TETANUS

DR . Rabie Zahran.
Tropical M . Consultant.
Damietta Fever
Hospital.
Egypt.
[email protected] 1
 Titles.
1) Introduction.
2) Causative organism.
3) Epidemiology
4) Pathogenesis .
5) Clinical Features .
6) Complications .
7) Diagnosis .
8) Medical Management .
9) Wound Management.
10) Prevention ( Tetanus Toxoid ) .
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 Introduction.
Definition
Tetanus is an acute , often fatal disease caused
by an exotoxin produced by the bacterium
Clostridium tetani. But prevented by
immunization with tetanus toxoid.
It is characterized by generalized rigidity and
convulsive spasms of skeletal muscles . The
muscle stiffness usually involves the jaw
(lockjaw)and neck and then becomes
generalized. [email protected] 3
Introduction (con ). History:
• Tetanus was first described in Egypt over
3000 years ago(Edwin smith papyrus).
• It was again described by Hippocrates
•Carle and Rattone in 1884 who first noticed
tetanus in animals by injecting them with
pus from a fatal human tetanus case.
•During the same year , Nicolaier produced
tetanus in animals by injecting them with
samples of soil.
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Introduction(con). History:
•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.
•Nocard demonstrated the protective effect of
passively transferred antitoxin,and passive
immunization in humans
•Passive immunization and prophylaxis for tetanus
during World War I
•Tetanus Toxoid was first widely used during
world war II
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 Causative Organism
Clostridium tetani

Acridine orange stain of characteristic C tetani with

endospores wider than the characteristic drumstick shape.
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 Clostridium tetani
• C.tetani is :
* a slender gram-positive, anaerobic rod that may
develop a terminal spore giving it a drumstick
appearance.
* It is sensitive to heat and cannot survive in the
presence of oxygen.
• It produces two exotoxins :
1) tetanolysin . its function of is not known
with certainty.
2) tetanospasmin is a neurotoxin and causes
the clinical manifestations of tetanus.
Tetanospasmin estimated Human lethal dose is 2.5
ng/kg ((a nanogram is one billionth of a gram)
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Courtesy : Google Image on tetanus
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Spores:
*very resistant to heat and the usual antiseptics.
•They can not survive autoclaving at (121 °C)for 20
minutes.
• relatively resistant to phenol & other chemical
agents.
• widely distributed in soil and in the intestines
and faces of horses, sheep, cattle , dogs , cats , rats,
guinea pigs , and chickens.
Manure-treated soil may contain large numbers of
spores. Spores may persist for months to years.
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 Epidemiology:
a:Occurrence.
b:Reservoir .
c:Mode of Transmission
d:Communicability

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Source : CDC.,google pictures
 Epidemiology:
• Tetanus - Greek Word -- Tetanos -to Contract
• Tetanus Remains a Major Public Health
Problem in the Developing World and Is
Still Encountered in the Developed World.
• There Are about 800 000 : 1 Million Deaths
Due to Tetanus Each Year.80% of These
Deaths Occur in Africa and South East Asia
and It Remains Endemic in 90 Countries
World Wide.
• 1998 - U.K,USA 7 Cases, 41 Cases Including One Neonate

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 Epidemiology(con):
•Occurrence: Tetanus occurs worldwide but is most
frequently encountered in densely populated regions in hot ,
damp climates with soil rich in organic matter.
•Reservoir : Organisms are found primarily in the soil and
intestinal tracts of animals and humans.
•Mode of Transmission: is primarily by:
* contaminated wounds,
*Tissue injury( surgery , burns , deep puncture
wounds , crush wounds , Otitis media ,dental infection ,
animal bites, abortion , and pregnancy).
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Epidemiology (contu ):

•Communicability
Tetanus is not contagious from person
to person .It is the only vaccine-
preventable disease that is :
“infectious but not contagious”.
Temporal pattern : Peak in winter and
summer season.
Incubation Period: 8 DAYS ( 3-21 DAYS)
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Source : CDC.,google pictures
Host Factors :
• Age : I t is the disease of active age (5-40 years),
New born baby, female during delivery or abortion
• Sex : males > females
• Occupation : Agricultural workers are at higher
risk
• Rural > Urban areas .
• Immunity : Herd immunity(community immunity)
does not protect the individual.
• Environmental and social factors: Unhygienic
custom habits , Unhygienic delivery practices.
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Pathogenesis .

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 Pathogenesis
*C. tetani usually enters the body through a wound.
*In the presence of anaerobic conditions, the spores germinate and
start to produce toxin and disseminated via blood and lymphatics.
*Toxin reaches the CNS . by passing along the motor nerves to the
anterior horn cells of the spinal cord .
(The shortest peripheral nerves are the first to deliver the toxin to the CNS, which leads to
the early symptoms of facial distortion and back and neck stiffness.)
*Toxins act at several sites within the central nervous system,
including :
1)peripheral motor end plates,
2)spinal cord,
3) brain,
4)sympathetic nervous system.
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 How tetanospasmin
reaches the CNS .
• Tetanospasmin is taken
up by motor neurons in
the peripheral nerve
endings through
endocytosis. It then
travels along the axons
until it reaches the
motor neuron cell
bodies in the spinal
cord, by fast retrograde
transport.
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Speed of toxin transport:
The toxin travels via intra
axonal transport at a rate of
75 -250 mm/day .
A process which takes 2 -14
days to reach the CNS.
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Pathogenesis (con )

The typical clinical manifestations of

tetanus are caused when tetanus toxin
interferes with release of neurotrans-
mitters blocking inhibitory impulses.
This leads to unopposed muscle contra-
ction and spasm. Seizures may occur,
and the autonomic nervous system may
also be affected.
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Mechanism of Action of
Tetanus Toxin

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 Why there is no loss of sensory function ?
• No loss in sensory function
because it only affects
inhibitory pathways.
• However, the disease is
very painful because it
affects our natural way to
control pain. The natural
pain controlling mechanism
uses inhibitory pathways. ,
and if those inhibitory
receptors are blocked the
Neuro-T’s can’t bind to
control pain
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Grand Synaptic Potential
Each motor neuron
is stimulated by a
large number of
presynaptic endings
releasing either
excitatory or
inhibitory chemical
messages.

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 Grand Synaptic Potential
If the SUM of the
potentials of all
inhibitory and
excitatory synapses
do not reach
threshold an action
potential will not be
triggered.
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SO :
• When no inhibitory messages are being received
by the motor neuron, the excitatory potentials
add up to reach threshold and send action
potentials much more frequently.

• Our ability to move smoothly relies upon

inhibitory chemical messages as well as
excitatory ones. When one muscle contracts the
opposing muscle must relax to allow the
movement.
• When all excitatory neurons are firing and no
inhibitory neurons are counteracting them, all of
the muscles are contracted and movement
becomes jerky or impossible.
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 Analogy
• Think of the Inhibitory pathway as your
parents, and the Excitatory pathway as your
friends.
– If a group of your parents’ friends take them away
for a weekend out, the friends are like
tetanospasmin because they are removing your
inhibitory control.
– When your friends come over for the party you’re
throwing. your excitatory pathway is uncontrolled
because your inhibitory pathway has been
incapacitated.
– This results in muscle spasms, and potentially
death. [email protected] 26
Clinical Features

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Incubation period :
I P. ranges from 3 to 21 days, usually about 8
days. In general :
*The further the injury site is from the CNS, the
longer the I P.
*The shorter the I P, the higher the chance of
death.
* In neonatal tetanus, symptoms usually
appear from 4 to 14 days after birth, averaging
about 7 days.
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 Types of tetanus:
(On the basis of clinical findings, three different forms of
tetanus have been described).

1) Local tetanus is an uncommon form of

the disease,in which patients have
persistent contraction of muscles in the
same anatomic area of the injury.
Local tetanus may precede the onset of
generalized tetanus but is generally milder
.Only about 1%of cases are fatal.
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Source : CDC.
Types of tetanus(con)
2)Cephalic tetanus is a rare
form of the disease, occasionally
occurring with otitis media(ear
infections)in which C. tetani is
present in the flora of the middle
ear , or following injuries to the
head . There is involvement of
the cranial nerves, especially in
the facial area.

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Types of tetanus(contu)

3) generalized tetanus
It is The most common type (about
80%)of reported tetanus .The disease
usually presents with a descending
pattern.
Neonatal tetanus is a form of
generalized tetanus
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 Sequence of events
Lock Jaw

Stiff Neck

Difficulty Swallowing

Muscle Rigidity

Spasms
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 Risus Sardonicus in Tetanus Patient

A person suffering from tetanus undergoes convulsive muscle

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contractions of the jaw--called LOCKJAW
 Opisthotonos in Tetanus Patient

The contractions by the muscles of the back and extremities may become so
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violent and strong that bone fractures may occur
Opisthotonos in Tetanus Patient

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Oposotinus postion in tetanus
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Neck rigidity & retraction.
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 Unfortunately, the
affected individual is
conscious
throughout the
illness,
but cannot stop these
contractions
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Rusty nail may cause prick &
transmit tetanus
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 Traumatic T.

Puerperal T.

Type of Otogenic T.
Tetanus
Idiopathic T.

T. Neonatorum
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Complications .

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Diagnosis

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 Laboratory diagnosis
*There are no laboratory findings characteristic
of tetanus.
*The diagnosis is entirely clinical and does not
depend upon bacteriologic confirmation.
•C. tetani is recovered from the wound in only 30%
of cases and can be isolated from patients who do
not have tetanus.
•Laboratory identification of the organism depends
most importantly on the demonstration of toxin
production in mice.
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 Clinically it is confirmed by noticing the
following features:
1. Risus sardonicus or fixed sneer.
2. Lock jaw.
3. Opisthotonos (extension of lower
extremities, flexion of upper extremities
and arching of the back. The examiners
hand can be passed under the back of the
patient when he lies on the bed in supine
position.)
4. Neck rigidity
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 Diagnostic tests for tetanus:
Spatula Test :
Apet and Kamad discribe a simple bedside test to diagnose tetanus :
the posterior pharyngeal wall is touched with a
spatula and a reflex spasm of the masseters
indicates a +ve.test.
This test shows 94 % sensitivity . and 100 %
specificity.
The altered whistle :
This explained as an early effect of tone in facial
muscles which causes the classic R . sardonicus47
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scale for the severity and the prognosis of tetanus:
Score :
One point for each of the following 7 items:
•I P. < 7 days
(period between injury and 1st.symptom.)
•Period of onset < 48 hours
(period between 1st. Symptom and 1st. Spasm. )
•Acquired from burns, surgical wounds, compound
fractures, or septic abortion .
•Addiction (Narcotics)
•Generalized tetanus
•Temperature greater than 104°F (40°C)
•Tachycardia greater than 120 beats per minute (>150
beats per min in neonates)
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Total score indicates the severity
and the prognosis as follows:

Severity Prognosis
Score (mortality rate)

0 -1 mild < 10 %

2 -3 moderate 10 : 20 %

4 severe 20 : 40 %

5:6 very severe > 50 %

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 Grading of tetanus severity(OXFORD )
Ablett Classification
Grade I (mild):
* mild to moderate trismus;
* general spasticity;
* no respiratory problems;
* no spasms;
* little or no dysphagia.

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Ablett Classification

Grade II (moderate):
* moderate trismus;
* well-marked rigidity;
*mild to moderate but short-lasting spasms;
* moderate respiratory failure with
tachypnoea 30-35/min;
* mild dysphagia.

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Ablett Classification

Grade III (severe):

* severe trismus;
*generalized spasticity;
*reflex and often spontaneous prolonged spasms;
*respiratory failure with :
tachypnoea >40/min;
apnoeic spells;
*severe dysphagia;
* tachycardia >120/min.

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Ablett Classification

Grade IV (very severe):

features of grade III +
violent autonomic disturbances involving
the CVS. These include:
episodes of severe hypertension and
tachycardia alternating with relative hypotension and
bradycardia;
severe persistent hypertension(diastolic >110
mmHg);
severe persistent hypotension (systolic <90)
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Imbaba Fever hospital Cairo Egypt
Grading:
We adopted a modification of
Ablett classification which
we consider to be more useful
in the prognosis and
management :
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Grade 1 ( mild )
Muscle rigidity affecting one
or more group of muscles sparing the
muscles of deglutition.
Grade 2 (moderate )
Muscle rigidity affecting
muscles of deglutition.
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Grade 3a (severe ):
muscle rigidity and reflex spasms.
Grade 3b ( very sever ):
Grade 3a
+
autonomic nervous system changes.

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1) Medical Management .
2) Wound Management .

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 Medical Management
Aim of TTT:
(1) provide supportive care (until the tetano-
spasmin that is fixed in tissue has been metabolized )
by:
• a: treatment of muscle spasm,
• b: prevention of respiratory complications.
• c: prevention of metabolic complications.
(2)neutralization of circulating toxin to prevent
the continued spread.
(3) elimination of the source of toxin.
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 How to treat :
1: Admit patients with Grade III (severe):
to the (ICU). For risk of reflex spasms .
2: maintain a dark and quiet room for the
patient.
3: Avoid unnecessary procedures .
4: Seriously consider prophylactic intubation
with succinylcholine in all patients with moderate-
to-severe clinical manifestations. Intubation and
ventilation are required in 67% of patients .
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How to treat :
5:Perform tracheostomy in patients requiring
intubation for more than 10 days. Tracheostomy has
also been recommended after onset of the first
generalized seizure.
7:Tetanus immune globulin (TIG)(passive
immunization) is recommended for treatment
of tetanus. TIG can only help remove unbound tetanus
toxin, but it cannot affect toxin bound to nerve endings.
A single IM. dose of 3000-5000 units is generally
recommended for children and adults, with part of
the dose infiltrated around the wound if it can be
identified.
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Marx: Rosen's Emergency
Medicine, 7th ed.2009
*Dosage recommendations vary (500–10,000 units of
TIG), but multiple injections are stimuli for spasm and
most authorities note that 500 units is as effective as
higher doses.
* Adult and pediatric doses are the same. If the larger
doses are used, they should be given in divided doses.
*Protective antibody levels are achieved 48 to 72
hours after administration of TIG.
* Because the half-life of TIG is 25 days, repeated
doses are not needed.
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 How to treat :
Recovered individuals :
do not necessarily develop “natural
Immunity” against the infection---
because of extreme potency of the toxin and
very small amount produced during the
infection, It does not elicit a strong ,
protective immune response which would
produce enough antibodies against future
re-infection.
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 How to treat :
SO Active immunization
with tetanus toxoid should
begin or continue as soon as the
person’s condition has stabilized.

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Drugs:
1) Penicillin G:
Adult
10-24 million U/d. ( IV/IM/6h. )
Pediatric
100,000-250,000 U/kg/d. (IV/IM/6h. )
( 10- to 14-d course of treatment is recommended.)

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Drugs:
2) Metronidazole :
*considered as a drug of choice by many.
* has a better safety profile, better tissue penetrability and
negligible CNS excitability.
(penicillin can cause seizures at high doses).
It can also be given rectally
Adult
500 mg orally/6h or 1 g IV /12h;
not to exceed 4 g/d
Pediatric
15-30 mg/kg/d IV divided /8-12h;
not to exceed 2 g/d
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( 10- to 14-d course of treatment is recommended.) 65
 Drugs:
3)Doxycycline :
Used when there is contraindication to penicillin
or metronidazol.
Adult
100 mg orally/IV /12h
Pediatric
<8 years: Not recommended
<45 kg : 4.4 mg/kg/d) PO/IV divided bid
> 45 kg: Administer as in adults
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Drugs: Anticonvulsants:
Sedative-hypnotic agents are the mainstays of
tetanus treatment.
1) Diazepam (Valium):
Depresses all levels of CNS, including limbic and reticular
formation, possibly by increasing activity of GABA(γ-Amino-butyric
acid ), a major inhibitory neurotransmitter.
Adult
Mild spasms: 5-10 mg PO /4-6h
Moderate spasms: 5-10 mg IV(diluted in 8 ml glucose 5% or saline )
Severe spasms: Mix 50-100 mg in 500 mL D5W and infuse at 40 mg/h
Pediatric
Mild spasms: 0.1-0.8 mg/kg/d PO divided tid/qid
Moderate or severe spasms: 0.1-0.3 mg/kg IV q4-8h
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2) Phenobarbital:
used to * prolong effects of diazepam.
* treat severe muscle spasms.
Adult
1 mg/kg IM q4-6h;
not to exceed 400 mg/d
Pediatric
5 mg/kg/d IV/IM divided tid/qid

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 Skeletal muscle relaxants
These agents can inhibit both monosynaptic and
polysynaptic reflexes at spinal level, possibly by
hyperpolarization of afferent terminals.
* Baclofen (Lioresal) a physiological GABA
agonist
Adult
<55 years: 1000 mcg IT(intrathecal)
>55 years: 800 mcg IT
Pediatric
<16 years: 500 mcg IT
>16 years: Administer as [email protected]
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 Consultations
After admission to the ICU Consult :
1:An intensive care medicine specialist
should be the primary physician
coordinating the patient's care.
2: A pulmonary medicine specialist for
patients with severe respiratory symptoms
or those requiring mechanical ventilation.
3: An anesthesiologist after if intrathecal
baclofen is to be administered.
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 Differential Diagnoses
Other Problems to Be Considered
Mandible dislocations, Intraoral disease
Stroke , Odontogenic infections
Encephalitis
Subarachnoid Hemorrhage
Globus hystericus
Hypocalcemia Hepatic encephalopathy
Dystonic Reactions Hysteria
Meningitis Strychnine poisoning
Peri-tonsillar Abscess
Rabies

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Wound Management .

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 All wounds should be
cleaned with H2O2&antiseptic.
 Necrotic tissue and
foreign material should be
removed.
Passive immunization.
Active immunization. Or Both.
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PREVENTION

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 PREVENTION

How to kill spores :

Spores are extremely stable ,but killed by:
• Immersion in boiling water for 15
minutes.
• Autoclaving for 15-20 minutes at 121°c.
• Sterilization by dry heat for 1 -3 hrs at
160 °C.
• Ethylene oxide sterilization is sporocid.

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PREVENTION
Fumigation
• Sterilization of operation theatre by :
* 500 ml of formalin , 200gms of Pot-
permanganate/30 cu . meters of space
*All windows and doors are closed except one .
*Fissures between the panels of the doors and
windows are closed with adhesive tape
*After 12 hours the doors and windows are
opened and the theatre is aired for 24 hours
before decommissioning it.
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PREVENTION:

• Active Immunization
• Passive Immunization
• Active and passive Immunization.

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Active Immunization
by using
tetanus toxoid

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TETANUS TOXOID

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TETANUS TOXOID
• Tetanus toxoid was developed by Descombey in 1924,
• Tetanus toxoid immunizations were used extensively in
the armed services during World War II.
• Tetanus toxoid consists of a formaldehyde-treated
toxin.
• There are two types of toxoid available —
1)adsorbed (aluminum salt precipitated)toxoid
2) fluid toxoid.
• Although the rates of seroconversion are about
equal,the adsorbed toxoid is preferred because the
antitoxin response reaches higher titers and is longer
lasting than that following the fluid toxoid.
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Tetanus Toxoid Adsorbed USP,for intramuscular use,is a sterile
suspension of alum-precipitated (aluminum potassium sulfate)toxoid in
an isotonic sodium chloride solution containing sodium phosphate buffer
to control pH.The vaccine,after shaking,is a turbid liquid,whitish-gray
in color.
Clostridium tetani culture is grown in a peptone-based medium and
detoxified with formaldehyde.The detoxified material is then purified by
serial ammonium sulfate fractionation,followed by sterile filtration,and
the toxoid is adsorbed to aluminum potassium sulfate (alum).The
adsorbed toxoid is diluted with physiological saline solution (0.85%)and
thimerosal (a mercury derivative)is added to a final concentration of
1:10,000.
Each 0.5 mL dose is formulated to contain 5 Lf (flocculation units)of
tetanus toxoid and not more than 0.25 mg of aluminum.
The residual formaldehyde content,by assay,is less than 0.02%.The
tetanus toxoid induces at [email protected]
2 units of antitoxin per mL in the guinea
81
pig potency test.
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 Doses to complete the primary series .

Immunization requires at least 3

doses of Td.
4-8 weeks
1st dose (at First visit) 2nd dose.

6 months Every 10 years

3rd dose. booster
dose throughout [email protected] 84
Passive Immunization

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Passive Immunization

1. ATS(equine)I g. 1500 IU/s.c

after sensitivity test
(or)
2. ATS(human)I g. 250-500 IU,
no anaphylactic shock, very
safe and costly.
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Assess
Wound

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 Tetanus Wound Management
Clean, minor All other
wounds wounds

Vaccination History Td* TIG Td* TIG

Unknown or less than 3 Yes No Yes Yes

doses
3 or more doses No+ No No** No

* Tdap may be substituted for Td if the person has not

previously received Tdap and is 10 years or older
+ Yes, if more than 10 years since last dose
** Yes, if more than 5 [email protected]
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MNT elimination
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The Maternal and Neonatal Tetanus elimination
initiative was launched by UNICEF, WHO and
UNFPA(The United Nations Population Fund Agency) in 1999,
revitalizing the goal of MNT elimination as a
public health problem - defined as
“ less than one case of neonatal tetanus per
1000 live births in every district of every
country”.
*Target estimated 100 million women at risk.
* 20 million women deliver in high risk areas
every year.
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•Maternal tetanus:
• defined as tetanus occurring
during pregnancy or within 6 weeks
after any type of pregnancy
termination,
•It is one of the most easily
preventable causes of maternal
mortality. [email protected] 91
• Maternal tetanus includes:
(i) postpartum or puerperal tetanus, usually
resulting from septic procedures during delivery,
(ii) post-abortal tetanus, following septic
maneuvers during induced abortion
(iii) tetanus during pregnancy, generally
resulting from inoculation through a non-genital
portal of entry

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 •Neonatal tetanus (NNT)
•It is a major problem and a leading cause of neonatal
mortality.
•It is easily preventable by 2 tetanus toxoid injections
and complete aseptic deliveries.
• 2 major programs are in operation for the prevention of
NNT in the country –
•the immunization of pregnant women with tetanus
toxoid vaccine (TT) under the expanded program on
immunization (EPI)
•and the training of dais under the rural health program.
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Tetanus Neonatorum.
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 Newborn
showing risus
sardonicus and
generalized
spasticity

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•NNT will be prevented:
•If the women and the dais (who are still
associated with almost 70-75% of the deliveries in
many areas with high NNT mortality rates) are:
1)convinced of the need for tetanus T.
vaccination during the antenatal period.
2)practice the basic principles of cutting
cord and keeping the umbilical stump
free of unclean dressings.
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 PREVENTION OF NEONATAL TETANUS
• 2 doses of T.T to all pregnant women between 16
to 36 weeks of pregnancy with an interval of 1 to
2 months between the two doses.
• The first dose as early as possible & the second
dose a month later preferably 3 weeks before
delivery.
• If the pregnant woman is previously immunized,
a booster dose is sufficient.
• If the pregnant woman is not immunized, then
the new born should be protected against tetanus
by giving tetanus human immunoglobulin 750 IU
within 6 hours of birth.
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 REFERENCE
• http://www.medindia.net/health_statistics/diseases/tetanusTetanus
J J Farrara b, L M Yenc, T Cookd, N Fairweathere, N Binhc, J Parrya b, C M
Parrya b
• http://www.who.int/immunization_monitoring/diseases/Tetanus_m
ap_cases.jpg
• Txt book of preventive and social medicine 18 th edition by K.PARK
• Text book of community medicine by T. Bhaskar Rao
• Management and Prevention of Tetanus
• Richard F.Edlich,MD PhD,?Lisa G..Hill,?Chandra A..Mahler, 툺 ary Jude
Cox,MD,?Daniel G..Becker MD,?Jed H..Horowitz,MD 4 Larry S.Nichter MD
MS,4 Marcus L.Martin,MD 5 &William C.Lineweaver MD6
. www.rxlist.com/cgi/generic/tettoxpi.htm - 22k
. Manson’s Tropical diseases 21 st edition
• www.emedicine.com
• Imbaba hospital web site
• CDC. Web site

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THANK YOU

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