1. Tetanus is caused by Clostridium tetani, which produces a potent neurotoxin called tetanospasmin that prevents inhibitory neurotransmitters, causing uncontrolled muscle contractions. 2. The spores can remain dormant in soil until transforming in an oxygen-poor environment, where the bacterium produces tetanolysin and tetanospasmin toxins. Tetanospasmin is transported to motor neurons and prevents inhibition, leading to tetanic spasms. 3. Treatment involves airway management, preventing further toxin absorption with antitoxin immunoglobulin, and relieving symptoms like spasms with benzodiazepines and antibiotics. Immunization with tetan

1. Fahad basheer

2. Tetanus is caused by CLOSTIDIUM TENATI
The organism produce a potent
NEUROTOXIN Known as TENATOSPASMIN.
Clostridium tetani
• Gram positive motile bacillus
• Found in human and animal feces
• Found commonly in areas where
soil is cultivated, in warm
climates and during summer
months

3. PATHOGENESIS
The spores of
the organism
remain non
pathogenic in
soil or
contaminated
tissues until
conditions are
favorable for
transformation
into vegetative
form.
Transformation
occurs in the
presence of locally
decreased oxygen
reduction potential
Part 1
When transformed
it produces 2 types
of TOXINS
1.Tetanolysin
2.Tetanospasmin

4. PATHOGENESIS
Part 2
Tetanolysin
Tetanospasmin
Hemolytic toxin
Binds to NM junction at the site of injury and
undergoes retrograde axonal transport to
reach presynaptic nerve terminal where it
prevents the inhibitory neurotransmitters
GLYCINE AND GABA.
Potentiates infection but does not cause
disease process
In normal states these neurotransmitters
prevent release of Ach from excitatory neurons
thus prevent muscle contraction.in the
presence of toxins these inhibitory impulses are
prevented leading to uncontrolled contraction
of muscles,

5. CLINICAL FEATURES
TETANUS
GENERALIZED
TETANUS
NEONATAL
TETANUS
LOCALIZED
TETANUS

6. – GENERALIZED TETANUS Incubation period is 8 days (2-14 days),
Incubation period depends on site of injury from
CNS
Diseases occurs after an initial injury.
Faster the onset of symptoms poor the prognosis.
The nature of paralysis is in descending form :
JAW muscles – Spasm of masseter leading to
Trismus and LOCK JAW
NECK
BACK
ABDOMINAL MUSCLES
WHOLE BODY.
COMPLICATES TO DEATH

7. – GENERALIZED TETANUS SPECIAL FEATURES
 SENSORIUM IS PRESERVED.
 DIFFICULTY IN SWALLOWING
 AUTONOMIC DYSFUNCTIONS:
HYPERTENSION,HYPOTENSION,DIAPHORESIS AND
ARRYTHMIAS
RECOVERY
Recovery usually begins in 3 weeks and approximately takes 4
weeks
Recovery occurs by sprouting new nerve terminals in the
spinal cord and leading to relaxation of contracted muscles.

8. – neonatal TETANUS  Results from unhygienic birth practices most commonly when umbilical cord is
contaminated at the time of cutting after delivery.
 Symptoms usually appear by the 3RD DAY after birth.
 Initial SYMPTOMS: Excessive unexplained crying followed by refusal of
feeds and apathy
 The baby develops progressive feeding difficulty
(reflex spasm of massetter makes feeding painful)
(pharyngeal muscles goes into spasm and cause dysphagia chocking)
Spasm of larynx and respiratory muscles are induced by stimuli such as
touch ,noise ,bright light, resulting in episodes of apnea and cyanosis.
Constipation persists until spasms are relieved,
becomes rigid ,develops paralysis , and may develop opisthotonic
posturing(in extension) and experience painful spasm.
Intercurrent infections, dehydration and acidosis complicate the clinical
picture:

9. – localized TETANUS  PAIN CONFINED TO INJURED REGION CHARECTERIZED BY
RIGIDITY
 IT MAY LEAD TO GENERALIZED TETANUS LATER.
 CEPAHALIC TETANUS IS A FORM OF LOCAL TETANUS WHICH
OCCURS DUE TO INJURY OF BULBAR MUSCLES.

10. – TREATMENT AIMS OF TREATMENT
Airway maintenance
Prevention of further
toxin absorption
Relieving clinical
symptoms : spasms,
autonomic instability

11. Aim 1
AIRWAY MANAGEMENT
• Intubation and mechanical
ventilation
• In severe cases , if the infant gets
frequent episodes of laryngeal
spasms, apneic attacks with cyanosis
or central respiratory failure.

12. Aim 2
PREVENTION OF FURTHER TOXIN ABSORPTION
• Neutralization of free toxin is done by administrating human
tetanus immunoglobulin ;however the anti toxin cannot dislodge
toxins in the nerve root.
• The route of administration is intra muscular or intra thecal.
• Dose:500 – 1000 IU
• Supportive care: maintain adequate hydration, early detection of
myoglobinuria , prevention of renal shutdown.
• Oropharyngeal secretions should be sucked periodically.
• Maintenance of oxygen is essential
• Oral feeding should be stopped and IV line should be established
for providing adequate fluids , calories , electrolytes and for
administration of various drugs.
• After 3 – 4 days of treatment milk feeding through nasogastric tube
may be started.

13. Aim 3
RELEIVING CLINICAL SYMPTOMS
• Spasms are precipitated by minimal stimuli therefore efforts
should be made to avoid noxious stimuli including bright
lights, pain , loud noises.
• So ,Patient should be kept in dark quiet and isolated rooms.
• I.M injections should be avoided.
• Temperature should be maintained within normal limits.
• Relief of symptoms is by using benzodiapenes.
• DIAZEPAM prevents spasms by causing GABA mediated
central inhibition.it promotes muscle relaxation.
• Antibiotic therapy is needed to abolish bacteria bacteria
from wound site. Commonly used: crystalline penicillin or
metronidazole
• ANS Instability treated by: alpha and beta blockers,i.v
magnesium.

14. – prognosis  The prognosis in neonatal tetanus is worse if
1.onset of symptoms occurs within 1st week of life
2.interval between lockjaw on onset of spasms is
less than 48
hours
3.high fever and tachyardia are present
4.spasms, especially of larynx resulting in apnea and are very
severe and frequent.
 All patient should receive a complete course of immunization with
tetanus toxoid once recovered.

15. -Prevention-
Part 1
 Prevention is by tetanus immunization.
 Using 2 doses of TT to immunize pregnant woman or
woman of child bearing age is an important strategy to
reduce the incidence of the disease , because IgG Abs are
transferred across the placenta to fetus and protect the
newborn.
 The last dose of TT should be received at least 2 wks prior
to delivery.this cause passive immunization to child.
 Scince tetanus can occur at any age: primary immunization
is essential for which 3 doses of DPT are given 1month apart
 Boosters are given at 18 th month, 5,10 and 16 years of age,
 For previously un immunized school children: 2 Doses of TT
given 1 month are sufficient.
 For previously immunized pregnant woman: 1 Dose of TT is
sufficient if the 2 nd pregnancy within the next 5 years

16. -Prevention-
Part 2
TETANUS TOXIN
• TT is highly toxic so it is inactivated by formalin
to make TT and adsorbed on to aluminum salts
to enhance its immunogenicity.
• TT vaccine contains 5 liters of toxoid
• It is heat stable vaccine that remain potent for
few weeks even at 37 degree Celsius
• Tetanus is administered along with Diphtheria
toxoid and pertussis killed vaccine as
combination called DPT.

17. -Prevention-
Part 3
Past doses of
TT
Clean minor
wound
Clean minor
wound
All other
wound
All other
wound
UNKNOWN/
Less than 3
doses
TT
TIG*
TT
TIG*
Greater
than/equal to
3 doses
YES
NO
YES
YES
NO**
NO
NO***
NO
*
**
TETANUS IMMUNOGLOBULIN (250IU i/m)
YES,IF GREATER THAN 10 YEARS SCINCE LAST DOSE
*** YES,IF GREATER THAN 5 YEARS SCINCE LAST DOSE

18. -------------------------------------------Tetanus