equis - Articles
Tetanus
Synonym(s): Lockjaw, Sawhorse stance
Introduction
- Tetanus is characterized by tetany, hyperesthesia and seizures; horses are highly susceptible.
- Cause: three exotoxins of Clostridium tetani Clostridium tetani.
- Signs: hyperesthesia and tonic spasm of muscle groups.
- Diagnosis: history and clinical signs.
- Treatment: antibiotics, antitoxin, supportive therapy.
- Prognosis: very guarded.
Presenting signs
- Hyperesthesia.
- Tonic muscle spasms.
- Stiff gait.
- Dysphagia.
- Dyspnea.
- Puncture wound may be found.
- Colic Abdomen: pain - adult, constipation and urine retention.
- Localized stiffness in groups of muscles.
- Recumbency.
- Pyrexia Pyrexia: overview in later stages.
Acute presentation
- Course of disease may take only 3 days in foals before death.
Geographic incidence
- Worldwide.
Age predisposition
- Foals - most adult mares adequately vaccinated.
- All ages if not vaccinated, but suggestions that young animals are affected more often and more severely by tetanus than older animals.
Cost considerations
- Most cases are fatal.
Special risks
- Affected animals should not undergo the stress of general anesthesia Anesthesia: general - overview.
Pathogenesis
Etiology
- Clostridium tetani Clostridium tetani: gram-positive, strictly anaerobic bacillus with terminal spore Clostridium tetani.
- Produces a protein exotoxin of 67,000 molecular weight with 3 components:
- Tetanospasmin.
- Tetanolysin.
- Non-spasmogenic toxin.
- Horses are sensitive to all of the components, but the clinical signs of tetanus are mainly due to tetanospasmin.
Predisposing factors
General
- Puncture wound contaminated with soil/spores.
- Contamination of uterus at parturition.
Specific
- Anerobic tissue environment.
Pathophysiology
- Spores of C. tetani Clostridium tetani → three exotoxins produced (tetanospasmin, tetanolysin and non-spasmogenic toxin) → CNS → muscle spasms.
- Spores from C. tetani carried into puncture wounds, uterus or umbilicus → germinate in anerobic tissue conditions → toxin production → toxin travels along peripheral nerves → CNS.
- Tetanospasmin binds to gangliosides in the CNS → inhibition of cholinesterase and prevention of release of inhibitory transmitter, glycine → abolition of synaptic inhibition of spinal motor neurones (GABA) → accumulation of acetylcholine → continued stimulation of neurones in motor and reflex arcs.
- Tetanospasmin also causes inhibition of protein synthesis.
- Tetanolysin causes tissue damage and necrosis at site of infection.
- Non-spasmogenic toxin may block transmission in peripheral neuromuscular junctions.
Timecourse
- Incubation period 7-21 days (possibly much longer, up to 2 months).
- Death may follow onset of clinical signs in 5-10 days (3 days in foals).
Epidemiology
- C. tetani spores are ubiquitous in soil and intestinal contents of horses.
- Clinical disease occurs sporadically.
- Infection occurs via a puncture wound, the umbilicus, or contamination of uterine contents during parturition.
Diagnosis
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Treatment
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Prevention
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Outcomes
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Further Reading
Publications
Refereed papers
- Recent references from PubMed and VetMedResource.
- Fisher R J (2005) The treatment of tetanus in horses using intrathecal injection of tetanus antitoxin. UK Vet 10 (6), 12-14.
- Steinman A, Haik R, Elad D & Sutton G A (2000) Intrathecal administration of tetanus antitoxin to three cases of tetanus in horses. Equine Vet J 12 (5), 237-240 VetMedResource.
- Sedrich S A, Seahorn T L & Martin G (1996) What is your neurologic diagnosis? Tetanus. JAVMA 209 (1), 57-58 PubMed.
- Abrutyn E & Berlin J A (1991) Intrathecal therapy in tetanus. A meta-analysis. JAVMA 266 (16), 2262-2267 PubMed.
- Wilkins C A, Richter M B, Hobbs W B et al (1988) Occurrence of Clostridium tetani in soil and horses. S Afr Med J 73 (12), 718-720 PubMed.