TETANUS

Dr. A.M IYAGBA,

Medicine Department,
Faculty of Clinical Sciences,
College of Health Sciences,
University of Port Harcourt
 Lecture outline
• Introduction • Differential diagnosis
• Definition • Investigations
• Epidemiology • Treatment
• Microbiology • Complications
• Portal of infection • Prognosis
• Clinical features • Prevention
• Clinical syndromes
 Historical perspective
“Tetanus is ……..characterized by persistent
tonic spasm with violent brief exacerbation.
The spasms almost commences in the muscles
of the neck and jaw, causing closure of the
jaws (trismus, lockjaw) and involves muscles
of the trunk more than those of the limbs”-
Gowers (1888)
 Definition
• Tetanus is a neurological disorder
characterized by increased muscle tone and
spasm caused by tetanospasmin, a powerful
neurotoxin produced by Clostridium tetani.
• A serious preventable disease caused by
infection of the skin and deep necrotic
wounds by Clostridium tetani, a Gram-positive
bacillus , which secrets a neurotoxin
• Lethal dose->500pg/kg i.e 25ng/70kg adult.
 Epidemiology
• 1st described 3000 years ago in Egypt.
• 1st passive immunization-1893.
• 1 million cases occur annually worldwide.
• Of these, 400, 000 cases in neonates.
• 80% of deaths occur in Africa and SE Asia.
• Age: > 50% of cases occur in persons >60 years.
• More common in males.
• Common in rural areas and warm climate.
It affects the following:
• Non-immunized.

• Partially immunized.

• Fully immunized who fail to maintain

adequate immunity with booster doses of
vaccine.
 Microbiology-1
• Organism
– Clostridium tetani
– Gram positive bacillus
– Spore forming, rod shaped, motile,
anaerobic
– Ubiquitous
– Sources
• Natural habitat is soil but it is present in
human and animal feces, house dust, air,
slums, marine and freshwater sediments
 Microbiology-2
– Spores may remain dormant for years.

– Spores become vegetative form in wounds under anaerobic

conditions, particularly when infected.

– Exotoxins-tetanospasmin and tetanolysin are produced

under anaerobic conditions.

– DNA for tetanospasmin is in a plasmid.

 Microbiology-3
• Spores germinate under anaerobic conditions
and produce two toxins:

-Tetanolysin (a haemolysin with recognized

pathologic activity).

-Tetanospasmin (which is responsible for the

clinical manifestations of tetanus).
 Portals of infection
• Wound on lower limb-often a minor one-thorn, splinter of
wood, piece of metal.
• Non-sterile intramuscular or intravenous injection
• Fracture.
• Chronic ulcers.
• Post-partum or post-abortal wound infection.
• Others
-Tooth picks
-Otitis media
-Accupuncture
• No obvious source (30%).
 Structure of tetanospasmin
• Tetanospasmin is a 151 KD chain.
• Cleaved into 2 chains joined by disulphide bond:
-Heavy chain (100kD) is responsible for binding to
neuronal cells & transport proteins.
-Light chain (50kD) is a zinc endopeptidase that
cleaves an integral membrane protein of small
synaptic vesicles, synaptobrevin at a single site &
blocks release of neurotransmitters.
 Pathogenesis-1
• Once synthesized, it moves from contaminated
site to the spinal cord or brainstem.
• Reaches CNS by intra-axonal transport, moving at
a rate of 75-350 mm (3-10 in)/day.
• Process takes 2-14 days (short with facial injuries)
• Once toxin reaches CNS, local or cephalic tetanus
may occur initially followed by generalized
tetanus.
 Pathogenesis-2
• Toxin produces presynaptic blockade of
inhibitory Renshaw cells and 1a fibers of the
alpha motor neurons that handle the
transmission of GABA and glycine.

• Instability of the ANS also occurs.

• Toxin binding may be reversible.

 Pathogenesis-3
• Affected neurons
– Masseter innervation is most sensitive
– Motor neurons of the spinal cord and brainstem
– Direct action at motor end-plate
– Cerebral cortex, hypothalamus
– Sympathetic neurons
• Effects of toxin
– Exaggerated effect of afferent stimuli
– Both agonists and antagonists co-contract
 Clinical features
• Incubation period-this is from inoculation to
1st symptom.
- 7-10 days.

• Period of onset-this is from 1st symptom to

start of spasm.
-1-7 days
• Localized tetanus

• Generalized tetanus

• Cephalic tetanus

• Neonatal tetanus
 Generalized tetanus
– May begin with trismus

– Stiffness and spasms of bulbar, neck, trunk and limb muscles

– Risus sardonicus

– Opisthotonos

– Board-like abdominal rigidity

– Spasms of laryngeal muscles may cause fatal asphyxia

– Consciousness is preserved
• Local tetanus
– This is usually benign
– Stiffness and tightness of muscles localized around
the wound followed by spasms

• Cephalic tetanus
– Follows wounds of the face and head
– Incubation period is usually short
– Affected muscles are weak or paralysed
 Cardiovascular and autonomic features
• Sustained tachycardia < 160 per min

• Persistent hypotension

• Labile or sustained hypertension

• Autonomic storms, hypertension alternating with hypotension

• Increased vagal tone, bradycardia

• Supraventricular arrhythmias

• Ventricular tachycardia

• Infranodal conduction defects

 Differential diagnosis
• Dystonic reactions to neuroleptic drugs.

• Strychnine poisoning

• Dislocation of mandible leading to ‘lockjaw’

• Facial or jaw trauma

• Rabies

• Hysteria

• Stiff-person syndrome
 Investigations
• Laboratory tests are of virtually no diagnostic
value.
• Blood counts & biochemistry are
unremarkable.
• Imaging of head and spine reveal no anomaly.
• LP is not necessary; the CSF is normal except
for raised opening pressure which occurs
during spasms.
 Diagnosis

This is purely clinical

 Treatment
1. Nurse in quiet, dark surroundings.

2. Remove source of toxin-excise and debride any wound.

3. Neutralize circulating toxin-Human anti-tetanus immune globulin (3000-

10,000 U)
-recommended
-controversial efficacy
4. Anti-tetanus toxin.

5. Control muscle spasms

-Benzodiazepines (GABA agonists that indirectly antagonize the toxin ) are
mainstay of Rx.
-10-40mg every 1-8 hrs.
6. Maintain ventilation & oxygenation and
prevent aspiration of gastric contents
-Tracheostomy if spasms can’t be controlled
-Paralysis of ventilation if spasms become
severe
7. Nutrition & fluid balance
-No nasogastric tube!
-IV fluids
8. Antibiotics
-Metronidazole 500 mg/6hr or 1 g/ 12 hr
-Penicillin G is no longer drug of choice
-Penicillin, just like tetanus toxin is a GABA
antagonist .

9. H2 receptor antagonists to prevent stress

ulcers
10. DVT prophylaxis-LMWH 5000 IU b.d

11. Control autonomic dysfunction-using beta

blockade or combined alpha & beta blockade
as necessary for labile blood pressure and
heart rate.
 Drugs used to control spasm
• Diazepam

• Baclofen

• Dantrolene

• Magnesium sulphate

• Propofol
 Complications
• Respiratory arrest/apnoea

• Autonomic dysfunction

• DVT

• Fracture of long bones

• Death
 Prognosis
• Disease progresses for about a week
• Stabilizes for another week.
• Recovers over several weeks.
• Severity is variable.
• Case fatality ranges from 10 to >50% worldwide.
• 50% of deaths occurs in neonates (preventable
through ante partum immunization)
 Poor prognostic features
• Short incubation period

• Short onset period

• Elderly

• Autonomic dysfunction

• Respiratory arrest
 Prevention
• Prevention
– Adsorbed tetanus toxoid
• Immunization after minor wounds
Thanks for listening!