In many areas of the world, most notably northern Europe and especially Great Britain, equine grass sickness (EGS) causes the sudden and devastating loss of horses grazing on grass. Although the disease was first identified in the early 1900s, the causative agent for EGS remains unclear. Several theories exist, including either a vitamin or mineral imbalance, or an overgrowth of Clostridium botulinum type C in the large intestine. This bacterium is believed to produce a toxin that damages nerves supplying the gastrointestinal tract, resulting in the classic clinical signs of disease: colic, excessive salivation, and difficulty swallowing.
Researchers from the Royal (Dick) School of Veterinary Studies located in Edinburgh, UK, recently suggested that an acute deficiency in dietary niacin, known also as vitamin B3 or nicotinic acid, was a possible culprit in EGS*.
“The researchers theorized that a sudden niacin deficiency would result in the degeneration of nerves supplying the gastrointestinal tract. Niacin is a central component of various compounds that play a role in the maintenance of nerve health,” explained Kathleen Crandell, Ph.D., a Kentucky Equine Research (KER) nutritionist.
Acute deficiencies could conceivably result after horses ingest certain compounds, such as products produced by some bacteria, including Fusarium spp. Bacteria are present in certain grasses and can therefore potentially result in EGS.
Researchers were unable to confirm the connection between acute niacin deficiency and EGS within the parameters of their research study. Specifically, there was no difference in blood concentrations of vitamins B1, B2, and B6 between horses that did and did not have EGS. The lack of evidence may have been compounded by the small number of horses in the study and insufficient data on what would be normal levels of niacin in horses.
In sum, an acute deficiency of niacin is an unlikely cause of EGS.
Source: Equinews
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