Tetanus in humans and animals: causative agent, symptoms and signs. Photo

The causative agent of tetanus

The causative agent of tetanus (Clostridium tetani) is a ubiquitous bacterium. It is an opportunistic microorganism that lives in the intestines of animals and humans, where it lives and reproduces. Bacteria enter the soil with feces, contaminating the soil of vegetable gardens, orchards and pastures.

The presence of oxygen and low ambient temperature are factors in the formation of spores, which exhibit tremendous stability in the external environment. They do not collapse when heated for 2 hours at a temperature of 90 °C, in dry form they remain viable when heated to 150 °C, and live in sea water for up to six months.

Rice. 1. The photo shows the causative agents of tetanus.

The causative agent of tetanus is a spore-forming bacterium. Under unfavorable environmental conditions, bacteria form spores that are extremely resistant to a number of chemical factors, disinfectants and antiseptics. Clostridium tetani persists as spores for many years.

Under favorable conditions (in the absence of free oxygen and sufficient humidity), the spores germinate. The resulting vegetative forms produce the exotoxin tetanospasmin and the exotoxin hemolysin. Tetanus exotoxin is a powerful bacterial poison, second in strength only to the toxin secreted by the spore-forming bacillus Clostiridium botulinum (botulinum toxin). Heat, exposure to sunlight and an alkaline environment have a detrimental effect on the exotoxin.

Rice. 2. The photo shows spore-bearing tetanus bacteria. They look like sticks with rounded ends (photo on the left). In unfavorable environmental conditions, bacteria form spores that resemble rackets in appearance (photo on the right).

Rice. 3. The photo shows a tetanus bacterium. The bacterium has up to 20 long flagella, as a result of which it has good mobility.

Dangerous splinter: Tetanus (7 photos)

Author: ScientaeVulgaris

13 December 2021 13:10

Community: Medicine on Chips

Tags: scientae vulgaris history history of medicine medicine popular science rare diseases

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Once upon a time, your Scientae Vulgaris was young and cheerful, could jump high, fresh traces of pioneers could still be found outside the window, and ordinary citizens did not yet know the current president. In those years of my glorious but unknown youth, during one of the nature trips conducted “from class,” I and a group of like-minded people went to explore an abandoned cowshed, similar to one of those in my previous posts, only without signs about foot-and-mouth disease.

See all photos in the gallery

Well, or they were nailed too high for short but inquisitive naturalists. My personal exploration ended with a big leap onto a huge rusty nail. The picture of how he pierced the boot and came out on top still sometimes excites my mind, when looking at particularly uncomfortable shoes. This is a light but scientifically bloody digression here for one reason. Then, in addition to the memory of the nail, I learned one new word. In a couple of days - carefully moving from hand to hand of adults all the way to the emergency room, I finally found myself in front of a huge doctor and a bunch of instruments, the doctor asked in a stern baritone - Have you been vaccinated against tetanus? And without waiting for an answer, he injected him with something childishly brutally painful. Meanwhile, behind this simple question lies a real titan in the closet. Or rather, not titanium, but Tetanus. Strange smile. Tetanus, comes from the Greek tein-ein - to stretch. And we will talk about Tetanus. This disease has been known to mankind for at least 24 centuries, and if we take into account the ambiguous descriptions of the Egyptians, even twice as long. Its first manifestations are associated primarily with military medicine. When particles of dirt and soil fell into puncture wounds, it didn’t matter whether it was an archer of Ramses’s chariot or a legionary of the “Illustrious Spanish”, this fate could have befallen anyone until literally yesterday. The disease in its maximum phase caused muscle contraction - trismus and cramps. First of all, the facial muscles suffered, a painful spasm twisted the face into an angry grimace of pain and despair, tightly clenched teeth creaked against each other, and the lips parted in a devilish grin, better known as a risus sardonicus, or sardonic smile. The eyebrows go up, the mouth stretches, and its corners go down. The grimace of a sadly laughing mime looks at us from the graves of the past, trying to remind us not to make mistakes in the future. The oldest description of Tetanus was found in papyrus recovered from the Pyramid of Cheops and dates back to 2600 BC. e.. Hippocrates, who lived in the 4th century. BC e. knew firsthand about the disease that took his son and describes it this way: “Tetanus leads to death in just four days, but if the patient manages to survive these days, he will recover. There are several types of the disease. The first is that it comes from a wound, the jaws are compressed like intertwined branches of a tree, it is impossible for the patient to open his mouth, even with iron. The unfortunate ones are constantly in tears. The back is straight, arms and legs are bent. Food previously consumed is expelled through the nose. The second type is opisthotonus. The disease occurs in the tendons of the neck, the tongue and ganglia become inflamed. The spasms are so strong that patients fall out of bed and break bones.” On soil and skin, in air and water, this bacterium has always been nearby. She is present with us from the cradle: the Chinese physician Hsueh Chi, in his book “Fundamentals of Obstetrics and Gynecology,” dating back to 1548, advised burning the umbilical cord in newborns and examining the umbilical wound several times a day so that it does not fester, arguing that this is the most important way prevention of tetanus in newborns; to the grave, almost literally, because the most common method of infection is a stabbing wound with the introduction of pathogens from the soil.

Disease history. Research into tetanus and the causes of its infections was inconclusive until the development of microscopy, although basic principles of hygiene, washing wounds with various solutions and amputation saved a certain percentage of the wounded from a terrible death. The causes and pathogen were unknown for a long time. The first advances in research come from Eastern Europe. Among the Slavs, information about this disease is given in a 16th century manuscript kept at the University of Belgrade. The first to suggest that Tetanus is an infectious disease was made in 1865 by the famous Pirogov Nikolai Ivanovich. Soon, in 1883, N.D. Monastyrsky, examining under a microscope smears taken from fluids discharged from a wound, finally discovered the tetanus bacillus and described it in detail. Just a year later, the Italians Carle and Ratton were able to infect experimental animals with similar secretions. The same results were obtained in 1884 by the Frenchman Nikolayer by introducing a soil-based suspension into experimental animals, thereby proving the presence of the disease in it. Do you understand? The fact that if you step on a dirty rake with your bare foot, or bring dirt into a wound and do not wash it, in the absence of vaccination and/or treatment, can lead to a disease that kills with almost the same probability as rabies was proven almost 150 years ago... Monastyrsky and Nikolayer reported their discoveries to the world in 1885, showing that tetanus was an infection caused by Clostridium tetani, which appeared in wounds and lived in the soil. Soon, the Italians Tizzoni and Cattani managed to isolate pure cultures of the microorganism, and in the same 1889, the Japanese Shibasaburo Kitasato, together with the German doctor Emil Adolf von Behring, discovered the antigenic properties of the toxin secreted by the bacterium, which made it possible to create anti-tetanus serum.

A year later, the ability of the pathogen to produce tetanospasmin (the toxin itself) was finally established; the discovery was made by K.H. Faber and V.D. Laird. And only in 1923, the French immunologist G. Ramon was able to create tetanus toxoid, necessary for the prevention and prevention of the disease. But what was its importance? And why are there two openings, one for treatment and the second for prevention? It's all in the details. There are two details. Bacteria and toxin. Let's start with the first one. If you google what tetanus bacillus is, you will see a cumbersome description: a gram-positive, spore-forming, obligate anaerobic bacterium. Translated into popular language: this garbage has an additional membrane, it can turn into spores and does not like open air. Survival in general is terrible. It can form terminal spores in order to survive unfavorable environmental conditions and travel. By the way, the spores give it the appearance of a stick. Sporification occurs in the presence of oxygen and temperatures above 4 °C. The spores are resistant to external influences: they can withstand heating up to 90 °C for 2 hours, when boiled they die only after 1-3 hours, in a dry state they can withstand heating up to 150 °C, and they live in salty sea water for up to 6 months. They persist in feces, soil, and on various objects for more than 100 years. The causative agent of tetanus itself belongs to the category of ubiquitous microorganisms, that is, ubiquitous. The spores are widespread in soil and manure; they are found in 50-60% of tested samples, and in some types of soil - in 100% of cases. Spores are present in the intestines and feces of horses, sheep, cattle, dogs, cats, rats, guinea pigs, chickens, people in general and you in particular, they can be carried with dust, penetrate into the home, get on outerwear, underwear , shoes and other objects.

But simply introducing bacteria into a wound is not enough. Not every such case will be accompanied by infection. Otherwise, we would all be extinct here by now. The disease occurs only if there are favorable conditions - warmth, lack of oxygen and the presence of a nutrient substrate (blood clots and tissue necrosis). If the stick does end up in a favorable environment, for example, in an inflamed wound cavity, the classic clinical picture of the disease develops. In the nature of the disease, much depends on how far the lesion is located from the central nervous system. The closer it is, the shorter the incubation period and the more severe the course of the disease. Typically the ripening period lasts up to 8 days. Then, at the site of infection, even if the wound has already healed, nagging pain appears. Chills, insomnia, sore throat, back pain. On the 2nd day after the start of the active phase - cramps of the masticatory muscles. Gradually, the number of muscles involved in spasms increases; the muscles of the back of the head, neck, back, abdomen and limbs are included. In severe cases, seizures last continuously. Patients scream and moan in pain, the temperature rises to 41-42 degrees, the functions of swallowing, defecation, urination, and breathing stop. Due to convulsions, the patient’s torso bends backward in an arched manner in the form of a column, which served as the basis for the Russian name of the disease. Due to uniform damage to the anterior and posterior muscle groups (opisthotonus), convulsions can reach such strength that they can be accompanied by fractures of the X-XII thoracic vertebrae. The next attack can lead to a complete stop of breathing due to the involvement of the muscles of the larynx (laryngospasm) and diaphragm in the process. Gradually, in severe cases, seizures, despite the administration of high doses of anticonvulsants, intensify and become more frequent, as a result of which the patient is intubated and placed on mechanical breathing. The heart begins to contract at a frequency of 130–160 beats/min, and blood pressure drops. Death occurs from the development of asphyxia, due to laryngospasm and spasms of the diaphragm. Simply put, patients, twisted by a painful spasm, suffocate. But it is not the bacteria itself that causes the attacks. Once it gets into the wound and attaches itself to the vessels that feed the muscle fibers, it wants nothing more than to multiply inside your body, in warmth and airless space. But while consuming something useful, it produces something that is useless, or rather harmful. And to be even more precise, tetanospasmin is a neurotoxic poison and tetanolysin, a hemolytic poison. Tetanospasmin ranks second among all organic poisons known to science. Second after botulinum, produced by a bacterium of the same family Clostridium botulinum. Think about it, we are talking about the most powerful organic poisons on the planet, and they are produced by bacteria living... everywhere. Deadly combo. The first toxin, tetanospasmin, is similar in properties to the botulism toxin and is an enzyme that breaks down proteins - proteinase. Released by the bacterium, it spreads through the lymphatic and circulatory systems, with almost no effect on them. It then travels to the terminal endings of the motor neurons that run through your muscles. Normally, neurotransmitters contained in neurons in special vesicles are released from these endings. They are secreted using a special protein - synaptobrevin, which is the target for tetanospasmin. Through neurotransmitters, an electrochemical impulse is transmitted from your brain to each specific muscle. The toxin binds the protein necessary for transmission and the first symptom of tetanus appears - flaccid paralysis. At this stage, the toxin acts similarly to butulinum toxin. But then the thing that turns tetanus into a special infection begins, the neurotoxin begins to spread throughout the nervous system all the way to the brain stem. Movement at a speed of about 1 cm/hour is carried out with the help of denin proteins and can occur from neuron to neuron only in the area of synapses, since the membrane of neurons is practically impenetrable to toxin molecules. In the central nervous system, the toxin continues to block synaptobrevin, and the transmission of impulses begins to be disrupted at the highest level, and the conduction of inhibitory signals is primarily disrupted. This denervation leads to hyperactivity of motor neurons, which is manifested by muscle spasms. The muscle tenses, but only at one end. The signal to relax no longer passes.

The second toxin in the deadly combo is tetanolysin. This is a membranotropic toxin; in other words, it destroys the membranes of the cells around it. In our case, red blood cells are susceptible to this. Essentially, the task of the toxin is to cause massive hemolysis (destruction of blood cells) and disrupt phagocytosis (cell nutrition), together they promote the spread of bacteria inside the body, creating comfortable conditions for them, with the necessary set of nutrients. The toxin is destroyed when heated, exposed to sunlight, or an alkaline environment. It is not absorbed through the intestinal mucosa and is therefore safe if swallowed. The lethal dose of the toxin for humans is 2 ng\1 kg of weight. Imagine, 100 billionths of a gram is enough to kill an adult man. Death, death, death. The mortality rate for tetanus is very high (higher only for rabies and pneumonic plague). With the use of modern treatment methods, 17-25% of patients die; these numbers cannot currently be reduced due to the development of complications such as pneumonia, sepsis and cardiac paralysis caused by bacterial toxin. In the absence of vaccinations and qualified medical care, the mortality rate is about 80%. Mortality in newborns reaches 95%. Of course, since the invention of the vaccine and toxoid, things have improved significantly.

According to approximate calculations carried out on the basis of the epidemiological model of B. D. Bychenko back in 1982, during 1951-1980. In the world, more than 1 million people fell ill with tetanus every year, most of whom were newborns. Moreover, for every person who died in industrialized countries, 135 died from this disease in developing countries. Observations conducted in Asia and the Mediterranean showed that in 1981, in 14 countries in these regions alone, at least 600,000 people fell ill with tetanus and 500,000 of them died. Europe had the lowest overall incidence between 1970 and 1981, less than 0.05 per 100,000 inhabitants. In 2010, there were approximately 61,000 deaths from Tetanus worldwide. However, taking into account the possibility of a large number of unregistered cases and unexpressed forms of the disease (especially in newborns), the total losses from tetanus on the planet can be estimated at 350-400 thousand people annually. The graph from the World Health Organization website does not require any special explanation: the columns are the number of disease cases, the line is the immunization of the population.

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Prevalence and incidence rate

Up to 400 thousand people die from tetanus every year. The prevalence of the disease on planet Earth is uneven. Hot and humid climate, lack of preventive work and medical care are the main reasons for the spread of the disease. In such regions, the mortality rate from tetanus reaches 80%, and in newborns - 95%. In countries where modern methods of treatment and prevention of tetanus are used, about ¼ of those affected die annually. This is due to severe complications of the disease caused by tetanus toxin that are incompatible with life.

Rice. 4. Dark red and red colors indicate incidence rates (very high and high, respectively) for the period from 1990 to 2004.

Treatment options

Treatment of tetanus is carried out in the intensive care unit under the supervision of an anesthesiologist-resuscitator. The main condition is that the patient must be absolutely at rest. There should be no tactile, visual or auditory stimuli. With the development of gastrointestinal paresis, the patient is fed by tube or parenterally. Prevention of bedsores is imperative.

The site of infection is injected with anti-tetanus serum, and if it heals, the same. This place is subjected to surgical treatment - stripe incisions are made so that the site of bacterial infection has access to oxygen, which will significantly reduce the development of anaerobic organisms. Manipulations are performed under mandatory anesthesia. The wound is treated with proteolytic enzymes.

To neutralize the effects of toxins secreted by bacteria, antitetanus serum and specific immunoglobulin are administered intramuscularly.

You must first do a sensitivity test. Early administration of drugs increases the effectiveness of treatment. Tetanus toxin circulates freely in the blood only during the first 2-3 days, and then it binds, and its neutralization becomes impossible. After administration of anti-tetanus serum, the patient should be monitored for an hour to exclude anaphylactic shock.

Epidemiology of tetanus

Tetanus bacteria are permanent inhabitants of the intestines of herbivores (herbivores, horses, sheep). Released into the external environment along with feces, microbes contaminate the soil. Tetanus most often affects older people. In regions where children are actively immunized, the disease develops extremely rarely.

The gates of infection are:

injuries, abrasions and splinters of the skin,
deep pyoderma in the form of boils and carbuncles,
skin damage due to bedsores, trophic ulcers and gangrene,
extensive wounds in wartime,
burns and frostbite,
postpartum and postoperative wounds, skin damage due to injections,
umbilical wound of newborns,
bites of poisonous animals and spiders.

Sometimes it is not possible to identify the entrance gates of infection.

The condition for the development of tetanus bacteria is an oxygen-free environment. These include puncture wounds and wounds with deep pockets.

Rice. 5. Injuries, abrasions and splinters of the skin are the main entry points for bacteria.

A sick person is not a spreader of infection.

Routes of infection

Tetanus bacillus, or rather its spores, are common in soil, in ordinary dust, in sea and fresh water. They are most often found in well-fertilized and moist forest soil. Due to its prevalence, tetanus has a high degree of danger.

When a person comes into contact with a contaminated environment, there is a risk of infection with this disease. A prerequisite for this is damage to the skin, through which the pathogen spores enter the human body.

Theoretically, a very small scratch is enough for infection to penetrate and the disease to begin to develop; in fact, this happens quite rarely.

Deep wounds that have torn edges and have pockets in them pose a significant threat, because spores for development require a temperature exceeding 37 degrees, humidity, lack of oxygen, and to create ideal conditions, the presence of staphylococcal infection.

Sometimes tetanus can develop even in small wounds if they are not treated and aerobic bacteria have developed in them. The umbilical wound in a newborn, theoretically, can also be one of the ways of transmitting tetanus.

Cases of infection are very rare these days. However, you can become infected during childbirth or abortions not performed in a hospital.

Important!!! Tetanus cannot be contracted from someone who is already sick. It does not spread this way. Infected people do not pose a danger to others.

Pathogenesis of tetanus

When spores of tetanus bacteria enter through damaged skin, they germinate. The resulting vegetative forms produce exotoxin. The exotoxin tetanospasmin is a high molecular weight protein consisting of 3 fractions - tetanospasmin, tetanohemolysin and protein.

The neurotoxin tetanospasmin is the most powerful of all exotoxins. The toxin passes through the blood and lymphatic vessels, along the perineural tract and is firmly attached to the cells of the nervous system. Tetanospasmin blocks the inhibitory effect of interneurons on motor neurons and impulses that spontaneously arise in motor neurons begin to be freely transmitted to the striated muscles, in which tonic tension occurs. Initially, muscle tension is recorded on the side of the affected limb. Next, muscle tension affects the opposite side. Next - the torso, neck and head. Tonic tension of the intercostal muscles and muscles of the diaphragm leads to impaired ventilation of the lungs, which leads to the development of metabolic acidosis.

When touched, loud sounds and the appearance of all kinds of odors, the patient experiences tetanic convulsions. Prolonged convulsions are accompanied by large expenditures of energy, which aggravates the development of metabolic acidosis. A block of neurons in the brain stem region leads to inhibition of the parasympathetic nervous system. The respiratory and vasomotor centers are affected. Spasm of the respiratory muscles and paralysis of the heart muscle are the main causes of death in tetanus.

Rice. 6. In the photo, signs of tetanus in a child are convulsions (left) and opisthonus (right).

Tetanus

The disease is classified as infectious; its causative agent is the bacillus Clostridium tetani. It has an acute nature, the blow is mostly on the nervous system.

It is classified according to the method of infection - cryptogenic, post-inflammatory, post-traumatic, and can also be local and generalized. Tetanus, which has a local form, is very rarely observed.

The causative agent is a gram-positive, motile, anaerobic, spore-forming rod-shaped microorganism. Outwardly, it is similar to drumsticks, because a spore is located on one edge of the bacterium.

Very stable: spores are viable for many years, they are destroyed only after two hours under the influence of a temperature of 90 degrees Celsius. The spore becomes active at 37 degrees without the presence of oxygen, but for its vital activity the presence of aerobic microflora - staphylococcus - is required.

The vegetative form of the bacterium dies in a matter of minutes when boiled. It takes 3 to 6 hours for disinfectants and antiseptics to have an effect on microorganisms.

Signs and symptoms of tetanus

Signs and symptoms of tetanus during the incubation period

The incubation period for the disease lasts from 5 to 14 days. Fluctuations range from 1 day to 1 month. Tetanus almost always begins acutely. The prodrome period is rare. Its main manifestations are restlessness and irritability, insomnia, yawning and headache. In the area of damage to the skin, nagging pain occurs. Body temperature rises. Appetite decreases.

The further the lesion is located from the central nervous system, the longer the incubation period. With a short incubation period, the disease is more severe. A short incubation period is observed for injuries to the neck, head and face.

Rice. 7. In the photo there is a “sardonic smile” with tetanus. With tonic tension of the facial muscles, the mouth stretches, its corners drop, the wings of the nose rise, the forehead wrinkles, and the palpebral fissures narrow.

Signs and symptoms of tetanus in the initial period

Tetanus almost always begins acutely. Its first symptom is a tonic contraction of the masticatory muscles, characterized by the inability to open the mouth. Trismus is often preceded by “fatigue of the masticatory muscles.” With tonic tension of the facial muscles, the mouth stretches, its corners drop, the wings of the nose rise, the forehead wrinkles, and the palpebral fissures narrow (“sardonic smile”). As a result of contraction of the pharyngeal muscles, dysphagia develops. The duration of the initial period is 1 - 2 days.

Rice. 8. The first symptom of tetanus is a tonic contraction of the masticatory muscles (trismus) and facial muscles (“sardonic smile”).

Trismus, "sardonic smile" and dysphagia are strictly specific symptoms of tetanus

Signs and symptoms of tetanus during the height of the disease

The duration of the peak period of the disease is from 8 to 12 days. In severe cases - from 2 to 3 weeks.

During the height of the disease, symptoms of skeletal muscle irritation appear. Muscle hypertonicity is accompanied by severe pain. Extensor reflexes predominate, which is manifested by stiffness of the neck muscles, throwing the head back, hyperextension of the spine (opisthonus), and straightening of the limbs. Hypertonicity of the muscles involved in breathing leads to hypoxia.

When touched, loud sounds and the appearance of all kinds of odors, the patient experiences tetanic convulsions. Prolonged convulsions are accompanied by large expenditures of energy, which contributes to the development of metabolic acidosis. During convulsions, body temperature rises, increased salivation and tachycardia are noted. Spasm of the perineal muscles is manifested by difficulties in urination and defecation. Convulsions last from a few seconds to one minute. Spasm of the respiratory muscles and paralysis of the heart muscle are the main causes of death in tetanus. In the absence of qualified medical care and preventive vaccinations, the mortality rate from tetanus reaches 80%. When vaccination is used and timely qualified medical care is provided, the mortality rate is 17 - 25%.

Rice. 9. The photo shows opisthonus (hyperextension of the spine) in a patient with tetanus.

Rice. 10. In the photo there is opisthonus in a child.

A patient with tetanus has no meningeal symptoms, and consciousness remains clear throughout the entire period of the disease.

Signs and symptoms of tetanus during recovery

The recovery period for tetanus lasts 3 to 4 weeks. In some cases - 8 weeks. Already on the 10th day of the disease, an improvement in the patient’s well-being is noted. Signs of infectious-toxic myocarditis and asthenovegetative syndrome appear.

Severity and prevalence of tetanus

The mild form of the disease lasts about 2 weeks. Patients with this form of the disease have partial immunity from tetanus. Muscle hypertonicity, tetanic convulsions and dysphagia are mild. Convulsions are rare or absent.
The moderate form of tetanus occurs with typical symptoms of the disease. The patient experiences convulsions every 1 to 2 hours. Their duration is short - 15 - 30 seconds.
In severe forms of tetanus, there is a high body temperature, frequent attacks of convulsions - every 5 - 30 minutes, their duration is 1 - 3 minutes. Hypoxia and cardiac weakness develop. Pneumonia occurs.
The encephalic form of the disease (Brunner's cephalic bulbar tetanus), which affects the medulla oblongata and the upper part of the spinal cord, is especially severe. The disease develops with injuries and injuries to the neck and head. The swallowing, respiratory and facial muscles are involved in the spasms. The incubation period for bulbar tetanus is short. Mortality is extremely high.
Local tetanus is very rarely observed. Its variety is facial paralytic tetanus (Rose's cephalic tetanus), which develops with injuries and wounds of the neck and head, sometimes with otitis media. It is characterized by trismus (contraction of the masticatory muscles), paralysis of muscles that are innervated by cranial nerves (either one or more). Most often, the disease affects the nervus facialis (facial nerve).

Rice. 11. The photo shows facial paralytic tetanus.

Complications of tetanus

Hypertonicity of the muscles involved in breathing leads to hypoxia. Mucus production increases. The drainage function of the bronchi is impaired. Against the background of congestion, bronchitis and pneumonia occur, complicated by pulmonary edema. Thrombosis of the pulmonary arteries develops.
The great strength of the muscles during the contraction period leads to the fact that they can be torn away from the place of attachment, fractures of the vertebral bodies, joint dislocations, ruptures of the muscles and tendons of the limbs and the anterior abdominal wall occur, compression deformation of the spine and muscle contractures develop.
Extensive wounds are often complicated by abscesses and phlegmon.
Later complications include spinal deformities, muscle contractures, and temporary cranial nerve palsies.

After recovery, the patient has been worried about general weakness, weakening of cardiovascular activity and stiffness of skeletal muscles for a long time.

In regions where there is no preventive work and proper medical care, the mortality rate from tetanus reaches 80%, and in newborns - 95%. In countries where modern methods of treatment and prevention of the disease are used, up to 25% of patients die annually. This is associated with severe complications of tetanus that are incompatible with life.

Rice. 12. In the photo, a child has tetanus. Above - opisthonus, below - tetanic convulsions.

Relapses of the disease are extremely rare. The reasons for their occurrence are unknown.

Diagnosis of tetanus

Epidemiological history

Epidemiological history when diagnosing tetanus is of paramount importance. Domestic injuries, burns, frostbite, criminal abortions and surgical interventions are most often the cause of the disease.

Clinical symptoms of tetanus during the height of the disease make it easy to make a diagnosis. Trismus, dysphagia and “sardonic smile” at the beginning of the disease, hypertonicity of skeletal muscles, periodic tetanic convulsions and opisthonus are the main diagnostic signs of the disease.

Rice. 13. The photo shows tetanus in adults.

Laboratory diagnostics

Laboratory diagnosis is of secondary importance. Tetanus toxin cannot be detected even when symptoms appear. Detection of antitoxic antibodies indicates previous vaccinations. The exotoxin does not cause an immune response, so there is no increase in antibody titer.

To diagnose the disease, microscopy of smears, histological examination of the material and culture of wound discharge on nutrient media are used.

Rice. 14. In the photo, terminal endospores of Clostridium tetani resemble a racket in appearance. Bacteria look like thin rods (microscopy).

Rice. 15. The photo shows the growth of colonies of tetanus bacteria in the form of a delicate coating, along the periphery of which processes are visible. A zone of hemolysis is determined around the colonies.

Treatment of tetanus

When treating tetanus, you must strictly adhere to the regime: patients are placed in the intensive care unit, in isolation wards with a minimum content of irritants. Nutrition – tube or parenteral (using a dropper), with special nutritional mixtures. The patients are monitored dynamically and are connected to a ventilator.

Etiotropic (elimination of the cause of the disease - the causative agent) treatment is limited, and it does not guarantee the prevention of the development of a severe clinical picture and death. Therefore, such treatment is carried out only if infection is suspected, when there are no symptoms yet, and this is done with the help of anti-tetanus immunoglobulin and anti-tetanus purified concentrated serum. In the treatment of tetanus, drugs that relax muscles, anticonvulsants, and narcotic painkillers are also used.