Clostridium tetani
Organism
-
Clostridium
tetani is a moderately-sized gram-positive,
endospore-producing bacillus.
- Motile with a peritrichous (def)
arrangement of flagella.
- Produce round, terminal endospores
that give the bacterium a "tennis-racquet" appearance.
- An obligate anaerobe(def).
Habitat
- Colonizes the intestinal tract
in humans and animals.
Source
- Endospores
found in fertile soil or feces.
Epidemiology
- Endospores are found in most soils
and in the intestinal tract of many animals and humans.
- Although exposure to endospores
is commom, disease is uncommon except in countries with poor medical care
and vaccination compliance.
- Fewer than 50 cases per year in
the U.S.; most in elderly individuals with waning immunity.
- It is estimated that there is
more than one million cases a year worldwide, with a mortality rate of 20%
to 50%.
- Most deaths occur in neonates
and originates from infection of umbilical stumps in mothers that have no
immunity.
Clinical Disease
- Generalized tetanus is most common.
Typical presenting symptoms include lockjaw and sardonic smile, arrising as
a result of spastic paralysis (def)
of the masseter muscles (def)
and other facial muscles. Difficulty in swallowing, drooling, irritability,
and persistent back spasms are other early symptoms. When the autonomic nervous
system is involved, symptoms include perfuse sweating, hyperthermia (def),
cardiac arrhythmias (def),
and fluctuations in blood pressure.
- Cephalic infection primarily infects
the head and involves cranial nerves.
- Localized infection involves the
muscles in the area of primary injury.
- Neonatal tetanus is in newborns
and originates from infection of umbilical stumps in mothers that have no
immunity.
- The infection begins when endospores
of C. tetani enter an anaerobic wound (def).
Since the bacterium is an obligate anaerobe, an anaerobic environment is needed
for the endospores to germinate and the vegetative bacteria to grow. Vegetative
bacteria eventually produce tetanospasmin, the toxin responsible for symptoms
of tetanus.
Pathogenicity
- Produces an A-B (Type III) (def)
toxin called tetanospasmin. This is a neurotoxin that binds to inhibitory
interneurons of the spinal cord and blocks their release of inhibitor molecules.
It is these inhibitor molecules from the inhibitory interneurons that eventually
allow contracted muscles to relax by stopping excitatory neurons from releasing
the acetylcholine that is responsible for muscle contraction. The toxin, by
blocking the release of inhibitors, keeps the involved muscles in a state
of contraction and leads to spastic paralysis (def),
a condition where opposing flexor and extensor muscles simultaneously contract.
Death is usually from respiratory failure.
- Endospores enable the bacterium
to survive indefinitely in soils and other environments.
Treatment
- Treatment involves debridement,
the antibiotic metronidazole* (see antibiotic
table), active immunization (def)
with tetanus toxoid (def),
and passive immunization (def)
with tetanus immune globulin (def).
- Prevention is through active immunization
with tetanus toxoid**. The toxoid stimulates the body to make neutralizing
antibodies against the binding component of the tetanus toxin. Once the antibody
binds to the toxin, the toxin can no longer bind to the receptors on the host
cell membrane.
*Drugs may change with time.
** CDC
Recommendations for tetanus prophylaxis.
For a more detailed article on tetanus,
see Tetanus,
by Daniel J Dire, MD, FACEP, FAAEM, Associate Professor, Department of Emergency
Medicine, University of Alabama at Birmingham and Daniel J Dire, MD, FACEP,
FAAEM, is a member of the following medical societies: American Academy of Clinical
Toxicology, American Academy of Emergency Medicine, Association of Military
Surgeons of the US, and Society for Academic Emergency Medicine
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Updated: January 7, 2005
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