Bovis ISSN 2398-2993

Oak poisoning

Synonym(s): Oak toxicity

Contributor(s): Nicola Bates , Mark Burnell

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Introduction

  • Cause: ingestion of acorns, buds or young leaves of Quercus species. 
  • Signs: gastrointestinal signs (constipation, then hemorrhagic diarrhea, abdominal pain) and renal dysfunction.
  • Diagnosis: based on history of exposure, clinical signs and post-mortem findings.
  • Treatment: supportive.
  • Prognosis: recovery is rare once renal dysfunction is advanced.

Pathogenesis

Etiology

  • There are hundreds of species of Quercus  including deciduous and evergreen species extending from cool temperate to tropical latitudes in the Americas, Asia, Europe and North Africa.
  • Poisoning is seasonal and occurs in the spring with ingestion of buds or young leaves and in the autumn from ingestion of acorns. 
  • Individual response is very variable. Some animals are severely affected and others not at all. It is unclear why this is the case.

Predisposing factors

General

  • Undernourishment.
  • Lack of or inability to access other forage.

Pathophysiology

  • The exact mechanism of poisoning is not fully understood.
  • Tannins (polyphenolic complexes) or their metabolites are thought to be the cause of the effects seen.
  • It is postulated that ingestion of a large quantity of oak has an astringent effect on the gut increasing absorption of toxic compounds. 
  • Tannins are metabolized to toxic components which results in tissue damage at the sites of highest concentration (e.g. the kidney).  Damage to the gut is exacerbated by the effects of uremia. 
  • Tannin compounds may combine with protein in the cell membrane or nutrients going into cells to form a precipitate. This results in sloughing of the epithelial cells and plugging of the loop of Henle resulting in renal failure.
  • Gallotannins are also present and these are hydrolyzed to gallic acid and pyrogallol in the rumen. These compounds are nephrotoxic.
  • Tannins also reduce dry matter and fibre digestion which will reduce growth and performance.
  • Toxicity is not reduced by drying or freezing.

Timecourse

  • Variable.
  • Sudden death may occur within 24 hours.
  • In other cases signs occur 2-10 after the start of exposure.
  • Less severely poisoned animals may survive for weeks or months before death occurs.

Epidemiology

  • Widespread, for example oak poisoning has been reported in livestock in the US, Europe, South Africa, the Middle East, India, New Zealand and elsewhere.
  • Some animals acquire a taste for oak and may consume large quantities. 

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.
  • Pérez V, Doce R R, García-Pariente C, Hervás G, Ferreras M C, Mantecón Á R, Frutos P (2011) Oak leaf (Quercus pyrenaica) poisoning in cattle. Research in Veterinary Science 91 (2), 269-277 PubMed.
  • Dunn K (2006) Oak poisoning in cattle. UK Vet 11 (5), 1-3 PubMed.
  • Spier S J, Smith B P, Seawright A A, Norman B B, Ostrowski S R, Oliver M N (1987) Oak toxicosis in cattle in northern California: clinical and pathological findings. Journal of the American Veterinary Medical Association 191 (8), 958-964 PubMed.
  • Neser J A, Coetzer J A W, Boomker J, Cable H (1982) Oak (Quercus robur) poisoning in cattle. Journal of the South African Veterinary Association 53 (3), 151-155.
  • Caedrvall A, Johansson H E, Jonsson L (1973) Acorn poisoning in cattle. Nordic Veterinary Medicine 25, 639-644.
  • Yeruham I, Avidar Y, Perl S, Yakobson B, Shlosberg A, Hanji V, Bogin E (1998) Probable toxicosis in cattle in Israel caused by the oak Quercus calliprinos. Veterinary and Human Toxicology 40 (6), 336-340 PubMed.

Other sources of information

  • Burrows G E, Tyrl R J (2013) Toxic Plants of North America, 2nd edition. Wiley Blackwell, Ames, Iowa.
  • Cooper M R, Johnson A W (1998) Poisonous Plants and Fungi in Britain, 2nd edition. The Stationery Office, London.

Organisation(s)


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