Aflatoxicosis: A Source of food poisoning in Dogs


What is aflatoxicosis?


Aflatoxicosis is a disease caused by the ingestion of highly poisonous fungal toxins in food or food scraps produced by a group of fungi called Aspergillus. These toxins, in few micrograms per kilogram (µg/kg) concentrations, have adverse effects on both livestock and humans, with the liver being the principal organ affected [1]; [2] [3]. There are four toxins out of the 17 aflatoxins that are important in causing the disease in animals and humans. These are B1, B2, G1 and G2, with B1 being the most important [4]. The strains that produce this toxin are Aspergillus flavus and Aspergillus parasiticus on peanuts, soybeans, corn (maize), and other cereals either in the field or during storage when moisture content and temperatures are sufficiently high for mould to grow. Additional strains include M1 and M2. Acceptable and tolerable values range from 0.05 ppb to 0.5 ppb in different countries. The fungi grow both as field fungi (infecting grains pre-harvest) and storage fungi (infecting grains and grain products in storage). Animals are poisoned by eating mouldy grain or by eating mouldy grain products, e.g., mouldy bread [3].

Which animals are affected by Aflatoxins?

Aflatoxicosis affects growing poultry (especially ducklings and turkey poults), young pigs, pregnant sows, calves, cats, dogs, cattle, sheep, and goats. [3].

What are the symptoms of aflatoxicosis in dogs and cats?

1. Anorexia

2. Weakness (lethargy),

3. Depression,

4. Vomiting,

5. Diarrhoea (melena, haematochezia),

6. Bleeding (haemorrhage or haemorrhagic diathesis),

7. Icterus (jaundice)

8. Abdominal effusion (accumulation of fluid in the abdomen)

9. Peripheral oedema, and

10. Terminal encephalopathy [2].

How does aflatoxicosis develop in animals (pathophysiology)?

Of all the animals, dogs are the most sensitive to aflatoxicosis. In the dog, aflatoxicosis is usually acute to subacute (a few days) in contrast to the chronic aflatoxicosis reported in livestock. The aflatoxins are converted to their toxic components by a cytochrome P450 in the liver cells. The highly reactive toxic elements (epoxides) bind to and damage DNA, proteins and other macromolecules throughout cells. Hepatocellular (liver cell) degeneration and death (necrosis) ultimately leads to impaired liver function, including synthesis of clotting factors [3].

How is aflatoxicosis detected or diagnosed?

1. Client history: access to mouldy dog food, mouldy food scraps, or use of mouldy bedding.

2. Clinical signs: Weakness, depression, vomiting, diarrhoea, melena (blood in stool), icterus.

3. Diagnostic investigation: food analysis, and clinical pathology including haematology, clinical chemistry and urinalysis. Typical findings are elevated liver enzymes, hypoalbuminemia, hyperbilirubinemia. In severe cases, results include prolonged bleeding times, thrombocytopenia, elevations in bile acids [5].

4. Confirmation of diagnosis:

  • Discriminatory diagnostic features: History of exposure to mouldy food or bedding.

  • Definitive diagnostic features: demonstration of the mycotoxin in the food, stomach contents, or bedding is definitive.

  • Gross autopsy findings: Icterus, widespread petechial and ecchymotic haemorrhage, ascites, subserosal oedema of the gallbladder. In severe cases, extensive haemorrhage and massive liver necrosis, while in longstanding cases, liver fibrosis [6].

  • Histopathology findings: Hepatocellular degeneration and necrosis, fatty change, megalocytosis, biliary hyperplasia, hepatic fibrosis. Renal proximal tubular necrosis may also be present [2].

How is aflatoxicosis treated?

  • Gastric decontamination may be relevant if ingestion is recent.

  • Remove the source of aflatoxins.

  • Cage rest

  • Avoid trauma

  • Offer high quality, readily digestible diet, i.e. liver failure diet. the dog may require a special diet and care for the rest of its life

  • If icteric, protect the dog from UV light.

  • A blood transfusion may be required.

  • Depending on the extent of liver damage, Anabolic steroid therapy may enhance liver regeneration [5].

  • Fluid therapy

  • Vitamin K1

  • Antiemetics

  • Gastrointestinal protectants

NB: While aflatoxicosis is fatal in most patients with overt signs of intoxication, some dogs may recover slowly with long-term care.

How is aflatoxicosis prevented?

  • Do not feed table scraps or mouldy dog food to dogs.

  • Do not allow dogs to have access to garbage containing food scraps.

  • Do not use beddings for dogs that look or smell mouldy [6].

What causes treatment failure?

  • Substantial liver failure.

  • Fibrotic disrepair (cirrhosis) of the liver.

  • Fatal haemorrhage [8].

References


[1] C. Mutegi, P. Cotty and R. Bandyopadhyay, “Prevalence and mitigation of aflatoxins in Kenya (1960-to date),” World Mycotoxin Journal, vol. 11, no. 3, pp. 341 - 357, September 2018.

[2] R. Dalefield and P. Talcott, “Mycotoxicoses,” Vetstream Ltd, 2020. [Online]. Available: https://www.vetstream.com/treat/canis/diseases/mycotoxicoses. [Accessed 28 June 2020].

[3] G. D. Osweiler, “Aflatoxicosis.,” Merck Sharp & Dohme Corp, 2016. [Online].

[4] D. Dhanasekaran, S. Shanmugapriya, N. Thajuddin and A. Panneerselvam, “Aflatoxins and aflatoxicosis in human and animals.,” in Aflatoxins-Biochemistry and Molecular Biology, R. G. Guevara-Gonzalez, Ed., 2011, pp. 221-254.

[5] P. B., “Mycotoxins.,” The Veterinary clinics of North America. Small animal practice, vol. 32, no. 2, p. 409–419., 2002.

[6] Peterson and Talcott, Small Animal Toxicology., P. a. Talcott, Ed., WB Saunders Company, 2001, pp. 593-599.

[7] W. E. Huff, J. A. Doerr, P. B. Hamilton, D. D. Hamann, R. E. Peterson and A. Ciegler, “Evaluation of bone strength during aflatoxicosis and ochratoxicosis.,” Applied and environmental microbiology, vol. 40, no. 1, p. 102–107, 1980.

[8] Farlex Partner Medical Dictionary, “aflatoxicosis,” 22 June 2012. [Online]. Available: https://medical-dictionary.thefreedictionary.com/aflatoxicosis.

[9] G. D. Osweiler, in Toxicology., Philadelphia: Williams & Wilkins, 1996.

[10] K. H. Plumlee, Clinical veterinary toxicology., 6th ed., St. Louis, Mo: Mosby, 2004.


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