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Most read articles
|0208 PD: Eliminate lame excuses: Maintain your cows’ feet and legs|
|Archives - Past Articles|
|Monday, 14 January 2008 10:57|
It has been long recognized that lameness in dairy cattle is important. It is usually recognized as coming third to infertility and mastitis as a reason for culling. So why, then, despite numerous workshops and reviews of papers on the subject do farmers still regularly cite it as being a critical issue on their farms, and why does the incidence appear to be increasing? (See Figure 1*.)
The problem with understanding “incidence” is in knowing what people mean by “lameness.” Are we measuring, on the one hand, “treated cows” or, at the other extreme, deviations from the ideal locomotion score? Are the reported figures from a small number of unrepresentative farms? The 70 percent incidence reported by Hedges from the U.K. seems staggeringly high, and the 60 percent reported by Ward is based on three herds, albeit over three years. However, studies in France, Florida and New York suggest a mean incidence of around 30 percent.
“Treated cows” is not an ideal measure. “The definition of clinical lameness in cattle is fraught with difficulty, even among specialists.” The same authors reported that clinically lame cows had a reduced milk yield for up to four months before diagnosis! This would suggest that earlier diagnosis would be beneficial, and locomotion scoring can provide an answer by identifying cow “discomfort” before they are actually “lame.” (See Table 1’s locomotion scoring guide.)
The key is to get the individual dairy producer to agree to monitor the incidence of lameness on his dairy. This is the first step to arriving at a plan of action that he will own and will follow.
Having agreed upon the incidence of lameness on a specific farm, the next part of the process is to work out how much the problem is costing that producer.
When you look to the literature for the cost of lameness, you get a confusing range. Esslemont in the U.K. suggested a total cost per case of $430.89 and applying a modest inflation rate of 3 percent, this equates to a 2006 value of $562.21, while Keating asserts that the total cost per case in the Southlands of New Zealand is $867.84. Wow!
Authorities in the U.S. have generally taken a more sanguine view. Ranging from a quoted minimum of $90 to $100 per case to Guard suggesting a figure of $302. Peter Robinson at the University of California, however, has developed a spreadsheet to predict milk loss associated with variations in locomotion score, and this would suggest that milk losses alone could cost $54.75 per cow over all cows in a herd with an 8 percent incidence of clinical lameness. This would equate to over $300 per clinical case, for lost milk alone.
Whatever the number quoted, it is irrelevant to the individual producer who needs to know how much lameness is costing him. Robinson’s spreadsheet will enable a producer to calculate the cost of milk loss. To this he will have to add his figure for the cost of treatments, reduction in fertility and increased culling.
Let’s take a 100-cow herd with a lameness incidence of 30 percent and assume that the cost of lameness has worked out at $21,000 per herd per year.
That is $700 per treated case (which would seem to be a reasonable assumption if it includes the lost milk production in the sub-clinical cases).
If the herd yield is 22,000 pounds, this equates to just under 1 cent per pound.
Clearly a reduction to 0 percent incidence is unrealistic. In Wisconsin, Cook and Nordlund have suggested that an incidence of 15 percent is what you would expect in well-managed herds. I think that this is still too high and that it is reasonable to expect to be able to reduce clinical lameness to 5 percent. This would still cost $3,500 per 100 cows, leaving a potential benefit of $17,500, 0.8 cents per pound part of which, obviously, would be invested in preventing lameness.
If the producer invests half of this, he is still 0.4 cents per pound better off, and this figure is net profit!
Now we can work out a plan of action. Ideally, this should involve a team consisting of the herdsman, the nutritionist, the vet and the hoof trimmer and it must take a holistic approach, dealing with all the issues.
I suggest that you identify all the issues and then score them on Figure 2*.
This approach recognizes that all issues are important and will be dealt with, as the time and money becomes available.
So what are the causes of lameness, and what can we do about them? I will briefly consider the following contributing factors, recognizing that they are all linked.
If you breed animals that have structurally unsound legs and feet, then the incidence of lameness in such cows is likely to be high. This will be accentuated by management and environmental issues. For instance, you are more likely to “get away” with genetic weaknesses in this area in tie-stall as opposed to freestall barns.
Particular problems to look out for are:
1. High pin bones – often associated with an incorrect leg-set at the thurl
2. Excessively narrow rumps which, in conjunction with the large udders associated with high yields, will tend to throw the legs out to the side, putting undue pressure on the inside claws.
Breeding companies have now recognized that locomotion score is associated with longevity and are building this into their indexes.
Lameness costs money. Make sure that you take account of this in your breeding program.
Lameness is often the result of an adverse interaction between the cow and her environment. In particular the type and design of her housing and the surface on which she is asked to walk.
Whatever the type of housing, it must allow sufficient comfortable lying time. Lameness is endemic in overcrowded freestall barns and those with poor stall design.
Cook and Nordlund have proposed a very useful flowchart for evaluating freestall, and the same authors have shown that, possibly counter-intuitively, sand provides a better surface than mattresses.
Curbs (the step-up to the stalls) should ideally be 5.9 inches (15 centimeters) high and certainly no more than 7.8 inches (20 centimeters). Apart from placing too much strain on the back feet when the cow stands half-in, half-out of the stall, too high a curb increases the risk of damage to the foot if the cow slips from the edge.
Farm tracks and paths should be free of mud and stones, and concrete surfaces should be well-maintained.
There is much more on this topic but, essentially, the rules here can be determined through the application of commonsense and close observation of the cows’ behavior.
I shall just make one point here. I was once asked by a farmer if I had anything he could add to his feed to “solve” the lameness problem on his farm. Looking across the yard, I could see the cows standing in three inches of slurry.
This includes “foul in the foot,” “digital dermatitis” and “heel wart.” The key lies in keeping the feet clean before and during the treatment with the antibiotic of choice. A common mistake is to use inadequate footbaths. Inadequate because they are allowed to get dirty (thus doing more harm than good) or typically because they are too short, not allowing enough contact time with the disinfectant.
Nutrition affects lameness in two main areas,
1. Quality of horn growth
Horn growth is influenced by trace elements, particularly zinc, through its involvement in keratinization. Supplementing the diet with a highly available organic form of zinc has been shown to have a significant effect, reducing lameness scores by 24 percent.
Laminitis has two main nutritional causes:
1. Excess protein in the diet
Both these issues are avoided by feeding a well-balanced diet, which should be the goal for reasons other than that of preventing lameness!
The mechanism whereby excess protein in the diet causes lameness is not fully understood. It may be that too much ammonia in the rumen can cause bacteria to die, leading to toxins in the blood similar to acidosis, or it may be that the breakdown products of excess protein themselves include histamines which can cause inflammation of the laminae.
Whatever the mechanism, Manson et. al. showed that cows on a lower protein diet with no foot trimming endured similar lameness to those on a higher protein diet with trimmed feet.
Since avoiding excess protein in the diet is also beneficial in terms of waste (both financial and environmental) and in terms of its effect on milk urea nitrogen (MUN), this is another no-brainer.
The issue of acidosis is well understood, and nutritionists should strive to avoid it through careful balancing of the diet with respect to rapidly fermentable carbohydrate and effective fiber. It is not always possible, however, to get this right for high-yielding cows under all circumstances, satisfying the nutrient demands of production being a priority.
In most parts of the world, it is thought that most cows in early lactation are suffering from sub-clinical acidosis. Under these circumstances, feeding a live yeast culture has been clearly demonstrated not only to increase, but to stabilize the rumen pH. The benefits of increased dry matter intake (DMI), forage digestibility and increased milk yield (at least 2 pounds per cow per day throughout the lactation) will be obtained on top of the reduction in lameness. So the lameness prevention is free. Yet another no-brainer. Suffice it to say that if you suspect that your cows might be at risk to sub-clinical acidosis, you should feed a live yeast.
The key objective of this article, however, was not to list the various causes and preventative treatments for lameness but to propose a mechanism whereby there would be a greater acceptance of the need for action and, indeed, a greater level of action itself. This consists of a way to make the issue of lameness more “real” for the individual farmer.
1. Identify incidence of lameness on the specific farm.
2. Attempt to apply a cost of lameness to the farm.
3. Devise a plan of action addressing all the possible causes.
If these are adopted, it will indeed result in no more lame excuses. PD