Background and history

Under certain conditions fungi multiply on cereals, corn, cotton seed and other food materials sometimes producing chemicals called mycotoxins. The common fungi causing disease (mycotoxicosis) in the pig include species of Fusarium, Aspergillus and Penicillium.

The presence of fungi including recognised toxic species however does not necessarily mean that the toxins are present.

Fungi require adequate moisture, oxygen and carbohydrates to multiply and temperatures from 10°C to 25°C (50°F to 77°F). Multiplication may still take place however outside these ranges and crops that are already diseased are more likely to succumb to fungal infection.

Fusarium species require high levels of moisture and relative humidity (>88 percent) for multiplication and toxin production whereas Aspergillus and Penicillium multiply at lower levels.

Each requires precisely the right substrate and environmental conditions to produce toxins. Toxins are not destroyed by heating but modern treatments used in the processing of animal feeds such as temperature and pressure may reduce the actual fungal load. Because of the variable requirements for growth and toxin production, particular species tend to predominate in certain geographical areas.

Clinical signs

There are many variations of mycotoxicity, related to the type of fungus, the toxin produced and the amounts present.

Zearalenone or F2 toxin (Fusarium poisoning)

The most important strand is F2 toxin or zearalenone is produced by a strain of Fusarium graminearum which is found in maize.

It is an oestrogenic toxin and is produced in high moisture environments in maize growing areas well before harvest.

Clinical Signs

All pigs

• Rectal and vagina prolapses are common symptoms in the young growing stock.
• The most striking clinical feature is the swollen red vulva of immature gilts.
• Stillbirths

The other signs are dependent up on the levels present in the feed and the state of pregnancy.
These include:

• Returns >23 days.
• Farrowing early.

Boars

• Semen may be affected with feed levels above 30ppm but not fertility.
• At higher levels poor libido, oedema of the prepuce and loss of hair may occur.

Gilts (pre puberty, 1­–6 months of age)

• 1 to 5ppm in feed causes swelling and reddening of the vulva and enlargement of the teats and mammary glands. Rectal and vagina prolapses also occur in young growing stock.

Gilts (mature)

• 1 to 3ppm will give rise to variable lengths in the oestrus cycle due to retained corpora lutea and infertility.

Sows

• Levels of 5 to 10ppm can cause anoestrus, which may also be associated with pseudo pregnancy due to the retention of corpus luteum. F2 toxin will not normally cause abortion however, if sows are exposed during the period of implantation litter size may be reduced. In lactation piglets may develop enlarged vulva.
• Embryo survival to implantation does not appear to be affected at levels less than 30ppm but above this complete loss between implantation and 30 days occurs, followed by pseudo pregnancies. Low levels of 3 to 5ppm do not appear to affect the mid part of pregnancy, but in the latter stages piglet growth in utero is depressed, with weak splay-legged piglets born. Some of these may have enlarged vulvas.
• 3 to 5ppm has no effect on lactation but the weaning to service interval may be extended.

Aflatoxins (Aspergillus poisoning)

These toxins are common and their effects are dependent upon the dose and age of the pig. Toxins are found in maize, peanuts and soya beans.

Clinical signs

Sows

• Abortion.
• No milk – agalactia.
• Liver damage.
• Reduced performance.
• Immuno-suppression.

Piglets, weaners and growers

• Unlikely to be any symptoms other than poor growth.

Ochratoxin and Citrinin (Aspergillus and penicillium poisoning)

The fungi are found in oats, barley, wheat and maize.

Clinical signs

Sows

• Liver/kidney damage.
• Jaundice.
• Reduced performance.

Weaners and growers

• Reduced growth.
• Kidney damage.

Ergotoxins (Ergot poisoning)

These toxins are produced from the fungus ergot found in wheat, oats and rye grass. They interfere with blood flow.

Clinical signs

• Poor growth.
• Increased respiration.
• Depression.
• Reduced blood supply due to blood vessel contractions. Blue skin.
• Gangrene at extremities.
• Tail, ear necrosis.

Diagnosis

Diagnosis is usually based upon the clinical signs and demonstrating the toxin in feed.

This can often be frustrating because although clinical signs may be suggestive they are rarely diagnostic. It may be impossible to detect the toxin in the feed because of patchy distribution and/or the samples taken are toxin free.

The effect of the toxin may have been delayed and the feed containing the toxin has been consumed. Alternatively the laboratory may be testing for the wrong toxin.

Causes

Factors that may increase the likelihood of mycotoxins in feed:

• Cereals left over after screening.
• Damaged or broken grains.
• Storage of moist grain.
• Storage in warm damp conditions.
• Damaged leaking feed bins.
• Fluctuating environmental temperatures.
• Fungal growth in liquid feeding systems.
• The mixing of contaminated and uncontaminated grains.
• Allowing grains to heat.
• Prolonged usage of feed bins, feed bridging across the bin and development of moulds.
• The bridging of feed in bins over long periods of time and their sudden descent.
• Prolonged use of automatic feeders and retention of mouldy feed.

Prevention

Wherever a fungal toxin is suspected consider the following actions:

• Immediately replace the feed or cereal sources by alternate ones.
• Examine carefully the meal or pellets for evidence of fungi.
• Empty all feed bins out and examine for bridging of feed or presence of mouldy feeds. If feed bins are contaminated, empty them and treat with a non-toxic fungicide.
• Examine all automatic equipment and in particular feed hoppers and automatic dispensers for evidence of mouldy feed.
• If wet moist grain is stored, mould inhibitors such as propionic acid, calcium propionate or sorbic acid will prevent growth.
• Once mycotoxins have developed in feed there are no methods that can destroy them. However their effects can be mitigated by regrinding the feed and mixing with an alternate source at a ratio of 1:10 and feeding to growing stock on a test basis first.
• A feed sample should be sent to a laboratory for examination.
• Check other sources of poisoning, including straw and wet bedding materials.

Treatment

There is no treatment. Focus on preventative measures.