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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; ...