Transcript Tetanus Reşat ÖZARAS, MD., Prof.

Tetanus
Reşat ÖZARAS, MD., Prof.
Infectious Dept.
Definition
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Tetanus is a toxin-mediated
infectious disease characterized by
increased muscle tone and spasms
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It is caused by tetanospasmin, a powerful
protein toxin elaborated by Clostridium tetani.
Etiology-1
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C. tetani
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anaerobic, motile gram-positive rod
forms a terminal spore: resembles a tennis
racket.
The organism is found worldwide
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in soil in animal feces,
occasionally in human feces.
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Spores may survive for years in
environments and are resistant to boiling
for 20 min.
Vegetative cells, however, are easily
inactivated and are susceptible to several
antibiotics (metronidazole, penicillin, and
others).
Etiology
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Tetanospasmin is formed in vegetative bacteria
under plasmid control.
It has a heavy chain, which mediates binding to
nerve-cell receptors and entry into these cells,
and a light chain, which acts to block
neurotransmitter release.
Epidemiology
Tetanus occurs sporadically
and always affects nonimmunized persons
 Tetanus is entirely preventable by immunization
 In countries without a comprehensive
immunization program, tetanus occurs
predominantly
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in neonates and
young children; an estimated ~500.000 neonates died
of tetanus worldwide in 1993.
Wound classification
Clinical features Tetanus prone
Age of wound
>6 hours
Configuration
Stellate
Depth
>1 cm
Mechanism of injury Missile, crush
burn, frostbite
Devitalized tissue
Present
Contaminants
Present
Non-tetanus prone
6 hours
Linear
1 cm
Sharp surface
(glass, knife)
Absent
Absent
Pathogenesis-1
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The injury may be major but often is trivial and,
in some instances no injury can be identified.
Tetanus is also associated with burns, frostbite,
surgery, abortion, and drug abuse
In some patients no portal of entry for the
organism can be identified.
Pathogenesis-2
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Contamination of wounds with spores of C.
tetani.
Germination and toxin production take place
only in wounds with devitalized tissue
Toxin released in the wound binds to peripheral
motor neuron terminals, enters the axon, and is
transported to spinal cord by retrograde
intraneuronal transport.
Pathogenesis-3
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The toxin then migrates across the synapse to
presynaptic terminals, where it blocks release of
the inhibitory neurotransmitters glycine and
gamma-aminobutyric acid (GABA).
Clinical forms of tetanus
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1-Generalized tetanus
2-Neonatal tetanus
3-Local tetanus
4-Cephalic tetanus
Generalized tetanus
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The most common clinical form of the disease
Characterized by increased muscle tone and
generalized spasms.
The median time of onset after injury is 7 days;
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15 percent of cases occur within 3 days and
10 percent after 14 days.
Typically, the patient first notices increased
tone in the masseter muscles (trismus, or
lockjaw).
Generalized tetanus
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Dysphagia, stiffness or pain in the neck, shoulder, and
back muscles appears concurrently or soon thereafter.
The subsequent involvement of other muscles produces
a rigid abdomen and stiff proximal limb muscles
The hands and feet are relatively spared.
Sustained contraction of the facial muscles results in a
risus sardonicus
These spasms occur repetitively and may be
spontaneous or provoked by even the slightest
stimulation.
Contraction of the back muscles produces opisthotonos
Generalized tetanus
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A constant threat during generalized spasms is reduced
ventilation or apnea or laryngospasm.
The severity of illness may be mild (few or no spasms),
moderate (trismus and dysphagia), or severe (frequent
explosive paroxysms).
Patients have no fever
Mentation is unimpaired.
Deep tendon reflexes may be increased.
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Dysphagia or ileus may preclude oral feeding.
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Generalized tetanus
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Autonomic dysfunction commonly complicates severe
cases and is characterized by
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labile or sustained hypertension,
tachycardia,
arrhythmia,
hyperpyrexia,
profuse sweating,
peripheral vasoconstriction, and
increased plasma and urinary catecholamine levels.
Other complications include pneumonia, fractures,
muscle rupture, deep vein thrombophlebitis, pulmonary
emboli, decubitus ulcer, and rhabdomyolysis.
Neonatal tetanus
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It usually occurs as the generalized form
It is usually fatal if left untreated.
It develops in children born to inadequately
immunized mothers, frequently after unsterile
treatment of the umbilical cord stump.
Its onset generally comes during the first 2
weeks of life.
Poor feeding, rigidity, and spasms are typical
features of neonatal tetanus.
Local tetanus
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It is an uncommon form in which manifestations
are restricted to muscles near the wound.
The prognosis is excellent.
Cephalic tetanus
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A rare form of local tetanus, follows head injury
Trismus and dysfunction of one or more cranial
nerves, often the seventh nerve, are found
The incubation period is a few days and the
mortality is high.
Diagnosis
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The diagnosis of tetanus is based entirely on
clinical findings.
CSF fluid examination yields normal results
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Muscle enzyme levels may be raised.
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The differential diagnosis-1
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The differential diagnosis includes local
conditions also producing trismus, such as
1-Abscess,
2- strychnine poisoning,
3-dystonic drug reactions (such as
phenothiazines and metoclopramide),
4-tetany.
The differential diagnosis-2
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Other conditions sometimes confused with
tetanus include;
1-meningitis
2-rabies, and
3-an acute intraabdominal process
(because of the rigid abdomen).
The differential diagnosis-3
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Markedly increased tone in central muscles
(face, neck, chest, back, and abdomen) with
superimposed generalized spasms and relative
sparing of the hands and feet strongly suggests
tetanus.
Treatment; the goals of therapy
1-To eliminate the source of toxin,
2-Neutralize unbound toxin,
3-Prevent muscle spasms,
4-Provide supportespecially respiratory supportuntil
recovery.
5-Patients should be admitted to a quiet room in an
intensive care unit
6-Cardiopulmonary monitoring can be maintained
continuously
7-Stimulation can be minimized
8-Protection of the airway is vital.
9- Wounds should be cleansed, and thoroughly debrided.
Antibiotic therapy
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Penicillin; 12 million units iv/day-10 days
Metronidazole; 500 mgx4 or 1 gx2/day and the
absence of the GABA antagonistic activity seen
with penicillin.
Clindamycin is alternative for the treatment of
penicillin-allergic patients.
Antitoxin
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Human tetanus immune globulin (TIG);
~5000 U IM, usually in divided doses because
the volume is large.
The value of infiltrating the wound is unclear.
Antibody does not penetrate the blood-brain
barrier.
Control of muscle spasms
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Diazepam, a benzodiazepine and GABA agonist,
is in wide use.
Barbiturates and chlorpromazine are considered
second-line agents.
Mechanical ventilation and therapeutic paralysis
with a neuromuscular blocking agent may be
required for the treatment of spasms
unresponsive to medication or spasms that
threaten ventilation.
Prevention; immunization
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1-Passive immunization with TIG
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2-Active immunization with vaccine, preferably
Td in persons over age 7
Prevention; active immunization
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All partially immunized and unimmunized adults should
receive vaccine,
The primary series for adults consists of three doses:
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the first and second doses are given 4 to 8 weeks apart,
the third dose is given 6 to 12 months after the second.
A booster dose is required every 10 years
Combined tetanus and diphtheria toxoid (Td) adsorbed
(for adult use), rather than single-antigen tetanus toxoid,
is preferred for persons over 7 years of age.
For clean minor wounds
Td is administered to persons who have
1-unknown tetanus immunization histories
2-received fewer than three doses of adsorbed
tetanus toxoid
3-received three or more doses of adsorbed
vaccine, with the last dose given more than 10
years previously
4-Passive immunization with TIG is not recommended for
clean minor wounds
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Contaminated or severe wounds
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Vaccine should be given to those; if more than 5 years
have elapsed since the last dose.
It is given for all other wounds if the patient's
vaccination history indicates unknown or partial
immunization.
The dose of TIG for passive immunization is 250 U IM ,
which produces a protective antibody level in the serum
for at least 4 to 6 weeks
Vaccine and tetanus antitoxin should be administered at
separate sites in separate syringes.
Preventing neonatal tetanus
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1-Maternal vaccination even during pregnancy
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2-Efforts to increase the proportion of births
that take place in the hospital
Prognosis
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The application of methods to support respiration has
markedly improved the prognosis in tetanus; mortality
rates as low as 10 % have been reported
The outcome is poor;
1-in neonates and the elderly
2-in patients with a short incubation period,
3-a short interval from the onset of symptoms to
admission,
4-or a short period from onset of symptoms to the first
spasm (period of onset).