UREA POISONING
citric acid cycle.
Urea and non-protein nitrogen have the
ability to liberate ammonia.
Urease present in plants and
microorganisms and hence in rumen.
Hydrolysis of urea is speeded up by urease
and an alkaline pH.
Excess urea liberates sufficient ammonium
ions making rumen contents more alkaline
and in turn further hydrolysis of urea.
Other factors, which enhance urea toxicosis,
are Rapid ingestion, A diet low in energy and
protein and high in fiber, Ingestion of urea
molasses mixtures,,High pH in the
rumen,High body temperature, Water
deficiency and Feed rich in urease.
Absorption and Fate
In the rumen, ammonia liberated is in the
form of ammonium ion and hence it cannot
be absorbed.
The rate of ammonia production depends
primarily on the amount of ration ingested,
amount of urease in the ruminal contents or
the diet and pH of the ruminal contents.
If rumen pH is elevated to 10.0 or above,
then ammonia will be in soluble form and
lacks charge and can be absorbed.
In the blood at a pH of 7.4, almost all the
ammonia is in the form of ions and cannot
cross the cell membrane.
In the liver ammonia is converted into urea
by the urea cycle or incorporated into
glutamic acid in the synthesis of glutamine.
Both these detoxification processes are
enzymatic and depend on substrates
produced by citric acid cycle.
Mechanism of Toxicity
Toxicity of urea and non-protein nitrogen is
due to ammonia absorbed from the
stomach.
When the level of ammonia is high, the
animal cannot detoxify ammonia fast
because the urea and glutamine synthesizing
mechanisms are saturated.
Increased ammonia leads to inhibition of
There is an increase in anaerobic glycolysis,
blood glucose and blood lactate.
Acidosis is manifested.
A decreased energy production and cellular
respiration leads to convulsions.
Clinical Symptoms
Sometimes affected animal is found dead
and sometimes the onset is slightly delayed.
The animal quickly dies after manifesting
weakness, dyspnoea, severe colic and
terminal toxic convulsions. In some
instances the onset of signs takes several
hours and a range of clinical symptoms are
seen.
Behavioural abnormalities like restlessness
and dullness initially, later signs of
excitation, head pressing, abnormal
posturing, jumping over unseen objects and
maniacal behaviour.Nervous phenomena
like initial hyperaesthesia, tremors, twitching
and spasm of muscles beginning from
eyelids and proceeding towards the tail are
noticed.Autonomic manifestations include
salivation, bradycardia, hypertension and
severe colic.
Gastrointestinal signs include rumen atony,
bloat, teeth grinding, groaning, kicking at
the abdomen and other evidence of colic.
Terminally ill animals may vomit and
aspirate the rumen contents.
Locomotor disturbances like initial
in-coordination and later staggering and
stumbling prior to collapse.
Diagnosis
Diagnosis is based on history, clinical
symptoms, post mortem lesions, laboratory
investigations like BUN, blood ammonia
concentration, ruminal pH, analysis of feed,
stomach and ruminal contents for urea or
ammonia.
Treatment
In animals that are not too ill, cold
water-acetic acid treatment can be given.
19-38 litres of water and 3.8litres of 5%
acetic acid can be administered to an adult
cow.
By diluting the ruminal contents and by
decreasing the ruminal pH and temperature,
hydrolysis of urea can be slowed.
Hastening formation of urea from ammonia
can decrease Blood ammonia level.
L-arginine and N-Carbamyl-L-glutamate can
stimulate urea cycle. But this treatment is
doubtful.
Emptying the rumen provides prompt relief
from urea toxicosis. But it is difficult to carry
out the emptying of ruminal contents.
Convulsions can be controlled by
pentobarbital sodium administration.