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aka Tropical Travel Trouble 003

A 65 yr old woman from Ethiopia is visiting her grandchild for the first time in Europe. She is normally fit and well, physically active with a small-holding in Ethiopia. She does not take any medication and cannot remember the last time she saw a doctor. She presents to you with difficulty chewing 3 days after arriving in the UK. She describes it as being “stiff in the mouth”


Q1. What is the differential diagnosis and how would you diagnose each?


  • Tetanus – clinical diagnosis and the one present in this case. Bacteriology is of little help, the organism is often not found and a positive wound culture for C. tetani does not prove that the organism is toxin producing.
  • Giant cell arterititis – ESR
  • Dental abscess – examination
  • Strychnine poisoning – history, most likely this will be of sudden onset and continuous, urinary levels can be obtained. Supportive care should be initiated. See Tox library – Strychnine poisoning.
  • Dystonic reactions – drug history, trial of benzatropine
  • Stiff person syndrome – most likely a diagnosis of exclusion but the presence of antibodies against GAD is the best indication of the condition that can be detected by blood and CSF. Anti-GAD65 is found in about 80 percent of SPS patients. Anti-thyroid, anti-intrinsic factor, anti-nuclear, anti-RNP, and anti-gliadin are also often present in blood tests. EMG can confirm the diagnosis by noting spasms in distant muscles as a result of subnoxious stimulation of cutaneous or mixed nerves.
  • Seizure disorder – EEG
  • Psychogenic – may have irregularities in their presentation or a history of recent stressors
  • Meningism – clinical signs, raised inflammatory markers

Q2. Why would the disease initially affect the muscles of mastication and what is the pathophysiology?


Generalised Tetanus with spasms is easy to diagnose but initially patients often have truisms because the muscles of mastication have the shortest motor nerves.

Clostridium tetani is a gram positive obligate anaerobe with a terminal spore (if seen in culture it is said to look like a tennis racket) which is ubiquitous in the environment. The spores are highly resistant to the environment and are transmitted to humans via wounds.

The bacteria produce two toxins: tetanolysin and tetanospasmin. Tetanispasmin binds to the presynaptic membrane of a nerve and prevents synaptic vesicle release of GABA and glycine (inhibitory transmitters). Tetanospasmin can travel retrogradely via axons to cell bodies and cross synapses to reach the spinal cord and the brain. This toxin can also enter the blood stream, spread to muscles and then into other nerve axons.

Q3. What is the average incubation time?


10 days on average but the range is from 1-2 days if the wound is on the face, to 21 days for more distal wounds with minimal inoculation.

Q4.What 4 disease syndromes can be present?


  • Gernalised (ROAST)
    • Rigidity
    • Opisthotonus
    • Autonomic dysfunction (hypertension, tachycardia, arrhythmias and hyperpyrexia)
    • Spasms – these are often an exaggeration of the underlying rigidity and occur in more severe disease either as a reflex response to stimuli (touch, sounds) or spontaneously.
    • Trismus (‘lock jaw’)
    • Recovery may take 4 weeks, case fatalities can reach 60% with death occurring due to respiratory, autonomic dysfunction or laryngeal spasm.
  • Neonatal – accounts for 50% of cases. In the context of lack of maternal immunity it occurs 1-10 days post partum and the mortality is 90%.
    • Infection is usually from a infected umbilicus (some cultures place dung on stump).
    • Initially irritable, poor feeding, generalised weakness, floppy.
    • Later spasms, opisthotonus, hypersympathetic state.
    • Survivors have mental retardation.
  • Localised
    • Muscle rigidity near the site of injury and occasionally weakness if the toxin acts on the neuromuscular junction.
    • Maybe mild and persist for months, can progress to the generalised form.
  • Cephalic (rare)
    • Associated with a head injury or middle ear infection. Incubation is 1-2 days.
    • Presents with cranial nerve palsies.

Q5. How would you treat this condition?


  • Tetanus immunoglobulin (human Ig 150 IU/kg intramuscular or equine tetanus Ig 10^4 – 10^6 IU intramuscular).
  • Wounds should be debrided to prevent further germination of spores.
  • Metronidazole (preferable) should be given to prevent multiplication of the bacteria. Penicillin is used throughout most of the world but is a GABA antagonist.
  • Supportive care – may require intubation with high dose benzodiazepines and baclofen. Non-deplarosing muscle relaxants should only be used if required. Autonomic dysfunction can be challenging and short acting agents should therefore be used, such as labetalol, esmolol, GTN. Atropine and pacing have sometimes been used for bradycardia. Intravenous magnesium has been used and may reduce the need for muscle relaxants and control some of the cardiovascular manifestations.

Q6. What are the indicators of a poor prognosis?


  1. Incubation of < 7 days
  2. Period of onset < 48 hours
  3. Portal of entry from umbilicus, uterus, burns, open fracture or IM injection
  4. Presence of spasms
  5. Temperature > 38.4
  6. HR > 120 (adults), > 150 (neonates)

Q7. How do you prevent this condition?


Vaccination – see vaccination page

Tetanus is a vaccine preventable disease. Most cases occur in south east Asia  and 90% of deaths are in the under 5 age group. Children should receive the vaccine as part of the routine diphtheria, tetanus and pertussis immunisation. Then a booster aged 4-7 years and one in adolescence. A single booster in adulthood leads to a lifetime protection. However, most countries recommend a booster every 10 years and if the wound is particularly tetanus prone, receiving a booster if none has been given within 5 years (this is not the case in the UK).

A single dose of tetanus toxoid in pregnancy leads to protective titres in a proportion of mothers and neonates; non-immunised mothers should ideally receive two doses four weeks apart during pregnancy.

Q8. What is a tetanus prone wound?


  • Wounds or burns that require surgical intervention that is delayed for more than 6 hours.
  • Wounds or burns that show a significant degree of devitalised tissue or a puncture-type injury, particularly where there has been contact with soil or manure.
  • Wounds containing foreign bodies.
  • Compound fractures.
  • Wounds or burns in patients who have systemic sepsis.


Q9. What would be a high risk wound that requires tetanus immunoglobulin?


High risk is regarded as a wound mentioned in Q7 that is heavily contained with material likely to contain tetanus spores and/or extensive devitalised tissue. These require tetanus immunoglobulin as a tetanus vaccine will not confirm enough protection within the incubation period of tetanus in some cases.

See tetanus immunoglobulin for further details.

Although any wound could give rise to tetanus, clean wounds are considered to be a low likelihood.

Case Resolution:
The patient was treated with metronidazole, tetanus toxoid but continued to have severe spasms on the ward. The patient was transferred to HDU and nursed in a quite dark room with moderate doses of benzodiazepines. She did not require intubation and at day 10 was discharged from hospital. At 3 month follow up she was still experiencing some stiffness.


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Last update: Mar 6, 2018 @ 3:10 am

Tropical Travel Trouble 003 Stiff in the Mouth
Neil Long

Article source here:Life in the Fast Lane