In line with our continued discussion of basic vaccinations and horse health upkeep, I wanted to complete our discussion of what we consider “core” vaccines.  Core vaccines are those that every equine (and equid for that matter!) should receive – they include EWT, Rabies, and West Nile Virus. We will continue our blogs with discussion of diseases whose vaccines are not considered part of a core program.  Today, we will close with the newest member of the core group – West Nile Virus.

West Nile Virus (WNV), like EEE and WEE, causes encephalitis (inflammation of the central nervous system) and results in neurological symptoms. Humans and other species can acquire this disease as well. West Nile was not found in the United States prior to its introduction to New York in 1999. Clinical signs usually progress back-to-front, meaning the hind-limbs are often affected first, then the forelimbs and so on forward. Early symptoms include inappetance, fever, hind-limb weakness and ataxia. Often the muscles of the muzzle twitch erratically, and they become hyper-excitable. Many horses with West Nile Virus are seen in a dog-sitting position early in the course of the disease, and it progresses to recumbency (lying down) and death. Other neurological signs seen with WNV include blindness, difficulty swallowing, head pressing, seizures, and aimless wandering.

Like EEE, birds keep the source of West Nile Virus alive in the United States, and mosquitoes feeding on the infected birds are the vectors that transmit it to the horse. There is no specific treatment for West Nile, other than supportive care for vital body functions. Recumbent horses must be supported in a sling or turned over every four hours until recovery occurs (if it does).  Like with other neurological diseases, when the horse becomes recumbent, euthanasia is generally recommended. Vaccination is recommended once yearly, but it is not a guarantee against infection. The goal of vaccination is to reduce the likelihood of infection, and minimize the clinical signs should infection occur. It is also crucial that you do your part in minimizing mosquito exposure for you and your horse!

You can minimize mosquito populations on your property by eliminating sources of stagnant water (or stocking them with fish), and cleaning out your clogged gutters!  Mosquitoes breed in any puddle that is left for more than four days.  Keep your barn lights out at night – mosquitoes are attracted by yellow incandescent bulbs. Placing these bulbs at sites away from your barn can draw them away from your horses. Report any dead birds you find on your property to the Alachua County Health Department (DO NOT pick up a carcass without gloves!), and eliminate roosting areas in your barn.

As you are probably wondering, my foot is doing well – the atrophied muscles are starting to come back and my limp is almost gone! I can’t tell you how wonderful it is to be prowling around the office again, inspecting your trailers and your horses. And it was fortunate my recovery happened at such an opportune moment – there’s a new stray lurking around the office that I must defend against!  Have a Happy Valentine’s Day, and we hope you can make it to our Senior Horse Seminar this Thursday at 6PM at Canterbury!  May your litter box be clean and your food bowl full!

After last week’s discussion on Rabies, I decided it was important to discuss another readily-controlled, animal-killing pathogen – Clostridium.  This genus, or group of bacteria has more species members than any other genus of bacteria.  A book could be, and probably has been, written about all of the Clostridial diseases that exist.  Clostridium bacteria produce neurotoxins or tissue toxins when seeded into wounds or ingested.  They generally favor environments that are anaerobic (without oxygen).  A few of the more notable diseases featured in this group include tetanus, botulism (limber-neck in poultry), gas gangrene, and overeating disease.  Others less commonly known include blackleg, red water, Tyzzer’s and black disease.  Many people (and foals, lambs, etc.) have been infected with, and killed by C. difficile diarrhea.  Any diarrhea, abscess (foot or otherwise), or hot, painful deep tissue infection in a vertebrate could well have a Clostridial source.

Many species in this genus live in the environment all around us, like Clostridium tetani, the organism that causes tetanus (not just on rusty nails!).  Some areas of the country (notably Kentucky and Texas), have high levels of botulism in the soil and are avoided.  Only a few years ago, C. botulinum bacteria growing in a batch of haylage produced a neurotoxin that, on ingestion, killed over 100 horses in the Ocala area.  Botulism is an important disease of foals in the Kentucky area, and vaccination is recommended for broodmares and foals in that area of the country.  As it causes flaccid (limp) paralysis, intensive care is required to support almost every bodily function during the weeks of recovery – eating, drinking, and breathing.

Tetanus, like botulism, can kill just about anything.  While botulism is usually ingested or inhaled, tetanus is usually associated with a wound, often a puncture wound that is allowed to heal over, creating the perfect warm, airless environment for it to multiple and produce toxins.  Its neurotoxin has the exact opposite effect than botulism: the uncontrolled paralysis is “tonic-clonic,” meaning the muscles undergo spasmodic continuous contraction.  Stiffness will first be noticed in the limb or area near the wound, and will become generalized in a matter of days.  The powerful clamping of the chewing muscles, often resulting in the subsequent starvation, dehydration and death of an animal affected by tetanus, is what gives rise to the term “lockjaw.” The body takes a rigid, arched position as the back muscles contract, overwhelming the abdominal muscles and pulling the head back.  There are no blood tests to diagnose tetanus, but often the characteristic symptoms readily point to this historic culprit.

Control of tetanus is easily achieved through annual vaccination.  A tetanus toxoid vaccine, given annually, is usually used for small ruminants, but can be given off-label to other species such as al pacas and llamas. Most horses receive their tetanus toxoid vaccine in the “EWT” (Eastern Encephalitis, Western Encephalitis, and Tetanus) combination product twice a year.  Ruminants (cattle, sheep, and goats) are usually are given a “seven way” vaccine as youngsters, then annually and pre-breeding that includes overeating disease (C. perfringens).  Generally vaccination is recommended starting at 4-6 months of age. The vaccines are inactive bacterial products, so unlike some vaccines, there is no risk of infection from vaccination. It is not uncommon for animals (and people) to be stiff for a day or two after vaccination.

If your animal receives a deep wound, call us immediately!  Antitoxin must be given to animals that are not vaccinated if they receive a deep puncture wound that will predispose to infection.  This antitoxin has been associated with reactions resulting in liver disease in horses, so regular vaccination is strongly recommended.  Like for Rabies, vaccination is cheap, easy and effective! Don’t overlook this important and easily preventable disease when taking care of your horses and livestock.

In the meantime, my spoon splint is finally off!!! …although I still have an annoying bandage on my foot (which I continue to shake at people), I feel like my stall-turned-paddock (when I get to go out in the barn aisle-way) rest is close to over! May your food bowl always be full, and your litter box be ever-clean!

We are very excited to start seeing our Wellness patients (new and old!) for their first visits! In addition, the staff, in particularly Dr. King, is ecstatic to be coming into breeding season.  She is ready for sleepless nights, bouncing foals, and the reward of pregnancy (for the mare)!! The year of 2012 promises to bring many exciting events for Springhill, continuing our old traditions, refining our current favorites, and adding new features to our packages and services. We can’t wait to see what new faces and old come through our doors this year!

The year of 2011 was a great one for Springhill as well, despite a rocky ending. An overall successful breeding season ended with the addition of Dr. King and our technician Danielle. Our other technician, Amber, moved into our office manager position, and has done a great job as our clinic crusader – along with our staff handling everything from answering your calls, preparing medications, and keeping your reminder cards coming! Our current team was complete with the addition of Michelle, who has worked for a long standing Springhill client for many, many years!  The overall excitement of the Springhill team, however, was sadly dashed to the ground in November when a tragic attack left me crippled for the remainder of the year. Hopefully the morale of the group will peak up a bit after my cast is removed in 2012.

Thanks for being loyal readers of my blog in 2011, and please help me come up with ideas of what you want to read about in 2012!  Feel free to email blog ideas to the clinic, vets@springhillequine.com.  I’m feeling quite comatose from all these cookies that you have been bringing by the office (THANK YOU!!!!!) – so I think I am going to tuck in for a warm winter’s nap and hibernate until 2012!!  May your litter box be clean until then, and your food bowl be exceptionally, holiday full!  See you next year!

Happy Thanksgiving from the counter top!!  I hope everyone had too much to eat.  I got a plate of leftovers from Dr. Lacher and boy they were good.  My broken foot is coming along well.  I have a recheck visit Tuesday to get my splint redone.  In the meantime I feel much better when my tummy is rubbed followed by treats in case you should stop by the office this week, hint…hint…Anyway on to the topic at hand this week:  Laminitis

Dr. Lacher and Shawn Jackson recently attended the Laminitis Symposium in Palm Beach.

We will start with new therapies.  There was lively discussion regarding Platelet Rich Plasma (PRP) and Stem Cells.  There was some excellent work showing Stem Cells to be a potentially effective part of therapy for the worst type of laminitis known as sinking.  This typically occurs in very sick horses.  This form of laminitis involves failure of the lamina around the entire hoof.  Stem Cells were one component of aggressive therapy and it is important to note success rates were still only around 40%.  Other treatments used alongside stem cells included very specific trimming methods based on x-rays of the hoof and full hoof casts.  PRP was also discussed as a therapy for laminitis both early in the disease and in older, chronic cases.  PRP is thought to provide the framework for a horse’s own stem cells to settle on.  PRP also releases signals which call stem cells to the area.

Foot casts were also talked about as a way to support the chronic laminitis horse.  In fact, Dr. Lacher has already placed them on one horse.  They allow us to fully support the foot and transfer weight to the fetlock.   Chronic laminitis is always about trying to get the foot to grow out, supporting the hoof and keeping infections at bay.  This leaves the infection part to deal with.  Maggots are excellent for use as a therapy in this area.  Dr. Lacher has used medical maggots for this purpose before and learned several new uses while attending the conference.  One case used maggots to treat a deep puncture wound from a nail!

Many of the laminitis cases we see are because our horses have a metabolic disorder such as Cushing’s or Equine Metabolic Syndrome (also known as Insulin Resistance).  Dr. Nicholas Frank, a leading researcher in this area, talked about his experience managing a herd of affected horses.  One of the biggest things he learned was that horses with Equine Metabolic Syndrome are MUCH more susceptible to Cushing’s disease at younger ages than normal horses.  He found Cushing’s in horses as young as 12 years!!  Dr. Frank believes this is secondary to oxidative changes or perhaps insulin stimulating overgrowth in the pituitary gland.  The important take home point was to monitor insulin levels in suspected horses, control diet in affected horses and test for Cushing’s early in this population.  Because of discussion with Dr. Frank, Dr. Lacher added our Senior Preventative Package to the Springhill Equine Wellness Program.  She feels this will help us identify Metabolic Syndrome and Cushing’s horses early.  Radiographs of the front feet are included to help us identify subtle coffin bone angle changes and institute therapeutic trimming or shoeing before your horse has a crisis.

That is just a start of what Dr. Lacher and Shawn learned at the Laminitis Symposium.  It was an amazing group of some of the best researchers on laminitis!  For an added bonus ask Dr. Lacher about the research on the wild horses of Australia.

That’s the musings from the counter top this week.  Well the bench actually.  I can’t jump all the way up to the counter top right now.  May your food bowl be full and your litter box clean!

Tony here.  Having a rough week at the office.  Teeny cat and I got into a fight last week – she bit my foot and the vets are saying I broke two bones!  I had to go to Newberry Animal Hospital, got put under anesthesia, and had a horrible splint put on my foot!!  Woe is me! On the upside, I spent a weekend in a bathroom kitty condo at Dr. King’s house, got a new fluffy bed, and am getting many pets.  ::Sigh::  Anyway, enough complaining, we’re supposed to be chatting about CSM – part two!

Last week, our blog was introducing CSM, a group of orthopedic disorders that happens in the neck of the horse, causing neurologic signs similar to EPM.  Scroll down to read last week’s blog on Type I, which generally occurs in young horses.  Type II CSM occurs in older horses as a result of arthritis that occurs at what is called the articular facets.  Facets are normal bony projections off the main body of the vertebra – in horses, the facet from one vertebra forms a joint with the facet from the next vertebra.  When arthritis forms at this joint, the horse becomes stiff and has a hard time turning his head from side to side.  Eventually, the arthritis becomes advanced enough that it results in compression of the spinal cord, causing neurologic signs. This type of impingement is static – meaning it does not generally change with head position.  Like type I, this is a problem with cartilage and bone development. The arthritic bone is very brittle and may fracture off small pieces, resulting in further pain and worsening of clinical signs.

Symptoms generally start with signs of ataxia, dragging the back feet, and hind end weakness, similar to type I.  A “pacing” walk may be seen, and the signs may be asymmetric (eg, your horse may be stiff turning his head one way, but not the other).  The horse may have trouble getting over fences or begin tripping in the front end.  In this respect, shoeing can help tremendously.  By using a world wide racing plate, you make it easier for the horse to pick his foot up (like when you wear a pair of Sketcher’s Shape Ups!), and often times, the greatly reduces how often the horse trips.  Like type I, diagnosis is based on neck radiographs that we perform at the clinic.  Treatment is palliative – anti-inflammatory medication such as phenylbutazone (Bute) or banamine help manage the pain and inflammation.  Facet injections (performed at the clinic under sedation, and with ultrasound guidance) help to reduce inflammation in the joint, and can make your horse more comfortable for months or even years.  If you are interested in having your horse evaluated for possible CSM type II, you should consider bringing your horse to the clinic for the neurologic evaluation.   as we can then perform neck radiographs and injections the same day!  Thanks for reading, may your litter box be clean and your food box be full!

Hello there!  Welcome back to my corner.  When it comes to neurological disease in the horse, there are two syndromes you should be familiar with. They are both diseases caused by spinal cord compression in the neck, and can exhibit symptoms very similar to EPM, West Nile Virus, and other infectious causes of neurologic disease. Cervical stenotic myelopathy (CSM), formerly known as “Wobbler’s syndrome,” exhibits two forms – type I and type II.  This week we will discuss Type I CSM, which is the “classic Wobbler’s,” and next week we will discuss type II – seen in older horses as a result of neck (cervical) arthritis.

Type I CSM, also called Cervical Vertebral Malformation, is most commonly seen in horses less than five years of age.  In every species, there is a canal that present in each vertebra, called the spinal canal, that houses the spinal cord. These holes must line up and be of sufficient width to allow the spinal cord to run straight through the spinal column without compression from the bony tunnel.  This is exactly what goes wrong in horse with Type I CSM.  Sometimes the canal in the vertebra narrows, sometimes it is shaped like a cone, or it can be elongated.  These changes are a result of a developmental orthopedic disease in the vertebra, in the same group as OCD, contracted tendons, and bone cysts.  As a result, the horse has compression of the nerves that run along the outside of the spinal cord to their legs.  In general, the nerve compression that occurs is worse in a flexed neck position, and so we call the narrowing “dynamic,” or changing.  Rapid growth and large size are risk factors for this type of CSM, as are high protein and caloric intakes.  There may be a genetic predisposition for this disorder as well. Thoroughbreds, Warmbloods, and Tennessee Walking horses are significantly more likely to be affected than Quarter horses, Standardbreds, and Arabians.

Clinical signs often manifest first as evidence of weakness in the hind end.  This is because the nerves running to the hind legs are to the outside of the nerves running to the front legs in the spinal cord.  Ataxia, spasticity of the limbs, and weakness may start insidiously or suddenly.  Sometimes a history of a fall confuses the diagnosis (was the fall the cause or result?), and clumsiness and tripping is commonly reported.  Changes may first be noticed by your farrier when he is trying to trim the back feet. A pacing gait may also be present. Diagnosis is based on a complete neurologic exam where the neurologic deficit is localized to the neck, followed by neck radiographs.  Sometimes it is necessary to inject contrast dye into the space outside the spinal cord (contrast myelogram), and then radiographs show a narrowed or “pinched off” area where the dye can’t pass through the compressed area.  Often the CSF analysis is normal.

Prevention of Type I CSM is aimed at limiting protein and caloric intake to regulate growth.  Suspected horses less than a year should be weaned and placed on a “Paced Diet,” including free choice grass hay and limited amounts of growth diet and/or ration balancer to provide necessary vitamins and minerals. Foals should be confined to a stall or small paddock to restrict exercise, certainly not free-choice pasture.  Intra-articular (joint) injections with steroids can be performed on the affected neck joints under ultrasound guidance, providing symptomatic relief (will be discussed in more detail next week).  Finally, surgical correction can be performed for affected horses.  A metallic (steel or titanium) cylinder or basket is placed between the vertebrae – the goal is to induce arthritis, fusing the joint between the neck vertebrae (as we fuse hock joints in cases of advanced arthritis).  This makes the joint more stable and minimizes dynamic compression. It has been found to improve the neurologic status in 44-90% of horses with dynamic compression.

Please contact us if you would like more information on diagnosis, prevention, and treatment of CSM Type I. As always, may your litter box be clean, and your food bowl be full.  Thanks for stopping by!