2/23/10 - Veterinary Specialists

Vet Tip of the Day: Understanding your Veterinarian's Training
Key Words: Diplomate, Board Certification, Residency, Internship

I've been looking at a horse with a challenging lameness problem for a couple of days.  This weekend I examined another horse with an unusual neck problem.  I obtained radiographs of both horses.  Tonight I will e-mail the x-rays of the lame horse to a board certified large animal surgeon for his opinion.  Yesterday I mailed a disc of the neck films to the radiology department at UC Davis where they will be reviewed by a board certified radiologist.  Last week a colleague of mine called me to ask for a consult on a horse with pleuropneumonia.  He was seeking my opinion on treatment options because I am board certified in Large Animal Internal Medicine.

What do you know about your veterinarian's training and post-doctoral experience?  All of us practicing veterinary medicine have completed a 4 year graduate veterinary degree program after our undergraduate college years.  When we graduate from veterinary school we receive a doctoral degree: DVM or VMD (if you graduate from the University of Pennsylvania your veterinary degree is awarded in latin so it ends up VMD instead of DVM).  In order to practice veterinary medicine we also have to pass the day long National Board Exam as well as an exam in any state in which we intend to practice.  With a DVM and passing scores on the National Board and state exams, we are licensed to practice all aspects of veterinary medicine according to the laws of the veterinary practice act in the state in which we work.

Unlike human medicine, veterinary medicine does not require an internship or residency after vet school.  However, many individuals choose to complete such post-doctoral training.  Most Colleges of Veterinary Medicine offer rotating small and large animal internship programs which provide a year of experience in medicine, surgery and reproduction under the supervision of experienced faculty members.  Many private practices also offer internship programs, but many of these programs do not fall under the guidance of any governing body.  While some private practice internships are of excellent quality and value, some are not.

After completing an internship, the final phase of advanced clinical training available to veterinarians is residency programs.  Most of these programs take place in a University setting, but there are private practice residency programs as well.  All residency programs must comply with rules and regulations set down by the Specialty College under which they operate.  The three main specialty colleges are the American College of Veterinary Internal Medicine (ACVIM),  the American College of Veterinary Surgeons (ACVS), and the American College of Theriogenology (ACT, reproduction).  There are many subspecialties in the Medicine college.  These include neurology, cardiology, oncology, and large and small animal internal medicine. There are also specialty colleges of Emergency Medicine, Exotic and Zoo Animal Medicine and Critical Care.

As you can see, there are many opportunities for advanced training after the Doctor of Veterinary Medicine is obtained.  My list above is far from complete.  All ACVIM and ACVS residency programs are at least 3 years long.  Some combine their clinical residency with a Masters or PhD program in a basic science.  My Large Animal Internal Medicine Residency was completed at the University of Georgia and was combined with a PhD degree program.  This combination training took 5 years to complete, and offered a great complementary combination of basic research and clinical training which in my case had a strong emphasis on colic, or equine gastrointestinal diseases.  It is important to remember that while we are completing residency programs, not only are we becoming highly skilled experts in our specialty field, but we also are working as practicing veterinarians in a teaching hospital, and so are interacting on a daily basis with other services, including surgery, lameness, reproduction, etc.

At the end of a residency program, the resident candidate's credentials must be approved by their resident mentor, and then they have the priviledge of taking a monster exam.  To give you an idea of how stringent our veterinary specialty residency programs are, when I took the ACVIM Large Animal Internal Medicine exam, the pass rate was 23%.  That means that only 1 of every 5 people who sat for the exam that year received board certification.    

If your veterinarian is a general practicioner, he or she may choose to consult with a specialist from time to time concerning certain issues with your horse, or in some circumstances may choose to refer you and your horse directly to a specialist.  As veterinarians, we have a strict code of referral ethics.  I encourage you to  follow your primary care veterinarian's advice, consult with the specialist, and return to your primary care veterinarian for follow up care.  It is important that specialist referral centers maintain open lines of communication both with their clients and with the referring veterinarians in order to provide the best care to your horse while maintaining continuity of service.

Now that you know a little bit about specialization within the veterinary profession, take advantage of your knowledge and ask your veterinarian any questions you may have about our profession.  Don't be afraid to ask any professional about their credentials and experience.  And if you do take your horse to see a specialist for any reason, be sure that that person is in fact a Diplomate of the Specialty College of Veterinary Medicine in which they are practicing.

To learn more about our specialty colleges, log on to ACVIM.org or ACVS.org

I am your Vet Tip of the Day Blogger,
Chrysann Collatos VMD (Veterinariae Medicinae Doctoris), PhD (Doctor of Philosophy in Physiology), DACVIM (Diplomate American College of Veterinary Internal Medicine)

2/22/2010 - Omega-3's & Colic

Vet Tip of the Day: The role of Omega-3 Fatty Acids in Colic prevention
Key Words: Colic, Polyunsaturated fat, fatty acid, cell membrane, endotoxin

Since you are now budding experts on the subject of endotoxemia and its devastating effects on horses with gastrointestinal disease, I thought we would conclude this segment on colic with a discussion of Omega-3 fatty acids.  You've may have heard a lot of buzz about these special fats; following are some facts about Omega-3's and how they can help protect your horse from some of the terrible consequences of endotoxemia.

Omega fatty acids - What are they?

This part is pretty dry, but it will only last a few sentences, so hang in there. Our bodies derive four types of fat from food:cholesterol, saturated fat, monounsaturated fat, and polyunsaturated fat. Omega-3 fatty acids are polyunsaturated fats. They are called omega-3 because a certain chemical bond between two carbon atoms occurs at the third carbon in this fatty acid chain of carbons. The other major polyunsaturated fat in our diet is Omega-6 fatty acid (first double bond at the sixth carbon).

Omega-3 and Omega-6 fatty acids are considered “essential” fatty acids, because neither horse nor human can construct these substances internally. They must be obtained in our diets. While both O-3 and O-6 are necessary for good health, we and our horses eat diets that are relatively high in Omega-6 fatty acid and deficient in Omega-3. As we will see, it appears that an ideal ratio of dietary O-3 to O-6 is about 2:1, while most of us are eating these fatty acids in a ratio more like 1:10 or even 1:20.

Omega fatty acids - What is their function?

Consider the building blocks of our bodies. We and our horses are amazing machines, composed of a group of organ systems that works in harmony to create life. Each of our organs is a mass of cells, and each organ has its own distinctive cell type. Liver, kidney, skin, nervous tissue, brain, blood vessel walls - each has its own unique cellular architecture. However, all of these cell types are encased in the same basic cell membrane. Guess what our cell membranes are made of? You’re right - they are made of fat!

Cell membranes are composed of a double layer of phospholipid, a complex fat containing Omega-3 and Omega-6 fatty acids. The cell membrane is like a telegraph system; signals from outside the cell are communicated to the inside through the cell membrane. The composition of the cell membrane determines in large part how signals are translated from outside to inside; the cell membrane makeup greatly influences the cell’s response to a given stimulus. Specifically, a cell membrane enriched in Omega-3 fatty acids is protected from many of the inflammatory responses to injury that are produced by an Omega-6 enriched membrane. 

If your horse experiences a serious colic in which gut motility is disrupted, remember that this leads to a die off of bacteria normally present within the bowel.  Some of these bacteria contain endotoxin, which is absorbed into the blood stream through the compromised gut wall of your colicky horse.  This endotoxin attaches to cell membranes in your horse's system, sending a series of telegraph signals across cell membranes and from cell to cell that lead to the production of many small molecules responsible for inflammation, shock, and cardiovascular collapse.  If your horse's cell membranes are enriched with Omega-3 fatty acids, the severity of the inflammatory response to these signals is dampened, resulting in less devastating effects on your horse's circulatory system.

Omega-3 Fatty Acids - Where do we find them?

Omega-3 fatty acids are relatively abundant in oily, cold water fish such as tuna, salmon, and mackerel. These fish contain large amounts of two Omega-3's, eicosapentaenoic acid (EPA) and docosahexanoic acid (DHA). Vegetable sources of Omega-3's include kelp, as well as flaxseed, canola, walnut, and soy oils. The latter 4 oils contain alpha-linolenic acid (ALA) the third major Omega-3 fatty acid. One should remember that all of these sources of Omega-3 fatty acid also contain Omega-6 fatty acid. Once ingested, the Omega-3 and Omega-6 fatty acids compete for the same processing sites in the body, emphasizing the importance of the balance of O-3 and O-6 in the diet.

For us, consumption of Omega-3's is easily achieved by eating fish. Since 2000, the American Heart Association’s dietary guidelines have recommended that healthy adults eat at least two servings of fish per week. Alternatively, there are many encapsulated fish oils available: people with existing cardiovascular disease are encouraged to take 1 gram of EPA and/or DHA daily.

For our horses, there are an increasing number of supplements and concentrate feeds on the market that are enriched with flaxseed oil to supply Omega-3 fatty acids. Unfortunately, we have no good information on how much a horse should eat to achieve a beneficial result. Therefore, while there is mounting evidence that dietary enrichment with Omega-3 fatty acids will improve your horse’s overall well-being, we are still guessing with our dietary supplementation. One positive note concerning flaxseed oil, the primary source of Omega-3 for horse consumption: flaxseed oil contains three times more Omega-3 than Omega-6 fatty acid, making it likely to shift the overall dietary balance of O-3 to O-6 in the right direction, toward 2:1.

How will Omega-3's help my horse?

We may not know how much to feed, but we do have some experimental evidence concerning the beneficial effects of Omega-3 fatty acids in horses. In the laboratory setting, researchers have looked at the effects of Omega-3 fatty acids on various equine cell types. Cells from joint linings, or cells from the abdominal cavity, for instance, can be grown and maintained in the lab. The cell cultures, as they are called, represent miniatures of the whole horse. Each cell type can be “fed” diets containing varying amounts of Omega-3 fatty acids. Then, cells can be subjected to an experimentally induced injury and the cell’s response to this injury can be measured. In fact, a beneficial effect of Omega-3 fatty acids on equine intestinal cells has been demonstrated in this experimental setting.  The presence of Omega-3 fatty acids in the cell membrane reduces the cell's inflammatory response when exposed to endotoxin.
There is much left to be learned concerning the role of Omega-3 fatty acids in our overall health plan, for our horses and our selves. However, early evidence weighs in strongly in favor of a beneficial effect with no apparent associated dangers. Educate yourself more about the world of Omega-3 fatty acids and make an informed decision concerning the inclusion of an increased amount of this essential fatty acid in your horse’s diet.

A bit of trivia: who remembers the heart-rending movie Lorenzo’s Oil? The story of a child with a degenerative nerve disorder. Guess what the magic oil was? Right again - Lorenzo’s Oil was an Omega-3 fatty acid.

Fri 2/19/10 - Colic - Clinical Case

Vet Tip of the Day: Fatal Colic
Key Words: Ischemia, Shock, Banamine, Heart Rate, Pain

My assistant Jessie and I had a hectic day - three emergencies, each in a different geographic area, on top of scheduled calls.  Our third emergency was the horse pictured here, who had an acute onset of abdominal pain.  Unfortunately, the outcome was not positive.  I am going to share this case with you so that perhaps by learning from this lovely old horse we can give some small value to his death.  The education he provides will be his last gift to us.

Chance was a 23 year old gelding.  His nutrition and preventive health care were excellent, and he was in very good condition.  He was used as a school horse for beginning riders and had no previous history of colic.  He was normal this morning, but suddenly around 2 PM began to look back at his abdomen  and paw at the ground.  Within 20 minutes these signs had progressed to the point that Chance would crumple to the ground and roll unless one person led him forward while a second person encouraged him to stay up with a longe whip.  We arrived 30 minutes after the onset of signs.

Chance's behavior is classic for acute, severe colic.  Mild signs of abdominal pain include looking back at the abdomen,  standing in a stretched out posture as if trying to urinate, loss of appetite, occasional pawing and spending unusual amounts of time lying down.  Moderate pain is characterized by persistent pawing, and frequent lying down and getting up.  As pain becomes severe, signs include falling suddenly to the ground and rolling violently.

When we arrived, it was impossible to perform a physical examination on Chance because as soon as he stood still he would attempt to throw himself down.  I administered a mild sedative intravenously as he was walking.  After 10 minutes this medication had had no effect so a second, more powerful sedative/analgesic combination was given.  Five minutes later Chance would stand without trying to roll, but was heavily sedated and not normally responsive to stimuli.  At this time his heart rate was moderately elevated (52 beats per minute/normal range 28-40), he had no gut sounds, and his gums were pale pink.  On rectal examination I could palpate an increased quantity of heavy ingesta in the large colon, which was displaced from its normal position.  A stomach tube was passed through the nose into Chance's stomach, and when a siphon was applied it was determined that there was no build up of fluid in the stomach.

Although I had not felt anything too alarming on rectal exam, at the time of our initial evaluation Chance has only been showing signs of discomfort for 30 minutes.  And in this time his degree of pain had escalated rapidly.  At this point my assessment was that Chance was suffering from an acute, severe colic.  Based on the severity of pain (which was only controlled temporarily by a very potent pain relieving injection) and the rapid progression of signs I was suspicious of a strangulating obstruction, or a twist in the bowel that had cut off blood supply to a section of the intestine.  These sudden strangulating lesions cause the most immediate, severe, and unrelenting pain of all forms of colic.  The strangulation can occur in either the large or small intestine.  Eventually the normal bowel becomes very distended in front of the strangulation, but this takes a few hours to develop, and during this time the rectal exam may be deceptively normal.  Unfortunately I couldn't accurately assess Chance's heart rate because I had to sedate him before I could listen to his heart and the sedative lowers heart rate significantly.  To answer one of yesterday's questions, of all the information we can gain from a colic, including sophisticated laboratory data, the two most sensitive indicators of the severity of the situation are heart rate and degree of pain.

At this point, Chance becomes a surgical candidate.  The only hope for horse's with strangulating lesions is rapid surgical intervention.  Once a significant portion of bowel looses blood supply,  endotoxic shock (see yesterday's blog) sets in very rapidly. Cardiovascular collapse and death can occur within 4-6 hours in the most severe cases. Because of Chance's age and economic constraints, surgery was not an option.  The only hope was that my assessment was incorrect.  I gave Chance a dose of flunixin meglumine (Banamine), a powerful anti-inflammatory medication which relieves gastrointestinal pain and combats the effects of endotoxemia, and we waited.

Within 30 minutes, when the sedative/pain killer was wearing off, Chance became very painful again.  With the recurrence of pain now Chance also exhibited an elevated heart rate (80 beats per minute), muscle tremors, a continued abscence of gut sounds, and deteriorating mucous membrane color.  His gums took on a grey/purple hue, which is hallmark indicator of cardiovascular compromise, or shock (see picture).

Euthanasia was performed 3 hours after the onset of Chance's colic.  Within that short time he had progressed from a healthy horse to one with multiple signs of severe endotoxic shock, the result of a strangulating intestinal lesion.

Long term (over 1 year) survival of horses with severe strangulating lesions after surgery ranges from 30 - 60%, depending on what study you read.  Estimated cost of surgery and hospitalization for these severe cases is 7,000 to over 10,000 dollars.  These are the worst case scenario colics, and they are by far the least common.  Colics requiring surgery that do not involve dead bowel, such as simple large colon displacements, have 85 - 90% long term survival rates, with cost estimate around 6,000 dollars.  And while Chance's story is a tragic one, remember that the vast majority of colics do not require surgery, and respond well to medical therapy.


The key to preventing colic is regular preventive health care, excellent quality diet, and a regular exercise program.  Unfortunately, colic can be an  indiscriminant killer, and as Chance showed us today, even horse's receiving the best of care can be stricken.  Chance was a wonderful horse, and will be sorely missed.  Hopefully by sharing his story he will help bring veterinary assistance to another horse with the chance for a better outcome.

Thurs 2/18/2010 - Colic

Vet Tip of the Day: What is Colic?
Key Words: gastrointestinal, endotoxin

I had a special visitor today.  Dr. James Moore, from the University of Georgia, was in Reno speaking at the AERC National Convention.  Dr. Moore was my major professor when I completed my doctoral research back in the early 90's.   He is a brilliant surgeon and researcher, and has spent much of his career investigating the factors that make colic such a deadly disease in horses.  As we ate pizza and swapped old stories this evening, I thought I would use his visit as inspiration for today's Vet Tip of the Day.

Colic is a very general term that refers to pain originating from the abdominal region.  In horses, colic has been associated with any disease of the gastrointestinal (GI) system that causes clinical signs of  GI pain.  The most common mechanisms of GI pain are distension and loss of blood supply.  Both of these occur when a section of bowel shifts into an abnormal position, or rotates on its own access.  The equine gastrointestinal system is composed of the esophagus, stomach, small intestine, cecum, large colon, small colon and rectum. The large colon is divided into 4 sections, which lie folded on each other, running along either side of the abdominal cavity. The intestinal tract of an adult horse, from stomach to rectum, is over150' in length!  Here's the most amazing part: the vast majority of the intestinal tract is free to move all over the abdomen,  only the cecum is attached at its base to the body wall.  Therefore, whenever the horse's complex intestinal motility pattern is upset, loss of coordination in progressive motility can lead to displacement of portions of the small intestine, or any of the colons.  When this occurs food material cannot move in an organized manner through the GI system.  When food transit is slowed, the bowel wall becomes distended.  This distension causes pain and further disrupts motility.  If the bowel rotates on itself (torsion or volvulus), a complete obstruction occurs, with loss of blood supply and severe distension, which can rapidly lead to death.

What kills horses with severe colic?  When a piece of the intestinal tract loses motility, becomes distended, or has reduced blood supply, several things happen.  First, the contents of the intestine stop moving. Second, the wall of the intestine begins to lose integrity as its oxygen supply is cut off due to lack of blood supply.  The intestinal contents are normally rich in bacteria which aid digestion.  However, when gut contents stop moving, the chemical environment in the gut contents is altered, resulting in bacterial death.  The dead bacteria decompose, and are absorbed across the now unhealthy gut wall into the blood stream.  One of the components of the bacterial cell wall is called endotoxin or lipopolysaccharide.  Endotoxin is a very powerful toxin to which horses are exquisitely sensitive.  Very small amounts of endotoxin in the equine blood stream cause severe inflammation, which leads to shock, cardiovascular collapse, and ultimately death.  So horses which die due to colic are actually poisoned by the contents of their own gastrointestinal tract.

Less serious colics, caused by temporary delay of transit through parts of the gut, such as large colon impactions, often respond to conservative treatment including anti-inflammatory analgesic medication such as flunixin meglumine (Banamine) combined with administration of fluid, and mineral oil via a naso-gastric tube.  When a complete obstruction occurs, however, surgical intervention is necessary to empty the affected bowel and return it to a normal position.  In the most severe cases, where segments of bowel have had severe compromise to their blood supply, surgical resection (removal of the affected bowel) may be necessary.

Can you list 5 signs of colic (gastrointestinal pain) in order or increasing severity?
Do you know what the 2 most reliable indicators are to determine whether a horse with colic requires surgery?

Answers in tomorrow's Tip of the Day.

2/16/10 All Vaccines are Not Equal

Vet Tip of the Day: How Vaccines Vary
Key Words: Antibody, Cell Mediated, Immune System, Virus, Bacteria, West Nile, DNA

We've looked at the factors that help you decide whether or not to vaccinate your horse against a certain disease.  Now let's examine how vaccines work.

All vaccines work by stimulating the immune system in some fashion.  We think most simply of a vaccine as something that stimulates the production of antibodies.  These antibodies then prevent invasion by either a bacterial or viral disease causing organism.  In fact, there are many different classes of antibodies in the equine immune system, and certain classes of antibody are more effective than others in fighting particular diseases.  For instance, IgA antibodies are very effective in fighting off infections that begin in the upper respiratory tract, such as Strangles.  Therefore, the intranasal Strangles vaccine was designed to stimulate a strong protective IgA reponse.  It does this by physically depositing live, chemically altered Strep Equi bacteria onto the back of the horse's pharynx when the vaccine is injected through the nasal passages.  This live bacteria mimics the actual Strangles organism and causes the horse to produce IgA antibodies in the upper airway which then combat the actual Strangles organism when your horse is exposed to it.  The protection is not absolute, and the antibody response to the vaccine is variable.  In addition, because the vaccine contains live, chemically altered organisms, there is a small risk of inducing a vaccine strain case of Strangles in response to the vaccine itself.

In addition to antibody production, the body has is a second, non-antibody dependent arm of the immune system.  It is called cell mediated immunity and is very important in the body's ability to fight viral diseases.  You may have read about the new technologies being used in some of the equine West Nile vaccines.  Instead of using an altered form of the disease causing organism to directly stimulate antibody production, these vaccine use a variety of technologies involving the actual genetic material (DNA) of the disease causing organism.  DNA based vaccines are more effective in stimulating all aspects of the immune system, thereby providing a stronger, more broad based protection against viral organisms, such as West Nile
Virus.  The Intervet DNA chimera vaccine is a fascinating cutting edge product with excellent safety and efficacy against the West Nile Virus.  To learn more about it, Google: Prevenile, Intervet, West Nile.

Finally, while the ideal vaccine will stimulate all arms of the immune system and prime it to rapidly eliminate an invading pathogen, it can only work if the organism causing disease can be consistently identified by the body.  For instance, the West Nile Virus is a very stable, unchanging organism that looks exactly the same to the horse in Massachusetts and the horse in California.  Influenza, on the other hand, is a viral organism that is constantly changing its appearance.  In exactly the same way our human flu produces new strains all the time, equine influenza undergoes small changes in its viral structure that allow it to evade the defenses of horses vaccinated with products produced using older strains of the virus.  So in the case of equine influenza, not only are we dealing with a viral disease, which challenges both the antibody and cell mediated arms of the horse's immune system, but we also are dealing with a disease that frequently alters its appearance, thereby posing one of the greatest challenges to researchers whose goal is to develop highly effective vaccines.

The subject of vaccines, the immune system, and disease prevention is extremely complex.  Luckily, those diseases which our horses may contract which are most deadly, are also the diseases against which it is possible to develop excellent, safe, and effective vaccines.  The prime examples of these are Tetanus and West Nile Virus.  Therefore, these are diseases against which ALL horses should be vaccinated.

The decision whether or not to vaccinate against influenza, rhinopneumonitis, and Strangles, should be made based on your individual horses risk of disease, and the impact that disease is likely to have on your horse's performance and well-being.  Refer to this past Saturday's blog to review the information that will help you make this decision, and then consult with your veterinarian as well.

Tuesday, 2/16/10 - Veterinary Tale Chapter 3 - A Man of Few Words

Sorry for no post yesterday - internet and telephone service to my valley were out for 48 hours. A transformer burned out and a new one had to be shipped in from who knows where before service could be restored.  That's the bad news - the good news is today's post is the latest chapter in Veterinary Tales.  I hope you enjoy it.   In case you missed the first two Veterinary Tales, you can find them in the blog archives from January 31st, and February 4th.  More on vaccinations and the immune system on tomorrow's Vet Tip of the Day.

Veterinary Tale Chapter 3 - A Man of Few Words
I excel in emergency situations. Throughout my life I’ve espoused the theory that there are basically two types of people. The ones who step forward toward crisis, and the ones who step back. Years ago a horse trailer pulled up in front of the large animal clinic at the University of Georgia where I was the resident on duty accepting emergencies. The driver jumped out of the truck, shouting over her shoulder as she rushed to the back of the trailer.

“It’s a really bad colic, and I think he just went down,” she said as she opened the door of the stock trailer before I could stop her.

I was standing about 6 feet away and what I saw was this woman standing there holding the door with her right hand, facing the open trailer. In the trailer, inches away from her face, was a horse in the process of throwing itself over backwards, its head and flying front feet coming directly at the woman. Without hesitation I jumped forward, shoving the gal to the side with my right arm while reaching up with my left arm and grabbing the horse’s lead rope. The rope was sailing through the air just ahead of the horse’s nose, following the trajectory caused when it snapped loose from the tie ring at the front of the trailer. As the horse’s owner went stumbling off to the right, I yanked the lead rope as hard as I could to the left, lunging in the same direction. The horse came tumbling out the back of the trailer, all 4 feet flying in the air, and hit the pavement left shoulder first. The owner was unhurt, the horse scrambled to his feet, and without pausing I headed into the clinic leading the horse to get emergency treatment started. James Bond eat your heart out.

This is the kind of thing I’m really good at – acting during a crisis. But the mass I’d discovered in my dog Sticky’s mouth was another matter all together. This was something I had time to think about, worry about, plan about – something that wasn’t going to be over and done within a short time, something that wasn’t going to go away. So I acted accordingly: I ignored it, just blocked it out, and when I did think about it, tried to convince myself that the mass was scar tissue that had formed at a tooth extraction site. I knew it had not been present 4 months ago, because Sticky had had her teeth cleaned by Dr. Mark Altman, my local small animal veterinary buddy, and a tooth had been extracted at that time. My denial continued for 5 days, and then I realized I had to face the music.

Here’s the thing. I’m a veterinarian, and while I don’t treat small animals, I am board certified by the American College of Veterinary Internal Medicine, and I’ve been practicing medicine for 22 years. I’ve seen my fair share of neoplasia (cancer) in large animal species, and I knew that the horrible thing growing in my dog’s mouth was not benign. On day 6, when Fern arrived at the office in preparation for the day’s calls, I asked for her help.

“Hey, Fern, I think we need to biopsy this thing in Sticky’s mouth,” I said, sounding all unconcerned.

“I was wondering what you were doing about it. I didn’t want to say anything, but it looks pretty bad, don’t you think?” Fern asked. Bless her heart; Fern is the soul of discretion. She’d come to work for 5 days without mentioning Sticky’s condition, even though I knew she’d been as upset by the discovery as I had. All nineteen year olds should have a fraction of her maturity and compassion.

Fern’s been one of my assistants since she was fifteen. She’s never wanted to be anything but a veterinarian, and I’ve been taking care of her horses since I met her family when Fern was eight. She announced she was ready to begin working for me when she was ten, and her mother and I struggled to dissuade her, pledging that if she was patient, she could start working at fifteen. Her intention never wavered, and for the past four years she’d been with me every summer and on weekends during the school year. We knew each other well, and worked in easy companionship most of the time. After all, I taught Fern early on my number one rule for employees: whatever goes wrong, it’s their fault. Once they get this down, the road smoothes right out.

I looked at Fern and nodded, “My small animal medicine is pretty rusty, but I do remember that oral tumors in dogs tend to be aggressive and malignant. But before we make assumptions, we need to submit a biopsy to be sure. They did pull a tooth right where the mass arises, so we cannot rule out that it is a mass of granulation tissue and not neoplastic.”

Fern gently held Sticky’s lip back while I took a scalpel blade and sliced off a small piece of the mass. My little PCD sat quietly, staring at me with absolute trust, without sedation or local anesthesia, as I performed the biopsy. She was just that kind of dog – she never made a big deal about anything. I knew the tumor would not have a nerve supply, so there would be no pain associated with the small biopsy, but most dogs would object to the restraint, especially around the mouth. But not Sticky, she didn’t move a muscle, just let Fern hold her lip back and wagged her tail slowly.

The biopsy safely stored in a submission jar filled with formalin, Sticky licked her bloody lips and jumped into the truck, ready to start the day. Fern and I looked at each other, hesitated a moment and then both burst out laughing.

“Sticky says, ‘come on you guys, let’s get going!’ “Fern said, her eyes shining with tears even as she smiled. “They just aren’t like us humans are they? No worries, just another day to live and enjoy. I don’t know, Dr. C, sometimes I’m just overwhelmed by how brave animals are.”

I climbed in and started the truck, motioning to Fern to join me. “I know, Fern, they teach us every day how to be better than ourselves, if we would just pay attention.” Sticky put her head in my lap, assuming her travel position. “Hand me a towel, will you – I’m going to have Sticky blood all over my pants for the rest of the day.”

“Here you go, Dr. C,” Fern said, handing me a blue surgical towel for my lap. “Maybe we should stop at the Frosty on the way to Roger & Barb’s and get her a soft cone – I bet that would feel good.”

“Good idea,” I agreed, “Today, whatever Sticky wants, Sticky gets.”

By the time we arrived at Roger Carlson’s cutting horse barn Sticky had lapped up her ice cream cone and was observing the world with her usual aura of ancient wisdom. Fern and I greeted Roger’s wife Barb and began preparations for the day’s procedure: castration of a two year old stallion.

Roger and Barb Carlson have been training cutting horses for over 30 years, almost as long as they’ve been married. They were high school sweet hearts, Barb the daughter of a local ranching family and Roger a Paiute Native American. They managed a training barn just over the California line, about 20 miles west of my office, in Sierra Valley. This was a picturesque area, located right at the transition elevation where desert and sage merged into aspen and pine stands peppering the steep Sierra Nevada foothills. I loved coming into this valley and had been excited about gaining the Carlson barn as an account. I inherited the work about a year previously from my friend Mark Altman when his small animal practice became so busy he no longer could provide adequate coverage to this area.

Mark was a real cowboy, a man’s man, a Deacon in the Church of the Latter Day Saints and one hell of an equine veterinarian. Guys like Roger Carlson and guys like Mark were born speaking the same language. When I first began working for the Carlson’s Roger’s wife Barb did all the talking, while Roger just watched me. I don’t think he said more than three consecutive words over the first year I came regularly to the barn. When he did finally begin talking to me, his dry humor and rare warm smile bowled me over. Roger had rich red skin, deep set dark eyes and a face etched by years riding outdoors in the high desert.

Today we were gelding one of his best young prospects. Roger brought the colt out into the center of the indoor arena and held him while I administered the first of two injections used for short term equine anesthesia. When my left hand closed around the colt’s neck to occlude the jugular vein I could feel his heart hammering through the skin against my thumb. I glanced at his eye to catch him glaring at me, his left ear cocked back and his expression saying loud and clear, “One wrong move and you are breakfast”. If only Sticky could talk to these young stallions and pass along some of her peaceful karma.

The first sedative successfully injected without incident, the colt began to relax, his head dropped, his lower lip drooped and he became wobbly. Ralph spoke to know one in particular,

“I guess this is the nicest colt I’ve ever raised.”

Silence.

“He certainly is a beauty, Roger,” I agreed. “Look at that hip, and the shoulder isn’t half bad either.” I added, thinking to myself – just lie down quietly and stay down until I’m done, you little monster.

Just as I pushed the plunger on the second syringe containing the ketamine that would cause the colt to drop, Ralph spoke again,

“You know when Dr. Mark used to do my colts he was done in no time at all.”

Silence.

“He’s quite a guy, that Dr. Mark” I mumbled, planning to wring his neck the next time I saw him.

“Why don’t you let me hold him while he goes down, Roger, “ I said, taking the lead rope into my left hand just as the youngster sank quietly to the ground with a deep groan. “How’s that for a smooth induction, oh Marvelous Mark?” I mentally complimented myself.

Fern moved in to tie up one hind leg, cover the colt’s eyes with a towel and scrub the scrotum while I gloved up and opened the emasculator and scalpel blade. I removed the first testicle and looked up to see where Sticky was. Don’t be too disgusted, but Sticky always knows when we are gelding a colt, and she is always sitting intently by the horse’s flank, waiting for her special treats. Soft ice cream cones are great, but they don’t compare to this. I spot her watchful eye and prepare to toss her the prize.

“Hold on there, doc!” Roger’s voice is actually raised a few notches, a new experience for me.

“I’m sorry Roger, I usually give these things to Sticky as a treat, but if you don’t want me too, that’s fine.”

“ I don’t care what happens to the damn things, but you move that dog up here by the colt’s head and throw ‘em forward to her – don’t you know that if you toss them over his head he’ll never look back?”

“Um, OK, no problem, come here Sticky,” I called, cursing Mark for not giving me a head’s up on this old western horseman’s tradition I’d certainly never heard before.

Sticky finished her hors d’oeuvres with relish, the colt recovered uneventfully from anesthesia, and Fern cleaned up and packed the truck while I stood with the now young gelding and Roger. More silence, but I figured I was better off saying nothing than trying to make conversation and sounding like an idiot. As I saw Fern finishing, I checked the colt’s incisions for bleeding and turned to Roger.

“Everything looks good Roger; he can go back to his stall now.”

Roger led the colt from the arena without a word and put him in his stall. I wrote up the bill and went out front to the travel trailer that served as an office to give it to Barb. We chatted as she wrote out the check and said thanks and good bye. I went out to the truck to leave. As I was pulling away from the barn Roger walked out. He spoke just loudly enough for me to hear.

“I guess Dr. Mark was right when he said you were OK.”

After a year, I was still thankful for small mercies.

Sat. Feb 13, 2010: Vaccination Protocols

Vet tip of the Day: Selecting Appropriate Vaccines
Key Words: West Nile, Tetanus, Influenza, Rhinopeumonitis, Encephalitis, Rabies, Strep Equi

Diseases are like brush fires.  Some smolder for awhile and are easily extinguished, others flare up and have devastating effects.  Choosing vaccinations for your horse has a lot to do with the nature of each disease we are attempting to prevent.  Toward this goal, here are the answers to yesterday's questions.  

Note: The answers about likelihood of exposure are only pertinent to horses in Northern Nevada.  Consult your veterinarian for other geographic regions.

1.     How likely is it that this horse will be exposed to Disease A?

• West Nile:  Likely
• Tetanus: Unlikely
• Influenza: Very Likely
• Rhinopnuemonitis: Very Likely
• Encephalitis: Very Unlikely
• Rabies: Very Unlikely
• Strangles: Likely

2.     Is Disease A a deadly disease, such as Tetanus? (this assesses risk to this horse)

• West Nile: Yes, 40% mortality
• Tetanus: Yes, 80+& mortality
• Influenza: No
• Rhinopneumonitis: No, but high risk abortion in pregnant mares
• Encephalitis: Yes, 85+% mortality
• Rabies: Yes, uniformly fatal
• Stangles: No, 10% complication rate, with fatality uncommon

3.     Is Disease A highly contagious, such as Influenza? (this assesses risk to neighboring horses)

• West Nile: No, is not transmitted horse to horse. Disease is transmitted from infected bird, to mosquito, to horse
• Tetanus: No, is not transmitted horse to horse. Tetanus bacteria lives in soil and usually gains access to horse through deep puncture wound that creates an oxygen free environment where bacteria can proliferate.
• Influenza: Yes! Transmitted directly horse to horse by aerosole (cough) and direct contact.
• Rhinopneumonitis: Yes! As for influenza.
• Encephalitis: Moderately, disease is not transmitted directly horse to horse, but is carried from horse to horse by a "vector", which for this disease is the mosquito.
• Rabies: No, is not transmitted horse to horse
• Stangles: Yes! Primarily transmitted by direct contact horse to horse AND by contact with contaminated "fomites": halters, lead ropes, hands, feet, water buckets, etc.

4.     Is the vaccine used to protect against Disease A highly effective?

• West Nile: Yes, Intervet DNA vaccine extremely safe and effective with minimal side effects
• Tetanus: Yes, killed vaccine 95+% safe and effective
• Influenza: Vaccines against influenza currently available are moderately effective, with relatively short lasting immunity provided. 
• Rhinopneumonitis/Equine Herpes type I and IV: There are 2 main Equine herpes viruses that cause upper respiratory disease in horses. They are also responsible for abortion and a neurologic disease which can be fatal.  Currently available vaccines are very effective in preventing abortion, moderately effective in preventing upper respiratory disease, and of questionable efficacy against the neurologic form of herpes virus.  More discussion on this in a later vet tip post.
• Encephalitis: Yes, killed vaccine very safe and effective
• Rabies: Yes, killed vaccine very safe and effective
• Stangles: The intranasal vaccine against Strep equi bacteria is moderately effective, and of all the vaccines discussed here has the highest complication rate.  We will discuss Strangles in more depth in a later vet tip post.

5.     What is the cost vs. effectiveness vs. safety value of the vaccine for Disease A?

• West Nile: Excellent
• Tetanus: Excellent
• Influenza: Moderate
• Rhinopneumonitis: Moderate, except very good against Equine Herpes induced abortion
• Encephalitis: Very Good
• Rabies: Excellent
• Stangles: Fair

 With this information, consider the following:
Your horse's age: the young and the old are always more susceptible to disease
Your horse's lifestyle: travel, stress of competition, and exposure to other horses always increase the risk of disease


Now decide which vaccines you think are appropriate for your horse.


More on Monday.  Have a wonderful weekend.


Chrysann