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Kansas State Veterinary Diagnostic Laboratory

Kansas State Veterinary Diagnostic Laboratory
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Diagnostic Insights for Veterinary Nurses
October 2019

Non-protein Nitrogen Ruminant Toxicosis

By Dr. Steve Ensley

Background: This is the time of year when the use of non-protein nitrogen (NPN) increases in ruminant diets. Ruminants have the ability to metabolize non-protein nitrogen like urea into protein. The non-protein nitrogens are a less expensive form of protein but must be used correctly. Urea is the predominate source of non-protein nitrogen but there are several others including biuret and ammonium salts. Urea (CH4N2O) is metabolized by urease present in the rumen into ammonia (NH3). The use of NH3 in the rumen is dependent on the availability of highly fermentable carbohydrates such as dietary starch. Ammonia from the metabolism of NPN is absorbed through the rumen wall and enters the blood stream. When the liver cannot metabolize the ammonia quickly enough, ammonia concentration in the blood stream increases to a toxic concentration. NPN toxicosis is actually an ammonia toxicosis. NPN toxicosis can also be seen when plastic tanks used to haul fertilizer are used to haul drinking water. 

History: The typical history with cases of non-protein nitrogen toxicosis involve over consumption of this form of nitrogen. A general guideline is to not use more than one third of the protein being fed as non-protein nitrogen. Ruminants need to acclimate to the NPN and if not consuming NPN they will lose their ability to metabolize NPN rapidly. Dietary urea at 0.3-0.5 grams/kg of body weight to unacclimated cattle can cause a toxicosis. In acclimated cattle, urea at 1-1.5 gram/kg can cause toxicosis. 

Clinical signs: Following the ingestion of large amounts of NPN a rapid release of ammonia occurs. This can happen in less than one hour after ingestion depending on the dose. Clinical signs include disorientation, aggressiveness, abdominal pain, increased respiratory difficulty, muscular tremors, bloat, recumbancy and rapid death. After recumbent animals are treated and become ambulatory they may become very aggressive so caution needs to be exercised when treating an animal with NPN toxicosis. 

Diagnostics: A quick field test for NPN toxicosis is to measure rumen pH. The more basic the pH the more likely the diagnosis is NPN toxicosis. Rumen pH > 7.4 is compatible with NPN toxicosis. If you have pH paper available you need to measure the rumen pH. If the yellow/orange pH paper strip turns dark green once it is in contact with rumen fluid, NPN toxicosis is a likely diagnosis. You can also collect rumen fluid and freeze it as soon as possible because urease in the rumen will continue to metabolize the NPN present. Ocular fluid and urine are also good samples to measure ammonia concentration with. Obtaining a feed sample is important to establish where the excess NPN came from. 

Treatment: Oral administration of 5% acetic acid. You need to use at least 2 quarts/ animal to be able to decrease the rumen pH. If you have more acetic acid you can dose with more. There is little risk of an adverse event because of excess ruminal acetic acid. When you run out of vinegar you can use cold water, < 50 °F. This will slow down the conversion of the NPN to ammonia. Rumen lavage has also been used to remove the NPN from the rumen. 

Outcome: Supportive care will be needed for acutely affected animals that survive the toxicosis. There is a potential for delayed abortions in animals late in gestation due to the stress of the toxicosis. 

Take home message: NPN is an excellent source of nitrogen for rumen organisms to convert into protein. The dose of NPN needs to be closely monitored to prevent overdosing. Continual use of NPN in the diet will prevent animals from losing the rumen adaptation that occurs. Don’t haul drinking water in plastic tanks that have been used to haul liquid nitrogen. 

 

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