Wednesday, March 31, 2010

3/31/2010 - Vaccination Reactions II

Vet tip of the Day: "Allergic" reactions to vaccination
Key Words: Urticaria, hives, hypersensitivity, anaphylaxis

Most importantly, remember that severe vaccination reactions are rare.  That's why it was difficult to find a decent picture - sorry for the quality of this one.  True hypersensitivity or anaphylactic reactions to vaccines, while rare, do occur and require immediate attention.  The physiology behind these reactions is very complex and poorly understood in horses. 

Anaphylaxis refers to a shock reaction by the body to some foreign substance.  In the case of vaccines, anaphylaxis can occur the first time a vaccine is administered.  An anaphylactic response can vary from mild hives that appear hours after a vaccine is given, to acute life-threatening cardiovascular collapse which can occur within minutes of vaccination.  Epinephrine is the preferrred initial treatment for severe anaphylasis.  It works by counteracting the immediately life-threatening components of the body's severe inflammatory response.  It is usually administered by intramuscular injection.  In the most severe cases, it may be given intravenously.  Administration may be repeated every 15-20  minutes if necessary.

Hypersensitivity and immune-mediated reactions to vaccines also occur and may have similar clinical signs to anaphylaxis.  When these reactions occur, they usually are less dramatic than acute, severe anaphylaxis.  Signs may include swelling of the muzzle, face and throat region, which can lead to respiratory distress, or may manifest as hives, or urticaria.  Depending on the severity and progression of the clinical signs, treatment may include steroidal or non-steroidal (phenylbutazone, flunixin/banamine) anti-inflammtory agents, and/or anti-histamines.

When a horse experiences an adverse reaction to vaccination, the question always arises, should the horse be vaccinated again?  If the reaction is a very sore neck, sometimes changing vaccine brands, and thus the adjuvant used, will help.  If the horse has a true anaphylactic or severe hypersensitivity response to vaccination, the problem is more complex and the decision to repeat vaccination should be made based on the severity of the reaction and consideration of the true risk of the disease against which vaccination is directed.

Finally, for those of you who adminster your own vaccines, be aware that storage conditions are extremely important for vaccines.  Vaccines that are not stored at proper temperatures are significantly more likely to cause adverse reactions than those kept cool at all times. Also, correct administration of intramuscular shots, both with respect to location of the injection and injection technique, play important roles in the safety of injections.  If you choose to vaccinate your own horses, be sure to obtain instruction from a licensed veterinarian or licensed veterinary technician concerning the correct administration of intramuscular injections.  And be sure that your vaccines have been properly stored before you purchase them, check the expiration date, and keep them carefully stored until they are administered.  Better yet, take advantage of the chance to visit with your vet and have a spring wellness check up and make an appointment with your veterinarian to give your spring vaccinations!

It's cold and snowy on March 31 in Northern Nevada.  What's it like where you are?  Looking forward to spring and good riding weather.

Tuesday, March 30, 2010

03/30/2004 - Vaccination Reactions

Vet tip of the Day: When Vaccinations go Wrong
Key Words: Vaccine, adjuvant, immune system, clostridium

Vaccination season is drawing to a close, but I thought I would return to this subject one more time to talk about vaccination reactions.  Of course I would like to tell you that I have never had a horse demonstrate an adverse response to vaccination, but that would be a big fat lie.  Fortunately, I can tell you that I have never had a horse suffer a serious vaccination reaction that didn't respond promptly to appropriate treatment. There are several types of adverse reactions to vaccination, and it is important that you understand how they differ, both in onset of signs, and seriousness of consequences.

By far the most common adverse reaction to vaccination is the simple sore neck.  I vaccinate hundreds (literally) of horses every spring, and this year to date I know of only two horses which developed significant signs of neck pain following vaccination.  Typically the day after vaccination the owner notices that these horses are unwilling to move their heads, show signs of pain if one of the vaccination sites is touched, and exhibit swelling at the vaccination site.  Occasionally the discomfort will be so severe that horses will not lower their heads to eat or drink, or will pull back if pressure is applied to a lead rope when they are haltered.  Years ago I had a client call to tell me that her horse was having a seizure when in fact the horse's neck was so painful that when the owner tried to lead her forward she reared over backwards in response to the pain.  The vast majority of inflammatory reactions after vaccination resolve within 48 - 72 hours with palliative therapy including warm compresses and phenylbutazone.

This "sore neck" reaction to vaccination is NOT an allergic response to the vaccine.  It is an exagerrated inflammatory response to the ingredient in the vaccine that stimulates the horse's immune system.  This ingredient is called an adjuvant, and is very important in causing vaccines to elicit a strong antibody response by your horse's immune system.  Without this response, the vaccine will not be effective in preventing the disease against which it is directed.  Drug companies spend a lot of time and money developing different adjuvants.  Their goal is to find an adjuvant that is a potent stimulator of the immune system but does not cause severe local soreness.  Over the years I have used many brands of vaccines, and have come to be a staunch supporter of Intervet vaccines.  I believe that their adjuvant causes very few advers reactions, and I have been impressed with the company's dedication to client education and with their committment to research and development of new products to protect horses' health, such as Prevenile, their DNA based West Nile vaccine.

When a horse develops a sore neck after vaccination, it is important to notice whether or not the horse is systemically ill.  Specifically, will the horse refuse food and water even when it is placed so that the horse can reach it without lowering its head? Is the horse's temperature over 102.5 degrees?  Is the swelling at the vaccination site severe and increasing over time?  When the swelling is palpated, is there a crackling feeling underneath the skin?  Does the horse appear markedly depressed?  If the answer to any of these questions is yes, then the horse should be examined by a veterinarian.  As stated earlier, the vast majority of inflammatory reactions after vaccination are not serious and resolve within 48 - 72 hours with palliative therapy including warm compresses and  phenylbutazone.  However, in rare cases, it is possible for a bacteria called Clostridium to grow deep in muscle tissue at a vaccination site. If this unlikely event does occur, it can be life-threatening.
Clostridial bacteria exist normally in the environment in a spore form which can only grow in the abscence of oxygen.  Even when a clean needle and syringe are used and the vaccination is administered correctly, it is possible for Clostridial spore sitting on the skin to be carried deep into the muscle tissue by the needle during vaccination.  When this happens it is a random, extremely unlucky event, and does not mean that the vaccine was administered improperly.  Clostridial infections can be life threatening and require prompt and aggressive treatment. The Clostridium bacteria grow rapidly in the abscence of oxygen and produce several toxins which invade the horse's blood stream and cause severe systemic illness which can be fatal. Therefore, it is always a good idea to contact your veterinarian if your horse has an adverse reaction to a vaccine and discuss your horse's specific clinical signs so that you and your vet can decide if your horse needs to be examined.  If you take your horse's temperature and do a physical examination (see blog on this!) and carefully observe your horse's behavior before you call your vet you will be best able to provide important information in making that decision.

In tomorrow's Vet tip of the Day I will discuss Allergic reactions to vaccination and the importance of careful storage and administration of  vaccines, for those of you who vaccinate your own horses.

Until then,

I believe that education is the key to evolution.
I believe that animals are the key to compassion.
I believe the learning never stops.

Thursday, March 25, 2010

4/25/2010 - How Diseases Spread

Vet tip of the Day: Infectious Disease Control/Equine Herpes Virus
Key Words: EHV-1, EHV-4, neurologic disease, upper respiratory virus

This story is loosely based on actual events that took place in 2007-2008, spanning from Europe to New York, then south to Florida, and west to California. The goal is not to alarm you, or make you an expert on Equine Herpes Virus type-1 (EHV-1), but to provide guidelines on how to protect your horse from infectious diseases. Developing an increased awareness of how diseases can change and spread rapidly will help you to improve the care and well-being of your equine companions. Our story:

An eight-year-old horse that received excellent care in Germany was purchased by a person in the United States. He was vaccinated and dewormed regularly, and received appropriate booster vaccinations three weeks before his transport by air to New York. Upon arrival he was quarantined according to federal regulations. Once released from quarantine, he was transported by truck to Kentucky with one group of horses, and then shipped on to Florida with a different group. When he arrived in Florida 10 days after leaving New York, a handler noticed he seemed depressed and unsteady on his feet. The owner was alerted and a veterinarian was contacted to evaluate the horse.

How are diseases spread?

How and why did the horse become ill? We know the horse received excellent management with booster vaccinations for appropriate infectious diseases three weeks before shipping overseas. The immune system takes at least 10 days to fully respond to a booster vaccine, so ideally they should be given two to four weeks before shipping or change of environment.

It would have been advisable to rest the horse in New York following the flight and quarantine before transporting to Florida, and to avoid the mixing of different groups of horses during travel. Research has shown that horses subjected to long-distance transport are at significantly greater risk of infection with respiratory tract pathogens compared to similar non-transported horses.

The veterinarian exam revealed the horse had a 102.5 ºF fever and neurologic signs manifested as weakness and incoordination of the hind limbs, and a rectal palpation determined the horse’s bladder was distended with urine. The owner was told that a neurologic form of EHV-1 was suspected and immediate isolation was recommended until a diagnosis could be confirmed because a new, highly contagious form of this disease had been reported in other U.S. locations.

What is EHV-1?

Equine Herpes Virus Type-1 (EHV-1) is an old and common disease in horses, most commonly causing an upper respiratory infection in young horses, but also responsible for late term abortion and a sporadic neurologic disease. Luckily, this veterinarian was aware of outbreaks in recent years of neurologic disease affecting multiple horses caused by EHV-1; most notably one in a university hospital in which 46 of 135 in-house patients developed neurologic signs, leading to death in 12 of those horses.

It was discovered that the EHV-1 virus had undergone a mutation in which a single element in the viral DNA code was altered. The resulting strain was more virulent, contagious, and specifically attacked the horse’s neurologic system. Therefore it was named neuropathogenic EHV-1. With the emergence of this mutated virus, the clinical form of EHV-1 associated with neurologic signs was becoming more common and more. This exemplifies how a tiny change in the genetic code of a virus can have far-reaching and dangerous effects.

In Florida, a nasal swab confirmed the diagnosis of neuropathogenic EHV-1. This first horse was treated and recovered. Meanwhile, another horse off-loaded from the original truck in Kentucky was arriving in Southern California, and a third horse that had accompanied our horse by van to Florida was taken to a farm, and later to a horse show facility nearby. The horse in California walked off the truck with clinical signs similar to the first index horse in Florida, and was quickly assessed and isolated. The third horse never showed signs of illness, but 10 days after arriving at the show grounds, other horses began to develop signs of neurologic disease. Subsequently, the presence of the neuropathogenic form of EHV-1 was confirmed, leading to an extended quarantine of the show grounds. No other cases were detected in Southern California after isolation of the index case, but within the month, a horse was confirmed infected at Golden Gate Race Track. There have been isolated confirmations of neuropathogenic EHV-1 in California horses since, but no multiple case outbreaks have occurred.

Disease control and prevention among horses

How could the spread to the show grounds have been prevented? First, when a contagious disease is suspected, the affected horse should be isolated and other in-contact horses should be quarantined and monitored for signs of disease for an appropriate duration. This would have meant immediately contacting the shipping company and identifying all the horses transported with the original horse in Florida with clinical signs. In the case of EHV-1, the incubation period is typically two to eight days, but can be as short as 24 hours – showing how quickly this becomes a logistical nightmare, and how critical every hour becomes. The horse in Southern California was traced back to the horse in Florida, which was connected to the air transport from Europe – tedious tracking, but important to successfully contain infectious diseases.

Second, rapid diagnosis is critical. Our astute veterinarian in Florida submitted the nasal swab for a state-of-the-art diagnostic technique called PCR (polymerase chain reaction). This test amplifies specific DNA segments in the sample and allows the detection and identification of minute amounts of viral DNA, confirming that this particular viral strain was present in the affected horse.

Finally, how can you as a horse owner reduce the spread of infectious disease? Your first goal is to protect your horse against infection by consulting with your veterinarian to ensure that your horse is appropriately vaccinated. Learn all you can about the safe and comfortable transporting of horses. With these good management techniques, you’re supporting your horse’s immune system and reducing the odds that he will succumb to an infectious disease, even in the face of exposure. Use common sense during competitive events: do not share water, tack, or grooming equipment. EHV-1 is spread primarily by horse to horse contact and by virus transported on equipment and the clothing, hands, and shoes of people moving between horses. If your horse is exposed to fewer viral particles and has a healthy immune system, illness is less likely.

When your horse is at high risk of contracting an infectious disease such as EHV-1, even the best management may not protect him completely. If he does become infected with a contagious disease, your goal is to protect him and other horses with early detection. Fever is the earliest sign of most viral diseases. The single most important thing you can do is to monitor your horse’s rectal temperature twice daily at shows, before and after shipping, and when new horses come on the property. Whenever your horse’s rectal temperature is 102.2 ºF or higher, contact your veterinarian and follow their recommendations.

Don’t abandon your equestrian activities for fear of infectious disease. Just stay informed and use common sense to guide you. Your veterinarian is your best resource for advice on the prevention and control of infectious diseases. Don’t hesitate to ask questions and continue your life-long education as a responsible and caring horse owner.

More Information on EHV-1

This story first appeared in Petfolio magazine, published in Reno, Nevada.

I believe that education is the key to evolution.
I believe that animals are the key to compassion.
I believe the learning never stops.

Wednesday, March 24, 2010

3/24/2010 Normal Physical Exam

Vet tip of the Day: The Normal Horse
Key Words: Heart rate, Respiratory Rate, Temp, Gut sounds, mucous membranes

I performed a prepurchase examination for a new horse owner this week.  She had lots of good questions about her horse husbandry.  One thing she was interested in was learning normal physical examination findings, so I thought I would go over some basics which all horse owners should know.  In case of emergency, or if your horse simply isn't feeling well, being able to do a basic asssessment of your horse's physical parameters can be extremely useful.  Not only does it give you factual information to convey to your veterinarian over the telephone, it also gives YOU factual information to allow you to determine just how serious your horse's condition may be.

First you need some equipment.  Go to any nursing supply store and by a CHEAP stethoscope.  The most basic model is perfectly adequate for obtaining a heart rate.  To listen to your horse's heart, place the flat side of the stethoscope bell against your horse's chest just behind the point of the elbow, then push the stethoscope head forward as far as you can so it slides in underneath the triceps muscle.  Close your eyes and listen carefully.  The heart beat has two parts - lubdub...lubdub...lubdub.  Practice until you can hear it clearly.

Next go to the drug store and buy a regular old human digital thermometer - I prefer the non-flexible ones. 

Finally, purchase a small, LED flashlight and cheap watch with a second hand and store them, along with your stethoscope, thermometer, and a small notebook with a pen attached to it by a piece of string in a handy place in your feed or tack room or horse trailer.

Here are some normal numbers - write them down in your notebook so in an emergency you don't have to remember them. 

Heart rate: 28- 44 beats per minute.  I usually count the heart rate for 15 seconds and multiply by 4 to get beats/minute. Heart rates over 52 beats per minute are definitely abnormal.  Heart rates over 80 beats per minute indicate severe cardiovascular distress.  Remember, exercise, nervousness or excitement may cause your horse's heart rate to be elevated without any serious illness present.
Respiratory rate: 8-16 breaths per minute.  The best way to count the respiratory rate is to stand back from the horse and watch the abdomen just behind the ribcage.  In a normal horse you will see a gentle rise of the abdomen with each breath.  Taking an accurate resting respiratory rate in a normal horse can be difficult, because as soon as you approach them they begin sniffing and snuffling, thereby disrupting the quiet, resting breathing rate.  If your horse has a wide flare to the nostrils with each breath and an deep movement of the abdomen with each breath coinciding with the nostril flare, this is a sign of labored breathing and is abnormal.
Gut Sounds: Using your stethoscope, listen to your horse's abdomen in 4 places - up high and down low on each side, behind the ribs and in front of the hip.  Gut sounds vary tremendously even in a normal horse, but if you listen for 30 seconds in each location, you should hear at least one good, rumbling gurgle in each of your 4 listening zones.
Mucous membranes: Standing beside your horse's head (not in front), lift your horse's lip just enough to see the gums above the incisors on one side.  Normal gums are quite pale pink, with a glistening surface.  If you press against the gums firmly with your finger for a few seconds, when you remove your finger the gums should be white, and should refill with the normal pale pink color in less than 2 seconds.  This is called the capillary refill time (crt).
Attitude:  When I record my physical examination findings, I will often note: BAR.  This is code for Bright, Alert, and Responsive.  When you do your physical exam, note your horse's attitude, expression, head position and body position. Look in the stall or pen and check for fresh manure, or signs of distress such as areas where your horse may have been pawing or rolling.  Check to see if the water trough is full and if the last feeding has been consumed.
Gait/Posture:  Finally, move your horse around a bit and check for lameness and willingness to move forward.

Now you are prepared to do a comprehensive physical examination on your horse.  The best way to recognize abnormal is to know normal, so practice performing physical examinations on your horse frequently so that when you are concerned that something isn't right, you will be confident in your assessment.


Sunday, March 21, 2010

3/28/2010: More on Vaccines

Vet Tip of the Day: Vaccinating old horses
Key Words:  geriatric, immune system
A client called this week asking about recommendations for vaccinating old horses and mules.  She was wondering if her old retirees still needed all the same vaccinations that her younger, active, travelling horses receive.  I thought I would answer her question with a blog post so you could all share this information.  Please first review the two previous blog entries on vaccinations posted earlier this spring.  To find them you can type  - vaccination - into the search bar at the top of the blog home page  OR click on - vaccination - in the label group in the top left margin on the blog home page.
Let me reiterate that the decision to vaccinate any horse should be made based on an assessment of risk of disease to that horse and to the other horses in that horse's population group.  With this in mind, let's look at the geriatric horse in particular.  Your old horse's immune system is likely to look pretty much like your old horse does: it ages along with the rest of his body, inside and out.  When deciding whether or not to vaccinate the old fellow, consider the following: his body condition, his mobility, and his population dynamics.  Then think about each disease against with we vaccinate in the terms discussed in the previous blog posts.
Let's consider a contagious disease (spread from horse to horse) such as the upper respiratory viruses - Flu/Rhino.  Keep in mind that immunity to these viruses in general is relatively short lived in all horses.  Should your old horse contract influenza it may take longer for him to recover, and, under certain circumstances he may be at greater risk of developing complications such as pneumonia.  What are these circumstances? Living as part of a  large group of horses in a small area is probably the most threatening to an old horse.  If your horse has chronic lameness issues that cause him to spend significant periods of time lying down, again he is at increased risk of  secondary pneumonia.  If your horse is in poor body condition or has poor dentition, he is at greater risk of having difficulty shaking the flu.  If, however, your retired horse or horses are in good health, living in a large field without much contact with other horses, then their liklihood of contracting a contagious disease such as influenza or rhinopneumonitis is decreased, and should they "catch a cold", it is likely it will run its course without complication.  Under these conditions, you may choose not to vaccinate against Influenza or Rhinopneumonitis.

Concerning Strangles (Strep Equi)  the situation is somewhat different.  While Strangles is a highly contagious disease spread from horse to horse, it also is a disease which causes a powerful and long-lasting immune response in those exposed to the disease.  Because Strangles is common in our area of northern Nevada, most older horses have good naturally aquired immunity.  Therefore, Strangles is uncommon in older horses.  Unfortunately,  old, debilitated horses which do contract Strangles are definitely at higher risk of potentially life threatening complications.  I recommend Stranges vaccination in old horses only if they are living in a high risk environment such as a concentrated boarding barn with high turnover of population or on a breeding farm with high number of foals in close contact.

All older horses should be vaccinated against West Nile Virus.  The disease is sporadic and unrelated to population dynamics.  To contract West Nile Virus, an infected bird flies over your horse's location, a mosquito bites the bird and within a short period of time that same mosquite flies down and bites your old horse.  Old horses definitely are at greater risk of death should they contract West Nile Virus.

Tetanus?  Sleeping Sickness?  The killed vaccines used against these diseases are very effective and afford long lasting immunity.  If you have owned your old friend for years and know for sure that annual tetanus/encephalitis vaccine has been administered, I would be comfortable decreasing the frequency of that vaccination to every 3 years rather than annually.  If you select this route, BE SURE that your horse receives a tetanus toxoid (not tetanus antitoxin) should he develop a foot abscess or deep puncture wound.

Hopefully this information will be of use to you when deciding which vaccines are appropriate for your old horses.

Forward this blog entry to all your friends with old horses.  Become a fan of HighDesertEquine on Facebook - and sign up as a follower of this blog! Your participation is vital to the success of these internet information efforts - every new fan and member moves us up on the search engine list and means that these educational articles will reach more people trying to become better informed caretakers to their horses. 

Wednesday, March 17, 2010

3/17/2010: New Foals Arriving!

Vet Tip of the Day: Keeping your Newborn Foal Healthy
Key Words: neonate, umbilicus, colostrum, IgG, plasma, passive transfer
It is spring, and for me that means lots of work related to reproduction.  Ironically, it seems like I'm either stopping reproduction (gelding colts) or enhancing reproduction (breeding mares) every day.  But the most fun for me is welcoming new equine lives into the world.

I strongly recommend that you look at the Mare & Foal page on our website (link at top of blog page).  There is an excellent revue of prepartions needed before your foal is born.  What I'd like to do  here is speak in a bit more depth about the equine neonate and its particular susceptibility to infection in the first few hours & days after birth.

Foals are born with naive immune systems.  This means that when they hit the ground, they have NO circulating antibodies.  Their bodies begin responding to challenges and producing antibodies immediately, but the development of a fully competent immune system takes time, and in the first hours and days of life an invading organism can quickly gain the upper hand.  Antibodies are the body's infantry in the fight against infection.  Without antibodies, we succumb to disease causing organisms and we die.  End of story.  No exceptions.  Foals obtain critical antibodies in colostrum, the first milk produced by their dams.  The absorption of colostral antibodies by the foal from the mare's milk is called passive transfer.  Two basic things have to happen for successful passive transfer to occur. 
1) The mare must be healthy and produce sufficient quantitiy and quality of colostrum.  Older mares, malnourished mares, and maiden mares all are at risk of producing poor quality colostrum.  The ideal high quality colostrum producer is a mare between 6-10 years of age, giving birth to her second foal, on an excellent diet, vaccinated 4-6 weeks before foaling to increase antibody production against common diseases
2) The foal must drink and abosrb the colostrum.  The antibodies in colostrum are very large molecules.  The foal is born with specialized cells in its small intestine which can absorb these antibody molecules.  These cells only function for 12-24 hours after the foal is born.  Therefore, the foal MUST consume adequate colostrum during the first 12 - 18 hours of life.  After this small window of opportunity closes, it doesn't matter how much colostrum the foal drinks, it will not be absorbed.

Sounds simple, but often it is not.  Maiden mares may be nervous about allowing foals to drink and they may have limited quantities of colostrum.  Foals born in severe cold may be slow to rise and may have delayed intestinal motility decreasing colostral absorption.  Foals born prematurely or with musculoskeletal abnormalities may also be slow to rise and nurse. All foals should be up and nursing within 2 hours.  If a foal is not nursing vigorously within 2 hours please contact your veterinarian immediately.  Foals are very delicate creatures and succumb rapidly to infections in the first few days of life, often with fatal consequences.

Let's assume your foal gets up and nurses appropriately and your mare has adequate colostrum.  Great! However, there are still risk factors which may predispose your foal to early infection.  The envivonment in which the foal is delivered should be clean and dry.  The foals' umbilicus is a little highway into the foal's blood stream for disease causing bacteria in the foal's environment.  The umbilicus should be dipped in 2% idodine or dilute chlorhexidine 3-4x in the first 24 hours of life to help minimize the chances of ascending infection through the umbilicus.

Even with successful passive transfer (absorption of colostral antibodies) if a foal is exposed to a large number of pathogenic (disease causing) bacteria in the first hours of life, they are at risk of developing a bactrial infection of the blood stream.  This is called neonatal septicemia, and is often fatal in foals.  The key to succeful treatment of neonatal septicemia is early detection and aggressive intervention. 

I cannot emphasize enough the importance of contacting your veterinarian IMMEDIATELY if any of the following is true:

Your foal is 2 hours old and is not up and nursing
Your foal shows signs of decreasing energy/lethary/depression at any time in the first week of life.
Your foal develops diarrhea.
Your foal shows signs of abdominal pain - foals with colic often roll up on their backs and lie like a dog with all 4 legs in the air, or they may roll and thrash like an adult horse with colic.
You notice that the mare's bag is full or is dripping milk and the foal is not nursing vigorously at least twice every hour.
You notice that your foal is constantly trying to nurse and does not lie down and sleep between nursing - this is hallmark sign that the mare does not have sufficient milk productio and the foal is hungry.

Please remember that foals are particularly delicate creatures - early intervention can often save them, but a delay of a few hours can mean the difference between life and death for a sick neonatal foal.

All foals should be examined by a veterinarian at 18-24 hours of age at which time a physical  examination and blood test to check for adequate colostral absorption is performed.

Don't be complacent about your newborn.  If you have any questions or concerns, call your veterinarian immediately - these precious lives are in our safekeeping, take the best care of them you possibly can.  Please read the mare/foal care information on our website.


Monday, March 15, 2010

3/14/2010 - Spring is Coming

Vet tip of the Day: Thinking about spring and your horse's feet
Wow, the sun came out and I wasn't wearing 4 layers today.  It was such a wonderful feeling not to feel that chill in my bones.  With spring come those freeze thaw cycles when the ground is frozen in sharp, uneven layers at night only to thaw and turn into a slippery slimey mess during the day.  For many of us our horse's turn out areas are a mess this time of year. Particularly around feeders and water troughs, footing tends to be wet during the day and frozen at night.

Because our soil is usually so dry, our horse's feet are adapted to a dry environment.  After a long wet winter as we've had this year, the manure and urine soaked into high traffic areas where horses stand a lot, combined with the freeze/thaw cycles, create a bad formula for our horses feet.  This time of year I see LOTS of severe subsolar abscesses, particularly in older horses.  Here's what happens: first, the horse living in a dry desert climate typically has a hard, somewhat brittle sole.  Over the winter, if the horse's environment is not kept clean and dry, then wet, manure packed material accumulates in the sole and along the sulci of the frog.  This material is full of bacteria.  It softens the frog which becomes recessed, thereby leaving the sole in direct contact with the ground.  The horse steps on a frozen jagged mud edge, creating a tiny defect in the sole which provides access for bacteria to infiltrate into the foot.  The bacteria become trapped beneath the hard sole where there is no air supply.  They begin to proliferate, spreading between the natural layers of the sole.  In response to the bacterial proliferation, the body mounts an inflammatory response, resulting in the accumulation of pus.  Eventually this pus produces enough pressure within the hoof that the horse becomes acutely severely lame.

At this point the sole must be removed to allow drainage of the dead tissue and expose the area to air.  In the worst case scenario, it is possible for the bacteria to migrate far enough into the hoof to cause infection of the coffin bone, although this is NOT the typical outcome.  Once the dead sole is removed exposing the area where the bacteria have infiltrated, with appropriate treatment the sole will harden and repair itself without long term complications.  However, subsolar abscesses are extremely painful, and can be frustrating and time consuming to treat, especially in horses living in outdoor settings.

Prevention is worth a pound of cure, and subsolar abscesses that occur secondary to poor footing conditions during the winter are preventable. First, be sure your horse has regular farrier care.  Second, PICK YOUR HORSES FEET OUT THOROUGHLY EVERY DAY!  Third, try to keep the area around feeders and water troughs as dry as possible, and remove manure from these areas.  If this is not possible,  using a tooth brush rub strong iodine (7%) into your horse's soles and frog several times a week after you clean out the feet.  Following these three simple rules may save you and your horse a major aggravation.  Again, this problem is especially prevalent in older, less active horses, so don't forget about the feet of the retirees, even though they are no longer performance horses.

Friday, March 12, 2010

3/12/2010 - Anatomy and OCD

Vet tip of the Day: Significance of OCD based on anatomic location
Key Words: Osteochondrosis, lameness, joint, anatomy

This cute foal picture is here to remind you that OCD is a developmental orthopedice disease.  In other words, it develops as a foal grows, although it may not manifest itself clinically until later in life when joints are subjected to the rigors of training and controlled exercise.  When we consider the prognosis of various OCD lesions, then, there is one common sense rule to keep in mind: foals that develop significant lameness early in life due to OCD are likely to have more severe lesions than animals that do not show any clinical signs until they are older and in training. 

Regardless of the anatomic location, the larger and deeper the OCD lesion is in a given animal, the less likely it is that surgical treatment will be successful.  In general, the degree of lameness and age at onset correlate with the severity of the lesion.  Consider our mare Classy, a five year old just completing 60 days of fairly rigorous training and only demonstrating a grade 1 lameness and mild joint swelling.  Even before examining her radiographs, one can be hopeful that her prognosis for full function would be favorable.  And this is in fact the case.  Classy has an excellent prognosis for a full athletic career following surgical debridement of her stifle lesions.  On the other hand, a 6 month old weanling with grade 3 lameness and severe swelling of the stifle joint undoubtedly has a more conservative prognosis for an athletic career, even with appropriate treatment.

OCD can occur in any joint in the body. The most commonly affected joints are the stifle, hock and fetlock, and less commonly the shoulder and cervical spine (neck).  Within each of these joints there are several locations where lesions can occur.  In addition, lesions may occur as mineralized cartilage fragments that have separated from the underlying bone (see Classy's x-ray's for a beautiful example) or they may appear as cyst-like lesions, where the cartilage lining the bone is still intact, but is no longer attached in one region, with fluid and tissue debris filling the area between the detached cartilage and underlying bone. Remember our jump painting analogy?  The detached lesions are like paint chips, leaving the wood of the jump exposed, the cyst-like lesions are like bubbles in the paint, detached from the wood, but with the paint surface still intact. 

The prognosis for full athletic function for OCD of the lateral trochlear ridge in the stifle and most locations in the hock is excellent in the majority of cases, particularly when lameness is not severe, and does not become apparent until the horse enters training.  OCD of the fetlock is often treated successfully, but caries a more conservative prognosis in general than lesions of the hock or stifle.  OCD of the shoulder and cervical spine in general carry a guarded prognosis. There are certain anatomic locations where OCD lesions may be detected radiographically in a sound horse during a pre-purchase examination, for example, and be considered clinically insignificant, depending on their severity, and the horse's level of performance.

While surgical debridement (scraping the lesion just as you would scrape the paint on your jumps before correctly applying fresh paint) remains the gold standard for treatment of OCD, there are many emerging treatments under investigation which may alter our approach to this complex disease.  Intra-articular stem cell therapy is one of the most promising of these.  And still, many foals and weanlings with early diagnosis of less severe forms of OCD respond well to simple rest and careful rehabilatation with intra-articular chondoprotective therapy, allowing mother nature to do her own magic in healing lesions.

I've barely scratched the surface of the subject of OCD in these past few posts, but hopefully you will take away the message that in most horses this diagnosis does not mean the end of an athletic career.

I'm off to dinner after a long, cold day of work in windy, 45 degree rain spitting Reno today.


Wednesday, March 10, 2010

3/9/2010 - Osteochondrosis - What is it?

Vet Tip of the Day: Osteochondrosis - Understanding the disease Process
Key Words: Bone, Cartilage, Mineralization, endochondral ossication

Yesterday I discussed the lameness workup on Classy, a 5 years old thoroughbred mare with OCD of the stifle.  So what is OCD anyway?
Today Iwill describe the disease process, and some of the factors we believe predispose juvenile horses to this problem.  Tomorrow I will go over some of the more common location for OCD lesions.

OCD stands for Osteochondrosis dissecans.  Just to give you a hint at how complex this disease is, there is still debate over whether this even is an accurate name for the problem.  To understand this disease at all, you must first understand how bones grow.  A joint is a moving part, consisting of bones that slide along each other, separated and lubricated by joint fluid.  The surface of the bone is covered by a layer of cartilage, which is softer and more compliant than bone, and therefore stands up better than more rigid bone to the forces exerted on joints during athletic activity. 

Think about it - how do your foal's bones get longer and thicker as the foal grows?  What happens is a process called endochondral ossification.  The bones grow from the surface cartilage toward the underlying bone.  The cartilage cells, called chondrocytes, divide and increase in number.  As they mature, they become mineralized and eventually transform into bone.  This is a rapidly ongoing process in the growing foal.  If the transition from young chondrocyte to mineralized chondrocyte to bone doesn't occur correctly, there is a defect in bone maturation.  Thus, osteochondrosis is a defect in endochondral ossification. 

Try this image to help you imagine what happens.  You are painting the jumps in your arena.  You are getting tired, so instead of putting on several thin coats of paint, and allowing each to dry in between, you start globbing on thick layers of paint, not letting each layer dry.  When you lay the paint on correctly, each layer adheres to the one beneath and you end up with a shiny surface of smooth paint that doesn't crack or peel.  If you glob the paint incorrectly, you end up with bubbles underneath the surface and cracks and flakes on the surface soon after the paint dries.  Exactly the same thing happens in foals with OCD.  The cartilage to bone development is abnormal, and the resulting defects include cysts (just like the bubbles under your paint surface) and cartilage flaps that detach from the underlying bone just like your flaky paint, because the attachment to the underlying layers is not healthy. 

Cysts lying just below a thin layer of unhealthy cartilage, flaky, cracked cartilage, and actual flaps of calcified cartilage that separate from the underlying bone are all manifestations of OCD.  In all three cases, the smooth, gliding surface that is critical to pain free, athletic joint function, is lost.  The result is swelling and pain during athletic activity.  Many factors predispose horses to develop OCD.  The particular combination of events in a given foal that result in OCD are complex and inter-related.  Some of the major forces at play are: genetics, rapid growth and large body size, excess feeding of carbohydrate, abnormal stress and trauma, and mineral imbalance, specifically copper deficiency.

This is a very basic overview of the disease process called OCD.  Tomorrow we will look at some of the most common sites in the body where OCD occurs, and the clinical significance of some of these sites.

Tuesday, March 9, 2010

3/9/2010 OCD

Vet Tip of the Day: Osteochondrosis Dissecans - More Lameness!
Key Words: OCD, stifle, developmental orthopedic disease

I'm going to continue discussing lameness today.  I'm also going to confuse you by presenting another case in which I did not follow the cardinal rules of lameness diagnosis: 1) physical examination 2) gait evaluation 3) diagnostic nerve blocks 4) diagnostic imaging.  In the horse I will discuss today, I skipped step 3, and will explain why.

In today's discussion I am simply going to present this case, and tomorrow will discuss the disease process in more detail.  Look at the x-ray here - this is the horse's stifle, the joint which corresponds to our knee.  The patella is the triangular shaped bone at top right of the picture.  It rests against the bottom of the femur (your thigh bone) and slides up and down on two ridges called the trochlear ridges.  These ridges end in the condyles, which on the x-ray are the two rounded knobs at the end of the femur.  Below the femur is the tibia (your shin bone). 

Look on the trochlear ridge just below the tip of the patella and you will see a small piece of bone separated from the trochlear ridge by a black shadow.  This is a classic lateral trochlear ridge OCD lesion.  Now here is the case presentation.

Classy is a 5 year old thoroughbred mare.  She never raced, but did train for the track as a 2 year old.  She was pulled from training due to "splint bone issues" and was turned out to pasture for a few years.  Recently she was sent out for 60 days basic flat work training which she completed successfully without complaint of lameness from the trainer.  Upon return to her owner's barn, both the owner and trainer at the barn noted that Classy would buck when asked to canter and just "didn't seem right behind".

On physical examination Classy had no remarkable abnormalities execept for moderate fluid filling in her femoropatellar joints on both hind legs.  The filling was soft and non-painful.  On gait evaluation Classy was grade 1 lame (see previous post on lameness grading) on her right hind.  She had a mild positive response to right hind hock/stifle flexion.  She was sound and negative to flexion of the left hind.  When observed on a longe line on a soft surface, Classy did not show overt lameness, but her hind limb gait was characterized by a shortened step and a rapid downward placement of her feet at the trot.  When asked to canter, she had obvious difficulty executing a canter departure.  When travelling to the right, she would only canter disunited, with the forelimbs following a right lead foot cadence and the hindlimbs following a left lead foot cadence.  Tracking to the left she would occasionally canter in a united left lead canter, but also frequently cantered disunited.  Her hind limb gait at all times during the canter was characterized by poor independent motion of her two hind legs - they tended to move together, suggesting a "bunny hop" quality.

The combination of physical examination findings and gait evaluation were suggestive of a stifle problem.  Radiographs were performed immediately for three reasons.  First, intra-articular anesthesia (joint block) of the femoro-patellar joint to identify subtle lameness such as Classy exhibited is not routinely reliable - horses will not always "block out" even though the stifle is the source of the lameness. In general, lameness should be at least a grade 2 before intra-articular anesthesia is relied upon as a diagnostic tool.  Secondly, from a strictly practical point of view, we were under time constraints, the intra-articular anesthesia would incur cost without a high likliehood of definitive results, and Classy was a somewhat fractious 5 year old likely to be uncooperative during placement of needles in her stifle without significant sedation.  Thirdly, OCD was the most likely presumptive diagnosis for Classy, and radiographic confirmation of this diagnosis in combination with Classy's signs is considered definitive without intra-articular anesthesia.

Classy was sedated and 3 views of each stifle were taken.  The radiographs confirmed OCD in both stifles, the right significantly worse than the left.  The x-rays were reviewed by a board certified surgeon and surgery is scheduled for next week!  Cost $2500 - prognosis for soundness and full athletic function excellent - layup time 6 weeks.

In Classy's case, the owner's astute attention to a relatively mild gait abnormality resulted in a timely diagnosis of a problem that left untreated would likely result in degenerative changes in the joint with resultant chronic lameness.  Over the next few days we will look at OCD in more depth, and then return to Classy's case and discuss why her particular manifestation of this developmental orthopedic disease carries with it an excellent prognosis following surgical repair.

Friday, March 5, 2010

3/5/2010 Winding up with Flash

.Vet tip of the Day:  Challenging lameness
Key words: Carpus, metacarpal bones

Finally I'm back after a few down days - my apologies to those of you following daily.

Let's finish up with Flash, the gelding with the challenging lameness.  Quick review: the take home messages you should remember from following this case are: the importance of client communication, the need to treat each lame horse individually, and the importance of patience and care to do know harm when approaching a challenging lameness.

Two weeks after my initial evaluation of Flash I returned to repeat x-rays and check on his progress.  His lameness was slightly improved, but he continued to be very uncomfortable when stepping down from his stall or turning.  Repeat x-rays of his splint bone in the area of the trauma still showed no fracture.  There still was no swelling in the joints above or below the site of trauma, but there continued to be some pitting edema (soft swelling) along the length of the medial splint bone (metacarpal II) and Flash continued to show a painful response when palpated along the proximal splint and at the back of the knee where the splint bone articulates with the second carpal bone (see red arrow on diagram).

Although Flash remained very lame, I decided to performa an abaxial sesamoid nerve block, which would remove sensation to structures below the fetlock.  There was no indication that the lameness originated in the area, but because I so far had failed to identify a definitive cause for the lameness, I wanted to be sure that I wasn't making a mistake concentrating on the splint trauma.  The foot block did not change Flash's gait.  I then did a local block, injecting local anesthetic directly into the region around the focal swelling which had orignially been so painful when the trauma occurred.  Again, no change in the lameness. 
At this point I decided to examine the leg more proximally - above the site of the injury.  We took several x-rays of the knee and found that there was evidence of trauma to the second carpal bone and extensive remodelling of the proximal second metacarpal bone (the medial splint).  Again, look at the red arrow on the diagram - the second carpal bone is the bone immediately above the arrow, sitting right on top of the head of the medial splint bone.  The radiographic changes appeared chronic - in other words the character of the abnormalities suggested they had been present for more than two weeks.  I e-mailed these x-rays to my consulting surgeons, who agreed that it appeared that some trauma involving the structures of the carpus in this region probably occurred at some time in the past and this recent injury led to a flare up of an old problem. 

It is important to remember that the x-ray only shows bones.  There is a very complex system of ligaments and tendon sheaths that overlies the medial aspect of the carpus exactly where the second carpal bone meets the medial splint.  Here is a somewhat out of focus (sorry, my limited tech skills showing through) diagram of these structures.  The boney remodelling present on the x-ray very likely is accompanied by additional damage to the associated soft tissue structures.  Ultrasound or MRI would be useful in further specifying such damage.

With these changes identified radiographically, and with the recommendation of the consulting surgeons, I went ahead and did an intra-articular block (use google bar at top of blog and search for "intra-articular block" and you'll find blog entry describing this) to anesthetize the carpo-metacarpal joint and Flash's gait improved about 75%.  With an articular injury, and likely additional pain arising from soft tissue structures outside the joint, this degree of improvement is considered diagnostic.

I felt comfotable that this unusual lameness story was finally coming to a conclusion.  The treatment would be rest and slow rehabilitation.  I left instructions for Flash to remain on stall rest for 60 days, at which time radiographs and full lameness exam would be repeated.  And in fact Flash's gait improved dramatically by 21 days post injury. I'll give you an update on his progress in May.

Please feel free to comment on these blog entries and let me know which are your favorites.  My goal is to provide continuing education that is both interesting and useful to you.  Give me some feedback to help direct my future efforts!

Monday, March 1, 2010

Monday, 2/1/2010 - Client communication and Flash

Vet Tip of the Day: Client Communication

Using Flash as an example, we've been discussing some of the principles of lameness evaluation used by veterinarians to make safe and accurate diagnoses for their equine patients.  There is a final element in this process that is critical not only to lameness exams but to every other facet of equine veterinary practice as well.  This element is client communication, and it is the subject of today's Vet Tip of the Day. 

For me, the most important goal when communicating with a client is to explain their horse's condition in the clearest terms possible.  Most of us have strong emotional ties to our horses.  At the same time, we know that our horses have an economic value, and that the cost of veterinary care can rapidly escalate.  When our horses are sick or injured, we immediately are concerned for their welfare while simultaneously wondering about associated costs.  Although we are uncomfortable facing it, for almost everyone there is a necessary balance between love and money where our animals are concerned.

As a veterinarian, I feel that the best service I can give my clients is to provide them with straightforward, understandable language describing their horse's injury, the prognosis for recovery, the treatment options and their associated costs. With a clear understanding of the facts surrounding their horse's problem, I believe my clients are best equipped to make informed decisions that are within their means and in their horse's best interest. 

Flash belongs to a very involved owner who has been breeding and showing performance horses for years.  Mary loves her horses, but is aware of the reality of economics when it comes to their maintenance.  Emotions can quickly cloud the picture when these two factors come into conflict.  She has a demanding job and juggles a heavy schedule to make time for her animals.  Many of my appointments with Flash take place without Mary being present.  It is very important to her that I contact her promptly after seeing Flash.  She expects a complete and definitive description of whatever has gone on with her horse so that she can stay on top of developments and make appropriate decisions as needed.  I appreciate these qualities because they reflect her concern for her animals and allow us to have an open, productive relationship.

Fulfilling such expectations is pretty easy when you are dealing with something like a simple skin laceration of the face.  All I have to do is remember to give clear instructions to the trainer and make the phone call to Mary as I leave the barn,  assuring her that Flash will be fine and I'll be out in 14 days to remove the sutures. With a lameness such as the one we are currently working through, it is more challenging.  I don't want Mary to worry unnecessarily, but it is important to convey my concern that the cause of Flash's lameness may be quite serious.  I am doing this based on my years of experience and my knowledge of anatomy and physiology but without a definitive diagnosis to offer Mary.

In this situation, because I cannot clearly define the problem, I explain the various possible causes of Flash's lameness to Mary without overwhelming and confusing her, and then focus on laying out a specific, structured plan explaining how we will go about narrowing down these possibilities.  This plan has a time line, it addresses Flash's care during that time, and it identifies specifically how I plan to go from "I don't know exactly what's wrong" to "OK, Mary, this is the problem."  Bringing in the opinions of outside experts, in this case ACVS board certified surgeons, to consult, is not only appropriate but, in my opinion, recommended, in this situation.

By approaching a challenging case with such an approach, I believe that the animal's best interest is protected, and I have the best chance of maintaining the trust I have established with my client and thereby minimizing her stress while we get to the bottom of Flash's problem.  As long as Mary is confident that her horse is safe and a time line has been defined, she can exercise her patience and allow me to continue down the path to figuring out Flash's lameness.

Tomorrow we will look at Flash's second set of x-rays and discuss his second lameness examination and the ongoing mystery, including the opinions of the outside experts.

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