59 

 granulomatous inflammation which was most likely due to 

 aspirated material or metabolic injury to lung collagen. The 

 liver showed a mild Kupffer cell hyperplasia. 



Discussion 



Serum Cu concentrations provide a good indicator of Cu 

 status of ruminants. The liver and kidneys of animal 77 could 

 not tolerate the dietary Cu as well as the others as indicated 

 by the relatively low levels of Cu the liver and kidney and 

 the high serum Cu at the time of death compared to animal 1. 



Animal 46 may not have died solely from a Cu toxicosis. 

 The factors which seem to substantiate this theory include the 

 low CK levels, the high GGT and AST levels (no decline) , the 

 failure of HCT to rise, and the absence of hepatitis at the 

 time of death compared to the animals which exhibited signs of 

 Cu toxicosis. 



Animal 288 was apparently never affected by Cu excess. 

 The exact cause of this is not known because the animal had 

 relatively similar liver Cu levels as the other animals but 

 showed no change in any of the serum enzymes. 



Blood HCT percentages show a slight increase in 

 erythrocytes during the days prior to death which might 

 reflect a decreased capacity to carry oxygen by the cells. A 

 dramatic decrease in HCT was seen in animal 77 which 

 represents the full onset of the hemolytic crisis. This 

 decline was not seen with the other animals perhaps because 



