Section 2: Metabolic Diseases of Ruminants: Ketosis (Donovan) Flashcards
Types of ketosis
1) starvation (uncommon in cattle)
2) primary (healthy high producing dairy cattle, or ewes carrying multiple feces)
3) secondary (to some other malady)
KET predisposing factors
cow: early lactation, high milk prod., high BCS
ewe: late gestation, low BCS
inappetence
low exercise
normal to have neg. energy balance during early lactation?
yes
KET etiology
- neg. energy balance of early lact.
- VFA prod. in rumen (acetic and butyric VFAs become ketone bodies)
propionate from grain usually goes to form:
glucose, lactose
acetate and butyrate from forage usually go to form:
activated acetate –> fat, energy in liver
if cow ingests CHO deficient in energy, what happens?
propionate goes down, so all of the propionate is utilized in milk and none goes to fat/energy. Cow wastes. Excess acetate and butyrate –> excess activated acetate –> converted to aceto-acetate and beta-hydroxybutyrate, which effect feed intake and neutrophil function
primary ketosis explained
high demand for energy depletes the body’s supply of free and stored glucose, dietary intake can’t keep pace with demand, and the body begins to use fatty acids and ketone bodies as its fuel source. Lipolysis depletes the body’s fat stores and results in rapid loss of body condition, particularly in cattle. Further, mobilization of lipids leads to accumulation and metabolism of free fatty acids in the liver, often resulting in excessive retention of lipid by the hepatocytes (fatty degeneration).
wasting vs. nervous form of ketosis explained
The wasting form involves mobilization of fat stores and loss of body condition. The nervous form involves the effects of ketones on the central nervous system. The presence of high levels of ketones leads to trembling, ataxia, and erratic behavior.
wasting form of KET: clinical signs
-dec. feed intake
-dec. milk yield
-weight loss
-ketone breath
(most common form)
nervous form of KET: clinical signs
- staggering
- abnormal stance
- apparent blindness
- pica
- uncommon
clin. path. of KET
- hypoglycemia
- hyperketonemia
- fatty liver ( a primary dz problem)
KET tx
-glucose solution IV
-propylene glycol oral
-Ca or Na-propionate oral
act to speed up Krebs cycle
last resort: glucocorticoids (facilitate breakdown of protein–>glucose)
KET prevention in dry cows
-maintain BCS, exercise, energy dense feed, dec. stress
KET prevention in lactating cows
-feed changes, DMI, energy dense feed, fiber
clin. signs of preg. tox. in SR
blind, demented, off feed, head pressing, CNS signs, DEATH. Necropsy: fatty liver, emaciation, multiple feti
