Portions of this article appeared in a two-part series in GREAT SCOTS MAGAZINE, Aug. - Sept., Vol. 13, No. 4 , and in Oct.-Sept. Vol 3., No. 5: “A Stone’s Throw: Ripples Across Time with Scottish Terriers.”
Bonnie Sue: One Scottish Terrier's Experience with Adrenal Exhaustion and SARDS
The Stone's Throw
Looking back over my life with Scotties, I realize that there have often been large, unforeseen consequences from small actions. You throw a small stone in a pond, but the ripples have a way of going far past the original point of impact, sometimes in a surprising way. My love of Scotties was started through a "small stone"--a gift for my graduation. I wandered into a pet store with my mother and grandmother and both noticed my interest in a young female Scottie. She'd been there a month or so past the cute puppy stage, so her price was reasonable and my grandmother decided to make this Scottie a gift to me. We'd owned a Poodle since I was eight years old so this young Scottish Terrier was a complete surprise. She had a saucy attitude from her months of confinement and made it clear she had no desire to sit quietly by my side or to gaze adoringly at anyone. No, she wanted to run and romp and see the world, and hey, if I wanted to come, great. If not, she'd just see me around. "Shock and awe" pretty much summed up my first impressions of "Babes," so named because she possessed the iron will, sense of humor and love of wandering that were found in Paul Bunyan's legendary pet, the Blue Ox, Babe. The name would have been more a more accurate reflection of all I didn't know about Scotties and my naivete' in supposing I would learn all I needed to know quickly.
Babes relented a bit and grew more loving as the years passed. In turn, I made a promise that she would have the best I could possibly provide. I had to learn exactly how to do that because it was not something I had been shown by example. Vet care was not something my kin thought much about, although my family did spay and neuter their pets and believed in the mercy of euthanasia administered through the hands of a professional, not a neighbor with a shotgun. In those beliefs and actions, we were exceptions.
I grew up in a rural coal-mining community in West Virginia. I was always concerned by the careless disregard for animals I witnessed in grownups and children alike. Where we lived, the possibility for pain animals could suffer was great. Ponies, horses, dogs, puppies, cats and kittens were all targets. If pets became ill or inconvenient, they might be shot, drowned or disposed of in some other way--perhaps being dropped by the side of the road in the dark of the night. Sometimes animals were hurt simply in the name of sport. A dog I had as a young girl was pushed off a large bridge by young men in our neighborhood. No reason was given, but a crowd witnessed the act and did nothing to stop it or assist the dog.
As I grew older, the empathy I felt for animals was such an integral part of my nature, I knew it was a God-given gift. The negative side of it was that I became sort of a bulls-eye for the neighborhood kids and they sought me out in particular to witness their more incredible acts of cruelty. One boy enjoyed watching my rising panic as he would hold a cigarette lighter beneath box turtles or other small animals. I attempted to avoid these scenes, reasoning that the violence escalated when witnesses were present. He soon retaliated by shooting our little 12-week-old puppy, Oscar, and leaving it in my parent's driveway. It was hard for me to understand why my parents did not take some kind of action. It maddened me that this kind of violence was easily accepted by the mainstream and consequences were nonexistent.
Viewing all this from the perspective of a powerless young girl in a community of strong-minded adults, I could only combat my feelings of helplessness by assuring myself that when I was older, I would do everything possible to protect and preserve the health of my own pets. It also led to a decision to be a vegetarian in my mid-twenties, a lifestyle change that sprang directly from this desire to protect the innocent. I was no longer able to mentally separate animals that were "pets" from animals designated "food." With that background, Babes was understandably a big part of my life as a young adult.
After I married, my husband Patrick spent many hours walking her and caring for her. When an independent dog like a Scottie turns to you for affection, you can't help but be flattered, and Pat soon fell into her fuzzy paws. I had long been suffering from her unique charm, but Babes gave Patrick the "Scottie flu" in a big way. That's how it all started for us as a family. We've had many Scotties and other pets since then, all unique, all wonderful, some with what you might think are impressive pedigrees, others without–but all united by the fact that they were sick for much of their all-too-short lives. That deep affection we both felt for them and the desire to create the best health for them has shaped many decisions in our life together.
Free to Good Home
After many years of owning Scotties and other kinds of cats and dogs, another Scottie--Bonnie Sue--came into our lives, I had no idea that in trying to care for her, I would stumble upon some particularly startling information that could impact the health of Bonnie and give me a new perspective on the health problems that plagued other animals we owned and those long gone.
In 2003, I was home nearly full-time. I had recently quit the job I'd had for 13 years and was doing some marketing for a friend who'd started a pet treat business. I was enjoying the freedom this break in the action offered, most especially the time with our pets. It was completely wonderful to have that uninterrupted time with them and they responded by following me around like sheep from the time I opened my eyes in the morning until we all went to bed at night.
One day, a lady from my former workplace who knew of my deep love of Scottish Terriers called to direct me to an ad in a local sales bulletin. The ad simply displayed the phone number and the words "Female Scottie free to good home, must be spayed." I wasn't looking for another Scottie, but I didn't think twice about making the call. I knew that if for some reason we could not keep this dog, I had contacts in Scottie rescue who would help me find just the right home.
Bonnie Sue: One Scottish Terrier's Experience with Adrenal Exhaustion and SARDS
The Stone's Throw
Looking back over my life with Scotties, I realize that there have often been large, unforeseen consequences from small actions. You throw a small stone in a pond, but the ripples have a way of going far past the original point of impact, sometimes in a surprising way. My love of Scotties was started through a "small stone"--a gift for my graduation. I wandered into a pet store with my mother and grandmother and both noticed my interest in a young female Scottie. She'd been there a month or so past the cute puppy stage, so her price was reasonable and my grandmother decided to make this Scottie a gift to me. We'd owned a Poodle since I was eight years old so this young Scottish Terrier was a complete surprise. She had a saucy attitude from her months of confinement and made it clear she had no desire to sit quietly by my side or to gaze adoringly at anyone. No, she wanted to run and romp and see the world, and hey, if I wanted to come, great. If not, she'd just see me around. "Shock and awe" pretty much summed up my first impressions of "Babes," so named because she possessed the iron will, sense of humor and love of wandering that were found in Paul Bunyan's legendary pet, the Blue Ox, Babe. The name would have been more a more accurate reflection of all I didn't know about Scotties and my naivete' in supposing I would learn all I needed to know quickly.
Babes relented a bit and grew more loving as the years passed. In turn, I made a promise that she would have the best I could possibly provide. I had to learn exactly how to do that because it was not something I had been shown by example. Vet care was not something my kin thought much about, although my family did spay and neuter their pets and believed in the mercy of euthanasia administered through the hands of a professional, not a neighbor with a shotgun. In those beliefs and actions, we were exceptions.
I grew up in a rural coal-mining community in West Virginia. I was always concerned by the careless disregard for animals I witnessed in grownups and children alike. Where we lived, the possibility for pain animals could suffer was great. Ponies, horses, dogs, puppies, cats and kittens were all targets. If pets became ill or inconvenient, they might be shot, drowned or disposed of in some other way--perhaps being dropped by the side of the road in the dark of the night. Sometimes animals were hurt simply in the name of sport. A dog I had as a young girl was pushed off a large bridge by young men in our neighborhood. No reason was given, but a crowd witnessed the act and did nothing to stop it or assist the dog.
As I grew older, the empathy I felt for animals was such an integral part of my nature, I knew it was a God-given gift. The negative side of it was that I became sort of a bulls-eye for the neighborhood kids and they sought me out in particular to witness their more incredible acts of cruelty. One boy enjoyed watching my rising panic as he would hold a cigarette lighter beneath box turtles or other small animals. I attempted to avoid these scenes, reasoning that the violence escalated when witnesses were present. He soon retaliated by shooting our little 12-week-old puppy, Oscar, and leaving it in my parent's driveway. It was hard for me to understand why my parents did not take some kind of action. It maddened me that this kind of violence was easily accepted by the mainstream and consequences were nonexistent.
Viewing all this from the perspective of a powerless young girl in a community of strong-minded adults, I could only combat my feelings of helplessness by assuring myself that when I was older, I would do everything possible to protect and preserve the health of my own pets. It also led to a decision to be a vegetarian in my mid-twenties, a lifestyle change that sprang directly from this desire to protect the innocent. I was no longer able to mentally separate animals that were "pets" from animals designated "food." With that background, Babes was understandably a big part of my life as a young adult.
After I married, my husband Patrick spent many hours walking her and caring for her. When an independent dog like a Scottie turns to you for affection, you can't help but be flattered, and Pat soon fell into her fuzzy paws. I had long been suffering from her unique charm, but Babes gave Patrick the "Scottie flu" in a big way. That's how it all started for us as a family. We've had many Scotties and other pets since then, all unique, all wonderful, some with what you might think are impressive pedigrees, others without–but all united by the fact that they were sick for much of their all-too-short lives. That deep affection we both felt for them and the desire to create the best health for them has shaped many decisions in our life together.
Free to Good Home
After many years of owning Scotties and other kinds of cats and dogs, another Scottie--Bonnie Sue--came into our lives, I had no idea that in trying to care for her, I would stumble upon some particularly startling information that could impact the health of Bonnie and give me a new perspective on the health problems that plagued other animals we owned and those long gone.
In 2003, I was home nearly full-time. I had recently quit the job I'd had for 13 years and was doing some marketing for a friend who'd started a pet treat business. I was enjoying the freedom this break in the action offered, most especially the time with our pets. It was completely wonderful to have that uninterrupted time with them and they responded by following me around like sheep from the time I opened my eyes in the morning until we all went to bed at night.
One day, a lady from my former workplace who knew of my deep love of Scottish Terriers called to direct me to an ad in a local sales bulletin. The ad simply displayed the phone number and the words "Female Scottie free to good home, must be spayed." I wasn't looking for another Scottie, but I didn't think twice about making the call. I knew that if for some reason we could not keep this dog, I had contacts in Scottie rescue who would help me find just the right home.
The woman who answered the phone was a longtime Scottie breeder not far from me in West Virginia. She bred not only Scotties, but other breeds as well. The breeder told me that "Bonnie Sue" was nearly seven years old, had come to her at about four years of age from another breeding facility in Kentucky, and had been bred by her every year since that time. My understanding was that Bonnie was at the end of her puppy-producing career, and as a result, she was being considered for placement in a pet home to live out her last days. The only requirement was that Bonnie be spayed, and as that was something I would have done anyway, I gladly arranged to meet this Scottie girl the following week.
My first impression of her was pretty much what you'd expect from a Scottie who had changed hands several times and produced puppies all her life. She was a cautious girl who showed little faith in humans or what they had to offer. She had been brought into the house from her kennel, bathed and brushed, and was allowed to get on the couch to sit with me. But she looked completely surprised and a little worried to be inside and in that particular spot. When I tried to let her sniff the back of my hand, she backed up to the furthest recesses of the couch and barked at me--a high, shrill bark that some Scotties have. She turned her head and gave me a sidelong Scottie inspection as if to say: "And what will you be wanting?" Given her history, I felt she had a complete right to wonder about that.
I learned that Bonnie was given access to a metal building when she had puppies, otherwise she was outdoors on a concrete pad that offered a simple doghouse as her only shelter. She was on a long leash that attached to a chain soldered around her neck. The kennel was beside a swampy area, so it was not a complete surprise to later discover at her first vet visit that she was suffering from heartworms. Bonnie had just given birth to puppies a few months before and was not looking her best as far as coat or weight, although she was nicely groomed. In light of her age and where she'd lived previously, I was advised that she probably could not be housebroken and that it would be fine if we wanted to keep her outside. In short, she did not have the hallmarks of a perfect pet, but people who feel as we do about Scotties are rarely deterred by simple things like housebreaking issues or old age. The hard life she had lived had not completely snuffed out the faint sparkle of Scottie liveliness I thought I could still see. I immediately felt that with some love, time and a spay procedure, she might relax and show more of her innate personality. I looked forward to seeing how I could shape the last chapter of Bonnie's life in a positive way and thought no more about sending her on to rescue.
All Because of Bonnie
Through that single phone call, we also learned about Charlie, Bonnie's ten-year-old breeding mate, burdened with a large aggressive soft-tissue sarcoma on his hind leg and also living outdoors. The breeder wasn't sure about what the tumor could be, but said that perhaps Charlie was too old or unhealthy to be adoptable. He had been through three different breeders and homes, but unlike Bonnie, he recognized a good thing when he saw it and loved us from the moment he met us. He was a large, handsome boy with an unforgettable face, who quickly chose my husband as his favorite person in the world. He fairly glowed when he met Patrick for the first time. Of course, when confronted with another Scottie in need, Patrick could not and would not leave him behind, even with the prospect of the heartache of another sick Scottie and the attendant veterinary bills. Money was tighter than it had been before I quit my job, but no matter. Patrick is a kind person, and so it was that Charlie came to live with us, too. I am happy to say that despite the worries and warnings, Bonnie and Charlie were soon housebroken, sleeping right beside us, and perhaps best of all, Charlie's cancer was successfully treated through surgery and chemotherapy.
The ripples from that first stone–that initial phone call to Bonnie's breeder--later appeared in the form of yet another Scottie boy who would come to live with us three years later, the last puppy Bonnie and Charlie produced, Bender. I had originally noticed him when we claimed Bonnie and Charlie years before. The breeder had held him back as a pet for her son, but he, too, was outdoors on a chain. As the son was growing up and had less time for Bender, she had inquired whether we might want to adopt him, and it didn't take us long to decide. He was a bit more of a challenge to socialize than either of his parents, but possessed the same good looks as his father and adored Patrick with equal devotion. Nowadays, he is just a big old bowl of sugar and is known as the "baby boy" of our home.
Still more ripples in the pond were appearing because at the time we obtained Bender, we learned through conversation with the breeder that two daughters produced by Bonnie and Charlie were now in a local puppy mill. Of course, I was completely distressed at that thought, so we contacted the puppy mill owner. He'd already made the decision to stop breeding Scotties, so we were able to work out a deal to buy all of the Scotties he had on the premises, not just the daughters we had originally discussed. Two of these Scotties were placed with veterinarians; one puppy, Miles, was adopted by my niece; the others were placed in homes through Wee Beasties in Virginia. Some folks would argue that putting money in the pocket of the folks who run puppy mills is not really making a change for the better, but I would argue that these Scotties didn't know that. Whether wrong or right, I could not possibly walk away from the offspring of two of the sweetest Scotties I'd ever known.
The rescue of those Scotties was best present my husband and I could have given one another. Motivated by our love for Bonnie, Charlie and Bender, we were able to do something tangible for their offspring and kin. Since that time, we've been able to aid in the rescue of two other Scotties that were related to Bonnie and Charlie.
Bonnie Makes a Home
In the first several months of her life with us, we saw Bonnie become more accustomed to human contact and display a more casual response to new experiences. She seemed to expect good things for herself and sometimes demanded it-- a reaction that never failed to delight us. Because I was home all day with her, she began to form a strong bond with me and desired to be with me at all times. Until the hormones wore off, she and Charlie romped through the house like rowdy school children and slept side by side. It seemed to me that Charlie's presence offered comforting continuity. He had no problem making the adjustment to our home, and it wasn't long before she learned to enjoy toys, hugs and long walks where she could investigate the scenery at her leisure. I felt as I watched her that she had come to realize that this life would not be taken from her and that she was finally in her forever-ever home.
The Aftermath of Stress
The year 2006 was a difficult one for everyone in our home and we were forced to endure many changes and much loss. We sadly said goodbye to many of our dearest pet friends. We've never had such a bad stretch of time; it left me so sick with grief, I felt like I would turn inside out with raw emotion. Kyle, my "heart dog," the one I called my forever beloved boy, my "Sunny D" (Sunshine-y Dog ), the one who had taught me the complete delight there is to be found in the company of male Scotties, was euthanized for advanced liver disease and bladder cancer. I don't think a single day has passed without a tear being shed for him.
"Charlie Bear Pants"--Patrick's name for him--was euthanized two months later for primary lung cancer. His loss was felt acutely by Patrick, who had the kind of relationship with Charlie that I'd had with Kyle. Several months later, we had to say good-bye to Brownie, our faithful, long-suffering red hound. After that, we lost two of our oldest cats, Dave, age 18 (my favorite cat of all time), and Red, a quirky and playful 15-year-old male. It was hard to let any of them go, but watching them suffer was simply not an option. We have always felt that euthanasia is the way of showing your protection and best wishes for your pets, and walking that final leg of our journey together is the last act of kindness.
We also had to part with adorable Amy Pie, a young Scottie we'd been fostering owing to an illness in her family. She came to our home late on the night of my birthday party that year. She was so utterly delightful, she seemed like a gift sent from Kyle. After five months in our care and her owner's move to California, she was requested to be shipped to her new home. I had hoped that I might be able to keep "The Pie," but it was not to be. Her destiny was to be reunited with her own young master who needed her to aid his own healing, as only a beloved Scottie can. Despite knowing that, I was ill-prepared for our final parting and found the experience uniquely painful.
Interspersed with these difficult losses, I was hospitalized for nearly two weeks to treat squamous cell oral cancer. It began with a small sore that my local oral surgeon said would be "fine." But six months later, a different surgeon removed much of the floor of my mouth, one-third of my tongue and 28 lymph nodes in my neck. I was a nonsmoker, a vegetarian and an organic gardener, so I was shocked with the diagnosis, not to mention the treatment. After the surgery, I was elated to learn that I was cancer-free and to realize how richly God had blessed me by granting me the continued ability to speak. There was no doubt I had been healed. But coping with the physical and emotional effects was harder than I had expected. I knew that stress could have a harmful effect on a person or pet's overall health and I believe I experienced this firsthand. I could see that our household stressors affected not only our human hearts, but those of our pets, too. Bonnie's declining health in the months to follow became an illustration that I could not ignore.
Bonnie's Symptoms
Sometime in the summer of 2007, we noticed that Bonnie was slowly losing the ability to hear or to see well. It was during the six-month period after we lost most of our six pets and I'd had surgery when I noticed that she became a little grumpy with the other dogs and was more reticent to be held. Normally, she wanted to be near me, so when she stopped going up and down the steps with me to my office, I attributed it to the first signs of arthritis and looked for natural supplements as a remedy. But as time passed, she changed in other ways, including excessive hunger, weight gain, intolerance to the slightest increase in temperature, excessive panting and increased water intake and output. She was also lethargic during the day, but unable to sleep well at night. She'd had an ultrasound within the year and had a complete CBC and thyroid test, too. Her thyroid response was in the gray zone and her alkaline phosphatase (liver) enzyme was high. It was not as high as we'd seen in some of our other Scotties, so we tried not to worry. I say "tried" because I've never been satisfied with that theory that high liver enzymes are just a Scottie thing. They've always signaled serious illness just down the road, and once I see the levels go up, I can never really relax and feel good about that pet's health. So, we started the natural liver-supportive things that Scottie people do and had an ACTH test done to rule out Cushings, which was of course my first thought. But it was negative. What else should we do? We kept the house cool and tried to make her comfortable, but I grew more concerned and found her behavior less easy to explain. There was also that matter of a mother's intuition that told me that I needed to pay attention to what was happening and seek answers quickly. My own health situation proved to me that waiting to see how things turn out isn't always the best plan.
Patrick has sweetly come to trust in that intuitive "Mom" part of my relationship with our pets and agreed to doing whatever I felt was right. Now, I just had to figure out what that might be.
We've often found ourselves with animals suffering from health issues that don't seem to find resolution on the first, second or tenth trip to the vet or specialist. This is no reflection on our vets; the medical problems our pets experience are rarely simple. Their proper health care sometimes requires a bit of detective work, a happy willingness to empty our pockets and travel to faraway specialists. Cushings disease, cerebellar abiotrophy, soft-tissue sarcoma, hemangiosarcoma, mammary cancer, bladder cancer, soft tissue cancer, lung cancer, heartworm, kidney failure, heart disorders, obsessive/compulsive disorders, collagen disorders, pancreatitis, diabetes, irritable bowel syndrome and food allergies, oral problems, gallbladder and liver disease were just a few of the items on the menu at the "House of Ill," (the name I mentally gave our home). Sometimes, despite all the special advice and tests and surgeries and hospitalizations and expensive medicines, we never found the answers we sought, as in Kyle's IBD or Brownie's collagen disorder, but merely muddled through these medical crises, managing each of them in turn as best we could.
Through the years of researching these problems and my own mysterious cancer, I became interested in the immune system and trying to learn how to aid, support or restore it. It seemed the key player in ensuring good health. I can't say I am the smartest person in even a very small group, but I may well be the most curious. I like to learn and discover new things, especially those that could offer happiness and vigor to my pets. But I came to realize somewhere in my journey of learning that not everyone shares this passion. Many people are simply content with status quo–even as it relates to their own health issues--and would rather keep the potentially hurtful things hidden from view. For those people, denial is an important coping mechanism.
"It is easy to dodge our responsibilities, but we cannot dodge the consequences of dodging our responsibilities." --Josiah Stamp
Even so, I have come to appreciate that everyone is on a different path and learn things in their own time. I hope that in reading Bonnie's story, someone will be inspired to start their own journey of discovery, just as I did long ago with Babes.
Cortisol and Disease
As I started searching for answers to address Bonnie's apparent illness, I found a resource that encouraged me to look deeper within the health problems suffered by not only Bonnie, but all of my pets. That resource was the book, "Pets at Risk" by Alfred J. Plechner with Martin Zucker.
This small, but ground-breaking book focuses on correcting the unrecognized endocrine-immune imbalance caused by a cortisol defect.
Dr. Plechner is a graduate of University of California-Davis Veterinary School and for many years had an interest in nutrition and the role of hormone and immunity imbalances in dogs, cats and horses. He helped formulate commercial diets for food-sensitive animals, among those the first lamb and rice varieties. His compassion for animals is all-inclusive; he worked for many years as a wildlife rescuer and owned and operated a wildlife relocation and rehabilitation center in California. He has now retired and lives in Idaho, but he is still quite active in helping pets and their people. He makes himself available to veterinarians and doctors who are interested in his theory of disease development, and he is a regular voice on radio stations devoted to alternative healthcare for pets and people. Through Dr. Plechner's years of observation, research and experience, he is most qualified to offer his opinions on the surge of medical problems seen in dogs and cats today.
Here is a list of some of the canine ailments that he observes can be caused by an adrenal hormone imbalance:
Allergies; viruses, bacteria and fungi (colds and flu, parvo, bacterial infections); malabsorption and digestive tract disorders (his studies show that food sensitivities occur only in animals with hormonal imbalances); autoimmune disease; cancer; kidney disease; chronic liver disease (endocrine and immune imbalances can "cause it to run in slow motion"); Von Willebrand's disease; behavioral problems; aggression; separation anxiety; hypersexuality of neutered or spayed animals; problems in reproduction, epilepsy; and obesity.
Plechner, Alfred J., Zucker, M. Pets at Risk From Allergies to Cancer, Remedies for an Unsuspected Epidemic. NewSage Press. Oregon, 2003. pp. 2, 3, 8.
Many of these ailments had been suffered by our own Scotties, and I was interested to see that some were mentioned in the 2005 GSM Scottie Health Survey.
"In my research I have learned that at a basal, or normal level, the body's own cortisol exerts a very discriminating regulatory effect on molecular 'mediators' that turn on or turn off activity related to immunity and inflammation. It is a very complex business. The bottom line is that a normal level of cortisol seems to be required for a normal immune response. A deficiency of cortisol may result in an unresponsive immune system, whereas too much cortisone medication or too much of the body's own active cortisol suppresses immune responses. An excess of active cortisol or cortisone drugs can lead to a condition known as Cushings syndrome. In Cushings, individuals develop severe fatigue, weak muscles, high blood pressure, high blood sugar, and fertility and menstrual problems, among other symptoms.
* * *
"Cortisol deficiency, the other side of the coin, tends to be overlooked in medical circles. A deficiency or ineffectiveness of cortisol certainly appears to cause many problems. I have seen this consistently in animals. Compared to healthy animals, I have found that sick and diseased pets often have too little cortisol, or the cortisol present is somehow in a bound or ineffective
state, resulting in system imbalances and chaos throughout the physiology. The particular problem I see does not relate to Addison's disease, a condition involving a deficiency or aldosterone, the hormone governing sodium and potassium levels in the body, and which is produced in the outer cortex layer of the adrenal glands. I have not found low levels of aldosterone in cortisol-deficient patients, nor have I seen any of the typical signs of Addisons."
Ibid. pp. 18, 19.
I was interested to read that Dr. Plechner believes that he has seen this hormonal imbalance in every animal with cancer he has ever treated. The causes he cites are contemporary breeding practices, leading to narrower gene pools, which in turn cause "compromised health and decreased life span." That certainly rang a bell for me because it was another area of concern I had felt since reading Dr. Harvill's "Deconstructing the Diehard" series, which laid bare the plain facts about the state of the Scottish Terrier's immune response.
Plechner has determined that the disease process in many pets can be corrected by addressing the issue of cortisol production and excess adrenal sex hormones. His protocol starts with specific testing he's developed ("Plechner endocrine-immune test") in order to determine a patient's precise point in the disease process. If hormonal imbalance is present, treatment is given through cortisol replacement. Most of the time, T-4 thyroid replacement is necessary, too, since thyroid hormones become bound to some degree because of the influence of "estrogen and cortisol abnormalities." A thyroid imbalance can be present even if the T3/T4 levels look normal, so it is important to use a lab that is particularly sensitive to this type of testing and aware of the correct range of these values. Plechner's E-1 test shows the values for T3,T4, cortisol, estrogen and three different antibodies or immunoglobulins (IgG, IgM, and IgA).
The prescription of steroid replacement that Dr. Plechner advocates is lifelong because the imbalance will return if treatment is stopped. He makes the important point that the animals he treats are not affected by the side-effects so often seen with steroids because he is providing the body with something it isn't producing on its own–and something it desperately needs. The oft-publicized immunosuppressive effects of these powerful drugs might make some veterinarians shy away from using them, but research has revealed that they can be healing and restorative to the immune system when properly used in small, physiologic doses for animals with a corresponding imbalance.
"In animals with healthy adrenals, sustained cortisone medication indeed has the potential to suppress the immune system and cause side effects because too much cortisol and cortisone are then present in the body. Remember that cortisone compounds convert in the body to cortisol. This is why treatment with potent, pharmacologic amounts of cortisone often has no long-lasting benefits and leads to problems. But in an animal with defective adrenals, cortisone at the proper low-dosage level does wonders. It may, in fact, be the only thing that can save the lives of very sick animals.
"My clinical practice and research have shown that the conservative use of cortisone makes up for the shortage in animals with an impaired ability to produce healthy amounts of cortisol. The replacement cortisone slows down ACTH, as would naturally happen if the animal had adequate
cortisol. This in turn stops the influx of unwanted extra estrogen. With cortisone now substituted for missing cortisol and with estrogen lowered, orderliness returns to the immune system allowing immune cells to protect the body."
Ibid. p. 25
There is a great online article, "Chaos in the Cortex," written by Dr. Plechner, wherein he explores his theories in an abbreviated, but readily understood format. The ideas he puts forth are worthy of consideration and make helpful reading for those with medically challenged Scotties, most especially those of us who have found no satisfying answers in what we've been told or the way some of our pets have been treated medically. I think many of us walk around feeling that something is not quite right, but we've exhausted our pet and vets with tests and ideas. We honestly don't know what to do next. In the end, I found Plechner's ideas extremely helpful in providing insight into how many of my past pets' "mysterious illnesses" could have been caused by abnormal cortisol and adrenal hormone levels. Dr. Plechner did not mention SARDS in his work but I realized that part of Bonnie's problems could include an adrenal imbalance, which would explain her Cushings-like symptoms.
In late spring 2007, I did an online search and came up with SARDS (Sudden Acquired Retinal Degeneration Syndrome, also known sometimes as simply "SARD"). When I thought of Bonnie in terms of the disease profile, it made a lot of sense.
As many as 4,000 dogs are diagnosed with SARDS each year, many suffering from the personality and medical changes we observed in Bonnie. SARDS is thought to begin through a biochemical process which ends in rapid death of neural cells (also known as massive apoptosis) and results in blindness. One of the difficult aspects for vets examining the potential SARDS dog is that the retina looks completely normal and intact upon examination. Sometime into SARDS–it could be a week or months later--the retina will visibly degenerate. I found a few sites that tantalizingly mentioned a connection between Cushings disease and SARDS, including the 2006 Edition of The Merck Veterinary Manual, which would implicate the endocrine system in the degenerative process. But no definite theories had been put forth about the connection. I would come to learn that a small number of SARDS dogs do have Cushings, but many more are suffering from adrenal exhaustion (which can look like Cushings). This confusion with Cushings disease can have disastrous results if a pet is incorrectly treated with Lysodren or Trilostane, which would further serve to suppress the already depleted cortisol levels in the case of a dog with adrenal exhaustion. This scenario can result in death.
My early research showed no hope for pets with SARDS and there were several web sites that suggested euthanasia for those affected. This was not what I was looking for, but I was not willing to give up. There had to be some hope on the horizon for Bonnie.
Examination Results Disappointing
In midsummer, our wonderfully intelligent and responsive vet, Dr. Shawn Sette of Hurricane Animal Hospital, gave Bonnie a thorough exam. He suggested that in order to have her eyesight properly assessed, we should take her to a specialty practice that offered ophthalmology services, MedVets of Ohio. We both felt that might give us a better idea of whether SARDS could be responsible for her decreased vision. In July 2007, Bonnie and I were off to get advice from the "experts."
At the specialty clinic in Ohio, Bonnie underwent a neurologic assessment for her hearing. She was given a Doppler blood pressure test to see if any undue pressure might be causing her sight problems. An ocular examination was also performed, including a Schirmer tear test, and an electroretinogram (ERG), which tests retinal function. In this test, special contact lenses were placed on Bonnie's eyes, and a series of flashing lights were directed toward them. A graph of the electrical impulses recorded electronic signals detected by the electrodes. In Bonnie's case, the ERG recorded barely any electrical responses, which meant her ERG was flat. When this happens and the blood pressure is normal, as it was with Bonnie, SARDS is the likely diagnosis.
As I was waiting on Bonnie's tests to be completed, I spent my time reading in the lobby, and was amazed to discover a timely article about a new and promising SARDS treatment for dogs that was being overseen by Dr. Sinisa Grozdanic at Iowa State University College of Veterinary Medicine. An intravenous treatment of immunoglobulin (IVIg, a human blood component that contains antibodies from the plasma of thousands of blood donors) was being used successfully to treat SARDS in dogs. This treatment was developed because Dr. Grozdanic believes that the sudden and painless onset of blindness is much like human antibody-mediated retinopathies. Dr. Grozdanic had already successfully restored limited vision to several canines. This treatment was quite new and could have side effects to dogs with pre-existing heart or kidney problems because the IVIg was produced with human plasma instead of canine plasma. Still, it was the only treatment I had found for SARDS anywhere. I was completely thrilled to find this possible treatment for Bonnie and was eager to discuss it with the doctors, certain as I was they would find Bonnie to have SARDS. But when I received the summarization of Bonnie's test results from the specialists, I learned that the Ohio group felt that Bonnie was not a candidate for SARDS treatment because she still retained some functional vision, and SARDS dogs, they told me, had none.
Her patient evaluation note from the ophthalmic group read: "Bonnie presented to the service for evaluation of profound visual deficits. She appears to have primarily lateral visual field deficits with preservation of vision in the central visual fields. She did have flat ERGs but does have some vision. Bonnie is poorly attentive to auditory stimuli with decreased attention to sound and localization of sound." The neurologist wrote: "I cannot find any neurologic deficits which would explain the visual loss. It is odd that she appears to have both visual and auditory changes, since these are both Special Somatic Afferents . . . . [h]owever, I know of no degenerative processes in dogs with a preferential effect on SSA fibers. If the auditory changes are real, a degenerative process would make the most sense, since there is not any evidence of vestibular dysfunction . . . I can't think of any additional testing to perform on Bonnie right now, but BAERS [Brainstem Auditory Evoked Response, used to detect retrocochlear pathology] would be interesting to perform to see if they show the same changes as the ERG. Nor can I think of any appropriate therapy for Bonnie."
These veterinary ophthalmologists said Bonnie's symptoms fit no particular category and felt her situation defied diagnosis. They called another veterinary ophthalmologist in their group to take a look at Bonnie because they found her symptoms and exam so perplexing. They all agreed that SARDS fit better than any other diagnosis but argued that she would be a very atypical case. Her ERG was flat but she still retained a small amount of functional vision that allowed her to navigate an exam room set up with obstacles. The neuro assessment pointed toward a degenerative process, but the veterinary ophthalmology team was not swayed toward the SARDS diagnosis. They pointed out that Bonnie's eyesight diminished over time, not overnight as they said is found in dogs with SARDS.
They could not offer any hope or treatment for her condition, but did suggest Occuvite as a nutritional supplement to slow down the loss of vision. They attempted to encourage me by saying that Bonnie would "adapt to her circumstances."
I'd found that annoying quote in much of the SARDS information I'd read and didn't enjoy having it repeated to me. I felt like it was just a way of excusing the absence of a diagnosis or treatment. I found myself lingering in the specialist's office, trying to gain more understanding and information. I just wasn't willing to accept that Bonnie would go blind--especially in light of the fact that she had been given no particular diagnosis. I protested that with neither sight nor hearing, it would be a difficult life for Bonnie. A blind dog can use its hearing to help navigate, and a deaf dog can use its sight to do the same–but a deaf and blind dog? I wondered aloud how happy Bonnie's future could be if she was isolated in her own little world, especially for a dog like Bonnie who had become so bonded to her humans.
When I mentioned to the ophthalmologist the article I had just read about ISU's IVIg treatment, she asked me if I felt like I needed to be referred to Iowa. She said could do that, but quickly assured me yet again that they didn't believe Bonnie to be a candidate for this therapy. I felt a little foolish for suggesting such an extreme measure. But in the end that is exactly what happened, because at least three of the things the Ohio "experts" told me turned out not to be true. Driving home from Ohio to West Virginia, I had the same nagging feeling I'd had all along, that something was being missed. The neurologist's mention of a degenerative process kept coming back to me. So, I turned to the Scottie network for help.
West Virginia is a sort of "Scottie hinterland" so sometimes my help for our dogs comes from turning to others who might be more knowledgeable. I couldn't even wait until I was home before I called several of my smartest Scottie pals and asked if they had ever encountered such a thing with their Scots. Once home, I e-mailed other friends. Those who responded said that they knew of situations where dogs had gone suddenly blind, but many were without known medical reasons. Some felt that it was caused by diabetes or was an old age-related problem. I was determined that after the hard life Bonnie had endured, her final years would not be spent in darkness. She'd been cold, she'd been alone, she'd been chained without freedom and I'd be danged if she would be blind on top of all of that. If she still had sight, then there was hope.
Once again at home, I did what I usually do when I am feeling pressed and stressed about my pets: I said a prayer and turned to the Internet for help. It is not always a prescription for success, but this time as I surfed once more for helpful SARDS resources, I found the Lantern Publications website. (Yes, God does love Scotties!) There, another qualified source showed a definite connection between SARDS and cortisol production, adrenal exhaustion and excess adrenal sex hormones. I also learned that: (1) a flat ERG with functional sight does not rule out SARDS; (2) SARDS dogs do not necessarily go blind overnight or even within a few weeks; and (3) there was a window of time where hope of restored sight was possible for SARDS-affected dogs. Ding! Ding! Ding!
The owner of Lantern Publications and author of many books and articles was Caroline D. Levin, R. N., an experienced nurse who had specialized in the fields of ophthalmology, family practice nursing and endocrinology. After a long career in human nursing, she left that field to manage an ophthalmic veterinary clinic. Her background provided her with particular insight into canine SARDS, and she has been published on this subject in The Journal of the American Holistic Veterinary Medical Association. In October 2007, she presented two reports at the 38th Annual Meeting of the American College of Veterinary Ophthalmologists, and will soon be addressing the Golden Retriever Foundation Health Symposium, in Longmont, Colorado.
Ms. Levin's ideas, perhaps novel to some veterinarians or specialists, are becoming better known. Still, don't be surprised if your veterinarian has never heard of the concept of adrenal exhaustion. Many have not, but they may be better familiar with the term Atypical Cushings:
"When clinical signs of hyperestrogenism are present in conjunction with normal cortisol values, a diagnosis of atypical Cushings disease is sometimes made. The author suggests that the terms atypical Cushings, hyperestrogenism, and adrenal exhaustion may all describe a similar state."
Levin, Caroline D. Environmental Factors and Signs of Hypercortisolism in Dogs Affected withSudden Acquired Retinal Degeneration (SARDS). The Journal of the American Holistic Veterinary Medical Association, 2006: Vol. 24 (4), 11-19
Levin has posted many of her best articles online for the benefit of the public. There was so much to read that I eventually found it simpler to print it and put in a notebook to study. She offered such useful information I'd never read anywhere else and I was completely blown away. Her web site included detailed case studies of dogs with SARDS, along with summaries in plain English–perfect for folks like me.
Levin eloquently puts forth some of the same ideas Plechner holds: that chronic irritation through commercial diet, stress, and excess vaccinations can lead to adrenal exhaustion. In the paper she presented before the American College of Veterinary Ophthalmologists, Levin offers a case report of a 9-year-old neutered Brittany Spaniel who had SARDS and adrenal exhaustion for three years, and the subsequent resolution of his adrenal symptoms through treatment. Because this dog was three years into his diagnosis, restoration of his vision was not possible. He had gone past his window of opportunity for limited restoration of sight.
In this well-researched report, she discusses the model that Hans Seyle set forth as it relates to stress adaptation and hypercotisolism. Seyle is referred to as the "Father of Endocrinology" and we are espousing his theories when we talk about the "fight or flight" mechanism.
"Dogs affected with SARD routinely present with signs suggestive of hypercortisolism, but only a minority are diagnosed with Cushing's disease. Early on, researchers speculated that this
hypercortisolism was the physiological response to some unidentified stress. SARD-affected dogs also demonstrate elevated levels of adrenal sex hormones (androstendione, estradiol, progesterones, and testosterone) within the first year of blindness. One explanation for this pattern of events is Selye's (1) model of stress adaptation, which describes the progression from adrenal gland hyperactivity (hypercortisolism) to adrenal gland exhaustion (cortisol insufficiency). In Selye's model, adrenal activity is marked by three stages: alarm, resistance, and exhaustion. "During the alarm phase the body responds to stressors with increased hypothalamic-pituitary-adrenal (HPA) activity and cortisol secretion. Cortisol production returns to normal when the stressor is resolved. This is the normal, healthy response to psychological and physical stressors (irritation).
"The resistance phase occurs following a prolonged period of stress. Elevated cortisol production continues but falls to a level only slightly above normal. The HPA feedback loop fails. Cortisol production continues unabated. Based on clinical signs and diagnostic tests, this dog experienced the resistance phase during the first year of SARD.
"In the final phase—exhaustion—the adrenal glands are unable to sustain elevated cortisol production. For a short time, declining levels of serum cortisol fall within the normal range giving the impression the dog has adapted. Clinical presentation may temporarily improve. Once cortisol production falls below normal, clinical signs resurface as a result of accumulating sex-hormones — progesterone, androgens, and adrenal estrogen.
"The dog described . . . first entered the adrenal exhaustion stage during the second year of blindness. As cortisol production began to fail, clinical signs improved. By the third year, the dog developed advanced adrenal fatigue with elevated estrogen levels. Note: This time frame, in the author's [Levin's] experience, is highly variable. The dog described here developed adrenal exhaustion several years subsequent to SARD-onset. Other dogs reach this stage within weeks or months.)
* * *
"This dog demonstrated an unmistakable pattern of stress adaptation during a three-year period following SARD onset. The period in which the dog was thought to have ‘adapted’ to SARD was merely a transitory phase preceding complete adrenal exhaustion. Low-dose glucocorticoid and thyroid hormone replacement had a significant positive effect on both clinical presentation and laboratory findings. Owners should be encouraged to pursue adrenal estrogen testing and hormone replacement therapy for signs of excessive adrenal activity."
(1) Selye H. The Stress of Life revised edition. McGraw-Hill, Incorporated: New York, 1976.
(2) Levin, Caroline D. Sudden Acquired Retinal Degeneration, associated pattern of adrenal activity, and hormone replacement therapy in a Brittany Spaniel. http://www.petcarebooks.com/pdf/acvo_caserpt_post.pdf
Levin outlines the signs of adrenal exhaustion in dogs. (Again, I think many Scottie owners will
see symptoms with which they are all too familiar):
"Signs/symptoms of elevated adrenal estrogen closely resemble those of excess cortisol including, fatigue, confusion, depression, incontinence, irritability, seizures, and darkening of the skin. Elevated estrogen raises liver/pancreas enzymes (serum amylase/alkaline phosphatase), cholesterol, and triglycerides. Elevated estrogen also results in kidney degeneration, bone marrow and immunoglobulin suppression (anemia, cancer), increased histamine activity (allergies/itching), and thyroid binding.
"Elevated levels of hormone precursors, such as progesterones and androgens cause impaired glucose tolerance (high blood glucose levels), obesity, increased body core temperature (heat intolerance/panting), increased hunger, aggression, thick coats, acne (small flesh-colored bumps), and bald patches. Severely depleted cortisol results in loss of appetite, vomiting, abdominal pain, diarrhea, weakness, organ failure, and death.
* * *
"Dogs other than SARD dogs can suffer from adrenal exhaustion, too. Dogs that will benefit from adrenal testing and treatment include those with:
*Poorly-controlled diabetes or pancreatitis (Elevated estrogen raises blood glucose, cholesterol, triglyceride, and lipase levels.)
*Poorly-controlled epilepsy (Elevated estrogen reduces the seizure threshold and increases nerve cell transmissions.)
*Poorly-controlled inflammatory bowel disease or allergies (Elevated estrogen suppresses immunoglobulin levels and increases histamine release, causing red, itchy, inflamed tissues and GI distress.)
*Poorly-controlled Cushing's disease or those dogs suffering from signs/symptoms of Cushing's disease but with normal results on standard Cushing's tests (Estrogen causes many effects similar to cortisol.)
***
"My thesis is that SARDS is first and foremost an adrenal problem that stems from the "modern-day lifestyle," that is — commercial pet food, annual vaccination, and chronic pesticide exposure — three modern-day elements that are physically irritating. After all, SARDS has only been diagnosed since the late 1970s.
"Of these three, I suspect diet is probably the biggest piece because it's something we do to the dogs twice a day every day. I do not believe it is any one thing in pet food, or any one type of vaccine, or a single chemical. They all irritate the body. Chronic irritation increases adrenal gland activity and the hormones that are produced there. In addition, there certainly must be an indirect genetic tendency to the problem, otherwise every dog in the America, and certainly every dog at the local dog pound would have SARDS.
* * *
"It seems that some dogs respond to chronic irritation gradually over time until they are either in overdrive (producing a lot of cortisol) or even into the exhaustion phase (producing a lot of adrenal estrogen) until these hormones reach a critical level. (Initially I suspected that SARDS occurred only when cortisol levels were very high, but increasingly I see dogs tested near the time of vision loss are already in adrenal fatigue, producing excess estrogen . . . . Both elevated estrogen and elevated cortisol have a similar affect on nerve/retinal cells. These individuals wear out their adrenal glands gradually over a very long time.
"Other dogs seem to reach the critical hormone levels after a spike in adrenal activity . . . . [S]ome proverbial straw that breaks the camel's back. These include vaccine incidents, intense psychological stressors (spending a week at a boarding kennel, home remodeling, etc.), pesticide application, or the arrival of spring (when adrenal activity normally increases) . . . . Dog #1 . . . has no identifiable trigger but gradually increases hormone levels until they reach a critical level. Dog #2 has an identifiable trigger and a spike in adrenal activity just prior to SARDS onset. Of course it's possible that all SARD dogs have a trigger and owners are just unaware of them. In either case, hormone levels crossed a critical threshold and damage the retina."
Levin, Caroline D. Frequently asked questions (FAQs) about SARDS and adrenal hormones.
http://www.petcarebooks.com/SARDS/FAQs.htm
Perhaps the most useful nugget of truth she offered was a simple way to distinguish a dog with Cushings from one suffering from adrenal exhaustion (or atypical Cushings). In either instance, the affected dog will gain weight, experience sleep pattern disturbances, suffer polyphagia, polydypsia and polyuria, show increased liver enzymes, confusion, lethargy, muscle weakness, intolerance to heat, but the dog who also has chronic irritation, i.e., itchy feet, itchy skin, irritable bowel syndrome, allergies--then that is the dog that is suffering from adrenal exhaustion, and therefore, producing excess estrogen. Why? Estrogen is a pro-inflammatory. If a dog were truly suffering from Cushings, it would be producing an excess of cortisol, which would soothe the itchiness and inflammation with its powerful steroidal anti-inflammatory effects. Makes a lot of sense, doesn't it?
In short, Levin's site was the first and only one I found that offered a wide variety of case studies of dogs suffering from SARDS and ideas about causes and treatment.
Iowa State University
Recalling the article I had read earlier in the specialty clinic's office about Dr. Sinisa Grozdanic's amazing breakthrough at ISU in treating dogs with SARDS, I thought perhaps he might help us determine a proper diagnosis for Bonnie. However, because of the non-SARDS diagnosis and conflicting information I had received in Ohio, I again turned to Dr. Sette to help me sort through the confusion. After considering all the information I had provided him about Grozdanic and Levin's work, as well as his own evaluation of Bonnie, Dr. Sette felt it most likely Bonnie did have SARDS. Dr. Sette contacted Dr. Grozdanic at ISU to determine if Bonnie might be a candidate for IVIg treatment.
Dr. "G" (as he is called by his co-workers) indicated to Dr. Sette that SARDS-affected dogs can suffer diminished hearing and sense of smell, along with retinal changes, and that it was not at all uncommon to see all these problems in the same dog. He also indicated that it was not completely true that blindness occurs suddenly in each case of dogs sufferings from SARDS. He said that it was a condition that could happen gradually, as I had witnessed with Bonnie. This again, was contrary to what I had been told previously by the specialists in Ohio. Dr. Grozdanic advised us to try a simple course of prednisone and doxycycline. He told Dr. Sette this was an inexpensive therapy that sometimes worked in treating pets with SARDS, and was worth a try before bringing her to Iowa. His advice was similar to the protocol provided by Levin because it provided for steroid treatment.
Ultimately, Bonnie was determined to be in early adrenal failure. Her cortisol level was normal, but both her estradiol and both progestins were in the high range. This along with her high alkaline phosphatase, cholesterol, calcium and albumin levels helped to verify the diagnosis, so replacement (steroid) therapy was indicated. Following Dr. Grozdanic's advice, Dr. Sette started her on doxycycline 10 mg/kg orally for 10 days and prednisone 1 mg/kg orally twice a day for five days, then once a day for five days, and finally every other day for five days. The plan was that if her vision had improved at the end of this loading period, then nothing more was needed. If there was no improvement, then she come to ISU for further evaluation and possible IVIg therapy. Would it be too much to hope for an inexpensive answer to this problem? As it turned out, no, but it also wouldn't be as easy as I thought to determine the overall results.
At the end of doxycycline/prednisone treatment cycle, I thought Bonnie's sight might be getting better, but when Dr. Sette reexamined Bonnie and performed a thorough eye exam, he felt she had not shown any true signs of improvement. Dr. Grozdanic had affirmed to Dr. Sette that SARDS dogs have a window of time where treatment is valuable, and past that, permanent changes to the retina take place, leaving the dog without IVIg as a treatment option. No one knows exactly how long this golden window of opportunity remains open, and fearing that our time was running out, I made an appointment for Bonnie with Dr. Grozdanic.
Bonnie Visits Iowa State University
Departing from Saint Albans, West Virginia, on a crisp October morning last year, Bonnie and I headed for Ames, Iowa, more than 800 miles away. My heart was full of hope for Bonnie's restored health as we set out with my mother, Jewel, and her gorgeous Papillon, Freddie.
It was a whirlwind tour of the heartland, but the weather was great and Bonnie was all that you could hope for in a pet passenger. Freddie was good in the car, but took a bit longer to do his business at the rest stops, and I couldn't help but brag on my nearly blind and deaf Scottie for being so cooperative. Secretly, I think she enjoyed the attention and time away from our herd at home. At night in the hotel when the chore of navigating a new room and a new place were behind her, she'd settle into bed with me. She'd offer up a contented Scottie sigh and fall sleep. Bonnie certainly seemed to have a high degree of trust in me and that made our journey more necessary than ever.
My experience at Iowa State University Small Animal Hospital was a positive one. I had a short
wait before I was ushered in for Bonnie's examination. Dr. Grozdanic easily conveyed both his concern for Bonnie and his expertise. As I chatted with him and his staff, I asked lots of questions and learned that people come from all parts of the country seeking Dr. Grozdanic's help for their blind dogs, so nobody was impressed by my mileage stats. There are many pet owners who feel the same desperation I felt when thinking of Bonnie's life without eyesight. Somehow I felt happier knowing that other pets were at the top of their owner's priority list, too. Bonnie's future treatment, Dr. Grozdanic explained, would depend on the results of her extensive evaluation by Iowa State University's Small Animal Ophthalmology Service, known for its state-of-the-art equipment and thorough ophthalmic testing.
Dr. Grozdanic's Assessment of Bonnie
Bonnie's final report was as follows: "On presentation, Bonnie was bright, alert and responsive and her physical exam was within normal limits. Ophthalmology exam revealed that there was vision present, as was demonstrated by Bonnie's ability to navigate two different obstacle courses despite absence of the menace response. Colorimetric evaluation of the pupil light reflect showed absence of pupillary light response to red light and good responses to the blue light in both eyes. Fundus examination revealed a pale optic nerve head (due to attenuated vasculature) with no hyper-reflectivity changes bilaterally, suggestive of advanced retinal degenerative changes. An electroreinogram was performed and revealed a complete absence of retinal electrical activity."
After the testing was complete, Dr. Grozdanic brought out his video camera and showed Bonnie's navigational abilities on an obstacle course and then played a video of a dog who had lost complete vision trying to do the same. Bonnie did quite well in comparison. It was not one of the more sophisticated tests Bonnie underwent, but Dr. Grozdanic finds the simple navigation test very useful.
He explained that standard eye tests normally performed by vets and even specialists are not always helpful in identifying good SARDS candidates. A dog may show little or even no retinal activity, as Bonnie did with her flat ERG, but they still retain an ability to see enough to let them get around. Many of the dogs they evaluate have gone completely blind, but others have not. Those who receive IVIg treatment are those dogs who have lost all vision, but whose retinas haven't undergone permanent changes. Hyper-reflective areas and thinning of the retina are usually observed in dogs with SARDS and can mean that a dog is not suitable for IVIg therapy. Dogs who do receive IVIg are usually restored to the level of vision which Bonnie now possessed.
Since Bonnie was still able to see, even in a limited way, Dr. Grozdanic felt she was not ready for IVIg. Much like my oncologist told me about my oral cancer: "Let's not do radiation now when something simpler like surgery might work--let's keep it in the back pocket in case we need it in the future." Similarly, Dr. Grozdanic advised keeping Bonnie on steroid therapy indefinitely, stopping only if it ceased being of benefit or she began to suffer from side effects, at which time we could consider the IVIg therapy. He understood that some owners might be concerned about long-term steroid therapy, but further advised that when owners try to wean their dog off steroids or decrease the dosage prescribed, they find that vision decreased to an unsatisfactory level. This condition is reversed once the steroid therapy is resumed. I was pleased to also learn that Dr. Grozdanic generously offers his protocol to any vet who requests it, and had already shared it with specialists who are much closer to our home in West Virginia.
Bonnie was sent home with a prescription and instructions for prednisone. She was to receive one 10 mg. pill once daily for seven days, followed by a pill every other day for 14 days, then one pill twice per week. We found that her eyesight was decreasing when we got to the maintenance dose of one 10 mg. pill twice a week, and so her prednisone was increased to one 5 mg. pill once a day. Some experts advise this schedule of steroid administration, also known as "pulsing." It is supposed to keep the body from forgetting how and why it needs to make cortisol. Other experts advise that pulsing will not prove totally successful (in Bonnie's case, this was absolutely correct), and that regular doses of cortisol are what the body would normally produce, and therefore, what is needed as a replacement. This idea made sense to me. Would those of us who need thyroid hormone supplementation feel well if we took our Synthroid or Levoxyl every other day or twice a week? Certainly not. I believe it is the same with administration of steroids for dogs who can't make it themselves and need it.
It is only acting out of extreme caution that we now supplement Bonnie's home-cooked diet with liver protective medication, Denomarin, a new product that is a combination of Denosyl and Marin. It contains milk thistle, s-adenosylmethionine (SAM-e) and other liver supportive ingredients in a form that is said to be more "bioavailable" than simple SAM-e or milk thistle alone. Bonnie should have blood work at regular intervals in order that her cortisol, hormone levels and liver status can continue to be monitored.
Stress and Disease Development
Caroline Levin has written that diet could be an irritant or a stressor that leads to adrenal exhaustion and she discusses this in depth in her book "Dogs, Diet and Disease: An Owner's Guide to Diabetes Mellitus, Pancreatitis, Cushing's Disease, and More." Although we had home-cooked for Bonnie at the beginning of her life with us, during the time I was ill, we had to abandon our regular home-cooking routine in favor of organic commercial dog foods--By Nature Organics and Karma. We are now back to cooking for our dogs and it is surprisingly cheaper, and no doubt, healthier. We haven't vaccinated our dogs in years and use organic products in our home and garden, so I think we've made every effort to minimize environmental stress as best we can. We have also decided we will be more reluctant to add new pets to our household. After watching the effects that new ones have had on all my old charges, I believe that this could be also be a huge stressor for some pets. The theory that young dogs bring new life back to old dogs may not be entirely correct in every case. For some pets (young or old), poised on the brink of illness, needing only some stressor to "pull the trigger," a more dominant pet, competing for affection, prized possessions, as well as primo sleeping spots, causing aggravation through typical playful or aggressive behaviors, may take years off the life of the submissive pet.
Consider the view of stress in submissive animals that has been studied by Dr. Carol A. Shively, Professor of Pathology and Psychology, Wake Forest University, and Assistant Director of the Wake Forest University Primate Center. Her work focuses on nonhuman primate response to social stress. She is evaluating the overall health effects of social stress on macaque monkeys, including atherosclerosis, coronary vasomotor reactivity, bone density and biochemistry, breast cancer risk, depression, lipid and carbohydrate metabolism, regional fat distribution and the metabolic syndrome and immune system function.
In 2005, Dr. Shively co-authored research that presented the first animal model of social stress-related depression and the first primate model of adult depression. She describes a behavior pattern in adult female cynomolgus monkeys that have several behavioral and physiological characteristics in common with human depression, including reduced body fat, low levels of activity, high heart rate, hypothalamic pituitary adrenal (HPA) axis disturbances, and increased mortality.
Shively CA, Register TC, Friedman DP, Morgan TM, Thompson J, Lanier T. Social stress-associated depression in adult female cynomolgus monkeys (Macaca fascicularis). Biol Psychol. 2005 Apr;69(1); 67-84.
Shively was recently featured in a PBS documentary called "Unnatural Causes . . . is Inequality Making Us Sick?" Part I explores the effect social stress has on human bodies using the model of stress adaptation. Shively explains what she has observed in her research: "A dominant animal has complete control over his life. He can go wherever he wants in the pen to do whatever he wants. That animal has all the control that it needs to create an optimal environment for himself. In contrast, subordinate animals have almost no control over what happens to them. They have to be watching all the time. With that high-level vigilance comes increases in heart rate. They have higher levels of cortisol circulating in their blood. It's the same chemical that is released in human beings in response to stress. And when it is sustained at high levels it starts having negative effects on cellular function and tissues."
Shively compare the arteries of dominant and submissive monkeys: "This is a cross-section of the artery of a dominant monkey. The hole in the center is large and that means that there's lots of room for blood to flow through. This is the artery of a subordinate animal. So what's happened here is that a subordinate monkey has developed a much larger atherosclerotic plaque than a dominant animal, who lived for the same amount of time, ate the same amount of diet and so on and so forth. And that is simply due to the stress of social subordination. Now, if this monkey keeps developing atherosclerosis at this increased rate relative to this monkey, this one is going to end up with an artery that is completely compromised and have a myocardial infarction."
Unnatural Causes: Is Inequality Making Us Sick? In Sickness and In Wealth – Episode 1. DVD. (2008; California Newsreel with Vital Pictures, Inc.)
www.unnaturalcauses.orghttp://www.unnaturalcauses.org/assets/uploads/file/UC_Transcript_1.pdf
“All animals that experience stressful events have physiologic responses that in the short term allow them to mobilize energy and resources to deal with the stress. But if the stress becomes chronic, and the physiologic responses to the stress continue unabated, health may be deleteriously affected. This is as true for Scotties as it is for people. Dogs, of course, are set up to find certain experiences more stressful then others. Since they are pack animals, being left alone may be quite stressful. Since they organize themselves along hierarchical lines, upheaval in their social hierarchy by the introduction of a new member, human (e.g., the new baby) or nonhuman (the new pet), may also be quite stressful. For most animals that live in a social status hierarchy, being the most subordinate is tolerable, but not optimal. Those low in the hierarchy, irrespective of species, are more likely to be less healthy.”
Carol A. Shively, Ph.D., personal e-mail to the author, April 7, 2008
Researching the Causes of SARDS
When I read of Dr. Grozdanic's work and then later when I was actually in Iowa, his advice was something akin to a miracle. He offers valuable service to the public by giving the hope of continued sight to pets and offering his protocol to others. I also appreciate the fact that he is working diligently on the SARDS problem and spreading the word that if treated promptly, some sight can be restored. There is so little hope offered for blind dogs. I appreciate every resource and expert. I believe his interest to be completely sincere; he has been nothing but gracious and responsive in his assistance to Bonnie, and I feel we owe him a great deal. Once back at home studying all the information I could locate on adrenal exhaustion, I began to think that the way that Dr. Grozdanic had helped Bonnie was through the simple advice to administer steroid therapy.
Clarification may be hard to come by–at least for now. It seems that even within the veterinary community, differing ideas are offered about why and how SARDS may begin and whether autoimmune disease has a role. These different ideas can dictate whether steroid therapy is used.
Dr. Grozdanic has recently published his findings about a new eye disease he has discovered, Immune-Mediated Retinopathy ("IMR"), which can cause blindness in dogs. It is similar to SARDS, one of the differences being that patients who have IMR always have detectable ERG amplitudes, whether they are "normal, supernormal or decreased." SARDS patients typically have flatline ERG. Dogs suffering from IMR always have a tiny pupil response to red light, but SARDS dogs do not. Both dogs respond to blue light of narrow wave length and high light intensity. SARDS dogs display no menace response, but do have phototopic blink or dazzle response (an involuntary blinking reaction to the sudden onset of bright light). Dr. Grozdanic connects both SARDS and IMR to an auto-immune process:
"Both diseases occur when the dog produces auto antibodies that attack the retinal cells. The antibodies mistake retinal cells for cancerous tumors or tissues that need to be destroyed. "In the process of attacking the retinal cells, the auto antibodies cause the retinal cells to lose function and the dog to lose some or all of its vision. The difference between IMR and SARDS that Grozdanic identified is that the auto antibodies that attack the retinal cells in SARDS patients are produced in the eye. In the newly identified IMR, Grozdanic found that these auto antibodies are produced elsewhere in the dog and travel to the eyes in the blood.
* * *
"Tests show SARDS-affected eyes have almost no electrical activity. IMR-affected eyes have some electrical activity, and the retinal cells are not destroyed but have only lost function. These are the retinal cells that Grozdanic thinks can function again now that the origin of the problem is known."
"Iowa State University researcher identifies eye disease in canines
"http://www.public.iastate.edu/~nscentral/news/2008/mar/disease.shtml
What Dr. Grozdanic had to say about IMR and SARDS caused me to wonder whether autoimmune disease truly played a part or did the autoimmune disease process occur because an endocrine disorder came first? Levin's work offers the following information on immune-mediated disease:
"Technically, 'immune-mediated' is a blanket term that covers three types of disease: 1) an allergic response that stems from some type of infection 2) antibodies that attack the patient's own body—an autoimmune reaction— or 3) antibodies that develop on surface tissue in response to an outside irritant, such as 'Farmer's lung'. "From past research done on SARDS, we know several things. To date, no bacterial, viral or protozoal infection has been associated with SARDS cases. This would suggest that SARD is not an infection-induced allergic response. In 2006, two independent studies found no autoimmune antibody activity specific to SARDS dogs. This would suggest that SARDS is not an autoimmune disease. Finally, the retina, located in a virtually closed system, is not in contact with outside irritants, which rules out item 3 as a cause. By these criteria SARDS doesn't qualify as an immune-mediated disease. Consequently, I suspect there may be some controversy in the veterinary community when SARDS is compared to immune-mediated retinopathy in humans.
"Why then, would immunoglobulin injections help some SARDS dogs? Well, research also tells us that immunoglobulins influence a vast number of functions in the body and one of those is to regulate how much calcium enters certain cells. When levels of steroid hormones (such as cortisol or estrogen) are elevated, excess calcium flows into nerve and retinal cells. Excess calcium damages the tiny organs inside the cells and the body eventually destroys these cells. Excess cortisol or estrogen also suppress immunoglobulin levels. So, by restoring normal immunoglobulin levels it may be possible to reduce calcium overload in retinal cells. This in turn, would reduce the resulting cellular damage."
Levin, Caroline D. Frequently asked questions (FAQs) about SARDS and adrenal hormones.
http://www.petcarebooks.com/SARDS/FAQs.htm
Bonnie's discharge papers from ISU contained the following notes, which I found somewhat puzzling: "After contacting ISU-Ophthalmology service and careful review of clinical data, it was decided to initiate [a] course of therapy with systemic steroids and doxycycline. Owner reported improvement of behavior with this therapy (which is highly unusual, since SARDS is a disease which does not respond to immunosuppressive treatment.)"
If it is so highly unusual to see a response, why were steroids offered? I wrote to Dr. Grozdanic to try and determine the reason steroids were tried and his reply indicates a completely different reason for using prednisone (and doxycycline) therapy than Plechner or Levin might advocate. While I was not aware at the time, he originally felt that Bonnie might have IMR, in which case he feels steroids and doxycycline would have been useful. But he disputes that hormonal disease can play a role in SARDS or IMR. He believes that both begin with an autoimmune process, so it follows that prednisone was used because of suspicion of auto-antibody induced damage to Bonnie's retinal neurons and "other neuronal populations," i.e., sense of hearing and smell. (Doxycycline is used because it has immunomodulatory properties.) Since he believes there is no evidence that SARDS dogs have decreased levels of cortisol, his approach to therapy with steroids (prednisone) is strictly for its more commonly understood immunosuppression purposes by using drugs which can alter the immune response by suppression.
He kindly provided me with research he co-authored regarding SARDS and IMR, published just this year. From a personal standpoint, I found it interesting reading, but also somewhat contradictory. (Yes, I admit it: like many Scottie owners, I play "armchair veterinarian.") I provide the following only to give readers a sense of the conflicting information they will find if they seek answers about the pathogenesis of SARDS or IMR. This from Grozdanic's recently published work:
"Although different hypotheses have been established as a possible explanation for SARDS etitology (exposure of photoreceptors to unidentified toxins, photoreceptor degeneration attributable to hormonal or metabolic abnormalities, and glutamate toxicity, the clinical appearance of sudden and painless onset of blindness is most similar to antibody-mediated retinopathies . . . in human beings. Early work . . . showed the possible presence of retinal autoantibodies in the serum of patients that had SARDS; however, these results have been disputed by recent studies demonstrating that patients that have SARDS do not have the detectable presence of retinal autoantibodies in serum or the presence of systemic neoplasia. Furthermore, Miller and colleagues demonstrated that retinas of dogs that have SARDS have extensive numbers of photoreceptors undergoing apoptosis, which is most likely responsible for the development of blindness. Because of the presence of metabolic and hormonal abnormalities in dogs that have SARDS, the most plausible hypothesis for photoreceptor damage in dogs that have SARDS was the presence of abnormal levels of hormones, which can have a toxic effect on photoreceptors. This hypothesis is not considered likely, however, because there is no published evidence demonstrating that hormonal abnormalities can have such a dramatic effect on retinal function."
[Emphasis added]
Grozdanic SD, Harper MM, Kecova H Antibody-mediated retinopathies in canine patients: mechanism, diagnosis, and treatment modalities. Vet Clin North Am Small Anim Pract 2008 Mar; 38(2):361-87; pp.367.
When reading this information, I noticed what I felt were inconsistencies. In one sentence this paper states that abnormal levels of hormones can have a toxic effect on photoreceptors, but in the next goes on to say that there is no published evidence demonstrating the same. I also didn't understand how one could say that metabolic and hormonal abnormalities were the most plausible hypothesis for the mechanism of SARDS, then go on to say that it's not considered likely. I am not sure what veterinarians or professors would consider published evidence, but Levin's case studies (presented before the American College of Veterinary Ophthalmologists) clearly reflect that metabolic and hormonal changes go hand-in-hand with SARDS development. Dr. Grozdanic compares the autoimmune process in human retinopathy to be similar to canine SARDS and IMR.
A cursory surf of the net will show many studies linking human retinopathy to both depressed
and elevated cortisol levels. Diabetes, the illness my Scottie friends mentioned as a possible cause for Bonnie's blindness, is a classic case of estrogens and protestogens affecting carbohydrate metabolism. Both dogs and humans develop diabetic retinopathy. I wrote to ask Ms. Levin if she knew of other eye diseases that might be linked to hormonal imbalance:
"We see a wide variety of ocular problems as the result of endocrine disease. Both dogs and humans develop diabetic retinopathy. Human hyperthyroid patients develop a number of occular problems. Elevated levels of estrogen during pregnancy can affect vision. And elevated cortisol can cause central serous retinopathy in men. None of these conditions mimic SARDS, but we know the anatomy of the canine retina differs from the human retina, and it may differ in physiology as well. But to the original point . . . there is certainly evidence that hormones affect the eye. And in the laboratory, steroids have long been linked with degenerative retinopathies.
Guarneri P, et al. Neurosteroids in the Retina. Annals of the New York Academy of Science 2003; 1007: 117-128.
C. Cascio, et al. Pregnenolone Sulfate, a Naturally Occurring Excitotoxin Involved in Delayed Retinal Cell Death. Journal of Neurochemistry 2000; 74: 2380-2391.
"There are certain contraindications (liver, kidney, or pancreatic disease) when prescribing traditional, large anti-inflammatory doses of steroids. But in cases of adrenal exhaustion (insufficient cortisol production which results in elevated estrogen production), it is this estrogen that actually causes kidney/liver degeneration, suppressed immunoglobulins, and chronic infections. And in these cases, low doses of cortisol can be life-saving. If practitioners are currently prescribing steroids to SARD patients in doses that are lower than in years past, it's possible they are achieving a hormone replacement effect rather than an anti-inflammatory one."
Caroline D. Levin, e-mail message to author, March 29, 2008.
Who Gets What
I wanted to try to determine which dogs would receive steroid therapy for SARDS or IMR at Iowa State and how that was decision was made. Grozdanic and his colleagues write: "SARDS has been considered an untreatable canine-blinding disease because of the complete lack of therapeutic response to anti-inflammatory, antimicrobial or immunosuppresive medications. Antibody-mediated retinopathy in human beings is frequently described as poorly responsive to medical treatment; however, high-dose steroids, plasmapheresis, and IVIg therapies have been described to reverse symptoms of blindness partially."
Ibid. p. 384
However, Grozdanic indicates that the general recommendation now is to initiate steroid and doxycyline therapy in SARDs and IMR dogs as a first step if there are no other associated organ problems. If the dog has liver disease, kidney failure, heart insufficiency or infectious disease, systemic steroids are thought to be contraindicated.
Sinisa Grozdanic, DVM, Ph.D., e-mail to the author, March 26, 2008.
According to Dr. Grozdanic, Bonnie and at least one other dog with SARDS had a positive response to steroid treatment, results he would expect to see in dogs with IMR instead of SARDS. His paper reflects that dogs receiving IVIg treatment for IMR will need long-term steroid/doxy treatment because a "decrease in the medication dose (especially steroids) can rapidly result in severe visual disturbances within 24 hours." So, IMR dogs are treated with steroids and doxycycline, sometimes for a lifetime. But SARDS dogs do not get steroids after IVIg treatment. Bonnie was a lucky exception, I guess. She got the steroids she needed in the beginning and because she responded, needed no further treatment.
Featured in Dr. Grozdanic's research are two photos of Bonnie, one showing her lack of menace response, the other in the visual maze, with the quote: "(A) Lack of menace response after treatment in a patient that has SARDS. (B) Excellent visual maze navigation is present despite the lack of a menace response (this patient did not have any detectable ERG activity before or after treatment)."
Ibid., p.370
I was delighted to see her memorialized in this research, but her picture is directly under the heading "Iowa State University Sudden Acquired Retinal Degeneration Syndrome Intravenous Immunogloublin Treatment Protocol." It seems important to note that Bonnie did not receive IVIg therapy as might be misinterpreted; her only treatment consisted of prednisone and doxcycline, and her vision is now sustained through continued treatment with prednisone, the prescription ISU provided for her.
It may be quite unfortunate that dogs with pre-existing organ problems are often unable to receive any kind of cortisol replacement therapy because of its supposed contraindication. These might be the very dogs who could most benefit from simple steroid treatment. This would only be true if those dogs were tested for and found to be in adrenal exhaustion–and if (1) you accept that adrenal exhaustion plays a role in the development of SARDS, and (2) that non-treatment of this imbalance results in other serious diseases, and (3) that steroid therapy is necessary in addressing this imbalance. Dogs who are suffering from these debilitating diseases and SARDS will have to find a sympathetic veterinarian willing to test for adrenal exhaustion and treat accordingly. This is difficult because conventional wisdom would hold that long-term steroid treatment is harmful, that it is immunosuppressive. So, it is indeed ironic that dogs who might truly need steroid treatment to address not only their SARDS, but also their other metabolic symptoms, are denied it because veterinarians and specialists might not completely understand the way in which these steroids could have a restorative instead of harmful effect.
Many of the metabolic symptoms of SARDS are not tracked at ISU. Excessive hunger, thirst and urination are mentioned as sometimes resolving after SARDS of long duration. (This finding is shown in Levin's work and is also probably part of the stress response.) But other abnormalities are present in dogs that are brought to ISU, even if they are not chosen to be completely addressed.
"Retrospective studies and the author's personal experience is that all symptoms of abnormal metabolic activity (eg, polyphagia, polydipsia, polyuria) resolve within 3 to 6 months after the onset of blindness in most patients. The results of the general physical examination are usually unremarkable, and serum analysis frequently shows the presence of elevated liver enzyme values, lipid abnormalities (predominantly increased cholesterol levels), increased levels of vitamins A and E, increased serum protein fractions . . . and increased levels of cortisol and sex hormones.”
Ibid, p.362
Dr. Grozdanic's work is aimed at showing how IVIg therapy works to restore vision, but is of course, shown through the lens of SARDS being an antibody-mediated process which must be suppressed. As I understand the role of adrenal exhaustion in SARDS as seen through the work of Levin, restoring the hormonal and cortisol balance through hormone replacement puts the immune response back to normal, which in turn stops the degenerative process going on within the retina. But if through IVIg injection, the inflammatory response is reduced, isn't hormone therapy aimed at doing the same thing, but using a different reasoning and less expensive method? In dogs that are given both IVIg and long-term steroid therapy both before and after treatment, how can you know which therapy is working its magic? Perhaps both are working together, but in a different way than those at ISU might propose.
Dr. Plechner writes of some of his more critical cases such as patients with cancer, malapsorption issues and viral diseases as needing more than an oral form of steroid treatment, which might not be absorbed or which could take weeks or months of oral treatment to correct. He then turns to intramuscular injections or, if the patient is hospitalized, a soluble cortisone preparation, along with certain vitamins, and if needed, an antibiotic. This in turn quickly restores normal levels of estrogen and cortisol, which in turn boost the immune system to its normal function. The administration of IVIg that ISU offers may actually be doing the same thing, just coming at it from another direction.
Dr. Grozdanic states the following: "In these diseases, however, it is not clear if the antibody production precedes the retinal disease or if the immune reactivity is a consequence of the retinal degenerative process."
Ibid. p. 381
Wondering if my questions about the cause of SARDS had any merit, I turned to the co-author of at least three studies Grozdanic cites in his research, Dr. Kenneth L. Abrams, DVM, DAVCO. Dr. Abrams is a board-certified veterinary ophthalmologist, practicing for the last 15 years in his own private referral ophthalmology practice, Veterinary Ophthalmology Services, Inc. He completed his small animal medicine and surgery internship at Angell Memorial Animal Hospital in Boston. He then pursued advanced training in his residency in comparative ophthalmology at the University of Tennessee but left the south to return to Boston, where he was the staff Ophthalmologist at Tufts School of Veterinary Medicine and Angell Memorial Animal. He is a past president of the American College of Veterinary Ophthalmologists and has authored several scientific articles and textbooks. However, from my perspective, his most valuable background comes through in his strong clinical interest in retinal disease, including SARDS.
Dr. Abrams co-authored a study that evaluated the blood of thirteen dogs affected by SARDS and five dogs with normal ocular examinations to determine the presence of antiretinal autoantibodies. The conclusion of this study was that "no antiretinal autoantibodies were identified in the serum of dogs affected by SARDS as compared to normal canine patients."
Keller RL et al. Evaluation of canine serum for the presence of antiretinal autoantibodies in sudden acquired retinal degeneration syndrome. Veterinary Ophthalmology 2006;9:195-2001
http://www.blackwell-synergy.com/doi/abs/10.1111/j.1463-5224.2006.00466.x?journalCode=vop
In his own practice, Dr. Abrams sees about 50 dogs a year with SARDS, and observes that Schnauzers, Brittany Spaniels and Dachshunds are the most affected breeds. He often sees a loss of the sense of smell in dogs with SARDS, but has not noticed the hearing loss that Bonnie experienced. He has also observed that stress is a precursor to this disease: "groomer, boarding, new house, new-born children." Both his research and personal experience point toward a corresponding hormonal imbalance. He indicated to me several theories had been put forth to explain the development of SARDS, including glutamate toxicity and autoimmune disease, but he did not believe these to be correct. "Many patients (70%) have an associated problem where they will drink lots of water, eat aggressively, and gain a lot of weight in recent times. These signs hint at a hormone disorder called Cushing's disease, a similar disease to diabetes. However, when patients are tested for Cushing's disease, the results are usually normal or borderline, therefore indicating that SARDS patients probably don't have true Cushings disease."
Common Eye Diseases, Sudden Acquired Retinal Degeneration
http://www.peteyespecialist.com/common.html#6
Clearly, the debate about whether IMR and SARDS are truly auto-immune diseases will persist, just as blindness in affected dogs will continue to occur. Even though it is helpful for owners of affected pets to understand the origin of these diseases and the factors which predispose pets toward them, it is perhaps far more important that we seek appropriate testing and demand proper treatment for any pet that might display the symptoms of adrenal exhaustion or SARDS.
The Future
Patrick and I intend to keep a firm eye on all our pets' endocrine function now as we see how important it is to overall health and well-being. About seven years ago, we began yearly health check ultrasounds for the dogs and the results sometimes identified problems before they got to the disaster stage. It is with hope for similar results that we will implement yearly testing to determine cortisol, hormone and immunoglobulin levels in all our pets. If I had to make a choice between the two, I think I would choose the blood work. In light of the new information I've been given, I now have confidence that hormone testing could have addressed much of the "junk"–the liver disease, the bladder cancer, the kidney disease–that we found through the ultrasounds. Since an ounce of prevention is worth a pound of cure, we plan to have complete blood work run for Bender, as evidence points to adrenal exhaustion being a heritable imbalance. I hope that this point does not escape the reader's attention.
Adrenal exhaustion is a real disorder, therefore breeders should begin testing for these imbalances and making choices based on the results. The buying public should insist on making our purchase decisions accordingly. We can no longer continue to accept genetic cripples.
"Indeed, the actions of breeders have given new–and literal–meaning to the term "killer looks."At great expense to the health of animals, breeding practices have taken a cosmetic/marketing path away from natural or functional criteria. As an example, this trend has converted hunting breeds of dogs into fashionable, nonhunting, household pets who have lost their field ability, nose, and hardiness. Pets have become more and more processed, unnatural, and unhealthy, and more like merchandise.
“I'm truly convinced that if current trends continue–emphasizing the latest fashion and ignoring the health of breeding stock–cats and dogs may simply be bred out of popularity. Whether they know it or not, breeders who worship at the altar of fashion and who relegate or ignore the health factor are compromising the survival of their breeds. They are, in a sense, practicing animal abuse. Their actions perpetuate unwellness and suffering. Their actions victimize buyers–innocent consumers who purchase puppies and kittens and who usually have no clue as to what may lie ahead in terms of sickness and veterinary bills.
* * *
"Irresponsible breeders are not interested in what I have to say. Responsible breeders are interested. "What can I do to correct this? they ask . . . . [T]herapy does not correct the genetics. It corrects the effects of the genetics that cause disease. If you breed two animals with the same degree of genetic flaws, even if both are corrected, then the genetic imbalances are merely passed on with more severe consequences for the offspring."
Plechner, A. J., Zucker, M. Pets at Risk From Allergies to Cancer, Remedies for an Unsuspected Epidemic.:NewSage Press. Oregon, 2003. pp. 153, 154
Bonnie Today
It has been six months since we started Bonnie's prednisone therapy. Simple observation of her behavior brings us much to be happy about. We once felt that Bonnie's touchiness with our other pets was because she had lost much of her sight and was feeling insecure. There are some resources that will point to that as the reason behind this behavior, and other sources indicate that treatment resolves the matter. I think her attitude was caused by the excess female hormones, or the "bitchy" hormones, as we like to refer to them. I am happy to say that since being treated, "Bitchy Bonnie" is gone. She's had to have some large skin tags removed and biopsied–also probably caused by the production of the excess female hormones. She has since healed nicely and the hair is growing back well in these areas. Her vision remains mostly stable, as does her hearing. We unfortunately ran out of prednisone while I was out of town recently, and I noticed as soon as I got home that her vision had suffered because she was bumping into things. When we returned to treating Bonnie with the steroids a few days later, we found we had to give her several days of higher dosages before her vision returned to the level it had been. Dr. Grozdanic's research indicates this to be typical in dogs with IMR dogs who are treated with long-term steroids. (She is still a dog with SARDS, but with responses that look more like a dog with IMR.)
In the last week, I have noticed that her vision seems a little off. She is not bumping into things, but not seeing all the things she'd been able to see before. Her sense of smell seems diminished, too. Will she need an increase in her steroid treatment? I won't know until I have her hormone panel run again in the next few weeks. Dr. Plechner indicates that each patient is biochemically unique and should be viewed as such when treated with hormone replacement. Large dogs can need a much smaller dosage of steroid replacement than a small dog might need. He believes it is all depends upon the amount of active cortisol that is able to be produced by the adrenal glands. So, it is possible Bonnie may need an increase in her steroid dosage.
Also, Dr. Sette just signed off on Bonnie being treated for thyroid supplementation. She had been in the gray zone and he had not felt she needed treatment before. But reflection on the fact that hormone replacement involves treatment of the thyroid, too, he decided to put her on Soloxine. The fact that she has not been on it might have some effect on the way her body is handling the prednisone. Dr. Plechner, when asked about Bonnie's adrenal exhaustion and my own hypothyroid condition, urged the following:
"Bonnie has an endocrine-immune imbalance that is caused by low or defective amounts of cortisol leading to an elevated Total Estrogen from the inner layer adrenal cortex which not only binds thyroid hormone,T3-T4, but further binds cortisol and DEREGULATES the immune system. These cells lose recognition of self tissue but the T-cell no longer protects the body from viruses etc. Long[-]term steroid can only work in dogs and people when used with thyroid hormone so that in 24 hrs the steroid is completely broken down. If thyroid is not used, then there will be daily steroid left and after this is occurring the steroid build up will be an over-dose and then hurt the patient . . . . The dose of steroid is determined by the immunoglobulin level reregulated by the B-cell. Bonnie may need to be on physiological levels of hormone replacement for good. By rechecking blood levels every 6-12 months you can determine if hormone replacement needs to be done. Remember, the blood sample must refrigerated immediately after being spun-down and kept refrigerated in travel and kept refrigerated until tested otherwise the test results are invalid."
Alfred J. Plechner, DVM, e-mail to the author, April 1, 2008.
Bonnie still feels sure enough of herself to get up alone during the night, navigate furniture in near darkness, go down a long hallway and out the pet door to do her business. This assures me that she has retained functional sight. At times, I find that she focuses on a spot where she thinks I am-- gazing with such an intensity--I am a little sorry to correct her. We have developed a system where I use a light touch to signal to her the direction I am heading. I give a light touch to her head if I am going forward or I will touch her back if I am heading in the opposite direction. Otherwise, she will sit and wait patiently and loyally for me in rooms I have long vacated, especially the kitchen. Another sad little sight is a Scottie begging thin air. Her tests would indicate that she has a kind of "peephole" where she is able to see, and so often I wave my arms or move around in a funny dance when I am far away so she can catch a glimpse of me in that little area of sight.
She is back to her routine of going with me to my office, and is sitting at my feet as I write these words, snoring away, oblivious of all the attention I am giving her as I type. She goes up and down stairs, albeit slowly, yet quite independently. She has suffered a few slips that found her on the landing looking a bit surprised. But when her dignity has been compromised, she accepts little sympathy. I can't help but be touched that she will make every effort to get to me, even if it means navigation through places where she can't see well or feel secure. I have found I am absolutely unable to slip out of bed at night for TV watching or late-night work without soon finding her at my side. I admire Bonnie's courage and determination to capitalize on what she can see instead of waiting to be carried around on a litter. It is the best of the Scottie spirit exemplified and just one of the many things I love about her. She won't give up or give in.
Bonnie's hearing is much better, but like those of some humans, is only really good within a certain range, so in addition to doing funny dances, I now can be heard talking to her in a high-pitched, sing-songy voice. Dancing and singing for your dog? Oh yes. That's me. I have resigned myself to being fodder for our guests' conversations on the way home. Now, if I could make my voice sound like a plastic bread bag being opened, I would have her complete attention every time I spoke.
Conclusion:
This is Bonnie's own story accompanied by my personal reflections. I have no formal education that qualifies me to sort through research and make assumptions based on what I find. I am simply an interested and loving pet owner, determined to learn and share all I can about a disease that is so devastating to the affected pets.
Bonnie Sue--our small stone--came to us through unexpected channels, led us to additional Scottie companions and inspired us to give aid to others in her situation. Through a simple phone call, we met her, loved her and vowed to protect her. That promise led to ripples in the pond, seeking real answers to her health problems in spite of mixed messages. Those ripples rebounded off the banks in ways we had not expected. We had to seek answers in a way that we had not in the past, going beyond what experts were telling us, to find the best information available. In the process, we met brilliant and gracious experts, gained a larger view of the beautiful and complicated mechanism that is the adrenal system, and best of all, maintained not just Bonnie's vision, but her overall continued good health. My hope is that her story will inspire others to seek the same sort of positive outcome for their pets.
It is the cycle of small actions leading to larger consequences. And as Robert Louis Stevenson said: "Sooner or later everyone sits down to banquet of consequences."
FIRST UPDATE ON BONNIE
Since April of 2008, Bonnie was retested using the E-1 adrenal panel offered through National Veterinary Diagnostic Services. While her values have improved and her cortisol is normal, her total estrogen was still too high 35.27 (normal 30.00-35.00) and her immunoglobulin levels were still very low. (IgA 50 (normal 100-200); IgG 1,089 (normal 1,250-2000); IgM 81 (normal 100-200). While the estrogen level may not look like it is off by much, Ms. Levin says that even small amounts like this can cause clinical symptoms like we have observed in Bonnie. Another reason we like the lab in California—they normal ranges are small and correspond well to what we observe as owners.
Because her values were not yet normal, and therefore her system not yet balanced, Bonnie was taken off prednisone and treated through weekly steroid injections. It was thought that she was not absorbing the oral medication as well as she might (adrenal exhaustion is often implicated in malabsorption problems) and so we did injections for a month. What we found was that sometime toward the end of the week, the steroids wore off and she would become almost completely blind, with much less functional sight than we’d been able to preserve up to this point. After consulting with Caroline Levin, it was determined that Bonnie should have one more initial injection of two steroids, then begin medrol at 4.mg daily. We were also advised to administer Sulfasalzine to increase absorption of the medrol. Bonnie also receives the supplement PS or Phosphatidylserine (which has the nice effect of also treating the gallbladder mucocele dysplasia she has), as well as a taurine/magnesium supplement designed to offer more protection to the retina. She is also receiving an oral form of Soloxine in the hopes that her thyroid meds will be absorbed better, too.
At this point, all of Bonnie’s outward symptoms have subsided and her vision is very stable. The only problem we are having currently is a recurrent bout of cystitis, which is probably caused because her IgA is so low, and her normal immunoglobulin protection is lacking in that area, leaving her susceptible to infection or attack of her mucosal surfaces (which obviously includes the bladder; a scary thought for any Scottie owner). Since any kind of invasive diagnostics are contraindicated to obtain a urine sample ((i.e., catheterization or cystocentesis) in a pet that might have transitional cell carcinoma—and that could be just about any Scottie—we’ve had to rely on repeated urinalysis tests. Bonnie has been on one antibiotic, and responded well at first, but her infection seems to have returned. We hope that she will soon be placed on a different antibiotic and that a trip to a specialist for an ultrasound to rule out bladder cancer isn’t a necessity.
The thing Patrick and I have learned in the last few months is that this is a difficult area to find good treatment. Most people who have a pet diagnosed or suspected of adrenal exhaustion and/or SARDS will have to be willing to be an informed consumer with their veterinary and to push for appropriate treatment. In our case that seems to involve contacting specialists for advice as each new problem arises and a combination of both diplomacy and pushiness with our local vet. We hope that the end result will prove Bonnie to be the big winner for our efforts.
SECOND UPDATE ON BONNIE
Since April of 2008, Bonnie was retested every few months using the E-1 adrenal panel offered through National Veterinary Diagnostic Services. While her values have improved and her cortisol was normal, her total estrogen was still too high 35.27 (normal 30.00-35.00) and her immunoglobulin levels were still very low. (IgA 50 (normal 100-200); IgG 1,089 (normal 1,250-2000); IgM 81 (normal 100-200). While the estrogen level was not off by much, even small amounts like this can cause clinical symptoms like we have observed in Bonnie. Another reason we like the lab in California—their "normal ranges" are small and correspond well to what we observe as owners and it is highly recommended by the experts in the field of canine endocrinology.
Because her values were not yet normal, and therefore her system not yet balanced, Bonnie was taken off oral prednisone and treated through weekly steroid injections and the thyroid supplement Soloxine compounded in liquid form was added. It was thought that she was not absorbing the oral medication as well as she might (adrenal exhaustion is often implicated in malabsorption problems) and so we did injections for several months. What we found was that sometime toward the end of the week, the steroids wore off and she would become almost completely blind, with much less functional sight than we’d been able to preserve up to this point.
After consultation with Dr. Plechner and Ms. Levin, it was determined that Bonnie should have one more initial injection of two steroids, then begin medrol at 4.mg daily. We were also advised to administer Sulfasalazine to increase absorption of the medrol. Bonnie also receives the supplement PS or Phosphatidylserine (which has the nice effect of also treating the gallbladder mucocele dysplasia she has), as well as a taurine/magnesium supplement designed to offer more protection to the retina.
After following these directions, nearly all of Bonnie’s outward symptoms subsided and her vision remained somewhat stable. She suffered with a recurrent bout of cystitis, probably caused because her IgA is so low, and her normal immunoglobulin protection is lacking in that area, leaving her susceptible to infection or attack of her mucosal surfaces (which obviously includes the bladder--a scary thought for any Scottie owner).
Since any kind of invasive diagnostics are contraindicated to obtain a urine sample (i.e., catheterization or cystocentesis) in a pet that might have transitional cell carcinoma—and that could be just about any Scottie—we’ve had to rely on repeated urinalyses. Bonnie has been on one antibiotic, and responded well at first, but her infection seems to have returned. We hope that she will soon be placed on a different antibiotic and that a trip to a specialist for an ultrasound to rule out bladder cancer isn’t a necessity.
The thing Patrick and I have learned in the course of fighting for Bonnie's health is that adrenal exhaustion is a difficult area to find good treatment locally. Most people who have a pet diagnosed or suspected of adrenal exhaustion and/or SARDS will have to be willing to be an informed consumer with their veterinarian and to push for appropriate treatment. In our case that seems to involve contacting specialists for advice as each new problem developed and a combination of both diplomacy and pushiness with our own local vet. We continue to hope that the end result will prove Bonnie to be the big winner for our efforts.
POSTSCRIPT:
After several months of steroid injections, we re-ran Bonnie's adrenal panel once more and found that she was still not in balance. We conferred with Dr. Plechner who indicated that perhaps higher doses of injectible steroids, using a different mix, might be indicated in Bonnie's case. Bonnie had two doses of these injections. We observed that she panted a lot and had a little bit of noisy breathing, but nothing serious. However, to take proper precautions, we took her to our local vet, who took x-rays and thought her heart was enlarged and her liver, too. We took her on to a cardiologist in Leesburg, Virginia, who assured us that her heart was not enlarged and that she simply had a "Scottie heart." He said that many broad-chested breeds like Scotties or Boxers have larger hearts simply because the chest cavity makes room for it.
Since her liver has been somewhat enlarged for the period we've owned her, we didn't feel we could do anything differently for Bonnie than we were at that time. So, we continued on with her treatment.
One night, after dinner, she seemed to have noisy breathing and didn't want to sit or lie down. After a satisfying meal, Bonnie normally goes straight to sleep. I noticed that she went out to potty, but produced bright red bloody diarrhea and seemed very uncomfortable.
I gave her some Loperimide (a medicine we had on hand for another Scottie we'd owned who suffered from IBD) and continued to watch her. As her breathing grew more labored, I noticed couldn't and wouldn't lie down. I quickly decided to take her to the Emergency Clinic, where the vet there gave her Cephalexin and was sending her home with me without any other treatment. I explained all about her adrenal exhaustion and offered a CD with all of Bonnie's records, but they weren't interested in seeing it or hearing about her problems. I wasn't with her when they were examining her for the hour she was there because all the client rooms were taken, so they took her to the back where they wouldn't permit me access.
I think they left her in a cage while they ran the CBC and she grew much worse during that period of time. Then the doctor trotted out and gave me some Cephalexin and said she'd be fine. I told them I didn't feel Cephalexin was strong enough to handle what I had observed. They reassured me it was and then brought Bonnie out to take home.
Obviously they didn't have a good look at her when they tried to give her back to me to take home. Nobody would have let a dog who looked like she'd had a major stroke go home with just antibiotics. She couldn't stand and her head was lolling around, her tongue was dark purple, her gums dark, too. She was gasping for breath and completely out of it. I said, "Hey, wait a minute, she can't go home like this!"
The vet tech told me she was so glad I questioned them and brought her back. She agreed with me that she had become much worse and that her gums had been a good color when she came in, but I pointed out they were now blue and her tongue was purple. I will never know why they didn't want to give her oxygen to begin with since she was having trouble breathing. They told me later--after all was said and done--that they "didn't want it to interfere with anything. "
I wondered later what oxygen could possibly interfere with in a dog that was gasping for breath. It seemed from my point of view, it interfered with her continuation of life!
But at that point, she was put on oxygen and in a very short while of observing her, the veterinarian suggested euthanasia. I asked for an x-ray, which the vet said (as did our earlier vet, but not the cardiologist) that she had an enlarged heart. Her lungs looked "crappy" he said, but didn't sound nearly as bad as they looked. The vet felt she had a "cardiac episode." We watched her for about an hour, and she got no better--really much worse. I explained to the vet again all about Bonnie's adrenal exhaustion, her SARDS and her enlarged liver. But the vet had no insight to offer and I felt like she was suffering so there was nothing else to be done. I am all about the ends justifying the means, but looking at her, it didn't seem the end was going to be much to be happy about. So, I chose to euthanize her at about 3:00 a.m.on the morning of November 10, 2008. I am sure, looking back, it was the right decision.
Distraught, my sole focus became trying to ensure that whatever could be learned from Bonnie's death would be brought to light.
A new vet we had switched to before Bonnie's death, Dr. Clara Mason, agreed to my request to do a necropsy for Bonnie. I actually ended up assisting Dr. Mason during the procedure, mostly labeling the specimens as she worked. I admit it was all a bit surreal and at times, painful to watch. However, knowing we own two of Bonnie's children and this was a heritable disorder kept me motivated to see it through. If there was anything to be learned from Bonnie in death, I felt I had an obligation to find out what it was. I also owed it to her.
What we learned was that her liver was huge, with lobes overlapping and some funny little lesions that I've read about on ultrasounds but never had a clear idea of how they might actually appear. Her liver was also quite thick. Dr. Mason said I should think of a normal liver being thin--like a beef or chicken liver. Bonnie's was clearly thin on the edges rising to a very fat middle.
Bonnie's gallbladder was one of the biggest Dr. Mason had ever seen in a dog. She was sure there would be stones, but there were none. Just a huge gallbladder. Bonnie had been diagnosed with gallbladder mucocele dysplasia and Dr. Mason saw no signs of that, but did say the gallbladder was grossly abnormal in size.. However, when she opened it up, it had all of this sludge in it that I also read about on our ultrasound reports for every Scottie we've owned. It looked like big pieces of black pepper. I had no yardstick for knowing whether it was a little or a lot, but Dr. Mason said in 20 years of practicing, she'd never ever seen that much in a dog or even heard of such a thing. She was at the top of her class at Michigan and won awards for her necropsy skills, so I suppose she is in a position to comment. I know the sludge is common in Scotties, but isn't supposed to be good. Kind of an indicator that the liver isn't working as well as it should.
One of my big regrets is that we forgot to get a bladder sample. A ridiculous omission in a Scottish Terrier, but I wasn't thinking well that day. Bonnie is even part of a special Ostrander Bladder Cancer study, searching for a genetic marker for transitional cell carcinoma, so it would have been good to have a sample to get a final determination on the status of her bladder. As it stands, her blood was sent in to several years ago to represent Scotties without bladder cancer.
Her heart was large, but showed no visible problems. Dr. Mason agreed with the cardiologist in Leesburg, VA, that her heart was just large because she is a Scottie, not because it was diseased in any way.
Her kidneys looked okay--not great--and her adrenals were small and hard and had an unusual texture, which really interested Dr. Mason. I had read before this could mean that they weren't working well, but she said she'd rather wait and get the report back before she made any comment about that.
Dr. Mason said--perhaps to make me feel better--that it appeared Bonnie had other issues going on that would have compromised any treatment plan to jump start her adrenals and that perhaps it was more merciful she died when she did.
I don't know about that. I just know I miss her a lot. She was one of those dogs you get really involved in caring for; it's kind of like a job. Most days revolved around what she needed or what help I could provide for her.
That night before I took her to the Emergency Clinic, I prayed with Bonnie at my side and asked God to heal her, to end her suffering, to delay it for another day. He answered my prayers, but not how I thought. Now, the hard part is accepting that He knew best.
NECROPSY RESULTS:
When we got the necropsy results back, I was surprised, to say the least. She had a lot of problems going on, but in the end, Bonnie died of end-stage kidney failure. But clearly, we were on the right track in believing her adrenals were a big part of the problem.
A summary of the results:
*Moderate subacute diffuse hepatopathy
*Marked acute to subacute focal hemorrhagic pancreatitis
*Adrenal atrophy
*Marked subacute diffuse membranous glomerulonephritis with interstitial fibrosis
The pathologist indicated that the "The kidney would be considered an end-stage type of kidney."
I found that surprising in that we never saw any indication of this in Bonnie's behavior. More significant and heartbreaking was the pathologist's last comment of all, which echoed quietly what Dr. Plechner has been preaching for years about the body-wide impact of adrenal failure. The pathologist simply wrote "Changes in the organs may be related to the adrenal atrophy."
So, we are left with proof through necropsy, not just blood work, that Bonnie did indeed have adrenal failure. When discussing these results with Dr. Mason, she tried to give me insight into the situation when I blamed myself for not being able to help Bonnie. She said that although we had made a valiant effort to help Bonnie's body heal, perhaps we were not successful simply because she was too far into the process to be able to receive that aid In effect, she said that to be able to regenerate and restore the body, the process has to begin before the end-stage, when the body is able to accept rejuvenation.
LAST THOUGHTS
Despite our best efforts to help Bonnie, we were unable to stop the degenerative process that caused her SARDS. However, we did give her a great year of limited vision with lots of love and attention and were able to learn a lot about how to help other dogs that were bred from her. I believe our experience with Bonnie will benefit her two offspring living with us, and hopefully, others. My deep desire is that owners with pets suffering from adrenal exhaustion will draw from our experiences and find motivation to seek treatment. Dr. Plechner's mechanism--his recognition of adrenal exhaustion--is the cornerstone of treatment of pets with adrenal exhaustion or SARDS, and I suggest to any owner seeking help for their pets suspected to suffer from these diseases to contact him immediately. His deep love of animals and his willingness to help owners goes above and beyond the average call of duty and I will be eternally grateful to him for his insight and aid in our time of need.
RESOURCES: If you are concerned that your pet might be suffering from endocrine-related disorders such as those described in this article, you may find your vet or specialist to be unacquainted with the diagnosis process or treatment information. Therefore, you may find the following web links and titles useful.
Caroline D. Levin, R. N 18709 S. Grasale Road Oregon City, OR 97045 Phone and fax: (503) 631-3491 Caroline Levin is available for phone consultations for a small fee, as well as speaking
engagements. She no longer replies to e-mails as a result of carpal tunnel tendonitis. Ms. Levin offers to consult free of charge by telephone with any Great Scots Magazine reader who has a newly diagnosed or suspected SARDS affected dog that has been blind for one to two weeks. Lantern Publications online resources for SARDS:
http://www.petcarebooks.com/research.htm
The Journal of the American Holistic Veterinary Medical Association, 2006: Vol. 24 (4), 11-19. "Environmental Factors and Signs of Hypercortisolism in Dogs affected with Sudden Acquired Retinal Degeneration (SARDS)" by Caroline D. Levin, R. N.
http://www.petcarebooks.com/pdf/SARDS_diet_study.pdf
For better endocrine testing with tighter "normal" ranges, Plechner and Levin recommend: National Veterinary Diagnostic Services (NVDS)29620 Ashdale Way Quail Valley, CA 92587-9511 Phone# 951-543-4678Web: www.national-vet.com Email: info@national-vet.com
Iowa State University Veterinary Teaching Hospital
College of Veterinary Medicine
Ames, Iowa 50011
Dr. Sinisa Grozdanic Veterinary Clinical Sciences
515-294-4900 or 515-294- 712
sgrozdan@iastate.edu
"Blind dogs can see after new ISU treatment for a sudden onset blinding disease"http://www.public.iastate.edu/~nscentral/news/2007/may/blind.shtm
"Iowa State University researcher identifies eye disease in canines "http://www.public.iastate.edu/~nscentral/news/2008/mar/disease.shtml
"New treatment for glaucoma shows promise in laboratory, say Iowa State researchers"
http://www.public.iastate.edu/~nscentral/news/2007/aug/glaucoma.shtml
"Pets at Risk: From Allergies to Cancer, Remedies for an Unsuspected Epidemic "Martin Zucker and Alfred J. Plechner, DVMNew Sage Press, 2003 $13.95
http://www.amazon.com/Pets-Risk-Allergies-Remedies-Unsuspected/dp/0939165481
"Chaos in the Cortex" by Alfred J. Plechner, DVM
http://www.drplechner.com/art-unrecimbal.html
The Plechner Protocol (links to much of Dr. Plechner's research and vets who embrace his theories):
http://www.drplechner.com/protocol.html
"Unrecognized Endocrine-Immune Defects in Multiple Diseases An Effective Veterinary Model May Offer Therapeutic Promise for Human Illness"Alfred J. Plechner, D.V.M.
http://www.drplechner.com/EI-Human-article.pdf
Dr. Kenneth L Abrams. DVM, DACVOhttp://www.peteyespecialist.com/abrams.html "When Blindness Strikes"http://www.alidas.com/articles/SARDS.htm
Canadian Diagnostic Veterinary JournalCan Vet J. 2002 September; 43(9): 729–730.
Diagnostic Ophthalmology http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=339566
