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Tetanus
Introduction
- Cause: Clostridium tetani.
- Signs: see below.
- Diagnosis: diagnosis is based on clinical signs.
- Treatment: see below.
- Prognosis: poor.
Public health considerations
- None.
Pathogenesis
Etiology
- Clostridium tetani Clostridium tetani are gram positive, anaerobic, spore forming rods which are ubiquitous in the environment, found in soil and are normal commensals of the ruminant gastrointestinal tract.
- Under the appropriate tissue anaerobic conditions and PH 7, sporulation can occur with the release of associated toxins tentanospasmin and tetanolysin causing the clinical signs associated with disease.
Predisposing factors
General
- A deep penetrating wound favouring anaerobic conditions.
- Dystocia Dystocia and retained fetal membranes Retained fetal membranes: removal.
- Surgical procedures where hygiene is compromised for example, castration Castration: surgical options.
- Sudden dietary change.
- Iatrogenic through the use of contaminated needles.
- Umbilical infection in neonatal animals through being born to an unhygienic environment Omphalophlebitis and omphaloarteritis.
Specific
- Poor hygiene during obstetrical or surgical interventions / procedures.
Pathophysiology
- Upon gaining entry to the body, often via a penetrating wound, tetanus spores remain quiescent until toxin production is triggered. An additional form idiopathic in origin has been described following a sudden dietary change where spore proliferation occurs within the intestinal tract (Thompson 1997).
- Two toxins are produced during the sporulation process, tetanospasmin and tetanolysin. Tetanospasmin causes the clinical signs attributed with disease, whilst tetanolysin is thought to facilitate tissue necrosis and promote favorable anaerobic conditions.
Timecourse
- The incubation period is extremely variable and does not reflect the speed of onset of disease.
- As C. tetani is ubiquitous it may reside within an animal for life without issue.
Epidemiology
- Normally only one or two animals are affected.
- However, outbreak situations have been documented in housed calves with no predisposing factors identified.
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.
- Niles G A (2017) Toxicoses of the Ruminant Nervous System. Vet Clin North Am Food Anim Pract 33, 111-138 PubMed.
- Mueller K (2015) Clostridial diseases in cattle and sheep. Cattle Practice 23 (1), 127-131.
- Otter A & Davies I (2015) Disease features and diagnostic sampling of cattle and sheep post mortem examinations. In Practice 37, 293-305.
- Harwood D G (2007) Clostridial Disease in Cattle: Part 2. UK Vet 12 (2), 21-24.
- Harwood D G & Watson E N (2004) Clostridial Infection In Young Cattle- An Update. Cattle Practice 12 (3), 219-227.
- Rings D M (2004) Clostridial disease associated with neurological signs: tetanus, botulism and enterotoxaemia. Vet Clin North Am Food Anim Pract 20 (2), 379-391 PubMed.
- Thompson R W (1997) Idiopathic tetanus in fattening cattle. Vet Rec 140, 435-436 PubMed.