Tetanus

TETANUS
Natia Shavgulidze , infectious disease specialist, M.D

N.Kipshidze Central University Clinic of Tbilisi State Medical Univeristy
Kutaisi State University After Ak. Tsereteli , medical faculty
 Tetanus is a neurologic disorder, characterized by increased muscle tone and
spasms, that is caused by tetanospasmin, a powerful protein toxin elaborated by
Clostridium tetani.
Tetanus occurs in several clinical forms, including generalized, neonatal, and
localized disease.
 Clostridium tetani is a slender gram-
positive rod with a terminal spore. It is an
obligate anaerobe, which is a commensal
of the human and animal gastrointestinal
tract and is widely distributed in the
environment, especially in manured soil.
 Spores are extremely resistant to heat and
light; autoclaving at 120°C (248°F), 1.5
bar for 15 minutes ensures sterility.
 Clinical disease follows inoculation of
spores into wounds and most cases occur
after an acute injury and injecting drug
use.
 The incubation period is typically
between 3 and 21 days, although it can
range from 1 day (cephalic tetanus) to
several months
 When spores of Clostridium tetani are inoculated into a wound, they can
germinate under anaerobic conditions into rod-shaped bacteria, which produce
tetanospasmin.
 This single-polypeptide toxin undergoes post-translational cleavage into heavy
and light chain fragments. The heavy chain attaches to gangliosides on peripheral
nerves.
 Toxin enters the presynaptic terminal and travels from the peripheral nerve
terminals to the central nervous system by retrograde axonal transport and trans-
synaptic spread.
 Free toxin can also enter the bloodstream and lymphatics, disseminating widely to
motor neurons at disparate sites. The light chain is a zinc metalloprotease that
cleaves synaptobrevin on the membrane of synaptic vesicles
 Synaptobrevin is required for the fusion of synaptic vesicles with the
presynaptic membrane. Cleavage of synaptobrevin prevents the synaptic
vesicles from releasing the inhibitory neurotransmitter gamma-
aminobutyric acid (GABA) into the synaptic cleft.
 Alpha-motor neurons therefore undergo uninhibited excitatory discharge
resulting in muscle spasms. Disinhibition of autonomic neurons causes
autonomic instability. Uncontrolled catecholamine release creates a hyper-
sympathetic state with sweating, tachycardia, and hypertension.
 Tetanospasmin-induced effects on the spinal cord, brain stem, and
peripheral and autonomic nerves are long-lasting; growth of new axonal
nerve terminals is necessary for recovery, which may take 4 to 6 weeks.
CLINICAL MANIFESTATION
 The most common clinical form,
frequently presenting with trismus
('lock jaw') due to spasm of the
masseter muscle.
 Repeated painful spasms occur
affecting any part of the body.
 Irritability, dysphagia, opisthotonus,
and seizures can be seen, as well as
respiratory failure due to vice-like
contraction of the intercostal muscles
or involvement of the glottis or
diaphragm.
 Severe autonomic dysfunction may
arise after several days.
CLASSIFICATION
Generalised tetanus can be further classified according to severity. The grading system
described by Ablett is the most widely used:
• Grade 1 (mild): mild/moderate trismus and general spasticity, little or no dysphagia, no

respiratory embarrassment, no spasms.
• Grade 2 (moderate): moderate trismus and generalised spasticity, plus mild dysphagia and
fleeting spasms. Moderate respiratory embarrassment may occur.
• Grade 3a (severe): severe trismus and generalised spasticity. Severe dysphagia and
respiratory difficulties. Severe and prolonged spasms (both spontaneous and on stimulation).
 Grade 3b (very severe): as for grade 3a plus marked autonomic dysfunction.
OPISTOTONUS
 Opisthotonus is defined as a dramatic
abnormal posture due to spastic
contraction of the extensor muscles
of the neck, trunk, and lower
extremities that produces a severe
backward arching from neck to
heel. In most cases, the trunk is
elevated off the ground by a few
inches.
 Autonomic dysfunction commonly complicates severe cases and is
characterized by labile or sustained hypertension, tachycardia,
dysrhythmia, hyperpyrexia, profuse sweating, peripheral vasoconstriction,
and increased plasma and urinary catecholamine levels.
 Periods of bradycardia and hypotension may also be documented.
 Sudden cardiac arrest sometimes occurs, but its basis is unknown.
 Other complications include aspiration pneumonia, fractures, muscle
rupture, deep-vein thrombophlebitis, pulmonary emboli, decubitus ulcer,
and rhabdomyolysis
 Neonatal tetanus usually occurs as the generalized form and 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.
 Local tetanus is an uncommon form in which manifestations are restricted
to muscles near the wound. The prognosis is excellent. Cephalic tetanus, a
rare form of local tetanus, follows head injury or ear infection and involves
one or more facial cranial nerves. The incubation period is a few days and
mortality is high.
DIAGNOSIS
 The diagnosis of tetanus is based entirely on clinical findings.
 Tetanus is unlikely if a reliable history indicates the completion of a
primary vaccination series and the receipt of appropriate booster doses.
 Wounds should be cultured in suspected cases.
DIFFERENTIAL DIAGNOSIS
 The differential diagnosis includes conditions also producing trismus, such

as alveolar abscess, strychnine poisoning, dystonic drug reactions and
hypocalcemic tetany.
 Meningitis/encephalitis, rabies
 An acute intraabdominal process (because of the rigid abdomen)

TREATMENT
1 st line
 Wound debridement : Prevention of tetanus is always preferable to management of the
clinical syndrome.
 Wounds or burns that are considered to be tetanus prone and high risk include the
following: requiring surgical management but delay in intervention of over 6 hours;
puncture-type injury or a significant degree of devitalized tissue (especially in contact
with soil or manure); foreign body-containing wounds; compound fractures;
concomitant systemic sepsis.
 All wounds should be thoroughly cleaned and debrided.
 Wound debridement removes spores and necrotic tissue, eradicating the anaerobic
conditions that facilitate clostridial growth. Antibiotic penetration into devitalised
tissue is likely to be poor, emphasising the importance of adequate wound debridement
+
PLUS – IMMUNISATION
The management of tetanus-prone wounds should take into account the patient's
immunisation status. Immunosuppressed patients may not be adequately protected and
additional boosting and/or immunoglobulin may be required :
 Patients with tetanus-prone wounds require an immediate reinforcing dose of vaccine
in the following scenarios: received adequate priming course of tetanus vaccine (at
least 3 doses at appropriate intervals) but last dose was more than 10 years ago, or
aged 5 to 10 years old and received an adequate priming course but no preschool
booster, or not received adequate priming course, or immunisation status is
uncertain.
 One dose of human tetanus immunoglobulin (TIG) is recommended in the
following:patients with tetanus-prone wounds who have not received adequate
priming course or immunisation status is uncertain; patients with high-risk tetanus-
prone wounds who have received adequate priming course of tetanus vaccine (at
least 3 doses at appropriate intervals) but last dose was more than 10 years ago, or
aged 5 to 10 years old and received an adequate priming course but no preschool
booster
HOW IT WORKS ?
 TIG neutralises toxin, reducing the duration and severity of tetanus. Toxin
binds irreversibly to tissues; therefore, only circulating and unbound toxin
can be neutralised.
 Tetanus antitoxin (equine) is more widely available in the developing world
(it may not be available or may be difficult to access in some countries), but
has a higher incidence of anaphylaxis (20% of cases)
ANTIMICROBIAL THERAPY
 ANTIBIOTIC THERAPY : is administered to eradicate vegetative cells—
the source of toxin. Penicillin (10–12 million units IV, given daily for 10
days) has been recommended, but metronidazole (500 mg every 6 h or 1 g
every 12 h) is preferred by some experts on the basis of this drug’s excellent
antimicrobial activity
SUPPORTIVE CARE
 RESPIRATORY CARE Intubation or tracheostomy, with or without
mechanical ventilation,may be required for hypoventilation due to
oversedation or laryngospasm or for the avoidance of aspiration by patients
with trismus, disordered swallowing, or dysphagia. The need for these
procedures should be anticipated, and they should be undertaken
electively and early.
PREVENTION
Vaccination according to the each country vaccination calendar
• Primary immunisation in infants and children aged <10 years: DTaP (D=diphtheria, T=tetanus,
) given in combination with inactivated polio vaccine
aP=acellular pertussis
(IPV)/Haemophilus influenzae type b (Hib)/hepatitis B at ages 2, 3, and 4 months.
• Primary immunisation in children aged >10 years and adults: 3 doses of Td (T=tetanus,
d=low-dose diphtheria ) given in combination with IPV, with an interval of 1 month between
each dose.
• First booster in children aged <10 years: DTaP (given in combination with IPV) ideally given at
least 3 years after completion of the primary immunisation course.
• First booster in people aged >10 years: Td (given in combination with IPV) for
those who have undergone primary immunisation, with the last dose 5 years or
more ago.
• Second booster, all patients: Td (given in combination with IPV), ideally given 10
years after the first booster.

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TETANUS

Natia Shavgulidze , infectious disease specialist, M.D

• Grade 1 (mild): mild/moderate trismus and general spasticity, little or no dysphagia, no

 The differential diagnosis includes conditions also producing trismus, such

 An acute intraabdominal process (because of the rigid abdomen)

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