Tetenus - Causes, symptoms and treatment. MF.

Tetanus is a particularly severe, acute, saprozonotic( soil inhabitant) bacterial infection with a contact mechanism of transmission, characterized by attacks of generalized seizures against a background of muscle hypertonia. Mortality in this disease reaches 85% after the onset of symptoms, even despite adequate treatment.

The description of this disease came from the treatise of Hippocrates, whose son died of tetanus. Only from the beginning of the 19th century the tetanus activator was actively studied, because they noticed that during the wars there is a mass infection with lethal outcomes among the military personnel. Later, a tetanus toxoid used for mass prophylaxis was created, which significantly reduced the risk of morbidity and mortality from tetanus.

The causative agent of tetanus

The causative agent of tetanus is the bacterium Clostridium tetani. In form it resembles a wand, with flags on each side( they cause active penetration and further movement through the body).The main distinguishing feature of the pathogen is the presence of the strongest exotoxin in the world, it is second only to botulinum toxin in strength. Its minimum lethal dose is 2ng / kg. This exotoxin consists of two fractions - tetanospasmin and tetanolysin.

Tetanolysin - is excreted from the cells of the pathogen from the first days, but its role in the development of pathogenesis still has no unambiguous explanation. It is only known that it destroys erythrocytes, thereby causing hemolysis, and suppresses phagocytosis( devouring the immune system of the pathogen itself) - these two directions predetermine the rapid penetration of the pathogen to the target( nervous system), which significantly shortens the incubation period and makes the development of symptoms moreimpetuous.

The tetranospasmin is the second component of exotoxin, which is released only after decay( ie after phagocytosis) and acts according to the following principle: it selectively affects synaptobrevin( this is a transmembrane protein carrier, secretory vesicle-vesicle cells involved in release of inhibitory mediators into the synapse), this leads to uncontrolled muscular contractions, because only excitation processes without inhibitory mediators go.

With regard to stability, the tetanus is one of the most hardy, because it forms a spore( it is round in shape, larger than the diameter of the cell, located terminal, which gives the causative agent a resemblance to the "drumstick") under adverse conditions and with access to oxygen.

Bacteria Clostridium tetani

In feces, soil and various contagious objects, spores persist for decades, so the soil is an inexhaustible reservoir of tetanus. It perishes within 14 hours from 1% solution of mercury, formalin and 5% solution of phenol. The action of UFI is stable.

Susceptibility to tetanus is high. There is no seasonality, no age and sex restrictions, and with respect to geographical boundaries - widespread distribution - the problem is of global importance, the mortality rate during infection always leaves high stability.

Causes of infection with tetanus

Source - soil and many species of animals in the digestive tract of which a tetanus pathogen is found, it is possible that the pathogen is found in the human intestine, but due to the integrity of the intestinal mucosa, further introduction of the pathogen does not occur( although there is always a risk!).

Paths - contact, infection through damaged skin or damaged mucous membranes. Basically, the entrance gate of the infection is considered to be: gunshot, stabbed, cut wounds, splinters, rubs, burns, frostbite, injured birth canals and umbilical wounds in unsanitary conditions.

But because the multiplication of the pathogen occurs in the entrance gate, then the primary treatment of the wound surfaces is very effective. If you are outside the hospital, use the most common disinfectants - hydrogen peroxide, alcohol, furacilin, chlorhexidine. Symptoms of tetanus

The incubation period of can last from 1 day to several months, but most often 3-14 days. At the same time, the shorter the incubation period, the heavier the disease progresses. This moment is considered from the beginning of the introduction of the pathogen to the first clinical signs. As soon as the pathogen contacts the open wound surface, it fixes and multiplies at the site of implantation, along the course of phagocytosis, a part of the exotoxin - tetanospasmin - is released from the cells of the pathogen. But the duration of the incubation period is explained by the fact that tetanospasmin can not directly reach the central nervous system from the blood, it has to go through a long and gradual path: from branches of blood vessels that supply blood to the muscle fibers, contact with the myoneural synapses( a connection between muscle fibers and motor neurons).The tetanospasmin binds first to the receptors, and then to the membranes of these nerve cells, penetrating it directly into the cell, advances through the fibers of these nerve cells to the next cells, thus achieving a CNS( moreover, the rate of advance of this toxin is 1 cm / h).After the gradual passage of a number of neurogenic structures, a "convulsive period" appears with the corresponding symptoms and signs.

The convulsion period begins with the onset of tetanospasmin. First, the symptoms develop locally, that is, at the site of implantation, in the form of blunt and drawing pains with muscle twitchings, then the symptoms gradually acquire a more widespread character, capturing ever larger muscular areas, with strict rigidity:

1. Trism is the tonic tension of the chewingmuscles, first obstructing the closure of the mouth, and then - making it impossible to open the teeth.

Trism in tetanus

2. Sardonic smile simultaneously expresses and weeping and irony, but sometimes it is also called maliciously mocking;

Sardonic smile

3. Dysphagia - difficulty swallowing due to spasm of the swallowing muscles, this leads in addition to exhaustion to hypersalivation( abundant salivation, without the possibility of swallowing).

The above triad of symptoms( trismus, sardonic smile, dysphagia) is a type-specific symptom complex that allows you to unmistakably put or even suspect a tetanus in the early stages.

4. Hypertonus of the muscles of the occiput, back and abdomen, with the gripping of the muscles of the limbs( arms and legs).The spread of muscle hypertonia follows a descending type and, due to the fact that the tone of the back muscles is developed more strongly than the abdomen, then opisthotonus appears, more rarely - emprostotonus( with a highly developed abdominal press, resulting in the patient's appearance as with severe abdominal pains).

Opistotonus is a view of the maximally unbent body, as a result of hypertension of the extensor muscles grouped mostly on the posterior surface of the trunk( neck and back muscles, extensor muscles of the limbs), the patient arches in the form of an arch, supported by the back of the head and heels.

Opistotonus at the time of muscle cramps, which can first be clonic( ie, relaxation after seizures), and then or bypassing the clonic stage, become titanic( i.e., there is no definitive relaxation after seizures, and they always remain in tension).They can be present in the patient at the same time, but in different parts of the body, so convulsions for tetanus are often called tonic-clonic. At the time of these convulsive seizures, complete stiffness occurs, the cramps are very painful, the possibility of movement remains only in the hands and feet - this is another important differential diagnostic feature, but at a later stage.

These cramps can occur as a result of any, even the most insignificant stimuli - tactile, auditory, visual. And the most terrible thing in this disease is that at the time of these incredibly painful convulsive attacks a person remains fully conscious and, with the addition of decompensation on the part of organs and systems, a slow and painful death sets in, but remains to the very end in the consciousness of .

5. Capture by tonic tension of intercostal muscles, diaphragm and glottis. Since this moment, the risk of death due to respiratory arrest due to spasm of respiratory muscles or as a result of direct involvement of the respiratory and vasomotor center in the medulla oblongata is high.

6. The formation of multi-organ failure is possible both at the height of clinical manifestations, and in the form of a consequence after the transferred disease. Changes in the KHS( acid-base state of the blood), also from the cardiovascular and respiratory systems:

• ↑ AD, tachycardia with possible development of arrhythmia;
• cyanosis develops due to respiratory arrest, and if the attacks are too frequent, acidosis is gradually formed( changes in the KSH), which aggravates the general condition and closes the formed vicious circle, namely, makes the excitability even easier and even more affects the center of the medulla oblongata,aggravated respiratory and cardiovascular disorders.

Newborn tetanus is a separate form of the disease, because the disease is more rapid and death occurs before the onset of typical clinical manifestations. Initially, the child is violated by the act of swallowing and sucking, there is a rejection of the breast. Aetanic convulsions are accompanied by screaming, tremor of the lower lip / chin and tongue, involuntary urination and defecation joins. During the attack, there is also cyanosis and blepharospasm( spasm of the eyelids - as a strong squeezing).Occurs in newborns whose mothers were not vaccinated, ie those children who did not receive passive immunity from mothers.

Diagnosis of tetanus

Often enough clinical data( examination), because the full clinic develops within 1-3 days, with the preservation of strict phase. From laboratory methods, bacteriological diagnostics are acceptable and most relevant, because it is aimed at isolating and identifying the pathogen and detecting its toxin in the material under investigation( microscopy of print smears, histological examination of tissues).In this case, there are no additional diagnostic methods, as in other diseases that are aimed at detecting antibodies, because in this case this increase in the antibody titer does not occur because even the minimal lethal dose of the causative agent does not elicit an immune response.

Treatment of tetanus

Treatment is inseparable from the regimen and diet for this disease: a therapeutic and protective regimen is needed to help reduce the frequency of seizures. For this, patients are placed in isolation chambers, thus preventing contact with external stimuli. In nutrition, it is necessary to switch to probe and / or parenteral nutrition( through a dropper) with special nutritional mixtures, amino acid mixtures and fatty emulsions. The food is made from the calculation 2500-3000kcal / day. With frequent convulsions, the KShS is diagnosed and then the nutrition is adjusted, for with convulsions there are large energy losses.

Treatment is carried out only in intensive care units, because almost all drugs are in the list of group A, dynamic control over laboratory changes is also necessary and the patient is on ventilators( they are necessarily catheterized)( because the act of urinating is grossly violated).

• Etiotropic therapy is very limited and at the moment of obvious symptoms already present, its effectiveness is minimized, so neither early nor repeated administration of these drugs does not prevent the development of severe clinical forms and death. To etiotropic drugs include antitetanus immunoglobulin and tetanus purified concentrated whey. They are used only in case of a suspected infection, until symptoms can be seen.

• Pathogenetic therapy is directed to the action of toxin and it is more effective in combination with etiotropic, which allows to improve the survival prognosis. These drugs include: muscle relaxants, the entire arsenal of anticonvulsants, narcotic analgesics, antihistamines, barbiturates, β-adrenoblockers to reduce the influence of the sympathetic nervous system. With prolonged heavy flow to the required list, antibiotics are added for the prevention / treatment of pneumonia and sepsis.

Complications of tetanus

• Of the complications, bone fractures, muscle tearing and tearing, muscle contractures, joint ruptures are more often than not.
• Of secondary complications of less dangerous and emerging at later stages, secondary bacterial infections( pneumonia, pyelonephritis, sepsis, lung atelectasis) are isolated.
• With extensive complications, abscesses and phlegmon appear in the gates of the infection. But in everyday life regarding the gate of infection, the picture is diametrically opposite - the gate of infection is often impossible to find at all.

The disease often ends in a lethal outcome.

Prevention of tetanus

Nonspecific - prevention of injuries and treatment of wound surfaces.

Specific - planned active immunization of children and adults and emergency post-traumatic prophylaxis. Active immunization of the population begins at 3 months of age → at 4.5 months → at 6 months → 18 months first revaccination → at 7 years old second booster → at 14 years old second revaccination → booster every 10 years from the last vaccination. You can be vaccinated with the following vaccines: DTP, ADS-M, Infanriks. Vaccination is carried out in accordance with the calendar of vaccinations, taking into account all indications and contraindications. In case of contraindications, vaccination manipulations are postponed, and an individual vaccination plan with preservation of time intervals( i.e., the difference between the first and subsequent vaccinations / revaccinations is preserved for about 1.5 months, etc.).

Emergency immunoprophylaxis is performed with trauma and, depending on the prescription of the previous vaccination with anatoxin, either passive immunization with antitoxic serum or active-passive immunization( tetanus toxoid or homologous immunoglobulin) or emergency revaccination with tetanus toxoid is carried out. It is better to choose the last 2 options, because when you introduce antitoxic serum, its level remains less than the incubation period can be. Therefore, passive immunization is only suitable for those who have completed the full course of immunization.

How much immunization helps to alleviate the disease?

Full and timely immunization of tetanus allows to completely eliminate the risk of the disease. If, for some reason, it was carried out more than 10 years ago, or if an emergency immunization was performed passive immunization with antitoxic serum, then the so-called "partial immunity" is formed in individuals, in which case the disease proceeds a little easier:

• the incubation periodis formed during 20 days;
• clinical triad( trismus, sardonic smile, dysphagia) is weakly expressed;
• Muscular tone increases within 6 days, while the ability to drink and eat is preserved;
• Seizures may be absent or occur only a few times a day;
• the temperature is normal or slightly raised;
• the duration of the disease is up to 2 weeks( while in non-vaccinated patients it reaches an average of a month, even if there is treatment);
• deaths are significantly less frequent.

With regard to postinfection immunity( i.e. those who have been ill), at the moment it is considered that it does not form and the risk of re-infection in case of survival remains also great. A patient with tetanus in the epidemic sense is not dangerous to others, ie is not contagious.

The disease is really terrible, I saw with my own eyes how people go through infernal torment, being in full consciousness. .. The treatment is practically meaningless, rarely anyone can survive, even despite modern technology and drugs.

Therapist doctor Shabanova I.Е.