Spring Crisis in the Bluegrass
Hanging by a Thread: Central Kentucky's Foaling Crisis
By Nathan M. Slovis, DVM, Diplomat American College
Veterinary Internal Medicine

photo by James Shambhu

"At first we thought of these as routine critical care cases but over the next three weeks the cases kept pouring on in. The clinic resembled a M.A.S.H. unit. The number of sick foals admitted to the hospital became so massive that we were hard pressed to find room for all of them. We made stalls out of the hay rooms, recovery rooms and even the aisleways."

-Dr. Fairfield Bain

Triage isn't usually the first word vets use to describe their clinics. Neither is "MASH unit." But those military-style terms couldn't help but come up in describing this past spring's foaling crisis.

At the end of April and beginning of May this year, Kentucky horse owners witnessed the worst disaster in the history of the state for fetal/foal losses. Never before in the history of veterinarian medicine had such a devastating group of syndromes hit a population of animals so fast and so hard. For 21 days, veterinarians were faced with a crisis of epic proportion. Horse hospitals throughout the state were set up like M.A.S.H. units, lining up the sick animals once they arrived, putting them wherever space would allow. Currently the cause of this crisis is still unknown, but scientists are collecting data and conducting experiments to hopefully reveal the cause of exactly what went wrong. What is known, however, is that whatever these horses were exposed to came and left in a hurry, but the devastating effects will be felt by the equine community for years to come.

Gail Murray, Supervisor of Nursing at Hagyard-Davidson-McGee.
The Crisis Unfolds

On April 26, the internal medicine department at Hagyard-Davidson-McGee saw its first case of excessive fluid in the sac around the heart (pericarditis) and a late term fetal loss mare.

Dr. Fairfield Bain recalls, "at first we thought of these as routine critical care cases but over the next three weeks the cases kept pouring on in. The clinic resembled that of a M.A.S.H. unit. The number of sick foals admitted to the hospital became so massive that we were hard pressed to find room for all of them. We made stalls out of the hay rooms, recovery rooms and even the aisleways."

Conversations with other equine hospitals in the area revealed that that they, too, were seeing an extraordinary number of fetal loss/weak foal syndrome cases. Similar deaths were also being documented in the neighboring states of West Virginia and Ohio.

On Derby Eve, Hagyard-Davidson-McGee reported that 14 red-bag foals had been presented to the clinic.

The following day, amid the excitement of the Kentucky Derby, the Kentucky Livestock Disease Diagnostic Center took in 73 [spontaneously] aborted foals and fetuses, marking a 700% increase in deaths for this year.

The late term foals were presented to the Neonatal Intensive Care Unit slightly premature (one to two weeks before their due dates) and with a history of a "red bag" delivery or premature separation of the placenta.

It is critical to assist these foals during delivery because many of them would die during the birth process. "Red Bag" foaling is not an uncommon complication associated with delivery, but it was the vast number of these complications that were occurring during such a distinct time period that concerned practitioners.

The majority of the foals that present as a "red bag" delivery are diagnosed with birth asphyxia. Most of the birth asphyxia foals respond favorably (up to 90%) to treatment and are discharged from the hospital.

The worrisome thing was that 50-60% of foals being diagnosed as "red bag" were dying. Plagued by low white blood cell counts (making them susceptible to bacterial infections), foals were also extremely dehydrated, hypoglycemic and had severe respiratory dysfunction which was not responding to conventional therapy.

Blood cultures and/or tissue cultures on the majority of these foals/aborted fetuses isolated a bacteria classified as an alpha-streptococcus. It was theorized that these foals/fetuses must have been immunocompromised to such an extent that this bacteria was able to gain entry into their system with minimal resistance.

“The inevitable is here... Ten days of treatment, all efforts spent, no plans left after Plan A, B, & C. …But I am a poor loser and don’t accept this well.”
—Nathan M. Slovis, DVM
Who, What, Why?

During late April and early May, these early fetal abortions were occurring in seemingly healthy mares throughout the bluegrass. The occurrence of these spontaneous abortions tended to be 35 days post breeding and prior to 120 days.

As the early fetal abortions and the later term pregnancy losses were occurring, two other syndromes were starting to be noticed. Opthalmologist Claire Latimer, DVM, Dipl. ACVO, noticed an extraordinary increase in eye problems this spring in Kentucky, affecting only one eye in older foals or adult horses (known as panopthalmitis). The inflammation was so severe that it didn't respond to treatment and the owners were left with a horse with only one seeing eye. Dr. Latimer stated that she has either seen or consulted on 30 +/- cases of these cases and that, "unfortunately none of these horses have regained vision in the affected eye."

At the same time, specialists at Hagyard-Davidson-Mcgee and Rood and Riddle Equine Hospitals were beginning to see an overwhelming amount of excessive fluid around the heart (pericarditis).

According to Dr. Doug Byars, a boarded internist and critical care specialist, his clinic sees usually two to three cases per year, but from early April to early June they "have seen 33 cases of pericarditis and eight of these cases came in over a 24 hour period."

Out of the 33 cases seen at HDM, four were either euthanized or died due to secondary constrictive pericarditis.

Rood and Riddle has seen 10 cases as of June and the Kentucky Livestock Disease Diagnostic Center has performed autopsies on another 10 cases.

The treatment plan for most of these pericarditis patients consisted of: placing an indwelling pericardial drain and the use of systemic steroids, antinflammatory drugs and antibiotics. Some horses had 5 gallons of fluid taken from the fluid surrounding the heart.

On average, 1 to 1.5 gallons of fluid have been drained from the pericardial space of adult horses.

The current survivors of the pericarditis syndrome are still being monitored closely because the tissue surrounding the heart will continue to mature and could cause constrictive pericarditis and right sided heart failure.

The prognosis for a horse with constrictive pericarditis is poor. Two pericardectomies (surgery to remove the constrictive pericardium around the failing heart muscle) have been performed by Dr. Scott Hopper of Lexington.

This difficult surgery is a last resort, available to veterinarians when they have a horse in constrictive heart failure. The prognosis for long term outcome from this surgery is considered guarded.

Of the two surgeries performed, only one horse has survived.

Ongoing research is still being pursued at the Gluck Center, Kentucky Livestock Disease Diagnostic Center and at Hagyard-Davidson-McGee and Rood and Riddle Equine Hospitals. The Kentucky Association of Equine Practitioners has recently acquired the assistance of an equine epidemiologist from Texas A&M Veterinary School to help pursue the epidemiological background for some of the other theories and potential causes of the bluegrass crisis.


All breeds were vulnerable to mare reproductive loss, pericarditis and uveitis syndrome. The following breeds were affected in Kentucky :



Tennessee Walking Horse

American Saddlebred

Quarter Horse


Rocky Mountain Horse





Paso Fino

Miniature horse




It is estimated that 5 percent of the 2001 Kentucky Thoroughbred foal crop and 20 percent of the 2002 foal crop has been lost. That will account for hundreds of millions of dollars in lost revenue for the Kentucky Thoroughbred Industry. -NS


Researchers and veterinarians are currently looking toward an environmental cause for these syndromes, since none of the signs pointed toward an infectious or contagious disease process.

The three syndromes of mare reproductive loss, pericarditis and uveitis appear to be linked to the same causative agent.

All of these syndromes occurred during the same time period and have a beginning and end documented by equine practitioners. Fetuses and foals have been tested for various heavy metals, leptospirosis, equine arteritis virus, equine herpes virus and adenovirus -all have been negative.

Here are some of the theories being tested by researchers:


Phytoestrogens are forages and feeds that have been known to cause hyperestrogenism in animals. Some common phytoestrogens are alfalfa, subterranean clover and red clover.

Signs of hyperestrogenism are nyphomania, cystic ovaries, swollen genitalia and in males, development of female characteristics. Horses are very resistant to these estrogenic compounds and as of now all samples tested for these phytoestrogens have been inconclusive, therefore they have been scientifically ruled out as a potential cause of these syndromes.


Mycotoxins are toxins produced by fungi. With the early spring freeze that occurred in April some of the forages were injured out in the pastures, therefore possibly allowing the growth of certain kinds of fungi that may produce certain toxins. Over 150 samples of forages, feeds and eastern tent caterpillars have been tested and have so far come up inconclusive. This theory has yet to be dismissed fully as the cause of the spring syndromes.


Fescue toxicosis is common throughout the United States. Fescue can be infected with an endophyte called Neophtodium coenophilum which has ergot alkaloids. These alkaloids can cause prolonged gestation, abortions, premature separation of the placenta, thick placentas, retained placentas and decreased to no milk production by the mare. However, the majority of the foals presented to the equine hospitals were premature in age (1-2 weeks early), the placentas were not all edematous and most of the mares had proper milk production. This does not fit a fescue toxicosis. Mare reproductive loss syndromes have been documented on pastures completely free of endophytes and fescue.


An agronomist from out of the state came to the bluegrass to help aid in the investigation of the syndrome. Unfamiliar with Lexington pastures, he spotted poison hemlock on the fence rows of some of the affected mares' pastures and thought that was the problem, sparking an investigation. The primary action of the hemlock is as a nerve depressant. Poison hemlock does not taste very good and a world authority on poison hemlock stated that he could not force horses to eat the plant even after he placed molasses on it, freeze dried it and even mixed it with other forages. All testing for the poison hemlock alkaloids have been negative.


The cyanide theory came into play when agronomists and farmers detected black cherry trees on their property where some of the mare losses where occurring. It is well known that black cherry tree leaves contain prunasin, a cyanide precursor that is non-toxic. However, when leaves are damaged (ie, the April frost) the prunasin molecule is split, allowing cyanide to be released. Cyanide causes the death of animals by keeping the body from being able to use oxygen at the cellular level and therefore causing "suffocation" of the tissues. Cherry trees were not detected in the pastures of some mares that had the syndrome.

Next came the theory of the Eastern Tent Caterpillars (ETC). ETC feed predominantly on black cherry tree leaves; they will search for these trees before going to another fruit tree to nest. ETC would then have cyanide in their digestive tract. Horses accidentally feeding on the caterpillars might be exposed to the cyanide. These low doses of cyanide would therefore cause fetal losses, uveitis and pericarditis in the affected horses.

A leading entomologist at UK has researched the physiologic perspectives and potential of the ETC to deliver cyanide to horses and thereby cause abortions. The results are consistent with the existing literature of insects feeding on cyanogenic plants and indicate that cyanogenic compounds are found only in newly ingested plant material, with ETC larvae rapidly detoxifying ingested plant material. Larvae on the ground, either starved or wandering, have little cyanogenic capacity and are unlikely to vector cyanide from plant material to vertebrate herbivores. Research is still being conducted at the Gluck Center to fully confirm or refute the entomologist's report. Cyanide has been detected in the hearts of two aborted fetuses.The main problem with this finding is that we do not know what the normal values are for fetal heart tissue. The theory of cyanide as the cause for mare reproductive loss syndrome is hanging on by a loose thread.


One researcher has recently claimed that he has noted increased fetal losses in pastures that have been fertilized with Pot Ash and/or fertilizers with a high potassium concentration. In those fields he noted an increase of the potassium to calcium ratio. Normal should be 1 to 2, but in these pastures it was 10 to 1. His theory was that with an increase in potassium you will have an anion and cation imbalance that could possibly make these animals vulnerable (immunosupressed) to various diseases or bacteria (ie, Streptococcus noted in the fetuses and foals). This theory is currently being investigated in an epidemiological report.