ruminant

 

 

Dairy cows and beef cattle are exposed to mycotoxins in a variety of ways:

• Growing pasture (fungal contamination of grasses)
• Silage
• Hay and straw (including bedding)
• Hard feed formulated with contaminated grain

Economic losses associated with mycotoxicoses include:

• reduced milk production
• poor fertility
•  increased somatic cell count (SCC)
• increased disease susceptibility
• reduced longevity.

In trials run with commercial dairy cows (Agovino and Andrieu, 2008a), exposure to mycotoxins resulted in losses in milk production of 1.5-2 l/h/d, increased SCC by 100,000 cells/ml and decreases of nearly 0.3% milk fat and 0.05% protein.

As ruminant diets generally include both concentrates and forages, which increase the risk of mycotoxin exposure compared with other animals that have less varied diets.

It has previously been thought that ruminants were not as affected by mycotoxins due to metabolism of these toxins in the rumen. However, although some detoxification may occur, the breakdown process can also result in the production of new and more toxic metabolites, making the problems more severe. Mycotoxin metabolism in the rumen is difficult to predict and is affected by the type of diet being fed to the cows. In general, the metabolism of toxins is more efficient at a more neutral rumen pH in comparison with acidic internal conditions, hence, cattle suffering from any level of acidosis will be more severely affected (e.g. those exposed to high grain diets, or lacking fibre in the diet).

Using a variety of feeds increases the probability of multiple mycotoxin contamination but decreases the risk of high mycotoxin concentrations because any one feed ingredient is diluted by the presence of other feedstuffs overall. This can be problematic, as sub-clinical mycotoxicoses can be much more difficult to diagnose.

 

 

Forage

The greatest exposure to toxins from moulds for cows comes from the forage they consume (grass, hays, silages). Most ruminants are maintained on pasture-based production systems around the world – where the climate permits such practises. Grazing systems are not safe from mycotoxin contamination - fresh grasses can be contaminated with several mycotoxins. These typically include fungal endophytes that produce mycotoxins, which protect the plant in some way, such as ergovaline and lolitrem B, as well as Fusarium mycotoxins, such as zearalenone or DON. Perhaps the most commonly recognised mycotoxicoses problem is that seen with Lolitrem infected ryegrass – which causes ‘ryegrass staggers’ (loss of co-ordination) in cattle.

Cattle are typically fed preserved forages (as silage) during times of the year when the grass growth is insufficient. Ensiled forages are more likely to harbour moulds and associated mycotoxins than dry forages, especially in poorly made silages where the fermentation and anaerobic conditions are not strictly controlled. Any silage showing signs of mould growth should be avoided.

 

Table 1. Identification of mould in silage (Mahanna, 2009)

Fungus	Mould colour	Associated toxin(s)
Penicillium	Green-blue	Ochratoxin, citrinin, patulin
Aspergillus	Yellow-green	Aflatoxin, ochratoxin
Fusarium	Pink-white	Zearalenone, DON, T-2, Fumonisin

 

 

 

Cheap Feedstuff

Other by-products (especially those that are moist or poorly kept) may harbour fungal contamination and include fruit pulp, palm kernel meal, copra and brewery wastes. As these materials are often handled in a wet form or are produced in poorer countries, where storage and management of materials is very basic, moulds have ample opportunity to grow and mycotoxins are often produced during storage and transport. In some countries, the use of these cheaper by-products has been limited for dairy diets, due to the high risk of mycotoxicoses, as well as the potential for contamination of milk.

 

 

Bedding

Although feed is the key vector bringing mycotoxins into the dairy production system and control strategies should focus mainly on optimising feed quality, cases have been reported where significant concentrations of mycotoxins have been introduced through the bedding. Straw quality should, therefore, also be considered as a risk factor especially in dry cows, which are fed below appetite and often consume straw bedding. Likewise, ‘store cattle’, maintained in barns ready for the spring market, can be affected by mycotoxins from deep litter straw systems.

 

Specific mycotoxins in dairy production

To effectively recognise mycotoxicoses, herds have to be carefully inspected for symptoms. Symptoms are often very general and can greatly vary according to the mycotoxins present, making proper diagnosis difficult. Careful recognition of symptoms and blood analyses in combination with adequate feed analyses, provide the most accurate diagnosis of mycotoxicoses.

 

 

Orchratoxin

Ochratoxins are produced during storage of feedstuffs by different fungi and are found in both temperate and tropical regions. Ochratoxin A is the most prevalent of the ochratoxins.  The primary effect of ochratoxin A is damage to kidneys (nephrotoxicity). In a correctly-functioning rumen, this toxin is known to be rapidly degraded and can, therefore, be assumed to be a lesser threat to cattle compared with other mycotoxins.

 

Clinical signs of ochratoxin toxicity include:

• Pulmonary oedema
• Increased mortality at very high inclusion levels (e.g. 3ppm)

 

 

Aflatoxin

Aflatoxins are of greatest concern in warm and humid climatic conditions. Although aflatoxins are not considered to be a major problem in cold or more temperate regions, caution must be exercised in colder climates when using feedstuffs imported from warm and humid countries (especially poorer countries producing by-products for cattle feed). Aflatoxins damage DNA, leading to cell death or its transformation into a tumour (cancer). Due to the transfer of aflatoxin into the milk (1.7% of dietary aflatoxin B1 is transferred as carcinogenic aflatoxin M1 in milk) most countries have regulated aflatoxin and have set upper legal dietary limits.

 

Clinical signs of aflatoxin toxicity include:

1. Reduced weight gain
2. Reduced milk production
3. Decreased feed intake
4. Decreased feed conversion efficiency
5. Reduce fertility
6. Mortalities at very high exposure levels gain
7. Liver lesions with congestion and bleeding
8. Fatty acid accumulation in the liver, kidney and heart leading to encephalopathies and oedemas.

Trials conducted in Italy with commercial dairy buffaloes (whose milk is used in Mozzarella cheese production) showed how aflatoxin M1 levels were elevated in the milk and affected other aspects of milk production in animals fed contaminated maize silage and ryegrass hay (Agovino and Andrieu, 2008b). The trial demonstrated how the use of Mycosorb™, a proven and effective toxin binder, reduced SCC counts from 247 to 219 x1000 cells/ml, increased milk yield by 0.13 l/h/d and reduced M1 in milk from 10 to 5 ng/kg milk (see below).

 

Figure 1. Effect of using a mycotoxin binder on M1 in buffalo milk (Agovino and Andrieu, 2008b)

 

 

Trichothecenes

Trichothecenes: T-2 toxin, diaceptoxyscripenol (DAS), deoxynivalenol (DON), HT-2 toxin

Trichothecenes are common ‘field’ toxins found on grain. They are produced on crops and enter the feed via contaminated ingredients. They can contaminate ruminant diets via concentrate or forages, although they can be partially metabolised in the rumen. As seen for ochratoxin, their breakdown can be inhibited by acidic rumen conditions (low pH). Research has shown differences in susceptibility between breeds, species and management systems, for example, beef cattle and sheep are more tolerant to DON consumption than dairy cattle.

Clinical signs of trichothecenes toxicity include:

• Reduced feed intake
• Reduced weight gain
• Reduced milk production
• Diarrhoea
• Emesis
• Reproductive failure
• Mortality
• Gastro-enteritis and lesions
• Intestinal haemorrhage

 

 

Zearalenone

Zearalenone often occurs in combination with DON in naturally contaminated cereals or in forages. This toxin mimics the activity of hormones (as an oestrogen analogue), which causes the majority of the reproductive-related symptoms seen, especially in pregnant animals. Zearalenone is partially metabolised in the rumen to alfa-zearalenol and, to a lesser extent, to beta-zearalenol. These breakdown compounds have shown no toxic effects on rumen bacteria, however, alfa-zearalenol is about four times more oestrogenic than the parent mycotoxin and so this rumen-mediated transformation actually causes greater toxicity. The rate of zearalenone transfer into the milk is low and is currently thought to present no real risk to consumers of dairy products.

 

Clinical signs of zearalenone toxicity include:

1. Abortions
2. Decreased embryo survival
3. Infertility and mammary gland enlargement of virgin heifers
4. Oedema and hypertrophy of the genitalia in pre-pubertal females
5. Vaginitis
6. Vaginal secretions
7. Feminisation of young males
8. Infertility of young males

Research trials with veal calves fed high grain diets contaminated with DON and Zearalenone showed that these animals appeared to able to handle a moderate level of exposure without suffering ill effects (Martin et al., 2009).

Other work conducted using dairy cows have shown that feeding a total mixed ration contaminated with DON (3.5 mg/kg dry matter in trial TMR versus 0.5 mg/kg in uncontaminated control diet) had an impact on metabolic and immune parameters (Korosteleva et al., 2009). The contamination was not severe enough to induce changes in milk production, so could be considered as proof of the negative impact of mycotoxicoses at sub-clinical levels of exposure. The researchers found that, although there was no significant loss in any milk production of feed intake seen for the cows, significant changes in the efficiency of the immune system (when tested by vaccination) were apparent and the cows drank less, resulting in changes in blood serum characteristics.

 

Table 2. Effect of feeding Fusarium contaminated feed to dairy cows on immune and metabolic parameters (Korosteleva et al., 2009)

Parameter	Control	Contaminated	P value
Phagocytotic activity (%)	64.0	53.3.	0.03
Primary antibody response (rel units)	0.86	1.15	0.028
Serum sodium *	138.7	141.6	0.02
Serum osmolarity *	275.9	281.2	0.02

*Measures of dehydration due to decreased water intake

 

 

 

Fumonisin

Fumonisins occur world-wide in feedstuffs. In contrast to other mycotoxins, fumonisin B1 (the most prevalent of the fumonsins) is relative slowly and poorly metabolised in the rumen. Despite this, fumonisin does not seem to affect rumen metabolism. Target organs damaged by these mycotoxins in ruminants include the liver and the kidney.

 

Clinical signs of fumonisin toxicity include:

• Reduced feed intake
• Reduce weight gain
• Reduce milk production
• Increased liver sphinganine : sphingosine ratio (biomarker

 

 

Patulin

 

Patulin is produced by certain fungal species of Penicillium, Aspergillus and Byssochlamys growing on fruit, including apples, pears and grapes. Fruits stored under conditions that promote bruising and rotting increase the probability of patulin formation. Penicillium expansum appears to be the mould usually responsible for patulin in apple juice and may contaminate the apple pumice waste sometimes used in animal feed.

Patulin was first isolated in the 1940's but is now known to occur world-wide in apple and apple products. Its potential danger to cattle is its presence within fruit pulp and waste products from the fruit industry. These can form a cheap feedstuff for inclusion in ruminant diets. Some fruit material is used as a flavouring agent – especially in cows, which are highly sensitive to changes in flavour, where fruit-based material is used to mask certain taints caused by e.g. medication.

The principal risk arises when unsound fruit is used for the production of juices and other processed products. Contamination with patulin has also been reported in vegetables, cereal grains and silage. Patulin, however, is not considered a particularly potent mycotoxin. The LD50 in rats has been reported as 15 mg kg1 body and 25 mg kg1after sub-cutaneous injection. Death was usually caused by pulmonary oedema. In long-term studies at lower dosage levels, these effects were not observed. It has also been shown to be immunotoxic and neurotoxic. Several studies have found that patulin is genotoxic, i.e. that it causes damage to DNA or chromosomes, in short-term studies. However, these studies were performed in bacterial or mammalian cell cultures and with doses of the toxin that are not relevant to human exposure levels. Based on reproduction and long-term carcinogenicity studies in rats and mice, the JECFA allocated a Provisional Tolerable Weekly Intake of 7 µg/kg body weight

Symptoms of patulin toxicity include haemorrhaging in the digestive tract in cattle. In 1954, patulin was implicated in the deaths of 100 cows in Japan that ate contaminated feed.

 

 

 

Symptoms

What are the symptoms of mycotoxins in your dairy herd?

It's nothing that you can quite put your finger on, but...

1. The cows don't seem to be milking quite as well as they should be
2. The dung is a little loose and variable
3. The butterfat is a bit lower than it could be
4. The cell counts have crept up and the fertility seems to be getting worse

A healthy rumen has an ability to protect against low levels of some mycotoxins, but not all, and the situation can be complex.

 

Common effects of mycotoxins

1. Variable feed intakes
2. Inconsistent milk yield
3. Reduced fertility
4. Scouring
5. Acidosis-type symptoms
6. Lethargy
7. Impaired immune function/poor response to disease or infections
8. Poor rumen function
9. Muscle tremors
10. Bloody faeces
11. Lower leg / teat swelling
12. Unsettled cows
13. General poor performance without any alternative explanation

Symptom: Swollen hock




Are there safe levels of mycotoxins for dairy?

Some of the factors that make diagnosis difficult also contribute to the difficulty of establishing levels of safety. Mycotoxin effects are moderated by factors such as sex, age, duration of exposure and environmental and production stresses.

One area of particular concern is that a low level of several mycotoxins can be more problematic than high levels of an individual mycotoxin, due to a synergistic relationship. So even if the feed samples tested come back as being ‘low’, there may still be an issue.

Partial degradation of certain mycotoxins in the rumen does mean that they are less toxic to cattle than to most other animals but some of these degradation products can be more toxic than the original mycotoxin.

 

Are dairy products contaminated when dairy cattle consume mycotoxin contaminated feed?

The majority of human health risk from mycotoxins is from the consumption of contaminated grains and nuts. Several mycotoxins have been shown to occur in the milk of dairy cattle, though concentrations are extremely low. Other than aflatoxin, they are not considered likely human health hazards in milk.

 

 

Silage

 

Managing silage to reduce mycotoxins exposure

In any fermentation storage system, temperature and the presence of moisture is sufficient for toxin production. But oxygen will act as the switch, which turns mycotoxin production on or off during storage. The amount of mycotoxin in contaminated silage samples increases as the ensilement method changes from airtight, upright silos to concrete capped and uncapped silos. The highest forage concentrations of mycotoxins are found in horizontal storage methods, such as bunker silos and feed piles, which are left open to oxygen.

Greater amounts of mycotoxins are found where there has been poor management of the upright or bunker silo, as this results in oxygen entering the stored feed. In scientific studies, well managed bunker silos, covered with plastic and weighted with tyres, did not have significantly greater levels of mycotoxins than well managed upright silos. In a plastic covered storage system, oxygen penetration is slowed but not eliminated. The longer the silage is stored, the greater the opportunity for significant fungus growth and mycotoxin contamination. In one study the levels of DON increased in the silo slowly over time even when properly covered.

There is no such thing as an oxygen-proof silo. We would all like to think this is true but, in practical terms, our current technologies are not perfect. If you examine a plastic layer under a microscope, you will see many tiny holes through which oxygen slowly flows. This is especially true of plastic that is stretched for wrapping bales. Any damage to the plastic further increases the flow of oxygen from a trickle to a river and must be repaired as quickly as possible.

 

A checklist of practices to prevent mycotoxin contamination in silage:

1. Purchase corn and other feed varieties resistant to foliar, ear rot, and stalk rot diseases
2. Purchase varieties resistant to ear and stalk boring insects.
3. Harvest corn and haylage at the recommended maturity and moisture level for your     storage system. DO NOT let corn stand in the field after reaching maturity
4. or killing frost.
5. Be sure chopper knives are sharp and cut at the correct length to improve packing
6. Harvest forages as quickly as possible and pack tightly with the proper weight of tractor matched to the right number of packing hours and filling rate.
7. Be sure the silo is sealed to exclude oxygen. Use plastic covers secured by tyres on bunkers.
8. Patch any holes in plastic covers, bags, or wrapped bails as soon as possible
9. Discard obviously spoiled feed or layers of feed.
10. Since mycotoxins are highly soluble in water, do not allow rain to wash through upper layers of spoiled feed.
11. Clean out leftover feed from feeding bunks regularly.
12. Consider the use of an inoculant in silage or acid additive in high moisture corn to enhance fermentation and control during storage.
13. Match the rate of feed removal from the silo face to the size of the herd. For example bunker silo faces should be removed at four to six inches and upright silo face at three to four inches per day. Use the higher rate during the warm seasons.
14. When confronted with a toxicity problem, stop feeding the contaminated feed.
15. In consultation with your veterinarian or nutritionist, consider the use of a mycotoxin adsorbent to be mixed with the feed. Contact your Alltech representative for more information.

If problematic levels of mycotoxins still occur despite preventative measures being taken in both field and silo, the only safe solutions are dilution or, preferably, complete removal of the contaminated ingredient. It must be remembered that dilution of contaminated ingredients is illegal in some markets and it is often not practical to completely remove certain ingredients due to associated cost.