CATEGORIES

SEARCH

CONTACT

25 Alderson Rd
Fairview Downs
Hamilton 3214
New Zealand
PH 64-212956469


proagcon@ozemail.com.au


“Every essential element either in our fertilizer or diet is a contaminant if over supplied.”

— Brian McLeod

Sheep Pasture Protein Foot Scald

imageLameness as foot scald is a continuing problem on many pastoral properties in New Zealand Australia. While the problem is often associated with wet weather the real coarse is high levels of dietary crude pasture protein and a resulting energy deficit further resulting in sub-clinical acidosis. Extensive trials in the USA, have confirmed 90% of all lameness in ruminant animals can be contributed to diet. This research has gone further and found that many foot injuries are also indirectly attributed to diet which result in the feet being more susceptible to damage.

In 1980 Dr Bob Scott of the USA lectured on the role Excess dietary Crude Protein (ECP) played in inducing lameness in the form of foot abscess or foot scald. Hot feet or muscle soreness are also a result of excess ECP. Dr Scott recommended iodine and high levels of vitamin A as a preventative against the incidence of lameness. Dr Scott’s work also showed the connection between ECP and infertility, abortion and full term deaths at lambing or calving. In Australia and NZ the assumption has always been, we are different here, we have pasture, and our stock are not subject to the same stresses as those fed high rates of grain. In fact our stock have higher dietary stress levels than those on total grain rations. Following rain, our pastures go from dry to very fresh in a matter of days. This means protein increases from 8 or 9% or lower to as high as 40%. Remember the ewe only requires approximately 12% to 14% crude protein in its diet, it has to dispose of the surplus. Pasture composition changes not only from paddock to paddock but also weekly and season to season.

A sudden increase in green feed can result in scouring, weight loss, breaks in the wool and even a reduced lambing percentage as well as lameness. The real issues leading to these symptoms include reduced rumination time, reduced rumen pH, reduced appetite, energy depletion as rumen organisms take part of the dietary energy for their own use when breaking down degradable protein and converting it to ammonia which ends up in the blood. Then we see the loss of body fat as it is used to produce urea from the ammonia and the urea is dispatched in the urine and shows as pasture burns. High protein diets result in the production of histamines in the body , causing dilation of the central arteries forcing blood to the outer extremities of the body, e.g. feet. With the resulting blood pooling in the feet we see animals with hot feet, which often results in infection and foot scald. Rams flushed in preparation for mating are a target for this type of lameness. Results published from dairy trials in England (2000) showed a direct relationship between ECP and lameness. As dietary crude protein increased above 19%, so did the incidence of lameness. The level of crude protein in winter, spring and irrigated pasture can range between 20% and 40%. Dry pastures will be lower. Urea applications can result in levels to the higher end of the scale. It is important to note that crude protein (CP) is the nitrogen content of a material multiplied by 6.25.

Nitrates

Another important issue is, nitrogen has different forms, some good and some toxic. Nitrogen readings do not identify the difference, so at times there are higher readings of toxic forms of N present. For ideal pasture growth pasture should contain 4 to 5% N or 25% to 31.25% CP. So there will always be a difference between pasture and animal requirements, the real issue is to understand. One fallacy often heard is that green pasture is high in vitamin A, when in fact it is only high in carotene, the precursor of vitamin A. This conversion takes place in the animal but is can suppressed by the presence of excess nitrogen in the body. So the animal is often vitamin A deficient, this is an induced deficiency. Bacteria are opportunists, blood pooling in the feet results in a breakdown of tissue allowing infection to occur. The infectious agents are secondary and may not be the normal dichelobater nodosus (Foot rot) organism. Autopsy of foot abscess has shown the presence of soil born staphlacocuss or spirochaete as well as the common foot rot organism.

If given the opportunity soil born organisms will invade hoof tissue. Dietary issues weaken tissue but if healthy will form an impregnable barrier to infection. Lameness is an important issue.  With the information we have it is possible to prevent or minimise clinical cases if not eliminate them from our property.

Bryan L McLeod