National Day of the Horse
— Read on www.nationaldayofthehorse.com/celebrate.html
National Day of the Horse
National Day of the Horse
— Read on www.nationaldayofthehorse.com/celebrate.html
Written by Dr. Tom Lenz on behalf of AQHA
Few horse owners are aware of this disease which is a progressive, paralyzing disease that is 80-100% fatal in affected horses. Botulism is sometimes referred to as “forage poisoning” in adult horses or “shaker foal syndrome” in foals. The disease is caused by a potent toxin that is produced by the bacterium Clostridium botulinum. This bacterium lives in the soil as well as the intestinal tract of many normal birds and mammals, including the horse. It produces dormant spores that can be found in 18.5% of soil samples tested in the United States. The disease is most prevalent in Kentucky, Ohio, Maryland, Pennsylvania, California, and Tennessee although it can occur in any state in the U.S. Clostridium botulinum produces several different toxins. Type A toxins are often implicated in human infant botulism and are most often found west of the Rocky Mountains. Types B, C, and D toxins are usually involved in cases of equine botulism, with Type B responsible for 85% of horse cases in the U.S.
Horses of any age are susceptible to botulism which may be initiated by one of three ways. In the case of “forage poisoning” the horse ingests toxins that are contaminating feedstuffs such as grain or hay. Feed contamination is most often due to putrefied carcasses of birds or rodents. A Type C botulism outbreak that killed a number of horses in California several years ago was traced back to hay that contained the infected carcass of a rabbit. The bacteria can also enter a horse’s body via contamination of a wound, especially a deep puncture wound. A good example is “Shaker foal syndrome” which is most frequently caused by the bacteria entering the newborn foal’s body through the foal’s moist navel. Something that can be minimized by dipping the foal’s navel in mild iodine solution soon after birth. The third method in which the disease can be initiated is by ingestion of the spores in the soil. The ingested spores activate in the horse’s intestinal tract where they produce potent toxins that are then absorbed. Regardless of the route, once the bacteria have entered the horse’s body they produce toxins that block transmission of nerve impulses to the horse’s muscles. This results in a progressive paralysis of all the major muscle groups and is concluded with paralysis of the diaphragm, which results in death. Once symptoms develop, death may ensue in several hours or take up to a week.
The disease is difficult to diagnose because it resembles several other medical conditions and diseases such as choke, colic, rabies, EPM, and sleeping sickness. Blood samples very rarely contain toxin and necropsy following the death of the horse usually does not provide a conclusive diagnosis. Because the bacteria often occur naturally in the horse’s intestinal tract, isolation of the organism from the sick horse’s intestine is not diagnostic.
Clinical signs of the disease in adult horses suffering from “forage poisoning” initially include loss of facial expression, a sleepy appearance, saliva drooling from the corner of the mouth, loss of tongue control and loss of tail tone. The horse’s appetite is good, but it has a great deal of difficulty in chewing food and appears to be “playing” in their feed and water buckets. As muscular weakness becomes more profound, the horse will experience muscle trembling, generalized sweating and labored breathing. A weakened, shuffling gait may develop and the horse may take stiff, short steps as if walking on eggs. Eventually, the horse goes down and death results due to paralysis of the respiratory muscles. “Shaker foal syndrome” is usually seen in foals one to two months of age but can develop as early as two weeks or as late as 8 months of age. Early signs in foals are similar to those seen in adults in that the foal shows generalized weakness, poor tail tone, and loss of tongue control. The foal will often dribble milk from the mouth and nostrils because of an inability to swallow. Because of muscle weakness, the foal will lie down frequently. When it does rise, it soon develops muscle tremors and collapses. Affected foals may die within 12 hours of exhibiting symptoms or may linger for as long as a week.
Botulism is usually fatal if left untreated. Prior to the advent of antitoxin, the death rate among affected foals was greater than 90%. With the use of antitoxins in conjunction with antibiotics and supportive therapy, the mortality rate can be reduced to less than 25%. Animals unable to swallow should be fed through a nasogastric tube and placed on IV fluids. Once the toxin produced by the bacteria is attached to the nerve ending it cannot be neutralized by the antitoxin. Therefore, early treatment is critical. Even with aggressive therapy, recovery is slow and may require up to two weeks before the affected horse recovers.
Because of the high death rate and the difficulty in diagnosing this disease, prevention through vaccination is critical. A Type-B Toxoid vaccine is available and is quite effective in preventing the disease. In areas where the disease is prevalent, pregnant mares should be initially vaccinated at the 8th, 9th and 10th month of gestation and thereafter at the 10th month of each pregnancy. Yearly vaccination of adults in areas where the disease frequently occurs is also recommended. If unable to vaccinate the mare prior to foaling, limited information suggests that foals vaccinated with the toxoid at 2 weeks, 4 weeks and at 8 weeks of age developed adequate protection, even in the presence of passive maternal antibodies. Currently, no licensed vaccines are available for preventing botulism due to Cl. botulinum types A or C or other subtypes of toxins. Cross-protection between subtypes does not occur.
As in all horse health issues, your local veterinarian is your best source of information.
ABOUT THE AUTHOR: Thomas R. Lenz, DVM, M.S., Diplomate of the American College of Theriogenologists, is a trustee of the American Horse Council, past chairman of AQHA’s research committee and past president of the American Association of Equine Practitioners. This article is provided courtesy of AAEP Alliance Partner, AQHA.
Reviewed and updated by original author in 2016.
Over the past 30 years the Grayson-Jockey Club Research Foundation has funneled nearly $20 million into studies aimed at improving horse health. This year the effort continues with funding for a dozen new projects in fields ranging from laminitis to lameness diagnosis. A sampling:
Detecting lameness at the gallop: Kevin Keegan, DVM, of the University of Missouri, is developing an objective method (using a calibrated instrument) for detecting obscure, subtle lameness in horses at the gallop. The goal is a low-cost method that can be used in the field to increase understanding of lameness in racehorses.
Deworming and vaccines: While it’s not unusual to deworm and vaccinate horses on the same day, recent findings have raised concerns about possible interactions. Martin Nielsen, DVM, of the University of Kentucky and Gluck Equine Research Center, is investigating whether deworming causes an inflammatory reaction that affects vaccination.
Imaging injured tendons: Horses recovering from tendon injuries are often put back to work too soon and suffer re-injury. Sabrina Brounts, DVM, of the University of Wisconsin–Madison, is exploring a new method developed at the university to monitor healing in the superficial digital flexor tendon. The technique, called acoustoelastography, relates ultrasound wave patterns to tissue stiffness: Healthy tendon tissue is stiffer than damaged tissue.
Detecting laminitis early: Hannah Galantino-Homer, VMD, of the University of Pennsylvania, is investigating possible serum biomarkers (molecular changes in blood) that appear in the earliest stages of laminitis. The goal is to develop tests for these disease markers so that treatment can start when laminitis is just developing, before it’s fullblown and damages the foot.
Other new studies include evaluations of a rapid test for salmonella; investigation of how neurologic and non-neurologic equine herpesvirus 1 (EHV-1) spreads cell-to-cell in the body; an effort to map the distribution of stem cells after direct injection into veins; and more.
This article originally appeared in the June 2013 issue of Practical Horseman.
Recently, I had to move to a new farm. And, if you are anything like me you loathe not only moving but moving your horse. The what-ifs running though my head- what if he won’t load? What if he hits his head? What if he freaks out? (Or to be completely transparent, what if I do?). What if he falls? Etc. Personally, when I am faced with a anxiety provoking situation, I need to have a sense of control however small it is. So, I did what I do best and planned and organized. Everything.
Chance had a bad prior experience with being trailered. Plus, with his age (31) and past health issues my anxiety was at an all time high. It was recommended that I plan to meet him at the new farm instead of being there for loading. Made sense. I scheduled the vet to be there in case medications were needed. And they scheduled a therapeutic trailering service with a large trailer that had an forward unloading ramp. The horse communicator was also scheduled as she knew of Chance’s past experience and did energy work.
The day arrived. I went to the farm early and wrapped Chance’s legs, brought he and Lucky inside, packed up all my stuff, and met with the horse communicator. She did some grounding exercises with Chance and myself. I left when everyone arrived and went to the new farm and unloaded our stuff. About 1 hour later the phone rang and of course, I thought the worse. Chance refused to load even after 2 rounds of medications. Lucky was on the trailer. They requested I come and try. I drove the 30 minutes back to the farm- praying to everyone and anything- that Chance would load. I read some tips on Google (yes, I’m ashamed to admit, while driving). One article suggested doing groundwork to get the horse to pay attention. For example, stop him, make him stand, back up, etc. Once he was listening that is when you try to load. The article went on to say that anger and frustration would not work. Because a horse is in sync with our emotions. And that physically, a horse has stamina that we as humans do not share. However, mentally the horse will give up quicker. Patience. Kindness. Persistence.
I arrived. I followed the advice of the article. I walked him and gave commands. I was cool, collected, firm, and kind. We tried once. He walked part way up the ramp, stopped, and backed up. Again, I did the commands. Tried once more. Same thing. The third time the lady who was there to Trailer him lightly smacked his butt with a crop and suddenly, he was on the trailer! I couldn’t believe it. We quickly shut the doors and off we went.
The trip was about 45 minutes. And, thankfully, uneventful. The trailering company was amazing and patient. I’m beyond grateful for everyone’s help!
Below is information for trailering issues, how-tos, and professionals that can make the transition 10000% easier and, almost, stress free.
1. True North Equine in Marshall, Virginia
2. Trailering service: Always There Horsecare: 703-915-6255 or http://www.alwaystherehorsecare.com
3. Article: Think like a horse
4. Article: The hard to load horse
5. Article: Lets Get Loaded
I had the opportunity to work with a “horse communicator” today. She was recommended to me by an equine vet who, after reading my blog, felt that I would be open to the idea, and introduced me to her via email. According to the vet, she often works with this particular equine communicator due to her ability to point out exactly where the horse’s issues are, allowing the vet to adjust/manipulate/treat the main issue.
I chatted with her at length a few days ago as she explained the process and we scheduled an appointment.
Today I gave her a call, as she explained, connecting remotely allows for the horse to be in his natural setting without the influence of an unknown person. That way the horse could be relaxed and the owner can observe, ask questions, and engage. So, that is what I did. She went onto explain that sometimes the horse needs energy work in order to open up to the process and that the horse must trust the process, her, and obviously, the owner.
I was asked to have questions ready to ask my horse, along with something I would like to tell him at the end of the session. (If you have been following this blog then you will know I had some difficulty narrowing down a couple of questions- I have a lot! 😉 ) She began connecting with Chance.
I will not be able to convey all the details of what was said, Chance’s reactions, or even mine…It is almost a blur… I wish I could.
I was asked to feel around Chance’s right forehead/eye area for a lump or bump. I did as I was asked and didn’t feel anything abnormal…but remembered he had a gash that was healing right above his right eye. She informed me that he had a “headache”. She continued to move over him and explained that his “energy” was “blocked” on his right side. This makes sense…Chance has a “swagger” at the walk- he pokes his butt to the side and has a twist on the back right leg (Chance’s swagger has gone up and down- it was worse when he had the tendon issues, resolved after stem cell injections, came back when he got EPM, went away ish, and came back with his Lyme). While she was working on his energy, I massaged Chance’s back, neck, hip, and shoulders. She went on to explain that Chance had some right shoulder pain. Thankfully, Chance allowed her to work on his jaw (he pretty much has TMJ), his head, his back, etc. The energy was “pouring out” even on the hind end which, if I recall correctly, is commonly seen on horses with head injuries.
This is where my one question came in…I wanted to know what happened to Chance when he came to my college. I didn’t give many details…I didn’t know many details but I always wondered what may have happened on Chance’s trip down to my college.
I had gone off to college in January and decided to have someone trailer Chance down (about 3 and a 1/2 hours) once I got settled and found a barn, etc. Two months later Chance was arrived at her new barn. Despite the cool March weather, he was covered in sweat and was visibly scared. I didn’t inquire too much since he was in one piece and I chalked up the sweating and fear to exactly that- fear and anxiety. However, as the months progressed, Chance began bucking and rearing while under saddle….this was really strange..When he had left home we were doing dressage and jumping and he was sound and calm. Once again, I chalked it up to being in a new place- a barn that hosted Friday night Bullbucking no less. I decided to switch to a different farm, one preferably without bulls, even though the show was awesome to go and see, and work with a trainer. Still the behaviors persisted and the episodes of lameness increased. The vet finally diagnosed Chance with arthritic changes in his back and suggested I no longer jump him. I decided that summer instead of bringing Chance home and have him endure another long trailer ride, to board him at my new vet’s farm. Chance had the summer to recuperate while under the care of an equine vet.
Anyways, after that summer, I decided to retire Chance for good. I would occasionally get home him to walk around, I still can and do today. But, that was the beginning of a chronic condition that was never given a diagnosis. Instead, Chance’s symptoms were treated as they came.
Back to my session with my very own horse whisperer..
Chance “showed” her what happened on his trip to college- a trailer wheel falling off the side of the road. His head hitting one side of the trailer and slamming the other side. The pain. The concussion. His neck and back becoming misaligned. His jaw coming out of position. His body compensating. He showed the decline of his once functioning body- starting with the hit on his head, to his jaw, and his neck. Down his neck and through his back towards his hips and down his legs. The wear and tear of his body. Chance stated that he is still angry with the person driving the trailer; he wasn’t ready to forgive. I have forgiven them. I have no doubt it was a mistake and that there was no ill intent. But, I am not the one feeling the pain that he is. I am not the one who went from a racehorse to a jumper to practicing dressage to retirement long before I should have. And like the “horse whisperer” said, she will “hold the forgiveness for him until he is ready.” I will do the same.
She spoke of his time on the racetrack. Chance was happy to hear that he was being remembered for who he once was, and will always be to me- a strong, beautiful and crazy talented 17.1 hand red-headed thoroughbred and not a “weak old man” as he put it. When asked what his name was during his time on the track, he said, “Hot Stuff”, which could be a nickname and not his actual race name.
At one point during Chance’s session he fell asleep; standing in an odd way- hind legs spread out. Suddenly, his body gave out and he caught himself from falling. This entire time his eyes were still closed! They remained closed for another minute after this. His body reacting to something, perhaps a shift in his energies, and all the while he was a a state of peace; trusting that nothing bad would happen to him.
The session lasted an hour and a half. Honestly, we could have continued because of all the “blockages” but decided to stop for the day and pick up again another day. I was told that the effects of the energy work or Reiki, would continued throughout the week and that he would be emotionally vulnerable. As the session wrapped up Chance apparently said that he was the lucky one because I found him all those years ago.
Energy Work and Reiki Resources
Head Trauma and Headaches in Horses
Past Treatments Tried
Chance showed decreased movement in his right hip and a audible cracking noise at the suspensory joint. He has edema of both hind fetlocks, Pastern, and Pastern Dermatitis. Chance was unshawed on both hinds due to his inability to stand for long periods of time and his decreased mobility. However, his front adorned clips.
Due to the length of Chance’s front toes and the height of his heels he was unable to evenly distribute his weight (60/40) to his front and hind ends. This would most likely cause increased tension on the DDFT tendons and corresponding ligaments resulting in an increased likelihood of tendon and ligament related injuries. The uneven distribution of weight could also inhibit the horse’s range of motion through his hips resulting in his body compensating for this injury and causing ataxia (balance issues), pain, arthritic changes, and cervical spine misalignment.
By shortening the toe of both front feet, the heel will rise allowing a more even distribution of his weight.
Final Product: Front
Trimmed feet to corrected to the following specifications:
Foot Beginning Angle & Toe Corrected Angles & Toe Total P.C.
L/F 47 Degrees at 3 7/8 inches 53 Degrees at 3 inches 6 Degrees
R/F 45 Degrees at 3 3/4 inches 54 Degrees at 3 inches 9 Degrees
Final Product: Hind
| Return visit to trim and shoe Chance’s hind feet with #2 OBRHB Wedge shoes.Trimmed hind feet and corrected to the following specifications:
Foot Beginning Angle & Toe Corrected Angles & Toe Total P.C.
L/H 48 Degrees at 3 7/8 inches 54 Degrees at 3 1/4 inches 6 Degrees
R/H 46 Degrees at 4 1/4 inches 55 Degrees at 3 1/4 inches 9 Degrees
Note: Chance needed to be sedated by veterinarian to complete the trim and shoe his hind feet due to preexisting hip and DDFT issues.
I have been trying for years to read Chance’s tattoo. Unfortunately, the tattoo was faded even back in 2000 and has become that much more over the years.
I have tried everything I can think of to figure out his tattoo or gain any information that I can about his racing name- video, photos, lots of light, a flashlight, a blue light, red light, asking vets and dentists, emailing his previous owner, the farm where I purchased him, my past trainers, rummaging through my old files…nada!
I have searched for hours on Jockey Club using his markings (white marks on his face and legs, different letter and number combinations based on his age, and different variations of what I thought was his “racing name”). I have even done a guided search that came back with nothing.
Chance’s racing records do not matter in the grand scheme of things…it is more curiosity then anything else. Plus, I think it would be pretty cool to find out more about my guy.
So far all I have is;
Tattoo Number: T_____
Foaling Year: 1990
Head: Patch of white hairs mid to top of eye level
Head Cowlick(s): Median cowlick at top of eye level.
Neck Cowlicks(s): Middle of front of neck
Left Fore Leg: cornet white left side of heel white
Left Hind Leg: none
Right Hind Leg: some white on cornet band
Right Fore Leg: none
Body: top of head off center/right behind right ear small white patch
Other: left foreleg inside firing markings
Chance has always been fighting “scratches” on his back legs. Frustrating, painful, and never seem to completely go away. Could scratches have caused this? My thoughts- scratches allowed bacteria to enter the leg, the infection settled on the DDFT sheath and caused the current flare up. Below is some research I found on possible conditions due to scratches that caused similar symptoms Chance had been experiencing.
CHRONIC PROGRESSIVE LYMPHEDEMA (CPL) due to Scratches
A condition characterized by progressive swelling, hyperkeratosis and fibrosis of distal limbs has been characterized in Shires, Clydesdales and Belgian Draft horses and unfortunately affects numerous horses within these breeds. The disease has also been recognized in Gipsy Vanners; however, only a few horses have been evaluated at this point of time. This chronic progressive disease starts at an early age, progresses throughout the life of the horse and often ends in disfigurement and disability of the legs, which inevitably leads to the horse’s premature death. The pathologic changes and clinical signs closely resemble a condition known in humans as chronic lymphedema or elephantiasis nostras verrucosa. The condition has therefore been referred to as chronic progressive lymphedema (CPL). The lower leg swelling is caused by abnormal functioning of the lymphatic system in the skin, which results in chronic lymphedema (swelling), fibrosis, decreased perfusion, a compromised immune system and subsequent secondary infections of the skin.
The clinical signs of this disease are highly variable. It is often first addressed as a marked and “therapy-resistant” pastern dermatitis (scratches). The earliest lesions, however, are characterized by skin thickening, slight crusting and possible skin folds in the pastern area. While readily palpable, these early lesions are often not appreciated visually as the heavy feathering in these breeds covers these areas. Upon clipping of the lower legs, it becomes obvious that the lesions are far more extensive than expected. Secondary infections develop very easily in these horse’s legs and usually consist of chorioptic mange and/or bacterial infections. Pigmented and non-pigmented skin of the lower legs are affected. Appropriate treatment of the infections (pastern dermatitis) is not successful as underlying poor perfusion, lymphedema and hyperkeratosis in association with the heavy feathering present perfect conditions for repetitive infections with both chorioptic mange as well as bacterial infections. Recurrent infections and inflammation will enhance the lymphedema and hence, the condition becomes more chronic. As a result, the lower leg enlargement becomes permanent and the swelling firm on palpation. More thick skin folds and large, poorly defined, firm nodules develop. The nodules may become quite large and often are described as “golf ball” or even “baseball” in size. Both skin folds and nodules first develop in the back of the pastern area. With progression, they may extend and encircle the entire lower leg. The nodules become a mechanical problem because they interfere with free movement and frequently are injured during exercise. This disease often progresses to include massive secondary infections that produce copious amounts of foul-smelling exudates, generalized illness, debilitation and even death.
Please keep in mind that none of these treatments listed below will “heal” chronic progressive lymphedema (CPL). However, a rigorous management following our suggestions below will assist you to slow down the process and even make some of the nodular lesions disappear. Your horse will need this management the rest of its life.
• Clipping of the feathers
Long and dense feathering makes management of lymphedema more difficult. We highly recommend clipping the feathers and keep them short, if horses are not presented at shows. If you have a show horse, we still recommend to clip the feathers to initiate a rigorous treatment. As the skin condition improves and the edema is reducing – you may have a better chance to keep the horse’s legs in better condition by. careful repetitive treatment, while the feathering is growing back. The feathers are usually back to their original length in about 10-12 months.
• Treatment of skin infections
Progression of lymphedema is also associated with deposition of fibrous tissue and formation of fibrotic nodules.. As a result, these horses have a poor blood circulation and immune response in the skin of their legs. They tend to built up a thick keratin layer. The long feathering further occludes the skin surface, which then remains humid. These factors provide the perfect culture environment for infectious pathogens. This explains why horses with CPL constantly battle recurrent infections with mites (Chorioptic mange) and bacterial infections (Staphylococcus, Dermatophilus).
Horses with CPL should consistently be treated against reinfestation of mites and bacteria:
• Careful washing, cleaning and drying of the legs on a routine basis is essential. Horses with long feathering may require blow-drying of their legs. We recommend using a product manufactured by HydroSurge Inc. ( http://www.hydrosurge.com ) called Apricot Sulfur Skin Treatment Shampoo.
• Frontline spray to treat chorioptic mange (do not use Frontline on pregnant and nursing mares)
• The best and most economical topical treatment is to find a source of wettable sulfur powder (“flowers of sulfur”). This can usually be found through a vineyard supply or at your local nursery (certain “rose dust” preparations). Mix this powder with mineral oil in to form a creamy paste. You can mix a moderate amount in a plastic lidded container or glass jar so that you have enough to last 2-4 weeks at a time. Apply this mixture to the ulcerated and/or affected areas of skin daily. This preparation is the best and most economical topical treatment we have found. You can use it indefinitely. Sulfur is safe to use in pregnant mares.
Systemic antiparasitic treatment: Frequent ivermectine treatment will also assist to keep the mites away.
Regular exercise is crucial. It will increase the circulation and the lymph drainage.
• Manual Lymph-drainage
Manual lymph-drainage is regularly used in humans with lymphedema as long as there is no inflammation present within the tissue. MLD has been successfully used in horses with more acute lymphedema, but has not been established yet in horses with progressed CPL. A massaging coldwater stream may assist a massage. It is important to dry the skin before applying anything else after massage and rinsing. If the feathers were not clipped this may take a long time and you may have to use a hair dryer. Your horse may become more compliant to this treatment as swelling reduces over time
• Bandaging and stockings
We have some limited experience with using special bandages developed for people with lymphedema. For horses, which always move around, “short-stretch” bandages should be used (example: Rosidal ®). Short stretch bandages have been successfully used in three horses with clipped feathering; but bandaging was not as successful on horses with long feathers. Of course it is crucial to have very good padding and keeping the bandages fairly tight. If tolerated, the best results will be achieved by keeping the bandages on 24/7. Of course they need to be redone at least every other day – better every day to control the legs. At first, there will be oozing from the lymphedema through the skin – so the bandages will get wet and have to be changed every day. With the reduction of the edema – this will stop. If the horse is only walked quietly the bandages can be left on for the exercise; very likely the legs have to be rewrapped after the exercise as the swelling will somewhat reduce. For more exercise it may be better to take the bandages off, use working bandages and then switch back to the short–stretch bandages after work. Again make sure the skin is dry when you rewrap.
After the edema has been reduced by using bandages – stockings are used for people to maintain avoid recurrence of lympedema. The use of such stockings in horses are currently under investigation.
It should be noted that horses suffering from CPL often are susceptible to reapeated bouts of “Thrush”. Consequently, thorough and routine foot trimming care is an essential part of the health care management for these horses.
After I left the barn, I drove home and went straight to my computer.
What was happening? What are the masses? Scar tissue? Nothing was able to be extracted out of them…How can I get rid of them in order to see behind them?
Again, I stayed up until the sun came out the next morning. I already had two binders full of research and now I had a third.
Research made me believe that C has an infection in the Synovial Tendon Sheath that was being masked by the masses on the outer lining of the SS. The masses could be scar tissue from his MANY past Lymphangitis flare-ups. Perhaps, his immune system was not able to fight last attack and the infection settled in the SS and was walled off. Thus his CBC & WBC were normal and no fluid was extracted from SS masses due to the large size of the scar tissue.
C has a major hx with his RH and “flare-ups” and lameness. I never realized this until I took the time to study his past records from the first 5 years I owned him.
Symptoms are similar to an infection- what if we proceeded as if it were?
Lack of a positive culture does NOT mean that there is not an infection in the sheath!
1. Swelling decreases after being active
2. Fails to extend fetlock
3. Lame- exasperated by flexion
4. Positioning for fetlock flexion
Septic Synovitis: Cartilage degradation ischemia, Fibrin deposition lead to lameness to pannus form and adhesive form
Most common is Staph
Systematic Procaine Penicillin 22000 iU/kg or Sodium Benzyl Penicillin & Gentamicin 6.6 mg/kg for 2-9 days
Then change to oral potentiated sulfonamides 5mg.kg Trimethoprim and 25 mg/kg of Sulphadiazine
Other potassium penicillin w/ Amikacin Cectiofur or Enrofloxacin
IV antibiotics for 7-10 days switch to oral for 2 weeks
Regional limb profusion or placement of impregnated Polymethyylmethacralate or PMMA
I immediately called Vet4 and told him my theory. He said that it was possible and that we should begin treatment asap. He was still out of town so I called Vet3 to order Baytril. Vet3 felt my theory was legit and immediately ordered the antibiotic!