3 Pathogenesis of Bovine and Ovine Ketosis

Transcript

So, in the second class, we have seen about the Etiology and also the Epidemiology. How and When Clinical Ketosis and Subclinical Ketosis will occur in the case of Bovine Ketosis and in the case of ovine Ketosis.

Now we will see something regarding the Pathophysiology. How Physiology becomes Pathology due to the presence of Ketosis. Whenever there is a demand for glucose there will be fat mobilization, this will lead to the Clinical ketosis in ruminants, especially during the early post partisan period.

In the case of ruminants, the energy is, or the energy requirement is met by the production of volatile fatty acids in the rumen. So, in the case of ruminants, very few carbohydrates are absorbed as hexose sugars and the remaining carbohydrates will be converted into or it will be fermented into short-chain volatile fatty acids like Acetate, Butyrate, and Propionate. In this Acetate, 70% of the acetate will be produced and this is mainly used for fat synthesis, and it is ketogenic whereas Butyrate again 20% it is produced it is again ketogenic this will be condensed into an acetyl-CoA, this will be either oxidized to ketone bodies or it will be transformed into acetyl- CoA and this acetyl-CoA will enter the TCA cycle for oxidation and the remaining Propionate that is only 10% is produced that is glycogenic, here it enters the TCA cycle at the level of the succinyl CoA. So, what happens is whatever the acetyl-CoA, I told in the previous slide whatever the acetyl- CoA that is formed it has to get oxidized via the TCA cycle, and this oxidation depends upon the adequate supply of oxaloacetate for which propionate is the main precursor for the production of the oxaloacetate. Once propionate is deficient, oxaloacetate will be insufficient this will make which will affect the oxidation of the TCA that is acetyl-CoA via the TCA cycle. So the acetyl[1]CoA will be diverted to the formation of ketone bodies, so to increase the gluconeogenesis and offset so this will result in, see this acetyl-CoA which is diverted to the formation of ketone bodies, so there will be insufficient glucose so the animal will enter into the state of negative energy balance and to offset this negative energy balance, more triglycerides will be mobilized from the adipose tissues as NEFA and free fatty acids to the liver. Once it enters the liver this will be converted again into triglycerides or triglycerides will be resynthesized from these free fatty acids and NEFA and the ketone bodies will be produced and in the liver triglycerides are resynthesized from the free fatty acids and will be stored by the liver or it will be exported as very-low-density lipoproteins.

But whereas in the case of Ruminants, Ruminants have inherently low capacity to export this VLDL, so what happens is excess of the free fatty acids or the NEFA that is that attempt to enter the TCA cycle through the acetyl-CoA in the absence of sufficient oxaloacetate, is partially oxidized to acetoacetyl-CoA which allows the formation of Ketone bodies and so the negative energy balance that occurs in the postpartum period, further reduces the available carbohydrates and this accelerates the further mobilization of the body fat and further production of the ketone body.

So all these together will cause Ketonemia, Ketonuria, Ketolactia, Hypoglycemia, and lower levels of the Hepatic glycogen.

In case how/ what is the path of Physiology in case of Ovine Ketosis? So there is an inadequate energy intake in the late pregnancy, which will lead to ineffective gluconeogenesis, so there will be hypoglycemia and lipid mobilization this will lead to the accumulation of ketone bodies and there will be an increase in the Cortisol level.

Bovine Ketosis: the principal metabolic disturbance will be Hypoglycemia and Ketonemia and the nervous signs that occur in the case of Bovine ketosis are mainly due to the production of Isopropyl alcohol which is a breakdown product of acetoacetic acid in the rumen and secondly because of the presence of Hypoglycemia, which is more important for the nervous function. And Ovine Ketosis: In the case of Ovine Ketosis Encephalopathy is mainly due to Hypoglycemia in the early stage of the disease. Once the Encephalopathy comes the disease is not reversible unless it is treated in the early stage. A high level of Cortisol and adrenal steroid diabetes contributes to the pathogenesis so adrenal cortical diabetes plays a major role by increasing the cortisol and it causes the remaining clinical signs or it is the cause of the clinical signs like Encephalopathy and other signs in Ovine ketosis.

To summarize this class, we have seen the Pathophysiology, how normal Physiology has become a Pathology because of the Ketosis, and How and why do those individual signs develop in Ketosis, especially in the case of Ovine Ketosis and in the case of Bovine Ketosis.

So, the factors that are causing the clinical signs in the case of Bovine and Ovine Ketosis have been seen. We have seen the cause for those things, and

Next class, we will see about the Clinical Findings and Treatment.

Thank you!