The Effects of Acute Ammonia Toxicity on Certain Blood Chemistries in Sheep

Protein has always been in short supply in the world. This will be even more evident when the world’s population reaches the projected 5.8 billion by the year 2000. Rosenfeld noted that not only will there be more mouths to feed, but there is also a decrease in cropland due to increased housing and industry. For these reasons, along with the monetary benefits, urea has been added to feeds for ruminants to prevent the waste of valuable protein. The Board on Agriculture and Renewable Resources cited several factors which may cause urea toxicity to develop: (1) lack of an adequate adaption period to urea-containing diets, suggesting that it was important to start feeding urea at low levels and increase gradually over a period of several days, especially if high levels of urea are fed; (2) fasting prior to urea consumption; (3) the feeding or urea in diets composed primarily of poor-quality roughages; (4) the feeding of diets that promote a high pH in ruminal fluid; and (5) low water intake. Errors in formulation and improper mixing of urea with other diet ingredients are probably the major factors causing urea toxicity in the feeding of ruminants. Toxicity occurs when excess ammonia produced by hydrolysis of urea accumulates in body fluids and tissues. Symptoms of acute ammonia toxicity in the ruminant appear to be progressive as follows: the animal becomes nervous and uneasy, salivates excessively, and demonstrates muscular tremors: these symptoms are followed by incoordination, respiratory difficulty, frequent urination and defecation; the front legs begin to stiffen, and the animal becomes prostrate; violent struggling, bellowing and terminal tetanic spasms occur on most animals; the jugular pulse is marked, and bloating is common; death occurs within 0.5 to 2.5 hours after the initial symptoms are observed. Treatment for urea toxicity is usually effective if applied before tetanic spasms occur. Therefore, it is important to be able to correctly diagnose toxicity. Blood ammonia levels can be used as a diagnostic tool but are difficult to determine. The purpose of this study was to measure the changes occurring in certain blood chemistries during acute ammonia intoxification. It was hoped that this study would provide information which would provide rapid diagnosis and a more effective treatment of urea toxicity. This information may also be used to develop more effective ways to use urea supplements, and therefore conserve the world’s supply of protein