The document discusses ammonia and urea toxicity, outlining their sources, mechanisms of toxicity, and clinical symptoms in animals. Ammonia exposure from various sources can lead to significant health issues, including blindness and convulsions, while urea can cause similar toxic effects when ingested in high quantities. Diagnosis and treatment strategies are also covered, primarily focusing on managing ammonia levels and relieving symptoms through various medical interventions.

1. AMMONIA AND UREA
TOXICITY
URUSHA GHIMIRE
ROLL NO 37​

2. AMMONIA
• Colorless gas with a pungent
ammoniacal smell
• Extremely soluble in water forming a
caustic alkaline solution of ammonium
hydroxide (NH4OH)
• Used as a refrigerant, fertilizer
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Source of ammonia poisoning
1.Gas leak.
2.Fertilizers.
3.The spillage of Household and industrial
cleaners
4.Ammonia is produced by decaying
manure.
5.Increased ammonia levels of 25–30 ppm
can damage the mucociliary apparatus of
the upper respiratory tract, and higher
levels (50–75 ppm) can cause decreased
feed intake as well as caustic burns to the
cornea, which can result in blindness.
Pullets exposed to high levels of ammonia in wet litter
developed blindness as a result of corneal ulcers.

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• Both ammonia and urea are nitrogen-containing compounds.
• Ammonia is the simplest nitrogen containing compound where
as urea is a derivative of ammonia.
• Because ammonia is toxic, it is excreted immediately by fish,
converted into uric acid by birds, and converted into urea by
mammals.
• Ammonia is smaller, more volatile and more mobile than urea. If
allowed to accumulate, ammonia would raise the pH in cells to toxic
levels.
Why does the body convert ammonia into urea?
Ammonia is produced from leftover amino acids, and it must be
removed from the body. The liver produces several chemicals
(enzymes) that change ammonia into a form called urea, which
the body can remove in the urine. If this process is
disturbed, ammonia levels begin to rise.

6. UREA
UREA
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Urea, also called carbamide, is an organic compound
with the chemical formula CO(NH2)2.
• Diamide of carbonic acid
• Easily soluble in water
• White crystalline powder and odourless
• Liberates ammonia smell
• Urea and other commonly used non-protein nitrogen
have the ability to liberate ammonia.
• Hydrolysis of urea is speeded up by urease and an
alkaline pH.

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UREA
Source of Urea poisoning
• Fertilizers
• Urea and other organic and
inorganic sources of nitrogen are
added to ruminant rations as a
source of non-protein nitrogen
• Ammonium salts
• Poachers use urea to kill wild
animals
• Toxic dose 100gms in cattle and 10-
25 gms in goat/sheep
• Blood ammonia nitrogen reaches
0.84mg to 1.3mg%

8. Toxicosis results from the accumulation of ammonia in the animal
factors, which enhance urea toxicosis, are
• Rapid ingestion
• A diet low in energy and protein and high in fiber
• Ingestion of palatable urea concentrate such as urea molasses
mixtures
• High pH in the rumen
• High body temperature
• Water deficiency and
• Feeds rich in urease like soyabeans
• Stress
• Hepatic insufficiency
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9. ABSORPTION AND FATE
• In the rumen, ammonia liberated is in the form of ammonium ion and
hence it cannot be absorbed.
• At rumen pH 6.2 charged ion is highly water soluble and poorly
absorbed.
• If rumen pH is elevated to 10 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 normal course, liver ammonia is converted into urea by the urea
cycle or incorporated into glutamic acid in the synthesis of glutamine.
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10. MECHANISM OF ACTION
• 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 citric acid cycle.
• There is an increase in anaerobic glycolysis, blood glucose and blood
lactate.
• A decreased energy production and cellular respiration leads to
convulsions.
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11. CLINICAL SYMPTOMS AND PM
LESIONS
• Sometimes affected animal is found dead
• Behavioural abnormalities like restlessness and dullness initially, later signs of
excitation, head pressing, abnormal posturing, jumping over unseen objects
• Nervous phenomena like tremors, twitching, and spasm of muscles beginning
from the 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.
• Locomotor disturbances like initial in-coordination and later staggering and
stumbling prior to collapse.
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12. POST MORTEM LESIONS
• No characteristic lesions are noticed in urea poisoning. Mild pulmonary
edema with lung congestion and petichiae are also noticed.
• Animals bloat rapidly and the carcasses decompose more rapidly.
• Liver is enlarged and pale
• Kidney cloudy and necrotic foci present
• Stomach- Hemorrhagic patches, ulceration and odema
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13. DIAGNOSIS AND TREATMENT
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Diagnosis is based on history, clinical symptoms, post mortem lesions,
laboratory investigations like BUN, blood ammonia concentration,
ruminal pH, and 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
• Intravenous fluids should be administered.
• Emptying the rumen provides prompt relief from urea toxicosis.
• Convulsions can be controlled by pentobarbital sodium administration.