4 of the total dose should be administered.

Antibiotics: for mild forms - erythromycin, rifampicin orally, for moderate and severe forms - injection of penicillins or cephalosporins. Course duration is 10–14 days. Antibiotics do not affect diphtheria toxin, but they reduce the number of bacteria that produce it.

Local treatment - rinsing and irrigation with disinfectant solutions.

Detoxification therapy - glucose-saline solutions, taking into account the daily need for fluid and its losses (moderate and severe forms).

Glucocorticosteroids – for moderate and severe forms.

Treatment of bacteria carriers is carried out with antibiotics: tetracyclines (children over 9 years old), erythromycin, cephalosporins against the background of general restorative therapy and elimination of chronic foci of infection.

Complications

Among the most serious complications of diphtheria on the cardiovascular system are myocarditis and heart rhythm disturbances.

Neurological complications of diphtheria are caused by damage to various cranial and peripheral nerves and are manifested by paralysis of accommodation, strabismus, paresis of the limbs, and in more severe cases, paralysis of the respiratory muscles and muscles of the diaphragm.

Secondary complications of diphtheria are such severe pathological conditions as acute disorders cerebral circulation(thrombosis, embolism), metabolic encephalopathy, cerebral edema, toxic kidney damage, diphtheria hepatitis, as well as infectious-toxic shock and DIC syndrome (disseminated intravascular coagulation syndrome - a severe disorder of the blood coagulation system). The toxic form of diphtheria can lead to acute renal, cardiovascular, respiratory or multiple organ failure.

Nonspecific complications of diphtheria are peritonsillar abscess, otitis media, and pneumonia.

Vaccination

Vaccination against diphtheria is carried out with toxoid, that is, an inactivated toxin. In response to its administration, antibodies are formed in the body not to Corynebacterium diphteriae, but to diphtheria toxin.

Diphtheria toxoid is part of the combined domestic vaccines DTP (associated, that is, complex, vaccine against whooping cough, diphtheria and tetanus), AaDPT (vaccine with an acellular pertussis component) and ADS (diphtheria-tetanus toxoid), as well as “sparing” vaccines ADS-M and AD-M. In addition, the SanofiPasteur vaccines are registered in Russia: Tetracok (against diphtheria, tetanus, whooping cough, polio) and Tetraxim (against diphtheria, tetanus, whooping cough, polio, with an acellular pertussis component); D.T. Vax (diphtheria-tetanus toxoid for vaccination of children under 6 years of age) and Imovax D.T. Adult (diphtheria-tetanus toxoid for vaccination of children over 6 years of age and adults), as well as Pentaxim (vaccine against diphtheria, tetanus, whooping cough, polio and Haemophilus influenzae infection with an acellular pertussis component).

According to Russian vaccination calendar, vaccination of children under one year of age is carried out at 3, 4–5 and 6 months. The first revaccination is carried out at 18 months, the second at 7 years, the third at 14. Adults should be revaccinated against tetanus and diphtheria every 10 years.