Diagnosis > Equine

Aflatoxin

Aflatoxins are of concern in warm and humid climatic conditions.  Aflatoxins may be produced by certain Aspergillus species of fungi at environmental temperatures greater than 70 degrees Fahrenheit and at moisture levels greater than 14%.  Although aflatoxins are not considered to be a major problem in cold or more temperate regions, care should be taken in colder climates when using feedstuffs such as maize, soya beans, oilseeds and other cereal grains, imported from warm and humid countries.

Aflatoxins are difuranocoumarin derivatives produced by many strains of Aspergillus parasiticus and Aspergillus flavus. Aflatoxin B1, B2, G1 and G2 are the only naturally-occurring compounds with aflatoxin B1 being the most common and biologically active. Aflatoxins are found in feedstuffs such as maize in the field and also when stored. Crops however may become contaminated with aflatoxin in the field when environmental conditions are right.

The biotransformation of AFB1 to AFB1-2, 3-epoxide involves a series of metabolic reactions including reduction, hydroxylation, hydration an epoxidation. The AFB1-2, 3-epoxide is the most reactive metabolite and is thought to be responsible for somatic mutation and carcinogenesis (Fung and Clark, 2004). Aflatoxins are readily absorbed into blood from the gastrointestinal tract and accumulate in most soft tissues including liver, kidney and body fat depots (Harland and Cardeilhac, 1975). The absorbed aflatoxins are biostransformed enzymatically by cytochrome P-450 into various metabolites and are rapidly excreted in urine and faeces (Sawhney et al., 1973).

Although limited information is available concerning the susceptibility of horses, ponies and other equids to aflatoxins, clinical signs, symptoms and necropsy and histological changes are summarised in table 2.

Table 2: summary of clinical signs, necropsy and histopathological changes due to aflatoxin B1 exposure in horses

Age and stage of horses	Nature of study	Source of mycotoxin	Mycotoxin levels	Clinical signs, necropsy and histological changes	References
15-year-old Arabian stallion	Case report	Unknown	58.4% μg/Kg	Severe weight loss, icterus and anorexia.  Firm enlarged black liver, bile duct hyperlasia, and deposition of the hemosiderin pigments nad congestion of renal tubules.	Greene, H. J., and Oeheme, F. W.1976" Clin. Toxicol., 9,25].
Adult horses	Case report	Moldy hay	not available	Poor body condition and bilateral congestion of eyes.  Animals experience colic before death.  Hepatic necrosis, hyperlasia of bile duct, dgeneration of the renal tubules and fatty degeneration of heart.	McGavin, M. D., and Knake, R. 1977, Vet. Patho!., 14, 182.
7-year-old thorough- bred stallion	Case report	Maize	300 μg/Kg	Icterus, depression,shifting lameness and subcutaneous hemorrhage	Asquith, R. L., and Edds, G. T. 1981, Proc. Am. Assoc. Equine PrllCt., 26, 193.
6-month-old pony	Research trial	Purified aflatoxin B1	5 mg/Kg	Increased body temperature, respiration and heart rate after administration of aflatoxin.  Pony was lethargic, ataxic, laterally recumbent with convulsions and comatosed before death	Asquith, R. L., and Edds, G. T. 1981, Proc. Am. Assoc. Equine PrllCt., 26, 193.
12 weamling ponies	Research trial	Purified aflatoxin B1	5 mg/Kg	Increased temperature and heart rate, ataxia, convulsions and blood in the feces, abdominal straining death.	Asquith, R. L., and Edds, G. T. 1981, Proc. Am. Assoc. Equine PrllCt., 26, 193.
Ponies	Research trial	Pure aflatoxin B1	0 to 6 mg/Kg	Aflatoxin  B1and M1 were recovered in large quantites from feces and gastrointestinal contents of treated animals. Prothrombin time, packed cells volume, hemoglobulin, red blood cells values, aspartate aminotransferase and gamma glutamyltransferase were elevated.  Visceral petechial hemorrhages and focal lesions, and various degrees of hemorrhage in skeltal muscle.	Bortell, R. 1981, M. S. thesis, Univ. of Florida, Gainesville.

From Smith and Girish, 2008

 

The most common characteristics of equine aflatoxicosis are liver damage and bile duct hyperplasia (Asquith, 1985). This might be considered as one of the pathognomonic lesions of equine aflatoxicsosis because the same gross and histopathological changes are characteristic of aflatoxicoosis in other species.

The feeding of infected corn on a farm in Arkansas resulted in the death of three horses and many others suffered health problems. Investigations showed severe hepatic necrosis suggesting involvement of aflatoxin. Further feed analyses showed the presence of numerous colonies of Aspergillus flavus and chemical analyses showed the presence of aflatoxin B1 B2 and M1, resulting in a total aflatoxin concentration of 130µg/kg. heptatocellular degeneration and necrosis, multinucleated giant cells and megalocytes and diffuse periportal fibrosis were observed.

In addition ponies fed diets containing 2ppm aflatoxin per day showed higher levels of liver enzymes including GGT (gamma glutamyl transferase) indicating liver damage. There are reports of much lower concentrations of 0.3 ppm causing death in horses.

In all species, aflatoxins are hepatotoxic and carcinogenic with fatty changes causing hepatocyte degeneration, necrosis, and altered liver function. Suppression of liver protein synthesis is the main factor resulting in growth suppression. Aflatoxin is also known to interfere with vitamin D metabolism, contributing to reduced bone strength. By reducing bile salt production, aflatoxin negatively affects lipid and pigment absorption. Additionally the metabolism of other minerals including iron, phosphorus and copper are also affected by aflatoxin.
Horses may also be exposed to AFB1 through inhalation in addition to ingestion of contaminated feed.

Clinical signs of aflatoxin toxicity include:

• Loss of weight / loss of appetite
• Reduce feed conversion efficiency
• Immune suppression and increased disease susceptibility
• Reduced fertility 
• Liver necrosis
• Death

 

Intervention level

The maximum aflatoxin levels suggested for mature horses should not exceed 50ppb and breeding stock and working horses should preferably be fed aflatoxin free diets. Other tolerance levels cited suggest 20ppb (0.02ppm) and so there is a wide range of levels associated with clinical symptoms.