NPN Toxicosis in Ruminants

Dr. A. Morrie Craig holds a doctor of philosophy in biophysics and is a research toxicologist who spent four decades as a professor of toxicology at Oregon State University. He also served as director of his institute’s endophyte lab. While teaching students in toxicology, Dr A. Morrie Craig concurrently oversaw research activities at OSU on plant toxicosis.

Livestock develop non-protein nitrogen (NPN) toxicosis when they ingest non-protein nitrogen-containing food or materials. In healthy animals, moderate levels of non-protein nitrogen are converted by ruminate microbes to ammonia, which is further combined with carbohydrates via metabolism to produce amino acids (protein building blocks). However, if the ruminal microorganisms (bacteria in the rumen that aid partial digestion of food) are not present in sufficient amounts to process all the ammonia into protein, the concentration of ammonia in the rumen will increase to dangerous levels.

Since ammonia is moderately alkaline, a large concentration can raise the pH of the rumen to above 7.5. The rumen is one of the four compartment stomachs of a ruminant animal where fermentation (initial digestion of ingested food in the absence of oxygen) occurs. High rumen pH hinders digestion because many useful microbes cannot survive in this condition.

Symptoms of NPN toxicosis include respiratory distress, abdominal pain, muscle tremors, and recumbency. Many animals die from this condition. Post-mortem diagnosis will reveal an abnormal rumen pH. The best way to save other animals in a location where animals are experiencing these symptoms is to completely remove the NPN sources. Typical sources are dry supplements and dry granular urea or ammonium-containing fertilizers.