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What causes tetanus?
Last reviewed: 04.07.2025
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Causes of tetanus
The cause of tetanus is Clostridium tetani (genus Clostridium, family Basillaceae) - a large gram-positive rod, polytrich, has more than 20 flagella, obligate anaerobe. With access to oxygen, it forms spores. During its life, it produces three toxic substances, has flagellar (H-Ag) and somatic (O-Ag) antigens. According to the flagellar antigen, 10 serovars of the pathogen are distinguished. The pathogenicity of the pathogen and all clinical manifestations of the disease are associated with tetanospasmin - a polypeptide weighing 150 kDa, the strongest poison, second in toxicity only to botulinum toxin.
Tetanus bacillus spores are extremely resistant to physical and chemical factors. In dry form, they die at a temperature of 155 °C after 20 minutes, and in a 1% solution of mercury chloride they remain viable for 8-10 hours. The vegetative form of the pathogen is unstable in the environment.
[ Pathogenesis of tetanus
Entering the body through damage to the outer covering, the spores of the pathogen remain at the entry point. In the presence of anaerobic conditions (necrotic tissue, blood clots, ischemia, foreign bodies, oxygen-consuming flora) and the absence of a sufficient level of immune protection, the spores germinate into vegetative forms. After this, intensive production of tetanus exotoxin begins. The toxin spreads throughout the body by hematogenous, lymphogenous and perineural routes and is firmly fixed in the nervous tissue. It selectively blocks the inhibitory effect of interneurons on motor neurons, primarily in the motor cells of the anterior horns of the spinal cord. Impulses that spontaneously arise in motor neurons are freely conducted to the striated muscles, causing their tonic tension.
It should be noted that first of all, the contraction of striated muscles occurs, which, on the one hand, are closer to the site of injury, and on the other hand, act as relatively (per unit area) "the strongest" in the human body (chewing and facial muscles). In addition, the blockade of neurons of the reticular formation of the brain stem contributes to the inhibition of the parasympathetic nervous system, which leads to the activation of the sympathetic nervous system, and this, in turn, causes an increase in body temperature, arterial hypertension and severe sweating, up to the development of dehydration.
Constant muscle tension is combined with microcirculation disorders. A vicious circle arises: metabolic acidosis and microcirculation disorders lead to the development of convulsions, and the convulsive syndrome in turn aggravates metabolic acidosis and microcirculation disorders. If the patient does not die at the "peak" of a convulsive attack from respiratory or cardiac arrest, then with the further course of the disease, the causes of death may be the direct effect of the toxin on the respiratory and vasomotor centers in combination with deep metabolic disorders, as well as purulent-septic complications.
Epidemiology of tetanus
The source of the pathogen is many species of animals, especially ruminants, in whose digestive tract spores and vegetative forms of the pathogen are found. The pathogen can also be detected in the human intestine. When spores of the tetanus bacillus enter the soil with excrement, they remain there for years, and under favorable temperature conditions, the absence of oxygen or its consumption by aerobic flora, they germinate, which leads to the accumulation of spores. An increase in the soil population of the pathogen is especially characteristic of tropical countries. Thus, the soil serves as a natural reservoir of the pathogen.
Infection occurs when spores penetrate tissues from wounds, especially shrapnel, household, industrial; agricultural injuries, together with soil particles and foreign bodies. In peacetime, the most common cause of infection is minor leg injuries, and in developing countries, the umbilical wound in newborns. Tetanus may develop after burns, frostbite, extra-hospital abortions, operations, childbirth, various inflammatory processes, trophic ulcers, and decaying tumors. Wartime tetanus is associated with extensive wounds. Sometimes the entry point of infection cannot be determined ("cryptogenic tetanus").
Susceptibility to tetanus is high. In countries with a temperate climate, summer seasonality is observed (agricultural injuries).
Post-infection immunity is not developed.
The disease is registered in all regions of the globe. The annual incidence rate largely depends on the vaccination coverage of the population, as well as on emergency prevention, and reaches 10-50 cases per 100,000 population in developing countries. The bulk of those infected in developing countries are newborns and infants. Up to 400,000 newborns die annually. In developed countries, where mass vaccination began in the 1950s, the incidence rate is almost two orders of magnitude lower. Patients do not pose an epidemiological danger.
A higher incidence rate is observed in hot, humid climates, which is associated with slow wound healing, increased contamination of the soil with the pathogen, and the widespread custom in a number of countries of treating the umbilical wound with soil or animal excrement.