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Tetanus is an acute illness caused by an exotoxin produced by the vegetative form of Clostridium tetani. The tetanus bacillus is an anaerobic, gram-positive, spore-forming organism. It is widely distributed in the soil in most parts of the world. Clostridium tetani is normally present in the intestines of horses, cattle, and other herbivora, and is found in 2% to 30% of normal human fecal flora. The highest number of colonized persons occurs in agricultural communities. The tetanus organism is a wound contaminant and does not cause tissue destruction or inflammation.

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Epidemiology and Pathophysiology

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Tetanus in children is rare in the United States, with fewer than 20% of cases in persons less than 20 years of age. Although it has been largely eliminated from the United States, neonatal tetanus causes more than 400,000 deaths annually worldwide because of the practice of applying animal excreta to the umbilical stump for hemostasis. Neonatal tetanus is the cause of 23% to 73% of neonatal deaths and 25% to 30% of deaths in the first year of life in developing countries. The increasing use of prophylaxis in the care of wounds of all kinds, and the widespread use of active immunization have greatly reduced the incidence in older children.

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Contamination of wounds by spores of the tetanus bacillus occurs without clinical signs of infection. Anaerobic conditions in the wound allow conversion of spores to the vegetative form and the subsequent production of a plasmid-encoded exotoxin, tetanospasmin, that acts at the myoneural junction of skeletal muscles and on neuronal membranes in the spinal cord, to block inhibitory pulses to motor neurons, producing spasms of muscles. This requires a low oxidation-reduction potential, which is achieved in deep puncture wounds, crushing injuries, and burns. Contamination with dirt, soil, or manure provides a heavy inoculum of organisms; however, C tetani spores are ubiquitous, and any wound has the potential to become contaminated.

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Although some toxin diffuses into the surrounding muscles, most toxin is distributed hematogenously to neural tissues. Some evidence suggests that tetanus toxin also travels along axis cylinders to reach the spinal cord and medulla. The exotoxin tetanospasmin consists of binding and toxin components. Tetanospasmin binding occurs to gangliosides at the myoneural junction and toxin interferes with neuromuscular transmission by inhibition of acetylcholine release. The toxin’s action in the central nervous system lowers the threshold of reflexes in which the lower motor neurons are involved, and induces susceptibility to reflex spasms and convulsions. The toxin combines with high affinity to neural tissue and binding is essentially irreversible by antitoxin. Thus, only toxin circulating in the blood can be neutralized by antitoxin. Tetanospasmin also affects the sympathetic nervous system, resulting in labile hypertension, tachycardia, profuse sweating, and increased urinary excretion of catecholamines.

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Clinical Manifestations

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Two clinical forms of tetanus are observed: generalized and local. The generalized form is the result of widespread distribution of toxin; ...

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