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
-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
-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.
-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 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.