Tetanus

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Introduction

Tetanus is a bacterial infection caused by clostridium tetani, which causes involuntary muscle spasm, and if untreated, is fatal in about 10% of cases.

The bacterium is widespread in the natural environment, particularly in soil, and is typically acquired through a penetrating injury.

The disease itself is actually caused by tetanus toxin, produced by the bacterium. The toxin is so potent, and the amount required to produce the disease is minuscule – so small that it in fact does not cause an immune reaction – and thus paradoxically survivors of tetanus do not typically have immunity to the disease.

A vaccine was developed in 1924. It is thinly vaccine preventable disease that is not readily transmitted between individuals. Immunity is not thought to be life-long, and repeat boosters in adulthood are required for continuing immunity. Typically in most developed nations, 3 doses are given during childhood, and re-vaccination is advisable for those at risk (e.g. manual workers) every 10 years.

Thanks to vaccination, the disease is now very rare in the developed world. In some developing countries it is a still seen frequently.

Most cases occur in people who have never been vaccinated. A small number of cases occur in those with prior vaccination, but whose vaccination has lapsed. It is most common in people aged >65.

Neonatal tetanus is particularly deadly, but even more rare in developed nations.

Treatment is with tetanus immunoglobulin, which can be given IV or IM. This binds to free tetanus toxoid, and prevent progression of the illness. Patients with severe disease, affected respiration, may required ventilation and PEG feeding – often for up to 8 weeks.

Organism

Clostridium tetani is a gram positive, anaerobic spore forming bacteria.
Incubation period; varies according to site of injury, 3-28 days, typically about 8 days. Shorter in severe disease.
It is found in soil all over the world, but is more common in hot and wet climates, where there is more organic matter in the soil.
It is also commonly found in the gut of mammals – where it does not cause disease.

Transmission

Spores of C. tetani live in faeces, soil and dust and can be introduced by small break in skin/via mucosa. Penetrating injuries (such as from thorns or other puncture wounds) are more prone to tetanus infection. Rarely, cases have been noted without a preceding injury – it is thought in these cases that very minor cuts and abrasions could be the cause.
  • Tetanus is only infectious vaccine preventable disease that isnt contagious

C. tetani will not grow in healthy tissuesFactors that are more likely to allow for tetanus infection include:

  • Co-infection with other bacteria
  • A foreign body
  • Localised ischaemia

As such, the types of injury that are more likely to be tetanus-prone include:

  • Splinters
  • Other puncture wounds
  • Burns
  • Unsterile injections (e.g. IV drug users)

Epidemiology

  • Occurs worldwide
  • Now almost exclusively affects those not vaccinated
  • In the US, there are about 30 cases per year
  • Worldwide, there are about 200,000 cases and 60,000 deaths per year
  • In Nigeria, tetanus is the second most common neurological disorder requiring hospital admission – after stroke
  • More common in
    • Hot, damp climates.
    • Those who work in agriculture (manure).
    • Heroin users (spores can be found in contaminated heroin)
WHO estimates 59,000 newborns worldwide died in 2008 as a result of neonatal tetanus.
 

Pathogenesis

Spores germinate in anaerobic conditions at wound site and produce neurotoxin (tetanus toxin). The toxin enters peripheral nerves – namely motor neurons, and then travels up peripheral nerves andante the spinal cord and brainstem. It the proximal end of the nerve it cleaves the protein that allows fusion of the synaptic vesicle with the membrane prevents neurotransmitter release – particularly of inhibitory neurons. This causes muscle spasm and over activation.
  • Primarily affects inhibitory glycine or GABA
  • Leads to less inhibition(relaxation), increased firing, contraction skeletal muscle

The longer the nerve, the longer it takes for tetanus to present. Hence wounds at the distal ends of the limbs could take several weeks, whilst wounds at the head and neck may present after only a few days.

The binding of tetanus toxin at the synapse is permanent. New synapses can grow, but this process typically takes 6-8 weeks. As such, the duration of symptoms is usually around 6-8 weeks.

Clinical features

  • Prodrome: fever, malaise, headache
  • Trismus (lock jaw)
  • Neck stiffness
  • Dysphagia
  • Risus sardonicus (grinding expression of facial muscles)
  • Opisthotonus (arching of body with neck hyper-extension)
  • Spasms – initially induced by movement/noise but later spontaneous
    • Muscle spasms can be so severe that they cause long bones to break
  • Autonomic dysfuction (arrhythmias and BP fluctuations)
  • Rigid board abdomen

Signs and symptoms can continue to progress for up two weeks after presentation, and can be variable, depending on the amount of toxin that reaches the CNS. Some studies have also suggested that the severity of symptoms is correlated to the previous level of vaccination – those with more up to date vaccination suffer less severe disease.

Symptoms can last for 4-8 weeks.


[image from Wikipedia]

 

Complications

Spasms may cause dysphagia, fracture of long bones, respiratory arrest and death – typically due to respiratory arrest.
 

Diagnosis

Usually a clinical diagnosis. There is a blood test, but it is unreliable – only typically only positive in about 30% of patients.
The “Spatula test” is believed to be the most reliable clinical sign for tetanus (high specificity and a high sensitivity). This ‘test’ involves touching the posterior pharyngeal wall with spatula (tongue depressor)
  • Positive = involuntary contraction of the jaw (biting down)
  • Negative = gag reflex
 Differential diagnosis
  • Dystonia – particularly drug induced
    • Causes eye deviation – unlike tetanus
  • Trismus from dental infection
  • Malignant neuroleptic syndrome

Treatment

Good quality published evidence for many of these interventions is lacking

  • Clean and debride the wound
  • Metronidazole (clears the bacteria but has no effect on toxin already produced)
    • If adequate wound debridement has not occurred, re-infection from spores in the wound can occur
    • IV 500mg TDS
    • Often a mixed infection is present – consider wound swabs for directed antimicobial therapy
  • Tetanus immunoglobulin IM/IV
    • 3000 – 6000 unit doses recommended
    • This neutralises the unbound toxin, but has no effect on the toxin that has already bound to synapses
  • Give a tetanus vaccine – e.g. DTaP
  • Diazepam/magnesium- to control muscle spasms
    • High doses may be required
    • Typical doses might include diazepam IV 10-30mg Q1H, maximum daily dose of 500mg
    • Continuous infusion of midazolam may be considered
    • In some cases, neuromuscular blockade – e.g. with vecuronium (traditionally used to paralyse patients for intubation) might be indicated
  • May require nutiritional and ventilator support, which will involve admission to ICU
    • In severe cases, ventilation and ICU admission for 6-8 weeks may be required
    • Nutritional demands are often very high due to prolonged muscle contractions. PEG feeding in ICU may be required if prolonged duration of illness
  • Control the autonomic dysfunction
    • Magnesium sulphate, often in combination with bet-blocker (often an IV infusion of labetolol) and morphine have been used

Prevention – Tetanus Vaccination

Vaccination
  • With tetanus toxoid (+booster every 10 years)
  • Part of the routine DTP vaccine in children in the UK

Assessing wounds for risk of tetanus

WOUNDVACCINE REQUIRED?Ig REQUIRED?
Has received at least 3 doses of tetanus vaccine in the past
<5 years since last doseAll woundsNo ❌No ❌
5-10 years since last doseClean, minorNo ❌No ❌
All otherYes ✅No ❌
>10 years since last doseAll woundsYes ✅No ❌
Has received <3 doses of tetanus vaccine in the past, or vaccine status unknown
Clean, minorYes ✅No ❌
All otherYes ✅Yes ✅

Source: Australian Immunisation Handbook. Refer there for most current advice.

References

Read more about our sources

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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University, and is studying for a Masters of Sports Medicine at the University of Queensland. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

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