Sweet potato poisoning

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 cells. 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 for cattle. The risk of fungal damages to tubers is higher in humid, warm, wet weather.