Electroarthrography to Predict Cartilage Quality

Article by Jackie Zions interviewing Dr. Adele Changoor and Dr. Judith Koenig

Researchers from the Ontario Veterinary College (OVC) and University of Toronto are developing a novel method to measure the quality of cartilage in horses using electroarthrography (EAG). EAG is a non-invasive technique that uses electrodes attached to the skin around a joint to detect electrical signals produced by the cartilage when it is loaded.

Dr. Adele Changoor, from the University of Toronto and Lunenfeld Tanenbaum Research Institute, and Ontario Veterinary College researcher Dr. Judith Koenig from the department of Clinical Studies, explain how EAG works and why it may become very useful for predicting cartilage quality and diagnosing osteoarthritis and other degenerative joints diseases in horses.

EAG is analogous to electrocardiography (ECG), which measures the electrical activity of the heart. Cartilage produces electrical signals during loading and these signals reflect its biomechanical properties, such as stiffness and permeability. 

“By measuring EAG signals, we can get an idea of how healthy the cartilage is,” said Changoor.

Healthy cartilage ensures joints can move without pain and has an important role preventing wear and tear on bone.  

Currently, there are no readily available tools to assess cartilage quality in horses with the exception of diagnostic arthroscopy – a minimal invasive surgery – under general anesthesia. X-rays and ultrasound are not sensitive enough to detect cartilage changes, and magnetic resonance imaging (MRI) is expensive, requires anesthesia and is often difficult to access. EAG offers a potential alternative that is fast, easy, and affordable.

“EAG is a promising tool for detecting cartilage damage early allowing intervention with treatments that can slow down or prevent further deterioration of the joint,” says Koenig “EAG could also help us monitor the effectiveness of treatments over time.”

EAG measurements were collected at the same time as the center of pressure (COP), which measures the distribution of force under the horse’s hoof when it stands or walks. 

“EAG is really tied directly to cartilage biomechanical properties,” says Changoor.   “We also needed to know about the joint biomechanics in order to interpret EAG properly.”  A custom, portable, force mat was developed by Dr. Changoor’s graduate students that included an array of force sensors to place under the horse’s hoof when measuring EAG. 

“Then we can measure how much compressive force or ground reaction force is being exerted on that joint” said Changoor.  “COP, is where the ground reaction force is acting.  The ground reaction force gives us the total load on the joint.  COP lets us figure out where on the hoof or where on the joint surface force is being concentrated.”

COP provides information about the joint biomechanics and the horse’s balance and stability.  EAG and COP testing were combined to get a comprehensive picture of the joint health and function in horses with osteoarthritis.  Results were compared with MRI imaging and it was found that EAG and COP testing correlated well with MRI and could detect differences in cartilage quality between healthy and osteoarthritic joints.

In the 2023 study involving horses with osteoarthritis in the fetlock joint; the horses were treated with MSCs to decrease inflammation and stimulate tissue healing. The researchers measured EAG, COP, and MRI before and after the treatment to evaluate its impact on cartilage quality.

“We observed that MSCs improved cartilage quality in some horses and EAG and COP testing were able to capture these changes and show the responses to treatment. This suggests that EAG and COP testing could be useful for selecting treatment options for the horse,” says Dr. Koenig.  “One of the biggest advantages of EAG is that it seems to correspond with our arthroscopic findings. It can perhaps evaluate the quality of the cartilage or cartilage defects, which we are at the moment only able to evaluate with arthroscopy.”

The researchers plan to conduct further studies in order to validate and refine EAG and COP testing for predicting cartilage quality in equines. They hope that these techniques will become widely available and accessible for veterinarians and horse owners in the future.

“This is an exciting and innovative research project that has the potential to improve the diagnosis and early management of osteoarthritis in horses,” says Dr. Koenig  “Osteoarthritis is a major health and welfare issue for horses and their owners, and we need better tools to detect it early and treat it. EAG and COP testing could provide a simple, affordable, and accurate way to assess cartilage quality and joint function in horses.”

Many thanks go to the graduate students who worked tirelessly on the EAG study:  Peter Suderman, PhD Candidate in the Department of Materials Science & Engineering at U of T, Jaylon Pascual, undergraduate co-op student finishing her fourth year in the Biomedical Engineering program at U of G, Dr Rodrigo Munevar Luque, Equine Sports Medicine Resident at OVC and PhD Candidate Biomedical Sciences  at U of G, Undergraduate Research Assistants in Clinical Studies Ashley Nixon, DVM 25 (OVC) , Pjotr Roest DVM 26 (OVC), and in Biomedical Sciences Axel Koenig Parris HBA 25 (Ivey School of Business, Western University) and Rebecca Mullin BSc OVC 25.

The study was funded by the Equine Guelph Research Fund and the Natural Sciences and Engineering Research Council of Canada (NSERC). 

The value of good hoof balance and how to evaluate this alongside your farrier

Article by Adam Jackson MRCVS

Introduction

The equine foot is a unique structure and a remarkable feat of natural engineering that follows the laws of biomechanics in order to efficiently and effectively disperse concussional forces that occur during the locomotion of the horse.  Hoof balance has been a term used by veterinarians and farriers to describe the ideal conformation, size and shape of the hoof relative to the limb.  

Before horses were domesticated, they evolved and adapted to survive without any human intervention. With respect to their hoof maintenance, excess hoof growth was worn away due to the varied terrain in their habitat.  No trimming and shoeing were required as the hoof was kept at a healthy length.

With the domestication of the horse and our continued breeding to achieve satisfactory performance and temperament, the need to manage the horse’s hoof became essential in order to ensure soundness and performance.  The horse’s foot has evolved to ensure the health and soundness of the horse; therefore, every structure of the foot has an essential role and purpose. A strong working knowledge of the biology and biomechanics of the horse’s foot is essential for the veterinarian and farrier to implement appropriate farriery.  It was soon concluded that a well-balanced foot, which entails symmetry in shape and size, is essential to achieve a sound and healthy horse.  

Anatomy and function of the foot

The equine foot is extremely complex and consists of many parts that work simultaneously allowing the horse to be sound and cope with the various terrains and disciplines.    Considering the size and weight of the horse relative to the size of the hoof, it is remarkable what nature has engineered.  Being a small structure, the hooves can support so much weight and endure a great deal of force.  At walk, the horse places ½ of its body weight through its limbs and 2 ½ its weight when galloping.  The structure of the equine foot provides protection, weight bearing, traction, and concussional absorption.  Well-balanced feet efficiently and effectively use all of the structures of the foot to disperse the forces of locomotion. In order to keep those feet healthy for a sound horse, understanding the anatomy is paramount.   

The foot consists of the distal end of the second phalanx (short pastern), the distal phalanx (pedal bone, coffin bone) and the navicular bone.  The distal interphalangeal joint (coffin joint) is found between the pedal and short pastern bone and includes the navicular bone with the deep digital flexor tendon supporting this joint.  This coffin joint is the center of articulation over which the entire limb rotates.  The navicular bone and bursa sits behind the coffin bone and is stabilized by multiple small ligaments. The navicular bone allows the deep digital flexor tendon to run smoothly and change direction in order to insert into the coffin bone.   The navicular bursa is a fluid-filled sac that sits between the navicular bone and the deep digital flexor tendon.

The hoof complex can be divided into the epidermal weight-bearing structures that include the sole, frog, heel, bulbs, bars, and hoof wall and the anti-concussive structures that include the digital cushion, lamina, deep digital flexor tendons, and ungual (lateral) cartilage.  The hoof wall encloses the dermal structures with its thickest part at the toe that decreases in thickness as it approaches the heel.  The hoof wall is composed of viscoelastic material that allows it to deform and return its shape in order to absorb concussional forces of movement.  There is enough deformation to diminish the force from the impact and load of the foot while preventing any damage to the internal structures of the foot and limb.  As load is placed on the foot, there is deformation that consists of:

• Expansion of the heels

• Sinking of the heels

• Inward movement of the dorsal wall

• Biaxial compression of the dorsal wall

• Depression of the coronary band

• Flattening of the sole

The hoof wall, bars and their association with the sole form the heel base with the purposes of providing traction, bearing the horse’s weight while allowing the stability and flexibility for the expansion of the hoof capsule that dissipates concussional forces on foot fall.  The sole is a highly keratinized structure like the hoof wall but made up of nearly 33% water so it is softer than the hoof wall and should be concave to allow the flattening of the sole on load application. The frog and heel bulbs serve a variety of special functions ranging from traction, protection, coordination, proprioception, shock absorption and the circulation of blood.  

When the foot lands on the ground, the elastic, blood-filled frog helps disperse some of the force away from the bones and joints, thus, acting as a shock absorber.  The venous plexus above the frog is involved in pumping blood from the foot back to the heart when the foot is loaded.  In addition, there is shielding of the deep digital flexor tendon and the sensitive digital cushion (soft tissue beneath the sole that separates the frog and the heel bulb from the underlying tendons and bones).  Like the heel bulbs, the frog has many sensory nerve endings allowing the horse to be aware of where his body and feet are and allows the horse to alter landing according to the condition of the ground (proprioception and coordination).  

The soft tissue structures comprise and form the palmar/plantar aspect of the foot.  The digital cushion lies between the lateral cartilages and above the frog and bars of the horse’s hoof.  This structure is composed of collagen, fibrocartilage, adipose tissue and elastic fiber bundles.  The digital cushion plays a role in shock absorption when the foot is loaded as well as a blood pumping mechanism.  Interestingly, it has been found that the digital cushion composition varies across and within breeds.  It is thought the variation of the composition of the digital cushion is partially dictated by a genetic predisposition.  In addition, the composition of the digital cushion changes with age.  As the horse ages the composition alters from elastic, fat and isolated collagen bundles to a stronger fibrocartilage.  Finally, the digital cushion and connective tissue within the foot have the ability to adapt to various external stimuli such as ground contact or body weight.   The lateral cartilage is a flexible sheet of fibrocartilage that suspends the pedal bone as well as acting as a spring to store and release energy. The lamina is a highly critical structure for hoof health.  The lamina lies between the hoof wall and the coffin bone.  There are two types of lamina known as the sensitive (dermal) lamina and insensitive (epidermal) lamina.  The insensitive lamina coming in from the hoof wall connects to the sensitive lamina layer that is attached to the coffin bone and these two types of lamina interdigitate with each other to form a bond.

Hoof and Musculoskeletal System

The hoof and the musculoskeletal system are closely linked and this is particularly observed in the posture of the horse when resting or moving.  Hoof shape and size and whether they are balanced directly affects the posture of the horse.  Ultimately, this posture will also affect the loads placed on the skeletal system, which affects bone remodeling. With an imbalance, bone pathologies of the limbs, spine and pelvis may occur such as osteoarthritis.  In addition, foot imbalances result in postural changes that lead to stress to the soft tissue structures that may lead to muscle injuries and/or tendon/ligament injuries.  

Conformation and hoof balance 

The terms balance and conformation are used frequently and used to describe the shape and size of the limb as a whole as well as the individual components of the limb and the spatial relations between them.  Balance is the term often used to describe the foot and can be viewed as a subset of conformation.  

Conformation should be considered when describing the static relations within the limb and excludes the foot.  Balance should be considered when describing the dynamic and static relationship between the horse’s foot and the ground and limb as well as within the hoof itself.  

These distinctions between conformation and balance are important to assess lameness and performance of the horse.  Additionally, this allows the veterinarian and farrier to find optimal balance for any given conformation.

The term hoof balance does lack an intrinsic definition.  The use of certain principles in order to define hoof balance, which in turn can be extended to have consistent evaluation of hoof balance as well as guide the trimming and shoeing regimens for each individual horse.  In addition, these principles can be used to improve hoof capsule distortion, modify hoof conformation and alter landing patterns of the foot.  These principles are:

• Evaluate hoof-pastern axis

• Evaluate center of articulation

• The need for the heels to extend to the base of the frog

Assessing the horse’s foot balance by observing both static (geometric) balance and dynamic balance is vital.   Static balance is the balance of the foot as it sits on a level, clean, hard surface.  Dynamic balance is assessing the foot balance as the foot is in motion.  However, horses normally do not resemble the textbook examples of perfect conformation, which creates challenges for the farriers and veterinary surgeons.  The veterinarian should instigate further evaluation of the foot balance and any other ailments, in order to provide information that can be used by the farrier and veterinarian in formulating a strategy to help with the horse’s foot balance. With the farrier and veterinarian working cooperatively, the assessment of the hoof balance and shoeing of the foot should deliver a harmonious relationship between the horse’s limb, the hoof and the shoe.  

Dynamic Balance

The horse should be assessed in motion as one can observe the foot landing and placement.  A balanced foot when in motion should land symmetrically and flat when moving on a flat surface.  When viewed from the side, the heels and toe should land concurrently (flat foot landing) or even a slight heel first landing.  It is undesirable to have the toe landing first and often suggests pain localized to the heel region of the foot.  When observing the horse from the front and behind, both heel bulbs should land at the same time.  Sometimes, horses will land first slightly on the outside or lateral heel bulb of the foot but rarely will a horse land normally on the medial (inside) of the foot.  If the horse has no conformational abnormalities or pathologies the static balance will achieve the dynamic balance.  

Static Balance 

Hoof –pastern axis (HPA)

The hoof pastern axis (HPA) is a helpful guideline in assessing foot balance. With the horse standing square on a hard, level surface, a line drawn through the pastern and hoof should be parallel to the dorsal hoof wall and should be straight (unbroken).  The heel and toe angle should be within 5 degrees of each other. An underrun heel has been defined as the angle of the heel being 5 degrees less than the toe angle. The heel wall length should be roughly 1/3 of the dorsal wall.  In addition, the cannon (metacarpus/metatarsus) bone is perpendicular to the ground and when observed from the lateral side, the HPA should be a straight line.  When assessing the foot from the side, the dorsal hoof wall should be aligned with the pastern.  The optimal angle of the dorsal hoof wall is often cited as being 50-54°. The length of the dorsal hoof wall is variable but guidelines have been suggested according to the weight of the horse. 

It is not uncommon that the hind feet are more upright compared to the fore feet at approximately 5 degrees.  A broken hoof-pastern axis is the most common hoof imbalance.  There are two presentations of a broken HPA known as a broken-back HPA and a broken-forward HPA.  These changes in HPA are often associated with two common hoof capsule distortions that include low or underrun heels and the upright or clubfoot, respectively.    

A broken-back hoof-pastern axis occurs when the angle of the dorsal hoof wall is lower than the angle of the dorsal pastern.  This presentation is commonly caused by low or underrun heel foot conformation accompanied with a long toe.  This foot imbalance is common and often thought to be normal with one study finding it present in 52% of the horse population.  With a low hoof angle, there is an extension of the coffin and pastern joints resulting in a delayed breakover and the heels bearing more of the horse's weight, which ultimately leads to excess stress in the deep digital flexor tendon as well as the structures around the navicular region including the bone itself.  

This leads to caudal foot pain so the horse lands toe first causing subsolar bruising.  In addition, this foot imbalance can contribute to chronic heel pain (bruising), quarter and heel cracks, coffin joint inflammation and caudal foot pain (navicular syndrome).   The cause of underrun heels is multifactorial with a possibility of a genetic predisposition where they may have or may acquire the same foot conformation as the parents.  There are also environmental factors such as excessive dryness or moisture that may lead to the imbalance.

A broken-forward hoof-pastern axis occurs at a high hoof angle with the angle of the dorsal hoof wall being higher than the dorsal pastern angle.  One can distinguish between a broken-forward HPA and a clubfoot with the use of radiographs.  With this foot imbalance, the heels grow long, which causes the bypassing of the soft tissue structures in the palmar/plantar area of the foot and leads to greater concussional forces on the bone.  This foot imbalance promotes the landing of the toe first and leads to coffin joint flexion as well as increases heel pressure.  The resulting pathologies that may occur are solar bruising, increased strain of the suspensory ligaments near the navicular bone and coffin joint inflammation.

Center of articulation

When the limb is viewed laterally, the center of articulation is determined with a vertical line drawn from the center of the lateral condyle of the short pastern to the ground.  This line should bisect the middle of the foot at the widest part of the foot and demonstrates the center of articulation of the coffin joint.  The widest part of the foot (colloquially known as “Ducketts Bridge”) is the one point on the sole that remains constant despite the shape and size of the foot.  The distance and force on either side of the line drawn through the widest part of the foot should be equal, which provides biomechanical efficiency.    

Heels extending to the base of the frog

With respect to hoof balance, another component of the foot to assess is that the heels of the hoof capsule extend to the base of the frog.  The hoof capsule consists of the pedal bone occupying two-thirds of the space and one-third of the space is soft tissue structures. This area is involved in dissipating the concussional and loading forces and in order to ensure biomechanical efficiency both the bone and soft-tissue structures need to be enclosed in the hoof capsule in the same plane. 

To achieve this goal the hoof wall at the heels must extend to the base of the frog.  If the heels are allowed to migrate toward the center of the foot or left too long then the function of the soft tissue structures have been transferred to the bones, which is undesirable.  If there is a limited amount to trim in the heels or a small amount of soft tissue mass is present in the palmar foot then some form of farriery is needed to extend the base of the frog (such as an extension of the branch of a shoe).    

Medio-lateral or latero-medial balance 

The medio-lateral balance is assessed by viewing the foot from the front and behind as well as from above with the foot raised.   To determine if the foot has medio-lateral balance, the hoof should be bisected or a line is drawn down the middle of the pastern down to the point of the toe.  

You should be able to visualize the same amount of hoof on both the left and right of that midline.  In addition, one should observe the same angle to the side of the hoof wall.  It is important to pick up the foot and look at the bottom.  Draw a line from the middle quarter (widest part of foot) on one side to the other then draw a line from the middle of the toe to the middle sulcus of the frog.  

This provides four quadrants with all quadrants being relatively the same in size (Proportions between 40/60 to 60/40 have been described as acceptable for the barefoot and are dependent on the hoof slope).  The frog width should be 50-60% of its length with a wide and shallow central sulcus.  The frog should be thick enough to be a part of the bearing surface of the foot.  The bars should be straight and not fold to the mid frog.  The sole should be concave and the intersection point of both lines should be the area of optimal biomechanical efficiency.  

The less concavity means the bone is nearer to the ground, thus, bearing greater concussional force.  Finally, assess the lateral and medial heel length.  Look down at the heel to determine the balance in the length of both heel bulbs.  Each heel bulb should be the same size and height.  If there are any irregularities with the heel bulbs then sheared heels may result, which is a painful condition.  Medio-lateral foot imbalance results in the uneven loading of the foot that leads to an accumulation of damage to the structures of the foot ultimately causing inflammation, pain, injury and lameness.   Soles vary in thickness but a uniform sole depth of 15mm is believed to be the minimum necessary for protection.  

Dorso-palmar/plantar (front to back – DP) balance

Refers to the overall hoof angle and the alignment of the hoof angle with the pastern angle when the cannon bone is perpendicular to the ground surface.  When assessing the foot from the side, the dorsal hoof wall should be aligned with the pastern.  The optimal angle of the dorsal hoof wall is often cited as being 50-54°.  The length of the dorsal hoof wall is variable but guidelines have been suggested according to the weight of the horse. 

The heel and toe angle should be within 5 degrees of each other. An underrun heel has been defined as the angle of the heel being 5 degrees less than the toe angle. The heel wall length should be roughly 1/3 of the dorsal wall.  

A line dropped from the first third of the coronet should bisect the base.  A vertical line that bisects the 3rd metacarpal bone should intersect the ground at the palmar aspect of the heels.

Radiographs

A useful way to assess trimming and foot balance is by having foot x-rays performed.  Radiography is the only thorough and conclusive method that allows one to determine if the foot is not balanced and the bony column (HPA) is aligned. 

Shoes should be removed and the foot cleaned before radiographs are executed.  The horse is often placed on foot blocks to elevate the feet off the ground so that the foot can be centered in the cassette and x-ray beam.  

Latero-medial view – The side view of the foot allows one to assess the dorsal and palmar aspects of the pedal bone as well as the navicular bone.  The horse should be standing squarely on a flat, level surface.  This projection is useful in determining the point of breakover and the hoof pastern axis should be parallel with the hoof wall.  The lateral view will demonstrate the length of the toe and the alignment of the dorsal surface of the pedal bone with the hoof wall, which should be parallel.  This view also allows one to determine the depth of the sole and inadequate solar depth is usually accompanied with excessive toe length (broken-back HPA). One may observe a clubfoot, broken forward.  

One can distinguish between a clubfoot and a broken-forward HPA with radiographs.  The broken-forward HPA the hoof angle of the heel is greater than the angle of the dorsal hoof wall.  The clubfoot also demonstrates these steep/high hoof angles but additionally the alignment of the coffin, short and long pastern bones are broken forward.

Dorsopalmar/plantar views - this “front to back” view is also performed with the horse standing squarely on 2 positioning blocks.  This projection allows the evaluation of medial to lateral balance and conformation of the foot with observation and measurement of the medial and lateral wall length and angle.  Horses with satisfactory conformation present with a parallel joint surface of the pedal bone to the ground.  The coffin joint should be even across its width.  In addition, the lateral and medial coronet and the lateral and medial walls are of equal thickness and the distance from the lateral and medial solar margins to the ground are similar. 

With foot imbalance, this author has observed that fore feet may have a higher lateral hoof wall, whereas, the hind feet may have a higher medial hoof wall.  It is worth noting that the pelvis, stifle and hocks are adapted to move laterally allowing a slight rotating action as it moves.  This action may cause uneven wear or poor trimming and shoeing may cause this limb movement to be out of line.  

Trimming

Often, trimming and shoeing are based on empirical experience that includes theoretical assumptions and aesthetic decisions.   The goals of trimming and shoeing are to facilitate breakover, ensure solar protection and provide heel support.  Trimming is the most important aspect of farriery because it creates the base to which a shoe is fitted.  Hoof conformation takes into account the function and shape of the foot in relation to the ground and lower limb both at rest and exercise.  Each individual foot should have a conformation that provides protection and strength while maximizing biomechanical efficiency often viewed as foot balance. 

An important question that initially needs to be addressed is whether the horse requires shoes or not.  The answer does depend on what type of work the horse performs, what is the amount of workload, the conformation of the horse (especially the limbs and foot) and are there any previous or current injuries.  It must be stressed that the most important aspect, whether the horse is shod or not, is that the trim ensures an appropriately balanced foot for the horse. If there is poor trimming then this may lead to uneven and increased workload on the limb leading to an increased strain of the hoof and soft tissues (i.e. ligaments, tendons) that increase the risk of injury and developing acute and chronic lameness. 

The foot can be evaluated, trimmed and/or shod in a consistent, reproducible manner that considers:

1. Hoof-pastern axis (HPA)

2. The center of articulation

3. Heels extending to the base of the frog

Appropriate trimming and shoeing to ensure the base of the foot is under the lateral cartilage; therefore, maximizing the use of the digital cushion, can help in creating a highly effective haemodynamic mechanism.  Shoeing must be done that allows full functionality of the foot so that load and concessional forces are dissipated effectively.  

To implement appropriate farriery, initially observe the horse standing square on a hard service to confirm that the HPA is parallel.  If The HPA is broken forward or backward then these balances should be part of the trimming plan.  To determine the location of the center of rotation, palpate the dorsal and palmar aspect of the short pastern just above the coronary band and a line dropped vertically from the center of that line should correlate with the widest part of the foot. 

Shoeing

When the shoe is placed on the horse, the horse is no longer standing on its feet but on the shoe; therefore, shoeing is an extension of the trim.  The shoe must complement  the trim and must have the same biomechanical landmarks to ensure good foot balance.  It is this author’s view that the shoe should be the lightest and simplest possible.  The shoe must be placed central to the widest part of the foot and the distance from the breakover point to the widest part of the foot should be equal to the distance between the widest part of the foot and the heel. 

It has been shown that the use of shoes that lift the sole, frog and bars can reduce the efficient workings of the caudal foot and may lead to the prevalence of weak feet.  A study by Roepstorff demonstrated there was a reduced expansion and contraction of the shod foot but improved functionality of solar and frog support.   With this information, appropriate shoeing should allow increased functionality of the digital cushion, frog and bars of the foot, which improves the morphology and health of the hoof and reduces the risk of exceeding the hoof elasticity.  

Disease associated with hoof imbalance

As seen in the figure above, foot imbalance can lead to multiple ailments and pathologies in the horse.  It must be noted that the pathologies that may result are not necessarily exclusive for the foot but may expand to other components to the horse’s musculoskeletal system.  In addition, not one but multiple pathologies may result.  Diseases that may result from hoof imbalance are:

Conclusion

Foot balance is essential for your horse to lead a healthy and sound life and career. With a strong understanding of the horse anatomy and how foot imbalance can lead to lameness as well as other musculoskeletal ailments, one can work to assess and alter foot balance in order to ensure optimal performance and wellbeing of the horse.  It is essential that there is a team approach involving all stakeholders as well as the veterinarian and farrier in order to achieve foot balance. With focus on foot balance, one can make a good horse into a great horse.

Gut issue biomarkers and their use in signalling dysbiosis

Article by Jackie Zions

Gastrointestinal issues (GI) are the number one cause of morbidity in horses other than old age.   An unhealthy digestive system can cause poor performance, pain, discomfort, diarrhea, and a whole host of issues that can sideline your horse.  It’s no wonder researchers are paying close attention to the ‘second brain’ and it’s billions of inhabitants.  Ontario Veterinary College (OVC) researcher, Dr. Luis Arroyo has been studying the equine gastrointestinal systems for many years with several research projects receiving funding from Equine Guelph.  Arroyo discusses what we know about equine gut health, causes of GI disorders and the extensive continuing research to understand what unstable and stable gut populations look like.

Starting with some basic anatomy Arroyo says, “The gastrointestinal tract of a horse is extremely large, and there are many things that can cause disturbances to the normal functioning or health of the gut.”  A healthy gut microbiome is essential for the horse’s entire body to function optimally.

Signs of GI issues

Common signs of disorders could include abdominal pain, bloating, changes in fecal consistency (including diarrhea or constipation), excessive drooling, decrease in water consumption, lack of or poor appetite, weight loss and low body condition score.  

“Some cases are more obvious to owners,” says Arroyo, “like poor performance, or acute or chronic diarrhea.” 

Changes of behaviour such as becoming cranky or moody can be tell-tale signs there is unrest in the GI system.  Biting at the flanks can signal abdominal pain as well as reactivity to being saddled.  When the horse stops wanting to perform and athletic abilities suddenly decline, if there is no obvious lameness, GI issues are high among the considerations.

“Horses are herbivores, designed to consume a diet of forage, and to break down complex sugars within that forage.” says Arroyo.  “The gut microbiota does this job and is very important for healthy digestion.”  Recent research is connecting the changes in diversity of microbial communities to conditions like colic, colitis, and gastric ulcers.

Causes of GI Issues

Colic is the number one clinical condition occurring in horses.  It is well-known that sudden dietary changes can be a major contributor as well as diets that are high in grain.  This can create changes in the volatile fatty acids produced in the GI system, which in turn can lead to the development of gas colic.  Arroyo provides the example of switching from dry hay fed in the winter, too rich, lush, spring grass as a big cause of rapid fermentation that can cause colic.  

Any abrupt change, even if it’s a good quality feed to a different good quality feed, can be a source of colic.  Then there is the more obvious consumption of moldy, poor, quality hay.  So not only the quality but the transition/adaptation period needs to be considered when making feed changes and this goes for both changes to forage or concentrates.

A table of feed transition periods on the Equine Guelph website states an adaptation period of at least 10 – 14 days is recommended.  Transition periods under seven days can increase colic risk over 22 times! 

“Decrease in water consumption can be an issue, especially in countries with seasons,” says Arroyo.  When water gets really cold, horses often drink less, and if it freezes, they don’t drink at all, which can lead to impaction colic.   Parasite burden can also cause colic. If your horse lives in a sandy environment, like California, ingesting sand can cause impaction colic.  

Non-steroidal anti-inflammatory drugs (NSAIDS) can cause colic or ulcers. NSAIDS can interfere with blood supply to the GI tract causing ulceration, for example in the mucosa of the stomach. Prolonged use can cause quite severe ulceration.

NSAIDS are not the only drugs that can contribute to GI issues.  “Antibiotics - as the name says - kill many kinds of bacteria,” says Arroyo. “They are designed for that!  Invariably they deplete some bacterial populations including in the intestine, and that is a problem because that may allow some other bacteria, potentially pathogenic or harmful, to overgrow, and that can cause dysbiosis.”  
In a recent study, by fellow OVC researcher, Dr. Gomez and co-workers, it was determined that damage to the intestinal microbiota could occur after only 5 days of administering antibiotics to horses.  Damage to the intestinal microbiota resembled dysbiosis that can potentially result in intestinal inflammation and colitis predisposing the horse to diarrhea.  Judicious use of antibiotics and antimicrobials are advised.

There are infectious and non-infectious causes of colitis.  Infectious examples include salmonella and then there is Neorickettsia risticii, which if ingested from contaminated sources, can cause Salmonellosis or Potomac horse fever, respectively.

“Any stress factors such as transportation, fasting or intense exercise like racing, can be a factor for developing stomach ulcers,” says Arroyo.  

Current Diagnostics

Putting together a picture of the horse’s health status includes gathering clinical history from the horse owner and performing a physical examination for motility and hydration status. A biochemistry profile and complete set count can be gathered from blood testing.

Gastric ultrasound allows veterinarians to view the wall of the intestine, noting if it has thickened or distended, which could occur in cases when there is colic.  They can assess appearance and find out if the intestine is displaced or if there is a twist.  Gastroscopy is commonly used to find ulcers in the stomach and can reach as far as the first part of the duodenum. 

GI Research

“DNA sequencing has been a breakthrough in science in terms of understanding the communities of different microorganisms living in many different niches from the skin to the lungs to the upper airways to the intestine,”  says Arroyo.

It has allowed in-depth study of the population of microorganisms, providing a big picture of the different inhabitants in various areas of the GI tract, such as the lumen of the small intestine and the small and large colon.  “The microorganisms vary, and they have different functions in each compartment,” says Arroyo.  

DNA sequencing has allowed researchers to study microbial populations and gather information on what happens to bacterial communities when impacted by diseases like colitis.  “We can see who is down, and who is up,” explains Arroyo, “and determine what populations have been depleted.”  It has led to a better knowledge of which of the billions of factors are harmful to the system and which can compromise the health of the horse.

Robo-gut is one example of a fantastic system where bacterial communities are being replicated in the lab to mimic what would be found in a natural environment.  

Researchers at the University of Guelph have measured metabolic profiles of the bacterial population after the addition of supplements like probiotics and prebiotics.  They found they can dramatically change the metabolites that are being produced, according to what is being added to the system.

Exciting new research that could impact the future of diagnostics includes screening for biomarkers as indicators of intestinal health among equine microbiota.  Dr. Arroyo is currently working with research partner, Dr. Marcio Costa, from the University of Montreal, looking for biomarkers that indicate changes in the inhabitants of the equine gut that take place during the early onset of illness.

“A biomarker is a biological molecule that you can find in different places,” explains Arroyo.  “For example, you might find them in tissue, blood, urine, or different body fluids.  They can signal normal or abnormal processes or could reveal a marker of a disease.  For example, a biomarker can be used to see how well the body might respond to a treatment or to a disease condition.”

“The objective of a dysbiosis index is quantifying ‘X’ number of certain bacteria that are important to us,” says Arroyo.  In this case, the dysbiosis derives from sequencing of the bacterial population in fecal samples.  

Changes in the intestinal microbiota (dysbiosis) are present before and during the outset of diseases and after treatment with antibiotics.  Arroyo cites the example of decreased Lachnospiraceae commonly observed when there is intestinal inflammation.  

Bacterial biomarkers are currently being used in other species to accurately predict intestinal dysbiosis, for example in cats and dogs.  One canine study quantified the number of seven different taxa of importance of the total bacterial populations.  This information is entered into a mathematical algorithm that comes up with results explaining which bacteria have increased or decreased.  Based on those numbers, one can use a more specific taxa to identify dysbiosis.  In a feline study, it was discovered that six bacterial taxa could be accurately used to predict diarrhea in 83% of cases.

It is hoped the same results could be accomplished for horses.  Developing PCR testing to screen for biomarkers could be a game changer that could potentially provide speedy, economical early diagnostics and early treatment.

So far, the most remarkable finding in the preliminary data reveals that in horses with colitis, the whole bacterial population is very depleted.

“At this stage we are in the process of increasing our numbers to find significant differences in which bacterial taxa are more important,” says Arroyo.  “Soon we hope to share which bacteria taxa are more promising for predicting dysbiosis in horses with gastrointestinal disease.”

The researchers are delving into a huge biobank of samples to identify potential markers of intestinal dysbiosis in horses, utilizing PCR testing as a faster and more economical alternative to the complex DNA sequencing technologies that have been used to characterize changes in microbiota thus far.  The goal is to develop simple and reliable testing that veterinarians can take right to the barn that will result in early treatment and allow closer monitoring of horses at the first onset of GI disease.

Top Tips to Protect Digestive Health

1. Horses are hind gut fermenters who rely on adequate amounts of fiber in the diet to maintain healthy gut function.

2. Make dietary changes slowly as abrupt changes disrupt the microbiota.

3. Avoid large grain meals as huge portions of highly fermentable diets can be quite harmful to the microbiota and can also be a source of risk for developing gastric ulcers.  Opt to spread out concentrates into several smaller rations.

4. Prevent long periods of fasting which can also lead to ulcers.  Horses are continuous-grazers, and they need to have small amounts of feed working through their digestive system to keep it functioning optimally.

5. Have a parasite prevention program.

6. Provide fresh water 24/7 to maintain good hydration and keep contents moving smoothly through the GI tract.

7. Keep up to date on dental appointments. 

8. Motion is lotion – turn out and exercise are extremely important to gut function.

In closing, Arroyo states, “These top tips will help keep the horse happy and the gastrointestinal tract functioning properly.”

Lower limb anatomy and how it can be conditioned for racing

Words - Adam Jackson MRCVS 

Better understanding the appropriate levels of exercise and training while the horse’s body grows and develops has been a topic of research for many years. Although it has been shown that young, growing horses are well-suited to adapt to conditioning, it is vital that continued research is performed in order to develop thoughtful and strategic training methods to promote healthy, fit and sound horses with long careers and lives.  

Horses’ limbs consist of dozens of muscles, bones, tendons, ligaments, and joints that allow the horse to move as well as support its body weight. The limbs function to provide thrust and movement while absorbing impact and bearing weight.  Most of the horse’s weight is supported by the fore limbs, while the propulsion of the horse is provided by the hind limbs. In addition, the horse has two apparatuses referred to as the stay apparatus and suspensory apparatus. The stay apparatus allows major joints in the limbs to lock so that the horse may rest and relax while standing. The suspensory apparatus is designed to absorb shock, carry the horse’s weight, and prevent the overextension of joints. Finally, the hooves are important structures that maintain support and traction as well as provide additional shock absorption.  

Since the cardiovascular system provides blood supply throughout the body, by responding to various stimuli, it can control the velocity and amount of blood carried through the vessels, thus, delivering oxygen, nutrients, hormones, and other important substances to cells and organs in the body.  It plays a very important role in meeting the body’s demands during exercise, stress, and activity.  

Exercise is used to increase the body’s ability to withstand repeated bouts of similar exercise with less impact.  With a strong and healthy cardiovascular system, there is an improved ability of the musculoskeletal system receiving oxygen, thus, allowing muscles to better their capacity to use oxygen and energy.  However, the adaptation period for each of these physiological systems do differ as the cardiovascular system adapts faster compared to the musculoskeletal system. This is often an overlooked consideration when developing training programmes for horses. 

It is important to understand the various functions, structures, and adaptive processes of the horse’s musculoskeletal system such as bone, articular cartilage, tendons, and ligaments in order to develop appropriate training regimens.  

Bone has many important roles that involve locomotion, the storage of minerals (especially calcium and phosphate), soft tissue and vital organ protection, and the support and containment of bone marrow. Bone is a specialized connective tissue, and together with cartilage forms the strong and rigid endoskeleton.  The bone is continuously altering through two processes called bone modeling and bone remodeling, involving four cells referred to as osteoclasts, osteoblasts, osteocytes and bone lining cells.  

Osteoblasts secrete bone matrix in the form of non-mineralized osteoid, which is then mineralized over a few weeks to form a bone matrix.  Osteoclasts are involved in resorption of bone as this process occurs faster than the formation of bone. When the bone surfaces are not in the development or resorption phase, the bone surface is completely lined by a layer of flattened and elongated cells termed bone-lining cells.  Osteocytes are derived from osteoblasts and are highly specialized to maintain the bone matrix.  They are designed to survive hypoxic conditions and maintain biomineralization of the bone matrix.  Osteocytes also control osteoblastic and osteoclastic activities allowing bone remodeling.

The function of bone modeling is to alter and maintain shape during growth. As the horse grows and develops, bone modeling occurs with the acquisition and removal of bone.  While the young horse grows and develops, bone modeling allows the bone to endure strains from everyday work and exercise. The adult skeleton undergoes a minimal amount of bone modeling. Due to the presence of the high frequency of bone modeling in young horses, their skeletal strength is highly influenced by strains to their bones during exercise and daily use. With this knowledge, it has been concluded and confirmed that short-term dynamic exercise of an adolescent can lead to beneficial changes to its bone morphology.  

Bone remodeling is a different process, in which old and damaged bone is renewed, which enables the bone to respond and adapt to changing functional situations. Bone remodeling is usually a coordinated relationship between bone resorption and bone formation. This process occurs throughout the horse’s life with the renewal of primary, damaged or old bone. Osteoclasts absorb old and damaged bone, and the osteoblasts form new bone and lay down new bone matrix until the earlier absorbed bone is replaced. In those animals with musculoskeletal disease or damage, there is an imbalance of osteoblast and osteoclast activity. With the knowledge that osteoblast activity to make new bone takes months whilst osteoclast activity of removing old and damaged bone only takes a few days to two weeks, bone that is being repaired is at a high risk of further injury as bone removed has not been completely replaced.   Multiple studies have shown that exercise while growing can provide lifelong benefits; however, it must be done with care and knowledge. In addition, many studies have shown that exercise of a dynamic nature in moderate distances, such as that achieved in the pasture or prescribed short-distance high-speed work is beneficial to musculoskeletal development and may prevent injuries when entering race training. It has also been observed that long slow work does not increase bone strength. Below is a summary of the young horse response of the various types of exercise.

Articular cartilage is a highly specialized connective tissue found in joints with the role of providing a smooth, lubricated surface of articulation and to help transmit loads with a low amount of friction. The articular cartilage is a hyaline cartilage (flexible and strong tissue providing a smooth, slippery surface) with a dense “ExtraCellular Matrix” (ECM) consisting of specialized cells called chondrocytes, collagen and proteoglycans. These components help to retain water in the ECM that is required for the joints mechanical properties. As age increases, hydration of the matrix does decrease, resulting in stiffness. Chondrocytes are residential cells in articular cartilage that play a role in the development, maintenance, and repair of the ECM. They do respond to a variety of stimuli, including mechanical loads, growth factors, hydrostatic pressures, piezoelectric forces (formation of electric charge with force). Because of the lack of blood vessels, lymphatics, and nerves as well as being a harsh biomechanical environment, there is a limited capacity to heal and repair. In addition, chondrocytes have limited potential for replication, thus, have limited healing capacity; and chondrocytes survival depends on an optimal chemical and mechanical environment.  

Maintaining joint health is vital, which requires the preservation of healthy cartilage tissue. Inactivity of joints is detrimental to articular cartilage; thus, regular movement of joints and dynamic loads is needed to provide a normal articular cartilage structure and function. Biochemical responses of the cartilage to exercise are not nearly as well known compared to bone. While the confinement of young horses stunts joint development, excessive straining of cartilage can also reduce joint development. It has been observed that pasture access was optimal for the development of joints and the confinement or excessive sprint exercise (12–32 sprints of 40 meters for 6 days a week for 5 months) causes detrimental effects on the joint and may be deemed as unnatural exercise.  It is also thought that exercise is needed well before two years of age to allow cartilage thickening as well as the avoidance of confinement. It can be concluded that further studies are required with respect to level of exercise and type of exercise in order to achieve healthy cartilage tissue as there is clearly a fine line between frequency and intensity of exercise.  

Tendons and ligaments are distinct but closely related tissues that have unique and important roles in musculoskeletal function and musculoskeletal disease. Tendons and ligaments are dense, fibrous connective tissues that connect muscle to bone or bone to bone, respectively.  These tissues transmit mechanical forces to stabilize the skeleton and allow body movement.  Tendons and ligaments consist mainly of collagen type I as well as small amounts of collagen III, IV, V, and VI. There are also various proteoglycans in tendons and ligaments that both organize and lubricate collagen fiber bundles. The elasticity of tendons and ligaments is due to the large amount of type I collagen. During locomotion, the tendon decreases energy cost to the horse by acting as a spring to store and release energy while stretching and recoiling in the stance and swing phases of each stride. Tendons and ligaments have blood vessels and nerves that allow the homeostasis and response to injury.  

Tenocytes are tightly regulated by a series of growth factors and transcription factors that allow the synthesis, maintenance, and the degradation of the tendon extracellular matrix. Tendons are elastic, but tearing may occur if there is excessive loading on the tendon and the repair of collagen is a slow process. In addition, tendons have crimp morphology where the tendons buckle in a state of relaxation and act as shock absorbers.  Unbuckling of the tendon occurs during loading.  This crimp morphology may be disturbed if an injury occurs and also is reduced in older horses.  

Due to the variation of activity of tenocytes in foals and young horses, it has been observed that both a lack of exercise and excess of exercise can impair tendon make-up and subsequent functionality. With the current data and research that has been gathered, it can be concluded that if horses take advantage of spontaneous exercise when in the paddocks (which they often do), the developing tendons may benefit and be at a lower risk of injury when racing training starts. 

Conclusion

It is clear that further research is needed in order to ascertain the optimal amount and type of exercise that is needed in order to provide a strong musculoskeletal system and functional performance. However, it has been shown that prescribed exercise during the growth of the horse can increase the longevity of the horse’s health and performance. It has been observed that confinement and the lack of loading can result in weaker tissues and the loss of function of none, tendons, ligaments and articular cartilage.  However, it must also be recognized that medical attempts to alleviate pain so that a horse can continue to train through an injury can greatly increase tissue damage which is detrimental to the horse’s health and career. It is far more beneficial to provide an adequate amount of time for the injury to heal, thus, putting the horse’s health and wellbeing as a top priority.  

Nutritional perspective

Bone development in yearlings from the sales ring to racing — nutritional perspective

Words - Des Cronin B.Ag.Sc, M.B.A

Maintaining the equine skeleton is vital to ensure optimal development of the young growing horse, minimize risk of injury in the performance horse, and promote longevity and soundness.

The skeletal development and health of a young horse begins in utero and ensuring the broodmare receives the correct intake of key nutrients will be critical to the growth of the unborn foal. Producing high-quality milk places a significant drain on the mineral reserves of the mare. Maintaining mineral intakes during peak lactation is vital to ensure the foal receives the best nutrition to support the rapid skeletal development in the early weeks and months of growth. During this time, bone formation, body size, and muscle mass greatly increase. Risk of defective bone and related tissue formation increases with one of more of the following:

• Poor diet with the incorrect balance of energy and nutrients in the daily ration

• Inadequate amounts of calcium (Ca) and phosphorus (P)

• A reversed Ca:P ratio

• Low zinc (Zn) or copper (Cu) in the diet

• Low Vitamin D

Feeding a young horse for a maximum growth rate is undesirable because bone hardening lags greatly behind bone lengthening. At 12 months old, the young horse could reach about 90 to 95 per cent of its mature height but only about 75 per cent of its mature bone mineral content.

Ideally, young horses should gain weight at a rate that their developing bones can easily support. Growing bones and connective tissues don’t have the strength to support rapid weight gain from overfeeding, especially energy. Rapid weight gain can also make other skeletal anomalies worse. In these cases the risk of developmental orthopedic disorders (DOD) and unsoundness increases.

DOD and unsoundness can also occur during uneven growth. For example, switching an underfed, slow-growing horse to a good diet that allows quick growth (compensatory growth), increases the risk of DOD. Foals between the ages of 3 and 9 months of age are at greatest risk of DOD.

Fresh forages, for example grazed grass, usually provide enough major minerals such as calcium (Ca) and phosphorus (P) for the growing horse. However, there can be significant variation in calcium and phosphorus levels in all forages but particularly preserved forages (hay and haylage). Forage analysis should always be undertaken to determine mineral composition. 

For young fast-growing horses, the diet must supply the quantities of calcium and phosphorus needed for normal bone formation. In terms of Ca:P ratio, the ratio must be positive in favor of calcium. Horses are much more tolerant of high-dietary calcium than other species. For practical purposes, a good guideline would be to keep the ratio Ca:P between 1.5 to 1 and 2.5 to 1.  Grains (e.g., oats) contain 10 per cent of the calcium level found in typical forages. Grains are poor sources of calcium, both in terms of the amount of calcium supplied and their effect on Ca:P ratio in the diet. Where grains are fed, supplementation will be necessary to balance the diet.  

While some forages may contain adequate calcium and phosphorus, they will typically supply less than 20 per cent of the daily requirements for trace elements. Supplementation of trace elements will generally be necessary to support normal bone development.

Where concentrates are fed (especially low levels), supplementation may still be necessary to balance the overall mineral and trace element intake. Nutritional advice should be sought to ensure the horse's diet is correctly balanced.

To meet the carefully balanced requirements of key minerals, it is advisable to supplement the daily rations of growing horses and young horses entering training with an appropriate nutritional product. 

Make sure that the supplement used contains the correct ratio of calcium and phosphorus, as well as other key nutrients such as vitamin D and chelated trace elements (copper, manganese, and zinc) to support normal bone development.

Supplementing branch chain amino acids in the diet ensures that growth is maintained. Lysine plays a key role when protein concentrations in the body are low. Vitamin A supports collagen formation, which is a key component of the supportive structures of joints (tendons and ligaments). Vitamin D3 is added to enhance calcium absorption.

Although growth rates slow after the age of two, they are still juvenile in their skeletal development with some growth plates, such as the shoulder and stifles, yet to completely close. Although they may look like fully grown adults, it is still important to meet nutritional requirements especially if starting training and work. With the addition of exercise and training, a young horse's nutritional needs change.  The added forces from groundwork on the long bones and increased requirements of other nutrients like electrolytes need to be considered. 

Finally, horses all grow and develop at different rates because of factors such as genetics. Some youngsters will need  more support for longer periods of time than others, so it is important to manage accordingly.

A New Look at Lameness

Words - Jackie Zions (interviewing Dr. Koenig)

Prevention is the ideal when it comes to lameness, but practically everyone who has owned horses has dealt with a lay-up due to an unforeseen injury at some point. The following article will provide tools to sharpen your eye for detecting lameness, review prevention tips and discuss the importance of early intervention. It will also begin with a glimpse into current research endeavouring to heal tendon injuries faster, which has obvious horse welfare benefits and supports horse owners eager to return to their training programs. Dr. Judith Koenig of Ontario Veterinary College (OVC) spends half of her time as a surgeon and teacher with a strong interest in equine sports medicine and rehabilitation, and the other half as a researcher at the OVC.

Lameness is a huge focus for Koenig, whose main interest is in tissue healing. “I think over the past 20 or 30 years we have become very, very good in diagnosing the cause of lameness,” says Koenig. “In the past, we had only radiographs and ultrasound as a diagnostic tool, but by now most referral centers also have MRI available; and that allows us to diagnose joint disease or tendon disease even more. We are much better now [at] finding causes that previously may have been missed with ultrasound.” 

Improvements in diagnostics have resulted in increased ability to target treatment plans. With all the different biologics on the market today, Koenig sees a shift in the management of joint disease with more people getting away from steroids as a treatment.

The following list is excerpted from Equine Guelph’s short course on lameness offered on TheHorsePortal.ca. It outlines the different diagnostics available:

Stem Cell Therapy
When asked for the latest news on research she has been involved in, Koenig proclaims, “I'm most excited about the fact that horses are responding well to stem cell treatment—better than I have seen any response to any other drug we have tried so far!”

Koenig has investigated the use of many different modalities to see if they accelerate tissue healing and has studied which cellular pathways are affected. Two recent collaborative studies have produced very exciting findings, revealing future promise for treating equine osteoarthritis with stem cell therapy.  

In a safety study, Koenig and her team at the Ontario Veterinary College have shown equine pooled cryopreserved umbilical cord blood, (eCB) MSC, to be safe and effective in treatment of osteoarthritis.  

“These cells are the ones harvested from umbilical cord blood at the time of foaling and then that blood is taken to the lab and the stem cells are isolated out of it,” explains Koenig. The stem cells are then put through a variety of tests to make sure they are free of infectious diseases. Once given a clean bill of health, they are expanded and frozen. 
The stem cells harvested from multiple donors of equine umbilical cord blood [eCB, (kindly provided by eQcell), MSC] were compared to saline injections in research horses. “This type of cells is much more practical if you have a cell bank,” says Koenig. “You can treat more horses with it, and it’s off the shelf.” There were no systemic reactions in the safety study. Research has also shown no different reactions from sourcing from one donor or multiple donors.  

In the second study, 10 million stem cells per vial were frozen for use in healing OA from fetlock chips in horses that were previously conditioned to be fit. After the fetlock chip was created, exercise commenced for six more weeks, and then osteoarthritis was evaluated by MRI for a baseline. Half the horses were treated with the pooled MSC stem cells, and the control group received saline before another month of exercise. Then MRI and lameness exams were repeated, and arthroscopy was repeated to score the cartilage and remove the chip.

Lameness was decreased and cartilage scores were improved in the group that received stem cell therapy at the time of the second look with arthroscopy.

Many diagnostics were utilized during this study. MRIs, X-rays, ultrasounds and weekly lameness evaluations all revealed signs of osteoarthritis in fetlock joints improved in the group treated with (eCB) MSCs. After six weeks of treatment, the arthroscopic score was significantly lower (better cartilage) in the MSC group compared to the control group. 

“Using the MRI, we can also see a difference that the horses treated with stem cells had less progression of osteoarthritis, which I think is awesome,” says Koenig. “They were less lame when exercised after the stem cell therapy than the horses that received saline.”
This research group also just completed a clinical trial in client-owned horses diagnosed with fetlock injuries with mild to moderate osteoarthritis changes. The horses were given either 10 million or 20 million stem cells and rechecked three weeks and six weeks after the treatment. Upon re-evaluation, the grade of lameness improved in all the horses by at least one. Only two horses presented a mild transient reaction, which dissipated after 48 hours without any need for antibiotics. The horse’s joints looked normal, with any filling in the joint reduced.
There was no difference in the 18 horses, with nine given 10 million stem cells and the other nine 20 million stem cells; so in the next clinical trial, 10 million stem cells will be used.

The research team is very happy with the results of this first-of-its-kind trial, proving that umbilical cord blood stem cells stopped the progression of osteoarthritis and that the cartilage looked better in the horses that received treatment. The future of stem cell therapy is quite promising!

Rehabilitation

Research has shown adhering to a veterinary-prescribed rehabilitation protocol results in a far better outcome than paddock turn out alone. It is beneficial for tendon healing to have a certain amount of controlled stimulation. “These horses have a much better outcome than the horses that are treated with just being turned out in a paddock for half a year,” emphasizes Koenig. “They do much better if they follow an exercise program. Of course, it is important not to overdo it.”

For example, Koenig cautions against skipping hand-walking if it has been advised.  It can be so integral to stimulating healing, as proven in recent clinical trials. “The people that followed the rehab instructions together with the stem cell treatment in our last study—those horses all returned to racing,” said Koenig.  

“It is super important to follow the rehab instructions when it comes to how long to rest and not to start back too early.”

Another concern when rehabilitating an injured horse would be administering any home remedies that you haven't discussed with your veterinarian. Examples included blistering an area that is actively healing or applying  shockwave to mask pain and then commence exercise.

Prevention and Training Tips

While stating there are many methods and opinions when it comes to training horses, Koenig offered a few common subjects backed by research. The first being the importance of daily turnout for young developing horses.  

Turnout and exercise
Many studies have looked at the quality of cartilage in young horses with ample access to turn out versus those without. It has been determined that young horses that lack exercise and are kept in a stall have very poor quality cartilage.
Horses that are started early with light exercise (like trotting short distances and a bit of hill work) and that have access to daily paddock turnout, had much better quality of cartilage. Koenig cited research from Dr. Pieter Brama and similar research groups.

Another study shows that muscle and tendon development depend greatly on low grade exercise in young horses.  Evaluations at 18 months of age found that the group that had paddock turnout and a little bit of exercise such as running up and down hills had better quality cartilage, tendon and muscle.  

Koenig provides a human comparison, with the example of people that recover quicker from injury when they have been active as teenagers and undergone some beneficial conditioning. The inference can be made that horses developing cardiovascular fitness at a young age stand to benefit their whole lives from the early muscle development.

Koenig says it takes six weeks to regain muscle strength after injury, but anywhere from four to six months for bone to develop strength. It needs to be repeatedly loaded, but one should not do anything too crazy! Gradual introduction of exercise is the rule of thumb.

Rest and Recovery

“Ideally they have two rest days a week, but one rest day a week as a minimum,” says Koenig. “I cannot stress enough the importance of periods of rest after strenuous work, and if you notice any type of filling in the joints after workout, you should definitely rest the horse for a couple of days and apply ice to any structures that are filled or tendons or muscles that are hard.” 

Not purporting to be a trainer, Koenig does state that two speed workouts a week would be a maximum to allow for proper recovery. You will also want to make sure they have enough access to salt/electrolytes and water after training.

During a post-Covid interview, Koenig imparted important advice for bringing horses back into work methodically when they have experienced significant time off.

“You need to allow at least a six-week training period for the athletes to be slowly brought back and build up muscle mass and cardiovascular fitness,” says Koenig.  “Both stamina and muscle mass need to be retrained.”

Watch video: “Lameness research - What precautions do you take to start training after time off?”

The importance was stressed to check the horse’s legs for heat and swelling before and after every ride and to always pick out the feet. A good period of walking is required in the warmup and cool down; and riders need to pay attention to soundness in the walk before commencing their work out.

Footing and Cross Training

With a European background, Koenig is no stranger to the varying track surfaces used in their training programs. Statistics suggest fewer injuries with horses that are running on turf, like they practice in the UK.  

Working on hard track surfaces has been known to increase the chance of injury, but delving into footing is beyond the scope of this article.

“Cross training is very important,” says Koenig. “It is critical for the mental and proper musculoskeletal development of the athlete to have for every three training days a day off, or even better provide cross-training like trail riding on these days." 

Cross-training can mitigate overtraining, giving the body and mind a mental break from intense training. It can increase motivation and also musculoskeletal strength. Varied loading from training on different terrain at different gaits means bone and muscle will be loaded differently, therefore reducing repetitive strain that can cause lameness.

Hoof care

Whether it is a horse coming back from injury, or a young horse beginning training, a proficient farrier is indispensable to ensure proper balance when trimming the feet. In fact, balancing the hoof right from the start is paramount because if they have some conformational abnormalities, like abnormal angles, they tend to load one side of their joint or bone more than the other. This predisposes them to potentially losing bone elasticity on the side they load more because the bone will lay down more calcium on that side, trying to make it stronger; but it actually makes the bone plate under the cartilage brittle.  

Koenig could not overstate the importance of excellent hoof care when it comes to joint health and advises strongly to invest in a good blacksmith. Many conformational issues can be averted by having a skilled farrier right from the time they are foals. Of course, it would be remiss not to mention that prevention truly begins with nutrition. “It starts with how the broodmare is fed to prevent development of orthopedic disease,” says Koenig. Consulting with an equine nutritionist certainly plays a role in healthy bone development and keeping horses sound.

Equine Neck CT: Advancing diagnostic precision in racehorses

Words - Rachel Tucker MRCVS

Introduction

When considering neck disorders in the racehorse, we most commonly think of severe conditions such as acute neck trauma and cervical vertebral myelopathy (Wobbler Syndrome). These represent the most severe end of the scale of orthopedic and neurologic injury to the neck; and a diagnosis, or at least prognosis, is usually clear. However, neck conditions encompass a far wider range of clinical presentations. 

At the milder end of the scale, signs may be subtle and easily missed, whilst still being responsible for discomfort and reduced performance. The recent ability to perform a computed tomography (CT) scan of a horse’s neck represents a major advancement in our ability to diagnose neck conditions. Timely and accurate diagnosis allows efficient and targeted treatment, the ability to plan schedules and improvement in welfare through the provision of appropriate treatment and earlier return to function. 

In neurologic cases, an accurate diagnosis facilitates risk management for both the horse, their handlers and riders, while improving safety for all.  As conditions and injuries of the neck are being better characterized using CT, new medical and surgical treatment options are being developed, giving the potential for improved outcomes and fewer losses from the racing industry. 

This article summarizes how CT is being increasingly used by vets to diagnose conditions of the neck and how it is revealing previously unknown information and providing exciting new treatment opportunities. 

Presentation

Conditions of the neck can cause a range of signs in the horse, which are wide-ranging in their presentation and variable in their severity. The manner in which these conditions present depends on which anatomical structures are affected. Issues affecting the bones, joints and/or soft tissues of the neck can all cause neck pain, which can manifest in a number of ways. Cases of neck pain can be severe, resulting in a horse with a rigid, fixed neck carriage, an unwillingness to walk and struggling to eat, perhaps due to a traumatic event. Neck fractures are thankfully uncommon but can be catastrophic. 

More moderate signs might be displayed as a stiff neck, with reduced range of movement and resentment of ridden work. There may be pain on palpation of the neck and changes in the neck musculature. Increasingly, we are seeing horses with far more subtle signs, which are ultimately revealed to be due to neck pain and neck pathology. Typically, these horses might have an acceptable range of motion of their neck under most circumstances, but they suffer pain or restriction in certain scenarios, resulting in poor performance. This may be seen as tension through the neck, resisting rein contact, a reluctance to extend the neck over fences, or they may struggle on landing. 

Riders might report a feeling of restriction or asymmetry in the mobility of the neck. In addition, these horses may be prone to forelimb tripping or show subtle forelimb lameness. 

Any condition, which causes injury or disease to the spinal cord or nerves within the neck, also causes a specific range of neurologic signs. Compression of the spinal cord is most commonly caused by malformations or fractures of the cervical vertebrae, or enlargement of the adjacent articular process (facet) joints. This results in classic ‘Wobbler’ symptoms, which can range from subtle weakness and gait abnormalities, through to horses that are profoundly weak, ataxic and uncoordinated. This makes them prone to tripping, falling, or they may even become recumbent. 

Peripheral nerve deficits are uncommon but become most relevant if they affect the nerves supplying the forelimbs, which can result in tripping, forelimb lameness, or local sensory deficits. This lameness might be evident only in certain circumstances, such as when ridden in a rein contact. This lameness is difficult to pinpoint as there will be no abnormality to find in the lame limb, indeed a negative response to nerve and joint blocks (diagnostic analgesia) will usually be part of the diagnostic process.

Horses can present with varying combinations and severities of neck pain, neurologic signs and peripheral nerve deficits, creating a wide range of manifestations of neck related disease. 

Diagnosis

A diagnosis of neck pain is based on careful static and dynamic clinical examination and may be supported by seeing a positive response to treatment. Neurologic deficits are noted during a specific neurologic assessment, which includes a series of provocation tests such as asking a horse to walk over obstacles, back up, turn circles and walk up and down a hill. Confirming neck pathology as the cause of signs can be difficult. Until recently, radiography has been the mainstay imaging modality. Radiographs are useful for assessment of the cervical vertebrae and continue to play an important role in diagnosis; however the complex 3-dimensional shape of these bones, the large size of the neck and an inability to take orthogonal (right-angled) x-ray views means that this 2-dimensional imaging modality has significant limitations. High quality, well-positioned images are essential to maximize the diagnostic potential of radiographs. 

A turning point in our diagnostic ability and understanding of neck dysfunction has been the recent adaptation of human CT scanners to allow imaging of the horse’s neck. A number of equine hospitals across the United Kingdom and Northern Europe now offer this imaging modality. We have been providing this service at Liphook Equine Hospital since 2017, with over 150 neck scans performed to date.

The CT procedure

A computed tomography (CT) scan combines a series of x-ray images taken from different angles around the area of interest to create a 3-dimensional volume of imaging data. This data is presented as a grayscale image which can be viewed in any plane and orientation. It provides excellent bone detail, and post processing techniques can provide information on soft tissue structures too. Additional techniques can be employed such as positive contrast myelography to provide greater detail about soft tissue structures. Myelography delineates the spinal cord using contrast medium injected into the subarachnoid space and is indicated in any case showing neurologic signs suggestive of spinal cord compression. 

Neck CT is performed under a short general anesthetic. Scans without myelography typically take less than 20 minutes to complete. The entire neck is imaged, from the poll to the first thoracic vertebra. The procedure is non-invasive and low risk, with anesthetic-related complication presenting the main risk factor to the procedure. We have not encountered any significant complications in our plain CT scan caseload to date. Horses showing ataxia, weakness and incoordination (Wobbler’s), undergo CT myelography which adds around 20 minutes to the procedure. These horses are exposed to a greater level of risk due to their neurologic condition, the injection of a contrast agent and the increased chance of destabilizing a more severe lesion during the procedure. 

CT is revealing more detailed information about ways that spinal cord compression can occur in Wobbler cases, about compression of spinal nerves resulting in forelimb gait deficits and precise detail about fracture configurations. It gives us detailed images of articular process joint disease, intervertebral disc disease, developmental conditions and anatomic variations. It is also revealing information about rare diseases such as vertebral abscesses or spinal neoplasia. As our caseload and confidence in the imaging modality grows, we are learning more about the value of CT in examining more subtle neck conditions. We are also bringing the benefit of a more accurate diagnosis, allowing precise targeted treatment and a better ability to provide a prognosis about outcomes—likely progression or safety factors. CT myelography allows circumferential imaging of the spinal canal and yields significantly more information than traditional x-ray myelography. As a result, we hope to enable better case selection of horses that may benefit from Wobbler surgery, with the goal of resulting in improved success rates of the surgery.

Innovations in treatment

New treatment options are emerging as a result of our more accurate diagnoses of neck pathology. Of the first 55 horses which underwent neck CT at our hospital, we were surprised to discover that 13 (24%) had some form of osteochondral fragmentation within the articular process joints of their neck. Some of these horses were young Thoroughbreds, bred to race but showing Wobbler signs. These tended to have convincing CT evidence of type 1 CVM (Wobbler Syndrome) and osteochondrosis affecting their neck. Others had fragments which were larger and more discrete, with evidence of articular process joint enlargement/arthritis but no other bony lesions. These horses were typically older and of a range of breeds and uses. 

In those horses presenting with signs of neck pain but no neurologic deficits, surgical removal of these fragments was proposed. Following further consideration and cadaver training, we have begun to offer this surgery for horses that fit the appropriate criteria and have surgically accessible fragments.  We have performed arthroscopic or arthroscopic-assisted fragment removal from eight articular process joints in six horses to date. No intraoperative or postoperative complications have been encountered; and five of six horses showed complete resolution of neck pain. In the sixth horse, full recovery was not anticipated due to the presence of additional neck pathology, but partial improvement occurred for two years.  Fragment removal has relieved signs of neck pain and stiffness and caused improved performance in these horses. 

Two procedures that are emerging to treat spinal nerve root impingement are a targeted peripheral nerve root injection and a keyhole surgical procedure to widen the intervertebral foramen. Nerve root injection is performed in the standing sedated horse under ultrasound guidance. Surgery is performed under anesthesia, using specialized minimally invasive equipment to widen the bony foramen using a burr. This surgery is in its infancy but offers an exciting treatment option.  

Additionally, CT gives us the ability to better plan for fracture repair, undoubtedly improving our case selection for Wobbler surgery; it more accurately guides intra-articular injection of the articular process joints. 

 Summary

Computed tomography is transforming our ability to diagnose conditions of the horse’s neck. The procedure is low risk and now widely available in the UK and other parts of Europe. It is driving the innovation of novel treatment options with the goal of improving outcomes and reducing losses to conditions of the neck. Our CT findings are posing new questions about neck function, pain and neurologic disease and is an active area of ongoing research.

References:

Schulze N., Ehrle, A., Beckmann, I and Lischer, C. (2021) Arthroscopic removal of osteochondral fragments of the cervical articular process joints in three horses. Vet Surg. ;1-9. 

Swagemakers J-H, Van Daele P, Mageed M. Percutaneous full endoscopic foraminotomy for treatment of cervical spinal nerve compression in horses using a uniportal approach: Feasibility study. Equine Vet J. 2023. 

Tucker R, Parker RA, Meredith LE, Hughes TK, Foote AK. Surgical removal of intra-articular loose bodies from the cervical articular process joints in 5 horses. Veterinary Surgery. 2021;1-9.

Wood AD, Sinovich M, Prutton JSW, Parker RA. Ultrasonographic guidance for perineural injections of the cervical spinal nerves in horses. Veterinary Surgery. 2021; 50:816–822. 

Air Quality and Air Pollution’s Impact on Your Horse’s Lungs

Article by Dr. Janet Beeler-Marfisi

There’s nothing like hearing a horse cough to set people scurrying around the barn to identify the culprit. After all, that cough could mean choke, or a respiratory virus has found its way into the barn. It could also indicate equine asthma. Yes, even those “everyday coughs” that we sometimes dismiss as "summer cough" or "hay cough" are a wake-up call to the potential for severe equine asthma. 

Formerly known as heaves, broken wind, emphysema, chronic obstructive pulmonary disease (COPD), or recurrent airway obstruction (RAO), this respiratory condition is now called severe equine asthma (sEA). These names reflect how our scientific and medical understanding of this debilitating disease has changed over the years. We now consider heaves to be most comparable to severe asthma in people.

But what if your horse only coughs during or after exercise? This type of cough can mean that they have upper airway irritation (think throat and windpipe) or lower airway inflammation (think lungs) meaning inflammatory airway disease (IAD), which is now known as mild-to-moderate equine asthma (mEA). This airway disease is similar to childhood asthma, meaning  that it can go away on its own. However, it is still very important to call your veterinarian out to diagnose mEA. This disease causes reduced athletic performance, and there are different subtypes of mEA that benefit from specific medical therapies. In some cases, mEA progresses to sEA.

Equine Asthma and  Air Quality
What does equine asthma have to do with air quality? A lot, it turns out. Poor air quality, or air pollution, includes the barn dusts—the allergens and molds in hay and the ground-up bacteria in manure, as well as arena dusts and ammonia from urine. Also, very importantly for both people and horses, air pollution can be from gas and diesel-powered equipment. This includes equipment being driven through the barn, the truck left idling by a stall window, or the smog from even a small city that drifts nearly invisibly over the surrounding farmland. Recently, forest-fire smoke has been another serious contributor to air pollution. 

Smog causes the lung inflammation associated with mEA. Therefore, it is also likely that air pollution from engines and forest fires will also trigger asthma attacks in horses with sEA. Smog and smoke contain many harmful particulates and gases, but very importantly they also contain fine particulate matter known as PM2.5. The 2.5 refers to the diameter of the particle being 2.5 microns. That’s roughly 30 times smaller than the diameter of a human hair. Because it is so small, this fine particulate is inhaled deeply into the lungs where it crosses over into the bloodstream. So, not only does PM2.5 cause lung disease, but it also causes inflammation elsewhere in the body including the heart. Worldwide, even short-term exposure is associated with an increased risk of premature death from heart disease, stroke, and lung cancer. This PM2.5 stuff is not trivial!

In horses, we know that PM2.5 causes mEA, so it’s logical that smog and forest-fire smoke exposure could exacerbate asthma in horses, but we don’t know about heart disease or risk of premature death.

Symptoms, Diagnostic Tests and Treatments

Equine asthma manifests with a spectrum of symptoms that vary in severity and the degree of debilitation they cause. Just like in people with asthma, the airways of horses with mEA and sEA are “hyperreactive.” This means that the asthmatic horse’s airways are extra sensitive to barn dusts that another horse’s lungs would just “ignore.” The asthmatic horse’s airways constrict, or become narrower, in response to these dusts. This narrowing makes it harder to get air in and out of the lungs. Think about drinking through a straw. You can drink faster with a wider straw than a skinnier one. It’s the same with air and the airways. In horses with mEA, the narrowing is mild. In horses with sEA, the constriction is extreme and is the reason why they develop the “heaves line”; they have to use their abdominal muscles to help squeeze their lungs to force the air back out of their narrow airways. They also develop flaring of their nostrils at rest to make their upper airway wider to get more air in. Horses with mEA do not develop a heaves line, but the airway narrowing and inflammation do cause reduced athletic ability.

The major signs of mEA are coughing during or just after exercise that has been going on for at least a month and decreased athletic performance. In some cases, there may also be white or watery nasal discharge particularly after exercise. Often, the signs of mEA are subtle and require a very astute owner, trainer, groom, or rider to recognize them.

Another very obvious feature of horses with sEA is their persistent hacking cough, which worsens in dusty conditions. “Hello dusty hay, arena, and track!” The cough develops because of airway hyperreactivity and because of inflammation and excess mucus in the airways. Mucus is the normal response of the lung to the presence of inhaled tiny particles or other irritants. Mucus traps these noxious substances so they can be coughed out, which protects the lung. But if an asthma-prone horse is constantly exposed to a dusty environment, it leads to chronic inflammation and mucus accumulation, and the development or worsening of asthma along with that characteristic cough.

Accurately Diagnosing Equine Asthma

Veterinarians use a combination of the information you tell them, their observation of the horse and the barn, and a careful physical and respiratory examination that often involves “rebreathing.” This is a technique where a bag is briefly placed over the horse’s nose, causing them to breathe more frequently and more deeply to make their lungs sound louder. This helps your veterinarian hear subtle changes in air movement through the lungs and amplifies the wheezes and crackles that characterize a horse experiencing a severe asthma attack. Wheezes indicate air “whistling” through constricted airways, and crackles mean airway fluid buildup. The fluid accumulation is caused by airway inflammation and contributes to the challenge of getting air into the lung. 

Other tests your veterinarian might use are endoscopy, bronchoalveolar lavage, and in the specialist setting, pulmonary function testing. They will also perform a complete blood count and biochemical profile assay to help rule out the presence of an infectious disease. 

Endoscopy allows your veterinarian to see the mucus in the trachea and large airways of the lung. It also lets them see whether there are physical changes to the shape of the airways, which can be seen in horses with sEA. 

Bronchoalveolar lavage, or “lung wash” is how your veterinarian assesses whether there is an accumulation of mucus and inflammatory cells in the smallest airways that are too deep in the lung to be seen using the endoscope. Examining lung wash fluid is a very important way to differentiate between the different types of mEA, between sEA in remission and an active asthma attack, and conditions like pneumonia or a viral lung infection. 

Finally, if your veterinarian is from a specialty practice or a veterinary teaching hospital, they might also perform pulmonary function testing. This allows your veterinarian to determine if your horse’s lungs have hyperreactive airways (the hallmark of asthma), lung stiffening, and a reduced ability to breathe properly. 

Results from these tests are crucial to understanding the severity and prognosis of the condition. As noted earlier, mEA can go away on its own; but medical intervention may speed healing and the return to athletic performance. With sEA, remission from an asthmatic flare is the best we can achieve.  As the disease gets worse over time, eventually the affected horse may need to be euthanized.

Management, Treatment and Most Importantly—Prevention
Successful treatment of mEA and sEA flares, as well as long-term management, requires a multi-pronged approach and strict adherence to your veterinarian’s recommendations.

Rest is important because forcing your horse to exercise when they are in an asthma attack further damages the lung and impedes healing.  To help avoid lung damage when smog or forest-fire smoke is high, a very useful tool is your local, online, air quality index (just search on the name of your closest city or town and “AQI”).  Available worldwide, the AQI gives advice on how much activity is appropriate for people with lung and heart conditions, which are easily applied to your horse. For example, if your horse has sEA and if the AQI guidelines say that asthmatic people should limit their activity, then do the same for your horse. If the AQI says that the air quality is bad enough that even healthy people should avoid physical activity, then do the same for you AND your horse. During times of poor air quality, it is recommended to monitor the AQI forecast and plan to bring horses into the barn when the AQI is high and to turn them out once the AQI has improved.

Prevent dusty air. Think of running your finger along your tack box – whatever comes away on your finger is what your horse is breathing in. Reducing dust is critical to preventing the development of mEA and sEA, and for managing the horse in an asthmatic flare. 

Logical daily practices to help reduce dust exposure:

• Turn out all horses before stall cleaning

• Wet down the aisle prior to sweeping

• Never sweep debris into your horse’s stall

• Use low-dust bedding like wood shavings or dust-extracted straw products, which should also be dampened down with water

• Reduce arena, paddock, and track dust with watering and maintenance

• Consider low-dust materials when selecting a footing substrate

• Steam (per the machine’s instructions) or soaking hay (15–30 minutes and then draining, but never store steamed or soaked hay!) 

• Feed hay from the ground

• Feed other low-dust feeds

• Avoid hay feeding systems that allow the horse to put their nose into the middle of dry hay—this creates a “nosebag” of dust

Other critical factors include ensuring that the temperature, humidity and ventilation of your barn are seasonally optimized. Horses prefer a temperature between 10–24 ºC (50–75 ºF), ideal barn humidity is between 60–70%. Optimal air exchange in summer is 142 L/s (300 cubic feet/minute). For those regions that experience winter, air exchange of 12–19 L/s (25–40 cubic feet/minute) is ideal. In winter, needing to strip down to a single layer to do chores implies that your barn is not adequately ventilated for your horse’s optimal health. Comfortable for people is often too hot and too musty for your horse! 

Medical interventions for controlling asthma are numerous. If your veterinarian chooses to perform a lung wash, they will tailor the drug therapy of your asthmatic horse to the results of the wash fluid examination. Most veterinarians will prescribe bronchodilators to alleviate airway constriction. They will also recommend aerosolized, nebulized or systemic drugs (usually a corticosteroid, an immunomodulatory drug like interferon-α, or a mast cell stabilizer like cromolyn sodium) to manage the underlying inflammation. They may also suggest nebulizing with sterile saline to help loosen airway mucus and may suggest feed additives like omega 3 fatty acids, which may have beneficial effects on airway inflammation. 

New Research and Future Directions

Ongoing research is paramount to expanding our knowledge of what causes equine asthma and exploring innovative medical solutions. Scientists are actively investigating the effects of smog and barn dusts on the lungs of horses. They are also working to identify new targeted therapies, immunotherapies and other treatment modalities to improve outcomes for affected horses.

Conclusion

Both mild and severe equine asthma are caused and triggered by the same air pollutants, highlighting the need for careful barn management. The alarming rise in air pollution levels poses an additional threat to equine respiratory health. Recognizing everyday coughs as potential warning signs and implementing proper diagnostic tests, day-to-day management practices and medical therapies are crucial in combating equine asthma. By prioritizing the protection of our horse’s respiratory health and staying informed about the latest research, we can ensure the well-being of our equine companions for years to come.

Highlights

1. Work to prevent dust and optimize barn air exchange.

2. Avoid idling farm equipment and trucks around horses.

3. Don’t ignore a cough—call your veterinarian.

4. Monitor your local air quality index—it’s a free and simple way to help prevent lung damage! 

Thermoregulation - Too hot to handle!

Article by Adam Jackson MRCVS

Exertional heat illness (EHI) is a complex disease where thoroughbred racehorses are at significant risk due to the fact that their workload is intensive in combination with the high rate of heat production associated with its metabolism.  In order to understand how this disease manifests and to develop preventative measures and treatments, it is important to understand thermoregulation in horses. 

What is thermoregulation?

With continuous alteration in the surrounding temperature, thermoregulation allows the horse to maintain its body temperature within certain limits.  Thermoregulation is part of the greater process of homeostasis, which is a number of self-regulating processes the horse uses to maintain body stability in the face of changing external conditions.  Homeostasis and thermoregulation are vital for the horse to maintain its internal environment to ensure its health while disruption of these processes leads to diseases. 

The horse’s normal temperature range is 99–101°F (37.5–38.5°C).  Hyperthermia is the condition in which the body temperature increases above normal due to heat increasing faster than the body can reduce it. Hypothermia is the opposite condition, where the body temperature decreases below normal levels as the body is losing heat faster than producing it.   These conditions are due to the malfunction of thermoregulatory and homeostatic control mechanisms.

Horses are colloquially referred to as warm-blooded mammals—also known as endotherms because they maintain and regulate their core body, and this is opposite ectotherms such as reptiles.  The exercising horse converts stored chemical energy into mechanical energy when contracting various muscles in its body. However, this process is relatively inefficient because it loses roughly 80% of energy released from energy stores as heat. The horse must have effective ways to dissipate this generated heat; otherwise, the raised body temperatures may be life threatening.

Transfer of body heat

There are multiple ways heat may be transferred, and this will flow from one area to another by:

1. Evaporation 

The main way body heat is lost during warm temperatures is through the process of evaporation of water from the horse’s body surface. It is a combination of perspiration, sweating and panting that allows evaporation to occur.

Sweating is an inefficient process because the evaporation rate may exceed the body heat produced by the horse, resulting in the horse becoming covered and dripping sweat. This phenomenon occurs faster with humid weather (high pressure).

Insensible perspiration is the loss of water through the skin, which does not occur as perceivable sweat. Insensible perspiration takes place at an almost constant rate and is the evaporative loss from skin; but unlike sweating, the fluid loss is pure water with no solutes (salts) lost. The horse uses insensible perspiration to cool its body.

It is not common for horses to pant in order to dissipate heat; however, there is evidence that the respiratory tract of the horse can aid in evaporative heat loss through panting.

2. Conduction

Conduction is the process where heat is transferred from a hot object to a colder object, and in the case of the horse, this heat transfer is between its body and the air.  However, the air has poor thermal conductivity, meaning that conduction plays a small role in thermoregulation of the horse.   Conduction may help if the horse is lying in a cool area or is bathed in cool water.  

The horse has the greatest temperature changes occurring at its extremities, such as its distal limbs and head.  The horse can alter its blood flow by constricting or dilating its blood vessels in order to prevent heat loss or overheating, respectively.

Interestingly, the horse will lie down and draw its limbs close to its body in order to reduce its surface area and to control conduction. There also have been some adaptive changes in other equids like mules and burros, where shorter limbs, longer ears and leaner bodies increase its surface area to help in heat loss tolerance.

3. Convection 

Convection is the rising motion of warmer areas of a liquid or gas and the sinking motion of cooler areas of the liquid or gas.  Convection is continuously taking place between the surface of the body and the surrounding air. Free convection at the skin surface causes heat loss if the temperature is low with additional forced convective heat transfer with wind blowing across the body surface.

When faced with cold weather, a thick hair coat insulates and resists heat transfer because it traps air close to the skin; thus, preventing heat loss. Whereas, the horse has a fine hair coat in the summer to help in heat loss.

4. Radiation

Radiation is the movement of heat between objects without direct physical contact.  Solar radiation is received from the sun and can be significant in hot environments, especially if the horse is exposed for long periods of time.  A horse standing in bright sunlight can absorb a large amount of solar radiation that can exceed its metabolic heat production, which may cause heat stress. 

How the horse regulates its body temperature

The horse must regulate its heat production and heat loss using thermoregulatory mechanisms.  There are many peripheral thermoreceptors that detect changes in temperature, which leads to the production of proportional nerve impulses. These thermoregulators are located in the skin skeletal muscles, the abdomen, the spinal cord and the midbrain with the hypothalamus being instrumental in regulating the internal temperature of the horse.   A coordinating center in the central nervous system receives these nerve incoming impulses and produces output signals to organs that will alter the body temperature by acting to reduce heat loss or eliminate accumulated heat.  

The racehorse and thermoregulation

The main source of body heat accumulation in the racehorse is associated with muscular contraction.  At the initiation of exercise, the racehorse’s metabolic heat production, arising from muscle contraction, increases abruptly.  The heat production does alter the level of intensity of the work as well as the type of exercise undertaken.  

During exercise, the core body temperature increases because heat is generated and the horse’s blood system distributes this heat throughout the body. Hodgson and colleagues have theorized and confirmed via treadmill studies that the racehorse has the highest rate of heat production compared to other sporting horses. In fact, the racehorse’s body temperature can rise 33°F (0.8°C) per minute, reaching 108°F (42.0°C). But what core temperature can the horse tolerate and not succumb to heat illness and mortality?  The critical temperature for EHI (exertional heat illness) is not known, but studies have demonstrated that a racehorse can be found to have core temperatures between 108°F - 109° F (42–43°C) without any clinical symptoms. Currently, anecdotal evidence is only available, suggesting that a core temperature of 110°F (43.5°C) will result in manifestation of EHI with the horse demonstrating central nervous system dysfunction such as ataxia (incoordination).  In addition, temperatures greater than 111°F (44°C) result in collapse. 

Heat loss in horses

A horse loses heat to the environment by a combination of convection, evaporation and radiation, which is magnified during racing due to airflow across the body. However, if body heat gained through racing is not minimized by convection, then the racehorse’s body temperature is regulated entirely by evaporation of sweat. This evaporation takes place on the horse’s skin surface and respiratory tract.  

The horse has highly effective sweat glands found in both haired and hairless skin, which produces sweat rates that are highest in the animal kingdom.   Efficient evaporative cooling is present in the horse because its sweat has a protein called latherin, which acts as a wetting agent (surfactant); this allows the sweat to move from its skin to the hair.

Because of the horse’s highly blood-rich mucosa of its upper respiratory tract, the horse has a very efficient and effective heat exchange system.  Estimates suggest this pathway dissipates 30% of generated heat by the horse during exercise.  As the horse exercises, there is blood vessel dilation, which increases blood flow to the mucosa that allows more heat to be dissipated to the environment. When the respiratory tract maximizes evaporative heat loss, the horse begins to pant. Panting is a respiratory rate greater than 120 breaths per minute with the presence of dilated nostrils; and the horse adopts a rocking motion. However, if humidity is high, the ability to evaporate heat via the respiratory route and skin surface is impaired. The respiratory evaporative heat loss allows the cooling of venous blood that drains from the face and scalp. This blood may be up to 37°F (3.0°C) cooler than the core body temperature of 108°F (42.0°C). And as it enters the central circulatory system, it can significantly have a whole-body cooling effect. This system is likely an underestimated and significant means to cool the horse.

Pathophysiology of EHI in the thoroughbred

Although it is inconsistent to determine what temperature may lead to exertional heat illness (EHI), it is known that strenuous exercise, especially during heat stress conditions leads to this disease.  In human medicine, this disease is recognised when nervous system dysfunction becomes apparent.  There are two suggested pathways that lead to EHI, which may work independently or in combination depending on the environmental factors that are present during racing/training.

1. Heat toxicity pathway

Heat is known to detrimentally affect cells by denaturing proteins leading to irreversible damage.  In general, heat causes damage to cells of the vascular system leading to widespread intravascular coagulation (blood clot formation), pathologically observed as micro thrombi (miniature blood clots) deposits in the kidneys, heart, lungs and liver.  Ultimately, this leads to damaged organs and their failure.

Heat tissue damage depends on the degree of heat as well as the exposure time to this heat. Mammalian tissue has a level of thermal damage at 240 minutes at 108°F (42°C), 60 minutes at 109°F (43°C), 30 minutes at 111°F (44°C) or 15 minutes at 113°F (45°C).  This heat damage must be borne in mind following a race requiring suitable and appropriate cooling methods, otherwise inadequate cooling may lead to extended periods of thermal damage causing disease. 

The traditional viewpoint is that EHI is caused by strenuous exercise in extreme heat and/or humidity.  However, recent studies have revealed that environmental conditions may only cause 43% of EHI cases, thus, suggesting that other factors are involved.

2. Heat sepsis pathway

In some instances. a horse suffering from EHI may present with symptoms and clinical signs similar to sepsis like that seen in an acute bacterial infection. 

A bacterial infection leading to sepsis causes an extreme body response and a life threatening medical emergency.  Sepsis triggers a chain reaction throughout the body particularly affecting the lungs, urinary tract, skin and gastrointestinal tract.

Strenuous exercise in combination with adverse environmental conditions may lead to sepsis without the presence of a bacterial infection— also known as an endotoxemic pathway—causing poor oxygen supply to the mucosal gastrointestinal barrier. Ultimately, the integrity of the gastrointestinal tract is compromised, allowing endotoxins to enter the blood system and resulting in exercise-induced gastrointestinal syndrome (EIGS).

However, researchers have observed that EHI in racehorses is unpredictable as EHI may develop in horses following exercise despite “safe” environmental conditions.  Even with adequate cooling and resuscitative therapies, tissue damage that occurs demonstrates that thermoregulatory and inflammatory pathways may vary, and hyperthermia may be the trigger but may not necessarily be driving the condition.

Diagnosis of EHI

The diagnosis of EHI is based on the malfunctioning of the central nervous system.

Initially, hyperthermia reduces the blood flow to the cerebrum of the brain, leading to a decrease of oxygen to that area—also known as ischemia. As a result, the clinical signs are:

• Extreme restlessness

• Confusion

• Substantial headache

If this hyperthermia continues, then the blood-brain barrier (an immunological barrier between circulating blood that may contain microorganisms like bacteria and viruses to the central nervous system) begins to leak plasma proteins, resulting in cerebral oedema (build up of fluid causing affected organ to become swollen). If treatment is not initiated at this point, then neuronal injury will result especially in the cerebellum.

EHI follows and involves serious CNS dysfunction.  The clinical signs associated with EHI are:

• Delirium

• Horses unaware of their surroundings

The final stage of EHI occurs when the swollen oedematous brain compresses vital tissue causing cellular damage. The clinical signs of end-stage EHI are:

• Collapse

• Unconsciousness

• Coma

• Death

Definition of EHI

EHI most commonly occurs immediately after a race when the horse is panting, sweating profusely and may be dripping with sweat. The most reliable indication of EHI is clinical signs associated with the dysfunction of the central nervous system in the presence of hyperthermia. Researchers have provided descriptions of levels of CNS dysfunction, ranging from level 1 to level 4.

Level 1 – The earliest recognizable signs of CNS dysfunction

The horse becomes restless, agitated and irritable. There is often head nodding or head shaking. The horse is difficult to restrain and will not stand still.  Therapeutic intervention such as cooling can resolve these clinical signs, but if the horse is inadequately cooled then the disease can escalate. 

Level 2 – Obvious neurological dysfunction

Often misdiagnosed as colic symptoms, the horse becomes further agitated and irritable with the horse kicking out without any particular stimulus present. This stage is dangerous to all handlers involved as the horse’s behavior is unpredictable. 

Level 3 – Bizarre neurological signs

At this stage, the horse has an altered mentation appearing vacant, glassy-eyed and “spaced-out”.  In addition, there is extreme disorientation with a head tilt and leaning to one side with varying levels of ataxia (wobbly).  It has been observed that horses may walk forward, stop, rear and throw themselves backwards.  It is a very dangerous stage, as horses are known to run at fences, obstacles and people. Horses may also present as having a hind limb lameness appearing as a fractured leg with hopping on the good limb.  These clinical signs may resolve with treatment intervention.

Level 4 – Severe CNS dysfunction

There is severe CNS dysfunction at this stage of EHI with extreme ataxia, disorientation and lack of unawareness of its surroundings. The horse will continuously stagger and repeatedly fall down and get up while possibly colliding with people or objects with a plunging action. Unsurprising, the horse is at risk of severe and significant injury.  Eventual collapse with the loss of consciousness and even death may arise.

Treatment of EHI

In order to achieve success in the treatment of EHI, it is imperative that there is early detection, rapid assessment and aggressive cooling. The shorter the period is between recognising the condition and treatment, the greater the chance of a successful outcome.  In particular settings such as racecourses or on particularly hot and humid days, events must be properly equipped with easily accessible veterinary care and cooling devices. It is highly effective if a trained worker inspects every horse in order to identify those horses at risk or exhibiting symptoms. 

If EHI is recognised, veterinary intervention will be paramount in the recovery to prevent further illness and suppress symptoms. It will be important to note any withdrawal periods of any non-steroidal anti-inflammatories (NSAIDs) and analgesics before returning to racing. There are a number of effective ways to cool the horse with easily accessible resources.

Whole body cooling systems

Cooling the horse with ice-cold water is an effective way to draw heat from the underlying tissues. In addition, cooling the skin redistributes cooled blood back to the central circulatory system thus reducing thermal strain with the cooling of core body temperature.

The system that works best for horses due to its size is spray cooling heat transfer. It is ideal to have two operators to spray either side of the horse. It is recommended to begin at the head and neck followed by the chest and forelimbs then the body, hind limbs and between the legs. Spray nozzles are recommended to provide an even coverage of the skin surface.   

Dousing is another technique in which horses are placed in stalls and showered continuously until the condition resolves. Pouring buckets over the entire body of the horse is not recommended as most of the water falls to the ground, thus, not efficient at cooling the horse. 

Because most horses suffer from EHI immediately after the race, the appropriate location for inspection, cooling systems and veterinary care should be in the dismounting yard and tie-up stalls.  There must be an adequate supply of ice to ensure ice-cold water treatment. 

When treating a horse with EHI, there must be continuous and uninterrupted cooling until the CNS dysfunction has disappeared. 

When the skin surface temperature decreases to 86°F (30°C), cutaneous skin vessels begin to disappear; CNS function returns to normal, and there is the normalization of behavior. Cooling can be stopped, and the horse can be walked once CNS abnormalities have resolved. It must remain closely monitored for a further 30 minutes in a well-ventilated and shaded region. It is important that they are not unattended.

Scraping sweat off of the horse must only be done if the conditions are humid with no airflow.  However, if it is hot and there is good airflow, scraping is unnecessary because the sweat will evaporate.

Cooling collars

During strenuous exercise, there is a combination of heat production in the brain, reduced cerebral blood flow, creating cerebral ischaemia as well as the brain being perfused with hot blood. It is believed that cooling the carotid artery that aids in blood perfusion of the brain might be a strategy to cool the brain. A large collar is placed on either side and around the full length of the horse’s neck and is cooled by crushed ice providing a heat sink around the carotid artery; and it is able to pump cooled blood into the brain. 

Another possible benefit of this device is the cooling of the jugular veins, which lie adjacent to the carotid arteries.  The cooled blood in the jugular veins enter the heart and is pumped to the rest of the body, hence, potentially cooling the whole body. In addition, it is thought that the cooling of the carotid artery causes it to dilate, allowing greater blood flow into the brain. 

Provision of shaded areas

Shaded areas with surfaces that reflect heat, dry fans providing air flow and strategically placed hoses to provide cool water is an important welfare initiative at racecourses in order to minimize risk of EHI and treat when necessary. 

Conclusion

The most effective treatment of EHI is the early detection of the disease as well as post-race infrastructure that allows monitoring of horses in cooling conditions, while providing easily accessible treatment modalities when they are needed.  

Evaluating the horse’s central nervous system dysfunction is essential to recognise both the disease as well as monitoring the progression of the disease. CNS dysfunction allows one to define the severity of the condition. 

Understanding the pathophysiology of EHI is essential. It is important to recognise that it is a complex condition where both the inflammatory and thermoregulatory pathways work in combination. With a better understanding of these pathways, more effective treatment for this disease may be found.

Why bucked shins are so prevalent in the racehorse

Article by Adam Jackson MRCVS 

One of the most common causes of lost days to training and racing in racehorses is dorsal metacarpal disease (DMD), often referred to as “bucked shins” or “sore shins.” 

Often a frustration to trainers and owners, this problem rears its ugly head at the time of highest expectations, such as arising the last day of work before a horse’s first race, right after a horse’s first victory or after a horse was purchased at a two-year-old sale.

This disease presents with heat, pain with or without inflammation (swelling) on the dorsal (front) surface or the dorsomedial (front inside) surface of the third metacarpal bone (cannon), which is referred to as acute periostitis. With rest and reduced exercise, the condition can improve, but catastrophic fractures of the cannon may occur at the site of previous DMD episodes. A good understanding of this disease and strategies of prevention are vital in order to improve the welfare of the horse and reduce the potential expenses to all shareholders.  

Introduction

The cannon bone is an important structure in the weight bearing and absorbing shock. As the horse moves, the bone bends a little and then returns to its original shape like an elastic band, which is often referred to as elastic deformation. In addition, it has been observed that horses that work slowly have tension on the front of the cannon bone; in other words, the bone is stressed by a stretching force rather than a compressing force. However, at higher speeds, these forces change from stretching to compressing forces.

Repeated bending forces (stress cycle) on the cannon bone causes dorsal metatarsal disease. When the horse is young, it has a thin bone cortex. As the horse grows and is repeatedly subjected to these forces, the bones remodel and the cortex thickens, making it stronger. However, if the bending forces exceed the bone’s ability to remodel, then this leads to stress fatigue and bone damage.

The occurrence of bucked shins is most common when horses are developing, typically at two to three years old as training becomes more intensive. But it must be noted that if the horse is not bone fit, any aged racehorse is susceptible to these diseases when they begin training. Roughly at the age of five years, when a horse is fit, they are at a low risk of this disease. Within the first six months of training, DMD may present in one or both front limbs. If the condition does occur in both front limbs and the horse is being trained on a circular track, then it is likely the inside leg is where it will occur first. In other words, if the training tends to be in a counterclockwise training circuit, then there are greater forces on the left limb than the right, thus the left is more likely to develop the disease before the right limb.

Risk Factors of DMD

1. Age: DMD occurs most commonly in two to three-year-olds often within their first six months of training. It is rarely seen in horses with a mature skeleton (age four and over). However, this disease has been seen in five-year-olds especially if they have been stalled for a long amount of time after weaning and not racing until that age.

2. Gender: It is believed that the gender of the horse does not alter its risk to DMD.

3. Breed: Most common in Thoroughbreds but may be seen in both Standardbreds and Quarter horses. 

4. Genetics: The risk of DMD is influenced by genetics as variation in limb bone geometry (inherited) behaves differently to force/strains on the bone. In addition, the longer the cannon bone, the greater the load is at flexion of the dorsal cortex of the bone, making it more susceptible to DMD.

5. Training and racing surfaces: The different types of training and racing surface alter the risk to DMD because there are variations in the force applied to limbs as well as the acceleration rates of hoof impact.  Furthermore, the impact of these forces is increased with greater speed.  Dirt tracks tend to be the hardest surface, whereas synthetic tracks reduce hoof and limb impact and loading force. However, it is important to remember that the hardness all of these surfaces can be altered by a number of other factors such as:

Training and racing surfaces

• Different surface materials

• Changes in weather, temperature and humidity

• Surface maintenance (i.e., soaking, harrowing)

• Changes in horse body weight

• Age of surface, wear and tear of surface

• Human opinion of condition of track

  6. Training: The length of time for bones to respond to different training practices is unknown. Although further research is required, it is suggested that fast work should be avoided in the early stages of training as it is thought that high-speed exercise introduced too quickly (within one month) was detrimental to bone health.

  7. Direction of training: Track direction varies globally. Thoroughbreds tend to lead with the inside forelimb around turns then switch to the outer forelimb on the straight. It has been suggested that due to greater forces on the leading limb on the turn, that limb is more at risk of bucked shins. However, more research is required to make accurate conclusions.

  8. Speed: Current research is contradictory. Some research indicates a reduction in the risk of DMD if the horse is trained at high speeds with every extra mile worked, and canter work increases the risk. However, other research suggests that short periods of work (< 1 month) at high speed increases the risk of DMD.

  9. Camber: In the U.S., tracks are usually flat in contrast with European tracks, which tend to vary in their design and often include slopes, twists, turns, uphill sections, and cambers, with turf being the prevalent surface.   In addition, races may be run straight, clockwise or counterclockwise.  Although it is known that this variation in track characteristics alters the horse’s gait, thus altering forces on the forelimbs, further research is needed to understand if these variations increase the risk of DMD.

How does DMD develop?

Bucked shin is the formation of tiny stress fractures on the front or inside of the cannon bone of the horse’s front legs. DMD occurs when the stress on the legs with high-speed training exceeds the bone’s ability to adapt to those stresses. 

Bone is a dynamic tissue that is constantly adapting its structure. Once the bone is formed in immature animals, the bone grows and changes shape by a process called modeling. Bone remodeling is different to modeling in that its function is to renew the skeleton and involves both bone resorption and formation to occur at the same location in a sequential manner.   

With high-speed training, there is high-strain fatigue, which causes excessive compression of the bone. During this compression, there is an insufficient amount of bone remodeling at the point of stress. At this site, this new bone is much weaker; thus, it is susceptible to inflammation, and pain and may lead to fractures.

Treatment of dorsal metacarpal disease

Treatment of DMD is designed to alleviate pain and inflammation while allowing the remodeling process of the bone to catch up with the damage that has been caused from stress cycling.

The core of the treatment is rest and providing pain relief, followed by a slow and gradual increase in exercise levels. 

Fractures of the bone cortex can be treated with surgery using lag screw fixation and osteostixis. Osteostixis is the drilling of many holes around the site of fracture in order to promote bone healing. Lag screw fixation is the drilling of a screw across the fracture line to compress and stabilize the bone. However, fracture recurrence is common with both techniques and requires five to six months out of training.

There are additional treatments that may be used to complement core treatments. Extracorporeal shock wave therapy (ESWT) is commonly used for treatment and involves a highly concentrated, powerful acoustic (sound) energy source being applied to the site of injury. The rationale is that ESWT increases blood flow, increases growth of new blood vessels and increases the production of natural healing factors in the treated area. The research findings are limited on its effectiveness but anecdotally among the veterinary profession, it seems to work on bucked shins and stress fractures. 

In North America, horses are not permitted to race or breeze for 30 days following treatment as per the Horseracing Integrity and Safety Authority’s (HISA) rulings. In Europe, horses must not have had shock wave therapy on the day of racing, or on any of the five days before the race day in which the horse is declared to run. 

With all treatment options, there must be a careful and considered discussion with the veterinarian and all stakeholders on the desired outcome while bearing in mind the important factor of the horse’s welfare and wellbeing.

What about bisphosphonates?

Some clinicians are using a combination of shockwave and bisphosphonates (TildrenTM, OsPhosTM) to treat DMD. Bisphosphonates were first seen in human medicine and used for osteoporosis. Bones are constantly remodeling in a process that removes old bone cells and deposits new ones. Bisphosphonates help prevent bones from losing calcium and other minerals by slowing or stopping that natural process that dissolves bone tissue, thus, helping bones remain strong and intact. Veterinary surgeons report mixed results with these therapies, and long-term use of bisphosphonates is expensive and has serious consequences. Bisphosphonates are toxic to the gastrointestinal and renal systems, thus, potentially causing colic and kidney disease. Their safety has not been evaluated for the use in horses younger than four years old nor in pregnant and lactating mares.

RULES ARE CHANGING - Bisphosphonates

HISA’s Anti-Doping and Medication Control (ADMC) Program came into effect on March 27 and with it, new regulations regarding the presence and use of bisphosphonates.

The Horseracing Integrity & Welfare Unit (HIWU) states “The ADMC Program regulations categorize bisphosphonates as a banned substance, meaning that they are prohibited from being administered to, or present in, covered horses at any time. Covered horses that test positive for bisphosphonates under the ADMC Program are subject to lifetime ineligibility, and associated covered persons may incur an Anti-Doping Rule Violation.”

“HIWU will not pursue disciplinary action against Covered Horses or their associated covered person(s) for the presence of bisphosphonates if the covered person(s) can provide documentation (e.g., medical records or a positive test result) to HIWU of the administration or presence of bisphosphonates prior to the implementation date of the ADMC Program.” 

In Europe, bisphosphonates are not to be administered to a racehorse under the age of three years and six months as determined by its recorded date of birth, on the day of the race or on any of the 30 days before the day of the race in which the horse is declared to run as per The International Federation of Horseracing Authorities rulings.

Training Regimens

With DMD, it must be remembered that it is an appropriate response for new bone formation when the cannon endures cyclic stress and injury. This injury cannot be ignored but addressed to reduce the risk of serious consequences.  Exercise is the root of the problem; therefore, the solution is to alter the patterns of exercise.   

Dr. David Nunamaker, DVM, of the University of Pennsylvania, has developed a training program, which is believed to reduce the risk of DMD. The rationale when developing this modified training program is that horses are not born with the right bone structure for racing.  The bones are to develop and adapt to racing. By providing training programs that mimic racing, the bones can adapt to the forces that are applied during racing, thus, reducing the risk of developing bucked shins.

When initiating this training regimen, it is assumed that young horses are broken to ride in autumn and able to gallop a mile by January so that training can start. 

Stage 1 (5-week duration) – Horses finish the gallops two times a week with the last 1/8th of the mile (last 200 meters of 1600 meters) completed in an open gallop in 15 seconds.

Stage 2 (5-week duration) – Twice a week, open gallops for ¼ of a mile (400 meters of 1600 meters) in 30 seconds including a one-mile (1600 meters) gallop.

Stage 3 (7-week duration) – The addition of speed work once per week.  Breezing (moderate speed) for ¼ mile (400 meters) and daily gallops lengthened to 1¼ miles twice per week for four weeks. In the following three weeks, the ¼ mile breeze is continued with a strong gallop out for another furlong (roughly 40 seconds total for a breeze). 

Conclusion

The findings of exercise research are often varied and contradictory due to many research variables, making comparisons and conclusions difficult. In addition, most of the research of musculoskeletal issues in racehorses uses racing data, but most injuries occur during training.

Because more research is needed, there remain conflicting views of the effects of racing on horses before skeletal maturity and the most effective and safe way to introduce speed exercise. At present, the data suggests that distance and speed should be implemented gradually and should include high-speed work at full racing speed.

The racing industry must continue to work cooperatively to address the welfare concerns associated with horses experiencing DMD.

EIPH - could there be links to sudden death and pulmonary haemorrhage?

Dr Peter W. Physick-Sheard, BVSc, FRCVS, explores preliminary research and hypotheses, being conducted by the University of Guelph, to see if there is a possibility that these conditions are linked and what this could mean for future management and training of thoroughbreds. 

"World's Your Oyster,” a three-year-old thoroughbred mare, presented at the veterinary hospital for clinical examination. She won her maiden start as a two-year-old and placed once in two subsequent starts. After training well as a three-year-old, she failed to finish her first start, easing at the top of the stretch, and was observed to fade abruptly during training. Some irregularity was suspected in heart rhythm after exercise. Thorough clinical examination, blood work, ultrasound of the heart and an ECG during rest and workout revealed nothing unusual. 

Returning to training, Oyster placed in six of her subsequent eight starts, winning the last two. She subsequently died suddenly during early training as a four-year-old. At post-mortem, diagnoses of pulmonary haemorrhage and exercise-induced pulmonary haemorrhage were established—a very frustrating and unfortunate outcome.

Across the racing world, a case like this probably occurs daily. Anything that can limit a horse's ability to express its genetic potential is a major source of anxiety when training. The possibility of injury and lameness is the greatest concern, but a close second is respiratory disease, with bleeding  from the lungs (most often referred to as exercise induced pulmonary [lung] haemorrhage or EIPH) being high on the list. 

EIPH is thought to occur in as many as 85 percent of racehorses, and may initially be very mild without obvious clinical consequences. In some cases it can be associated with haemorrhage of sufficient severity for blood to appear at the nostrils, even at first occurrence. In many racing jurisdictions this is a potentially career-ending problem. In these horses, an impact on performance is unquestionable. Bleeding from the lungs is the reason for the existence of ‘Lasix programs,’ involving pre-race administration of a medication considered to reduce haemorrhage. Such programs are controversial—the justifications for their existence ranging from addressing welfare concerns for the horse to dealing with the performance impacts. 

Much less frequently encountered is heavy exercise-associated bleeding from the nostrils (referred to as epistaxis), which can sometimes be accompanied by sudden death, during or shortly after exercise. Some horses bleed heavily internally and die without blood appearing at the nostrils. Haemorrhage may only become obvious when the horse is lying on its side, or not until post-mortem. Affected animals do not necessarily have any history of EIPH, either clinically or sub-clinically. There is an additional group of rare cases in which a horse simply dies suddenly, most often very soon after work and even after a winning performance, and in which little to nothing clearly explains the cause on post-mortem. This is despite the fact most racing jurisdictions study sudden death cases very closely.

EIPH is diagnosed most often by bronchoscopy—passing an endoscope into the lung after work and taking a look. In suspected but mild cases, there may not be sufficient haemorrhage to be visible, and a procedure called a bronchoalveolar lavage is performed. The airways are rinsed and fluid is collected and examined microscopically to identify signs of bleeding. Scoping to confirm diagnosis is usually a minimum requirement before a horse can be placed on a Lasix program. 

Are EIPH, severe pulmonary haemorrhage and sudden death related? Are they the same or different conditions? 

At the University of Guelph, we are working on the hypothesis that most often they are not different—that it’s degrees of the same condition, or closely related conditions perhaps with a common underlying cause. We see varying clinical signs as being essentially a reflection of severity and speed of onset of underlying problems. 

Causes in individual cases may reflect multiple factors, so coming at the issues from several different directions, as is the case with the range of ongoing studies, is a good way to go so long as study subjects and cases are comparable and thoroughly documented. However, starting from the hypothesis that these may all represent basically the same clinical condition, we are approaching the problem from a clinical perspective, which is that cardiac dysfunction is the common cause. 

Numerous cardiac disorders and cellular mechanisms have the potential to contribute to transient or complete pump (heart) failure. However, identifying them as potential disease candidates does not specifically identify the role they may have played, if any, in a case of heart failure and in lung haemorrhage; it only means that they are potential primary underlying triggers. It isn't possible for us to be right there when a haemorrhage event occurs, so almost invariably we are left looking at the outcome—the event of interest has passed. These concerns influence the approach we are taking.

Background

The superlative performance ability of a horse depends on many physical factors:

• Huge ventilatory (ability to move air) and gas exchange capacity

• Body structure including limb length and design - allows it to cover ground rapidly with a long stride

• Metabolic adaptations - supports a high rate of energy production by burning oxygen, tolerance of severe metabolic disruptions toward the end of race-intensity effort

• High cardiovascular capacity - allows the average horse to pump roughly a brimming bathtub of blood every minute

At race intensity effort, these mechanisms, and more, have to work in coordination to support performance. There is likely not much reserve left—two furlongs (400m) from the winning post—even in the best of horses. There are many wild cards, from how the horse is feeling on race day to how the race plays out; and in all horses there will be a ceiling to performance. That ceiling—the factor limiting performance—may differ from horse to horse and even from day to day. There’s no guarantee that in any particular competition circumstances will allow the horse to perform within its own limitations. One of these factors involves the left side of the heart, from which blood is driven around the body to the muscles.

A weak link - filling the left ventricle

The cardiovascular system of the horse exhibits features that help sustain a high cardiac output at peak effort. The feature of concern here is the high exercise pressure in the circulation from the right  ventricle, through the lungs to the left ventricle. At intense effort and high heart rates, there is very little time available to fill the left ventricle—sometimes as little as 1/10 of a second; and if the chamber cannot fill properly, it cannot empty properly and cardiac output will fall. The circumstances required to achieve adequate filling include the readiness of the chamber to relax to accept blood—its ‘stiffness.’ Chamber stiffness increases greatly at exercise, and this stiffened chamber must relax rapidly in order to fill. That relaxation seems not to be sufficient on its own in the horse at high heart rates. Increased filling pressure from the circulation draining the lungs is also required. But there is a weak point: the pulmonary capillaries.

These are tiny vessels conducting blood across the lungs from the pulmonary artery to the pulmonary veins. During this transit, all the gas exchange needed to support exercise takes place. The physiology of other species tells us that the trained lung circulation achieves maximum flow (equivalent to cardiac output) by reducing resistance in those small vessels. This process effectively increases lung blood flow reserve by, among other things, dilating small vessels. Effectively, resistance to the flow of blood through the lungs is minimised. We know this occurs in horses as it does in other species; yet in the horse, blood pressure in the lungs still increases dramatically at exercise. 

If this increase is not the result of resistance in the small vessels, it must reflect something else, and that appears to be resistance to flow into the left chamber. This means the entire lung circulation is exposed to the same pressures, including the thin-walled capillaries. Capillaries normally work at quite low pressure, but in the exercising horse, they must tolerate very high pressures. They have thin walls and little between them, and the air exchange sacs in the lung. This makes them vulnerable. It's not surprising they sometimes rupture, resulting in lung haemorrhage.

Recent studies identified changes in the structure of small veins through which the blood flows from the capillaries and on toward the left chamber. This was suspected to be a pathology and part of the long-term consequences of EIPH, or perhaps even part of the cause as the changes were first identified in EIPH cases. It could be, however, that remodelling is a normal response to the very high blood flow through the lungs—a way of increasing lung flow reserve, which is an important determinant of maximum rate of aerobic working. 

The more lung flow reserve, the more cardiac output and the more aerobic work an animal can perform. The same vein changes have been observed in non-racing horses and horses without any history or signs of bleeding. They may even be an indication that everything is proceeding as required and a predictable consequence of intense aerobic training. On the other hand, they may be an indication in some horses that the rate of exercise blood flow through their lungs is a little more than they can tolerate, necessitating some restructuring. We have lots to learn on this point.

If the capacity to accommodate blood flow through the lungs is critical, and limiting, then anything that further compromises this process is likely to be of major importance. It starts to sound very much as though the horse has a design problem, but we shouldn't rush to judgement. Horses were probably not designed for the very intense and sustained effort we ask of them in a race. Real-world situations that would have driven their evolution would have required a sprint performance (to avoid ambush predators such as lions) or a prolonged slower-paced performance to evade predators such as wolves, with only the unlucky victim being pushed to the limit and not the entire herd. 

Lung blood flow and pulmonary oedema

There is another important element to this story. High pressures in the capillaries in the lung will be associated with significant movement of fluid from the capillaries into lung tissue spaces. This movement in fact happens continuously at all levels of effort and throughout the body—it's a normal process. It's the reason the skin on your ankles ‘sticks’ to the underlying structures when you are standing for a long time. So long as you keep moving a little, the lymphatic system will draw away the fluid. 

In a diseased lung, tissue fluid accumulation is referred to as pulmonary oedema, and its presence or absence has often been used to help characterise lung pathologies. The lung lymphatic system can be overwhelmed when tissue fluid is produced very rapidly. When a horse experiences sudden heart failure, such as when the supporting structures of a critical valve fail, one result is massive overproduction of lung tissue fluid and appearance of copious amounts of bloody fluid from the nostrils. 

The increase in capillary pressure under these conditions is as great as at exercise, but the horse is at rest. So why is there no bloody fluid in the average, normal horse after a race? It’s because this system operates very efficiently at the high respiratory rates found during work: tissue fluid is pumped back into the circulation, and fluid does not accumulate. The fluid is pumped out as quickly as it is formed. An animal’s level of physical activity at the time problems develop can therefore make a profound difference to the clinical signs seen and to the pathology.

Usual events with unusual consequences 

If filling the left ventricle and the ability of the lungs to accommodate high flow at exercise are limiting factors, surely this affects all horses. So why do we see such a wide range of clinical pictures, from normal to subclinical haemorrhage to sudden death? 

Variation in contributing factors such as type of horse, type and intensity of work, sudden and unanticipated changes in work intensity, level of training in relation to work and the presence of disease states are all variables that could influence when and how clinical signs are seen, but there are other considerations.

Although we talk about heart rate as a fairly stable event, there is in fact quite a lot of variation from beat to beat. This is often referred to as heart rate variability. There has been a lot of work performed on the magnitude of this variability at rest and in response to various short-term disturbances and at light exercise in the horse, but not a lot at maximal exercise. Sustained heart rate can be very high in a strenuously working horse, with beats seeming to follow each other in a very consistent manner, but there is in fact still variation. 

Some of this variation is normal and reflects the influence of factors such as respiration. However, other variations in rate can reflect changes in heart rhythm. Still other variations may not seem to change rhythm at all but may instead reflect the way electrical signals are being conducted through the heart. 

These may be evident from the ECG but would not appear abnormal on a heart rate monitor or when listening. These variations, whether physiologic (normal) or a reflection of abnormal function, will have a presently, poorly understood influence on blood flow through the lungs and heart—and on cardiac filling. Influences may be minimal at low rates, but what happens at a heart rate over 200 and in an animal working at the limits of its capacity?

Normal electrical activation of the heart follows a pattern that results in an orderly sequence of heart muscle contraction, and that provides optimal emptying of the ventricles. Chamber relaxation complements this process. 

An abnormal beat or abnormal interval can compromise filling and/or emptying of the left ventricle, leaving more blood to be discharged in the next cycle and back up through the lungs, raising pulmonary venous pressure. A sequence of abnormal beats can lead to a progressive backup of blood, and there may not be the capacity to hold it—even for one quarter of a second, a whole cardiac cycle at 240 beats per minute. 

For a horse that has a history of bleeding and happens to be already functioning at a very marginal level, even minor disturbances in heart rhythm might therefore have an impact. Horses with airway disease or upper airway obstructions, such as roarers, might find themselves in a similar position. An animal that has not bled previously might bleed a little, one that has a history of bleeding may start again, or a chronic bleeder may worsen. 

Relatively minor disturbances in cardiac function, therefore, might contribute to or even cause EIPH. If a horse is in relatively tough company or runs a hard race, this may also contribute to the onset or worsening of problems. Simply put, it's never a level playing field if you are running on the edge.

Severe bleeding

It has been suspected for many years that cases of horses dying suddenly at exercise represent sudden-onset cardiac dysfunction—most likely a rhythm disturbance. If the rhythm is disturbed, the closely linked and carefully orchestrated sequence of events that leads to filling of the left ventricle is also disturbed. A disturbance in cardiac electrical conduction would have a similar effect, such as one causing the two sides of the heart to fall out of step, even though the rhythm of the heart may seem normal. 

The cases of horses that bleed profusely at exercise and even those that die suddenly without any post-mortem findings can be seen to follow naturally from this chain of events. If the changes in heart rhythm or conduction are sufficient, in some cases to cause massive pulmonary haemorrhage, they may be sufficient in other cases to cause collapse and death even before the horse has time to exhibit epistaxis or even clear evidence of bleeding into the lungs. 

EIPH and dying suddenly

If these events are (sometimes) related, why is it that some horses that die of pulmonary haemorrhage with epistaxis do not show evidence of chronic EIPH? This is one of those $40,000 questions. It could be that young horses have had limited opportunity to develop chronic EIPH; it may be that we are wrong and the conditions are entirely unrelated. But it seems more likely that in these cases, the rhythm or conduction disturbance was sufficiently severe and/or rapid in onset to cause a precipitous fall in blood pressure with the animal passing out and dying rapidly. 

In this interpretation of events, the missing link is the heart. There is no finite cutoff at which a case ceases to be EIPH and becomes pulmonary haemorrhage. Similarly, there is no distinct point at which any case ceases to be severe EIPH and becomes EAFPH (exercise-associated fatal pulmonary haemorrhage). In truth, there may simply be gradation obscured somewhat by variable definitions and examination protocols and interpretations.

The timing of death

It seems from the above that death should most likely take place during work, and it often does, but not always. It may occur at rest, after exercise. Death ought to occur more often in racing, but it doesn't. 

The intensity of effort is only one factor in this hypothesis of acute cardiac or pump failure. We also have to consider factors such as when rhythm disturbances are most likely to occur (during recovery is a favourite time) and death during training is more often a problem than during a race. 

A somewhat hidden ingredient in this equation is possibly the animal's level of emotional arousal, which is known to be a risk factor in humans for similar disturbances. There is evidence that emotions/psychological factors might be much more important in horses than previously considered. Going out for a workout might be more stimulating for a racehorse than a race because before a race, there is much more buildup and the horse has more time to adequately warm up psychologically. And then, of course, temperament also needs to be considered. These are yet further reasons that we have a great deal to learn.

Our strategy at the University of Guelph

These problems are something we cannot afford to tolerate, for numerous reasons—from perspectives of welfare and public perception to rider safety and economics. Our aim is to increase our understanding of cardiac contributions by identifying sensitive markers that will enable us to say with confidence whether cardiac dysfunction—basically transient or complete heart failure—has played a role in acute events. 

We are also looking for evidence of compromised cardiac function in all horses, from those that appear normal and perform well, through those that experience haemorrhage, to those that die suddenly without apparent cause. Our hope is that we can not only identify horses at risk, but also focus further work on the role of the heart as well as the significance of specific mechanisms. And we hope to better understand possible cardiac contributions to EIPH in the process. This will involve digging deeply into some aspects of cellular function in the heart muscle, the myocardium of the horse, as well as studying ECG features that may provide insight and direction. 

Fundraising is underway to generate seed money for matching fund proposals, and grant applications are in preparation for specific, targeted investigations. Our studies complement those being carried out in numerous, different centres around the world and hopefully will fill in further pieces of the puzzle. This is, indeed, a huge jigsaw, but we are proceeding on the basis that you can eat an elephant if you're prepared to process one bite at a time.

How can you help? Funding is an eternal issue. For all the money that is invested in horses there is a surprisingly limited contribution made to research and development—something that is a mainstay of virtually every other industry; and this is an industry. 

Look carefully at the opportunities for you to make a contribution to research in your area. Consider supporting studies by making your experience, expertise and horses available for data collection and minimally invasive procedures such as blood sampling. 

Connect with the researchers in your area and find out how you can help. Watch your horses closely and contemplate what they might be telling you—it's easy to start believing in ourselves and to stop asking questions. Keep meticulous records of events involving horses in your care— you never know when you may come across something highly significant. And work with researchers (which often includes track practitioners) to make your data available for study. 

Remember that veterinarians and university faculty are bound by rules of confidentiality, which means what you tell them should never be ascribed to you or your horses and will only be used without any attribution, anonymously. And when researchers reach out to you to tell you what they have found and to get your reactions, consider actually attending the sessions and participating in the discussion; we can all benefit—especially the ultimate beneficiary which should be the horse. We all have lots to learn from each other, and finding answers to our many challenges is going to have to be a joint venture.  

Finally, this article has been written for anybody involved in racing to understand, but covering material such as this for a broad audience is challenging. So, if there are still pieces that you find obscure, reach out for help in interpretation. The answers may be closer than you think!

Oyster

And what about Oyster? Her career was short. Perhaps, had we known precisely what was going on, we might have been able to treat her, or at least withdraw her from racing and avoid a death during work with all the associated dangers—especially to the rider and the associated welfare concerns. 

Had we had the tools, we might have been able to confirm that whatever the underlying cause, she had cardiac problems and was perhaps predisposed to an early death during work. With all the other studies going on, and knowing the issue was cardiac, we might have been able to target her assessment to identify specific issues known to predispose. 

In the future, greater insight and understanding might allow us to breed away from these issues and to better understand how we might accommodate individual variation among horses in our approaches to selection, preparation and competition. There might be a lot of Oysters out there!

For further information about the work being undertaken by the University of Guelph

Contact - Peter W. Physick-Sheard, BVSc, FRCVS.

Professor Emeritus, Ontario Veterinary College, University of Guelph - pphysick@uoguelph.ca

Research collaborators - Dr Glen Pyle, Professor, Department of Biomedical Sciences, University of Guelph - gpyle@uoguelph.ca

Dr Amanda Avison, PhD Candidate, Department of Biomedical Sciences, University of Guelph. ajowett@uoguelph.ca

References

Caswell, J.I. and Williams K.J. (2015), Respiratory System, In ed. Maxie, M. Grant, 3 vols., 6th edn., Jubb, Kennedy and Palmer’s Pathology of Domestic Animals, 2; London: Elsevier Health Sciences, 490-91.

Hinchcliff, KW, et al. (2015), Exercise induced pulmonary hemorrhage in horses: American College of Veterinary Internal Medicine consensus statement, J Vet Intern Med, 29 (3), 743-58.

Rocchigiani, G, et al. (2022), Pulmonary bleeding in racehorses: A gross, histologic, and ultrastructural comparison of exercise-induced pulmonary hemorrhage and exercise-associated fatal pulmonary hemorrhage, Vet Pathol, 16:3009858221117859. doi: 10.1177/03009858221117859. Online ahead of print.

Manohar, M. and T. E. Goetz (1999), Pulmonary vascular resistance of horses decreases with moderate exercise and remains unchanged as workload is increased to maximal exercise, Equine Vet. J., (Suppl.30), 117-21.

Vitalie, Faoro (2019), Pulmonary Vascular Reserve and Aerobic Exercise Capacity, in Interventional Pulmonology and Pulmonary Hypertension, Kevin, Forton (ed.), (Rijeka: IntechOpen), Ch. 5, 59-69.

Manohar, M. and T. E. Goetz (1999), Pulmonary vascular resistance of horses decreases with moderate exercise and remains unchanged as workload is increased to maximal exercise, Equine Vet. J., (Suppl.30), 117-21.

The Often Overlooked Equine Sacroiliac Joint

Horses that present as sore in the hindquarters can be perplexing to diagnose. Sometimes the problem is found in the last place you look – the sacroiliac joint.

Article by Annie Lambert

Even though the sacroiliac joint (SI) was on veterinary radars long ago, due to its location buried under layers of muscle in the equine pelvic region, the joint and surrounding ligaments were tough to diagnose and treat.

The sacroiliac joint is often a source of lower back discomfort in race and performance horses. Trainers may notice several clinical signs of a problem. These hints include sensitivity to grooming, objections to riders getting legged up, stiffness of motion, pain to manual palpation of the rump or back, resistance to being shod behind and poor performance.

Of course, those symptoms could describe other hind limb soundness issues, making the origin of the problem arduous to ascertain. A thorough physical examination with complete therapeutic options can relieve sacroiliac pain. The treatments are complicated, however, by the anatomy of the SI area. 

The equine pelvis is composed of three fused bones: ilium, ischium and pubis. The sacrum, the lower part of the equine back, is composed of five fused vertebrae. The sacroiliac joint is located where the sacrum passes under the top of the pelvis (tubera sacrale). The dorsal, ventral and interosseous sacroiliac ligaments help strengthen the SI joint. 

The SI and surrounding ligaments provide support during weight bearing, helping to transfer propulsive forces of the hind limbs to the vertebral column—creating motion much like the thrust needed to break from the starting gate.

Sound complicated? It certainly can be.

Diagnosing Dilemmas

It wasn’t until modern medical technology advanced that the SI could be explored seriously as a cause of hind lameness.

“The sacroiliac is one of the areas that’s very hard to diagnose or image,” explained Dr. Michael Manno, a senior partner of San Dieguito Equine Group in San Marcos, California. “[Diagnostics] of the area probably correlated with bone scans or nuclear scintigraphy. You can’t really use radiographs because the horse is so massive and there is so much muscle, you can’t get a good image.

“About the only time you can focus on the pelvis and get a decent radiograph is if the horse is anesthetized—you have a big [x-ray] machine and could lay the horse down. But, it’s hard because with anything close to a pelvic injury, the last thing you want to do is lay them down and have them have to get back up.”  

The nuclear scintigraphs give a good image of hip, pelvis and other anatomical structures buried deep in the equine body, according to Manno, a racetrack practitioner. “Those images can show areas of inflammation that could pretty much be linked right to the SI joint.”

The other modern technological workhorse in the veterinary toolbox is the digital ultrasound machine. Manno pointed out that veterinarians improved diagnostics as they improved their ultrasounding skills and used those skills to ultrasound areas of the body they never thought about before. Using different techniques, frequencies and various heads on the machine’s probe, the results can be fairly remarkable.

“The ultrasound showed you could really image deeper areas of the body, including an image of the sacroiliac joint,” Manno said. “It can also show some ligament issues.”

Where the SI is buried under the highest point of a horse’s rump, and under heavy gluteal muscles, there are two sets of ligaments that may sustain damage and cause pain. The dorsal sacroiliac ligaments do not affect the sacroiliac joint directly, but help secure the ilium to the sacral spine. The ventral sacroiliac ligaments lie deeper, in the sacroiliac joint area, which they help stabilize. These hold the pelvis tight against its spine. The joint itself, being well secured by these ligaments, has little independent movement and therefore contains only minimal joint fluid.

Diagnosing the SI can be complex because horses often travel their normal gait with no change from normal motion—no signs of soreness. Other horses, however, are sore on one leg or another to varying degrees, sometimes with a perceptible limp. 

“I don’t know that there is a specific motion,” Manno explained. “You just know that you have a hind end lameness, and I think a lot of performance horses have mildly affected SI joints. 

“The horses that are really severe become acutely lame behind, very distinct. You go through the basic diagnostics, and I think most of these horses will show you similar signs as other issues behind. We palpate along the muscles on either side of their spine and they are sore, or you palpate over their croup and you can get them to drop down—that kind of thing. Other times you do an upper limb flexion on them and they might travel weird on the opposite leg. So, it can be a little confusing.” 

In the years prior to the early 2000s, the anatomical location of the SI hindered a definite diagnosis; decisions on hind soreness were more of a shrug, “time and rest” treatment evaluation. As one old-time practitioner called it, a SWAG – “Scientific Wild Ass Guess.”

Even with modern tools, making a conclusive diagnosis can be opaque.

“The less affected horses, through exercise and with medications like Robaxin [muscle relaxer] or mild anti-inflammatories, seem to be able to continue to perform,” Manno said. “I don’t know how you can be perfectly sure of an inside joint unless you try to treat it and get results.”

“That’s why bone scans came into play and are really helpful,” Manno added. “You can image that [SI] area from different angles with the machine right over the path of the pelvis, looking down on it or an angle view into it, and then you see it from the side and the back very often. We can get an idea from the different views and angles of where the inflammation is and pinpoint the problem from that.” 

Once Manno has a generalized idea of where the problem is, he fine-tunes his hypothesis using more diagnostics with a digital ultrasound machine. 

“You can ultrasound from up above and see the joint that way,” he said. “As ultrasound has progressed, we’ve found that the rectal probes the breeding vets have used can also be tuned in to start looking for other things. If you turn them upwards, you can look at the bottom of the pelvis and the SI joint. You can see things through the rectum by just looking straight up. That is a whole new thing that we probably never thought about doing. I don’t profess to be very great at it; it’s not something I do a lot, but there are people that are just wonderful at it.” 

Treating a Theorem

But, if the diagnosis is incorrect, the prescribed treatment may be anything but helpful.

“In many cases, if a horse is really sore, you need to be very careful,” cautioned Manno. “What you don’t want to do is go from a strain or some sort of soft tissue injury into a pelvic fracture by trying to keep them going. In many cases you are back in the old rest and time type of treatment.”

Manno pointed out one treatment that has advanced over many years is injecting the SI joint directly. There are a couple of techniques used when injecting the SI. With a blind injection the practitioner directs a long, straight needle into the joint by relying solely on equine anatomy. The other technique employs an ultrasound machine to guide the placement of the needle into the joint.

“Normally we are just injecting cortisone in those cases,” Manno noted. “We are trying to get the inflammatory response to settle down. Hopefully that gives the horse some relief so that they’re a bit more relaxed in their musculature. You know how it is when you get a sore back; it’s hard to keep yourself from cramping, which makes everything worse.”

A slight tweak of that technique is to use a curved needle. When you are positioning the curved needle, it follows the curve of the horse’s anatomy and helps the practitioner direct the injection into the joint.

“It curves right into position for you; it gives you a little help,” Manno confirmed of the curved needle. “Some people are really good with that technique; others still like to go to the straight needle. [The curved needle] helps you approach the site without interference from the bones in that area.”

SI joint injuries affect most performance horses, including Standardbred trotters and pacers, Western performance athletes as well as hunters, jumpers and dressage horses.

The older show horses are often diagnosed with chronic SI pain, sometimes complicated by arthritis. These chronic cases—and admittedly some racehorses—are treated with different therapies. These conservative, nonsurgical treatments have been proven effective.

In addition to stall rest and anti-inflammatories, physical training programs can be useful in tightening the equine patient’s core and developing the topline muscles toward warding off SI pain. Manno, a polo player who also treats polo ponies, believes the hard-working ponies avoid having many SI injuries due to their fitness levels. 

“I think these polo horses are similar to a cross between a racehorse and a cutting horse,” Manno opined. “They are running distances and slide stopping and turning.”

Other treatments utilized include shockwave, chiropractic, acupuncture, therapeutic laser and pulsed electromagnetic therapy.

Superior Science

With the new diagnostic tools and advanced protocols in their use, veterinarians can pinpoint the SI joint and surrounding areas much closer. This gives them an improved indication that there definitely is an issue with the sacroiliac. 

When there is a question about what is causing hind end lameness, most practitioners begin with blocking from the ground up.

“In many cases with hind end lameness that we can’t figure out, we block the lower leg; if it doesn’t block out down low, we conclude the problem is up high,” Manno said. “Once you get up to the hock you’re out of options of what you can figure out. You start shooting some x-rays, but by the time you get to the stifle, you’re limited. Bone scans and ultrasounds have certainly helped us with diagnosing.”

Manno doesn’t see a lot of SI joint injuries in his practice, but he noted there were cases every now and again. He also opined that there were probably other cases that come up in racehorses on a short-term basis. He also noted that, although it may not be a real prominent injury, that’s not to say it has not gone undiagnosed.

“I think we realize, in many of the horses we treat, that the SI joint is something that may have been overlooked in the past,” Manno concluded. “We just didn’t have the ability to get any firm diagnosis in that area.”

Racetrack Fracture Support Equipment - coming to North America this summer

Words - Ian Wright

Over the last six months, British racecourses have taken a major step forward in racehorse welfare by being provided with fracture support systems (Figure 1). These consist of two sizes of compression boots and flexion splints, both for use in the forelimbs; and a set of modular adjustable splints. Together, these provide appropriate rigid external support for the vast majority of limb fractures that occur during racing. The general principles are that management of all fractures is optimized by applying rapid and appropriate support to provide stability, reduce pain and relieve anxiety. 

Figure 1

The fracture support systems are about to make their debut in North America with trials due to take place this summer and fall with the support of the National HBPA.

The fracture support system is provided in two mobile impact resistant carrying boxes that protect the equipment and allow it to be checked before racing. All boots and splints are permanently labeled with individual racecourse identification to ensure return of equipment if it leaves the racetrack. 

In the last 25 years there have been major improvements in fracture treatment due to significant advances in surgical techniques (particularly with internal fixation), minimally invasive approaches (arthroscopy) and the use of computed tomography (CT). Arthroscopy and CT allow accurate mapping and alignment of fractures, which is important for all and critical for athletic soundness. All have contributed to improvements in survival rates; and it is now safe to say that with correct care, the vast majority of horses that sustain fractures in racing can be saved. Equally importantly, many can also return to full athletic function including racing. 

Fracture incidences and locations vary geographically and are influenced by race types, track surfaces and conditions. There is good evidence that the majority of non-fall related fractures, i.e. those occurring in flat racing and between obstacles in jump racing, are caused by bone fatigue. This is determined by the absolute loads applied to a bone, their speed/frequency and the direction of force application. As seen with stress or fatigue failure in other high-performance working materials in which applied forces are relatively consistent, fractures in racehorse bones occur at common sites, in particular configurations, and follow similar courses. Once the fracture location has been identified, means of counteracting forces which distract (separate) the bone parts can therefore be reliably predicted and countered. 

Worldwide, the single most common racing fracture is that of the metacarpal/metatarsal condyles (condylar fracture). In Europe, the second most common fracture is a sagittal/parasagittal fracture of the proximal phalanx (split pastern). Both are most frequent in the forelimbs. 

In the United States, particularly when racing on dirt, mid-body fractures of both proximal sesamoid bones, which destabilize the fetlock (almost always in the forelimbs), are the most common reason for on-course euthanasia. They occur less frequently when racing on turf. 

There is no specific data documenting outcomes of horses that have sustained fractures on racecourses. However, there is solid data for the two most common racing injuries. The figures below are a meta-analysis of published data worldwide.

CONDYLAR FRACTURES

• Repaired incomplete fractures: 80% returned to racing

• Complete non-displaced fractures: 66% of repaired fractures returned to racing

• Displaced fractures: 51% raced following repair

• Propagating fractures: 40% raced following repair

SPLIT PASTERN

• Short incomplete fractures: 65% returned to racing

• Long incomplete fractures: 61% returned to racing

• Complete fractures: 51% returned to racing

• Comminuted fractures in most circumstances end racing careers but with appropriate support and surgical repair, many horses can be saved. There is only one comprehensive series of 64 cases in the literature of which 45 (70%) of treated cases survived.

MID BODY SESAMOID FRACTURES

• Uni-axial (single) fractures: 53% raced following screw repair

• Bi-axial (both) fractures are career ending but can be salvaged with appropriate emergency support and arthrodesis (fusion) of the fetlock joint. Results of a single series of 52 cases are available in which 65% of horses were able to have unrestricted activity post-operatively primarily as breeding animals

The science behind the development of the fracture support systems comes from two directions. The first is data collected from racecourse injuries and the second, improved understanding of fracture courses and behavior. Data collected from UK flat racecourses between 2000 and 2013 demonstrated that 66% of fractures occurred in the lower limb (from knee and hock down) and of that over 50% of fractures involved the fetlock joints. Condylar fractures are most common, representing 27% of all reported fractures; and of these, approximately two thirds occurred in the forelimbs. Split pasterns were the second most common, accounting for 19% of all fractures with three quarters of these occurring in the forelimbs. These fractures have predictable planes and courses, which means that once recognized, they can effectively be immobilized in a standard manner that is optimal for each fracture type. For condylar fractures and split pasterns, this principally involves extension of the fetlock joint. By contrast, in order to preserve soft tissues and blood supply to the lower limb, fractures of the sesamoid bones require fetlock flexion. 

Figure 2

Figure 3

The compression boot is readily applied “trackside” and can be used to stabilize most distal forelimb fractures sufficiently for horses to be humanly moved off the course. It is the temporary immobilization of choice for forelimb condylar fractures and split pasterns (Figure 3). Radiographs can be taken with the boot in place (Figure 4), and this can be maintained for transport. The boot is a rigid construct of fiberglass made from a single mold. The divided front portion is contiguous with a foot plate on which the back of the boot is hinged.  Two sizes are available with internal foot widths of 135 and 160mm (5–6 inches). Removable foot inserts are also provided to make minor adjustments for hoof size. The boot is lined with foam rubber and has a rubber sole plate that protects the shell and provides a cushion grip for the foot. When the boot is opened, the injured limb is placed into the front of the boot while the back is closed and secured by sequential adjustment of ski boot clips. When the boot edges are apposed (it cannot be over tightened), immobilization is secure. It is made with a fixed fetlock angle of 150o which counteracts distracting forces and allows horses to weight-bear and load the limb to walk. 

Figure 4

Flexion splints (Figure 5) are critical for the survival of horses with breakdown injuries such as sesamoid fractures. They are also suitable for other lower limb injuries, which are supported by fetlock and pastern flexion such as tendon and suspensory ligament injuries and lacerations. The splints are made of aluminum alloy with a secure work-hardened foot plate and conjoined compressed foam-lined front splint, which is angled 30o at the level of the coffin joint and extends to the top of the cannon. Here, there is a shallow foam-covered concavity in which the upper cannon sits, allowing the horse to lean into the splint and load the leg while flexed. The splint is secured to the leg with nylon and Velcro straps. Splints are provided with internal foot widths of 135 and 160mm (5–6 inches) to accommodate variations in horse/hoof sizes.

The modular adjustable splints (Figure 6) are made from heat-treated aluminum alloy. They are lightweight and can be configured to fit the individual horse and regional needs. The splints are 38x19mm (1.5x0.75in) rectangular tubes with an enclosed locking screw I beam. They are light but rigid and secure and are tolerated well. In the hindlimb, the reciprocal apparatus which combines stifle, hock and fetlock joint positions precludes use of a compression boot. However, modular splints provide rigid support for condylar fractures and split pasterns in hindlimbs and are secured—over a bandage to create a parallel sided tube—on the inside and outside of the limb. The splints can also be adjusted and assembled to splint fractures that occur above the fetlock (Figure 7). 

Figure 7

Appropriate immobilization effectively stops fracture progression (i.e., getting worse) which not only improves the horse's prospects for recovery but also provides effective relief from pain and anxiety. As flight animals, loss of limb control or function is a major contributor to stress. The relief provided by effective immobilization is substantially greater than provided by any pain killer or sedative. It is also recognized that when fractures occur in the high-adrenaline environment of racing, horses exhibit latent pain syndrome. Application of appropriate rigid support at this time (i.e., on the track) limits pain generation and allows humane movement for considered evaluation, X-ray, etc., away from the racetrack. 

In the UK, techniques for application of the boots and splints are taught to racetrack veterinary surgeons at annual seminars run by the Association of Racecourse Veterinary Surgeons (ARVS). The Racecourse Association (RCA) has provided forms to record use and to collect data centrally which, in the fullness of time, will determine impact and help to guide future welfare strategies. 

Providing modern, scientifically rational equipment to racecourses has done two things in the UK. First, injured horses are optimally cared for immediately and secondly, it sends out a strong positive public relations message that people involved in racing care. The initiative has been widely welcomed by the British racing industry. “This new equipment will provide the best possible chance for an injury to be properly assessed while discomfort to the horse is significantly reduced and give the best chance of future rehabilitation” Caroline Davies, RCA (Racecourse Association) - Racecourse Services Director.

“The fracture support [system] kit is a major advance in the treatment of horses on the racetrack. It allows immediate effective support to be applied to an injured horse, resulting in pain control and stability, facilitating safe transport from the racecourse to a center of excellence without risk of exacerbating the injury. This will optimize the chance of horses to return to athletic function. This innovation must be seen as a major step forward in horse welfare for the participants in racing and all other equine disciplines.” Simon Knapp, Horse Welfare Board.

What's that noise? An overview of exercise-induced upper airway disorders

by Kate Allen and Geoffrey Lane

The majority of upper airway (‘wind’) disorders affect the regions of the pharynx and larynx. Most of these conditions are only present during exercise, when the upper airway is exposed to large changes in pressures associated with increased breathing rate and effort. This is the reason why performing endoscopy at rest may not give an accurate diagnosis. Endoscopy during strenuous exercise (overground endoscopy) has become key for veterinary surgeons to be able to give an accurate interpretation of upper airway function.

There are many different forms of upper airway disorders. They occur when part of the pharynx or larynx collapses into the airway, causing an obstruction to airflow. This obstruction causes turbulence to airflow, which in turn creates the abnormal noise. Observations of upper airway function during exercise enable veterinary surgeons to estimate the impact of the abnormalities with respect to race performance. Generally speaking, the more the structure collapses and the more the airway is narrowed, the greater the detrimental effect to performance. The mechanisms by which upper airway disorders affect performance are surprisingly complex, but in brief they influence the amount of air the horse can breathe in and also how hard the horse has to work to get that air into the lungs. 

A full understanding of an individual horse’s upper airway function allows targeted treatments to be performed. Although the more common treatments have been included here for completeness, it is important for you to discuss individual horses with your own veterinary surgeon. 

Understanding the anatomy is the first step to interpreting upper airway function during exercise. When looking at an endoscopic image, the left side of the horse is on the right side of the image as we look at it, and vice versa (figure 1). 

Figure 1: Most disorders of the upper airway are named according to the structure that is collapsing. Therefore, understanding the anatomy of the airway will help to understand the individual conditions.

  ← Horse’s RIGHT side : Horse’s LEFT side →

Fig 2a

Fig 2b

With good upper airway function, we are looking for full abduction (which means opening) of the arytenoid cartilages while the vocal cords and aryepiglottic folds remain stable, and the epiglottis retains a curved shape; the soft palate and pharyngeal walls also remain stable. This gives a wide opening called the rima glottidis for air to enter the lungs (Figure 2 a, b, c).  

Figure 2 a, b, Images showing good upper airway function.

Palatal instability and dorsal displacement of the soft palate

In the normal horse, the soft palate is positioned beneath the epiglottis. Palatal instability comprises billowing movement of the soft palate and often coincides with flattening of the shape of the epiglottis. The appearance of palatal instability can differ between horses (Figure 3 a, b, c). Palatal instability often causes an inspiratory noise.

Fig 3a

Fig 3b

Fig 3c

Figure 3 a, b, c: Images showing different types of palatal instability.

Dorsal displacement of the soft palate (DDSP) occurs when the free border of the soft palate becomes displaced and comes to lie above the epiglottis (Figure 4 a, b, c). In this displaced position, there is a substantial obstruction of the rima glottidis. Sudden onset ‘gurgling’ expiratory noises are characteristic of DDSP. Palatal instability almost invariably precedes DDSP, and it is thought these conditions may arise through weakness of the muscles within the palate itself.

Fig 4a

Fig 4b

Figure 4 a, b : Images showing dorsal displacement of the soft palate (DDSP). The epiglottis is no longer visible as the soft palate is now positioned on top of it.

Thus, in younger racehorses, palatal instability and DDSP will often improve with fitness and maturity. In the UK, the two most commonly performed surgical treatments are soft palate cautery and laryngeal tie-forward. The purpose of the soft palate cautery is to induce scar tissue to tighten the soft palate. The tie-forward has a different rationale. In some horses, the larynx slips backward just prior to DDSP, therefore the tie-forward holds the larynx in a more forward position, thereby inhibiting displacement. 

Arytenoid cartilage collapse

This condition is also called recurrent laryngeal neuropathy, laryngeal hemiplegia or laryngeal paralysis because it is caused by nerve damage to the muscles of the larynx. During exercise, we observe collapse of the arytenoid cartilage almost always on the left side. In the context of sales, most trainers are familiar with laryngeal function grading applied during resting endoscopy. The purpose of this is to predict what is likely to happen to arytenoid function during exercise. During exercise, arytenoid function is typically graded as A, B or C where A is full abduction, B is partial collapse and C is complete collapse (Figure 5 a, b, c). The majority of horses with grade 1 or 2 laryngeal function at rest have grade A function during exercise (96% and 88% respectively). Arytenoid cartilage collapse causes a harsh inspiratory noise, often termed ‘roaring’. 

Fig 5a

Fig 5b

Fig 5c

Figure 5 a, b, c: Images from 3 different racehorses, showing the variations in position of the left arytenoid. The first image shows a good position, followed by horses with increasing severity of collapse. In the last image, there is virtually no opening remaining for airflow.

Arytenoid cartilage collapse occurs when the nerve supply to the left side of the larynx is damaged. The most frequent surgery to improve complete collapse is a ‘tie-back’, which fixes the collapsing left side into a semi-open position. The potential limitation of this surgery is that if the arytenoid is fixed open, it cannot close to protect the rima glottidis during swallowing. Therefore, horses that have had a tie-back are susceptible to inhaling food into the lower airways leading to coughing. The tie-back is associated with a higher risk of complications than all other upper airway surgeries. More recently a nerve grafting surgery has been developed in which a normal local nerve is detached from a local muscle and then implanted into the laryngeal muscles. This avoids the potential complications of food inhalation but does take a few months to take effect. Both of these surgeries can be combined with ‘Hobday’ surgery. 

Arytenoid Subluxation 

This condition seems to be observed with increasing frequency. We see it most commonly in young flat racehorses; it is far less common in National Hunt horses, which probably reflects maturity of the laryngeal structures. One arytenoid subluxates or slips underneath the other arytenoid (Figure 6 a and b). The full name for this condition is ventromedial luxation of the apex of the corniculate process of the arytenoid cartilage (VLACPA). This condition appears to lead to instability of several other areas of the larynx, most commonly the vocal cords and aryepiglottic folds (Figure 7 a and b). There is limited scientific evidence for the best way to manage this disorder, and at present there is no effective surgical treatment. The instability within the larynx can be exacerbated the more the horse is exercised, therefore limiting the intensity of training to allow the larynx to mature may be recommended. 

Fig 6a

Fig 6b

Figure 6 a and b: Images to show a closeup of the arytenoid cartilages. The image on the left is normal, and the two arytenoid cartilages meet in the middle. The image on the right shows that one side of the larynx has subluxated or slipped underneath the other side. 

Fig 7a

Fig 7b

Figure 7 and b: Images to show arytenoid subluxation which has led to aryepiglottic fold collapse and vocal cord collapse.

Vocal cord collapse

Vocal cord collapse is often described as mild, moderate or severe, and typically causes a high-pitched inspiratory ‘whistle’ noise. Vocal cord collapse will almost always occur if arytenoid cartilage collapse occurs (Figure 8) but can also occur without arytenoid cartilage collapse (Figure 9). The traditional treatment for vocal cord collapse is the ‘Hobday’ procedure, which aims to remove the mucosal pocket to the side of the vocal cord along with the cord itself. 

Figure 8: Image showing left arytenoid cartilage collapse with vocal cord collapse. 

Figure 9: Image showing severe bilateral vocal cord collapse.

Aryepiglottic fold collapse

Aryepiglottic fold collapse is when the folds of tissue on the side of the larynx get sucked into the airway (Figure 10 a , b, c). This condition also causes a high-pitched inspiratory noise. It is typically graded as mild, moderate and severe. It most often occurs in conjunction with other conditions that alter the normal conformation of the arytenoid or epiglottis (i.e., palatal instability, arytenoid subluxation, arytenoid cartilage collapse). Treatment aims to remove a section of the folds.

Fig 10a

Fig 10b

Fig 10c

Figure 10 a, b, c: Images showing aryepiglottic fold collapse.

Pharyngeal wall collapse 

Pharyngeal wall collapse is when the roof or sides of the pharynx collapse, which tends to obscure the larynx from clear view (Figure 11 a and b). It occurs more commonly in sport horses than racehorses due to head and neck position; the more flexed the head and neck position, the harder it is for the walls to remain stable. The time that we most often observe it in racehorses is at the start of the gallops if they are restrained, and often it will improve as the horse is able to extend its head and neck. This condition also causes a coarse inspiratory noise. 

Fig 11a

Fig 11b

Figure 11 a and b: Images showing pharyngeal wall collapse.

Epiglottic entrapment

Although included here for completeness, epiglottic entrapment can usually be diagnosed during a resting endoscopic examination, particularly if the horse is triggered to swallow. The epiglottis becomes enveloped in the excess tissue that should lie underneath it (Figure 12 a and b). Sometimes the epiglottis remains entrapped, but sometimes it will entrap and release on its own which can make the diagnosis more difficult. The noise caused by epiglottic entrapment can vary, depending on the thickness of the entrapping tissue and whether DDSP occurs concurrently. Treatment involves releasing or resecting the excessive tissue.

Fig 12a

Fig 12b

Figure 12 a and b: Images showing epiglottic entrapment in two different horses. The image on the right shows an epiglottic entrapment that is more long standing, and the tissue has become swollen and ulcerated.

The disorders outlined above are described as if they are isolated single entities, but it is commonplace for horses to sustain complex collapse, which means collapse of multiple structures at the same time. Other less common disorders are epiglottic retroversion (when the epiglottis flips up to cover the rima glottidis), and cricotracheal membrane collapse (when there is collapse between the larynx and the trachea). On occasion obstructions to breathing can also occur in the nasal passages and the trachea (i.e., masses, ethmoid haematoma, sinusitis), but are far less common than those of the pharynx and larynx. 

Looking forward it is unlikely that any new conditions remain to be discovered. Research now centres around better understanding of the causes of these disorders and how best to prevent and treat them. A particular area of investigation amongst several research groups is understanding how to train the upper airway muscles more appropriately to reduce the prevalence of these disorders and to investigate methods to strengthen the muscles. This would have the potential to reduce the number of horses needing surgical treatments.  

Antimicrobials in an age of resistance

By Jennifer Davis and Celia Marr

Growing numbers of bacterial and viral infections are resistant to antimicrobial drugs, but no new classes of antibiotics have come on the market for more than 25 years. Antimicrobial-resistant bacteria cause at least 700,000 human deaths per year according to the World Health Organization (WHO). Equivalent figures for horses are not available, but where once equine vets would have very rarely encountered antimicrobial-resistant bacteria, in recent years this serious problem is a weekly, if not daily, challenge. 

The WHO has for several years now, designated a World Antibiotic Awareness Week each November and joining this effort, British Equine Veterinary Association and its Equine Veterinary Journal put together a group of articles exploring this problem in horses.

For more information:  https://beva.onlinelibrary.wiley.com/hub/journal/20423306/homepage/sc_antimicrobials_in_an_age_of_resistance

How do bacterial populations develop resistance?

Certain types of bacteria are naturally resistant to specific antimicrobials and susceptible to others. Bacteria can develop resistance to antimicrobials in three ways: bacteria, viruses and other microbes, which can develop resistance through genetic mutations or by one species acquiring resistance from another. Widespread antibiotic use has made more bacteria resistant through evolutionary pressure—the “survival of the fittest” principle means that every time antimicrobials are used, susceptible microbes may be killed; but there is a chance that a resistant strain survives the exposure and continues to live and expand. The more antimicrobials are used, the more pressure there is for resistance to develop.

The veterinary field remains a relatively minor contributor to the development of antimicrobial resistance. However, the risk of antimicrobial-resistant determinants traveling between bacteria, animals and humans through the food chain, direct contact and environmental contamination has made the issue of judicious antimicrobial use in the veterinary field important for safeguarding human health. Putting that aside, it is also critical for equine vets, owners and trainers to recognize we need to take action now to limit the increase of antimicrobials directly relevant to horse health.

How does antimicrobial resistance impact horse health?

Fig 1. This mare’s problems began with colic; she underwent surgery to correct a colon torsion (twisted gut). When the gut wall was damaged, bacteria easily spread throughout the body. The mare developed an infection in her surgical incision and in her jugular veins, progressing eventually to uncontrollable infection—resistant to all available antimicrobials with infection of the heart and lungs.

The most significant threat to both human and equine populations is multidrug-resistant (MDR) pathogens, including methicillin-resistant Staphylococcus aureus (MRSA), extended-spectrum beta-lactamase (ESBL) producing Escherichia coli, MDR Klebsiella pneumoniae, Pseudomonas aeruginosa, Enterococcus faecium, and rising MDR strains of Salmonella spp. and Clostridium difficile. In an analysis of 12,695 antibiograms collected from horses in France between 2012-2016, the highest proportion (22.5%) of MDR isolates were S. aureus. Identification of ESBL E.coli strains that are resistant to all available antimicrobial classes has increased markedly in horses. In a sampling of healthy adult horses at 41 premises in France in 2015, 44% of the horses shed MDR E.coli, and 29% of premises shedding ESBL isolates were found in one third of the equestrian premises. Resistant E. coli strains are also being found in post-surgical patients with increasing frequency.

Fig 2. Rhodococcus equi is a major cause of illness in young foals. It leads to pneumonia and lung abscesses, which in this example has spread through the entire lung. Research from Kentucky shows that antimicrobial resistance is increasingly common in this bacterial species.

Of major concern to stud owners, antimicrobial-resistant strains of Rhodococcus equi have been identified in Kentucky in the last decade, and this bacteria can cause devastating pneumonia in foals. Foals that are affected by the resistant strains are unlikely to survive the illness. One of the leading authorities on R.equi pneumonia, Dr. Monica Venner has published several studies showing that foals can recover from small pulmonary abscesses just as quickly without antibiotics, and has pioneered an “identify and monitor” approach rather than “identify and treat.”  Venner encourages vets to use ultrasonography to quantify the infected areas within the lung and to use repeat scans, careful clinical monitoring and laboratory tests to monitor recovery. Antimicrobials are still used in foals, which are more severely affected, but this targeted approach helps minimize drug use.

What can we do to reduce the risk of antimicrobial resistance?

The simple answer is stop using antimicrobials in most circumstances except where this is absolutely avoidable. In training yards, antimicrobials are being over-used for coughing horses. Many cases are due to viral infection, for which antibiotics will have little effect. There is also a tendency for trainers to reach for antibiotics rather than focusing on improving air quality and reducing exposure to dust. Many coughing horses will recover without antibiotics, given time. Although it has not yet been evaluated scientifically, adopting the identify and monitor approach, which is very successful in younger foals, might well translate to horses in training in order to reduce overuse of antimicrobials.

Fig 3. Faced with a coughing horse, trainers will often pressure their vet to administer antibiotics, hoping this will clear up the problem quickly. Many respiratory cases will recover without antibiotics, given rest and good ventilation

Vets are also encouraged to choose antibiotics more carefully, using laboratory results to select the drug that will target specific bacteria most effectively. The World Health Organization has identified five classes of antimicrobials as being critically important, and therefore reserved, antimicrobials in human medicine. The critically important antimicrobials which are used in horses are the cephalosporins (e.g., ceftiofur) and quinolones (e.g., enrofloxacin), and the macrolides, which are mainly used in foals for Rhodococcal pneumonia. WHO and other policymakers and opinion leaders have been urging vets and animal owners to reduce their use of critically important antimicrobials for well over a decade now. Critically important antimicrobials should only be used where there is no alternative, where the disease being treated has serious consequences and where there is laboratory evidence to back up the selection. The British Equine Veterinary Association has produced helpful guidelines and a toolkit, PROTECT-ME, to help equine vets achieve this.

How well are we addressing this problem?

Disappointingly, in a recent review of prescribing behavior of three “reserved” antimicrobials at first-opinion equine practices in the USA and Canada between 2006-2012 published in Equine Veterinary Journal, only 5% of prescriptions for the reserved antimicrobials enrofloxacin, ceftiofur and clarithromycin were informed by culture and sensitivity testing. There was also an overall trend of increased prescribing of enrofloxacin across the study period, and despite increasing awareness of the challenge of antimicrobial resistance, a decreasing proportion of enrofloxacin prescriptions were based on culture and sensitivity results.

Judicious use of antimicrobials for surgical patients

Antimicrobials are commonly used in the perioperative period. In both human and veterinary medicine, antimicrobial use for surgical prophylaxis has been a target for reducing or eliminating inappropriate antimicrobial administration. The British Equine Veterinary Association recommends administration of penicillin pre- and post-operatively for 24 hours for clean surgeries; penicillin and gentamicin pre- and post-operatively for five days for contaminated surgeries; and penicillin and gentamicin pre- and post-operatively for 10 days for complicated surgeries. Furthermore, for uncomplicated contaminated wounds (e.g., hoof abscesses), antimicrobial therapy is not recommended. A 2018 survey of perioperative antimicrobial use among equine practitioners in Australia revealed that most equine vets selected an appropriate antimicrobial agent. However, the dose of penicillin chosen was often suboptimal, and therapy was frequently prolonged beyond recommendations in all scenarios except for castration. 

Judicious use of antimicrobials through appropriate routes of administration

Fig 4. Using antimicrobials as effectively as possible helps to reduce their use overall. For septic arthritis, intravenous regional perfusion of antimicrobials can achieve very high concentrations within a specific limb. This involves placing a temporary tourniquet to reduce blood flow away from the area while the antimicrobial is injected into a nearby blood vessel. The technique is suitable for some but not all antimicrobial drugs.

Due to increasing isolation of MDR organisms, research into local therapy of “reserved” classes of antimicrobials is of interest. Intravenous regional limb perfusion of ceftiofur sodium may be appropriate for septic arthritis but is less clear cut for osteomyelitis. 

Oral and rectal administration of antimicrobials are common means to provide cost-effective and convenient treatment options for owners. However, these routes of administration can lead to variable absorption and therefore have the potential for subtherapeutic concentrations. Rectal administration of some antimicrobials has been explored in order to provide antimicrobials to horses with diseases that prevent oral administration, such as small intestinal problems or to provide an alternative for horses that find drugs unpalatable and go off their feed. Metronidazole is one of the few drugs for which pharmacokinetic data following rectal administration have been published, but the optimal dosing regimens via this route have yet to be determined.

Clinical conclusions

Given the increasing prevalence of resistant bacteria affecting the equine population, judicious use of antimicrobials is necessary. Trainers and vets must work together to implement this, otherwise before long, we will find we have no effective drugs left. Firstly, in any given situation, we should question whether antibiotics are really necessary.

Appropriate antibiotic selection, as well as choosing the correct dose, frequency, duration and route of administration should all be considered. Veterinarians should encourage culture and sensitivity testing to allow for guided and narrow spectrum therapies whenever possible. It is also important to keep up-to-date with the latest information on drug treatment schedules and be prepared to modify and adapt as new information becomes available. Appropriate antimicrobial stewardship in veterinary medicine will ensure the availability and legal use of antimicrobials remains an option for our equine patients.

Experiences with a new surgical technique for ‘Wobblers’ horses

By Lynn Pezzanite

Wobbler syndrome, also known as cervical vertebral compressive myelopathy (CVCM),  is the most common cause of neurological disease in horses and affects many breeds. Although numerous spinal surgeries are performed on humans, this is the only condition of the spinal cord for which surgery in horses is often performed. 

Wobbler syndrome involves compression of the spinal cord due to narrowing or abnormal development of the spine in the neck, which results in neurologic deficits—specifically ataxia. Ataxia is a term used by veterinarians to describe incoordination and inability of an animal to properly place their legs and maintain balance when they are standing and walking. It is easy, therefore, to see why horsemen describe CVCM horses as “wobblers.” CVCM has been described in many breeds, and it was estimated to affect up to 3% of thoroughbreds in one UK study. There is a high prevalence in young male horses, and these horses comprise 75 to 80% of cases. The condition negatively affects athletic performance, and up to 2/3 of horses diagnosed with CVCM are euthanised due to severity of the ataxia or perceived poor response to therapy and subsequent loss of use of the horse. Treatment recommendations are controversial due to the fear that horses cannot recover function when diagnosed with this condition, as well as concerns regarding the cost of treatment, its invasiveness and complications associated with current surgical procedures. Also, at the current time, it is still very unlikely a veterinarian can accurately predict the degree of improvement and prognosis for a specific horse undergoing treatment. Furthermore, veterinarians do not always agree amongst themselves how severe the ataxia is, which makes it even more difficult to measure improvement following treatment and compare treatments. Despite these concerns, there are many horses that do improve and return to athletic use after neck spinal surgery. 

What are the current options for spinal surgery?

The goal of spinal surgery for CVCM is to remove the ability of two vertebral bodies to move by fusing the two adjacent bones together. The result is that over time, the two bones and joints will change in configuration, the fused bones shrink and more space becomes available for the spinal cord. By removing the compression of the spinal cord, neurological function improves. Current surgical treatments for CVCM include methods for ventral interbody fusion: kerf cut cylinders and ventrally placed locking compression plate and dorsal laminectomy (the top portion of the vertebral body is removed entirely to reduce any compression on the spinal cord). Fusion with using the kerf cut cylinder remains the most commonly performed surgical procedure for cervical stabilisation, but this does not provide stability when the spine is in extension. Locking compression plate technologies are difficult to apply due to the shape of the vertebral body and limited flexibility in placement of the fusion construct and the associated screws. Despite great advancements in equine surgery over the past years, these surgical methods for equine cervical stabilisation require specialised equipment and extensive surgeon experience and still have a high risk of complications, including implant migration or failure and vertebral fracture with a high chance of associated horse fatality. 

The goal of spinal surgery for CVCM is to remove the ability of two vertebral bodies to move by fusing the two adjacent bones together

Recent developments in spinal surgery

Because CVCM is relatively common and there is huge interest in returning affected horses to athletic function, there is a demand to develop surgical techniques that are less technically challenging while reducing complications associated with surgery to safely return horses affected by CVCM to their intended use. Overall, there remains room for improvement in surgical treatment of CVCM to both increase biomechanical stability and reduce complications associated with implant placement.

A new technique for spinal surgery

In a recent pilot study by our group at the PreClinical Surgical Research Laboratory at Colorado State University (Fort Collins, CO, USA), a new technique using advanced surgical implants known as pedicle screws and connecting rods with an interbody fusion device (IFD) were evaluated as an alternative to current techniques for cervical fusion in horses. The idea to use these novel implants came from human surgery, where interbody fusion devices are considered the standard technique for lumbar spine fusion in people, resulting in improved success rates in neurologic function and return to activity. The IFD device was evaluated initially in four horses, showing that the construct integrated with surrounding bone within eight months and did not result in any severe complications, such as implant failure, migration or fracture (as has been reported with other techniques). In addition, we noted that the polyaxial pedicle screw head allowed for increased screw placement options compared to previously described techniques. In particular, this is an improvement compared to the locking compression plate technology, which is limited by the conformation of the ventral keel of the cervical vertebrae. The results obtained in this pilot study prompted further investigation of polyaxial pedicle screw and rod technology in equine patients clinically affected by CVCM. 

The Colorado team’s results

We found 10 horses at the Colorado State University Veterinary Teaching Hospital that were diagnosed with Wobbler syndrome based on examination and diagnostic imaging including x-rays, myelogram, and CT scan. The owners of the horses approved to have them undergo this new surgery with placement of the IFD and polyaxial pedicle screw and rod construct. The 10 horses were closely followed, and clinical outcomes and owner reports were recorded and described in our recent publication in Equine Veterinary Journal. 

The breeds of horses treated included warmbloods, Tennessee Walkers, Arabians and quarter horses. No horses in this case population were intended as racehorses. The median age of horses at the time of surgery was two years (24 months, range 12-168). Male horses were overrepresented as is typical for CVCM, with four geldings, four stallions and two mares treated. Preoperative grade of ataxia ranged from 1 to 3 out of 5 based on the Modified Mayhew neurological grading scale. Surgical fusion was performed at one site in three horses and two sites in seven horses. In 6 out of 8 horses with ≥1-year follow-up, ataxia improved by 1–3 grades, with an average improvement of 1.25 grades. In four horses, ataxia improved to grade 0 (normal) or 1 (mild ataxia). In two horses, the gait was unaffected, but neck comfort improved according to owner follow-up. There were no fatal complications associated with the placement of implants. Complications encountered included swelling around the incision site (seroma), pain and fever. Although we found more serious complications including screw breakage in two horses, a vertebral fracture in one horse, and implant infection in one horse, none of these horses required additional surgical procedures to remove the implants. Two horses were euthanised within the first year after surgery. In one horse with severe neurological deficits preoperatively, surgery did not result in improvement of signs; and the horse was euthanised at six weeks postoperatively. The second horse developed upper respiratory tract obstruction immediately following general anesthesia and was euthanised at the time. 

Long-term follow-up with owners was performed by phone and survey consultation. All eight owners for which at least one year follow-up after surgery was available, reported that their horse’s clinical signs and quality of life were improved, and for all horses the level of exercise was increased since surgery. Five horses were being ridden at the time of follow-up, and one additional juvenile horse was beginning training. All four horses that had been ridden before surgery had improved under saddle. Overall, owner satisfaction with the procedure was reported as excellent in five cases or good in two cases, with one owner not responding to the question. All eight owners reported that they were overall positive about the procedure and would recommend this surgery to other horse owners in the future.

This new surgical technique to treat horses with Wobbler syndrome resulted in at least one grade of gait improvement in 6/10 cases and 6/8 cases for which ≥1-year follow-up was available, which is a similar result when compared to other methods. Advantages of this surgical procedure over others to treat this syndrome in horses include that this technique requires less bone removal from the vertebral column and that the implant itself (polyaxial screw head) may be more easily applied to the vertebral body, as its shape can be varied and so can be tailored to each individual horse. Importantly, this technique offers greater stability in two planes (tension and compression), which is not provided by other techniques such as the Bagby basket or kerf cut cylinder. There were no fatal complications related to implant placement in this procedure. This is in contrast to other techniques such as the basket or kerf cut cylinder, where euthanasia of the horse is the more typical outcome if the implant fails and vertebral fracture occurs due to the extent of damage that usually results in spinal cord injury with subsequent severe neurologic signs. In summary, this technique may represent a safer alternative to current techniques of ventral interbody fusion while achieving similar outcomes in performance. Polyaxial pedicle screw and rod systems for cervical fusion should be considered as an alternative to minimise fatal complications associated with surgery while achieving one to three grades of improvement in neurological signs in horses with Wobbler syndrome. However, this study was performed in a small number of horses, so continued study of this method remains critical, as well as further development and optimisation of other surgical techniques that may result in lower frequency of complications and greater neurologic improvement.

Pezzanite, et al, Outcomes after cervical vertebral interbody fusion using an interbody fusion device and polyaxial pedicle screw and rod construct in 10 horses (2015-2019) https://beva.onlinelibrary.wiley.com/doi/10.1111/evj.13449

Orthopaedic problems in young Thoroughbreds

Helping these future athletes achieve a protective conformation is vital with respect to their welfare, athletic career and sales potential: Orthopaedic conditions have the potential to blight a promising athletic career and prevent young horses reach their full potential. Early diagnosis and management are critical if horses are to be given the best chances of a successful and long career. And this, of course, depends on horsemen being able to pick up on problems as early as possible so they can be dealt with effectively. The Beaufort Cottage Educational Trust is a charity that aims to help disseminate knowledge in the Thoroughbred breeding and racing communities with the ultimate goal of improving horse welfare.

Each year, the charity organizes the Gerald Leigh Memorial lectures which are fantastic resources for horsemen. The lecture series is supported by the Gerald Leigh Trust in honor of Mr. Leigh's passion for the Thoroughbred horse and its health and welfare. Most years, the lectures are presented in person in an event at the UK’s National Horseracing Museum in Newmarket; but for 2021, an in-person gathering was not possible and instead, the lectures are available online. For 2021, the charity chose the theme of orthopaedic problems, which are such a common challenge in young Thoroughbreds.

Angular Limb Deformities: Evaluation and treatment in foals and yearlings

Recognizing, diagnosing and understanding angular limb deviations in young Thoroughbreds are critical skills for horsemen and an important part of both stud management and veterinary care. Angular limb deformities (ALD) refer to deviation of the limb in its frontal plane, or side to side when evaluating the individual from the front or back. A varus deformity is a medial deviation of the limb below the location of the problem (e.g., toeing in), whereas a valgus deformity is a lateral deviation of the limb below the location of the deformity (e.g., toeing out). Angular limb deformities must be distinguished from a flexural limb deformity, which is in the sagittal plane, i.e., from front to back when evaluating the individual from the side.  

How do ALD occur?

ALD can be both congenital and acquired. Congenital means the condition has been present from birth and causes include incomplete ossification or immaturity of the small cuboidal bones, which make up the hocks and knees as well as weakness of the ligaments supporting the joints and periarticular laxity. These issues tend to result in valgus knees and hocks. We also know that ALD can be inherited and that as a breed, Thoroughbreds tend to be varus (toe in). 

Acquired ALD develop after birth and come about through overloading of the physis (growth plate), which is usually caused either from hard ground, an over-conditioned foal or a combination of the two. The biomechanics of equine limb lead horses to bear more weight through the inside of the leg; therefore, the inside of the growth plate, which is inhibited more than the outside and when there is overloading the net effect is that the foal will toe in.

How do ALD impact a foal’s future career?

Carpal and fetlock injuries in racing Thoroughbreds account for a large majority of the reasons racehorses spend time out of training. Intervening while foals are growing and developing to help them achieve a protective conformation gives them the best chance of maximizing their potential and enjoying their racing career. 

Diagnosis of ALD

Evaluating young stock is certainly best achieved using a team approach involving owners/managers, farriers and veterinarians. Regular evaluation from a young age is key, as is examination of the foal while static and while walking. Severe deviations should also be evaluated radiographically.

Treatment of ALD

Conservative treatment options can include exercise restriction, corrective farriery and nutritional management. Hoof correction and toe extensions can be extremely helpful in managing foals and yearlings with minor deviations; and farriery can often correct such issues without needing to resort to surgical treatment options.

The surgical treatment of choice for correcting ALD is the transphyseal screw. In general, it achieves the most effective and cosmetic outcome of the surgical options. The procedure involves placing a screw across the growth plate on the side of the leg that is growing too fast. For example, for a foal that is toeing in, the screw is placed on the outside of the leg. This allows the inside of the growth plate to grow faster and so correct the deviation. The screws are placed under a short general anesthetic. The screw does need to be removed to avoid over-correction, but often they can be removed with the horse standing using a mild sedative once the desired correction is achieved.

Osteochondrosis – recent advances and diagnosis

Osteochondrosis is one of the most important developmental diseases in young athletic horses. It occurs in young, large-breed horses, including Thoroughbreds, and can cause a variety of clinical signs. The age at which the disease starts to cause clinical signs varies from a young foal to horses over 10 years old. This is because lesions can remain silent and only cause clinical signs later on in life. But even in the absence of any clinical signs, the pathological lesions will have been present since the horses reached skeletal maturity. 

How does osteochondrosis affect athletes?

Osteochondrosis often starts to cause problems when the horse is put into training—when they are athletically challenged. This age will differ for different populations, starting earlier in Thoroughbred racehorses than in Warmbloods destined for sports horse disciplines. Often the horse will be sound, or can experience different degrees of lameness and may present with joint effusion. This disease affects more than one joint in an individual in over 50% of cases, and it usually occurs in the same joint on the contralateral limb; but it can also affect multiple different joints. 

How does osteochondrosis develop?

In foals, areas of growth cartilage within the joints will continue to ossify (become bone) after birth. When this process is complete and the animal is skeletally mature, a thin layer of normal articular cartilage will remain supported by subchondral bone. Osteochondrosis is caused by a “failure of endochondral ossification,” which simply means the growth cartilage fails to become healthy bone. A defect, with or without a fragment, is then created in the articular surface of the bone. This dynamically changing area is susceptible to trauma or high biomechanical loads. Recent advances in research, carried out in Norway by Dr. Olstad, suggest that failure of endochondral ossification is likely caused by loss of blood supply to these areas of growth cartilage, which prevents it from ossifying. This has been linked to a heritable predisposition, among other factors such as rapid growth, dietary imbalance, exercise, environment and prior joint sepsis.

Diagnosis of osteochondrosis

Thorough clinical examination and radiography remain at the forefront of osteochondrosis diagnosis. This disease occurs at joint-specific predilection sites as a result of site-specific biomechanical forces and differences in the age at which that site becomes skeletally mature. For example, in the femoropatellar joint (pictured), the most common site of osteochondrosis is the lateral trochlear ridge of the femur. This is predilected by the thick cartilage surface, later age of maturation/ossification, and by the shear forces the patella exerts on the ridge as the stifle flexes and extends. Ultrasonography can also be very sensitive in detecting osteochondrosis in the stifle. Research performed by Dr. Martel in Canada suggests early detection of subclinical lesions in the stifle have been found in foals aged 27-166 days old.  

Management of osteochondrosis

Lesions can spontaneously resolve, and the majority will have done so by 12 months old. Otherwise, management recommendations to limit lesion development include keeping horses exclusively at pasture up to 1 year old, not using rough terrain, in large group sizes (>3 brood mares) or in a large pasture size (large pasture size > 1 hectare before 2 weeks old and > 6 hectare before 2 months old). Strict box rest is discouraged, and a convalescence paddock of 33ft x 56ft (10m x 17m) for 60-90 days may help stabilize lesions. 

Conclusion

Gerald Leigh was an incredibly successful Thoroughbred breeder and owner based in the UK. The 2021 lectures honoring his passion for the Thoroughbred provide a useful update for horsemen on two common conditions of the young Thoroughbred and add to the contribution the charitable trust established by Mr. Leigh’s family, which continues to make in supporting the Thoroughbred industry.

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Can we use biomarkers to predict catastrophic racing injuries?

By Holly Wiemers

University of Kentucky study shows association between mRNA biomarkers and catastrophic injuries in Thoroughbred racehorses— a positive step forward in the development of a pre-race screening tool.

Catastrophic injuries in Thoroughbred racehorses is a top-of-mind concern for the global racing industry and its fans. That sentiment is shared by researchers at the University of Kentucky and their collaborators, who are working to learn more about changes happening at a cellular level that might indicate an injury is lurking before it becomes career or life ending. Could it be possible to identify an early marker or signal in horses at risk of catastrophic injury, allowing for intervention before those injuries happen? And, if so, might this type of detection system be one that could be implemented cost effectively on a large scale?

According to Allen Page, DVM, PhD, staff scientist and veterinarian at UK’s Gluck Equine Research Center, the short answer to both questions is that it looks promising.

Allen Page

To date, attempts to identify useful biomarkers for early injury detection have been largely unsuccessful. However, the use of a different biomarker technology, which quantifies messenger RNA (mRNA), was able to identify 76% of horses at risk for a catastrophic injury. An abstract of this research was recently presented at the American Association of Equine Practitioners’ annual meeting in December 2020 and the full study published January 12 in the Equine Veterinary Journal (www.beva.onlinelibrary.wiley.com/journal/20423306).

In this initial research—which looked at 21 different mRNA markers selected for their roles in encoding proteins associated with inflammation, bone repair and remodeling, tissue repair and general response to injury— three markers showed a large difference in mRNA levels between injured and non-injured horses.

For almost four years, Page and his University of Kentucky colleagues have been analyzing blood samples from almost 700 Thoroughbred racehorses. These samples, collected by participating racing jurisdictions from across the United States, have come from both catastrophically injured and non-injured horses in a quest to better understand changes that might be happening at the mRNA level and if there are any red flags which consistently differentiate horses that suffer a catastrophic injury. …

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Roarers - surgery for recurrent laryngeal neuropathy -impact and outcomes

By Safia Barakzai

Recurrent laryngeal neuropathy (RLN), more commonly known as “roaring”, “laryngeal paralysis” and “laryngeal hemiplegia” is a disorder affecting primarily the left recurrent laryngeal nerve in horses >15hh. This nerve supplies the muscles that open and close the left side of the larynx. The right recurrent laryngeal nerve is also now proven to be affected, but only very mildly, thus affected horses very rarely show signs of right-sided dysfunction. Horses with RLN become unable to fully open (abduct) the left side of their larynx. During exercise they then make abnormal inspiratory noise due to collapse of both the vocal fold(s) and the left arytenoid cartilage (Fig. 1), and airflow to the lungs can become severely obstructed in advanced cases. There is a proven genetic component to RLN, but in many cases the disease progresses over months or years. The age at which clinical signs become apparent is highly variable. Foals can show endoscopic and pathologic evidence of RLN, but some horses do not develop clinical disease until >10 years old. Severity of disease can be reasonably estimated using endoscopy in the resting horse (grades 1-4), but the gold standard for assessing this disease is endoscopy during exercise, when the high negative pressure—generated when breathing—test the affected laryngeal muscle, which is trying its best to resist the “suctio”’ effect of inspiration (Fig. 1).

Horse undergoing exercising endoscopy to ascertain how the left arytenoid performs when the airway is under pressure. Inset photos show resting (top) and then exercising endoscopy (bottom) of a larynx with grade D arytenoid collapse (green arrow) with additional deformation of the arytenoid cartilage shape and bilateral vocal fold collapse (red arrows).

During exercise, RLN is graded from A to D, depending on how much the left side of the larynx can open (Table 1).

• Treatment of RLN

TABLE 1: Grades A-D of laryngeal abduction during exercise. Figures c/o F. Rossignol.

Traditionally, left-sided ventriculocordectomy (“Hobday”/ ventriculectomy plus vocal-cordectomy surgery) and laryngoplasty (“tie-back”) surgeries have been used to treat the disorder, depending on which structures are collapsing and how severely. The intended use of the horse, the budget available and other concerns of the owner/trainer also come into play. New techniques of providing a new nerve supply (“re-innervating”) to the affected muscle are now being trialled in clinical cases. Pacing the muscle with an implanted electronic device has also been attempted in research cases.

• Ventriculocordectomy

Ventriculocordectomy is commonly now referred to as a “Hobday” operation; however, the “Hobday” actually only refers to removal of the blind ending sac that constitutes the laryngeal ventricle. Currently, surgeons tend to remove the vocal cord as well as the ventricle, because it is vocal cord collapse that creates the “whistling” noise. It is a relatively straightforward surgery to perform with minimal risks and complications for the patient. In the last 15 years, there has been a shift to performing it in a minimally invasive way, using a diode laser under endoscopic guidance in the standing sedated horse rather than with the conventional method, via an open laryngotomy incision on the underside of the neck with the horse under a general anesthetic. However, transendoscopic laser surgery is technically difficult with a very steep learning curve for the surgeon. All ventriculocordectomies are not equal (Fig. 2) and for both laser and ‘open surgery’ methods, incomplete resection of the fold can leave behind enough tissue to cause ongoing respiratory noise and/or airway obstruction after surgery.

Two horses after ventriculocordectomy surgery. The horse on the left has an excellent left-sided ventriculocordectomy, with complete excision of the vocal fold tissue (black arrow). The right cord is intact, but the right ventricle has been removed (‘Hobday’). The horse on the right has bilaterally incomplete vocalcordectomies, with much of the vocal fold tissue left behind (green arrows).

Sports horses, hunters and other non-racehorses were often previously recommended to have a ventriculocordectomy performed rather than a laryngoplasty, even if they had severe RLN. This decision was often made on the grounds of cost, but also due to fear of complications associated with laryngoplasty (‘tie-back’ surgery). A new study has shown that for horses with severe RLN, a unilateral ventriculocordectomy is actually extremely unlikely to eliminate abnormal noise in severely affected horses, because the left arytenoid cartilage continues to collapse.3 The authors recommended that laryngoplasty plus ventriculocordectomy is a better option than ventriculocordectomy alone for all grade C and D horses if resolution of abnormal respiratory noise and significant improvement of the cross sectional area of the larynx are the aims of surgery.3

Advancements in laryngoplasty (‘tie-back’) surgery

Laryngoplasty is indeed one of the most difficult procedures that equine surgeons perform, and suffice to say that with such an advanced surgery, using a registered specialist veterinary surgeon that has considerable experience in airway surgery will likely minimise the chances of a negative outcome. Laryngoplasty surgery has an unjustified poor reputation in my opinion, …

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The differences between a healthy / unhealthy biome. We learn how gene sequencing technology can reveal common gastrointestinal disease.

By Carol Hughes PhD

Gastrointestinal diseases and upsets are common in Thoroughbred racehorses, causing discomfort, loss of performance and even mortality. Every common gastrointestinal disease can be linked back to disturbances (dysbiosis) of the gut bacteria. Currently, new gene technology is driving research at an intense rate, providing new insights into the equine microbial community (1) and providing both trainer and the vet with a powerful and accurate analytical tool to improve health and manage disease. The gastrointestinal tract of the horse is colonized by trillions of microorganisms, which includes 1,000-1,500 different species, making up around 95% of the biome; the other 5% are made up of archaea, protozoa, fungi and viruses. Though most studies concentrate on identifying species of bacteria and linking to health and disease. Other members of the biome have equally important roles to play. In the racehorse, a major player is the Enterobacteria phage PhiX174, which is a bacterial virus that protects the horse against E-coli.(2) The microbial community has co-evolved with the host, performing essential and vital activities such as the extraction of energy and nutrients from foodstuff, synthesis of vitamins, interaction with the immune system and cross talk with the brain, which is thought to affect temperament and behavior. Taxonomic and functional compositions of the gut microbiome are rapidly becoming viable indicators of horse health and disease. Each member of the microbial community has a different but synergistic role, which is beneficial to the health of the horse; e.g., the fungi break down the indigestible parts of forage plants, such as the polysaccharides, while the ciliate protozoa contribute to the process by producing a wide range of enzymes that the horse is unable to make, impacting and benefitting the immune system. Microbial fermentation of cellulose, hemicellulose and lignin reduces the structural and non-structural plant wall material into carbohydrates, proteins (amino acids) and lipids, and produces volatile and short chain fatty acids,(2a) which are the primary source of energy for the horse. The bacteria contribute the most to the degradation of ingested food, producing the final components of the fermentation process, which are acetic, propionic and butyric acid, methane and carbon dioxide. The gastrointestinal tract of the horse is sensitive to change, stress, environment and medication, which cause imbalances or dysbiosis.(3)

Fig 1: Image of the analysis of the microbiome of a Grade 1 horse, compared to a non-group horse.

Establishing or profiling a healthy baseline in the horse is difficult as variations exist between individuals, breeds, diets and locations; the Thoroughbred racehorse is a very different animal to the Shetland pony or an Irish Draught. Fitness training alters the microbiome further; for these reasons it is important to study the Thoroughbred as a population separate from other breeds and to analyze, where possible, racehorses training in a similar environment and location. With this in mind, since 2017 there has been an ongoing project to study and profile the microbial populations of over 1,000 racehorses based in Newmarket, throughout the racing season; and the data produced has been used to develop profiles of the differences between a healthy/unhealthy biome. The project utilizes the cutting-edge Illumina MiSeq technology, which is the most accurate and up-to-date, preferred by genomic researchers around the world.

THE BIOME IN HEALTH ELITE RACEHORSES HAVE HIGHER LEVELS OF A SUPER-PHYLUM BACTERIA

Questions asked...

Elite racehorses are trained to achieve peak fitness, but is it possible that they can gain an extra edge from the input of the hind gut bacteria?

How different is the microbiome of a Grade 1 horse, and is it possible to identify the bacteria responsible for the extra edge?

Answers found...

Human scientists have known for some time that the microbiome of an elite human athlete is different,(4) with faster metabolic pathways (amino acids and carbohydrates) and higher levels of fecal metabolites (microbial-produced short-chain fatty acids) acetate, propionate and butyrate associated with enhanced muscle fitness. The human and elite equine athlete do share similar microbial profiles, having higher percentages of the bacteria that manufacture short-chain fatty acids and higher levels of the super-phylum verrucomicrobia; these increase as the season/training progresses. What is known about this super-phylum? It has two main members: Methylacidiphilaceae and Akkermansia

1) Verrucomicrobia Methylacidiphilaceae thrive and proliferate on the ammonia produced from the degradation of starch and protein,(5) whereas starch produces very high levels of ammonia. The bacteria make enzymes (ammonia monooxygenase),(6) which convert ammonia into nitric oxide.(7) The nitric oxide has three major benefits to a racehorse:

a. Helps repair and renew the gut wall (8)

b. Enhances performance and increases exercise tolerance (9)

c. Improves vascular function and metabolism (10)

2) Verrucomicrobia Akkermansia is a mucus-eating specialist, living and thriving within the gut wall, digesting mucin from the mucosal lining (10a) with a unique ability to metabolise galactose and melibiose (11) for energy. Akkermansia in the human biome significantly increases the numbers of metabolic pathways. Horses with gastric ulcers have very low levels, perhaps indicating its function in both performance and disease. …

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Outlook for stem cell therapy - its role in tendon regeneration - different treatments for horse tendon injuries

By Dr Debbie Guest

Tendon injuries occur very commonly in racing thoroughbreds and account for 46% of all limb injuries. The superficial digital flexor tendon (SDFT) is the most at risk of injury due to the large strains that are placed upon it at the gallop. Studies have reported that the SDFT experiences strains of up to 11-16% in a galloping a thoroughbred, which is very close to the 12-21% strain that causes the SDFT to completely rupture in a laboratory setting.  

An acute tendon injury leads to rupture of the collagen fibres and total disruption of the well organised tendon tissue (Figure 1). There are three phases to tendon healing: an inflammatory phase that lasts for around one week, where new blood vessels bring in large numbers of inflammatory blood cells to the damaged site—a proliferative phase that lasts for a few weeks, where the tendon cells rapidly multiply and start making new collagen to replace the damaged tissue; and a remodelling phase that can last for many months, where the new collagen fibres are arranged into the correct alignment and the newly made structural components are re-organised.

Figure 1. A) The healthy tendon consists predominantly of collagen fibres (light pink), which are uniformly arranged with tendon cells (blue) evenly interspersed and relatively few blood vessels (arrows). B) After an injury the collagen fibres rupture, the tissue becomes much more vascular, promoting the arrival of inflammatory blood cells. The tendon cells themselves also multiply to start the process of rebuilding the damaged structure.

After a tendon injury occurs, horses need time off work with a period of box rest. Controlled exercise is then introduced, which is built up slowly to allow a very gradual return to work. This controlled exercise is an important element of the rehabilitation process, as evidence suggests that exposing the tendon to small amounts of strain has positive effects on the remodelling phase of tendon healing. However, depending on the severity of the initial injury, it can take up to a year before a horse can return to racing. Furthermore, when tendon injuries heal, they repair by forming scar tissue instead of regenerating the normal tendon tissue. Scar tissue does not have the same strength and elasticity as the original tendon tissue, and this makes the tendon susceptible to re-injury when the horse returns to work. The rate of re-injury depends on the extent of the initial injury and the competition level that the horse returns to, but re-injury rates of up to 67% have been reported in racing thoroughbreds. The long periods of rest and the high chance of re-injury therefore combine to make tendon injuries the most common veterinary reason for retirement in racehorses. New treatments for tendon injuries aim to reduce scar tissue formation and increase healthy tissue regeneration, thereby lowering the risk of horses having a re-injury and improving their chance of successfully returning to racing.

Over the past 15 years, the use of stem cells to improve tendon regeneration has been investigated. Stem cells are cells which have the remarkable ability to replicate themselves and turn into other cell types. Stem cells exist from the early stages of development all the way through to adulthood. In some tissues (e.g., skin), where cells are lost during regular turnover, stem cells have crucial roles in normal tissue maintenance. However, in most adult tissues, including the tendon, adult stem cells and the tendon cells themselves are not able to fully regenerate the tissue in response to an injury. In contrast, experimental studies have shown that injuries to fetal tissues including the tendon, are capable of undergoing total regeneration in the absence of any scarring. At the Animal Health Trust in Newmarket, we have an ongoing research project to identify the differences between adult and fetal tendon cells and this is beginning to shed light on why adult cells lead to tendon repair through scarring, but fetal cells can produce tendon regeneration. Understanding the processes involved in fetal tendon regeneration and adult tendon repair might enable new cell based and/or therapeutic treatments to be developed to improve tendon regeneration in adult horses.

In many tissues, including fat and bone marrow, there is a population of stem cells known as mesenchymal stem cells (MSCs). These cells can turn into cells such as bone, cartilage and tendon in the laboratory, suggesting that they might improve tendon tissue regeneration after an injury. MSC-based therapies are now widely available for the treatment of horse tendon injuries. However, research has demonstrated that after injection into the injured tendon, MSCs do not turn into tendon cells. Instead, MSCs produce factors to reduce inflammation and encourage better repair by the tissue’s own cells. So rather than being the builders of new tendon tissue, MSCs act as the foreman to direct tissue repair by other cell types. Although there is some positive data to support the clinical application of MSCs to treat tendon injuries in horses, placebo controlled clinical trial data is lacking. Currently, every horse is treated with its own MSCs. This involves taking a tissue biopsy (most often bone marrow or adipose tissue), growing the cells for 2-4 weeks in the laboratory and then injecting them into the site of injury. This means the horse must undergo an extra clinical procedure. There is inherent variation in the product, and the cells cannot be injected immediately after an injury when they may be the most beneficial. 

To allow the prompt treatment of a tendon injury and to improve the ability to standardise the product, allogeneic cells must be used. This means isolating the cells from donor horses and using them to treat unrelated horses. Experimental and clinical studies in horses, mice and humans suggest that this is safe to do with MSCs, and recently an allogeneic MSC product was approved for use in the EU for the treatment of joint inflammation in horses. These cells are isolated from the circulating blood of disease-screened donor horses and are partially turned into cartilage cells in the laboratory. They are then available “off the shelf” to treat unrelated animals. Allogeneic MSC products for tendon injuries are not yet available, but this would provide a significant step forward as it would allow horses to be treated immediately following an injury. However, MSCs exhibit poor survival and retention in the injured tendon and improvements to their persistence in the injury site, and with a better understanding of how they aid tissue regeneration, they are required to enable better optimised therapies in the future.

Our research has previously derived stem cells from very early horse embryos (termed embryonic stem cells, ESCs. Figure 2). ESCs can grow in the laboratory indefinitely and turn into any cell type of the body. These properties make them exciting candidates to provide unlimited numbers of cells to treat a wide range of tissue injuries and diseases. Our experimental work in horses has shown that, in contrast to MSCs, ESCs demonstrate high survival rates in the injured tendon and successfully turn into tendon cells. This suggests that ESCs can directly contribute to tissue regeneration.

Figure 2. A) A day 7 horse embryo used for the isolation of ESCs. Embryos at this stage of development have reached the mare’s uterus and can be flushed out non-invasively. B) “Colonies” of ESCs can grow forever in the laboratory.

To understand if ESCs can be used to aid tendon regeneration, they must be shown to be both safe and effective. In a clinical setting, ESC-derived tendon cells would be implanted into horses that were unrelated to the original horse embryo from which the ESCs were derived. The recipient horse may therefore recognise the cells as “foreign” and raise an immune response against them. Using laboratory models, we have shown that ESCs which have been turned into tendon cells do not appear recognisable by the immune cells of unrelated horses. This may be due to the very early developmental stage that ESCs originate from, and it suggests that they would be safe to transplant into unrelated horses. 

To determine if ESCs would be effective and improve tendon regeneration, without the use of experimental animals, we have established a laboratory system to make “artificial” 3D tendons (Figure 3).

Figure 3. Artificial 3D tendons grown in the laboratory are used to study different sources of tendon cells and help us work out how safe and effective an ESC-based therapy will be. A) Artificial 3D tendons are 1.5 cm in length. B) a highly magnified view of a section through an artificial tendon showing well-organised collagen fibres in green and tendon cells in blue.

ESC-tendon cells can produce artificial 3D tendons just as efficiently as adult and fetal cells, and this system allows us to make detailed comparisons between the different cell types. …

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