The first signs of tetanus. The first signs of tetanus in humans

  • What is Tetanus
  • What causes Tetanus
  • Symptoms of Tetanus
  • Diagnosis of Tetanus
  • Treatment of Tetanus
  • Prevention of Tetanus
  • Which doctors should you contact if you have Tetanus?

What is Tetanus

Tetanus (lat. Tetanus)- zooanthroponotic bacterial acute infectious disease with a contact mechanism of pathogen transmission, characterized by damage to the nervous system and manifested by tonic tension of the skeletal muscles and generalized convulsions.

Brief historical information
The disease has been known since ancient times; its occurrence has long been associated with injuries and wounds. The name of the disease and the first description of its clinical manifestations were given by Hippocrates. Tetanus bacillus was first discovered by N.D. Monastyrsky (1883) in the corpses of dead people and A. Nikolayer (1884) in abscesses in experimental tetanus in animals. A pure culture of the pathogen was isolated by the Japanese bacteriologist Sh. Kitazato (1887). Later, he obtained tetanus toxin (1890) and, together with E. Bering, proposed an antitoxic serum for the treatment of tetanus. The French immunologist G. Ramon developed a method for producing tetanus toxoid (1923-1926), which is still used to prevent the disease.

What causes Tetanus

Pathogen- obligate anaerobic gram-positive spore-forming motile rod Clostridium tetani of the Bacillaceae family. The spores are located terminally, giving the bacteria the appearance of “drumsticks” or “tennis rackets.” C. tetani produces a potent exotoxin (tetanospasmin), a cytotoxin (tetanolysin) and a so-called low molecular weight fraction. In soil, feces and on various objects, spores can persist for years. Maintain a temperature of 90 ° C for 2 hours. Under anaerobic conditions, at a temperature of 37 ° C, sufficient humidity and in the presence of aerobic bacteria (for example, staphylococci), spores germinate into vegetative forms. Vegetative forms of tetanus bacillus die within a few minutes when boiled, after 30 minutes - at 80 °C. Antiseptics and disinfectants kill the tetanus pathogen within 3-6 hours. In countries with warm climates, spores can grow directly in the soil. In C. tetani, two types of antigens are detected: somatic (O-antigen) and flagellar (H-antigen). Based on the structures of flagellar antigens, 10 serovars are distinguished. All serovars produce tetanospasmin and tetanolysin, which are identical in antigenic properties.
- Tetanospasmin- one of the most powerful biological poisons. It is a polypeptide with a “distanced” mechanism of action, since bacteria rarely leave the primary site of infection. The toxin is fixed on the surface of the processes of nerve cells, penetrates them (due to ligand-mediated endocytosis) and enters the central nervous system through retrograde axonal transport. The mechanism of action is associated with suppression of the release of inhibitory neurotransmitters (in particular, glycine and γ-aminobutyric acid) in synapses (the toxin binds to synaptic proteins synaptobrevin and cellubrevin). Initially, the toxin acts on peripheral nerves, causing local tetanic muscle contractions. In cultures, the toxin appears on the 2nd day, reaching its peak formation by the 5-7th day.
- Tetanolysin exhibits hemolytic, cardiotoxic and lethal effects, causes the development of local necrotic lesions. This toxin plays a less important role in the pathogenesis of the disease. The maximum accumulation of the toxin in the culture is observed after 20-30 hours. The processes of its formation are not associated with the synthesis of tetanospasmin. The low molecular weight fraction enhances the secretion of mediators at neuromuscular synapses.

Epidemiology
Reservoir and source of infection- herbivores, rodents, birds and humans, in whose intestines the pathogen lives; the latter is released into the external environment with feces. Tetanus bacillus is also widespread in soil and other environmental objects, where it can multiply and persist for a long time. Thus, the pathogen has two interconnected and mutually enriching habitats, and, consequently, two sources of the pathogen - the intestines of warm-blooded animals and the soil. The significance of a particular source is apparently largely determined by the climatic and geographical conditions of the area. The most favorable soils for vegetation and preservation of the microorganism are chernozem and red soil soils rich in humus, as well as soils well fertilized with organic matter. From soil with dust, bacteria can enter any premises (including dressing rooms and operating rooms), onto various objects and materials used in surgical practice (various powders, gypsum, talc, medicinal clay and mud, cotton wool, etc.).
The frequency of carriage of tetanus bacillus spores by humans varies from 5-7 to 40%, and an increased degree of carriage is noted among persons who professionally or at home come into contact with soil or animals (agricultural workers, grooms, milkmaids, sewer workers, greenhouse workers, etc.). C. tetani is found in the intestinal contents of cows, pigs, sheep, camels, goats, rabbits, guinea pigs, rats, mice, ducks, chickens and other animals with a frequency of 9-64%. The contamination of sheep droppings reaches 25-40%, which is of particular epidemiological significance due to the use of the small intestine of sheep for the production of surgical catgut.

Transmission mechanism- contact; The pathogen penetrates through damaged skin and mucous membranes (wounds, burns, frostbite). Infection of umbilical wounds if asepsis is not observed during childbirth can cause neonatal tetanus. The entry point for the pathogen can be open wounds of different nature and location (punctures, splinters, cuts, abrasions, crushes, open fractures, burns, frostbite, bites, necrosis, inflammatory processes); in these cases, post-traumatic tetanus develops. Surgical wounds, especially on the colon and ischemic extremities, can become an entry point for infection with the subsequent development of postoperative tetanus. Abortion interventions outside of health care facilities may cause post-abortion tetanus. There is no possibility of transmission of the pathogen from a sick person to a healthy person.

Natural sensitivity of people high. Those who have recovered from tetanus do not develop immunity to the disease, since a very small dose of the toxin that can cause the disease is not sufficient to ensure an immunological response.

Basic epidemiological signs. The incidence is sporadic in the form of unrelated cases. The zonal spread of infection is determined by both climatic and geographical and socio-economic factors. The seasonality of the disease is spring and summer. Among the cases, residents of rural areas, children and the elderly predominate; It is in these groups that the majority of deaths are recorded. Due to the widespread implementation of active immunization, tetanus in newborns is not currently registered. The presence of a permanent reservoir of infection in the soil determines the possibility of infection as a result of minor household injuries. There are still cases of nosocomial tetanus infection during operations on the extremities, gynecological operations and surgical interventions on the gastrointestinal tract.

Pathogenesis (what happens?) during Tetanus

The pathogen in the form of spores enters the human body through damaged skin and mucous membranes. Under anaerobic conditions (deep puncture wounds, wounds with deep pockets or necrotization of crushed tissue), the development and reproduction of vegetative forms in wounds occurs, accompanied by the release of exotoxin. Along the motor fibers of peripheral nerves and with the bloodstream, tetanospasmin penetrates into the spinal cord, medulla oblongata and reticular formation of the trunk, where it is fixed mainly in the interneurons of polysynaptic reflex arcs. The bound toxin cannot be neutralized. Paralysis of interneurons develops with suppression of all types of their synaptic inhibitory effect on motor neurons. As a result, the uncoordinated flow of motor impulses from motor neurons to muscles through neuromuscular synapses increases. The throughput of the latter increases due to increased secretion of acetylcholine under the influence of the low molecular weight fraction. A continuous flow of efferent impulses maintains constant tonic tension in the skeletal muscles.

At the same time, afferent impulses increase in response to the influence of tactile, auditory, visual, olfactory, gustatory, temperature and barometric stimuli. In this case, tetanic convulsions periodically occur.

Muscle tension leads to the development of metabolic acidosis. Against this background, both tonic and tetanic convulsions intensify, cardiac activity worsens, and preconditions are created for secondary bacterial complications. Cardiovascular disorders (tachycardia, arterial hypertension, arrhythmia, ventricular fibrillation) are aggravated due to the hyperactivity of the sympathetic nervous system that develops during tetanus. The excitability of the cortex and reticular structures of the brain increases. Possible damage to the respiratory and vasomotor centers and nuclei of the vagus nerve (bulbar tetanus), which often leads to the death of patients. Other causes of death may be associated with asphyxia due to seizures and the development of complications (pneumonia, sepsis).

Post-infectious immunity does not develop in tetanus. Specific pathological changes are scant (venous stagnation, minor hemorrhages, in rare cases, muscle ruptures and muscle hematomas).

Symptoms of Tetanus

Taking into account the entrance gates of infection, they are distinguished:
- traumatic tetanus;
- tetanus that developed as a result of inflammatory and destructive processes;
- cryptogenic tetanus (with unknown portal of entry).

According to the prevalence of the process, the disease is divided into general (generalized) and local tetanus. The latter is rarely observed.

Incubation period varies from several days to 1 month, on average not exceeding 1-2 weeks. The disease begins acutely, only sometimes prodromal phenomena are noted in the form of tension and muscle twitching at the site of injury, malaise, headache, sweating, and irritability.

IN initial period of tetanus In some cases, its earliest sign may appear - dull nagging pain in the area of ​​the entry gate of infection, even in already completely healed wounds. The main specific symptoms that occur during this period are trismus, sardonic smile, dysphagia and stiff neck. These signs appear early and almost simultaneously.
- Lockjaw- tension and convulsive contraction of the masticatory muscles, which leads to difficulty opening the mouth.
- Tonic spasms of facial muscles are expressed in a “sardonic smile” (risus sardonicus), which gives the patient’s face a peculiar expression: wrinkled forehead, narrowed palpebral fissures, stretched lips, drooping corners of the mouth.
- Dysphagia (difficulty and painful swallowing) caused by convulsive spasm of the pharyngeal muscles. The combination of trismus, “sardonic smile” and dysphagia is characteristic only of tetanus.
- Stiff neck, caused by tonic spasms of skeletal muscles, in tetanus is not a meningeal symptom and is not combined with other meningeal signs (Kernig's, Brudzinsky's symptoms, etc.).

IN the height of the disease painful tonic spasms spread to the muscles of the trunk and limbs (without involving the hands and feet). Tonic muscle tension is constant; muscle relaxation, as a rule, does not occur even in sleep. The contours of large skeletal muscles are clearly outlined, especially in men. From the 3-4th day of illness, the muscles of the abdominal wall become hard as a board, the legs are often extended, and movements in them are limited. At the same time, the intercostal muscles and diaphragm are involved in the process, breathing becomes shallow and rapid. Tonic tension of the perineal muscles leads to difficulty defecating and urinating. As a result of severe tension and soreness of the back muscles in severe tetanus, opisthotonus develops: when the patient is positioned on his back, his head is thrown back, the lumbar part of the body is raised above the bed in such a way that you can stick your hand between the back and the bed.

Against the background of constant tonic tension of the skeletal muscles, tetanic convulsions occur periodically with varying frequencies. Their duration initially ranges from a few seconds to a minute. Most often they are provoked by auditory, visual and tactile stimuli. In mild cases of the disease, 1-2 attacks of convulsions per day are observed; in severe cases of tetanus, they can be repeated up to tens of times within an hour, becoming longer and more widespread. Seizure attacks occur suddenly. In this case, the patient’s face takes on a pained expression and becomes cyanotic, the contours of the muscles are more clearly outlined, and opisthotonus increases. Patients moan and scream because of the pain, trying to grab the headboard of the bed with their hands to ease their breathing. Body temperature rises, the skin (especially the face) becomes covered with large drops of sweat, hypersalivation, tachycardia, shortness of breath are noted, heart sounds are loud, blood pressure tends to increase. The convulsive syndrome develops and intensifies while the patient maintains a clear consciousness; confused consciousness and delirium appear only shortly before death.

The period from the end of the first week to the 10-14th day of illness is the most dangerous for the patient’s life. Metabolic acidosis and a sharp increase in metabolism cause hyperpyrexia and increased sweating. It is difficult to produce sputum because coughing provokes tetanic convulsions. Deterioration of pulmonary ventilation often contributes to the development of secondary bacterial pneumonia. The heart is dilated due to both ventricles, the sounds are loud. The liver and spleen are not enlarged. Deep intoxication of the brain stem causes depression and arrhythmia of breathing, weakening of cardiac activity; possible cardiac paralysis. Due to frequent and prolonged tonic convulsions, painful insomnia and irritability develop, and the threat of asphyxia increases.

In cases of a favorable outcome, the period of convalescence is long; Gradually weakening clinical manifestations of the disease persist for 2-4 weeks, recovery is delayed up to 1.5-2 months.

The severity of tetanus is determined by a combination of several indicators.
- At mild current The disease incubation period often exceeds 20 days. Trismus, “sardonic smile” and opisthotonus are moderate, hypertonicity of other muscle groups is weak. Tonic convulsions are absent or insignificant, body temperature is normal or subfebrile. Symptoms of the disease develop within 5-6 days.
- In cases moderate course the incubation period is 15-20 days. The main clinical signs of the disease increase over 3-4 days. Convulsions occur several times a day, tachycardia and sweating are moderate, body temperature is low-grade or (less frequently) high.
- Severe form Tetanus is characterized by a shortened incubation period to 7-14 days, a rapid (over 1-2 days) increase in symptoms, a typical clinical picture with frequent and intense tetanic convulsions (several times within an hour), expressed by sweating and tachycardia, high fever.
-Very severe course are distinguished by a shortened (less than a week) incubation period and fulminant development of the disease. Tonic convulsions occur several times within 3-5 minutes. They are accompanied by hyperpyrexia, severe tachycardia and tachypnea, cyanosis, and threatening asphyxia.

One of the most severe forms of generalized descending tetanus is Brunner's cephalic (“bulbar”) tetanus. It occurs with primary damage to the muscles of the face, neck and pharynx, with spasms of the swallowing and intercostal muscles, muscles of the glottis and diaphragm. Usually the respiratory, vasomotor centers and vagus nerve nuclei are affected. Gynecological tetanus and neonatal tetanus, which is one of the important causes of child mortality in developing countries, are also distinguished by the severity of their course and unfavorable prognosis. It is associated with unsatisfactory conditions for the provision of obstetric care and the lack of immunization programs for women.

Ascending tetanus, observed in rare cases, first manifests itself as pain, tension and fibrillary twitching in one group of muscles; later, as new overlying parts of the spinal cord are affected, the disease acquires the typical features of a generalized process.

Local tetanus is rare. One of its typical manifestations, developing after wounds to the face and head, is facial paralytic tetanus Rose. Trismus, stiff neck, and “sardonic smile” occur, accompanied by paresis of the cranial nerves. The lesion is usually bilateral, more pronounced on the side of the wound.

When determining the prognosis of tetanus, much attention is paid to the period between the appearance of the first signs of the disease (lockjaw, etc.) and the onset of seizures. If this period is less than 48 hours, the prognosis of the disease is extremely unfavorable.

Complications
One of the dangerous complications of tetanus is asphyxia. At the same time, there is an opinion that asphyxia and cardiac arrest are not complications, but manifestations of a symptom complex of a severe course of the disease. Complications also include pneumonia, muscle ruptures, bone fractures, and compression deformities of the spine. Hypoxia that increases during convulsions can contribute to the development of coronary vascular spasm and myocardial infarction, and cardiac arrest. During the recovery period, muscle contractures and paralysis of the III, VI and VII pairs of cranial nerves are possible. Neonatal tetanus can complicate sepsis.

The prognosis of the disease is always serious.

Diagnosis of Tetanus

Tetanus should be distinguished from hysteria, epilepsy, strychnine poisoning, tetany, encephalitis and other diseases with convulsive syndrome.

The diagnosis of tetanus is made based on clinical findings. Specific symptoms of tetanus that occur already in its initial period are dull nagging pain in the area of ​​the wound (even already healed), trismus, “sardonic smile”, dysphagia and stiff neck. The combination of these symptoms is characteristic only of tetanus. During the height of the disease, painful tonic convulsions of the muscles of the trunk and limbs (not involving the hands and feet) occur, and against their background - periodic, suddenly occurring tonic convulsions, the frequency and duration of which largely determines the severity of the disease.

Laboratory diagnostics
When the blood thickens due to severe and constant excessive sweating, as well as secondary bacterial complications, neutrophilia is possible. If a typical clinical picture develops, isolation of the pathogen and its identification may not be necessary. Material from a patient or corpse, dressing and suture surgical material, as well as soil, dust and air are subject to research. Bacteria are usually found at the point of entry into the patient's body. Therefore, it is most rational to study various material taken from the wound site. In cases where the entrance gate is unknown, the patient should be carefully examined to identify abrasions, scratches, catarrhal and inflammatory processes. Particular attention should be paid to old scars after wounds, since the pathogen can persist in them for a long time. In some cases, mucus from the nose, bronchi, pharynx, plaque from the tonsils, as well as discharge from the vagina and uterus (for postpartum or post-abortion tetanus) are examined. When bacteriological examination of corpses, the possibility of generalization of infection is also taken into account. For analysis, blood (10 ml) and pieces of liver and spleen (20-30 g) are taken. To isolate the pathogen, methods common to obtaining pure cultures of anaerobic bacteria are used.

When examining material taken from a patient or a corpse, in parallel with the bacteriological analysis, tetanus exotoxin is detected in a biological sample on mice. To do this, the material is crushed, a double volume of physiological solution is added, incubated for an hour at room temperature, and filtered. Part of the filtrate is mixed with antitetanus serum at the rate of 0.5 ml (200 AE/ml) of serum per 1 ml of extract and incubated for 40 minutes. Then one group of animals is injected with the extract without prior incubation with serum, and the other group is injected with the incubated mixture. In the presence of C. tetani, animals of the first group develop symptoms of tetanus.

Treatment of Tetanus

Treatment of tetanus carried out in the intensive care and resuscitation department with the participation of an anesthesiologist. It is necessary to provide a protective regime that excludes auditory, visual and tactile stimuli. Patients are fed through a tube or parenterally (for gastrointestinal paresis). They carry out the prevention of bedsores: frequently turning the patient in bed, smoothing out crumpled bed and underwear, cleaning them and periodically changing them. An infected wound, even a healed one, is injected with antitetanus serum (at a dose of 1000-3000 IU), then a thorough inspection and surgical treatment of the wound is carried out with wide striped incisions (to create aerobic conditions), removal of foreign bodies, contaminated and necrotic tissue. To prevent seizures, all these manipulations are best performed under anesthesia. In the future, it is advisable to use proteolytic enzymes (trypsin, chymotrypsin, etc.) to treat wounds.

To neutralize tetanus exotoxin in the bloodstream, 50,000 IU of antitetanus serum or 1,500-10,000 IU (average dose 3,000 IU) of specific immunoglobulin is injected intramuscularly once, with preliminary testing of individual sensitivity to them. These drugs should be administered as early as possible, since tetanus toxin circulates freely in the blood for no more than 2-3 days, and the associated toxin is not inactivated, which reduces the therapeutic effect. After administration of heterogeneous antitetanus serum, it is necessary to monitor the patient for 1 hour due to the risk of developing anaphylactic shock.

The fight against convulsive syndrome is carried out using sedatives and narcotics, neuroplegics and muscle relaxants. Recently, diazepam 5-10 mg orally every 2-4 hours has been widely used; in severe cases, it is administered intravenously at 10-20 mg every 3 hours. For children, the drug is prescribed intravenously or intramuscularly at 0.1-0.3 mg/kg every 6 hours (maximum up to 10-15 mg/kg/day). You can use injections of a mixture of 2.5% solution of aminazine, 1% solution of promedol and 1% solution of diphenhydramine (2 ml of each drug) with the addition of 0.5 ml of 0.05% solution of scopolamine hydrobromide. Also prescribed are seduxen, barbiturates, sodium hydroxybutyrate, and in severe cases, droperidol, fentanyl, curare-like muscle relaxants (pancuronium, d-tubocurarine). In case of lability of the sympathetic nervous system, α- and β-blockers are sometimes used. In case of breathing disorders, intubation or tracheotomy is performed, muscle relaxation is combined with mechanical ventilation, and clearing the airways with an aspirator; Patients are given humidified oxygen. There are reports of the effectiveness of hyperbaric oxygen therapy.

Laxatives are prescribed in small doses, a gas outlet tube and a catheter are placed in the bladder (if necessary). To prevent pneumonia, frequent turning of the patient, forced breathing and coughing are necessary.

To prevent and treat bacterial complications, antibiotics are used - benzylpenicillin 2 million units intravenously at intervals of 6 hours (children up to 200,000 units/kg/day), tetracycline 500 mg 4 times a day (children up to 30-40 mg/kg/day ). The use of antibiotics does not exclude the possibility of developing pneumonia and other secondary infections.

The fight against hyperthermia, acidosis and dehydration is carried out with intravenous infusions of 4% sodium bicarbonate solution, polyionic solutions, hemodez, rheopolyglucin, albumin, plasma.

Prevention of Tetanus

Epidemiological surveillance
To identify patterns in the spread of tetanus and rational planning of preventive measures, an in-depth epidemiological analysis of the incidence and the preventive measures used is necessary. To assess the quality of medical care for injuries, it is necessary to analyze its timing, volume and nature. When analyzing the effectiveness of emergency prevention, you should pay attention not only to its volume, but also to the timing of its implementation (the time elapsed after the injury and seeking medical help). Of particular relevance in connection with cases of diseases in previously vaccinated people is the analysis of the immune status of the sick. The immunization of the population against tetanus and the implementation of the vaccination plan for individual age, socio-professional groups, including the rural population, are subject to detailed analysis. Immunological control is an integral part of epidemiological surveillance of tetanus. It allows you to assess the security of various populations, reliably judge the level of vaccination and the quality of immunization, as well as the duration of immunity, identify the most affected groups of the population and characterize areas with varying degrees of risk of infection.

Preventive actions
Nonspecific prevention of tetanus is aimed at preventing injuries at home and at work, eliminating infection of operating rooms, as well as wounds (umbilical and others), early and thorough surgical treatment. Specific prevention of tetanus is carried out on a planned and emergency basis. In accordance with the vaccination calendar, children from 3 months of life are vaccinated 3 times with 0.5 ml of DTP vaccine with the first revaccination after 12-18 months and subsequent revaccinations every 10 years with associated drugs (ADS or ADS-M) or single drugs (AS) . After a completed course of immunization, the human body for a long period (about 10 years) retains the ability to quickly (within 2-3 days) produce antitoxins in response to repeated administration of drugs containing AS toxoid.

Emergency prevention of tetanus is carried out according to the scheme for any injuries and wounds with a violation of the integrity of the skin and mucous membranes, burns and frostbite of II-IV degrees, animal bites, penetrating intestinal injuries, out-of-hospital abortions, childbirth outside of medical institutions, gangrene or tissue necrosis of any type, long-term current abscesses, carbuncles. Emergency prevention of tetanus includes primary wound treatment and simultaneous specific immunoprophylaxis. Depending on the previous vaccination status of patients, a distinction is made between passive immunization, active-passive prophylaxis, consisting of the simultaneous administration of tetanus serum and toxoid, and emergency revaccination with AS to stimulate immunity in previously vaccinated individuals. Emergency immunoprophylaxis of tetanus should be carried out as early as possible and up to the 20th day from the moment of injury, taking into account the length of the incubation period for tetanus.

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The content of the article

Tetanus(synonyms for the disease: tetanus) is an acute infectious disease from the group of wound infections, which is characterized by tetanus clostridia, characterized by damage to the central nervous system, mainly interneurons of polysynaptic reflex arcs, exotoxin of the pathogen, characterized by constant tonic tension of skeletal muscles and periodic generalized tonic-clonic convulsions, which may lead to asphyxia.

Historical data of tetanus

The clinic of tetanus was known for 2600 BC. e., in the 4th century. BC That is, it was described by Hippocrates in the 2nd century. BC e. - Galen. The number of cases of tetanus increased during the wars. In 1883 p. N. D. Monastyrsky discovered the tetanus bacillus during microscopy of smears of wound discharge from a patient with tetanus. In 1884 p. A. Nicdaier first caused tetanus in an experiment on laboratory animals. A pure culture of the pathogen was obtained in 1887 p. S. Kitasato. In 1890 p. E. Behring developed a method for producing tetanus antitoxic serum, and during 1922-1926 pp. G. Ramon received tetanus toxoid and worked on a method for specific prevention of the disease.

Etiology of tetanus

The causative agent of tetanus, Clostridium tetani, belongs to the genus Clostridium, family Bacillaceae. This relatively large, thin rod, 4-8 microns long and 0.3-0.8 microns wide, forms spores that are resistant to physical and chemical environmental factors and remains viable in the soil for decades. At 37°C, sufficient humidity and lack of oxygen, the spores germinate, forming vegetative forms. Clostridia tetanus is motile, has peritrichial flagella, is good, stains with all aniline dyes, and is gram-positive. Belongs to obligate anaerobes. The pathogen has a group somatic O-antigen and a type-specific Basal H-antigen, which distinguishes 10 serotypes. Toxin formation is an important biological feature of the vegetative form of CI. tetani.
Tetanus exotoxin consists of two fractions:
1) tetanospasmin with neurotoxin properties that affects the motor cells of the central nervous system,
2) tetanohemolysin, which causes hemolysis of red blood cells. Tetanus exotoxin is unstable, quickly inactivated under the influence of heat, sunlight, and an alkaline environment.
It is one of the strongest bacterial toxic substances, second only to botulinum toxin in toxicity.

Epidemiology of tetanus

. The source of the pathogen is mainly herbivores and people in whose intestines it is located. Clostridium tetanus is found in the intestines of horses, cows, pigs, goats and especially sheep. The pathogen enters the soil with animal feces.
Tetanus is a wound infection. The disease develops only when the pathogen enters the body parenterally (sometimes through the umbilical wound) during wounds, operations, injections, bedsores, abortions, childbirth, burns, frostbite, and electrical injuries. In all cases, the factors of transmission of infection are objects contaminated with spores, causing injuries, as well as unsterile instruments during criminal abortions and assistance to women in labor. Injuries to the feet when walking barefoot (minor injuries) often lead to the disease, which is why it is called barefoot disease (60-65% of cases). With dust, spores, and sometimes vegetative forms, fall on clothing, shoes, skin, and even with minor damage to the skin and mucous membranes, this can lead to disease. In temperate latitudes, an increase in the incidence of tetanus is detected during the period of agricultural work - April - October.
Immunity in those who have recovered almost does not develop due to the weakness of antigenic irritation; the lethal dose of the toxin is less than the immunogenic one.

Pathogenesis and pathomorphology of tetanus

Tetanus refers to neuroinfections with damage to the corresponding structures of the central nervous system (spinal and medulla oblongata, reticular system). The entry point for infection is damaged skin, less often mucous membranes. Wounds in which anaerobic conditions are created are especially dangerous - puncture wounds, with necrotic tissue, etc. Tetanus with an unknown source of infection is classified as cryptogenic, or hidden. Under conditions of anaerobiosis, vegetative forms germinate from spores, multiply and release exotoxin. The toxin spreads in the body in three ways: through the circulatory, lymphatic system and along the course of motor nerve fibers, reaching the spinal and medulla oblongata, reticular formation, where it causes paralysis of interneurons of polysynaptic reflex arcs, removing their inhibitory effect on motor neurons. Normally, interneurons carry out the correlation of biocurrents arising in motor neurons. Due to paralysis of interneurons, uncoordinated biocurrents from motor neurons flow to the periphery of the skeletal muscles, causing the characteristic tetanus constant tonic tension. Periodic convulsions are associated with increased efferent, as well as afferent, impulses, which is caused by nonspecific stimuli - sound, light, tactile, gustatory, olfactory, thermo- and baropulses. The respiratory center and nuclei of the vagus nerve are affected. A significant increase in the reactivity of the sympathetic nervous system leads to arterial hypertension, tachycardia, and arrhythmia. Convulsive syndrome leads to the development of metabolic acidosis, hyperthermia, impaired respiratory function (asphyxia) and blood circulation.
Pathomorphological changes in the body occur mainly due to increased functional load during seizures. Coagulative necrosis is found in skeletal muscles, which often leads to muscle rupture with the formation of hematomas. Sometimes, especially in children, compression fractures of the thoracic vertebrae are observed due to seizures. Histological changes in the central nervous system are insignificant: edema, congestive plethora of the brain and its soft shell. Most anterior horn neurons are well preserved, but acute swelling of groups of cells is noted at various levels of the spinal cord.

Tetanus clinic

According to the clinical classification, generalized (generalized) and local tetanus are distinguished. More often the disease occurs in a generalized manner; Local tetanus, main, or facial, Rose tetanus and other forms are rarely observed.

Generalized tetanus

The incubation period lasts 1-60 days. The shorter it is, the more severe the disease and the higher the mortality rate. If the incubation period lasts more than 7 days, mortality is reduced by 2 times. There are three periods of the disease: initial, convulsive, recovery.
In the initial period, nagging pain, burning in the wound area, fibrillary twitching of adjacent muscles, sweating, and increased irritability are possible. Sometimes Lorin-Epstein symptoms are detected, which are important for the early diagnosis of tetanus: 1) convulsive contraction of muscles when massaging them proximal to the wound, 2) contraction of the masticatory muscles and closing of the half-open mouth. Impact with a spatula or finger on the inner or outer surface of the cheek or on a spatula placed on the lower teeth (chewing reflex).
The disease usually begins acutely. One of the early symptoms of the convulsive period is trismus - tonic tension and convulsive contraction of the masticatory muscles, which makes it difficult to open the mouth. Next, spasms of the facial muscles develop, as a result of which the face acquires a peculiar appearance of a smile along with crying - a sardonic smile. At the same time, the mouth is stretched, its corners are lowered, the forehead is wrinkled, the eyebrows and wings of the nose are raised, narrowed and squinted. At the same time, difficulty swallowing appears due to convulsive contraction of the muscles of the pharynx, painful rigidity of the muscles of the back of the head, which spreads to other muscle groups in a descending order - neck, back, abdomen, limbs.
Tonic contraction of predominantly extensor muscles predetermines the patient's bent position with his head thrown back, resting only on the heels and back of the head - opisthotonus. In the future, tension in the muscles of the limbs and abdomen is possible, which from the 3-4th day of illness becomes hard as a board. Tonic tension applies mainly to the large muscles of the limbs.
The muscles of the feet, hands, and fingers can be free from tension.
At the same time, the process involves the intercostal muscles and the diaphragm. Their tonic tension leads to difficulty in breathing and rapid breathing. Due to tonic contraction of the perineal muscles, difficulty urinating and defecating is observed. If tonic contraction of the flexor muscles predominates, a forced position of the body occurs with the body bent forward - emprostotonus, and if the muscles on one side contract, the body is bent to one side - pleurostotonus.
Constant symptoms of the disease include intense pain in the muscles due to their constant tonic tension and excessive functioning.
Against the background of constant increased muscle tone, common ONICO-tonic convulsions appear, which last from several seconds to 1 minute or more with a frequency ranging from several times during the day to 3-5 times per 1 minute. During convulsions, the patient’s face swells, becomes covered with drops of sweat, has a pained expression, the features are distorted, the body is elongated, the abdomen tenses, opisthotonus becomes so significant that the patient bends in an arc, the contours of the muscles of the neck, torso and upper limbs become clear. Due to the high excitability of the nervous system, convulsions intensify when touched, light, sound and other irritations. Severe attacks of spasms of the respiratory muscles, larynx and diaphragm sharply disrupt breathing and can lead to asphyxia and death. Respiratory and circulatory disorders cause the occurrence of congestive pneumonia. Spasm of the pharynx disrupts the act of swallowing, which, together with trismus, leads to starvation and dehydration. The patient's consciousness is not impaired, which increases his suffering. Painful cramps are accompanied by insomnia, in which sleeping pills and narcotics are ineffective. Constant general hypertonicity, frequent attacks of clonic-tonic convulsions lead to a sharp increase in metabolism, profuse sweating, hyperthermia (up to 41 - 42 ° C).
Changes in the circulatory system are characterized from the 2-3rd day of illness by tachycardia against the background of loud heart sounds. The pulse is tense, blood pressure is increased, and symptoms of overload of the right side of the heart appear. From the 7-8th day of illness, heart sounds become muffled, the heart is enlarged due to both ventricles, and paralysis of its activity is possible. There are no characteristic changes in the blood, although sometimes there may be neutrophilic leukocytosis.
The severity of the disease depends on the frequency and duration of seizures.
Patients have a mild form of tetanus, which is rare, symptoms of the disease develop within 5-6 days, trismus, sardonic smile and opisthotonus are moderate, dysphagia is minor or absent, body temperature is normal or subfebrile, there is no tachycardia or it is insignificant, there is no convulsive syndrome for it manifests itself rarely and insignificantly.
Moderate forms In addition, it is characterized by moderate tonic muscle tension and infrequent clonic-tonic convulsions.
If the course of the disease is severe, the full clinical picture develops within 24-48 hours from the onset of its first signs - pronounced trismus, sardonic smile, dysphagia, frequent intense convulsions, severe sweating, tachycardia, high body temperature, constant increased muscle tone between frequent attacks of convulsions.
In patients with a very severe form, all symptoms of the disease develop within 12-24 hours, sometimes from the first hours. Against the background of high body temperature, severe tachycardia and tachypnea, convulsions appear very often (every 3-5 minutes), accompanied by general cyanosis and the threat of asphyxia. This form includes the main Brunner's tetanus, or bulbar tetanus, which occurs with primary damage and a sharp spasm of the muscles of the pharynx, glottis, diaphragm and intercostal muscles. In such cases, death is possible from respiratory or cardiac paralysis.
Very heavy is the course of gynecological tetanus, which develops after criminal abortions and childbirth. The severity of this form is due to anaerobiosis in the uterine cavity and the frequent accumulation of secondary staphylococcal infection, which leads to sepsis. The prognosis for these forms is almost always unfavorable.
A typical manifestation of local tetanus is facial paralytic tetanus, or Rose major, which develops when infected through a wound surface of the head, neck, or face. Paresis or paralysis of the facial nerve of a peripheral type occurs on the affected side, often muscle tension with trismus and a sardonic smile on the second half of the face. Ptosis and strabismus occur when infected during an eye injury. Disorders of taste and smell are possible. In some cases, convulsive contraction of the muscles of the pharynx is observed, as in rabies, which is why this form was given the name tetanus hydrophobicus.
The duration of tetanus is 2-4 weeks. The acute period of the disease is especially dangerous - up to the 10-12th day. Death often occurs in the first 4 days of illness. After the 15th day of illness, we can talk about the beginning of the recovery period, the course of which is very slow. Increased muscle tone lasts for about a month, especially in the abdominal, back, and calf muscles. Trismus also goes away slowly.
Depending on the speed of development of symptoms, fulminant, acute, subacute, and recurrent forms of tetanus are distinguished.
Lightning form begins with painful general clonicotonic convulsions that occur continuously, the activity of the heart quickly begins to weaken, the pulse increases sharply. The attacks are accompanied by cyanosis and during one of them the patient dies. The fulminant form of tetanus is fatal in 1-2 days.
In patients with acute tetanus, convulsions develop on the 2-3rd day of illness. At first they are infrequent, not intense, then they become more frequent, become longer, the process covers the muscles of the chest, pharynx, and diaphragm. Sometimes a reverse progression of the disease is observed.
The subacute form of tetanus is observed with a long incubation period or when the patient received anti-tetanus serum after an injury. Characterized by a slow increase in symptoms.
Muscle tension is moderate, cramps are rare and weak, sweating is insignificant. Recovery occurs within 12-20 days from the onset of the disease.
Recurrent form. Sometimes, after almost complete recovery, convulsions develop again, which can in some cases lead to asphyxia and death. In general, relapses of tetanus are very rare, their pathogenesis is unclear. This may also be a new activation of the encapsulated pathogen.
The course of tetanus in newborns has some peculiarities. The entry point for infection is often the umbilical wound, sometimes macerated skin or mucous membrane. The course is very severe, although the main symptoms of tetanus (trismus, sardonic smile) are less pronounced than in adults. Increased tone and tonic convulsions in newborns often manifest themselves in the form of blepharospasm, tremor of the lower lip, chin, and tongue. Attacks of tonic convulsions generally end in respiratory arrest (apnea). Often apnea develops without convulsions and is like the equivalent of a convulsive attack.

Complications of tetanus

The early ones include bronchitis and pneumonia of atelectatic, aspiration and hypostatic origin. The consequence of tetanic spasms can be ruptures of muscles and tendons, most often of the anterior abdominal wall, bone fractures, and dislocations. Due to prolonged tension of the back muscles, compression deformation of the spine is possible - tetanus-kyphosis. Hypoxia that occurs during seizures causes spasm of the coronary vessels, which can lead to myocardial infarction and contributes to the development of paralysis of the heart muscle. Sometimes after recovery, contractures of muscles and joints, paralysis of the III, VI and VII pairs of cranial nerves are observed for a long time.

Tetanus prognosis

With a relatively low incidence, mortality during editing is quite high (up to 30-50% or more), especially in newborns (up to 80-100%). Prevention of tetanus in all injuries and timely administration of antitoxic serum help reduce mortality.

Diagnosis of tetanus

The main symptoms of clinical diagnosis of tetanus in the early period are nagging pain in the wound area, Lorin-Epstein symptoms (muscle contractions during massaging proximal to the wound and chewing reflex). Of the typical symptoms of the height of the disease, the most important are trismus, a sardonic smile, significant sweating and increased reflex excitability. The presence of clonic-tonic convulsions against the background of tonic muscle tension makes the diagnosis of tetanus probable.
If the clinical picture of tetanus is typical, the diagnosis is established accurately in most cases, but during the initial examination the disease is not diagnosed in 30% of patients. In 20% of patients, tetanus is not recognized in the first 3-5 days. The reasons for late diagnosis are mainly related to the episodic nature of the disease. The occurrence of the disease after wounds and trauma deserves special attention.
Specific diagnostics usually not carried out. To confirm the diagnosis, sometimes (rarely) a biological test is used, which is carried out on white mice, just like the neutralization reaction for botulism.

Differential diagnosis of tetanus

Maintaining full consciousness in patients with tetanus allows one to immediately discard suspicion of certain diseases accompanied by convulsions.
Differential diagnosis is carried out with meningitis, encephalitis, rabies, epilepsy, spasmophilia, strychnine poisoning, hysteria, and in newborns - with intracranial trauma. Difficulty opening the mouth is observed with general diseases of the pharynx, lower jaw, and parotid glands, but there are also other symptoms of the corresponding disease. In case of strychnine poisoning, there is no trismus, convulsions are symmetrical, begin from the distal parts of the extremities, and between convulsive attacks the muscles completely relax. There is no tonic muscle tension in other diseases accompanied by convulsions. In patients with epilepsy, in addition, they experience loss of consciousness during an attack, foam at the mouth, unauthorized defecation and urination. Spasmophilia is distinguished by a characteristic position of the hands (symptom of the obstetrician's hand), symptoms of Chvostek, Trousseau, Lust, Erb, laryngospasm, absence of trismus, normal body temperature. With hysteria, “convulsions” of the type of tick-like and trembling movements, there is no sweating, the connection of the disease with a psychotraumatic situation, effective psychotherapeutic measures are characteristic.

Treatment of tetanus

The principles of treating patients with tetanus are as follows.
1. Creating conditions to prevent exposure to external stimuli (silence, darkened rooms, etc.).
2. Surgical treatment of the wound with previous injection of anti-tetanus serum at a dose of 10,000 AO per Bezredka.
3. Neutralization of freely circulating toxin. Antitetanus serum with previous desensitization for Bezredka (1500-2000 AO / kg) is administered intramuscularly, and in very severe cases and early hospitalization - intravenously. Anti-tetanus human immunoglobulin from immunized donors is also used at 15-20 IU / kg, but not more than 1500 IU. , 4. Administration of primordial toxoid 0.5-1 ml intramuscularly every 3-5 days 3-4 times per course.
5. Anticonvulsant treatment, which is carried out in the following average therapeutic daily doses of drugs: chloral hydrate - 0.1 g / kg, phenobarbital - 0.005 g / kg, aminazine - 3 mg / kg, sibazon (Relanium, Seduxen) - 1-3 mg/kg. A lytic mixture is prescribed: aminazine 2.5% - 2 ml, diphenhydramine 1% - 2 ml, promedol 2% - 1 ml, or omnopon 2% 1 ml, scopolamine hydrobromide 0.05% - 1.0 ml; 0.1 ml/kg of mixture per m injection. The frequency of administration and dosage (including per dose) of these drugs is determined individually depending on the severity of the patient’s condition, the frequency and duration of seizures, as well as the effectiveness of the drugs. In severe cases, muscle relaxants are used in combination with artificial ventilation.
6. Antibacterial therapy - benzylpenicillin, tetracycline, chloramphenicol for 7-15 days in fairly large doses.
7. Fight against hypertremia.
8. Symptomatic treatment.
9. Providing nutrition to patients - liquid, pureed food, if necessary - feeding through a tube.
10. Organization of supervision and care for the patient.

Prevention of tetanus

Prevention involves preventing injuries and immunization. Specific prevention of tetanus is carried out both routinely and urgently. Active routine immunization is carried out with DPT (adsorbed pertussis-diphtheria-tetanus), ADS, AP vaccines - for children, as well as young people of secondary and higher educational institutions, workers of construction enterprises and railways, athletes, Grabar. In areas with high incidence, vaccination against tetanus is mandatory for the entire population. Routine DTP immunization is given to children from 3 months of age three times with 0.5 ml of vaccine with an interval of 1.5 months. Revaccination is done after 1.5-2 years once in a dose of 0.5 ml, as well as ADP at 6, 11, 14-15 years, and then every 10 years once in a dose of 0.5 ml. Emergency immunization is carried out for wounds, especially with soil contamination of wounds, frostbite, burns, electrical injuries, operations on the stomach and intestines, home births and out-of-hospital abortions. Vaccinated persons are administered a single dose of 0.5 ml of tetanus toxoid (TA). Unvaccinated persons undergo active-passive immunization: 0.5 ml of tetanus toxoid is administered subcutaneously and 3000 AO anti-tetanus serum or 3 ml of anti-tetanus donor immunoglobulin for Bezredka is administered intramuscularly. In the future, only toxoid is used according to the general scheme.

Tetanus is an infectious disease of the sapronosis type (the name comes from the Greek sapros, meaning rotten, and nosos, meaning disease). Characteristic of this group of diseases is the contact mechanism of transmission of the pathogen and its habitat.

The habitat for tetanus bacteria is objects (not the human or animal body) located around us - for example, water, soil, chair, table. Thus, the causative agent of Legionnaires' disease, which belongs to this group of diseases, chose an air conditioner, shower and similar objects as its habitat.

Tetanus is not characterized by an epidemiological nature of spread, since the patient does not pose a danger to others - he is not contagious. Although immunity to tetanus does not develop after illness.

For reference. Tetanus is an acute saprozoonotic infectious disease caused by Clostridium tetani. The pathology is manifested by severe damage to nervous tissues by tetanus toxins, leading to the development of severe muscle hypertonicity and tetanic convulsions.

Tetanus infection is one of the most ancient diseases. The first detailed description of pathology belongs to Hippocrates. After his son died of tetanus, he compiled a detailed description of this infection, giving it the name tetanus.

The infection is also mentioned in books such as Ayurveda and the Bible. It should be noted that in all descriptions of tetanus, its development was always associated with contamination of the open wound surface with soil. In some countries, soil contaminated with feces was even treated with weapons instead of poisons.

For reference. For a long time, tetanus was considered an absolutely incurable disease with a 100% mortality rate. At the moment, tetanus is considered a curable disease (subject to early adequate wound treatment and administration of anti-tetanus serum). However, severe tetanus is still accompanied by a high mortality rate. Hospitalization for tetanus is strictly mandatory.

Self-medication is impossible, and the only effective specific remedy against tetanus is antitetanus serum, which must be administered no later than 30 hours from the moment the first symptoms of the disease appear. Later administration of the drug is ineffective.

Why is tetanus dangerous?

For reference. The disease is known all over the world. Sensitivity to tetanus bacillus is high in people of all races and ages. The mortality rate for tetanus (in the absence of timely specific treatment) is ninety-five percent for adults and one hundred percent for newborns.

Before the development of a specific serum by Gaston Ramon (1926), obstetric tetanus was one of the main causes of death in mothers and infants in maternity hospitals.

At the moment, tetanus is quite rare. This is due to the fact that in 1974, WHO introduced a special strategy to reduce the incidence and completely eradicate vaccine-preventable diseases (diphtheria, tetanus, polio, etc.).

Attention. Currently, a high incidence of tetanus is observed only in developing countries, with low economic levels and insufficient coverage of the population with preventive vaccinations. This applies to tourists traveling to such countries.

The leading causes of death in patients with tetanus are:

  • respiratory arrest or cardiac arrest at the peak of seizures;
  • severe metabolic and microcirculatory disorders leading to multiple organ failure;
  • secondary purulent complications, sepsis with septic shock.

The causative agent of tetanus

Clostridium tetani belongs to the large gram+ rods of the genus Clostridium. Tetanus clostridium is a strict obligate anaerobe, that is, for adequate development and reproduction it requires conditions with a complete lack of oxygen access.

Vegetative toxin-producing forms are absolutely not viable in the environment. Therefore, under unfavorable conditions, the tetanus bacillus turns into spores, characterized by the highest level of resistance to physical and chemical influences.

The tetanus spores themselves are not pathogenic. They are not capable of producing a toxin (tetanospasmin) and, in the absence of favorable conditions, do not cause disease.

This explains the fact that, depending on the area of ​​residence, approximately five to forty percent of people are carriers of tetanus bacilli in the intestines. Such carriage is transient, is not accompanied by clinical symptoms and does not lead to the development of the disease.

However, when exposed to anaerobic (oxygen-free) conditions, spores are able to transform back into pathogenic, toxin-producing forms.

Attention. In terms of toxic properties, tetanospasmin produced by tetanus bacilli is second only to botulinum toxin. This toxin is produced and is considered the strongest poison known.

How can you get tetanus?

The source of infection for tetanus is animals. Clostridia in the form of vegetative forms or spores is found in the stomach and intestines of many ruminants. The causative agent of tetanus is released into the environment along with feces.

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In the soil (especially in a humid, warm climate), the pathogen can remain viable for a long time, and under adequate conditions (lack of direct access to oxygen) can actively reproduce. In this regard, soil is the most significant natural reservoir of tetanus bacillus.

Infection occurs when soil containing tetanus spores comes into contact with a damaged skin surface (wound). The highest incidence of tetanus occurs during wartime. With shrapnel wounds, crush wounds and gunshot wounds, the most favorable (oxygen-free) conditions are created, allowing the pathogen to actively multiply.

For reference. In peacetime, the most common causes of tetanus are various leg injuries (puncture of the heel with a rusty nail, thorn, damage to the legs with a rake while working in the country, etc.). Tetanus can also occur when soil gets into a burn wound, contamination from frostbite or trophic ulcers, after illegal (out-of-hospital) abortions, etc. In developing countries, there is still a high rate of neonatal tetanus infection due to infection of the umbilical wound.

Susceptibility to the causative agent of tetanus is extremely high in all age groups and does not depend on gender, but most often the disease is registered in boys under 10 years of age (due to frequent injuries during outdoor games).

How the disease develops

After contact with the wound surface, spore forms of clostridia tetanus remain in it.
The transition to the vegetative form, with the further development of the infectious process, is possible only if oxygen-free conditions are created in the wound:

  • deep puncture injuries with a long wound channel;
  • entry into the wound of pyogenic flora, which actively consumes oxygen;
  • unprofessional wound treatment;
  • blockage of the wound lumen with crusts, blood clots, etc.

For reference. After the spores transform into pathogenic forms, they begin to actively multiply and produce tetanus toxins (tetanospasmin). Toxins quickly spread throughout the body and accumulate in nerve tissues.

Subsequently, the transmission of inhibitory impulses is blocked, as a result of which spontaneous excitatory impulses begin to continuously flow to the striated muscle tissue, causing its tonic tension.

The first signs of tetanus are always manifested by damage to the striated muscles, as close as possible to the wound, as well as facial and masticatory muscles.

Sympathetic signs of tetanus in adults and children include:

  • high body temperature,
  • high blood pressure,
  • severe profuse sweating,
  • profuse salivation (against the background of pronounced sweating and salivation, dehydration may develop).

Against the background of constant tonic convulsive syndrome, a severe disturbance of microcirculation occurs in organs and tissues, leading to the development of metabolic acidosis.

For reference. As a result, a vicious circle is formed: metabolic acidosis contributes to increased seizures, and seizures support the progression of metabolic and microcirculatory disorders.

Tetanus – incubation period

The incubation period of tetanus is from one to thirty days. Usually the disease manifests itself a week or two after clostridia enter the wound.

Attention. It must be borne in mind that minor wounds may heal by the time the first symptoms appear, so it is possible to identify the entrance gates for infection only by collecting an anamnesis.

The severity of the disease is directly related to the length of the incubation period. The shorter it is, the more severe the tetanus.

Tetanus symptoms

Most often, the first symptoms of the disease are:

  • the appearance of nagging and aching pain in the wound area;
  • stiffness and difficulty swallowing;
  • slight twitching of muscles in the wound area.

In some cases, there may be a short period of prodromal manifestations, occurring with fever, chills, weakness, irritability, and headaches.

Important. The first highly specific symptom of tetanus is the appearance of chewing trismus (tonic tension of the chewing muscles, leading to difficulty, and subsequently complete impossibility, to open the teeth).

In the initial stages of the disease, this symptom can be identified by a special technique that provokes muscle spasm: they rest a spatula on the teeth of the lower jaw and begin to tap on it.

Subsequently, progressive damage to nerve fibers by toxins leads to severe and specific damage to the facial muscles:

  • distortion of facial features;
  • the appearance of sharp wrinkles on the forehead and around the eyes;
  • stretching the mouth in a tense, forced smile;
  • raising or lowering the corners of the mouth.

Tetanus (jaw lockjaw) is a serious bacterial infectious disease that affects the muscles, nerves and respiratory functions of a person. Tetanus bacillus ( Clostridium tetani) can enter the body through a cut or wound and spread throughout the body in less than three days. Early symptoms (appearing between three days and three weeks after infection) include headache, difficulty swallowing, and stiffness in the neck and jaw. If you think you have tetanus, seek medical help immediately before it's too late!

Steps

Part 1

Symptoms

    Recognize the early signs of tetanus. At first, you will feel a headache and muscle stiffness in the jaw area. You will have difficulty opening and closing your mouth. Symptoms usually appear eight days after infection, although the first signs of illness may appear between three days and three weeks after the bacteria enters the body.

    • A shorter incubation period indicates a more severe infection of the wound. It is worth noting that the further the wound is from the central nervous system, the longer the incubation period will last. Seek immediate medical attention if you experience symptoms of tetanus in the first eight days after exposure.
    • Headaches and impaired jaw mobility in themselves should not scare you. The presence of these symptoms does not mean anything. If you are still concerned about this, we advise you to consult your doctor.
  1. Beware of developing symptoms. As the disease worsens, you will develop a stiff neck and have difficulty swallowing. Other symptoms also include:

    Beware of possible complications. Advanced cases of tetanus can seriously impair your breathing with spasms in the throat and vocal cords. These spasms can lead to fractures and muscle tears. Your blood pressure may increase and your heartbeat may become irregular. If tetanus is not treated, the patient may develop pneumonia, develop blood clots in the lungs, or even fall into a coma. Despite medical innovations, 10-30% of tetanus patients die from the disease.

    Take a dose of antitoxins immediately. If possible, obtain a prophylactic dose of tetanus immunoglobulin from human serum (or equine tetanus serum). This will help stop the spread of tetanus throughout the body.

    • Don't wait until symptoms become severe before going to the hospital. If you are not vaccinated against the disease and think you may have been exposed to tetanus bacteria, you will need to get an antitoxin injection.
  2. Ask your doctor about taking antibacterial medications. Penicillin, chloramphenicol, and other antimicrobial drugs are often prescribed to treat tetanus. You may also be prescribed medications to help stabilize muscle spasms.

    Know what to do for severe cases of tetanus. In case of serious tissue damage, drug treatment may be accompanied by the removal of necrotic, damaged or infected tissue. The decision on such treatment can only be made by an experienced, highly qualified doctor. It is resorted to only in cases where the infection has spread too much and nothing else can be done other than removing tissue.

    Get vaccinated when you are well. Be aware that even after you recover from tetanus, you can get sick again. Get vaccinated as soon as your symptoms go away. This will reduce the chance of tetanus recurring. Get booster immunization every ten years (at least) to protect yourself from this disease.

Part 3

Preventing Infection

    Know how tetanus is transmitted. The tetanus bacterium enters the body through cuts and breaks in the skin. Tetanus bacillus lives in soil, dust and animal feces. When bacteria enter a deep wound, the spores can produce a powerful toxin, tetanospasmin, which harms motor neurons, the nerves that control muscles. The incubation period is 3-21 days, after which the patient begins to show symptoms of the disease.

  • Always wash cuts, punctures and breaks in the skin thoroughly. If you get injured, you need to disinfect the wound as soon as possible.
  • If you have an open wound, do not touch fertilizer or soil that may contain contaminated fertilizer.
  • The standard incubation period for tetanus is 3-8 days. However, symptoms can occur even 3 weeks after infection. The more serious the infection, the shorter the incubation period will be.

Warnings

  • Thanks to widespread immunization, tetanus is now quite rare. However, if the disease is neglected, the consequences can be very serious. If you think you have contracted tetanus, contact your doctor immediately.

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Tetanus

What is Tetanus -

Tetanus (lat. Tetanus)- zooanthroponotic bacterial acute infectious disease with a contact mechanism of pathogen transmission, characterized by damage to the nervous system and manifested by tonic tension of the skeletal muscles and generalized convulsions.

Brief historical information

The disease has been known since ancient times; its occurrence has long been associated with injuries and wounds. The name of the disease and the first description of its clinical manifestations were given by Hippocrates. Tetanus bacillus was first discovered by N.D. Monastyrsky (1883) in the corpses of dead people and A. Nikolayer (1884) in abscesses in experimental tetanus in animals. A pure culture of the pathogen was isolated by the Japanese bacteriologist Sh. Kitazato (1887). Later, he obtained tetanus toxin (1890) and, together with E. Bering, proposed an antitoxic serum for the treatment of tetanus. The French immunologist G. Ramon developed a method for producing tetanus toxoid (1923-1926), which is still used to prevent the disease.

What provokes / Causes of Tetanus:

Pathogen- obligate anaerobic gram-positive spore-forming motile rod Clostridium tetani of the Bacillaceae family. The spores are located terminally, giving the bacteria the appearance of “drumsticks” or “tennis rackets.” C. tetani produces a potent exotoxin (tetanospasmin), a cytotoxin (tetanolysin) and a so-called low molecular weight fraction. In soil, feces and on various objects, spores can persist for years. Maintain a temperature of 90 ° C for 2 hours. Under anaerobic conditions, at a temperature of 37 ° C, sufficient humidity and in the presence of aerobic bacteria (for example, staphylococci), spores germinate into vegetative forms. Vegetative forms of tetanus bacillus die within a few minutes when boiled, after 30 minutes - at 80 °C. Antiseptics and disinfectants kill the tetanus pathogen within 3-6 hours. In countries with warm climates, spores can grow directly in the soil. In C. tetani, two types of antigens are detected: somatic (O-antigen) and flagellar (H-antigen). Based on the structures of flagellar antigens, 10 serovars are distinguished. All serovars produce tetanospasmin and tetanolysin, which are identical in antigenic properties.

  • Tetanospasmin- one of the most powerful biological poisons. It is a polypeptide with a “distanced” mechanism of action, since bacteria rarely leave the primary site of infection. The toxin is fixed on the surface of the processes of nerve cells, penetrates them (due to ligand-mediated endocytosis) and enters the central nervous system through retrograde axonal transport. The mechanism of action is associated with suppression of the release of inhibitory neurotransmitters (in particular, glycine and γ-aminobutyric acid) in synapses (the toxin binds to synaptic proteins synaptobrevin and cellubrevin). Initially, the toxin acts on peripheral nerves, causing local tetanic muscle contractions. In cultures, the toxin appears on the 2nd day, reaching its peak formation by the 5-7th day.
  • Tetanolysin exhibits hemolytic, cardiotoxic and lethal effects, causes the development of local necrotic lesions. This toxin plays a less important role in the pathogenesis of the disease. The maximum accumulation of the toxin in the culture is observed after 20-30 hours. The processes of its formation are not associated with the synthesis of tetanospasmin. The low molecular weight fraction enhances the secretion of mediators at neuromuscular synapses.

Epidemiology

Reservoir and source of infection- herbivores, rodents, birds and humans, in whose intestines the pathogen lives; the latter is released into the external environment with feces. Tetanus bacillus is also widespread in soil and other environmental objects, where it can multiply and persist for a long time. Thus, the pathogen has two interconnected and mutually enriching habitats, and, consequently, two sources of the pathogen - the intestines of warm-blooded animals and the soil. The significance of a particular source is apparently largely determined by the climatic and geographical conditions of the area. The most favorable soils for vegetation and preservation of the microorganism are chernozem and red soil soils rich in humus, as well as soils well fertilized with organic matter. From soil with dust, bacteria can enter any premises (including dressing rooms and operating rooms), onto various objects and materials used in surgical practice (various powders, gypsum, talc, medicinal clay and mud, cotton wool, etc.).

The frequency of carriage of tetanus bacillus spores by humans varies from 5-7 to 40%, and an increased degree of carriage is noted among persons who professionally or at home come into contact with soil or animals (agricultural workers, grooms, milkmaids, sewer workers, greenhouse workers, etc.). C. tetani is found in the intestinal contents of cows, pigs, sheep, camels, goats, rabbits, guinea pigs, rats, mice, ducks, chickens and other animals with a frequency of 9-64%. The contamination of sheep droppings reaches 25-40%, which is of particular epidemiological significance due to the use of the small intestine of sheep for the production of surgical catgut.

Transmission mechanism- contact; The pathogen penetrates through damaged skin and mucous membranes (wounds, burns, frostbite). Infection of umbilical wounds if asepsis is not observed during childbirth can cause neonatal tetanus. The entry point for the pathogen can be open wounds of different nature and location (punctures, splinters, cuts, abrasions, crushes, open fractures, burns, frostbite, bites, necrosis, inflammatory processes); in these cases, post-traumatic tetanus develops. Surgical wounds, especially on the colon and ischemic extremities, can become an entry point for infection with the subsequent development of postoperative tetanus. Abortion interventions outside of health care facilities may cause post-abortion tetanus. There is no possibility of transmission of the pathogen from a sick person to a healthy person.

Natural sensitivity of people high. Those who have recovered from tetanus do not develop immunity to the disease, since a very small dose of the toxin that can cause the disease is not sufficient to ensure an immunological response.

Basic epidemiological signs. The incidence is sporadic in the form of unrelated cases. The zonal spread of infection is determined by both climatic and geographical and socio-economic factors. The seasonality of the disease is spring and summer. Among the cases, residents of rural areas, children and the elderly predominate; It is in these groups that the majority of deaths are recorded. Due to the widespread implementation of active immunization, tetanus in newborns is not currently registered. The presence of a permanent reservoir of infection in the soil determines the possibility of infection as a result of minor household injuries. There are still cases of nosocomial tetanus infection during operations on the extremities, gynecological operations and surgical interventions on the gastrointestinal tract.

Pathogenesis (what happens?) during Tetanus:

The pathogen in the form of spores enters the human body through damaged skin and mucous membranes. Under anaerobic conditions (deep puncture wounds, wounds with deep pockets or necrotization of crushed tissue), the development and reproduction of vegetative forms in wounds occurs, accompanied by the release of exotoxin. Along the motor fibers of peripheral nerves and with the bloodstream, tetanospasmin penetrates into the spinal cord, medulla oblongata and reticular formation of the trunk, where it is fixed mainly in the interneurons of polysynaptic reflex arcs. The bound toxin cannot be neutralized. Paralysis of interneurons develops with suppression of all types of their synaptic inhibitory effect on motor neurons. As a result, the uncoordinated flow of motor impulses from motor neurons to muscles through neuromuscular synapses increases. The throughput of the latter increases due to increased secretion of acetylcholine under the influence of the low molecular weight fraction. A continuous flow of efferent impulses maintains constant tonic tension in the skeletal muscles.

At the same time, afferent impulses increase in response to the influence of tactile, auditory, visual, olfactory, gustatory, temperature and barometric stimuli. In this case, tetanic convulsions periodically occur.

Muscle tension leads to the development of metabolic acidosis. Against this background, both tonic and tetanic convulsions intensify, cardiac activity worsens, and preconditions are created for secondary bacterial complications. Cardiovascular disorders (tachycardia, arterial hypertension, arrhythmia, ventricular fibrillation) are aggravated due to the hyperactivity of the sympathetic nervous system that develops during tetanus. The excitability of the cortex and reticular structures of the brain increases. Possible damage to the respiratory and vasomotor centers and nuclei of the vagus nerve (bulbar tetanus), which often leads to the death of patients. Other causes of death may be associated with asphyxia due to seizures and the development of complications (pneumonia, sepsis).

Post-infectious immunity does not develop in tetanus. Specific pathological changes are scant (venous stagnation, minor hemorrhages, in rare cases, muscle ruptures and muscle hematomas).

Symptoms of Tetanus:

Taking into account the entrance gates of infection, they are distinguished:

  • traumatic tetanus;
  • tetanus, which developed as a result of inflammatory and destructive processes;
  • cryptogenic tetanus (with unknown portal of entry).

According to the prevalence of the process, the disease is divided into general (generalized) and local tetanus. The latter is rarely observed.

Incubation period varies from several days to 1 month, on average not exceeding 1-2 weeks. The disease begins acutely, only sometimes prodromal phenomena are noted in the form of tension and muscle twitching at the site of injury, malaise, headache, sweating, and irritability.

IN initial period of tetanus In some cases, its earliest sign may appear - dull nagging pain in the area of ​​the entry gate of infection, even in already completely healed wounds. The main specific symptoms that occur during this period are trismus, sardonic smile, dysphagia and stiff neck. These signs appear early and almost simultaneously.

  • Lockjaw- tension and convulsive contraction of the masticatory muscles, which leads to difficulty opening the mouth.
  • Tonic spasms of facial muscles are expressed in a “sardonic smile” (risus sardonicus), which gives the patient’s face a peculiar expression: wrinkled forehead, narrowed palpebral fissures, stretched lips, drooping corners of the mouth.
  • Dysphagia (difficulty and painful swallowing) caused by convulsive spasm of the pharyngeal muscles. The combination of trismus, “sardonic smile” and dysphagia is characteristic only of tetanus.
  • Stiff neck, caused by tonic spasms of skeletal muscles, in tetanus is not a meningeal symptom and is not combined with other meningeal signs (Kernig's, Brudzinsky's symptoms, etc.).

IN the height of the disease painful tonic spasms spread to the muscles of the trunk and limbs (without involving the hands and feet). Tonic muscle tension is constant; muscle relaxation, as a rule, does not occur even in sleep. The contours of large skeletal muscles are clearly outlined, especially in men. From the 3-4th day of illness, the muscles of the abdominal wall become hard as a board, the legs are often extended, and movements in them are limited. At the same time, the intercostal muscles and diaphragm are involved in the process, breathing becomes shallow and rapid. Tonic tension of the perineal muscles leads to difficulty defecating and urinating. As a result of severe tension and soreness of the back muscles in severe tetanus, opisthotonus develops: when the patient is positioned on his back, his head is thrown back, the lumbar part of the body is raised above the bed in such a way that you can stick your hand between the back and the bed.

Against the background of constant tonic tension of the skeletal muscles, tetanic convulsions occur periodically with varying frequencies. Their duration initially ranges from a few seconds to a minute. Most often they are provoked by auditory, visual and tactile stimuli. In mild cases of the disease, 1-2 attacks of convulsions per day are observed; in severe cases of tetanus, they can be repeated up to tens of times within an hour, becoming longer and more widespread. Seizure attacks occur suddenly. In this case, the patient’s face takes on a pained expression and becomes cyanotic, the contours of the muscles are more clearly outlined, and opisthotonus increases. Patients moan and scream because of the pain, trying to grab the headboard of the bed with their hands to ease their breathing. Body temperature rises, the skin (especially the face) becomes covered with large drops of sweat, hypersalivation, tachycardia, shortness of breath are noted, heart sounds are loud, blood pressure tends to increase. The convulsive syndrome develops and intensifies while the patient maintains a clear consciousness; confused consciousness and delirium appear only shortly before death.

The period from the end of the first week to the 10-14th day of illness is the most dangerous for the patient’s life. Metabolic acidosis and a sharp increase in metabolism cause hyperpyrexia and increased sweating. It is difficult to produce sputum because coughing provokes tetanic convulsions. Deterioration of pulmonary ventilation often contributes to the development of secondary bacterial pneumonia. The heart is dilated due to both ventricles, the sounds are loud. The liver and spleen are not enlarged. Deep intoxication of the brain stem causes depression and arrhythmia of breathing, weakening of cardiac activity; possible cardiac paralysis. Due to frequent and prolonged tonic convulsions, painful insomnia and irritability develop, and the threat of asphyxia increases.

In cases of a favorable outcome, the period of convalescence is long; Gradually weakening clinical manifestations of the disease persist for 2-4 weeks, recovery is delayed up to 1.5-2 months.

The severity of tetanus is determined by a combination of several indicators.

  • At mild current The disease incubation period often exceeds 20 days. Trismus, “sardonic smile” and opisthotonus are moderate, hypertonicity of other muscle groups is weak. Tonic convulsions are absent or insignificant, body temperature is normal or subfebrile. Symptoms of the disease develop within 5-6 days.
  • In cases moderate course the incubation period is 15-20 days. The main clinical signs of the disease increase over 3-4 days. Convulsions occur several times a day, tachycardia and sweating are moderate, body temperature is low-grade or (less frequently) high.
  • Severe form Tetanus is characterized by a shortened incubation period to 7-14 days, a rapid (over 1-2 days) increase in symptoms, a typical clinical picture with frequent and intense tetanic convulsions (several times within an hour), expressed by sweating and tachycardia, high fever.
  • Very severe course are distinguished by a shortened (less than a week) incubation period and fulminant development of the disease. Tonic convulsions occur several times within 3-5 minutes. They are accompanied by hyperpyrexia, severe tachycardia and tachypnea, cyanosis, and threatening asphyxia.

One of the most severe forms of generalized descending tetanus is Brunner's cephalic (“bulbar”) tetanus. It occurs with primary damage to the muscles of the face, neck and pharynx, with spasms of the swallowing and intercostal muscles, muscles of the glottis and diaphragm. Usually the respiratory, vasomotor centers and vagus nerve nuclei are affected. Gynecological tetanus and neonatal tetanus, which is one of the important causes of child mortality in developing countries, are also distinguished by the severity of their course and unfavorable prognosis. It is associated with unsatisfactory conditions for the provision of obstetric care and the lack of immunization programs for women.

Ascending tetanus, observed in rare cases, first manifests itself as pain, tension and fibrillary twitching in one group of muscles; later, as new overlying parts of the spinal cord are affected, the disease acquires the typical features of a generalized process.

Local tetanus is rare. One of its typical manifestations, developing after wounds to the face and head, is facial paralytic tetanus Rose. Trismus, stiff neck, and “sardonic smile” occur, accompanied by paresis of the cranial nerves. The lesion is usually bilateral, more pronounced on the side of the wound.

When determining the prognosis of tetanus, much attention is paid to the period between the appearance of the first signs of the disease (lockjaw, etc.) and the onset of seizures. If this period is less than 48 hours, the prognosis of the disease is extremely unfavorable.

Complications

One of the dangerous complications of tetanus is asphyxia. At the same time, there is an opinion that asphyxia and cardiac arrest are not complications, but manifestations of a symptom complex of a severe course of the disease. Complications also include pneumonia, muscle ruptures, bone fractures, and compression deformities of the spine. Hypoxia that increases during convulsions can contribute to the development of coronary vascular spasm and myocardial infarction, and cardiac arrest. During the recovery period, muscle contractures and paralysis of the III, VI and VII pairs of cranial nerves are possible. Neonatal tetanus can complicate sepsis.

The prognosis of the disease is always serious.

Diagnosis of Tetanus:

Tetanus should be distinguished from hysteria, epilepsy, strychnine poisoning, tetany, encephalitis and other diseases with convulsive syndrome.

The diagnosis of tetanus is made based on clinical findings. Specific symptoms of tetanus that occur already in its initial period are dull nagging pain in the area of ​​the wound (even already healed), trismus, “sardonic smile”, dysphagia and stiff neck. The combination of these symptoms is characteristic only of tetanus. During the height of the disease, painful tonic convulsions of the muscles of the trunk and limbs (not involving the hands and feet) occur, and against their background - periodic, suddenly occurring tonic convulsions, the frequency and duration of which largely determines the severity of the disease.

Laboratory diagnostics

When the blood thickens due to severe and constant excessive sweating, as well as secondary bacterial complications, neutrophilia is possible. If a typical clinical picture develops, isolation of the pathogen and its identification may not be necessary. Material from a patient or corpse, dressing and suture surgical material, as well as soil, dust and air are subject to research. Bacteria are usually found at the point of entry into the patient's body. Therefore, it is most rational to study various material taken from the wound site. In cases where the entrance gate is unknown, the patient should be carefully examined to identify abrasions, scratches, catarrhal and inflammatory processes. Particular attention should be paid to old scars after wounds, since the pathogen can persist in them for a long time. In some cases, mucus from the nose, bronchi, pharynx, plaque from the tonsils, as well as discharge from the vagina and uterus (for postpartum or post-abortion tetanus) are examined. When bacteriological examination of corpses, the possibility of generalization of infection is also taken into account. For analysis, blood (10 ml) and pieces of liver and spleen (20-30 g) are taken. To isolate the pathogen, methods common to obtaining pure cultures of anaerobic bacteria are used.

When examining material taken from a patient or a corpse, in parallel with the bacteriological analysis, tetanus exotoxin is detected in a biological sample on mice. To do this, the material is crushed, a double volume of physiological solution is added, incubated for an hour at room temperature, and filtered. Part of the filtrate is mixed with antitetanus serum at the rate of 0.5 ml (200 AE/ml) of serum per 1 ml of extract and incubated for 40 minutes. Then one group of animals is injected with the extract without prior incubation with serum, and the other group is injected with the incubated mixture. In the presence of C. tetani, animals of the first group develop symptoms of tetanus.

Treatment of Tetanus:

Treatment of tetanus carried out in the intensive care and resuscitation department with the participation of an anesthesiologist. It is necessary to provide a protective regime that excludes auditory, visual and tactile stimuli. Patients are fed through a tube or parenterally (for gastrointestinal paresis). They carry out the prevention of bedsores: frequently turning the patient in bed, smoothing out crumpled bed and underwear, cleaning them and periodically changing them. An infected wound, even a healed one, is injected with antitetanus serum (at a dose of 1000-3000 IU), then a thorough inspection and surgical treatment of the wound is carried out with wide striped incisions (to create aerobic conditions), removal of foreign bodies, contaminated and necrotic tissue. To prevent seizures, all these manipulations are best performed under anesthesia. In the future, it is advisable to use proteolytic enzymes (trypsin, chymotrypsin, etc.) to treat wounds.

To neutralize tetanus exotoxin in the bloodstream, 50,000 IU of antitetanus serum or 1,500-10,000 IU (average dose 3,000 IU) of specific immunoglobulin is injected intramuscularly once, with preliminary testing of individual sensitivity to them. These drugs should be administered as early as possible, since tetanus toxin circulates freely in the blood for no more than 2-3 days, and the associated toxin is not inactivated, which reduces the therapeutic effect. After administration of heterogeneous antitetanus serum, it is necessary to monitor the patient for 1 hour due to the risk of developing anaphylactic shock.

The fight against convulsive syndrome is carried out using sedatives and narcotics, neuroplegics and muscle relaxants. Recently, diazepam 5-10 mg orally every 2-4 hours has been widely used; in severe cases, it is administered intravenously at 10-20 mg every 3 hours. For children, the drug is prescribed intravenously or intramuscularly at 0.1-0.3 mg/kg every 6 hours (maximum up to 10-15 mg/kg/day). You can use injections of a mixture of 2.5% solution of aminazine, 1% solution of promedol and 1% solution of diphenhydramine (2 ml of each drug) with the addition of 0.5 ml of 0.05% solution of scopolamine hydrobromide. Also prescribed are seduxen, barbiturates, sodium hydroxybutyrate, and in severe cases, droperidol, fentanyl, curare-like muscle relaxants (pancuronium, d-tubocurarine). In case of lability of the sympathetic nervous system, a- and ß-blockers are sometimes used. In case of breathing disorders, intubation or tracheotomy is performed, muscle relaxation is combined with mechanical ventilation, and clearing the airways with an aspirator; Patients are given humidified oxygen. There are reports of the effectiveness of hyperbaric oxygen therapy.

Laxatives are prescribed in small doses, a gas outlet tube and a catheter are placed in the bladder (if necessary). To prevent pneumonia, frequent turning of the patient, forced breathing and coughing are necessary.

To prevent and treat bacterial complications, antibiotics are used - benzylpenicillin 2 million units intravenously at intervals of 6 hours (children up to 200,000 units/kg/day), tetracycline 500 mg 4 times a day (children up to 30-40 mg/kg/day ). The use of antibiotics does not exclude the possibility of developing pneumonia and other secondary infections.

The fight against hyperthermia, acidosis and dehydration is carried out with intravenous infusions of 4% sodium bicarbonate solution, polyionic solutions, hemodez, rheopolyglucin, albumin, plasma.

Prevention of Tetanus:

Epidemiological surveillance

To identify patterns in the spread of tetanus and rational planning of preventive measures, an in-depth epidemiological analysis of the incidence and the preventive measures used is necessary. To assess the quality of medical care for injuries, it is necessary to analyze its timing, volume and nature. When analyzing the effectiveness of emergency prevention, you should pay attention not only to its volume, but also to the timing of its implementation (the time elapsed after the injury and seeking medical help). Of particular relevance in connection with cases of diseases in previously vaccinated people is the analysis of the immune status of the sick. The immunization of the population against tetanus and the implementation of the vaccination plan for individual age, socio-professional groups, including the rural population, are subject to detailed analysis. Immunological control is an integral part of epidemiological surveillance of tetanus. It allows you to assess the security of various populations, reliably judge the level of vaccination and the quality of immunization, as well as the duration of immunity, identify the most affected groups of the population and characterize areas with varying degrees of risk of infection.

Preventive actions

Nonspecific prevention of tetanus is aimed at preventing injuries at home and at work, eliminating infection of operating rooms, as well as wounds (umbilical and others), early and thorough surgical treatment. Specific prevention of tetanus is carried out on a planned and emergency basis. In accordance with the vaccination calendar, children from 3 months of life are vaccinated 3 times with 0.5 ml of DTP vaccine with the first revaccination after 12-18 months and subsequent revaccinations every 10 years with associated drugs (ADS or ADS-M) or single drugs (AS) . After a completed course of immunization, the human body for a long period (about 10 years) retains the ability to quickly (within 2-3 days) produce antitoxins in response to repeated administration of drugs containing AS toxoid.

Emergency prevention of tetanus is carried out according to the scheme for any injuries and wounds with a violation of the integrity of the skin and mucous membranes, burns and frostbite of II-IV degrees, animal bites, penetrating intestinal injuries, out-of-hospital abortions, childbirth outside of medical institutions, gangrene or tissue necrosis of any type, long-term current abscesses, carbuncles. Emergency prevention of tetanus includes primary wound treatment and simultaneous specific immunoprophylaxis. Depending on the previous vaccination status of patients, a distinction is made between passive immunization, active-passive prophylaxis, consisting of the simultaneous administration of tetanus serum and toxoid, and emergency revaccination with AS to stimulate immunity in previously vaccinated individuals. Emergency immunoprophylaxis of tetanus should be carried out as early as possible and up to the 20th day from the moment of injury, taking into account the length of the incubation period for tetanus.

Activities in the epidemic outbreak

The patient is hospitalized in specialized (intensive care) departments for treatment. Dispensary observation of the patient is carried out for 2 years. Separation of contact persons is not carried out, since the patient is not dangerous to others. Disinfection is not carried out in the outbreak.

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