Abstract

In late April/early May of 2001, for the equine industry in Kentucky, a previously unknown factor led to the loss of up to 40% of the new pregnancies (20-60 days) for that year, with a following significant number of late abortions and ill new born foals. In addition, encephalopathy, ocular lesions, pericarditis, laminitis, and other diseases were suspected to be associated with the syndrome. This occurrence was known as the mare reproductive loss syndrome (MRLS). On examination of the weather data, this period was seen to have an unusual pattern of severe late spring frost. Acute changes in the pasture diet affected the horses gut microflora, allowing the overgrowth of opportunistic pathogens and resulting in the excessive absorption of nitrogen and ammonia from the large bowel. Clinical blood chemistries from the horses on pasture at this time showed abnormally high levels of blood urea nitrogen (BUN). Elevated blood ammonia levels were found in mares and newborn foals affected with MRLS. Ammonia is metabolically one of the most toxic substances to the body. It is present naturally as a breakdown product of nitrogen turnover. If the body nitrogen balance is disturbed for any reason, with nitrogen accumulation exceeding the body's ability to excrete it as urea (BUN), ammonia will accumulate in toxic levels. Ammonia toxicity can cause all the symptoms that were observed in the horses exhibiting MRLS.

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