51
but at a basic level it contains elements of truth. Calving is somehow involved and diet is important.
Understanding of the condition and its causes is now much better, although still incomplete. The multifactorial nature of the condition and its causes is better appreciated with ketosis, milk fever and toxaemia all having an important role to play and all influencing each other. The theory is now vastly more complex. Much has been written about the ‘energy gap’ experienced by most modern dairy cows during early lactation leading to a period of negative energy balance and mobilisation of body fat reserves. This is exacerbated by a period of appetite depression around calving and further exacerbated in over-conditioned cows. This all results in increased levels of circulating β hydroxy-butyrate and NEFAs which have a deleterious effect on abomasal motility. To counter this highly
fermentable, energy dense diets are fed in early lactation and the ‘leakage’ of either diet from the rumen into the abomasum where it may continue to ferment or of VFAs, the products of dietary fermentation in the rumen, may further compromise abomasal motility. What is needed is to maximise appetite while feeding a sufficiently energy dense diet, to minimise the ‘energy gap’, containing an adequate amount of long fibre to optimise rumen function.
Milk fever also needs to be addressed. Calcium reserves
will always be adequate given the enormous amount of this mineral stored within the skeleton. This calcium cannot, however, be released immediately. Systems need to be primed and the sudden demand for calcium at the start of a lactation is massive. Even when this acute situation can be managed, traditionally perhaps by feeding a low calcium/high magnesium dry cow ration to ensure the enzyme systems necessary to mobilise skeletal calcium are primed prior to the demand at calving. Or, more recently, by paying attention to the DCAB of the transition ration to ensure maximum absorption of dietary calcium at the vital time, the published literature continues to show most of our dairy cows persist in being subclinically hypocalcaemic during the early part of their lactation. Just as an adequate calcium status is needed to maintain skeletal muscle function, this is why cows with clinical milk fever cannot stand, it is also needed to maintain smooth muscle, which is found in gut wall, function. As a result subclinical hypocalcaemia will further compromise abomasal motility. It will also compromise food intake at its most extreme. A cow that cannot stand because of milk fever will not be able to walk to feed to eat which will exacerbate negative energy balance and subclinical ketosis which will further affect abomasal motility. Calcium metabolism around the time of calving also, therefore, needs to be managed carefully if
herd management to prevent displaced abomasums is to be successful. Toxaemia will also affect abomasal motility both directly and indirectly through its effects on appetite and dietary intake. Of particular concern in the immediate post-partum period and during early lactation are uterine infections and mastitis. Every effort should be made to avoid calving problems; bulls with known difficult calving tendencies should be avoided and cows should be in a ‘fit- not-fat’ body condition. Fat cows tend to have more difficult calvings and so more post- partum uterine infections, are likely to suffer greater appetite depression at calving than thinner cows and have more fat to mobilise exacerbating any subclinical ketosis that may be present.
Care should also be taken to maintain cows and their environment in as clean and as dry a condition as possible to minimise the risk of toxic mastitis and where this does occur it should be treated aggressively with fluids and calcium as well as more traditional treatments and regular stripping of the affected quarter(s) to minimise its impact.
All of this adds up to paying the greatest attention to ensuring transition cow management is as good as it can possibly be and even then the odd displaced abomasum should still, perhaps, be expected.
Page 1 |
Page 2 |
Page 3 |
Page 4 |
Page 5 |
Page 6 |
Page 7 |
Page 8 |
Page 9 |
Page 10 |
Page 11 |
Page 12 |
Page 13 |
Page 14 |
Page 15 |
Page 16 |
Page 17 |
Page 18 |
Page 19 |
Page 20 |
Page 21 |
Page 22 |
Page 23 |
Page 24 |
Page 25 |
Page 26 |
Page 27 |
Page 28 |
Page 29 |
Page 30 |
Page 31 |
Page 32 |
Page 33 |
Page 34 |
Page 35 |
Page 36 |
Page 37 |
Page 38 |
Page 39 |
Page 40 |
Page 41 |
Page 42 |
Page 43 |
Page 44 |
Page 45 |
Page 46 |
Page 47 |
Page 48 |
Page 49 |
Page 50 |
Page 51 |
Page 52 |
Page 53 |
Page 54 |
Page 55 |
Page 56 |
Page 57 |
Page 58 |
Page 59 |
Page 60 |
Page 61 |
Page 62 |
Page 63 |
Page 64 |
Page 65 |
Page 66 |
Page 67 |
Page 68 |
Page 69 |
Page 70 |
Page 71 |
Page 72 |
Page 73 |
Page 74 |
Page 75 |
Page 76 |
Page 77 |
Page 78 |
Page 79 |
Page 80 |
Page 81 |
Page 82 |
Page 83 |
Page 84 |
Page 85 |
Page 86 |
Page 87 |
Page 88 |
Page 89 |
Page 90 |
Page 91 |
Page 92 |
Page 93 |
Page 94 |
Page 95 |
Page 96 |
Page 97 |
Page 98 |
Page 99 |
Page 100 |
Page 101 |
Page 102 |
Page 103 |
Page 104 |
Page 105 |
Page 106 |
Page 107 |
Page 108 |
Page 109 |
Page 110 |
Page 111 |
Page 112