Review/Oorsig Volume 22, Issue 03 - Page 25

Volume 22 • Issue 03 • 2018 PART 03 COMMON PRODUCTION DISEASES: KETOSIS OR ACETONAEMIA Ketosis or acetonaemia Ketosis in dairy cows can broadly be classified into either type I or type II ketosis, based on the underlying pathophysiology, with some similarities to that of type I and type II diabetes. Type I ketosis is a metabolic disorder of high yielding lactating dairy cows caused b y an imbalance in the energy metabolism. It is characterized by ketonaemia, ketonuria, hypoglycaemia, depression and anorexia. It is most often seen from the third to the sixth week of lactation. The key factor in the occurrence of ketosis in dairies, is sufficient intake of a properly balanced ration (Dry Matter Intake). Feedbunk management, as mentioned before in the case of hypocalcaemia, is of particular importance. Type I ketosis can be sub-classified into primary and secondary, where primary ketosis occurs due to a severe negative energy balance (NEB) that leads to a substrate (oxaloacetate) deficiency in the absence of any other disease. Secondary ketosis is the accumulation of ketone bodies in the body due to anorexia secondary to a disease process. Any disease process that reduces dry matter intake (DMI) in early lactation may cause secondary ketosis. The prevalence of primary ketosis is relatively low in southern Africa. Subclinical ketosis can often be detected in cows from high producing dairy herds if body fluids are tested for ketone bodies. Most cases occur between the 3rd and 6th week of lactation. Many cases (50%) will spontaneously recover within days and mortalities are rare loss of production is more important, especially where cows do not respond well to treatment. High producing cows and cows in their 3rd lactation and older have an increased risk for type I ketosis. Physiological background Carbohydrates and fibre compounds in the feed are broken down in the rumen by rumen microbes. The end products of rumen digestion are the volatile fatty acids acetate (average 70%), propionate (average 20%) and butyrate (average 10%). Propionate can enter the citric acid cycle (CAC) directly and its carbon atoms can move through the cycle to enter the gluconeogenic pathway to form new glucose (propionate is thus glucogenic). Acetate may also enter the CAC through acetyl CoA (small amounts) but only if there is enough C4 atoms (oxaloacetate) available in the CAC. Most of the acetate will, however, be used in fat synthesis, or if the body is in a catabolic state with fat being broken down, acetate will be used to form ketone bodies (aceto acetate, ß hydroxy butyric acid and acetone). Aceto-acetate and ß hydroxy butyrate have 4-carbon atoms, but they cannot be interchanged with the C4 units in the CAC. Acetone is a C3 compound that is formed slowly and spontaneously from aceto-acetate. Ketone bodies form an important energy source. They can enter the CAC via acetate and be oxidized for energy in heart, kidney, skeletal muscle and lactating mammary glands if there is sufficient C4 units (oxalo-acetate) available. If the C4 units concentration of the mitochondria becomes sufficiently depleted, there will not be enough C4 units to condense with C2 (acetyl CoA) to allow the initiation of the CAC. When this occurs, C2 units accumulate in the mitochondria and are 25