Tetanus Flashcards
Define Tetanus, probable tetanus by CDC
It is an acute disease manifested by skeletal muscle spasm and autonomic nervous system disturbance.
The CDC defines probable tetanus as an acute illness with muscle spasms or hypertonia in the absence of a more likely diagnosis.
Define neonatal tetanus
Neonatal tetanus is defined by WHO as an illness occurring in a child who has the normal ability to suck and cry in the first 2 days of life but who loses this ability between 3 and 28 days of life and becomes rigid and has spasms.
Define tetanus
Maternal tetanus is defined by WHO as tetanus occurring during pregnancy or within 6 weeks after conclusion of pregnancy (whether with birth, miscarriage and abortion.
What is the epidemiology of tetanus
Tetanus is a rare disease in the developed world.
In a 14 year prospective study carried out in a tertiary health facility in Northwest Nigeria, they found a prevalence of 6.5 cases per year with a complication rate of 71.4% and a mortality rate was 48.4%.
Globally, 7% of neonatal deaths was as a result of tetanus, but the incidence is up to 20% in Nigeria.
Almost always affects the non-immunized
Common in
areas where soil is cultivated
rural areas
warm climate
during summer months
among males
What is the aetiology of tetanus?
Causative organism is Clostridium tetani.
Poorly motile, spore-forming, anaerobic obligate , non encapsulated gram-positive bacillus
Sources: soil, human and animal feces, house dust, clothing, air, slums, marine and freshwater sediments.
Neonatal tetanus , source of infection is following infection of umbilical stump, open dirty wound, otitis media and circumcision or ear piercing.
What are the Risk Factors?
Acute injury (puncture wound, laceration, abrasion, etc
may be major or trivial
No identifiable injury or portal in some cases (20-30%)
Chronic conditions: skin ulcers, abscesses, and gangrene
Burns, frostbite, middle-ear infection, surgery, abortion, childbirth, body piercing, “skin popping
Discuss clostridium, what exotoxins does
Clostridium produces two exotoxins: Tetanolysin and tetanospasmin.
- Tetanolysin: increases tissue necrosis and optimises condition for multiplication of bacteria.
- Tetanospasmin: implicated in tetanus.
Very low concentrations of this highly potent toxin can result in tetanus (minimal lethal human dose is 2.5ng/kg).
What is the pathogenesis of tetanus?
Spores may remain dormant for years
Spores become vegetative form in wounds under anaerobic conditions
Spores are resistant to heat, desiccation and disinfectants.
Discuss Tetanospasmin
Tetanospasmin is a 150 kDa polypeptide heteromer ;2 chains - 100kDa(heavy chain) & 50kDa (light chain) chains joined by a disulphide bond.
Tetanospasmin is intra axonally transported to the motor nuclei of cranial nerves or anterior horn of spinal cord.
What is the process?
- Heavy chain binds to the lower portion of the terminal neuron
- Leading to uncontrolled disinhibited discharge from motor neurons
- Tetanospasmin is intra axonally transported to the motor nuclei of cranial nerves or anterior horn of spinal cord.
- Once inside, the neuron toxin enters a retrograde transport pathway whereby it is carried proximally to the motor neuron body.
- In the anterior horn of the spinal cord, it is then taken by presynaptic terminals of the inhibitory spinal interneurons with the aim of inhibiting the release of inhibitory neurotransmitters (glycine and GABA).
- This results in excessive discharge from the alpha motor neurons.
- This leads to intense muscular rigidity and spasm.
- Muscles of the jaw, face, and head often involved first due to shorter axonal pathways.
- Once the toxin becomes fixed to neurons, it cannot be neutralized with antitoxin. (Neuronal binding of toxin is irreversible).
- Recovery requires the growth of new nerve terminals
What occurs afterwards?
- Loss of reflex inhibition of antagonist muscle groups
- Co-contraction of agonist and antagonist muscles
- intensely painful spasms, may lead to fractures & tendon rupture
What causes the autonomic tetanus symptoms?
Pre-ganglionic sympathetic neurons in the lateral horns and the parasympathetic centers are later affected
This leads to disinhibited autonomic discharge resulting in sympathetic over activity and excessive plasma catecholamine levels resulting in the autonomic symptoms.
What is the natural history of the disease?
Incubation period :time from injury to first symptom
Averages 7–10 days, with a range of 3days–3weeks
Period of onset (onset time): time interval between trismus and first spasm
1st week - muscle rigidity and spasms, which increase in severity.
Autonomic disturbance usually starts several days after the spasms and persists for 1–2 weeks
Spasms reduce after 2–3 week
Rigidity may persist considerably longer
What are the clinical forms of tetanus?
Generalized
Localized
Cephalic
Neonatal
What is Generalized tetanus?
Most common form
Characterized by generalized rigidity & spasms
Trismus (lockjaw)
usually the 1st
Due to masseter rigidity
Risus sardonicus
a grimace or sneer
from sustained contraction of the facial muscles
