Tetanus - Horse

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Also known as: Lockjaw


Tetanus is a highly-fatal infectious disease caused by the neurotoxin of the gram-positive bacterium Clostridium tetani, resulting in spastic paralysis of affected animals. The bacteria causes infection via contamination of wounds and deposition of bacterial spores in tissue. Deep puncture wounds, cuts and surgical sites may all provide sites of entry for infective spores due to the requirement for anaerobic conditions to allow bacterial germination. C. tetani produces tetanospasmin, a neurotoxin that is transferred to distant sites via the vascular system. This causes inhibition of the release of GABA and glycine from interneurons in the spinal cord and brain, resulting in tetanic spasm of striated muscle. The incubation period varies from one to four weeks depending on the suitability of the wound environment for bacterial multiplication.


All species of all ages may be affected but horses are the most sensitive of the domestic species. Foals may be particularly susceptible due to the risk of infection via the umbilicus. Mares with a retained placenta post-foaling may also be affected. Cats and dogs have a higher natural resistance to tetanus toxin, and these animals may have a longer incubating period and a localised (rather than generalised) tetanus.


Diagnosis is often based on a history of a penetrating wound, often to the foot, and clinical signs. Affected animals may have no history of vaccination against tetanus. In cases in which an obvious wound is visible, demonstration of C. tetani in gram-stained smears and by anaerobic culture may be attempted. Severe cases may be easily diagnosed but mild cases may need differentiating from exertional rhabdomyolysis, laminitis, hypocalcaemia and heat stroke.

Clinical Signs

  • Sudden onset stiff gait
  • Rigid posture ('sawhorse stance')
  • Protrusion of the third eyelid, particularly after mild stimulation
  • Trismus (lockjaw)
  • Flaring of the nares
  • Retracted lips
  • Elevated tail head
  • Dysphagia
  • Tetanic spasms of the neck, trunk, masseter and limb muscles
  • Third eyelid paralysis

Cases may vary from mild signs of a short, stilted gait, to complete recumbency with spastic paralysis. Progression of the disease may lead to involvement of the pharyngeal and laryngeal muscles leading to aspiration pneumonia. Recumbency may be followed by paralysis of the respiratory muscles, leading to death due to hypoxia or respiratory arrest due to diaphragmatic spasm.


Treatment may be attempted but consideration must be given to severely affected cases (e.g. recumbency, severe muscle spasms) that usually carry a grave prognosis. The horse should receive as little external stimuli as possible, ideally by keeping it in a darkened, quiet stable. Packing of the ears with cotton wool may help to minimise auditory stimulation. Administration of acetylpromazine may provide both sedation and a reduction in muscle spasm. Diazepam may be used alone or in combination with other sedatives to reduce severe muscular spasm. The use of an intravenous catheter is recommended to further reduce external stimulation. Any obvious wounds should be thoroughly debrided and flushed using 1% hydrogen peroxide, and parenteral penicillin should be administered. Tetanus antitoxin may be adminstered intravenously at the onset of clinical signs and is especially important in horses with no history of tetanus vaccination. Foals and horses with obvious wounds should also receive tetanus antitoxin.

Affected horses may require intensive supportive and nursing care. Intravenous fluid and electrolytes should be administered if the horse is unable to drink or dehydrated. Dysphagic horses may require feeding via a nasogastric tube, particularly in the case of foals. Horses that are able to eat may be fed soft and moist feed in order to aid prehension and swallowing. Feed and water containers should be raised above ground height. Adequate bedding consisting of peat or shavings must be provided, particularly in the case of recumbent horses when decubital ulcers must be avoided. In severe cases the use of slings may be employed to provide support and prevent self-trauma. Catheterisation of the bladder may be required as well as manual evacuation of faeces from the rectum.


The prognosis is variable according to the severity of clinical signs. Horses that are able to eat and drink generally have a favourable prognosis providing nursing care is available. Recumbent horses with severe muscular spasm and trismus carry a grave prognosis with a mortality rate of approximately 80%. Horses that recover may be normal but some may be left with persistent neurological deficits.


Effective prevention is obtained via vaccination with the tetanust toxoid vaccine. Brood mares may be vaccinated one to three months prior to foaling in order to maximise passive immunity to the foal. Recovery from the disease does not provide protection from further infection, therefore the horse must still be vaccinated.

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Tetanus in horses publications


  • Blood, D.C. and Studdert, V. P. (1999) Saunders Comprehensive Veterinary Dictionary (2nd Edition) Elsevier Science
  • Mair, T., Love, S., Schumacher, J. and Watson, E. (1998) Equine Medicine, Surgery and Reproduction WB Saunders Company Ltd
  • Knottenbelt, D.C. A Handbook of Equine Medicine for Final Year Students University of Liverpool
  • Pearce, O. (1994) Treatment of Equine Tetanus In Practice November 1994 pp 322-325.
  • Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition) Merial
  • Bodecek, S., Jahn, P., Dobesova, O., and Vavrouchova, E. (2010) Equine cyathostomosis: case reports Veterinarni Medicina, 55, 2010 (4): 187–193

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