What is Tetanus?

Tetanus (lat. Tetanus) is a zoo-anthroponic bacterial acute infectious disease with a contact mechanism of transmission of the pathogen, characterized by lesions of the nervous system and manifested by the tonic stress of skeletal muscles and generalized convulsions.

Brief historical information

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

Causes of Tetanus

The causative agent is obligately anaerobic gram-positive spore-forming movable bacillus Clostridium tetani of the Bacillaceae family. The spores are located terminal, giving the bacteria the appearance of “drumsticks” or “tennis rackets”. C. tetani form a potent exotoxin (tetanospasmin), cytotoxin (tetanolysin) and the so-called low molecular weight fraction. In the soil, feces and on various objects disputes can persist for years. Maintain a temperature of 90 ° C for 2 hours. In 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. The vegetative forms of tetanus sticks die within a few minutes during boiling, after 30 minutes at 80 ° C. Antiseptics and disinfectants kill the causative agent of tetanus within 3-6 hours. In countries with a warm climate, spore vegetation is possible directly in the soil. In C. tetani, two types of antigens are detected: somatic (O-antigen) and flagellate (H-antigen). According to the structures of flagellated antigens, 10 serovars are isolated. All serovars form tetanospasmin and tetanolysin identical in antigenic properties.

  • Tetanospasmin is one of the most powerful biological poisons. It is a polypeptide with a “distanced” mechanism of action, since bacteria rarely leave the primary source of infection. The toxin is fixed on the surface of the processes of nerve cells, penetrates into them (due to endocytosis mediated by ligands) and via retrograde axonal transport enters the central nervous system. The mechanism of action is associated with the suppression of the release of inhibitory neurotransmitters (in particular, glycine and γ-aminobutyric acid) in synapses (the toxin binds to synaptic proteins synaptobrevin and celbyurvein). Initially, the toxin acts on peripheral nerves, causing local tetanic contractions of the muscles. In cultures, toxin appears on the 2nd day, reaching a peak of formation by the 5-7th day.
  • Tetanolizin exhibits hemolytic, cardiotoxic and lethal effects, causes the development of local necrotic lesions. In the pathogenesis of the disease, this toxin plays a less important role. The maximum accumulation of toxin in culture is observed already in 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 in the neuromuscular synapses.

The reservoir and source of infection – herbivores, rodents, birds and humans, in the intestines of which the pathogen lives; the latter is released into the external environment with faeces. The tetanus rod is also widely distributed in the soil and other environmental objects, where it can multiply and persist for a long time. Thus, the pathogen has two interconnected and mutually enriched habitats, and, consequently, two sources of the pathogen – the intestine of warm-blooded animals and the soil. The significance of one or another source seems to be largely due to the climatic and geographical conditions of the area. The most favorable for the growing season and the preservation of the microorganism are chernozem and red earth soils that are rich in humus, as well as soils that are well fertilized with organic matter. Bacteria from soil with dust can get into any premises (including dressing and surgical blocks), various objects and materials used in surgical practice (various powders, gypsum, talc, therapeutic clay and mud, cotton wool, etc.).

The carrier rate of tetanus wand spores varies from 5–7 to 40%, with a higher degree of carrier noted in persons who professionally or at home are in contact with the soil or animals (agricultural workers, grooms, milkmaids, cesspool cleaners, 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%. Sheep litter contamination reaches 25-40%, which has a special epidemiological significance in connection with the use of sheep’s small intestine for the manufacture of surgical catgut.

Transmission mechanism – pin; the pathogen penetrates through the damaged skin and mucous membranes (wounds, burns, frostbite). Infections of umbilical wounds with non-observance of asepsis at birth can cause tetanus in newborns. The location of the entrance gate of the pathogen can be open wounds of different nature and localization (punctures, splinters, cuts, chafing, crush injuries, open fractures, burns, frostbite, bites, necrosis, inflammatory processes); in these cases, post-traumatic tetanus develops. Surgical wounds, especially on the colon and ischemic limbs, can be the entry gate to infection with the subsequent development of postoperative tetanus. Abortion interventions outside of medical facilities can cause post-abortion tetanus. The possibility of transmission of the pathogen from a patient to a healthy person is missing.

The natural susceptibility of people is high. In tetanus patients, immunity to the disease is not formed, since a very small dose of toxin capable of causing the disease is insufficient to provide an immunological response.

Major epidemiological signs. The incidence of sporadic in the form of unrelated cases. Zonal distribution of infection is due to both climatic and geographical, and socio-economic factors. Seasonality of the disease spring-summer. The majority of cases are dominated by rural dwellers, children and the elderly; It is in these groups that most of the deaths are recorded. Due to the widespread active immunization, neonatal tetanus is currently not registered. The presence of a permanent reservoir of infection in the soil determines the possibility of infection due to minor household injuries. There are still cases of nosocomial infection with tetanus during operations on the limbs, gynecological operations and surgical interventions on the gastrointestinal tract.

Pathogenesis during Tetanus

The causative agent in the form of spores penetrates the human body through damaged skin and mucous membranes. Under anaerobic conditions (deep puncture wounds, wounds with deep pockets or necrotization of crushed tissues), development and reproduction of vegetative forms occur in wounds, accompanied by exotoxin release. Through the motor fibers of the peripheral nerves and with blood flow, tetanospasmin penetrates into the dorsal, medulla and reticular formation of the trunk, where it is fixed mainly in the intercalated neurons of the polysynaptic reflex arcs. Bound toxin can not be neutralized. Paralysis of intercalary neurons develops with the suppression of all types of their synaptic inhibitory effect on motor neurons. As a result, uncoordinated movement of motor impulses from motor neurons to muscles through neuromuscular synapses is enhanced. The capacity of the latter increases due to increased secretion of acetylcholine under the action of the low molecular weight fraction. The continuous flow of efferent impulses maintains a constant tonic tension of the skeletal muscles.

At the same time, afferent impulses are intensified in response to the impact of tactile, auditory, visual, olfactory, gustatory, temperature, and bar-reflectors. At the same time there are tetanic convulsions.

Muscle tension leads to the development of metabolic acidosis. Against this background, both tonic and tetanic convulsions intensify, cardiac activity worsens, and prerequisites for secondary bacterial complications are created. Cardiovascular disorders (tachycardia, arterial hypertension, arrhythmia, ventricular fibrillation) are aggravated by the sympathetic nervous system developing in tetanus hyperactivity. 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 with tetanus. Specific pathological changes are scarce (venous congestion, minor hemorrhages, in rare cases, muscle breaks and muscle hematomas).