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Sweet potato poisoning

obovis
Contributor(s):

Nicola Bates

Mike Reynolds

Synonym(s): Sweet potato (Ipomoea batatas), Yam (North America – not related to the yam, Dioscorea spp), Kumara


Introduction

  • Cause: ingestion of moldy sweet potato tubers.
  • Signs: severe respiratory distress.
  • Diagnosis: based on history, clinical signs and ruling out of other causes of pneumonia.
  • Treatment: supportive.
  • Prognosis: poor in animals with severe respiratory effects.

Pathogenesis

Etiology

  • An herbaceous, perennial vine native to South America. It is cultivated in many countries for its large, starchy, sweet tasting tuberous roots that are an important root vegetable for humans .
  • The tuberous roots also used as cattle food, because of their palatability and high energy content.

Predisposing factors

General

  • Poor storage of tubers.
  • Inadequate alternative forage.

Pathophysiology

  • Ingestion of moldy tubers causes atypical interstitial pneumonia resulting from acute, diffuse damage to alveolar septa and subsequent influx of protein-rich fluid into the airspaces.
  • The toxic compounds in sweet potato are ipomeanols, which are generated by metabolism of damaged tuber tissue by certain fungi, particularly Fusarium solani and Fusarium oxysporum.
  • The fungi metabolize plant stress metabolites (3-substituted furans) such as ipomeamarone (itself a hepatotoxin) that are produced in response to mechanical injury, microbial infection or insect damage. This results in the production of several related furanoterpinoid toxins (ipomeanine, 1-ipomeanol, 1,4-ipomeanol, 4-ipomeanol).
  • All these compounds produce the same effect in the lungs of experimental animals, but 4-ipomeanol (1-(3-furyl)-4-hydroxypentanone) is thought to be the most important in sweet potato poisoning. These compounds are inactive until activated by pulmonary microsomal enzymes, which results in a toxic lung edema factor, which produces the pulmonary pathology observed in sweet potato poisoning. The fungi themselves are not toxic.
  • In mammals 4-ipomeanol is converted to a reactive metabolite via cytochrome P450 in the non-ciliated (Clara) bronchial epithelial cells in the lungs. In experimental animals, injection of 4-ipomeanol has been shown to cause extensive degeneration and necrosis of Clara calls. At higher doses both ciliated and non-ciliated cells are destroyed. It is tightly bound to tissue macromolecules and depletes lung glutathione without affecting liver or kidney concentrations.
  • Hepatic and renal damage has been observed in experimental animals. Hepatic damage is due to ipomeamarone and renal effects (tubular nephrosis and accumulation of intratubular debris) may be due to 1-ipomeanol and 1,4-ipomeandiol.
  • Cooking (baking or boiling) does not destroy the toxins.
  • Tubers that appear relatively undamaged can still cause poisoning.

Timecourse

  • Various time frames have been reported and onset is influenced by the extent of damage and fungal infection.
  • Poisoning could occur days after starting to eat a supply of sweet potatoes as the tubers start to degrade.
  • Clinical signs can occur within a few hours of ingestion of damaged potatoes, 24 h or several days after ingestion.
  • Recovery can take 4-12 days.
  • Death can occur within a few hours after onset of signs, and usually within 24 h.

Epidemiology

  • Sweet potato poisoning can occur anywhere the tubers are used as cattle. The risk of fungal damages to tubers is higher in humid, warm, wet weather.

Diagnosis

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Treatment

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Prevention

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Further Reading

Publications

Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Mawhinney I, Trickey S, Woodger N & Payne J (2009) Atypical interstitial pneumonia associated with sweet potato (Ipomea batatas) poisoning in adult beef cows in the UK. Cattle Pract 17 (1), 96-99 PubMed.
  • Fighera R A, Rozza D B, Piazer J V et al (2003) Pneumonia intersticial em bovinos associada à ingestão de batata-doce (Ipomoea batatas) mofadaPesquisa Veterinária Brasileira 23 (4), 161-166.
  • Medeiros R M, Simões SV, Tabosa I M et al (2001) Bovine atypical interstitial pneumonia associated with the ingestion of damaged sweet potatoes (Ipomoea batatas) in Northeastern Brazil. Vet Human Toxicol 43 (4), 205-7 PubMed.
  • Hill B D & Wright H F (1992) Acute interstitial pneumonia in cattle associated with consumption of mould-damaged sweet potatoes (Ipomoea batatas). Aust Vet J 69 (2), 36-37 PubMed.
  • Li X & Castleman W I (1991) Effects of 4-ipomeanol on bovine parainfluenza type 3 virus-induced pneumonia in calves. Vet Pathol 28 (5), 428-437 PubMed.
  • Doster A R, Mitchell F E, Farrell R L & Wilson B J (1978) Effects of 4-ipomeanol, a product from mold-damaged sweet potatoes, on the bovine lung. Vet Pathol 15 (3), 367-375 PubMed.
  • Boyd M R, Burka L T, Harris T M & Wilson B J (1973) Lung-toxic furanoterpenoids produced by sweet potatoes (Ipomea batatas) following microbial infection. Biochim Biophys Acta 137 (2), 184-195 PubMed.
  • Peckham J C, Mitchell F E, Jones O H & Doupnik B Jr (1972) Atypical interstitial pneumonia in cattle fed moldy sweet potatoes. JAVMA 160 (2), 169-172 PubMed.
  • Wilson B J, Boyd M R, Harris T M & Yang D T C (1971) A lung oedema factor from mouldy sweet potatoes (Ipomoea batatas). Nature 231 (5297), 52-53 PubMed.
  • Wilson B J, Yang D T C & Boyd M R (1970) Toxicity of mould-damaged sweet potatoes (Ipomoea batatas). Nature 227 (5257), 521-522 PubMed.

Other sources of information

  • Andrews T (2019) Sweet potato use and poisoning. In: Vet Times 49 (42) VetTimes.

Organisation(s)

  • ASPCA Animal Poison Control Center. Tel: +1 (888) 426 4435; Website: www.aspca.org.
  • Veterinary Poisons Information Service (VPIS). Tel: +44 (0)2073 055 055; Website: www.vpisglobal.com.
  • Animal and Plant Health Agency (APHA), the UK. https://www.gov.uk.

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