Disease factsheet about tetanus

Tetanus is caused by a neurotoxin produced by the spore-forming bacterium Clostridium tetani. Tetanus is unique among the vaccine preventable diseases in that it is not communicable. Disease occurs when the ubiquitous C. tetani spores are introduced into the hypo-aerobic conditions of devitalized tissue and puncture wounds, where they germinate and produce a neurotoxin. The inactivated toxin, termed tetanus toxoid, effectively induces antibody production and vaccines became commercially available already in 1938.

Military recruits were among the first to be routinely immunised in Europe and the vaccine was later introduced to childhood immunisation programmes. Tetanus is rare in Europe today and predominantly a disease of unvaccinated or partly vaccinated risk groups.

The pathogen

• Clostridium tetani is an obligate anaerobic Gram-positive bacillus.
• The tetanus bacillus forms spores that can be found in soil and house dust, and in animal and human faeces. The spores remain viable for years in the environment and are resistant to boiling and freezing. 
• Direct contamination of wounds with C. tetani spores results in germination of the spores under hypo-aerobic conditions. The spores develop into a vegetative form of the bacilli which produces and releases a neurotropic exotoxin called tetanospasmin. 
• Tetanus toxin is one of the most potent toxins known in relation to its weight. It is transported with blood and lymph, and taken up via endocytosis by nerve cells at the neuromuscular junctions after which it is transported centripetally inside the axons.
• Once inside the neurons, tetanus toxin cannot be neutralised by antitoxin. The tetanus toxin acts on four areas of the nervous system: a) the motor end plates in the skeletal system; b) the spinal cord; c) the brain; and d) the sympathetic system. 
• The toxin blocks the release of the inhibitory neurotransmitters glycine and gamma-amino-butyric acid in the central nervous system. This leaves excitatory nerve impulses unopposed resulting in muscle spasms.   

Clinical features and sequelae

• There are three clinical presentations of tetanus:
  • generalized tetanus, which is the most common form;
  • localised tetanus; and
  • cephalic tetanus.
• In generalized tetanus, the presenting symptoms include trismus (‘lock jaw’), episthotonus, facial grimacing (risus sardonicus), spasms, back and neck stiffness, muscle rigidity, dysphagia, and restlessness. Reflex spasms are triggered by minor external stimuli such as noise, light or touch. 
• Tetanus neonatorum is a generalised form of tetanus in newborns. Contamination of the cord stump with C. tetani spores occurs as a result of unclean delivery and cord care practices. Newborns of unimmunised mothers lack passive protection from maternal antibodies to the tetanus toxin and are at high risk. The typical case is a previously well and feeding newborn who presents at age 3-14 days with symptoms of irritability, inability to suck, muscle rigidity, facial grimacing, opisthotonos and severe spasms elicited by sound, light and sensory stimuli. The case definition for surveillance includes newborns aged 3-28 days.
• Localised tetanus is an uncommon presentation localised to the site of spore entry, with weakness of the involved extremity and intense, painful spasms in severe cases. 
• Cephalic tetanus is the result of inoculation by way of head injury or middle ear infection and presents as motor cranial nerve palsies—commonly affecting the facial nerve. 
• Maternal tetanus typically develops in unimmunised women as a result of unsafe abortions and unclean deliveries.
• There is a direct relationship between the distance from the inoculation wound to the central nervous system and the onset of symptoms. 
• Tetanus is a clinical diagnosis and there are no definitive laboratory tests. 
• The diagnosis is supported by an incomplete or out-of-date vaccination status, culture of C. tetani from the wound, detection of circulating tetanus toxin and the absence of tetanus toxin antibodies.
• Complications of tetanus arise either as a direct result of the disease or due to the intensive care management. Direct complications include the following:
  • respiratory compromise because of chest wall muscle rigidity, spasm and diaphragmatic dysfunction;
  • airway obstruction due to laryngeal spasm and respiratory apnoea;
  • aspiration pneumonia;
  • fractures associated with severe muscle spasm.
• Autonomic dysfunctions, often exacerbated by intensive care interventions, can cause labile hypertension, hypotension, tachycardia, bradycardia and arrhythmias which can result in hemodynamic instability and cardiac arrest. 
• The clinical course of generalised tetanus is variable and reported case fatality ratios for hospitalised cases range from 20–70%. Short incubation and early manifestations of autonomic dysfunction, young age, and old age are associated with more severe disease and higher case fatality. 
• Sequelae of neonatal tetanus: Studies have linked neonatal tetanus to neurological disabilities ranging from cerebral palsy and severe psychomotor retardation to subtle intellectual and behavioural abnormalities but it has not been established how much is caused by the neurotoxin and how much is the result of compromised respiration and hypoxia.

Epidemiology

• Soil is the main reservoir of C. tetani but many animals, both herbivores and omnivores, carry the bacilli in their intestines and excrete the spores in their faeces.
• Tetanus spores have a worldwide distribution and the incidence of tetanus in a population primarily reflects the effectiveness of the immunisation program. 
• Tetanus remains common in countries with inadequate immunisation coverage, low antenatal care attendance, unsafe traditional cord care practices and where women deliver without the assistance of trained health professionals.
• It is estimated that tetanus causes 213 000 – 293 000 deaths worldwide each year and that it is responsible for 5–7% of all neonatal deaths and 5% of maternal deaths globally.
• Neonatal tetanus has been eliminated from Europe and the overall number of tetanus cases has declined sharply since the 1950s. Tetanus is today a rare disease in Europe.
• The highest tetanus risk in Europe is found in the elderly unvaccinated or partially vaccinated population and among injecting drug users. Induced tetanus immunity wanes with increasing age and this partly explains the higher incidence in higher age groups.
• The EU case definition of tetanus for the purpose of reporting communicable diseases to the community network can be reviewed  here: EU case definition of tetanus.
• Annual updates on tetanus incidence in the European Union are presented in ECDC’s Annual epidemiological report on communicable diseases in Europe.

Transmission

• Tetanus is spread by the direct transfer of C. tetani spores from soil and excreta of animals and humans to wounds and cuts. It is not transmitted from person to person.
• Contaminated puncture wounds, compound fractures, burns, frostbites, ulcers, gangrene, unclean deliveries and unhygienic cord care practices are risk factors for tetanus in unvaccinated or partly vaccinated populations. 
• The time from inoculation with tetanus spores to the first symptoms can be from one day to one month with a median of 7 days.
• The incubation period for neonatal tetanus (age at first symptom) is between the first 3–14 days of life, and is most common between days 6–8.

Prevention

• Immunisation is the only effective prevention of tetanus. Tetanus toxoid is an effective, safe, stable and inexpensive vaccine that can be given to all ages, to pregnant women and to immunocompromised individuals.
• Most countries recommend a minimum of five doses of tetanus toxoid vaccine over 12–15 years, starting in infancy. Further booster doses can be given at regular intervals in adulthood, to ensure long-lasting protection. 
• Opportunistic immunisation of people who are treated for wounds and cuts is important for maintaining high protection levels, as is targeted vaccination of population groups born before general immunisations programmes started.
• Tetanus antibody levels decline with increasing age which helps explain why the highest tetanus incidence in Europe is among the elderly. Booster vaccination of elderly people can improve protection against tetanus.
• Maternal tetanus antibodies passively protect newborns, and immunising pregnant women remain an important intervention for the prevention of neonatal tetanus in countries with low protection levels in the adult population.  
• Vaccination schedules for the European countries can be reviewed in the Vaccine Scheduler.

Management and treatment

• Although tetanus has become an uncommon disease in Europe, it remains an important differential diagnosis, particularly in elderly patients and intra-venous drug users.
• Tetanus immunoglobulin should be given to individuals with high-risk conditions, such as: wounds requiring surgical intervention which is delayed for more than six hours; burns and injuries with significant devitalised tissue, especially where there has been contact with soil or manure; wounds containing foreign bodies; compound fractures; wounds or burns in septic patients, injecting drug users with multiple skin abscesses.
• Human anti-tetanus immunoglobulin can neutralise circulating toxin but will not pass the blood-brain-barrier and has no effect on already bound toxin.
• The benefit of intrathecal administration of antitoxin has not been proven. 
• Toxin production at infection site is reduced by proper wound care and the administration of appropriate antibiotics.
• Treatment should be started on clinical suspicion. Wound swabs should be sent for culture but the results should not delay the onset of therapy. 

Note: The information contained in this fact sheet is intended for the purpose of general information and should not be used as a substitute for the individual expertise and judgement of healthcare professionals.