Difference between revisions of "Ketosis of Cattle"
Line 38: | Line 38: | ||
Treatment is aimed at restoring normal blood glucose levels. | Treatment is aimed at restoring normal blood glucose levels. | ||
− | A bolus of Intravenous dextrose (50%) has been the treatment of choice for years. This | + | A bolus of Intravenous dextrose (50%) has been the treatment of choice for years. This often results in a quick recovery however animals may relapse. |
− | Glucocorticoids also act to increase blood glucose but tend to have longer acting effects and can be given intramuscularly once daily. | + | [[Adrenal Glands - Anatomy & Physiology#Glucocorticoids|Glucocorticoids]] also act to increase blood glucose but tend to have longer acting effects and can be given intramuscularly once daily. |
Propylene glycol can be administered orally and it acts as a precursor to glucose. This can be administered twice daily. | Propylene glycol can be administered orally and it acts as a precursor to glucose. This can be administered twice daily. | ||
Revision as of 20:42, 3 August 2010
This article is still under construction. |
Also known as: | Acetonemia Ketonemia |
See also: | Ketosis |
Description
A metabolic disease of adult dairy cattle which often occurs in association with metritis or another infectious disease process. The exact cause is unknown however the disease occurs when cows are in a negative energy balance and are rapidly mobilising adipose tissue. As a result blood levels of Nonesterified fatty Acids (NEFAs) are raised.
It normally affects cows during lactation however it can also occur in late gestation where it presents similarly to pregnancy toxaemia.
Signalment
Most commonly occurs in high yielding dairy cows a few weeks postpartum. Cows with a higher body condition score are more at risk.
Diagnosis
Can often diagnose this condition on clinical signs combined with a history of concurrent disease. It is possible to test milk or urine on the farm for the presence of ketone bodies. These are often dipsticks which change colour in the presence of ketone bodies. False positives can occur with these tests and they should be used in conjunction with clinical signs suggestive of ketosis.
Additionally, serum concentrations of NEFAs will be high and glucose levels will be low.
Clinical Signs
Reduced feed intake is often the first clinical sign to be noted. Other signs include decreased milk yield, lethargy and an “empty” appearing abdomen. Rumen motility is variable, but often hypoactive following reduced feed intake. Rarely cases present with central Nervous System signs and include incoordination, aggression, excesssive licking and chewing and occassionally bellowing.
Additionally ketosis produces a characteristic 'pear drop'(acetone) smell on the breath of affected cattle.
Treatment
Treatment is aimed at restoring normal blood glucose levels. A bolus of Intravenous dextrose (50%) has been the treatment of choice for years. This often results in a quick recovery however animals may relapse. Glucocorticoids also act to increase blood glucose but tend to have longer acting effects and can be given intramuscularly once daily. Propylene glycol can be administered orally and it acts as a precursor to glucose. This can be administered twice daily.
Prevention and Control
If many cases of ketosis are occuring on one farm this suggests that the nutrition of the cows must be studied. Cows should not be a high body condition score when they calve as these cows mobilise more adipose tissue and are at a greater risk of ketosis. Cows should be encouraged to eat and maintain a high feed intake in the late gestation and transition period to avoid entering a negative energy balance state.
Prognosis
If clinical signs are recognised early and cases are treated correctly the prognosis is good.
References
Andrews, A.H, Blowey, R.W, Boyd, H and Eddy, R.G. (2004) Bovine Medicine (Second edition), Blackwell Publishing
Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition) Merial