Tetanus
Brief history of disease
5th century BC: Hippocrates first described
the disease
1884: Carle and Rattone discovered the etiology
(cause/origin of disease)
p
Produced tetanus by injecting pus from a
fatal human case
p
Nicolaier was able to do the same by
injecting soil samples into animals
1889: Kitasato isolated the organism from
human victim, showed that it could produce disease when injected into animals.
Reported that toxin could be neutralized by specific antibodies.
1897: Nocard demonstrated the protective
effect of passively transferred antitoxin à
used in WWI
1924: Descombey developed tetanus toxoid for active
immunization à
used in WWII
Causative agent
Clostridium tetani
Morphology & Physiology
Relatively
large, Gram-positive, rod-shaped bacteria
Spore-forming, anaerobic.
Found in soil, especially
heavily-manured soils, and in the intestinal tracts and feces of various
animals.
Strictly fermentative mode of
metabolism.
Virulence & Pathogenicity
Not pathogenic to humans and
animals by invasive infection but by the production of a potent protein toxin
tetanus toxin or tetanospasmin
The second exotoxin produced is
tetanolysin—function not known.
Tetanus toxin
Produced when spores germinate
and vegetative cells grow after gaining access to wounds. The organism
multiplies locally and symptoms appear remote from the infection site.
One of the three most poisonous
substances known on a weight basis, the other two being the toxins of botulism
and diphtheria.
n
Tetanus toxin is produced in vitro in amounts
up to 5 to 10% of the bacterial weight.
n
Estimated lethal human dose of Tetanospamin =
2.5 nanograms/kg body
Because the toxin has a specific affinity for
nervous tissue, it is referred to as a neurotoxin. The toxin has no known
useful function to C. tetani.
Initially binds to peripheral nerve terminals
Transported within the axon and across
synaptic junctions until it reaches the central nervous system.
Becomes rapidly fixed to gangliosides at the
presynaptic inhibitory motor nerve endings, then taken up into the axon by
endocytosis.
Methods of
transmission
C. tetani can live for
years as spores in animal feces and soil. As soon as it enters the human body
through a major or minor wound and the conditions are anaerobic, the spores
germinate and release the toxins.
Tetanus may follow burns, deep
puncture wounds, ear or dental infections, animal bites, abortion.
Only the growing bacteria can
produce the toxin.
It is the only vaccine-preventable
disease that is infectious but not contagious from person to person.
Symptoms
Tetanic
seizures (painful, powerful bursts of muscle contraction)
if
the muscle spasms affect the larynx or chest wall, they may cause asphyxiation
stiffness
of jaw (also called lockjaw)
stiffness
of abdominal and back muscles
contraction
of facial muscles
fast
pulse
fever
sweating
Types of tetanus:
local, cephalic, generalized, neonatal
Incubation
period: 3-21 days, average 8 days.
Uncommon types:
Local
tetanus: persistent muscle contractions in the same anatomic area as the
injury, which will however subside after many weeks; very rarely fatal; milder
than generalized tetanus, although it could precede it.
Cephalic
tetanus: occurs with ear infections or following injuries of the head;
facial muscles contractions.
Most
common types:
Generalized tetanus
-
descending pattern: lockjaw à stiffness of neck à difficulty swallowing à rigidity of abdominal
and back muscles.
-
Spasms continue for 3-4 weeks, and recovery can
last for months
-
Death occurs when spasms interfere with
respiration.
Neonatal tetanus:
-
Form of generalized tetanus that occurs in
newborn infants born without protective passive immunity because the mother is
not immune.
-
Usually occurs through infection of the unhealed
umbilical stump, particularly when the stump is cut with an unsterile
instrument.
Methods
of diagnosis
Based
on the patient’s account and physical findings that are characteristic of the
disease.
Diagnostic
studies generally are of little value, as cultures of the wound site are
negative for C. tetani two-thirds of the time.
n When
the culture is positive, it confirms the diagnosis of tetanus
Tests
that may be performed include the following:
n Culture
of the wound site (may be negative even if tetanus is present)
n Tetanus
antibody test
n Other
tests may be used to rule out meningitis, rabies, strychnine poisoning, or
other diseases with similar symptoms.
Clinical
treatment
If
treatment is not sought early, the disease is often fatal.
The
bacteria are killed with antibiotics, such as penicillin or
tetracycline; further toxin production is thus prevented.
The
toxin is neutralized with shots of tetanus immune globulin, TIG.
Other
drugs may be given to provide sedation, relax the muscles and relieve pain.
Due
to the extreme potency of the toxin, immunity does not result after the disease.
Method
of prevention - immunization
A
person recovering from tetanus should begin active immunization with tetanus
toxoid (Td) during convalescence.
The
tetanus toxoid is a formalin-inactivated toxin, with an efficiency of approx.
100%.
The
DTaP vaccine includes tetanus, diphteria and pertussis toxoids; it is routinely
given in the US during childhood. After 7 years of age, only Td needs to be
administered.
Because
the antitoxin levels decrease over time, booster immunization shots are needed
every 10 years.
What else can be
done?
Remove
and destroy the source of the toxin through surgical exploration and cleaning
of the wound (debridement).
Bedrest
with a nonstimulating environment (dim light, reduced noise, and stable
temperature) may be recommended.
Sedation
may be necessary to keep the affected person calm.
Respiratory
support with oxygen, endotracheal tube, and mechanical ventilation may be
necessary.
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