TETANUS

TETANUS
 Tetanus
merupakan kondisi
medis yang ditandai
olrh perpanjangan
kontraksi serabut
otot skeletal.
Introduction

 Primary symptoms by-tetanospasmin, a

neurotoxin produced by the Gram-positive,
obligate anaerobic bacterium Clostridium
tetani.
 Infection generally occurs through wound
contamination, & often involves a cut or deep
puncture wound.
Introduction
 As the infection progresses, muscle spasms
in the jaw develops, hence the common
name, lockjaw.
 This is followed by difficulty swallowing &
general muscle stiffness & spasms in other
parts of the body.
 Infection can be prevented by proper
immunisation & by post-exposure
prophylaxis.
Epidemiology
 World wide
distribution- higher in
developing countries
due to warm climate,
unhygienic practices
& poor medical
services.
Clostridium tetani

 Cl.tetani is widely
distributed in soil &
in intestine of
human beings &
animals.
 They cause tetanus
in both man &
animal.
Morphology
 Gram-positive, 4-
8µm×0.5µm
bacillus.
 Has straight axis,
parallel sides &
rounded ends.
 Occurs singly &
occasionally in
chains.
Morphology
 It is capsulated & motile with peritrichate
flagella (except typeVI Cl. tetani-
nonflagellar strain).
 Young cultures are strongly Gram positive
but older cells show variable staining &
may be even Gram negative.
 Spore
 The spores are
spherical, terminal &
bulging, giving the
bacillus the
characteristic
‘drumstick’
appearance.
 Morphology depends
on stage of
development.
 Young spore may be
oval rather than
spherical.
Resistance
 Spore resistance to heat show strain
variation.
 Majority are killed by boiling for 15min.
 Some withstand boiling for 3hr & dry heat
at 160°C for 1hr.
 Spores can survive in soil for years & are
resistant to most antiseptics.
 Not destroyed by 5% phenol or 0.1% HgCl2
solution in 2 weeks or more.
Toxins
 All types produce same toxins which are
pharmacologically & antigenically
identical.
 Plasmid mediated.
 1.Tetanolysin
 2.Tetanospasmin
Tetanolysin
 Heat & O2 labile hemolysin.
 Cause red cell lysis.
 Pathogenic role not clear.
 May act as leucocidin.
Tetanospasmin
 O2 stable & heat labile neurotoxin.
 Good antigen & specifically neutralised
by antitoxin.
 Similar to botulinum toxin in str.
 Gets toxoided spontaneously or in
presence of formaldehyde.
Incubation Period
 Varies from 1 day to several months. It is
defined as the time from injury to the
first symptom.
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.
PATHOGENESIS
 1. C. tetani enters 2. Stays in sporulated
body from through form until anaerobic
conditions are
wound.
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

5. Travels along the
for inhibiting skeletal muscle
axons to the spinal cord. contraction.
Causes
 Tetanus spores are found throughout the
environment, usually in soil, dust, and animal waste.

 Tetanus is acquired through contact with the

environment; it is not transmitted from person to
person.
 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.
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
Signs and Symptoms
Other symptoms include:
 Drooling
 Excessive sweating
 Fever
 Hand or foot spasms
 Irritability
 Swallowing difficulty
 Uncontrolled urination or defecation
1. Local tetanus
 Persistent spasm of
musculature at site of
primary infection (injury
site).
 Contractions persist for
weeks before subsiding.
 Its generally milder, 1%
cases are fatal but may
precede the generalised
tetanus.
2.Cephalic tetanus
 Primary site of infection is head injury or
otitis media.
 Associated with disfunction of 1 or more
cranial nerves, most commonly facial
nerve.
 Poor prognosis.
3.Generalised tetanus
 Most common form(80% of
cases).
 Presents with a descending
pattern.
 1st sign is trismus(lockjaw) -
due to spasm of masseter
muscles.
 Followed by stiffness of the
neck, difficulty in
swallowing, rigidity of
abdominal muscles.
Risus sardoricus
 Characteristic sardonic
smile in tetanus
 Results from sustained
contraction of facial
muscles.
Opthisthotonus
 Back spasm seen in
tetanus
4.Tetanus neonatorum
 It is the generalised
tetanus that occurs
in newborn infants.
 Occurs in infants of
non-immunised
mothers.
Tetanus neonatorum
 Occurs from infection
of un-healed umbilical
stump particularly when
stump is cut with non-
sterile instrument.
 Very poor prognosis
Differential Diagnosis
 Masseter muscle spasm due to dental abscess
 Dystonic reaction to phenothiazine
 Rabies
 Hysteria
 Laboratory diagnosis
 Diagnosis made based on
clinical presentation.
 Specimen: Wound swab,
exudate or tissue from the
wound.
 1.Direct smear & gram
staining
 2.Culture
 3.Animal inoculation
Prophylaxis
 1.Surgical attention
 2.Antibiotics
 3.Immunisation-passive,active or combined.
 Surgical Prophylaxis
 Aims at
 removal of foreign bodies,
necrotic tissue & blood
clots,
 To prevent an anaerobic
envt favourable for the
Clostridium tetanae
Antibiotic prophylaxis
 Aims at destroying or inhibiting tetanus
bacilli & pyogenic bacteria in wounds so
that toxin production is prevented.
 Long-acting Penicillin is the drug if choice.
Erythromycin is an alternative.
 Bacitracin or neomycin can be applied
locally.
 Has no action on toxin.
Immunisation
 Combined immunisation:
Tetanus
immunoglobulin(TIG) &
tetanus toxoid are given on
different arms.
 Provides both passive &
long-lasting immunity.
Treatment
 Isolate pt. from noise &
light which may provoke
convulsions.
 Followed by supportive
care.
 TIG is infused.
 Antibacterial therapy
started.
Prevention & control
 By active immunisation with
tetanus toxoid.
1.TT-2 doses for pregnant
women,
2.DPT at 6, 10, 14 weeks after
birth,
3.DPT booster at 18 months
4.DT at 5yrs.
5.TT boosters at 10 & 16 yrs.
Thank You