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18. Tetanus. Etiology
Epidemiology. Pathogenesis. Pathomorphology
Tetanus is an acute toxemic disease caused by the action of an exotoxin (tetanospasmin) produced by the bacteria Clostridium tetani. The toxin is produced by vegetative forms of the microorganism at the site of its penetration into the tissues of the body, and then enters the central nervous system and is fixed there.
Etiology. The causative agent of tetanus is an obligate anaerobe, a thin Gram-positive mobile non-encapsulated rod that forms terminal spores, which give it a resemblance to a drumstick.
Vegetative C. tetani are sensitive to heat and disinfectants.
Tetanus bacilli are themselves harmless, their disease-causing effect is associated with two toxins they produce: tetanospasmin and tetanolysin.
Epidemiology. The sources of infection are animals and humans, in the intestines of which tetanus bacillus saprophytes, which enters the soil with the feces of animals and disperses in the environment.
Tetanus is a wound infection, the disease occurs when the pathogen enters the body through the wound surface. In newborns, the umbilical wound, infected in violation of the rules of asepsis and antisepsis, can serve as an entrance gate.
Pathogenesis. The disease develops after tetanus spores that have fallen into damaged tissues begin to germinate, multiply and produce tetanospasmin. Germination and reproduction of spores occurs at the site of the entrance gate of infection and only when the level of oxygen in the tissues decreases.
From the site of the entrance gate, the infection spreads throughout the body:
1) on the surrounding tissues;
2) through the lymphatic system;
3) along the nerve trunks.
Tetanospasmin acts on motor nerve endings at myoneural synapses, on the spinal cord and brain, and on the sympathetic nervous system. At neuromuscular synapses, the toxin inhibits the destruction of acetylcholine, causing disturbances in the processes of neuromuscular transmission. Disruption of inhibitory mechanisms in the spinal cord itself significantly weakens the inhibitory influence of the higher parts of the central nervous system. The toxin causes an increase in the activity of the sympathetic nervous system: tachycardia, unstable hypertension, arrhythmia, peripheral vascular spasms, profuse sweating, hypercarbia and an increase in the excretion of catecholamines in the urine.
Tetanospasmin, adsorbed in the tissues, binds strongly with them, and is not subsequently destroyed or neutralized by antitoxin. Tetanus antitoxin may prevent the binding of tetanospasmin to the CNS if the latter is located in the peripheral nerve trunks.
Pathomorphology. C. tetani infection remains localized and causes minimal inflammatory changes in damaged tissues. Local pathological changes are secondary.
Author: Pavlova N.V.
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