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Ammonia (Urea) Toxicosis In Ruminants

Typical presentation:   A client calls and reports that 20 of his dairy cows were found dead this morning. Four cows are still alive, but are recumbent and paddling. They are exhibiting signs of dyspnea and CNS stimulation including dilated pupils, ear twitching, and rapid eye blinking. If prodded to get up, the cows become rigid, and experience tetanic convulsions. The cows were supplemented with a liquid molasses-based NPN concentrate for the first time yesterday.

Physiology of toxicosis: Nitrogen in ruminant rations is derived from two sources: 1) Natural plant and animal protein, and 2) Non-protein nitrogen (NPN), such as urea or ammonia. Non-protein nitrogen is used as an economical supplement for nitrogen in poor ruminant rations. Rumen microbes convert NPN to ammonia via urease. The ammonia is then combined with ketoacids by the microbes to produce amino acids. Urease in the rumen will continue to convert urea to ammonia even if there is a lack of keto acids. If the rate of ammonia production (i.e., urea via urease breakdown to ammonia) or ingestion of ammonia (i.e., ammoniated feeds) exceeds the microbes ability to utilize it to form amino acids, there is an accumulation of ruminal ammonia. Ammonia absorbed from the rumen into systemic circulation is normally detoxified by the liver via the urea cycle. This detoxification system can be overwhelmed resulting in elevated blood ammonia levels.

Causes of toxicosis:   The most common causes of toxicosis from NPN supplementation include:

-Improper mixing of NPN resulting in concentrat­ed pockets.

-Calculation error resulting in excessive supple­mentation.

-Inadequate adaptation period. Cattle require at least five to seven days of small increases in concentration. This adaptation period needs to be repeated even if NPN is removed for a very short time.

-NPN rations low in carbohydrates prevent proper formation of keto acids.

-Free-choice access to NPN rations.

There are several factors which make animals more prone to ammonia toxicosis:

-Hungry animals will consume excessive amounts.

-In an alkaline rumen urease is more efficient. There is also more ammonia in the NHs form, which is readily absorbed across the rumen wall.

-Decreased water intake.

-Elevated body temperature increases urease activity.

-Liver disease.

-Stressed animals (recently shipped, castrated or vaccinated).

Clinical signs: The animals are often found dead as the progression of ammonia toxicosis is very rapid. The onset of clinical signs may vary from a matter of only 15 minutes to several hours. Death usually occurs around 24 hours following ingestion, but can range from less than one hour to three to four days. Clinical signs include ear twitching, pupil dilation, rapid eye blinking, dyspnea,    excessive    salivation,    frequent urination/defecation,ataxia, and tonic convulsions induced by stimuli. Death of affected animals may result from multiple factors and is a somewhat inconsistent finding. Hypeikalemia may occur due to metabolic acidosis since the primary mechanism of ammonia toxicosis appears to be an inhibition of the citric acid cycle with resulting compensatory anaerobic glycolysis.Hyperkalemia can induce cardiac failure. Respiratory paralysis or anoxia from prolonged seizure activity as well as CNS dysfunction from the direct actions of ammonia can also result in death of the animal.

Diagnosis:    Unfortunately there are no characteristic gross or microscopic lesions. Non­specific lesions such as pulmonary edema, hydrothorax, and visceral congestion may be seen. Ammonia toxicosis is a very difficult diagnosis unless there is a history of NPN supplementation. Feed samples should be taken for NPN analysis. Whole blood, rumen fluid, vitreous fluid, and cerebrospinalfluid should be collected in sterile containers and submitted frozen for ammonia analysis.   Normal   blood/vitreous   ammonia concentrations should be less than 0.5 mg/dl. Clinical signs appear when blood ammonia levels reach approximately 1.0 mg/dl. Death usually occurs at blood ammonia concentrations greater than 2.0 mg/dl.

Treatment:  Because of the rapid clinical course of NPN (i.e., urea) induced ammonia toxicosis, treatment often is not possible. If confronted with such a diagnosis, several modes of treatment have been suggested in the literature. Acidify the rumen by infusing two to six liters acetic acid (vinegar) per animal (cattle) or 0.5-1 liter in sheep and goats. Follow the vinegar with large volumes (20-30L [adult cattle]) of cold water. This should act to convert most of the ammonia into the NR^ form, which is not readily absorbed across the rumen wall. Emergency rumenotomywith removal of contents has also been suggested as a treatment Regardless of the treatment attempted, the prognosis is poor for recumbent animals. The prognosis improves for animals that survive the acute phase of the condition.

Additional Note: A unique and clinically distinct central nervous system disorder in cattle, anunoniated feed toxidty (a.k.a.. Bovine Bonkers Syndrome) is associated with NPN but is not related to the liberation of free ammonia. It is related to the formation of imidazoles; a by product formed during the ammoniation of feed. The most characteristic clinic sign is hyperexcitability. Affected animals suddenly stampede, run in circles and often collide with fences. Diagnosis is made by a combination of clinical signs with a history of feeding anunoniated feeds. Blood and rumen ammonia levels are in the normal range. There is no known specific treatment for this syndrome at this time.

- Dustin Decker, Class of 1997

• edited by MelissaPopielarczyk


Veterinary Clinics of North America, Food Animal Practice, 1989, vol. 5:2, 237-249.

Whitehair,  C.K.  DVM,  PhD.,  Bovine Practitioner.1989, vol. 24: 67-73.



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