Dr DHARMINDER
TETANUS
What is Tetanus?
Tetanus is an illness characterized by an acute onset
of hypertonia, painful muscular contractions (usually
of the muscles of the jaw and neck), and generalized
muscle spasms without other apparent medical
causes.
TETANUS
caused by
contamination of wounds from the
bacteria Clostridium tetani,
or the spores they produce that live in the soil,dust
and animal feces
is acquired through
contact with the environment
not transmitted from person to person.
TETANUS CAUSED BY…
Clostridium Tetani
Gram positive
Spore-forming
Anaerobic bacilli
Characterized by:
Muscular rigidity present throughout the illness
Paroxysmal spasm of voluntary musle.
1. Masseter (lock jaw or trismus )
2. Facial muscle (risus sardonicus)
3. Muscle of back and neck(opisthotonus)
4. Muscle of lower limb and abdomen
Mortality is very high(40-80%)
TYPES OF TETANUS
Traumatic
Puerperal
Otogenic
Idiopathic - microtrauma, absorption of tetanus toxin from intestine,
inhalation of tetanus spores.
Tetanus neonaturum
Tetanus clinical features
Incubation period 8 days (range, 3-21 days)
Three clinical forms:
Local (uncommon),
cephalic (rare),
generalized (most common) ,
neonatal
Nerves with short axons are affected initially, so symptoms appear first in
the facial muscles, with descending progression to the muscles of the neck,
trunk, and extremities
Generalized tetanus: descending symptoms of trismus (lockjaw), risus
sardonicus (sardonic smile) difficulty swallowing, muscle rigidity, spasms
Spasms continue for 3-4 weeks; complete recovery may take months
CLINICAL FEATURES
Risus sardonicus: Contraction of the muscles at the angle of mouth and frontalis
Trismus (Lock Jaw): Spasm of Masseter muscles.
Opisthotonus: Spasm of extensor of the neck, back and legs to form a backward
curvature.
Prolonged muscular action causes sudden, powerful, and painful contractions of
muscle groups. This is called tetany. These episodes can cause fractures and
muscle tears.
If respiratory muscle is involved – apnoea
MODE OF TRANSMISSION
The range of injuries and accident that lead to tetanus can be
Pin prick
Skin abrasion
Puncture wound
Burns
Human bite
Animal bite
Sting etc
ROUTE OF ENTRY
Apparently trivial injuries
Animal bites/human bites
Open fractures
Burns
Gangrene
In neonates usually via infected umbilical stumps
Abscess
Parenteral drug abuse
TETANUS PATHOGENESIS
Anaerobic conditions allow germination of spores
and production of toxins.
Toxin binds in central nervous system
Interferes with neurotransmitter release to block
inhibitor impulses.
Leads to unopposed muscle contraction and
spasm.
2. Stays in sporulated
1. C. tetani enters body form until anaerobic
from through wound. conditions are
presented.
3. Germinates under 4. Tetnospasmin spreads
using blood and lymphatic
anaerobic conditions and system, and binds to motor
begins to multiply and neurons.
produce tetnospasmin.
6. Binds to sites responsible for
5. Travels along the axons
inhibiting skeletal muscle
to the spinal cord. contraction.
•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.
Toxin and C.tetani
•Tetanospasmin ( exotoxin ) produced locally , released into
bloodstream .
•Binds to peripheral motor neuron terminals & nerve cells of
ant.horn of spinal cord
•The toxin after entering axon , transported to nerve cell body
in brain stem & spinal cord – retrograde intraneuronal transport
•Toxin – migrates across synapse – presynaptic terminals-
blocks the release of Glycine & GABA from vesicles.
How the toxin acts?
Blocks the release of inhibitory neurotransmitters
(glycine and gamma-amino butyric acid- GABA) across the
synaptic cleft, which is required to check the nervous impulse.
If nervous impulses cannot be checked by normal inhibitory
mechanisms, it leads to unopposed muscular contraction and
spasms that are characteristic of tetanus.
DIAGNOSIS
There are currently no blood tests that can be used to
diagnose tetanus. Diagnosis is done clinically.
Tetanus prone wounds
compound fractures
deep penetrating wounds
wounds containing foreign bodies (especially wood splinters)
wounds complicated by pyogenic infections
wounds with extensive tissue damage (eg. contusions or burns)
any wound obviously contaminated with soil, dust or horse manure
(especially if topical disinfection is delayed more than 4 hours).
Re-implantation of an avulsed tooth is also a tetanus-prone event
PREVENTION
Tetanus is completely preventable
by active tetanus immunization.
Immunization is thought to provide
protection for 10 years.
Begins in infancy with the DTP
series of shots. The DTP vaccine is
a "3-in-1" vaccine that protects
against diphtheria, pertussis, and
tetanus.
History of tetanus vaccination Type of wound Tetanus vaccine Tetanus
booster immunoglobulin
(see below)
3 or more doses < 5 years since last dose All wounds NO NO
5-10 years since last dose Clean minor wounds NO NO
All other wounds YES NO
> 10 years since last dose All wounds YES NO
< 3 doses or uncertain Clean minor wounds YES NO
All other wounds YES YES
