Tetanus (Lockjaw)

Tetanus (lockjaw) is an acute disease caused by neurotoxins from the bacterium Clostridium tetani. C. tetani is ubiquitous in spore form and enters the body through broken skin (e.g., deep puncture wounds). Its toxins then cause uncontrolled activation of alpha motoneurons, leading to muscular rigidity and convulsive spasms. Patients classically present with a triad of trismus, risus sardonicus, and opisthotonus. Despite treatment with anti-tetanus toxoid immunoglobulin and antibiotics (e.g., metronidazole), the overall prognosis is poor once symptoms begin. Therefore, vaccination as primary prevention is crucial.

• Pathogen
  • Clostridium tetani, gram-positive rod, obligate anaerobe, spore-forming
  • Produces neurotoxins
  • Ubiquitous (especially animal feces and soil)
• Route of infection
  • Clostridial spores contaminate the wound (e.g., through dirt, saliva, feces)
  • Wounds with compromised blood supply create anaerobic conditions that are ideal for the multiplication and germination of C. tetani.
    • Deep, penetrating wounds (e.g., knife, gunshot, animal bites)
    • Open fractures
    • Surgical procedures (e.g., bowel and biliary tract surgery, septic abortion)
    • Burns
    • Umbilical stump infections
    • Often associated with contamination; (dirt, saliva, feces), foreign bodies; , localized ischemia; , necrosis; , and/or coinfection with other bacteria
• Groups with a higher risk: non-immunized individuals; , diabetics, neonates, drug abusers, certain patient groups (i.e., postsurgical, obstetric, dental) ^[1]

Ubiquitous C. tetani spores contaminate a wound → bacteria reproduce under anaerobic conditions → production of toxins tetanospasmin and tetanolysin

• Tetanospasmin reaches the CNS through retrograde axonal transport; → the toxins bind to receptors of peripheral nerves and are then transported to the CNS via vesicles ^[2][3] → prevents the release of inhibitory neurotransmitters (i.e., GABA and glycine) from interneurons (Renshaw cells); → uncontrolled activation of alpha motor neurons; → tonic and clonic spasms (spastic paralysis) + autonomic instability
  • Renshaw cells are found in the gray matter of the spinal cord and inhibit alpha motor neurons. ^[4]
• Tetanolysin causes hemolysis and has cardiotoxic effects

Neurotoxins cause tetanus (not the pathogen itself)!

• Incubation period: 3–4 days (up to several weeks in rare cases)
• Initial presentation: flu-like symptoms and headache
• Painful descending muscle stiffness and spasm
  • Trismus; : lockjaw due to tonic spasms of the jaw musculature
    • Commonly the first tetanus-specific sign
  • Risus sardonicus; : grinning caused by tonic cramps of the facial muscles
  • Neck stiffness
  • Opisthotonus; : backward arching of spine, neck, and head caused by tonic spasms of the back muscles
  • Abdominal rigidity
• Life-threatening complications
  • Laryngospasm and/or respiratory muscles spasms → respiratory failure ^[5]
  • Autonomic dysfunction → circulatory arrest and shock ^[5]
• Although generalized tetanus accounts for over 80% of cases, localized and cephalic forms are possible

Neonatal tetanus

• Occurs in infants of poorly immunized mothers after unsterile management of the umbilical stump
• Typically occurs 5–8 days after birth, but could be up to a few weeks
• Typically a rapid onset of symptoms as axonal length in infants is shorter than in adults
• Symptoms include difficulty opening the mouth and feeding; due to trismus, risus sardonicus, and/or clenched hands

In addition to initial supportive care, management should focus on controlling the infection, eliminating toxin production, and neutralizing circulating toxins.

• Wound cleaning and debridement
• Antibiotic treatment
  • Drug of choice: metronidazole
  • Alternative: penicillin G
• Active and passive immunization
  • Single IM dose of human tetanus immunoglobulin (HTIG)
  • Tetanus toxoid-containing vaccine: for example, TdaP, Td, DTaP, DT; , DPT, or tetanus toxoid, depending on age, previous immunization, or allergies (see tetanus prophylaxis after injury in “Prevention” section below for details)
    • Inject in separate site from HTIG
    • If patient has not received initial immunization before infection: second and third dose 1–2 months and 6–12 months later, respectively
    • The still intact receptor binding site of the tetanus toxoid induces antibody production and memory cell formation (active immunity).
• Supportive care: transfer to ICU, ventilation, benzodiazepines and/or paralytics for control of muscle spasms

Tetanus vaccination ^[7]

• Tetanus toxoid-containing vaccines according to age groups
  • For children < 7 years of age
    • DTaP (diphtheria, tetanus, and acellular pertussis)
    • DT (diphtheria, tetanus): for children who cannot tolerate the pertussis vaccine
  • For adolescents and adults
    • Tdap (tetanus, diphtheria, pertussis): recommended for patients 11–64 years of age, but may be considered for children > 7 years old
    • Td (tetanus, diphtheria): for patients > 11 years old
• Initial immunization recommendations: children < 7 years of age → 5 doses of DTaP (see “Immunization schedule”):
  • 2 months
  • 4 months
  • 6 months
  • 15–18 months
  • 4–6 years
• Booster recommendations
  • Children 11–12 years of age: single dose of Tdap^[8]
  • Adults 19–64 years of age: single dose of Tdap^[8]
  • Adults ≥ 19 years of age: Td (tetanus, diphtheria) every 10 years

Since recovery from infection does not confer immunity following recovery, routine immunization is generally recommended!

Tetanus prophylaxis after injury

Vaccination history	Clean, minor wounds	All other wounds
Unknown or < 3 tetanus toxoid doses	Active immunization with tetanus toxoid (Td or Tdap)	Active immunization with Td or Tdap and passive immunization with TIG
≥ 3 tetanus toxoid doses	Active immunization with Td or Tdap if last vaccination ≥ 10 years ago	Active immunization if last vaccination ≥ 5 years ago