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Flexure Deformity, written by Dr John Doyle DVM, PhD

As a veterinarian, I believe the severe contracted tendon syndrome (i.e. foal tendons not relaxing) has multiple causes and cannot be singularly related to a single mineral or vitamin deficiency (e.g. Se & vitamin E). The following are some thoughts related to newborn foal (1-3mo).

Most veterinarians observing contracted tendons in foals reference the cause as abnormal positioning of foal during the last weeks of the pregnancy in the uterus. This may be the situation when the foal responds with normal limb articulation and mobile within a week of birth. However, when newborn foal tendon contraction persists for longer suspect an underlying cause as genetic and/or physiologically related.

Physiologic cause is related to nutritional foetal programming or mobilization of nutrients from maternal to developing foetus (well documented in several species). Formation of normal bones, cartilage and tendons requires adequacy of all nutrients (i.e. carbohydrates, fats, proteins/amino acids, major, trace minerals and vitamins) at specific time periods during gestation. The brain and/or hormones regulates nutrient partitioning into maternal and foetal tissues. Inadequate maternal consumption of protein/amino acids, imbalanced major minerals (Ca:P:Mg) or elemental (natural & pollutant)/chemical (poisonous plants) antagonism may inhibit 1 or more trace minerals can result abnormal tissues deposition.

Forages absorb minerals for their growth and reproduction, not that of an animal. Hence, dependency upon forages to supply all required nutrients for their animals is naïve management. Forages uptake elemental minerals (i.e. essential and toxic) not required for their growth as opportunist.

Selenium is not required for grass growth and deficient in some areas of Australia (e.g. as are copper & cobalt). Toxic Se levels can be achieved Se supplementation or exposure to natural sources (e.g. WA, plant accumulator). The yeast Se chelated forms appear to be more bioavailable as well as possessing low toxicity. Hence, if supplementing would select chelated trace mineral products. Major minerals such as calcium, phosphorus and magnesium inorganic sources supplemented in feed have good bioavailability.

Blood is the carrier of major/trace minerals, not a storage site. Blood and hair are weak methods in identifying mineral deficiencies. The 1st item I analyse for animals with suspected mineral imbalance is their primary water source. Water assay is an inexpensive assay, best assessed once a year and good first rule out. Animals consume more water than feed on a weight basis. I observe water quality problems causing mineral imbalances on a sporadic basis over the year. Droughts do have a major impact on water quality.

Trace mineral storage sites (e.g. liver) must be frequently replenished to supply adequate levels, especially for the pregnant animal. A little daily supplementation of balanced feed with minerals/vitamins is much better for the animal than large slugs of supplements on an infrequent basis.

Hope this short review stimulates some new thoughts concerning foal contracted tendon problem.

John Doyle DVM, PhD

Consulting Nutritionist


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