2. Introduction
• 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 due to an infection of anaerobic bacilli, Clostridium tetani.
• Tetanos – a Greek word – to stretch
• First described by Hippocrates & Sushruta
• It is caused by a powerful neurotoxin produced by the bacterium Clostridium
tetani and is completely preventable by vaccination. C. tetani is found throughout
the world, and tetanus commonly occurs where the vaccination coverage rate is low.
3. History
• Tetanus was first described in Egypt over 3000 years ago (Edwin smith papyrus).
• 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.
• Nocard demonstrated the protective effect of passively transferred antitoxin, and
passive immunization in humans
• Tetanus Toxoid was first widely used during World War II
4. Epidemiology
• Tetanus is important endemic infection in India
• Factors contributing for endemicity are:
• Unhygienic Hand washing
• Unhygienic delivery practices
• Traditional birth customs
• Less Interest of people towaerds immunization
• Prior to the National Immunization Programme an estimated 3.5 lac children die annually.
• 70,000 cases continue to occur largely in the BIMAROU states (Empowered Action Group States)
where TT Immunization coverage is less than national average (70%).
6. Epidemiology
• More common in areas where soil is cultivated, in rural areas, in warm
climates, during summer, among males.
• 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).
7. Epidemiology
• 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)
8. Host Factors
• Age : It 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.
9. Causative Organism
Acridine orange stain of
Clostridium tetani with
endospores wider than bacterial
body giving the characteristic
drumstick shape.
10. Clostridium tetani
• It’s a slender gram-positive, anaerobic bacilli 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 :
• Tetanolysin : its function of is not known with certainty.
• Tetanospasmin : is a neurotoxin and causes the clinical manifestations of tetanus.
• Tetanospasmin estimated Human lethal dose is 2.5ng/Kg Body Wt.
11. Clostridium tetani
Gram Stain of C.
tetani with
spores giving
Drumstick or
Tennis Racket
Appearance.
13. C. tetani Spores
• It’s 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 feces 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.
14. C. tetani Spores
C. tetani
Spores
magnified to
about 4000 times
their actual size
15. 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 lymphatic system.
• 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 :
• Peripheral motor end plates,
• Spinal cord,
• Brain,
• Sympathetic nervous system.
16. Pathogenesis
• How Tetanospasmin reaches 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.
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.
17. Pathogenesis
The typical clinical manifestations of
tetanus are caused when tetanus toxin
interferes with release of
neurotransmitters, blocking
inhibitory impulses. This leads to
unopposed muscle contraction and
spasm. Seizures may occur, and the
autonomic nervous system may also
be affected.
18. Pathogenesis
• The blocking of neurotransmitter release by Tetanospasmin involves cleavage of
Synaptobrevin – essential for proper functioning of synaptic vesicle release
apparatus
• With diminished inhibition – resting firing rate of alpha motor neurons increases –
causes Muscle Rigidity
• Lessened activity of reflexes which limit polysynaptic spread of impulses, causing
agonists & antagonists getting recruited – thereby causes Muscle spasms
• Loss of inhibition of preganglionic sympathetic neurons – causes Sympathetic
Hyperactivity
19. Why there is no Sensory Deficit?
• 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
Neurotransmitters can’t bind to control
pain.
20. Grand Synaptic Potential
• Each motor neuron is stimulated
by a large number of presynaptic
endings releasing either excitatory
or inhibitory chemical messages.
• If the SUM of the potentials of all
inhibitory and excitatory synapses
do not reach threshold an action
potential will not be triggered.
21. 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.
22. Analogy of Tetanospasmin
• 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.
23. Clinical Features
• The further the injury site is from the CNS, the longer the Incubation Period.
• The shorter the Incubation Period, the higher the chance of death.
• In Neonatal Tetanus, symptoms usually appear from 4 to 14 days after birth,
averaging about 7 days.
• On the basis of clinical features, 3 types of tetanus has been described,
• Local Tetanus
• Cephalic Tetanus
• Generalized Tetanus
24. Other Types of Tetanus
• Traumatic Tetanus
• Puerperal Tetanus
• Otogenic Tetanus
• Idiopathic Tetanus
• Tetanus Neonatarum
25. Local Tetanus
• 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.
26. Cephalic Tetanus
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.
27. 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
• Increased muscle tone & generalized spasms
• Median time of onset after injury – 7 days
• Patient first notices increased tone in masseter muscles causing Trismus, called as lock jaw
• Dysphagia
• Stiffness/pain in neck, shoulder, back muscles appear concurrently/or soon thereafter
• Rigid abdomen & stiff proximal limb muscles.
• Hands, feet spared.
28. Neonatal Tetanus
• Form of generalized tetanus that occurs in
newborn infants born without protective passive
immunity because the mother is not immune.
• Usually occurs through infection of the
unhealed umbilical stump, particularly when the
stump is cut with an unsterile instrument.
• During 1st 2 weeks of life.
• Usually fatal if untreated
• Poor feeding, rigidity and spasms usually occur.
29. Symptoms
• Tetanic seizures (painful, powerful bursts of muscle contraction)
• If the muscle spasms affect the larynx or chest wall, they may cause asphyxiation
• Stiffness of jaw (also called lockjaw)
• Stiffness of abdominal and back muscles
• Contraction of facial muscles
• Fast pulse
• Fever
• Sweating
30. Symptoms
• The contractions by the muscles of the back and extremities may become so
violent and strong that bone fractures may occur.
• The affected individual is conscious throughout the illness, but cannot stop these
contractions
• Some patients develop paroxysmal, violent, painful, generalized muscle spasms and
cyanosis. Spasms occur repetitively & may be spontaneous/provoked by slightest
stimulation.
• Constant threat during generalized spasm is reduced ventilation,
apnea/laryngospasm.
32. Signs
• Opisthotonus : Painful spasms
of neck, trunk and extremity
producing characteristic bowing
and arching of back
• The back muscles are more
powerful, thus creating the arc
backward
33. Signs
Lock Jaw : Increased tone in
masseter muscles causing Trismus,
and called as Lock Jaw.
34. Signs
• Neck Rigidity & Retraction :
Stiffness/pain in neck,
shoulder, back muscles
36. 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.
• As a result, diagnosis is made on the basis of clinical findings and history
37. Indirect Investigations
• Done Rarely.
• Wound cultures : In suspected cases, C. tetani can be isolated from wounds of
patients without tetanus & frequently cannot be isolated from wounds of those with
tetanus
• Electromyograms : Continuous discharge of motor units, shortening / absence of
silent interval seen after AP.
• Muscle enzymes : Raised
• Serum Anti toxin levels >= 0.1 IU/ml : Protective & makes tetanus unlikely .
38. Clinical Diagnosis
• Clinically it is confirmed by noticing the following features,
• Risus Sardonicus or fixed sneer.
• Lock jaw.
• Opisthotonus (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.)
• Neck rigidity
39. Bedside Diagnostic Tests
• Spatula Test :
• Apet and Kamad described 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 positive test.
• This test shows 94 % sensitivity and 100 % specificity.
• The altered whistle :
• This explained as an early effect of increased tone in facial muscles which causes the
classical Risus Sardonicus.
40. Grading and Prognosis
• Give One point for each of the following 7 items if present:
• Incubation Period < 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)
41. Grading and Prognosis
• Total score indicates the severity and the prognosis as follows,
SCORE GRADE PROGNOSIS (in terms
of MORTALITY)
0-1 MILD <10%
2-3 MODERATE 10-20%
4 SEVERE 20-40%
5-6 VERY SEVERE >50%
42. Albett Classification of Severity
• Grade I (mild):
• Mild to Moderate Trismus
• General Spasticity
• No Respiratory Problems
• No Spasms
• Little or No Dysphagia
43. Albett Classification of Severity
• Grade II (moderate):
• Moderate Trismus
• Well-marked Rigidity
• Mild to Moderate but short-lasting Spasms
• Moderate Respiratory Failure with Tachypnea of 30-35/min
• Mild Dysphagia
44. Albett Classification of Severity
• Grade III (severe):
• Severe Trismus
• Generalized Spasticity
• Spontaneous prolonged Spasms
• Respiratory failure with tachypnea >40/min and apneic spells
• Severe Dysphagia
• Tachycardia >120/min.
45. Albett Classification of Severity
• 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)
47. Treatment
• It includes,
• General Measures
• Wound Management
• Medical Management
• Control of Spasms
• Neutralizing remaining Toxin
• Elimination of Source of toxin (Elimination of C. tetani from body)
• Prevention of Tetanus
48. General Measures
• Goal is to eliminate the source of toxin, Neutralize the unbound toxin & prevent muscle spasm
& providing support especially respiratory support.
• Admit in a dark and quiet room in ICU.
• Continuous careful observation & cardiopulmonary monitoring.
• Minimize stimulation.
• Protect airway
• Explore wounds – debridement
• Seriously consider prophylactic intubation with succinylcholine in all patients with moderate-to-
severe clinical manifestations. Intubation and ventilation are required in 67% of patients.
49. Wound Management
• All wounds should be cleaned with Hydrogen Peroxide & Antiseptics.
• Necrotic tissue and foreign material should be removed.
• Wound is then lightly bandaged to prevent formation of local anaerobic
environment which is conducive for growth of C. tetani.
50. Control of Spasms
• Nurse in a quiet dark room
• Avoid noise & other stimuli
• IV Diazepam/Lorazepam/Midazolam – 1st Drug of Choice.
• Barbiturates & Chlorpromazine –2nd line drugs
• Continued spasms : Intubate & ventilate
• Propofol, Dantrolene, Intrathecal Baclofen, Succinylcholine & Magnesium
Sulfate can be tried.
51. Control of Spasms
• Sedative-hypnotic agents are the mainstays of tetanus spasms treatment.
• 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 Dose:
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 Dose:
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
52. Control of Spasms
• Phenobarbital: used to
• Prolong effects of diazepam
• Treat severe muscle spasms.
Adult Dose: 1 mg/kg IM q4-6h; not to exceed 400 mg/day
Pediatric Dose: 5 mg/kg/d IV/IM divided tid/qid.
53. Control of Spasms
• 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 Dose:
<55 years: 1000 mcg IT(intrathecal)
>55 years: 800 mcg IT
• Pediatric Dose:
<16 years: 500 mcg IT
>16 years: Administer as in adults
54. Neutralizing remaining Toxin
• Tetanus immune globulin (TIG) (passive immunization) :
• 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.
• 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.
55. Neutralizing remaining Toxin
• 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.
• So, Active immunization with tetanus toxoid should begin or continue as
soon as the person’s condition has stabilized.
56. Elimination of C. tetani
• Penicillin G:
• Adult Dose:
• 10-24 million U/d. ( IV/IM/6h)
• Pediatric Dose:
• 100,000-250,000 U/kg/d. (IV/IM/6h)
• 10 to 14 day course of treatment is recommended.
57. Elimination of C. tetani
• Metronidazole :
• Considered as a drug of choice by many as it 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 Dose:
• 500 mg orally/6h or 1 g IV /12h; not to exceed 4 g/d
• Pediatric Dose:
• 15-30 mg/kg/d IV divided /8-12h; not to exceed 2 g/d
• 10 to 14 day course of treatment is recommended.
58. Elimination of C. tetani
• Doxycycline:
• Used when there is contraindication to penicillin or metronidazol.
• Adult Dose:
• 100 mg orally/IV /12h
• Pediatric Dose:
• <8 years: Not recommended
<45 kg : 4.4 mg/kg/d) PO/IV divided bid
• > 45 kg: Administer as in adults
61. Prevention
• It includes,
• Active Immunization
• Passive Immunization
• Elimination of Spores
62. Active Immunization
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 —
• Adsorbed (aluminum salt precipitated) toxoid
• 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.
63. Active Immunization
Tetanus Toxoid:
• Tetanus Toxoid Adsorbed, 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.
• 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.
64. Active Immunization
Tetanus Toxoid:
• Immunization requires at least 3 doses of Td.
• 1st dose at First visit
• 2nd dose after 4-8 weeks
• 3rd dose after 6 months
• Booster dose throughout life every 10 years.
66. Passive Immunization
• ATS (equine) Immunoglobulin - 1500 IU/ Subcutaneously,
• After sensitivity test
• ATS (human)Immunoglobulin - 250-500 IU/ Subcutaneously,
• No anaphylactic shock, very safe
• Very Costly
67. Elimination of Spores
• 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 sporocidal.
68. 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.
69. References
• Centre For Disease Control, Atlanta, USA
• Management and Prevention of Tetanus, Richard F. Eldritch, MD PhD, Lisa Hill, Chandra A Mahler, Larry 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
• Current Medical Diagnosis & Treatment, 2011
• Harrison’s Principles of Medicine, 22nd Edition.
• Text of Emergency Medicine, S. David, 1st Edition
• Manson’s Tropical diseases 21st edition
• Txt book of preventive and social medicine 18th edition by K.PARK
• http://www.who.int/immunization_monitoring/diseases/Tetanus_map_cases.jpg
• Tetanus By J J Farrara b, L M Yenc, T Cookd, N Fairweathere, N Binhc, J Parrya b, C M Parrya b
