In the spring of 2013, one of our favorite mares gave birth to her first foal, a strapping bay colt we named Winston. At first, Winston was strong and athletic. We taught him to lead, longe and respond to other handling while his watchful mother stood nearby. On all counts, he seemed a healthy and promising baby. After just a few weeks, however, we could see that something was wrong with Winston—he was becoming weak and uncoordinated. We called our veterinarian out for an examination.
The diagnosis was cervical vertebral compressive myelopathy (CVCM), commonly called wobbler disease. A catchall term for compression of the spinal cord, “wobbles” in older horses is often related to arthritic changes or trauma, but in foals as young as Winston the condition is typically due to malformations and abnormalities of the vertebrae. Winston’s condition deteriorated rapidly, and soon he began to have difficulty lying down and getting up on his own. At this point, our family made the grim decision to end his suffering and euthanize him.
Several veterinarians we consulted told us that Winston’s case was an anomaly and extremely unlikely to reoccur on our farm. And we had no reason to doubt that. We’d had two or three homebred foals annually on our farm for the previous nine years and not one had any known neurological issues. So, after a year of rest, we decided to give Winston’s dam another chance at motherhood, matching her with a different stallion. We wanted this healthy, kind and wonderfully bred mare to have the opportunity to raise a foal. In the spring of 2015, Hope was born. Her name symbolized the bright future that seemed to stretch ahead of her.
Hope was beautiful in every respect. She had a bright dun coat and her classically athletic stock horse build was evident from the beginning. As the months passed, we watched her grow, and her health appeared to be excellent. But when she was 3 months old, Hope started showing signs of uncoordination. We began to fear that she had a milder form of the condition that had plagued Winston. We consulted the same veterinarian, who told us that we were again dealing with a case of wobbler disease. As time passed and her condition deteriorated, Hope struggled to get up on her own. By the time she was a weanling, we saw no other option but to end her discomfort. We had no faith that she could have had a comfortable life.
We decided that Winston and Hope’s dam must not be a broodmare. Even lacking scientific proof that wobbles is a heritable condition, the only logical explanation to us seemed to be that our mare was, due to some genetic or reproductive issue, producing offspring with this problem. Luckily, the mare was well-trained as a riding horse, so we were able to find her a wonderful home with owners who agreed to our stipulation that she never be bred again. We were overjoyed at her opportunity to begin a lovely new life.
Life on our farm went back to normal. We watched our remaining group of homebred yearlings, 2- and 3-year-olds flourish, trying to heal from the loss of Winston and Hope.
More heartbreak
Then in 2016, as usual, we had a small group of spring foals. One, a filly named Peach, was the first foal born to Plum, one of our favorite riding mares. At first everything seemed fine. When Peach was only a few days old we practiced putting a lead on her and asking her to walk along next to her mother. She seemed more sensitive than the average foal and was prone to pulling back. This did not appear terribly abnormal at first, but over the next month it became apparent that she lacked coordination and balance.
We started to panic. Peach’s disability was frighteningly similar to those we had seen before. But how could it be the same issue? Everything we’d been told pointed to Winston and Hope being unfortunate, isolated cases. Yet here we were again.
Consulting a different equine veterinarian this time, we explained the entire series of events in detail. At this point, we were convinced there was an underlying cause. One small farm having three cases of wobbler disease in four years seemed improbable. Our first suspicion was an environmental toxin or a nutritional deficiency, but the veterinarian thought these were unlikely because we feed high-quality hay and a commercially produced feed formulated for breeding horses. The veterinarian did find a sore area on Peach’s neck and proceeded to take x-rays. A possible area of inflammation was found near a growth plate, and the veterinarian recommended that we give her a few months to improve. Over the next two months, her condition continued to deteriorate. We were at our wits’ end.
In search of an answer, we began scouring the internet for scientific literature that might shed some light on what we were dealing with. Soon we came across research conducted by C.J. Finno, DVM, PhD, at the University of California—Davis. In one of her studies, Finno described a Paint Horse breeding farm with a situation that mirrored our own. The horses on that farm had a vitamin E deficiency, which triggered the development of clinical signs associated with a hereditary condition known as equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy (eNAD/EDM). We become convinced we were dealing with the same situation. We contacted Finno and she generously agreed to fly from California to examine Peach for herself.
By the time Finno arrived at our farm with her research assistants, Peach was having trouble standing. After only a short neurological exam, Finno told me that she thought our filly could have eNAD/EDM—a disease she has dedicated her career to researching—and began to fill me in on the details of this devastating condition.
A confluence of conditions
Equine NAD/EDM, Finno told me, develops in very young horses when two very specific conditions are met: a genetic susceptibility and vitamin E deficiency. That was surprising to hear, given that we always fed high-quality hay and grain. But without regular access to good pasture, horses can quickly become deficient in this nutrient. We proceeded to check the vitamin E levels of Peach, her dam and several other horses on the property. All were low or even critically low. The normal range of vitamin E in blood is 2 to 4 µg/mL. Peach had a blood level of 0.6 µg/mL.
Vitamin E is an antioxidant, protecting cells from the action of “free-radical” oxygen molecules that steal electrons. This is a crucial function in rapidly growing foals. Without adequate antioxidant protection, neurons and axons throughout the body degrade, leading to incoordination and progressive weakness. Mildly affected foals may have lesions consistent with only eNAD (i.e., the mildest version of the disease) whereas moderate to severely affected foals have more extensive lesions consistent with EDM. Foals can show signs of impairment as early as one month of age, and signs are usually progressive, beginning as clumsiness and advancing to severe disability. Affected horses may have trouble backing up and rising from a lying position. In severe cases, weakness is most easily seen in the hind legs.
Not every foal deficient in vitamin E, however, will develop eNAD/EDM. Foals must also have a genetic predisposition to develop the disease. Although the exact gene has yet to be located in horses, it is clear from Finno’s research that there is a heritable component to eNAD/EDM, not just in Quarter Horses but also in many other breeds. This genetic predisposition likely explains why Peach was affected by eNAD/EDM while other foals born on our farm that year were not, even though they all had low vitamin E levels.
The necessity of these two factors also explains why the condition hardly ever appears in foals born in areas of the country where lush pasture is readily available. Even if they have the predisposing genetic defect, their dams have plenty of vitamin E to deliver to the foal via colostrum0, and then pasture provides enough supply as the foals’ diet shifts from milk to forage. The abundance of lush pasture protects the youngster until the window of risk —thought to be about a year—passes. As Finno put it, “You probably won’t see this disease very often in Kentucky, where lush pasture is available for pregnant mares and young foals.”
Finno went on to explain that there is an identical syndrome in children, who appear normal at birth but develop progressive neurological symptoms due to a defect in the gene responsible for vitamin E transport into cells. Analysis of the same gene in affected horses hasn’t turned up a cause for the defect, but Finno and her team are continuing to look. Once the genetic component responsible is identified and the heritability understood, sires and dams can be tested to determine the risk of producing an affected foal. Then a different pairing with a lower risk could be made, or other preventive measures could be taken— namely supplementing the dam and newborn foal with vitamin E. An additional supply of the vitamin may protect an affected foal’s neurons and axons through the critical growth period.
Leaving a legacy
All of this, however, was too late for Peach. Finno indicated that once neurological signs of eNAD/EDM appear, there is no way to reverse them. The damage was done, and no amount of vitamin E at this point could fix it. Further, the only way to know for sure if Peach had eNAD/EDM would be a necropsy, which would have to be performed immediately after she died. With that information, we made the gut-wrenching decision to send Peach back to California with Finno. We also sent another homebred horse, a 7-year-old gelding with a pedigree similar to that of Winston and Hope. When put in training, the gelding seemed so clumsy that we had decided he was not safe to ride. Finno had performed a neurological exam on the gelding and told us she suspected that he may have eNAD/EDM as well. Now they would both be part of her essential research.
A week after she left our farm, Finno called to confirm that Peach and the gelding both had damage in the region of the brainstem and spinal cord specific to eNAD/EDM. Neither horse had any pathological evidence of wobbler disease. Their tissues and genetic material would become clues in the search for the gene responsible for this terrible disease. As horrible as it was to lose them, we take some comfort in knowing they contributed to this effort.
Without necropsies, there is no way to know for certain whether Winston and Hope also had eNAD/EDM, but in our minds, there is no doubt. Finno explained that many cases of eNAD/EDM are misdiagnosed as wobbler disease or, in older horses, equine0 protozoal myeloencephalitis (EPM) that doesn’t respond to treatment or “returns” repeatedly. Many of these horses manage well enough at liberty but are too uncoordinated to carry a rider. They are labeled “clumsy” or “unathletic” when, in reality, they actually have a serious problem.
Since discovering the cause of Peach’s disease, we’ve changed the way we manage our horses. We regularly check their vitamin E levels, and we supplement all horses, especially broodmares, to ensure their colostrum is rich with the vitamin. Because the milk that follows colostrum doesn’t contain much vitamin E, we supplement all newborns with a liquid form of the nutrient until they are a year old. We are also taking steps to improve our pastures and provide our horses with more access to fresh grass, but living where we do, we will never be comfortable relying on grass alone to fulfill this crucial need.
We’ve also become advocates for eNAD/EDM awareness and preventive measures in our local horse community. We share our message with anyone who will listen: Horses who don’t have regular access to high-quality pasture are likely to become vitamin E deficient, which can have serious consequences even in those not susceptible to eNAD/EDM. In our area, this is especially important to know. No one here has abundant pasture and, if they rely on baled forage, they need to be aware of the risks. We encourage horse owners to raise the question of eNAD/EDM with their veterinarians because, unfortunately, this disease is not widely recognized. We also promote supplementation of horses and broodmares with vitamin E. Supplementation is relatively easy and we’ve already seen the benefits on our farm—we had two foals born this past year who are growing into perfectly coordinated, strong, beautiful horses.
This article first appeared in the September 2017 issue of EQUUS (Volume #380)In the spring of 2013, one of our favorite mares gave birth to her first foal, a strapping bay colt we named Winston. At first, Winston was strong and athletic. We taught him to lead, longe and respond to other handling while his watchful mother stood nearby. On all counts, he seemed a healthy and promising baby. After just a few weeks, however, we could see that something was wrong with Winston—he was becoming weak and uncoordinated. We called our veterinarian out for an examination.
The diagnosis was cervical vertebral compressive myelopathy (CVCM), commonly called wobbler disease. A catchall term for compression of the spinal cord, “wobbles” in older horses is often related to arthritic changes or trauma, but in foals as young as Winston the condition is typically due to malformations and abnormalities of the vertebrae. Winston’s condition deteriorated rapidly, and soon he began to have difficulty lying down and getting up on his own. At this point, our family made the grim decision to end his suffering and euthanize him.
Several veterinarians we consulted told us that Winston’s case was an anomaly and extremely unlikely to reoccur on our farm. And we had no reason to doubt that. We’d had two or three homebred foals annually on our farm for the previous nine years and not one had any known neurological issues. So, after a year of rest, we decided to give Winston’s dam another chance at motherhood, matching her with a different stallion. We wanted this healthy, kind and wonderfully bred mare to have the opportunity to raise a foal. In the spring of 2015, Hope was born. Her name symbolized the bright future that seemed to stretch ahead of her.
Hope was beautiful in every respect. She had a bright dun coat and her classically athletic stock horse build was evident from the beginning. As the months passed, we watched her grow, and her health appeared to be excellent. But when she was 3 months old, Hope started showing signs of uncoordination. We began to fear that she had a milder form of the condition that had plagued Winston. We consulted the same veterinarian, who told us that we were again dealing with a case of wobbler disease. As time passed and her condition deteriorated, Hope struggled to get up on her own. By the time she was a weanling, we saw no other option but to end her discomfort. We had no faith that she could have had a comfortable life.
We decided that Winston and Hope’s dam must not be a broodmare. Even lacking scientific proof that wobbles is a heritable condition, the only logical explanation to us seemed to be that our mare was, due to some genetic or reproductive issue, producing offspring with this problem. Luckily, the mare was well-trained as a riding horse, so we were able to find her a wonderful home with owners who agreed to our stipulation that she never be bred again. We were overjoyed at her opportunity to begin a lovely new life.
Life on our farm went back to normal. We watched our remaining group of homebred yearlings, 2- and 3-year-olds flourish, trying to heal from the loss of Winston and Hope.
More heartbreak
Then in 2016, as usual, we had a small group of spring foals. One, a filly named Peach, was the first foal born to Plum, one of our favorite riding mares. At first everything seemed fine. When Peach was only a few days old we practiced putting a lead on her and asking her to walk along next to her mother. She seemed more sensitive than the average foal and was prone to pulling back. This did not appear terribly abnormal at first, but over the next month it became apparent that she lacked coordination and balance.
We started to panic. Peach’s disability was frighteningly similar to those we had seen before. But how could it be the same issue? Everything we’d been told pointed to Winston and Hope being unfortunate, isolated cases. Yet here we were again.
Consulting a different equine veterinarian this time, we explained the entire series of events in detail. At this point, we were convinced there was an underlying cause. One small farm having three cases of wobbler disease in four years seemed improbable. Our first suspicion was an environmental toxin or a nutritional deficiency, but the veterinarian thought these were unlikely because we feed high-quality hay and a commercially produced feed formulated for breeding horses. The veterinarian did find a sore area on Peach’s neck and proceeded to take x-rays. A possible area of inflammation was found near a growth plate, and the veterinarian recommended that we give her a few months to improve. Over the next two months, her condition continued to deteriorate. We were at our wits’ end.
In search of an answer, we began scouring the internet for scientific literature that might shed some light on what we were dealing with. Soon we came across research conducted by C.J. Finno, DVM, PhD, at the University of California—Davis. In one of her studies, Finno described a Paint Horse breeding farm with a situation that mirrored our own. The horses on that farm had a vitamin E deficiency, which triggered the development of clinical signs associated with a hereditary condition known as equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy (eNAD/EDM). We become convinced we were dealing with the same situation. We contacted Finno and she generously agreed to fly from California to examine Peach for herself.
By the time Finno arrived at our farm with her research assistants, Peach was having trouble standing. After only a short neurological exam, Finno told me that she thought our filly could have eNAD/EDM—a disease she has dedicated her career to researching—and began to fill me in on the details of this devastating condition.
A confluence of conditions
Equine NAD/EDM, Finno told me, develops in very young horses when two very specific conditions are met: a genetic susceptibility and vitamin E deficiency. That was surprising to hear, given that we always fed high-quality hay and grain. But without regular access to good pasture, horses can quickly become deficient in this nutrient. We proceeded to check the vitamin E levels of Peach, her dam and several other horses on the property. All were low or even critically low. The normal range of vitamin E in blood is 2 to 4 µg/mL. Peach had a blood level of 0.6 µg/mL.
Vitamin E is an antioxidant, protecting cells from the action of “free-radical” oxygen molecules that steal electrons. This is a crucial function in rapidly growing foals. Without adequate antioxidant protection, neurons and axons throughout the body degrade, leading to incoordination and progressive weakness. Mildly affected foals may have lesions consistent with only eNAD (i.e., the mildest version of the disease) whereas moderate to severely affected foals have more extensive lesions consistent with EDM. Foals can show signs of impairment as early as one month of age, and signs are usually progressive, beginning as clumsiness and advancing to severe disability. Affected horses may have trouble backing up and rising from a lying position. In severe cases, weakness is most easily seen in the hind legs.
Not every foal deficient in vitamin E, however, will develop eNAD/EDM. Foals must also have a genetic predisposition to develop the disease. Although the exact gene has yet to be located in horses, it is clear from Finno’s research that there is a heritable component to eNAD/EDM, not just in Quarter Horses but also in many other breeds. This genetic predisposition likely explains why Peach was affected by eNAD/EDM while other foals born on our farm that year were not, even though they all had low vitamin E levels.
The necessity of these two factors also explains why the condition hardly ever appears in foals born in areas of the country where lush pasture is readily available. Even if they have the predisposing genetic defect, their dams have plenty of vitamin E to deliver to the foal via colostrum0, and then pasture provides enough supply as the foals’ diet shifts from milk to forage. The abundance of lush pasture protects the youngster until the window of risk —thought to be about a year—passes. As Finno put it, “You probably won’t see this disease very often in Kentucky, where lush pasture is available for pregnant mares and young foals.”
Finno went on to explain that there is an identical syndrome in children, who appear normal at birth but develop progressive neurological symptoms due to a defect in the gene responsible for vitamin E transport into cells. Analysis of the same gene in affected horses hasn’t turned up a cause for the defect, but Finno and her team are continuing to look. Once the genetic component responsible is identified and the heritability understood, sires and dams can be tested to determine the risk of producing an affected foal. Then a different pairing with a lower risk could be made, or other preventive measures could be taken— namely supplementing the dam and newborn foal with vitamin E. An additional supply of the vitamin may protect an affected foal’s neurons and axons through the critical growth period.
Leaving a legacy
All of this, however, was too late for Peach. Finno indicated that once neurological signs of eNAD/EDM appear, there is no way to reverse them. The damage was done, and no amount of vitamin E at this point could fix it. Further, the only way to know for sure if Peach had eNAD/EDM would be a necropsy, which would have to be performed immediately after she died. With that information, we made the gut-wrenching decision to send Peach back to California with Finno. We also sent another homebred horse, a 7-year-old gelding with a pedigree similar to that of Winston and Hope. When put in training, the gelding seemed so clumsy that we had decided he was not safe to ride. Finno had performed a neurological exam on the gelding and told us she suspected that he may have eNAD/EDM as well. Now they would both be part of her essential research.
A week after she left our farm, Finno called to confirm that Peach and the gelding both had damage in the region of the brainstem and spinal cord specific to eNAD/EDM. Neither horse had any pathological evidence of wobbler disease. Their tissues and genetic material would become clues in the search for the gene responsible for this terrible disease. As horrible as it was to lose them, we take some comfort in knowing they contributed to this effort.
Without necropsies, there is no way to know for certain whether Winston and Hope also had eNAD/EDM, but in our minds, there is no doubt. Finno explained that many cases of eNAD/EDM are misdiagnosed as wobbler disease or, in older horses, equine0 protozoal myeloencephalitis (EPM) that doesn’t respond to treatment or “returns” repeatedly. Many of these horses manage well enough at liberty but are too uncoordinated to carry a rider. They are labeled “clumsy” or “unathletic” when, in reality, they actually have a serious problem.
Since discovering the cause of Peach’s disease, we’ve changed the way we manage our horses. We regularly check their vitamin E levels, and we supplement all horses, especially broodmares, to ensure their colostrum is rich with the vitamin. Because the milk that follows colostrum doesn’t contain much vitamin E, we supplement all newborns with a liquid form of the nutrient until they are a year old. We are also taking steps to improve our pastures and provide our horses with more access to fresh grass, but living where we do, we will never be comfortable relying on grass alone to fulfill this crucial need.
We’ve also become advocates for eNAD/EDM awareness and preventive measures in our local horse community. We share our message with anyone who will listen: Horses who don’t have regular access to high-quality pasture are likely to become vitamin E deficient, which can have serious consequences even in those not susceptible to eNAD/EDM. In our area, this is especially important to know. No one here has abundant pasture and, if they rely on baled forage, they need to be aware of the risks. We encourage horse owners to raise the question of eNAD/EDM with their veterinarians because, unfortunately, this disease is not widely recognized. We also promote supplementation of horses and broodmares with vitamin E. Supplementation is relatively easy and we’ve already seen the benefits on our farm—we had two foals born this past year who are growing into perfectly coordinated, strong, beautiful horses.
This article first appeared in the September 2017 issue of EQUUS (Volume #380)
