IT CONTAINS ALL THE RELEVANT INFORMATIONS REGARDING TETANUS.

1. TETANUS
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2. HISTORY
 During the same year, Nicolaier
produced tetanus in animals by
injecting them with samples of soil.
 In 1889, Kitasato isolated the
organism from a human victim,
showed that it produced disease
when injected into animals, and
reported that the toxin could be
neutralized by specific antibodies.
 In 1897, Nocard demonstrated the
protective effect of passively
transferred antitoxin, and passive
immunization in humans was used for
treatment and prophylaxis during
World War I.
 A method for inactivating tetanus
toxin with formaldehyde was
developed by Ramon in the early
1920's which led to the development
of tetanus toxoid by Descombey in
1924. It was first widely used during
World War II.
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3. What is Tetanus?
 An infectious disease caused by
contamination of wounds from the
bacteria Clostridium tetani, or the
spores they produce that live in the
soil, and animal feces.
 Greek words -“tetanosand teinein”,
meaning rigid and stretched, which
describe the condition of the
muscles affected by the toxin,
tetanospasmin, produced
by Clostridium tetani. 3

4.  The usual locations for the bacteria to enter the
body:
 Puncture wounds (such as those caused by rusty
nails, splinters, or insect bites.).
 Burns, any break in the skin, and IV drug access
sites are also potential entryways for the bacteria.

5. Route of Entry
i. Apparently trivial injuries.
ii. Animal bites/human bites.
iii. Open fractures.
iv. Burns.
v. Gangrene.
vi. In neonates usually via infected umbilical stumps.
vii. Abscess.
viii.Parenteral drug abuse.

6. Incubation Period
 Varies from 1 day to several months. It is
defined as the time from injury to the
first symptom.

7. Period of onset
 It is the time from first symptoms to the reflex
spasm.
 An incubation period of 4 days or less
or A period of onset of less than 48 hr is
associated with the development of severe
tetanus.

8. Clostridium Causing Tetanus
Cl. tetani
 Gram positive, straight, slender rod
with rounded ends.
 All species form endospore.
(drumstick with a large round end)
 Fermentative.
 Obligate anaerobe.
 Motile by peritrichous flagella.
 Grows well in cooked meat broth
and produces a thin spreading film
when grown on enriched blood agar.
 Spores are highly resistant to
adverse conditions.
 Iodine (1%) in water is able to kill
the spores within a few hours.
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9. Clostridium tetani — agent of tetanus
Morphology and Physiology-
• long thin gram-positive organism that stains gram negative in old cultures
• round terminal spore gives drumstick appearance
• motile by peritrichous flagella
• grow on blood agar or cooked meat medium with swarming
• beta-hemolysis exhibited by isolated colonies
• spores resist boiling for 20 minutes
Antigenic Structure-
flagella (H), somatic (0), and spore antigens. Single antigenic toxin characterizes all strains.
Pathogenicity Determinants"
• play a role in local infection only in conjunction with other bacteria that create suitable
environment for their invasion
• systemic-acting, plasmid-mediated A-B neurotoxin (tetanospasmin) produced intracellularly
 Mode of Action — one of most poisonous substances
• binds gangliosides in synaptic membranes (synapses of neuronal cells) and blocks
release of inhibitory neurotransmitters; continuous stimulation by excitatory transmitters
• muscle spasms (spastic paralysis) (trismus (lockjaw), risus sardonicus, opisthotonos),
cardiac arrhythmias, fluctuations in blood pressure
Lab Identification"
• use characteristics of resistance to heat, motility, and toxin production to help identify
Diagnosis/Treatment/Prevention
• empirical diagnosis on basis of clinical manifestations
• treat to prevent elaboration and absorption of toxin
 clean wound (debridement), control spasms
 metronidazole administered to eliminate vegetative bacteria that produce neurotoxin
 passive immunity (human tetanus immunoglobulin); vaccination (active) as preventative
 antitoxin administered to bind free tetanospasmin
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10.  Toxins
Cl. tetani produces two types of
toxins:
Tetanolysin, which causes lysis of RBCs.
Tetanospasmin , is neurotoxin and essential
pathogenic product. Heat-labile (65℃, 30min).
Tetanospasmin is toxic to humans and various
animals when injected parenterally, but it is not toxic
by the oral route.
Tetanospasmin which causes increasing excitability of
spinal cord neurons and muscle spasm.
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 Mechanisms of tetanospasmin
 toxin → peripheral nerve fibers / lymph
and blood → spinal cord and brain stem →
inhibitory interneuron → blocks the release of
neurotransmitters from the presynaptic
membrane of inhibitory interneurons→ inhibit
the motor neuron → spastic paralysis (rigid
paralysis).
excitatory transmitter: acetylcholine
inhibitory transmitter: glycine and γ–aminobutyric acid(GABA)

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 Mechanisms of tetanospasmin(Contd…)
spastic paralysis (rigid paralysis)NORMAL

13.  Mechanism of Action of Tetanus Toxin(Contd…)
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14. 1. C. tetani enters
body from through
wound.
3. Germinates under
anaerobic conditions and
begins to multiply and
produce tetnospasmin.
2. Stays in sporulated
form until anaerobic
conditions are presented.
4. Tetnospasmin spreads using
blood and lymphatic system,
and binds to motor neurons.
5. Travels along the axons
to the spinal cord.
6. Binds to sites responsible for
inhibiting skeletal muscle
contraction.
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15.  Laboratory Diagnosis of Tetanus
 The diagnosis of tetanus depends primarily upon the
clinical manifestation of tetanus including muscle
spasm and rigidity.
 Specimen: Wound exudates using capillary tube.
 Culture:
 On blood agar and incubated anaerobically.
 Growth appears as a fine spreading film.
 Gram stain is a good method for identifying
Clostridium
 Cl. tetani is Gram positive rod motile with a round
terminal spore giving a drumstick appearance
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16.  Clinical Forms of Tetanus
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17. 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.
 Muscle spasticity
 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.

18. Opisthotonos in Tetanus
Patient

19. Risus Sardonicus in Tetanus
Patient

20. TRISMUS(LOCK JAW)
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21.  Signs and Symptoms

22. TETANUS COMPLICATIONS
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23. Diagnosis
 There are currently no blood tests that can be used
to diagnose tetanus. Diagnosis is done clinically.
Differential Diagnosis
 Masseter muscle spasm due to dental abscess.
 Dystonic reaction to phenothiazine.
 Rabies.
 Hysteria.

24. Principle of Treatment
1. Neutralization of unbound toxin with Human tetanus immunoglobulin.
2. Prevention of further toxin production by
-Wound debridement.
-Antibiotics (Metronidazole).
3. Control of spasm
- Nursing in quiet environment
- avoid unnecessary stimuli
- Protecting the airway
4. Supportive care
- Adequate hydration
- Nutrition
- Treatment of secondary infection
- prevention of bed sores.

25. Prevention
 Tetanus is completely preventable
by active tetanus immunization.
 Immunization is thought to provide
protection for 10 years.
 Begins in infancy with the DPT
series of shots. The DPT vaccine is
a "3-in-1" vaccine that protects
against diphtheria, pertussis, and
tetanus.

26. Prevention(Contd…)
 Can be achieved by active immunization by tetanus
toxoid (5 doses – 0 day, 1 month, 6 month, 1 year, 1
year).
 Older teenagers and adults who have sustained
injuries, especially puncture-type wounds, should
receive booster immunization for tetanus if more than
10 years have passed since the last booster.
 Clinical tetanus does not produce immunity to further
attacks. Therefore, even after recovery patients must
receive a full course of tetanus toxoid.

27. TETANUS TOXOID
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28. Epidemiology
 Tetanus is an international health problem, as spores
are ubiquitous. The disease occurs almost exclusively
in persons who are unvaccinated or inadequately
immunized.
 Tetanus occurs worldwide but is more common in hot,
damp climates with soil rich in organic matter.
 More common in developing and under-developing
countries.
 More prevalent in industrial establishment, where
agriculture workers are employed.
 Tetanus neonatorum is common due to lack of MCH
care.

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