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SPECIALS & CLOSEOUTS

NITRATES

Why should we be concerned about nit­rate problems? After all some authorities state that nitrates are of little consequence and we should ignore them. The other extremists accuse nitrates of being respon­sible for everything that happens from mastitis to death losses and everything in between.

Neither position is correct. One can nei­ther ignore nitrates nor blame nitrates as being directly responsible for all his prob­lems. However, for too long, we have been guilty of overlooking some of the chronic difficulties, particularly in dairy herds that are directly traceable to nitrates as the primogenitor. If animals ingest an acute level of nitrates, the effects are swift, there will be a high mortality rate. However, if animals are constantly sub­jected to a chronic level of nitrates in their daily diet, the results may not be as dramatic but are nonetheless, devastating, especially economically.

In a dairy herd the noticeable symptoms of a chronic nitrate problem is a reduction of milk yields. This, for no apparent reason. Secondly, problems may be encounter with reproduction. In-calf percentages drop. The number of insem­inations per cow in rises dramatically. Calves born apparently healthy may be dead in two or three days. The incident of stillborn calves will increase. All this may occur without any visible symptoms being manifest in the dam. However, later it may be noticed that the cows have ketosis more frequently and more contract pneumonia and other respiratory diseases, especially during cold weather. There are logical explanations for all such occurrences. If the rumen cannot convert the nitrates fast enough, nitrites are formed which enter the blood stream where they cause methemoglobinemia; and if severe enough, death ensues from anoxia. What is not too well understood are some other effects which occur when animals ingest nitrates over a long period. One of the main effects is that the thyroid gland becomes hypertrophied. As the thyroid gland is the governing body for the regulation of the metabolic functions, it then becomes apparent why we encounter more frequent ketosis and lowered bodily resistance to respiratory diseases.

To get things into perspective we must go right back to the beginning where all things are created. The world and life around us could be said to be divided into three major categories, Animal, Vegetable and Mineral.

Each has a specific role to play in the overall scheme of things. Obviously the largest of the three kingdoms is mineral. Included in this kingdom is soil. Soil in its truest sense contains elements of all three kingdoms and could be classed as a junction between the living and the dead. While the greater bulk of soil is composed of non-living minerals, a healthy soil is teaming with life of both vegetable and animal, as well as any plants that may be growing in it at the time. We usually refer to these life forms as bacteria, yeast and fungi. Also present are many forms of animal life including microscopic unicell­ular ones as well as nematodes and earth­worms which are all natural inhabitants of the soil. The vegetable and animal kingdom representatives in the soil aid in making many of the non-living mineral elements available to plants growing in the soil. Time does not permit a detailed study of the intricacies of these processes; it is a study in itself.

Of the three kingdoms, only the vegetable kingdom has the ability to make food. Plants can literally manufacture carbohy­drates fats and proteins from carbon, hydrogen and oxygen obtained from air and water, plus nitrogen obtained from the air and the soil using sunlight as an energy source. Chlorophyll is the catalyst to trigger this action.

Not only do plants produce carbohydrates fats and proteins from such simple and readily available raw materials; they also produce a fantastic array of very complex chemicals. Hence, we look to plants not only for food but for fibre, fuel, drugs, dyes, antibiotics and a host of other categories too numerous to mention.

Animals cannot make their own food, let alone make a surplus for use by others. Animals are dependent upon plants for

food. Not until you reach a limited and specialized group of animals called carnivores, do you find those that derive their food from eating other animals.

Other differences between plants and animals are evident. What about control of vital functions? In animals they are controlled by a nervous system. Plants are regulated and controlled chemically. Herein lays one of the reasons for a nitrate problem.

Plants take nitrogen from the soil in the form of NITRATE. (NO3) By means of a plant enzyme known as Nitrate Reductase, the nitrate form is broken down into a lower oxidized state. Other enzyme systems then further reduce the highly oxidized form of nitrogen to NH2 and NH3. From this form of nitrogen the plant can proceed with the building of amino acids and proteins provided there is an abundance of nitrogen, carbohydrates and energy.

Nitrate Reductase is an enzyme contain­ing iron in its molecular structure. There­fore iron must be present and available in order for this system to function. Also experimental evidence has indicated that potash, while not part of the Nitrate Reductase molecule, must be present in abundance if the convert ion of nitrates is to take place at anything like the normal rate. It is as if the system must operate in a high flux of potassium ions. Potassium is a catalyst and is essential in the combining of amino acids to full proteins. it is indispensable to this reaction. It is quite possible that other ions as well are needed in this reaction. However as the application of potassium and iron have succeeded in reducing nitrate content of plants to zero levels, in some cases, it would appear that any other ions would assume only minor roles.

We have established that in the plant the reduction of nitrates to ammonia is accomplished by a system of enzymes. Enzymes are very specific in what they do. Each enzyme has only one function. Further, the conditions under which it performs that function, best are also very specific. For instance, the temperature must be right, the pH of the substrate must be right, the minerals essential to its processes must be present and in sufficient supply to their requirement. In other words all variables must be right for the enzymes to produce a maximum yield of its particular product. The chemical, phy­sical and biological status of the soil that the plant is growing in must be correct so that there is no plant stress.

As enzymes are so specific in their requir­ements, we can understand why plants, under adverse conditions, can become toxic to grazing animals. Such things as mineral imbalances, shading, crowding, wet and cold weather, hot and dry weather, compaction etc. can all have an adverse effect on the enzyme system, upsetting nitrate conversion. Nitrates not converted will remain in the plants system building up to toxic levels. As nitrates concentrate mostly in the stems, less in the leaf and least in the fruit, it is the forage animals such as cattle that are affected by nitrate build up.

To sum it up, nitrate problems are caused by stress. Stress can be caused by many things. We have already mentioned a few, such as too much water, not enough water, crowding, shading etc. Stress can be poor plant nutrition due to the lack of or shortage of minerals. In our experience, this constitutes the greatest single source of stress. Fortunately this problem can usually be fixed. Correcting weather stresses is limited.

Certain other types of stress-producing conditions should be mentioned. Luxury use of nitrate-containing fertilizers is certainly one major cause. Another cause is the accumulation of large amounts of animal manure on the soil. Animal manure is high in nitrate nitrogen. Another stress source is weed killers and herbicides such as 24D and 245- T, but particularly the auxins or plant hormone type. Auxins are plant hormones that promote growth. The hormone causes a plant to literally grow itself to death by depleting all its energy reserves, such as stored carbohydrates. This is an extreme source of stress. All other vital life functions comes to a halt, and no nitrates are converted. The nitrate may even become doubly high from two causes. Not only is the nitrate conversion slowed down or even halted, but the actual rate of uptake from the soil may be greatly in­creased in an attempt by the plant to meet the increased demand for nitrogen and all other nutrients.

ATMOSPHERIC NITROGEN GAS (N2)

It will be seen that a nitrate problem can be the result of (1) stress: slowing down nitrate conversion rates; (2) an excess of readily available N. in the soil: allowing rapid uptake of nitrates in excess of the plants conversion capabilities, even though healthy; (3) a deficiency of iron or potas­sium in the reductase enzyme. Another cause of nitrate build up is tied to natural events or diurnal-nocturnal fluctuation. At night, the plants rest. Their respiratory functions, transpiration rates and photo­synthetic processes either cease or are greatly reduced. This means that some work is left undone at night, such as converting nitrates. In the meantime, the plant continues to absorb nitrates from the soil; some authorities believe that this build up of nitrates destroys the entire Vitamin A. If this is so it could explain the reproductive problems bought on by high nitrate levels.

Lowered resistance to disease, and ill thrift, can be blamed in part on the fact that nitrates are lowering the blood's ability to carry oxygen. If the oxygen­ carrying power of the blood is reduced too much, cellular tissues die, and eventually the animal succumbs. If the nitrate levels are not high enough to kill the animal outright, but keep the oxygen-carrying capacity of the blood at a below-normal level for a prolonged period, many compli­cations will set in. These include reduced resistance to disease, lack of protection against other forms of stress particularly in cold weather. In fact the animal would have an induced and chronic anemia.

Correcting the source of stress depends on controlling the amount of residual nitrates in the plant. But what do we do when faced with a whole season's production of a forage or roughage which has a high nitrate content? Is there anything we can do? Fortunately there is. However, as with most cases of this kind where we treat symptoms instead of curing the cause, the treatment is expensive. We list below some adjustments that must be made in the total ration if faced with high-nitrate roughage as the only source of fibre.

1. Raise the energy in the ration.

2. Raise the Vitamin A levels.

3. Raise the iodine content of the ration. 4. Eliminate urea from the ration.

5. Eliminate tetracycline antibiotics from, the ration.

These five adjustments will help to greatly increase an animal’s ability to tolerate high-nitrate roughage.

There is a level of nitrate beyond which nothing will help. However, we wish to make one point perfectly clear. There is no such thing as anyone particular level of nitrates which can be considered safe. Toxicity depends entirely upon the plane of nutrition, both past and present. We have seen animals die which were eating nothing but poor quality Bermuda grass pasture with a nitrate level of only 500

ppm. (0.9128%) with no ill effects other than poor weight gains. It all depends upon the energy levels, carbohydrates, vitamins and minerals in the ration. We have not seen any cases where animals could tolerate nitrate levels in the range of 1,000 ppm. of NO3 (1.63% KNO3) regardless of the type of ration. Therefore raising energy levels of feed is a good protection against nitrate toxicity.

Regarding the second recommendation, we have pointed out that high nitrates destroy or render inactive Vitamin A. We are also aware of the necessity of Vitamin A in rations. When feeding high-nitrate roughage, it is not uncommon to raise the Vitamin A levels to 5 to 10 times higher than NCR (National Research Councils) recommendations.

The reason for raising iodine levels in the ration is to protect the thyroid gland against hypertrophy. This reduces the secondary effects such as onset of ketosis and other metabolic dysfunctions.

With regard to the last two recommen­dations (No’s 4 and 5), these two are negative in character. The first three are positive. Also these last two are somewhat controversial in nature. Suffice it to say,

that if practiced, greater results will be obtained. Actually, the two are somewhat akin as we shall see below.

Urea is broken down in the rumen into ammonia and carbon dioxide very quickly. Quite literally, this is true if hydrolyzed. The carbon dioxide gas is eliminated by the bovine's eruction mechanism, but the ammonia can be converted by certain bacteria and protozoa in the rumen into useful amine acids if given sufficient time. Other conditions necessary are an adequate supply of carbohydrate energy and certain key minerals such as sulfur, Zinc, iron and cobalt. As the rate of release of ammonia in the rumen from urea is rapid, and the rate of tie-up of this ammonia by certain rumen microorganisms is slow, there occurs a buildup of ammonium ions in the rumen.

Also in the rumen are present other types of bacteria which possess the ability of converting nitrates to nitrites, nitrites to hydroxylamine and hydroxylamine to ammonia which is then used by the aforementioned microorganisms to pro­duce useful amino acids. However, if the concentration of ammonia from urea is already high in the rumen, the conversion of nitrates to ammonia is blocked at the nitrite stage. This situation is in accord with a well-known chemical principle known as solubility product constant (KSP) or "common ion effect." In simple terms, it states that if there is already a surplus of a certain ion present, the system will not accept any more of that particular ion, as "enough is enough." What nitrates are present are converted to nitrites and not ammonia and as nitrites are ten times as toxic as nitrates, we can begin to see the dangers involved in feeding urea in conjunction with a nitrate containing roughage. Many cases are on record where­in animals were able to get along fairly well on a nitrate-containing roughage until urea was introduced into the ration, then they died; not of urea poisoning, as such, but of nitrate poisoning outright. Urea, then, can complicate a nitrate problem.

Now for the last recommendation (No.5) which states that we remove any tetracycline-type antibiotics from the ration. Reference was made above to certain bacteria in the rumen which can convert nitrates to ammonia in a series of steps. These are all Gram-negative notile rods. This happens to be the group that is most sensitive to the effects of tetracycline type antibiotics. So, by its use, what happens is that you are eliminating the only built-in defense system the animal has against nitrates.

We are speaking here particularly about the custom of feeding tetracycline-type antibiotics daily in the ration at a sub clinical level. We are not an advocate of such a practice for several reasons apart from the reason explained above. Apparently the FDA agrees as the practice is not condoned by them, either. We are not condemning the use of tetracycline-type antibiotics. They are wonderful indeed and in many cases they have been responsible for saving the lives of countless thousands of livestock and humans. What we are saying is that they should be saved for use against the day when a real outbreak of disease occurs whereupon their use will be more effect­ive due primarily to the fact that no resistance by bacteria will have been built up against them as would be the case if these same antibiotics has been fed daily over a long period of time.

No discussion of nitrates would be complete without mentioning water. Large animals, especially cattle, and more particularly dairy cattle, can consume large quantities of water. Any farm boy who ever had the chore of watering the family milk cow on a hot day can attest to this fact. While the level of nitrates and nitrites in water may be small in compar­ison to levels found in feedstuffs, by sheer volume alone the total nitrate intake from water may be quite significant. It is not uncommon for a dairy animal to drink 50 gallons of water on a hot day. If this water has a nitrate-nitrite content of 100 p.p.m. we are talking about a total intake of nitrates from water alone of very nearly 19 grams of nitrates. To be the equivalent of this same amount from 20lbs of dry matter feed, the total nitrate content of that feed would have to be 2086p.p.m. N03 or 3400% KNO3. If the water were 150 ppm. or 200 ppm. N03 then we can begin to appreciate what would happen. To further compound the situation, let us assume that the water does contain as much as 100 ppm total nitrates, and the feed contains around 2,100 ppm total nitrates and that the animal eats 20lbs of such roughage on a dry matter basis. Such an animal is ingesting a total of nearly 38 grams of nitrates expressed as NO3 or nearly 62 grams expressed as KNO3. now suppose further that there is urea in the grain portion of the ration. What do you suppose will happen? Suppose further that the owner notices his animals are sick and decides they need medication, so he uses a tetracycline-type antibiotic. He does not raise energy, Vitamin A or iodine in the ration. Will these animals be more resistant to diseases such as pneumonia? Can they endure cold weather stress? Will his veterinary bills be reduced? Will his milk cheque pay for all the extra problems he has encountered? .

Diagnosis of a nitrate problem can best be accomplished by an appreciation of the level of nitrates being ingested from all sources, in both feed and water. This can best be done by laboratory tests. Tests are now available which can differentiate between urea poisoning and nitrite poisoning where both are being ingested. What is needed in addition to feed and water samples is a sample of well-oxalated venous blood drawn from an affected animal and a sample of the rumen contents of that same animal. Samples of blood and rumen contents are useless if taken as much as 2 hours after death.

The visual symptoms of nitrate poisoning are not always absolutely definitive as many other causes can produce the same effect. In acute nitrate poisoning, the cause of death is anoxia, but then several other things can produce anoxia such as cyanide poisoning.

Postmortem findings are also vague and indefinite. Typical gross pathological findings may include mild congestion in the gut with some inflammation of epithe­lial tissues. There may be petechial hemorrhages in lungs and heart, but many other things can cause these same symp­toms. Only good laboratory analysis can be relied upon to get a "feel" for nitrate involvement. In addition to laboratory test results, some idea about the feeding regimen must be used as collateral information. What was the energy level? What was the Vitamin A level? What was the iodine level? Was urea being fed in any form? Were tetracycline-type antibiotics being used? Had pastures recently been fertilized or heavily manured? What about the water supply? Could it be contaminat­ed from runoff from a farm above that has received urea or where cattle may have contaminated the supply? Is the soil texture such that percolation of manure-contain­ing cow excretory in the water could easily get into the water-bearing strata that supplies the well? Is runoff a problem in the pond or tank or dam where animals drink? These and other questions are pertinent to an accurate diagnosis of a nitrate problem, in addition to the laboratory tests.

Prophylaxis for nitrates includes the removal of the source or at least the dilution of the source as greatly as poss­ible with either feed or waters of as low nitrate content as possible. Also the administration of 250 cc's of 2% ethylene blue in glucose solution intravenously and repeated if necessary every 48 hours is of benefit in acute cases. Great care must be exercised in accurately diagnosing a true case of nitrate poisoning. As mentioned earlier, cyanide can also produce anoxia. The prophylaxis for cyanide poisoning includes the admin­istration of a solution of sodium nitrate intravenously. What happens if we are faced with a case of nitrate poisoning wherein we already have too much nitrite in the blood stream converting oxyhem­oglobin to methemoglobin, and we assume the animal is dying of cyanide poisoning and administer sodium nitrite? Death follows swiftly and surely!

In summary we have:

1. Introduced the problem of nitrates and their origin.

2. Discussed the problem of nitrates in livestock feeding.

3. Discussed the cause of nitrates, namely stress.

4. Discussed the cure for the problem, or relieving stress.

5. Recommended remedial measure.

6. Discussed diagnostic techniques and prophylaxes.

7. Warned against making the wrong diagnosis.

8. Explained what samples are necessary to properly diagnose a nitrate problem.

9. Explained the importance of conside­ring water as a source of nitrates.

10. Given some guidelines as to what constitutes a toxic dose, the range usually encountered, and the con­ditions under which those levels may or may not produce problems.

 

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