Pork Feeding Sprouted Grain and Ergot Disease
Variable weather conditions within Western Canada can present challenges in acquiring a consistent volume of high quality feed grains. Rainfall during the harvesting period can result in bleaching and pre-harvest sprouting in some grains (barley, wheat). Can these sprouted grains be effectively incorporated into swine diets, and what impact is there on feed efficiency and growth rate?
Nutrient profile of sprouted barley does change. A study by Peer and Leeson examined spouted barley undercontrolled conditions. They reported decreased digestible energy levels resulting from starch being used as an energy source in the
sprouting process. Crude protein concentration, in partic ular lysine concentrations increased in the sprouted barley, and experienced lower concentrations of methionine, phenylalanine and threonine. Fiber concentration increased resulting from an increase in the number and size of cell walls during growth. Therefore, digestibility of nutrients decreased with increased sprouting time.
In an Alberta study (Plett and Ahrene) with grower pigs, sprouted barley did not differ significantly in average daily gain and average daily feed intake from non-damaged barley. However, the study did report lower digestibilities for
dry matter, protein and energy (3, 4 and 5% respectively).
The feeding value of sprouted wheat did not vary significantly from that of regular wheat in a French study.The results demonstrated that the feeding value of partially sprouted wheat was similar, or even better when compared toregular soft wheat.
Ergot is a fungal disease that most often affects rye and triticale, but may also affect barley and wheat. Oats is the least susceptible cereal grain. Many wild and cultivated grasses may also become infected with ergot. Ergot is of concern to pork producers because the feeding of contaminated grain can lead to significant production losses.
Infection and Life Cycle
Fungi of the genus Claviceps are responsible for ergot infection. The most common and most damaging species is Claviceps purpurea. The mycelium of the fungus attacks the ovaries of the infected plant, resulting in the formation of sclerotia or ergot bodies in place of grain kernels. These ergot bodies are dark in colour, have a rough surface and may be as much as four times as large as the grain kernels they replace. The ideal conditions for ergot contamination is a wet, cool spring. These conditions extend the flowering period, the stage when the plant is most susceptible to infestation.
Ergot sclerotia survive in and on the soil over winter. In the spring, the sclerotia germinate, producing spores which become airborne and infect grasses and certain crops. Grasses may act as a reservoir for ergot. However, sclerotia apparently
do not remain viable more than one year. Thus, certain agronomic practices may help to control ergot infection.
The ergot bodies contain ergot alkaloids and amines which, when consumed in sufficient quantity, cause health problems in both animals and people. The amines and alkaloids which are found in ergot produce clinical signs that are generally
the result of vasoconstriction and psychoactive activity. Ergot alkaloids cause a constriction of smooth muscle fibres and the walls of small blood vessels. This explains why ingestion of toxic quantities of ergot cause lameness and may ultimately
result in sloughing of hooves as well as the tips of tails and ears.
Animals can be affected either by feeding of low quantities of ergot for long periods of time, or by feeding higher levels for a shorter period of time. Clinical symptoms include reduced feed intake, convulsions, incoordination, respiratory distress, rapid pulse, salivation, vomiting, diarrhoea, tremors, abdominal cramps, physical and mental depression, pupils first contracted but later dilated, numbness and coldness of extremities.
In severe cases, gangrene may occur. Because ergot toxicity impairs blood flow to the extremities, the breeding herd is particularly affected. Pregnant sows may abort spontaneously, and nursing sows may dry up, seemingly overnight. Even if sows do not dry up completely, their litters often decline in vigour and growth, as milk production is impaired. When ergot toxicity has been diagnosed, and the source of infection removed, neurological symptoms may be reversed. Unfortunately, recovery from damage due to blood vessel constriction is less likely to be corrected. This is particularly true if gangrene is observed. Ergotism in humans is sometimes called St. Anthony’s fire, presumably due to the burning sensation which occurs in the extremities. It was not uncommon among humans in the Middle Ages, when contamination of rye flour lead to thousands of deaths. Ergotism in humans now is almost an historical anecdote, due to much more stringent controls in our food delivery system.
While ergot alkaloids are better known for their toxicity, they also have pharmaceutical properties. For example, ergotamine tartrate is used in the treatment of migraines. LSD, the drug made famous, is chemically related to one of the ergot alkaloids.
It is extremely important for grain to be visually inspected for ergot at the time of combining or delivery to the feed mill. Prior to grinding, the sclerotia are readily visible, and the degree of infestation determined. However, once the grain is ground, the only option is laboratory analysis for the ergotoxins. The level of ergot infection is relatively easy to determine in raw grain. A 500 g grain sample is weighed, the ergot sclerotia are then removed and weighed separately and finally, the portion of the sample which is ergot is calculated as a percent of the total sample weight. In the absence of scales, the number of sclerotia in a 1000 kernel sample can be counted as an estimate of ergot levels. For official grading of grains, dockage is removed prior to weighing. If the grain is to be fed with dockage included, then dockage should be included in the estimate of ergot content.
In Canada, the Canadian Grains Commission has developed a grading system that includes standards for ergot. To be graded No. 1, most varieties of wheat can have no more than 0.01 % ergot bodies and to be graded as No. 2, the maximum level changes to 0.02 %. Hulless barley is graded as Select CW/CE two row and six row if there are less than 3 kernels ergot bodies per 500 g grain sample. Grains with more than 0.04 % and less than 0.10 % ergot bodies are classified as feed grade. Because other factors affect grain grades, a sample may be classified as “feed” and have no ergot present. Use of Ergot-Infected Grain There has been very little recent research conducted on the impact of ergot on pig performance and health. The most common recommendation is to avoid ergot altogether in feeds destined for use in the breeding herd, and to limit the concentration of ergot in diets for growing pigs to 0.1%, or approximately 1 kernel per 1,000.
If ergot infected grain must be used, it should be diluted with clean grains or other ingredients to bring the total content in the diet to less than 0.1%. Thus, if a contaminated grain contains 0.3% ergot, it could make up one-third of the total diet and still fall within the 0.1% tolerance. However, even diluted grains should not be fed to the breeding herd. Gravimetric grain cleaning systems are able to remove ergot, at least to some extent. Other methods of detoxification of grains would be highly desirable.
However, there is no reliable evidence of the existence of products that bind or otherwise render ergot toxins inactive in livestock feeds.
Ergot control is aided by crop rotation. If the rotation cycle can include a noncereal or non-grass, the number of infectious spores will be reduced when cereal grains are planted in subsequent years. Deep tillage is also beneficial. Burying sclerotia more than 2” deep prevents the formation of infectious perithecia and reduces the spread of spores. Clean seed must be used to prevent direct contamination of the new crop. Also, mowing of grass in pastures and roadsides before flowering may be beneficial as it helps to break the life cycle of the ergot fungi.
Source: Prairie Swine Centre