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Published by the Florida Association of Equine Practitioners, an Equine-Exclusive Division of the FVMA

Issue 1

2021

PRACTICAL ULTRASOUND OF THE EQUINE STIFLE PART TWO SUZAN C. OAKLEY

DVM, DACVSMR, DABVP (Equine), Certified Member ISELP

INFECTIOUS GASTROINTESTINAL ILLNESS IN HORSES NATHAN M. SLOVIS

DVM, DACVIM, CHT

TOOLS OF REHABILITATION PART TWO SARAH PLEVIN

BVMS, MRCVS, CVA, DABVP, DACVSMR, RCVS Specialist


The President's Line EXECUTIVE COUNCIL RUTH-ANNE RICHTER

BSc (Hon), DVM, MS FAEP COUNCIL PAST PRESIDENT

rrichter@surgi-carecenter.com

ADAM CAYOT DVM

adamcayot@hotmail.com

SALLY A. L. DENOTTA

Hello fellow practitioners, I hope everyone has a busy and productive spring. Hopefully, the COVID-19 situation continues to improve and your lives begin to resemble ‘normal’ once more. Spend time outside this summer recharging with your people. Enjoy Florida’s natural treasures and take some time to look after yourself. The pandemic has been hard on so many of us, but you are important to the people and animals around you. We are all here to help support each other and this profession we all love.

DVM, PhD

s.denotta@ufl.edu

AMANDA M. HOUSE DVM, DACVIM

housea@ufl.edu

As a part of our return to ‘normal,’ we are excited to announce that the 2021 Promoting Excellence Symposium (PES) is scheduled for October 21-24 in beautiful Naples, Florida. The Naples Grande Beach Resort is a phenomenal venue, and we have a roster of incredible speakers and topics. Additional safety measures will be in place to help ensure the health of our attendees. We look forward to seeing you all once more! You can learn more and register for PES 2021 at cvent.me/XkgqRZ

cmiller@emcocala.com

If you can’t attend PES this fall, the 2022 Ocala Equine Conference (OEC) is currently being scheduled for January 21-23, 2022. It is shaping up to be another great conference, and we will be sure to let everyone know when registration opens.

ANNE L. MORETTA

Take some time to enjoy life. Remember how great our profession is, and how lucky we are to be taking care of such incredible animals.

COREY MILLER DVM, MS, DACT

VMD, MS, CVSMT, CVA

maroche1@aol.com

Armon Blair, DVM FAEP Council President

JACQUELINE S. SHELLOW DVM, MS REPRESENTATIVE TO FVMA EXECUTIVE BOARD

jackie@shellow.com

If anyone is feeling too stressed or mentally unwell, please do not hesitate to reach out to colleagues, friends, or the FAEP (call 800.992.3862).

Opinions and statements expressed in The Practitioner reflect the views of the contributors and do not represent the official policy of the Florida Association of Equine Practitioners or the Florida Veterinary Medical Association, unless so stated. Placement of an advertisement does not represent the FAEP’s or FVMA’s endorsement of the product or service. FAEP | 7207 MONETARY DRIVE, ORLANDO, FL 32809 | PH: 800.992.3862 | FAX: 407.240.3710 | EMAIL: INFO@FVMA.ORG | WEBSITE: WWW.FAEP.NET

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PRACTICAL ULTRASOUND OF THE EQUINE STIFLE Part Two: Lateral and Flexed Approaches

SUZAN C. OAKLEY | DVM, DACVSMR, DABVP (EQUINE), CERTIFIED MEMBER ISELP INTRODUCTION

Part One of this article discussed the medial and cranial ultrasound approaches to the stifle joint. Part Two covers the commonly examined structures in the lateral and flexed approaches.

LATERAL APPROACH – LATERAL FEMOROTIBIAL JOINT The lateral aspect of the stifle is easy to examine once basic anatomical landmarks are identified. The combined tendon of the long digital extensor/peroneus tertius (LDE/PT), lateral meniscus (LM), lateral collateral ligament (LCL), origin of the popliteus tendon, and the subextensor recess of the lateral femorotibial joint (LFTJ) can be evaluated with the lateral approach. It can be helpful to use two hands when imaging the lateral aspect of the stifle. One hand can be used to stabilize the probe on the leg and prevent slipping, and the other hand can be used to change probe angle. A high-frequency linear probe is used to examine the lateral structures of the stifle. The depth must be increased to six centimeters. The probe is placed in long-axis over the palpable extensor groove on the proximal tibia (probe position A1 in Figure 2) to image the LDE/PT origin. Keep the bone lines of the femur and tibia in view and angle the beam approximately 70 degrees caudomedially without moving the probe on the leg to image the lateral meniscus (probe position A2 in Figure 2). Follow the lateral meniscus caudally, changing the angle of the probe to remain perpendicular to the curved surface of the lateral meniscus until you reach the lateral collateral ligament. Each time you move the probe caudally, keep the bone lines of the femur and tibia in the image, then adjust the angle of the probe until the lateral meniscus is back in view. The lateral collateral ligament is easily palpable and is parallel to the tibia (NOT perpendicular to the ground). An important landmark to recognize is the tibiofibular junction. If it is in your image, you just need to adjust the angle of your probe so that it is parallel to the tibia to image the LCL. Once you have the LCL in view, follow it proximally to its origin on the femur and distally to its insertion on the tibia (probe position B in Figure 2). At the origin of the LCL, angle the probe more horizontally (Photo A in Figure 5) to image the origin of the popliteus tendon. The LCL should also be imaged in short-axis view. The subextensor recess of the LFTJ is easiest to image in short-axis view over the LDE/ PT tendon distal to its origin (Photo B in Figure 3). The recess normally has no fluid in it. 4  The Practitioner 

Figure 1. Anatomical specimen showing the lateral aspect of the stifle joint. Image courtesy of Dr. Suzan Oakley.

Legend pertains to the anatomical dissections and ultrasound images. 1. Femur 2. Tibia 3. Fibula 4. Combined tendon of the long digital extensor/peroneus tertius 5. Lateral meniscus 6. Lateral collateral ligament 7. Popliteus tendon 8. Subextensor recess of lateral femorotibial joint 9. Superficial digital flexor muscle (gastrocnemius has been removed)

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Figure 2. Photographs illustrate probe positions to image the origin of the long digital extensor/peroneus tertius, lateral meniscus, and lateral collateral ligament. Positions A1, A2, and B pertain to the ultrasound images below. Image courtesy of Dr. Suzan Oakley.

Reference images

Figure 3. (a) Long-axis image of the origin of the combined tendon of the LDE/PT on the femur. (b) The probe is kept in the same position on the leg and the beam is angled approximately 70 degrees caudomedially to image the lateral meniscus. Image courtesy of Dr. Suzan Oakley.

Figure 4. Composite long-axis image of the lateral collateral ligament. The lateral meniscus and distal aspect of the lateral collateral ligament appear hypoechoic due to beam angle not being perpendicular to those structures. Image courtesy of Dr. Suzan Oakley.

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A

B

Figure 5. Photo A illustrates probe position for the long-axis image of the origin of the popliteus. Photo B shows position for the transverse image of the extensor recess of the LFTJ. Image courtesy of Dr. Suzan Oakley.

Figure 6. (a) Long-axis image of the origin of the lateral collateral ligament, oblique image of popliteus tendon. (b) Short-axis image of lateral collateral ligament (outlined by the yellow dotted line), longitudinal image of the origin of popliteus. (The angle of the popliteus varies between horses.) Image courtesy of Dr. Suzan Oakley.

Figure 7. (a) Short-axis image of the extensor recess of the LFTJ containing a small amount of fluid. (See Photo B in Figure 5.) (b) Long-axis image of the long digital extensor muscle (superficial) and peroneus tertius (between arrows). The extensor recess of the LFTJ is not visible because no fluid is present. Image courtesy of Dr. Suzan Oakley.

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FLEXED APPROACH The flexed approach allows the evaluation of the weight-bearing surfaces of the femoral condyles (MFC), the cranial aspect of the medial meniscus and the meniscotibial ligaments. The flexed views should be done on every exam of the stifle because they provide valuable clinically relevant information and are easy to do. The hoof can be placed in a hoof stand, or an assistant can hold the leg in a flexed position with the tibia parallel to the ground. Alternatively, the operator can sit on a stool and bring the leg forward in a flexed position. (Please note that ultrasound evaluation of the cruciate ligaments is not discussed in this article.)

MEDIAL FEMORAL CONDYLE Palpate the medial femoral condyle when the limb is in a flexed position (it is further distal than it appears when the limb is flexed). Evaluate the cartilage and subchondral bone in a grid-like pattern in both short and long axes (Photo A in Figure 9).

MEDIAL MENISCOTIBIAL LIGAMENT AND CRANIAL HORN OF MEDIAL MENISCUS Slide the probe distally from the MFC in a horizontal orientation to evaluate the medial meniscotibial ligament (MMTL). Alternatively, the MMTL can be located by putting the probe in horizontal orientation against the medial border of the tibial insertion of the intermediate (middle) patellar ligament and rotating the medial aspect of the probe 10 degrees dorsally (Photo B in Figure 9). Rotate the probe 90 degrees to evaluate the MMTL in short-axis. With the probe in a vertical orientation, follow the MMTL medially to evaluate the cranial (a) horn of the medial meniscus.

Figure 8. Anatomical specimen showing the cranial aspect of the stifle joint in a flexed position. Image courtesy of Dr. Suzan Oakley.

Legend pertains to the anatomical dissections and ultrasound images. 1. Medial femoral condyle 2. Medial meniscotibial ligament 3. Cranial aspect of medial meniscus 4. Lateral meniscotibial ligament 5. Cranial aspect of lateral meniscus 6. Tibia

(b)

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A

B

Figure 9. Photo A shows probe position for short-axis image of medial femoral condyle. Photo B shows probe position to evaluate the medial meniscotibial ligament. Image courtesy of Dr. Suzan Oakley.

Figure 10. (a) Short-axis image of normal medial femoral condyle (Photo A). (b) Long-axis image of normal medial femoral condyle. Cartilage is the hypoechoic line between the arrows. Image courtesy of Dr. Suzan Oakley.

Figure 11. (a) Normal long-axis image of the medial meniscotibial ligament and cranial aspect of medial meniscus (Photo B). (b) Long-axis image of cranial aspect of medial meniscus. Note: Long-axis and short-axis orientation are in reference to the structure, not the limb. Image courtesy of Dr. Suzan Oakley.

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ABNORMAL EXAMPLES

Figure 12. (a) Normal medial femoral condyle. Arrow indicates normal subchondral bone margin. (b) Abnormal subchondral bone margin. Arrow indicates a cyst in the medial femoral condyle. Image courtesy of Dr. Suzan Oakley.

Figure 13. (c) Normal medial meniscotibial ligament (between arrows). (d) Abnormal medial meniscotibial ligament showing enlargement, change in shape, mottled echogenicity, and loss of fiber pattern. Image courtesy of Dr. Suzan Oakley.

Ultrasound imaging of the stifle is easy to learn when you have a thorough knowledge of the regional anatomy, good probe handling skills, and an understanding of the controls on the ultrasound machine. Ultrasound allows the evaluation of all of the soft tissues of the joint and is more sensitive than radiography to changes in the bone surface. This article was written to provide a user-friendly reference for the gross and ultrasonographic anatomy of the stifle and common areas of pathology. Ultrasound is easy to do, and when combined with radiology, provides more complete information to diagnose and treat conditions of the stifle.

References

1. Werpy NM. Equine Imaging Modalities. In: Proceedings AAEP 2010; 56:300 2. Denoix JM, Audige,F. (2004) Imaging of the Musculoskeletal System in Horses. In: Equine Sports Medicine and Surgery (pp 166-171)

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3. Denoix JM, Audige, F. Ultrasonographic Examination of Joints in Horses. In: Proceedings AAEP2001; 47:374 4. Werpy NM, Axiak L. Review of Innovative Ultrasound Techniques for the Diagnosis of Muscu-loskeletal Injury. In: Proc AAEP 2013; 59: 209-219. 5. Bourzac C, Alexander K, Rossier Y, Laverty S. Radiography and Ultrasonography for Diagnosis of Osteochondritis Dissecans in the Femoropatellar Joint. In: Proc AAEP 2009; 55:454 6. Budras KD, Sack WO, Rock S. (2011) Anatomy of the Horse. (p. 24) 7. Cauvin ERJ (2014). Ultrasonography of the Stifle. In: Kidd, Lu and Frazer (Ed.), Atlas of Equine Ultrasonography (pp. 161-181) Recommended Reading • Busoni V. Ultrasonographic Assessment of Cranial Meniscal Ligaments in the Horse. In: Proceedings of the European Association of Vet Diagnostic Imaging 2003; 39 • Budras KD, Sack WO, Rock S. (2011) Anatomy of the Horse.

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• • • • • • •

(p. 24) Cauvin ERJ (2014). Ultrasonography of the Stifle. In: Kidd, Lu and Frazer (Ed.), Atlas of Equine Ultrasonography (pp. 161-181) Denoix JM. Ultrasonographic Examination of the Stifle in horses. In: Proceedings of the Annual Meeting of the ACVS 2003; 122. Dik K. Ultrasonography of the Equine Stifle. Equine Vet Educ 1995; 7:154-160 Dyson SJ. Normal Ultrasonographic Anatomy and Injury of the Patellar Ligaments in the Horse. Equine Vet J 2002; 34:258-264 Hoegarts M, Saunders JH. How to perform a Standard Ultrasonographic Examination of the Equine Stifle. In: Proc AAEP 2004; 50:212-218. Werpy NM, Axiak L. Review of Innovative Ultrasound Techniques for the Diagnosis of Musculoskeletal Injury. In: Proc AAEP 2013; 59: 209-219. Whitcomb MB, Review of Techniques to Improve Musculoskeletal Image Quality. In Proc AAEP 2009; 55: 431437

Notes • All ultrasound images were obtained by Dr. Oakley with a SonoSite Edge II or SonoSite Edge. • All anatomical dissections were done by Dr. Oakley.

Anatomical dissections and ultrasound images were not enhanced.

Dr. Suzan C. Oakley, DVM, DACVSMR, DABVP (Equine), Certified Member ISELP Dr. Suzan Oakley is a 1991 graduate of the University of Florida. She is the owner of a sports medicine practice in Wellington, Florida. Dr. Oakley is board certified by the American College of Sports Medicine and Rehabilitation and the American Board of Veterinary Practitioners in Equine Practice and is a certified member of the International Society for Equine Locomotor Pathology (ISELP). Dr. Oakley has an avid interest in sport horses, lameness, and the use of ultrasound as a diagnostic tool.

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Update

INFECTIOUS GASTROINTESTINAL ILLNESS IN HORSES NATHAN M. SLOVIS | DVM, DACVIM, CHT

CORONAVIRUS Equine Coronavirus (ECoV) is responsible for fever, depression, anorexia, and occasional colic and diarrhea in adult horses. Interestingly, in a study on infectious foal diarrhea in central Kentucky, the author noted that coronavirus does not appear to be a primary pathogen. Sporadic cases and outbreaks have been documented with increased frequency since 2010 in the United States and Japan. Coronaviruses are members of the coronaviridae family, all of which are single-stranded, positive-sense, non-segmented, enveloped RNA viruses responsible for enteric, respiratory, hepatic, and neurologic disease in a variety of mammalian and avian species. A closely-related coronavirus is Bovine Coronavirus (BCoV), known as winter dysentery in cattle. The epidemiologic information at this time is sparse and most of the information is based on BCoV or on published preliminary observations. Since 2010, the number of positive qPCR samples submitted to Cornell, Hagyard Equine Medical Institute IDEXX, and UC Davis has been on a steady rise. These laboratories have noted the majority of the cases are in adult horses from a wide geographic range across the US, with the number of cases being higher during the colder months of the year (October–April). The majority of the cases/outbreaks appear to be predominately in riding, racing, and show horses. There have only been a few cases (published and unpublished) on breeding farms. It has been speculated that on these breeding farms there are asymptomatic horses spreading the virus, conferring protection of clinical disease. Preliminary studies have shown that the feco-oral route of transmission has been successful in Japan utilizing three nineto 10-month-old Japanese draft horses. Unlike BCoV that is considered a pneumoenteric virus, ECoV has only been detected by qPCR in 17/2,437 nasal secretions from horses showing signs of fever and/or upper respiratory infections. A French study had similar preliminary findings. Morbidity can range from 10-83% with mortality rates considered low, but some published outbreaks were as high as 27% in American Miniature horses. Mortality has been associated with endotoxemia, septicemia, and hyperammonemia. The incubation period noted after natural and experimental infection is short with clinical signs developing 48-72 hours after exposure, which 12  The Practitioner 

can last a few days to a week. The illness is usually mild and tends to resolve with minimal supportive care. Shedding of the virus in feces ranged from 10 to 12 days in experimentally unaffected animals while, in one outbreak, fecal shedding was reported to last as long as 25 days and, in a 28-year-old, for up to 99 days. In two experimental infection model studies in horses, it has been documented that some horses can intermittently shed the virus in their feces. This finding indicates the importance of repeated testing before reintroducing the horse to a herd. We currently do not know how long ECoV can persist in the environment, but it can be speculated from severe acute respiratory syndromeassociated (SARS-associated) virus, that it is a short period in warm weather (two-three days) and longer in colder (4°C) weather (14-17 days). Clinical presentation collected by 16 outbreaks showed that 30% of the horses showed clinical signs. The primary clinical signs were anorexia (98%), lethargy (89%), and pyrexia (101.5 to 105.8 F: 84%). Colic was observed in 18% of the cases while change in fecal consistency was noted in 25%. A few of the horses showed signs of encephalopathy, which has been speculated to be associated with hyperammonemia. Antemortem diagnosis based primarily on hematological changes is not recommended. Observations noted on the complete blood cell count (CBC) are leukopenia characterized with a neutropenia and/or lymphopenia, which tends to resolve in five to seven days. Dr. Nicola Pusterla noted that in 73 diseased horses the CBC was unremarkable in only 11%. Serum biochemistries performed on diseased horses may be unremarkable. Horses that are exhibiting neurological signs should have a blood ammonia level performed as hyperammonemia has been reported in a ECoV case that developed encephalopathy and subsequently died. For an accurate diagnosis, the presence of ECoV in feces should be determined by qPCR. Interestingly, the viral load measured by qPCR in foals (up to six months of age) appears to be lower compared to horses older than 12 months of age, although the difference was not significant. Horses that died secondary to ECoV had severe diffuse necrotizing enteritis with marked villus attenuation, epithelial necrosis in the tips of the villi, neutrophilic and fibrin extravasation into the Issue 1 • 2021


membranes and the perineum/udder of the mare was possible if Salmonella was in the feces. During udder seeking, foals will have extensive contact with the perineum and therefore may be at risk of Salmonella ingestion. Most immune-competent adults can be exposed to Salmonella and not succumb to clinical disease. It is not uncommon for a mare with a sick salmonellosis foal to have no clinical signs of illness and yet be shedding Salmonella in the feces. The exact number of organisms needed to cause clinical disease in an adult animal is unknown because of the multitude of intrinsic and extrinsic factors that are responsible for the overall health and immunity of the animal. Once Salmonella has overcome the host defense mechanisms (gastric acidity, intestinal flora, peristalsis, intestinal mucus, and lactoferrin) the Seven-month-old weanling with chronic salmonellosis. The weanling was bacteria migrate through the enterocytes and placed on enrofloxacin and subsequently removed. access the lamina propria where they stimulate an Image courtesy of Dr. Nathan Slovis. inflammatory response. Both phagocytized and free Salmonella organisms travel via the lymphatics small intestinal lumen, as well as crypt necrosis, microthrombi, to regional lymph nodes where they persist in stimulating an and hemorrhage. inflammatory response. Salmonella can also reach circulation from efferent lymphatics. The neonate predisposition toward Treatment is usually not necessary for the majority of the cases bacteremia and septicemia may be because of factors such as and horses tend to recover spontaneously in a few days. If delayed gut closure at birth, immature cellular immune response, pyrexia and depression are noted, then the use of nonsteroidal and decreased complement activity. Salmonella enterotoxins, anti-inflammatory drugs may be warranted for two to three days. cytotoxins, and generalized inflammation within the bowel Horses that suffer from colic, dehydration, and diarrhea may induces secretions of fluid from the intestinal epithelium. require the addition of oral or IV fluid and electrolyte support. The issue of antimicrobials is under debate with this illness. Unless the Salmonella enterica can be an important factor in healthcareanimal is severely neutropenic broad spectrum antimicrobials are associated epidemics and zoonotic disease in veterinary usually not recommended. If the horse has hyperammonemia or hospitals. Outbreaks associated with multidrug resistant (MDR) signs consistent with hyperammonemia, then the use of lactulose Salmonella among equine patients can result in high case fatality (0.1 to 0.2 ml/kg PO or per rectum) or fecal transfaunation will be rates and substantial financial cost. As such, routine surveillance recommended. to detect this organism among equine patients is commonly performed on targeted high-risk subgroups (e.g., gastrointestinal The epidemiology and pathogenesis of ECoV infection in horses disease) and upon recognition of epidemic disease, and less is currently being investigated. commonly performed continuously on all equine inpatients. While there are many reports suggesting patients are more likely to shed Salmonella in their feces at times of stress or systemic SALMONELLA compromise, there are no reports that indicate what factors may Salmonella are gram negative, facultative, anaerobic bacteria, be important to horses shedding MDR-strains; something that which usually can access the intestinal tract via the fecal-oral can result in infections that are much more difficult to treat in route. Salmonella commonly infects foals between 12 hours horses and humans alike. Drs. Paul Morley, Brandy Burgess, and and four months of age. Young animals are more susceptible to myself recently investigated some of the factors associated with Salmonella infections, maybe because of a less sophisticated or the shedding of multidrug-resistant Salmonella. The below gives less well-established microflora within the gastrointestinal tract. a summary of our findings: The most common source of exposure and infection in the foal is another horse. Often, the mare herself is an asymptomatic Background: Salmonella enterica can be an important factor carrier. Mares have been shown to shed Salmonella at or shortly in healthcare-associated epidemics and zoonotic disease in after parturition despite having as many as 19 negative cultures veterinary hospitals—with outbreaks of multidrug-resistant before foaling. Observations of foalings revealed that all mares (MDR) Salmonella among equine patients resulting in high case defecate during stage two labor and that contamination of fetal fatality rates and substantial financial cost.

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Hypothesis/Objectives: The objectives of this study were: • 1) to determine factors associated with fecal shedding of MDR- • Salmonella; and 2) to determine what effect Salmonella shedding may have on health outcomes of previously hospitalized horses • and their stablemates.

Lameness associated with septic arthritis or physitis Abnormal lung sounds associated with pneumonia of hematogenous origin Lethargy, stupor, or seizures associated with meningitis (or from severe electrolyte derangements, e.g., hyponatremia)

Materials and methods: Patients eligible for this case-control

Laboratory findings may be characteristic of a leukopenia as a study included those having fecal cultures for S. enterica as part result of neutropenia. The neutrophils frequently demonstrate of a surveillance program from January 2011 through December toxic changes and may be immature (Bands). Fibrinogen 2012. Data regarding exposures of interest were collected concentration may be elevated. Low platelet count may indicate retrospectively from medical records. Information on long- the presence of disseminated intravascular coagulation. term outcomes was obtained by administering a phone survey Hyponatremia, hypochloremia, acidosis, and azotemia are the to horse owners. Multivariable regression techniques were used most common findings in regards to lab work. to determine factors associated with shedding MDR-Salmonella • Acidosis may mask life-threatening hypokalemia. and subsequent health outcomes. • Low serum potassium may result from a combination of decreased intake, increased loss in diarrheic feces, and polyuric acute renal failure. Results: Equine patients enrolled in this study included 94 culture-positive (29 MDR and 65 susceptible) and 279 culturenegative (on at least three fecal samples) horses from 199 different Diagnosis of Salmonella is conducted by testing fecal samples farms. Horses experiencing diarrhea during hospitalization using bacteriologic procedures in the laboratory. The samples were more likely to shed Salmonella (OR 1.88; 95% CI 1.02, are initially plated to a hektoen agar and inoculated in a selenite 3.45) compared to horses without diarrhea; and horses having broth. However, it can take up to three to five days to obtain decreased feed intake during hospitalization were more likely to the culture results. Several laboratories have developed PCR shed MDR-strains (OR 5.95; 95% CI 1.21, 29.20) compared to tests for detection of Salmonella spp. in fecal and environmental horses with normal feed intake. In general, shedding Salmonella samples, but there is evidence of an increased frequency of did not increase the long-term risk for non-survival, colic, or Salmonella-PCR positive results in horses without clinical signs abnormal feces after discharge of hospitalized horses, nor did of Salmonellosis that test negative to Salmonella spp. by culture it increase the risk for hospitalization or abnormal feces in on multiple fecal samples, perhaps due to the use of primers stablemates. targeting a non-specific Salmonella spp. gene fragment that may cross-react with other enteric or non-enteric organisms. There is a novel enhanced detection test (Reveal® 2.0 Salmonella Conclusions and clinical relevance: Horses experiencing a test system) for the detection of Salmonella spp. in fecal and diarrhea during hospitalization were less likely to shed MDRenvironmental samples. This test appears to help shorten the strains; while horses having decreased feed intake during time period to obtain laboratory results from our culture samples. hospitalization were more likely to shed MDR-strains. Interestingly, receiving antimicrobial therapy during hospitalization was not associated with shedding Salmonella, nor was it associated with We have had foals present with fevers of unknown origin with shedding of MDR-strains. In general, shedding Salmonella did no signs of diarrhea that have had positive blood and fecal not decrease long-term survival or increase the occurrence of cultures for Salmonella. Intermittent shedding of Salmonella is colic or abnormal feces in the hospitalized horse nor increase the common, and therefore, a minimum of three to five consecutive risk for hospitalization or abnormal feces in stablemates. Despite 1-gram fecal cultures taken 24 hours apart are recommended. A these findings, in order to mitigate the exposure risk to other current Morris Animal Foundation funded study is investigating horses and personnel, it is still recommended to manage horses how long horses will shed Salmonella in their feces. Preliminary shedding Salmonella separately from other resident horses and to data presented at the ACVIM forum in 2019 demonstrated that most animals will stop shedding Salmonella by six to eight employ rigorous personal and environmental hygiene. weeks. Horses that have been on systemic antibiotics tend to shed Clinical signs of Salmonellosis are variable and can range from Salmonella for a longer duration. We have noted in our clinic mild enteritis to severe septicemic shock. The diarrhea may that as long as farms implemented proper biosecurity measures be scant or profuse, watery, or hemorrhagic. Fevers, if present, (hand hygiene and personal protective equipment) the incidence are usually > 103° F. Other clinical signs that can be noted are of spreading clinical disease on a farm has been 0%. anorexia, tachycardia, tachypnea, and abdominal pain. These signs often related to bacteremia/endotoxemia rather than Treatment for Salmonella is non-specific and is aimed at electrolyte derangements and dehydration. Other signs of maintaining hydration and electrolyte balance. Antibiotic therapy, even though it does not alter the clinical course of diarrhea or bacteremia include the following (especially in foals): shedding of the organisms, should be initiated in foals to help prevent bacteremia. In adults, the use of antimicrobials is usually • Green-tinted iris (presumed septicemia-induced uveitis), not warranted unless the total neutrophil count is < 1000/ml. Fluid injected sclera, and mucous membranes

14  The Practitioner 

Issue 1 • 2021


therapy usually consists of polyionic fluids such as lactated Ringers, Normosol-R, and PlasmaLyte, because sodium chloride is an acidifying solution. Use hypertonic saline if polyionic fluids do not alleviate hypotension associated with severe disease. It can be administered in 1to 2-ml/kg boluses at 30- to 60-minute intervals for severe hyponatremia (no more than 2L a day given to an adult horse). Goal for initial correction of severe hyponatremia should be a sodium concentration of 125 to 130 mEq/L, no higher. Potassium chloride should be added to fluids (20 mEq/L) if the animal can urinate properly and serum potassium is < 3.0 mEq/L. Remember potassium administration should not exceed 0.5 mEq/kg/h. If acidosis remains in the face of adequate fluid therapy, add sodium bicarbonate to fluids. General rule in bicarbonate administration is to give as a bolus half of the calculated deficit and then to correct remaining deficit over 12 to 24 hours. If sodium bicarbonate is used, more potassium supplementation is necessary.

Two-day-old TB foal with necrotizing enteritis from clostridium perfringens. The foal survived with the use of oral and IV metronidazole and supportive care including TPN nutrition. Image courtesy of Dr. Nathan Slovis.

Polymyxin B (6,000 IU/kg IV TID) diluted in 1 L of fluids, flunixin meglumine (0.25mg/kg TID IV) and pentoxifylline (7.5mg/kg PO BID) all have been shown to reduce the effects of endotoxemia. Bismuth subsalicylate (1-3ml/ kg PO Q4-8 hrs) is also commonly used as a gastroprotectants secondary to its endotoxic and antiprostaglandin properties. J-5 plasma may also be given to aid in decreasing the systemic endotoxin level. The author usually adds 4,000 IU of heparin to each liter of plasma administered in order to activate AT3. Theoretically, you do not want to add more “clotting factors” into an animal already at risk (or has developed) of disseminated intravascular coagulation. Prevention of Salmonella consists of proper hygiene. Before the foal is able to nurse, the udder and perineal regions of the mare are to be thoroughly washed with dilute chlorohexidine or Ivory soap and water. During an outbreak situation, foals should also be intubated with six-eight ounces of colostrum prior to contact with the mare. A conditionally approved inactivated bacterin (Salmonella typhimurium and Newport) vaccine that is approved in the state of Kentucky has been developed by Hagyard Equine Medical Institute and Dr. John Timmoney at the Gluck Research Center in Lexington, Kentucky. We have currently been using this vaccine on endemic farms since 2007. Farms that have incorporated the vaccine into their herd health have not had any cases of clinical Salmonellosis. Veterinarians can obtain this vaccine in their state once their state veterinarian gives conditional approval. Veterinarians demonstrating the need for this vaccine will need to obtain the necessary paperwork from their state veterinarian’s office to obtain conditional approval.

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ENTEROCOCCUS DURANS (GROUP D STREPTOCOCCUS)

Enterococcus durans is a gram-positive coccus in the alimentary tract that has been implicated as a cause of enteritis in foals, piglets, calves, and puppies. The author has documented Enterococcus durans as a cause of diarrhea in five of seven foals that had developed diarrhea during the first 10 days of life. In one study conducted in Australia, seven foals were experimentally infected (via stomach tube) by E. durans (isolated from a foal that had severe diarrhea). All seven foals developed profuse watery diarrhea within 24 hours of inoculation with varying degrees of depression, anorexia, abdominal tenderness, and dehydration. The pathogenesis of diarrhea and enteric disease remains unknown. Diarrhea induced by E. durans is not associated with enterotoxin production or substantial mucosal injury. However, decreased activity of brush border digestive enzymes such as lactase and alkaline phosphatase suggest that there is a direct mechanical interference with digestion and absorption at the brush border. Treatment for E. durans has not been adequately investigated, but subjectively, the β-lactams appear to help decrease the duration of the diarrhea (Ampicillin or Penicillin). The ideal treatment is to improve husbandry on the farm.

CLOSTRIDIUM DIFFICILE

Clostridium difficile is the agent that causes pseudomembranous colitis associated with antibiotics in humans. It is now being identified in recent years as a significant nosocomial pathogen

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@FLORIDA_VMA | The Practitioner  15


for equine as well as human patients. First described in 1935 by Hall and O’Toole, this gram-positive anaerobic bacillus was named “the difficult clostridium” because it resisted early attempts at isolation and grew very slowly. The organisms were found in stool specimens from healthy human neonates (up to 50%), which led to its classification as a commensal and was subsequently ignored as a potential pathogen. In the 1960’s and 1970’s, antibiotic-associated pseudomembranous colitis became a major clinical problem, which was attributed to mucosal ischemia or viral infection. In 1977, Larson et al. reported that stool specimens from affected patients contained a toxin that produced cytopathic changes in tissue culture cells. C. difficile was identified as the source of the cytotoxin. It is now clear that C. difficile is responsible for virtually all cases of human pseudomembranous colitis and 20% of the cases of antibioticinduced colitis. Pathogenesis of antibiotic-associated diarrhea/colitis begins with a disruption of colonization resistance (disruption of the normal colonic flora) of C. difficile. Colonization occurs by the oral-fecal route. C. difficile forms heat-resistant spores that can persist in the environment for years. These spores can survive the acid environment of the stomach and convert to vegetative forms in the colon. Environment contamination by C. difficile is particularly common in human hospitals that have reported isolation rates of 11.7% to 29%. Health care personnel may carry bacteria on their hands, under rings, or on stethoscopes, but fecal carriage by staff is rare. High rates of infection can be isolated from stalls (hospital rooms), scales, thermometers, and surgical preparation rooms. Clostridium difficile has also been implicated in an outbreak of colitis among horses at veterinary teaching hospitals. When established in the colon, pathogenic strains of C. difficile produce toxins that cause diarrhea and colitis. Strains that do not produce toxins are not pathogenic. Two large exotoxins, toxin A (enterotoxin) and toxin B (cytotoxin), are produced by C. difficile. Toxins A and B appear to act synergistically which cause fluid secretion, mucosal damage, and intestinal inflammation. Toxin A is also a chemoattractant for human neutrophils in vitro. Recently, a third toxin, an actin-specific ADP-ribosyltransferase (binary toxin), has been identified in certain strains of C. difficile isolated from human patients. The role and the pathogenesis of binary toxin is unclear, but it may act synergistically with toxins A and B. The toxic effects appear to follow binding of toxins to membrane receptors. After binding to its intestinal receptor, toxin A enters the cell and alters the actin cytoskeleton, leading to cell rounding. Toxin B causes the identical rounding. Clinical presentation of C. difficile in horses range from anorexia and pyrexia to fulminate colitis with ileus. The foals with severe colitis become anorexic and dehydrated. In addition to the diarrhea, foals become tachypneic, which may be secondary to discomfort associated with the enteritis, pyrexia, metabolic acidosis, or the anxiety of being in the hospital. Hypoproteinemia is also a feature of C. difficile secondary to the effects of toxins A and B leading to extravasation of plasma proteins. Metabolic

16  The Practitioner 

ELISA TEST: tech lab C. diff quick check complete. Illustrates clostridium difficle, positive antigen, and toxin noted in the feces. Image courtesy of Dr. Nathan Slovis.

acidosis is also consistent with clostridial enterocolitis and hypovolemia or gastrointestinal tract loss of bicarbonate. Hyponatremia may also be attributable to the gastrointestinal tract losses, as well as to an excess of free water associated with water consumption by these foals. In Kentucky, there has been recognition of an increased incidence of C. difficile infection (CDI) in the equine community over the past several years, with increased disease on farms and an increase in the number of foals arriving to a hospital setting without enteric disease that later develop clinical disease (e.g. pyrexia, leucopenia, and colic) usually after 48 hours of hospitalization. CDI is often subtle initially and not consistent with classical CDI, with a lower incidence of overt diarrhea but commonness of fever, depression, and decreased appetite. This is consistent with recognition in humans that CDI is not always accompanied by overt diarrhea, as discussed above. In a recent study conducted at our hospital, we noted that fifteen of 96 (15.6%) mares and 31 out of 113 (27%) foals admitted into the NICU had communityassociated C. difficile shedding (positive on admission samples). Twenty-three different ribotypes were identified, with ribotype 078 predominating. The rate of C. difficile shedding at the time of admission was high in this study; however, the study population must be considered. All mares were in the immediate post-partum period and alterations in the gut microbiota in the peripartum period has been reported in mares, something that would likely predispose to transient shedding of C. difficile. Further, higher rates of C. difficile shedding have also been reported in neonates of various species. Clostridium difficile is an important pathogen in adult horses and foals, and this study highlights the complexity surrounding the epidemiology of this opportunistic pathogen. It can be commonly found and transiently present in the absence of identifiable disease occurrences. Diagnosis of C. difficile infection depends on the demonstration of C. difficile toxins in the stool. The cytotoxin assay that uses

Issue 1 • 2021


tissue cell culture had been the gold standard for diagnosis. It is the most sensitive test (sensitivity 94-100% and specificity 90%), detecting as little as 10pg of toxin B. This test is not used commonly because it is time consuming and expensive. A stool culture of C. difficile is a less efficient method of establishing a laboratory diagnosis, since some strains of C. difficile are nontoxigenic (approximately 25%). Two enzyme immunoassays have been introduced that 1) detect toxin A/toxin B (Clostridium difficile TOX A/B test, Techlab®, Blacksburg, Virginia) or 2) detect antigen of Clostridium difficile and toxin A (TRIAGE® Micro; BIOSITE, San Diego, California, 1-888-BIOSITE). These tests have a good sensitivity (69-87%) and specificity (99 to 100%). Clostridium difficile TOX A/B test, Techlab® has been validated for use in feces of horses. The C. difficile toxins have been found to be stable in fecal samples which were refrigerated at 4˚C for 60 days. (DO NOT USE STYROFOAM CUPS to submit a fecal sample because they can bind the toxins.) PCR techniques can also be used to differentiate toxigenic strains from nontoxigenic strains in feces or among bacterial isolates. However, PCR methods can detect toxigenic C. difficile organisms that are present in low and clinically irrelevant levels. A related issue is the accuracy of testing in foals. The author has noted an increased number of C. difficile enterocolitis cases that have tested positive for the C. difficile glutamate dehydrogenase antigen (a highly sensitive test that detects the organism) and negative for toxins A and B utilizing a commercially available Rapid Membrane Enzyme Immunoassay. Results from 2013 and 2014 at HEMI revealed 11.6% (34/291) and 15.6% (71/454), respectively, samples that were antigen positive but toxin negative. This could be caused by a few different reasons, each with different clinical implications. It could indicate the presence of C. difficile in the absence of relevant toxin production. It could also result from sub-optimal sensitivity of the assay. Another possible cause is presence of high levels of toxin in the proximal intestinal tract with disease at that location (e.g. accounting for fever and colic) but little toxin in feces. It could also result from the presence of strains that are nontoxigenic (and therefore clinically irrelevant). Understanding which of these occur is critical because of the marked differences in clinical relevance of test results in those situations. A pilot study of discrepant results has been performed. In 10 antigen positive, toxin negative cases, enrichment culture for C. difficile was performed, and C. difficile that possessed genes encoding toxins A and B genes were isolated in nine (90%). A separate subset of 30 antigen-positive/toxin-negative samples were submitted for commercial PCR for toxin A and B genes, with 74% (22/30) being positive. Clearly, much remains to be understood about diagnosis of CDI and the relative performance of different tests. Accurate detection of potentially pathogenic Clostridium difficile shedders and individuals with CDI is imperative for adequate disease control and biosecurity measures. Prompt and accurate diagnosis of CDI is needed for prompt treatment and understanding of the epidemiology and pathophysiology of equine CDI. Hence, further evaluation of the efficacy of these test methods is warranted.

therapy, if possible. Specific therapy is aimed at eradicating C. difficile from the intestinal tract. Oral metronidazole is the drug of first choice. Adult horses are dosed at 15mg/kg PO TID-QID and foals less than six months of age are dosed at 10-15mg/kg BID-TID. The response rate for C. difficile in patients (humans) taking metronidazole is 98%. Patients who cannot tolerate oral medication because of an ileus may either receive the same dose per rectum or can be effectively treated with intravenous metronidazole at 10mg/kg TID to QID. Excretion of the drug into bile and exudation from the inflamed colon results in bactericidal levels in the feces. Metronidazole-resistant strains of C. difficile have been isolated, and there are even reports of metronidazole inducing colitis. For resistant strains of C. difficile, the use of vancomycin orally is indicated. The dose is 4mg/kg PO loading dose then 2mg/kg PO Q6h. When oral vancomycin is prescribed, I recommend the use of the parenteral solution because of the expense. It is recommended that treatment be continued for five days past the resolution date of the diarrhea. A substantial number of human patients 10-20% will have a relapse of C. difficile diarrhea. Various other approaches have been suggested for the management of relapses, including slow tapering of metronidazole therapy, bacteriotherapy with the use of nasogastric fecal transfaunation or fecal enemas, oral administration of nontoxigenic C. difficile, and treatment with the yeast Saccharomyces boulardii (may compete with C. difficile toxin A for binding sites on the intestinal epithelium). Saccharomyces boulardii anecdotally can be given to a foal at dose rate of five billion colony-forming units orally two times a day. One novel treatment plan currently used as an adjunctive treatment for both viral and bacterial causes of diarrhea is the use of bentonite clay. Bentonite is effective because it bonds to a variety of toxins and prevents the absorption of toxins by coating the intestinal wall. Not all bentonite clay is created equally and currently there is an ultra-purified bentonite clay that is available for use in our equine patients.a There is a hyperimmunized Clostridium difficile Toxin A and B plasma that is currently available.b The efficacy of the plasma in resolving diarrhea/toxic insult is currently anecdotal.

CLOSTRIDIUM PERFRINGENS Clostridium perfringens is a relatively ubiquitous bacterium that has been associated with enteric diseases in a number of diverse species. It is widespread in the soil and is found in the alimentary tract of nearly all warm-blooded species. Clostridium perfringens is a frequent postmortem invader in the alimentary tract’s tissues of bloating cadavers. Therefore, one must be cautious about drawing conclusions based on the presence of the organisms in the tissues of these animals. Types of C. perfringens are differentiated (five major types A, B, C, D, and E) based on the production of four major toxins; alpha, beta, epsilon, and iota. In addition, isolates may have the gene known as C. perfringens enterotoxin (CPE). Toxins are produced by sporulating cells in an alkaline environment and is released upon lysis of these cells.

Treatment in managing diarrhea and colitis with confirmed or suspected C. difficile infection is to discontinue antibiotic

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Continued on page 20

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Continued from page 17 It is resistant to proteolytic enzymes and will bind and insert on the brush border membrane causing pore formation in cells leading ultimately to cell lysis. Enterotoxin can be produced by all types of Clostridium perfringens but is most commonly associated with type A. Many factors are involved in the production of enterotoxin by C. perfringens. In one study, the prevalence of CPE in feces of adult horses with diarrhea was 16% and detected in only 10% of the horses with colic regardless of whether or not they had diarrhea. Studies investigating CPE in feces of adult horses and foals with diarrhea have produced variable results. CPE has been detected in the feces of 7% to 33% of adult horses with diarrhea and 28% of the foals with diarrhea. Furthermore, out of 843 C. perfringens type A isolates from dogs, people, and horses that were genotyped, only 62 (7.3%) contained the CPE gene. An unassigned type of C. perfringens that produces alpha-toxin Foal with clostridium perfringes and netF toxin with bloody diarrhea. and a β2-toxin was described. It was isolated from piglets Image courtesy of Dr. Nimet Browne. with necrotic enterocolitis and was also found in horses with enterocolitis. Since the alpha toxin, which is produced by all types of C. perfringens including non-pathogenic type A strains, disease caused by this toxin. Most of the affected foals in one is not considered a primary cause of digestive lesions, it was study had serum IgG concentrations of >800mg/dl, indicating suggested that the β2-toxin, which is present in this type of C. adequate passive transfer. This finding helps support a theory perfringens, is responsible for the lesions. A recent study found that trypsin inhibitor in the dam’s colostrum, which protects that β2-toxin was detected in 52% of the horses with typical and immunoglobulins from gastrointestinal breakdown, may atypical typhlocolitis. To a lesser extent, they were also isolated potentially allow C. perfringens type C β-toxin to persist in foals from horses with other intestinal disorders, in which they with adequate passive transfer and may allow type C bacteria represented 37% of the isolates. No β2-toxinigenic C. perfringens to overgrow. has been found in healthy horses or in horses hospitalized for reasons other than intestinal problems. Recently, the group at Clinical appearance of the disease is usually associated with foals Guelph has identified toxin genes encoding proteins related to < five days of age with a history of being obtunded, colicky, and/ the pore-forming Leukocidin/Hemolysin superfamily; these or diarrhea for less than 24 hours. The animals usually present were designated netE, netF, and netG. NetF is a new toxin that dehydrated with a severe colitis. Some of the animals may develop has been documented to cause hemorrhagic diarrhea in dogs and an ileus with evidence of colonic distention. In adults, the author horses. has documented cases of chronic colic associated with lowgrade clostridial enterocolitis. Clinical pathology work-up for a Pathogenesis of C. perfringens is based on their production of majority of these cases reveals that the animal is acidotic (HCO3 one or more of the four major exotoxins or enterotoxin. The 10-15 Meq/L), azotemic, and occasionally hypoglycemic. The factors that lead to the development of disease are not clear, but complete white blood cell count is characterized as a leukopenia it is believed that there is an alteration of the normal flora that with a toxic left shift. Some of these animals may develop a allows overgrowth of the clostridia. Proposed causes include diet protein-losing colitis secondary to severe intestinal inflammation. changes, antibiotic therapy, stress, or concurrent infection. In adult ponies, enterocolitis has been produced when antibiotics Specific diagnosis and definitive diagnosis of equine clostridial (clindamycin or lincomycin) were given to the animals orally enterocolitis requires both identification of toxins and isolation of with a fecal cocktail containing clostridium. However, the fecal the organism from intestinal contents. Isolation of the organism cocktail alone did not cause disease. Other factors that may play without the analysis for toxins is considered inappropriate a role in the development are host factors such as age, immunity, because of the possibility of isolating a non-enterotoxigenic and the presence or absence of intestinal receptors for the C. perfrigens type A which can be isolated from normal horses’ perfringens toxins. Beta toxin-producing types of C. perfringens manure. In a population study of fecal shedding of C. perfringens (type C) appear to cause enterocolitis in neonatal animals only. in 128 broodmares and foals, C. perfringens was isolated from The digestive enzyme trypsin is produced by older animals and 90% of the normal three-day-old foals. 85% were identified as can inactivate the toxin. Neonatal animals have a less developed type A; 12% of the samples had type A with the β2-toxin gene digestive enzyme production, thus may be more susceptible to isolated, C. perfringens with the enterotoxin gene was identified

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in 2.1% of samples and C. perfringens type C was identified in < 1% of the samples. A presumptive diagnosis may be made (until culture and toxin analysis) by demonstration of abundant grampositive bacteria in a fecal smear. However, this test did not appear to be sensitive because C. perfringens was isolated from 59% of samples in which no gram-positive rods were seen. The diagnosis is supported by culture of fecal clostridia and further verify the isolates as C. perfringens by the use of a polymerase chain reaction method that incorporated primers that allowed for classification of C. perfringens types A, B, C, D, and E, as well as genes for β2-toxin, enterotoxin (CPE), and recently netF. Toxin detection kits are commercially available for identification of C. perfringens enterotoxin (C. perfringens enterotoxin test, ELISA, Techlab®, Blacksburg, Virginia).

of metronidazole (10mg/kg PO BID) has also been instituted after birth. In mares that have a good history of milk production, a ration containing low to moderate amounts of digestible energy should be fed beginning one week before parturition and one week after parturition to aid in the prevention excessive milk production and, thus, excessive milk intake by the foal. Specific preventative methods addressing C. perfringens include immunization of mares with the use of a toxoid vaccine (aluminum hydroxide adsorbed culture supernatant PLUS recombinant β2-toxoid: vaccine strain is Clostridium perfringens Type A and carries genes for Alpha, β2 , netF, and CPE) that has recently been developed (2007) by Hagyard Equine Medical Institute (www.hagyardpharmacy.com). We have currently been using this vaccine on endemic farms since 2007. Veterinarians can obtain this vaccine in their state once their state veterinarian gives conditional approval. Veterinarians demonstrating the need for this vaccine will need to obtain the necessary paper work from their state veterinarian’s office to obtain conditional approval. Other oral enteric protectants include the oral and/or administration of hyperimmunized plasma which was previously mentioned. Specific immune treatments for C. perfringens types C and D do provide some protection against alpha-toxin, but it is generally believed that this protection would be inadequate against C. perfringens type-A organisms.

Treatment for neonatal C. perfringens is considered a medical emergency. Even with the best care, many foals can die if infected with C. perfringens type C. Neonates with clostridiosis are at a higher risk for the development of peritonitis. When there is a large volume of peritoneal exudate, the prognosis is grave and euthanasia would be recommended. If attempted, the treatment plan should be aggressive and aimed at the following areas: abdominal pain, septic shock, clostridial infection and toxin production, and maintenance of nutrition. The use of oral metronidazole 10-15mg/kg three-four times daily (dose depends on severity) for foals and 15mg/kg three-four times daily for adults. If the animal has an ileus and is intolerant of oral feeding, then NEORICKETTSIA RISTICII the use of intravenous metronidazole is recommended at a dose Equine neorickettsiosis is caused by the bacterium Neorickettsia of 10mg/kg IV four times daily. Should the foal develop an ileus risticii (formerly Erlichia risticii) and is a common cause of with marked colonic distention, we have used neostigmine 1-2mg equine colitis in endemic areas. Neorickettsia spp. are obligatory (2mg for foals greater than 250 pounds) SQ with good clinical intracellular bacteria of digenean trematodes, a kind of fluke, response. The author will administer two-three doses at one-hour which are transmitted through all developmental stages of the intervals and then use it as needed. Oral and IV administration of trematodes and vertically through generations of trematodes. C. perfringens type A, C, and D hyperimmunized plasma may be The trematode host of N. risticii in the eastern United States given to the neonate. The oral dosage would range from 50-100cc was identified morphologically and molecularly defined as the every six hours for 48-72 hours. If the animal is severely ill, the digenetic trematode Acanthatrium oregonense. A. oregonense has author would nasogastrically intubate the foal with 250-500ml of a complex life cycle involving miracidia and sporocysts in its snail the hyperimmunized plasma. So far, subjectively, foals given the host (Elimia virginica), free-swimming cercariae, metacercariae hyperimmunized plasma appeared to have their manure become in aquatic insects (example: caddisflies and mayflies), and adults formed faster than the patients not treated with the plasma. that lay eggs in the intestinal lumen of insectivorous bats. Upon ingestion of N. risticii-infected metacercarial trematodes within Bentonite clay can also be used for treatment since it has been their insect hosts, N. risticii is horizontally transmitted from the shown to adsorb Clostridium perfringens alpha, beta, and trematodes to horses (unlike the Cercariae, the metacercariae beta-2 exotoxins without interfering with absorption of equine can survive the pH in the horse’s stomach), and the bacterium colostral antibodies. then replicates within inclusion bodies inside monocytes, macrophages, mast cells, and intestinal epithelial cells. A recent Numerous prophylactic measures can be instituted on farms report in 2020 noted a new Neorickettsia species found in two with a history of C. perfringens-associated enterocolitis in foals. locations in eastern Ontario, Canada, in 2016 and 2017. Animals Optimal hygiene efforts to ensure cleanliness of the foaling affected with this new species exhibited the same clinical signs as stall and the mare (clean udder before and after birth, clean horses infected with N. risticii. Interestingly some of the horses the perineal and hind limb region) at parturition should be did test positive for N. risticii on whole blood or fecal PCR. For undertaken to decrease the degree of exposure of the foal to this study, the authors were able to culture 12 Neorickettsia strains pathogens in the feces. Some farms have stopped their outbreak from the blood of horses with typical PHF clinical signs. Because of foal diarrhea by foaling the mares out in pasture. Oral both blood and fecal samples were real-time N. risticii PCR administration of lactobacillus acidophilus (found in yogurt and negative for some horses, the 12 culture isolates were analyzed commercial probiotics) have been successfully used in chickens by PCR of four genes, P51, 16S rRNA, Ssa3, and Ssa1, followed to minimize the overgrowth of C. perfringens. Prophylactic use by sequencing. Phylogenetic analysis revealed that only 10 of

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the isolates were N. risticii strains, whereas the remaining two isolates (Fin17 and Tom16) were a previously uncharacterized Neorickettsia spp. This is important as the author has had many horses with typical signs of N. risticii that tested PCR negative on both whole blood and feces. This new uncharacterized Neorickettsia spp. could be a plausible explanation. More research is being conducted by Hagyard Equine Medical Institute and Oklahoma State University’s National Center for Veterinary Pathology (Dr. Kathryn Duncan) to better understand the life cycle and diagnostic challenges for uncharacterized Neorickettsia spp.

• •

In a study conducted at our Hagyard Equine Medical Institute • and Purdue Veterinary School, horses affected can range in age from four months to 29 years of age. The most common clinical • signs included diarrhea (66%), fever (48%), anorexia (42%), depression (40%), colic (38%), and lameness (18%). The median duration of hospitalization was six days and 76% of horses • survived to discharge. Laminitis was confirmed in 26% and suspected in 36% of cases. A diagnosis of PHF can be made on the presence of positive blood (Buffy Coat) or fecal PCR, an IFA titer >1:2,560 in nonvaccinated horses with compatible signs, or a four-fold increase between acute and convalescent titers. Treatment consists of the use of Oxytetracycline, Minocycline or Doxycycline. Four R. risticii vaccines containing a liquid suspension of inactivated N. risticii have been licensed for use in the United States with one vaccine currently available. It has been demonstrated, however, that administering killed N. risticii bacterin fails to mitigate clinical signs and reduce treatment costs. Vaccine failure is due, at least in part, to various strains of N. risticii expressing different major antigens such as 51 kD and 55 kD. Vaccine failure has been reported to be as high as 89% and is associated with relatively low levels of vaccine-induced antibodies. There are some regions of the United States where veterinarians are very pleased with its use. a Resolvet Relieve, Hagyard Pharmacy, Lexington KY 40511 USA, www. hagyardpharmacy.com b Lake Immunogenics Clostridium difficle Toxin a and B Antibody Select HI Plasma, Ontario NY 14519 USA

References • • • • •

Nicola Pusterla UC Davis, Personal Communication August 2015 Coronavirus Pusterla N, Mapes S, Wademan C, White A et al. Emerging outbreaks associated with equine coronavirus in adult horses. Vet Microbiol. 2013; 162:228-231 Oue Y, Morito Y, Kondo T, Nemoto M. Epidemic of equine coronavirus at Abihiro Racecourse, Hokkaido , Japan in 2012. J Vet Med Sci. 2013; 75:1261-1265 Fielding CL, Higgins JK, Higgin JC, McIntosh S et al. Disease associated with equine coronavirus infection and high case fatality rate. J. Vet Intern. Med. 29, 307-310 Goodrich EL, Mittel AD, Glaser A, Ness SL, Radcliffe RM and Divers TJ. Novel findings in a beta coronavirus outbreak on an American Miniature breeding farm in upstate New York. Equine Vet Ed. 2020; 32: 3: 150

22  The Practitioner 

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Schaefer E, Harms C, Viner M, Barnum S, Pusterla N. Investigation of an experimental infection model of equine coronavirus in adult horses. J Vet Intern Med. 2018 ;32;6:2099 2104. Burgess BA, Bauknecht K, Slovis NM, Morley PS.. Factors associated with equine shedding of multi drug resistant Salmonella enterica and its impact on health outcomes. Equine Vet J;2018;50;5:616 623. BA Burgess, H Aceto, EA Barrell, S Braultf EK Cook, RS McConnico, NM Slovis, PS Morley. How long will my horse shed Salmonella?. 2019 ACVIM Forum, Phoenix Arizona Tzipori S, Hayes J and et al. Streptococcus durans: an unexpected enteropathogen of foals Jones JM, Adney WS, Alexander AF, et al. Hemorrhagic necrotizing enterocolitis associated with Clostridium difficile infection in four foals. J Am Vet Med Assoc 1988;193:76-79. Magdesian KG, Hirsh DC, Jang SS, et al. Characterization of Clostridium difficile isolates from foals with diarrhea: 28 cases (1993-1997). J Am Vet Med Assoc 2002;220:67-73. Weese JS, Staempfli HR, Prescott JF. A prospective study of the roles of Clostridium difficile and enterotoxigenic Clostridium perfringens in equine diarrhoea. Equine Vet J 2001;33:403-409. Pepin J, Alary M-E, Valiquette L, et al. Increasing risk of relapse after treatment of Clostridium difficile colitis in Quebec, Canada. Clin Infect Dis 2005;40:1591-1597. Pépin J, Valiquette L, Alary M-E, et al. Clostridium difficileassociated diarrhea in a region of Quebec from 1991 to 2003: a changing pattern of disease severity. CMAJ 2004;171:466472. Mulvey MR, Boyd DA, Gravel D, et al. Hypervirulent Clostridium difficile strains in hospitalized patients, Canada. Emerging Infect Dis 2010;16:678-681. Pépin J, Valiquette L, Gagnon S, et al. Outcomes of Clostridium difficile-associated disease treated with metronidazole or vancomycin before and after the emergence of NAP1/027. Am J Gastroenterol 2007;102:2781-2788. Vohra P, Poxton IR. Comparison of toxin and spore production in clinically relevant strains of Clostridium difficile. Microbiology (Reading, Engl) 2011;157:1343-1353. Medina-Torres CE, Weese JS, Staempfli HR. Prevalence of Clostridium difficile in horses. Veterinary Microbiology 2011. Schoster A, Staempfli HR, Arroyo LG, et al. Longitudinal study of Clostridium difficile and antimicrobial susceptibility of Escherichia coli in healthy horses in a community setting. Veterinary Microbiology 2012. Songer JG, Trinh HT, Dial SM, et al. Equine colitis X associated with infection by Clostridium difficile NAP1/027. J Vet Diagn Invest 2009;21:377-380. Rodriguez C, Taminiau B, Avesani V, et al. Multilocus sequence typing analysis and antibiotic resistance of Clostridium difficile strains isolated from retail meat and humans in Belgium. Food microbiology 2014;42:166-171. Magdesian KG, Leutenegger CM. Real-time PCR and typing of Clostridium difficile isolates colonizing mare-foal pairs. Veterinary journal (London, England : 1997) 2011;190:119123. Medina-Torres CE, Weese JS, Staempfli HR. Validation of a Commercial Enzyme Immunoassay for Detection of Clostridium difficile Toxins in Feces of Horses with Acute Diarrhea. J Vet Intern Med 2010. Schoster A, Arroyo LG, Staempfli HR, et al. Longitudinal study of Clostridium difficile, Clostridium perfringens, Issue 1 • 2021


• • •

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Salmonella and Escherichia coli in healthy horses. Annual Forum of the American College of Veterinary Internal Medicine. Denver, CO, 2011. Weese JS, Staempfli HR, Prescott JF. Isolation of environmental Clostridium difficile from a veterinary teaching hospital. J Vet Diagn Invest 2000;12:449-52. F.R. Bertin, A. Reising, N.M. Slovis, P.D. Constable, and S.D. Taylor . Factors Associated with Survival in 50 Horses with Potomac Horse Fever. J Vet Intern Med 2013 Teymournejad O, Lin M, Bekebrede H, Kamr A, Toribio RE, Arroyo LG, Baird JD, Rikihisa Y. Isolation and molecular analysis of a novel Neorickettsia species that causes Potomac horse fever. 2020. mBio 11:e03429-19. https://doi. org/10.1128/mBio.03429-19. Madewell BR, Tang YJ, Jang S, et al. Apparent outbreaks of Clostridium difficile-associated diarrhea in horses in a veterinary medical teaching hospital. J Vet Diagn Invest 1995;7:343-6. Kelly CP, Pothoulakis C, LaMont JT. Clostridium difficile colitis. N Engl J Med 1994;330:257-62. Magdesian G, Hirsh D, Jang S, et al. Clostridium difficile and horses: a review. Reviews in Medical Microbiology 1997;8:S46-S48 Weese JS, Parsons DA, Staempfli H : Association of Clostridium difficile with enterocolitis and lactose intolerance in a foal. J Am Vet Med Assoc. 214;2:229 232, 1999 Magdesian G, Hirsh D, Jang S, et al. Charcaterization of Clostridium difficile isolates from foals with diarrhea: 28 cases (1993-1997). JAVMA 2002;220:67-73. Gohari IM, Parreira VR, Nowell VJ, Nicholson VM, Oliphant K, Prescott JF. A Novel Pore-Forming Toxin in Type A Clostridium perfringens Is Associated with Both Fatal Canine Hemorrhagic Gastroenteritis and Fatal Foal Necrotizing Enterocolitis. 2015 PLoS ONE 10(4): e0122684. doi:10.1371/ journal.pone.0122684

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Nathan M. Slovis, DVM, DACVIM, CHT Dr. Nathan Slovis is the director of the McGee Medical and Critical Care Center at the Hagyard Equine Medical Institute located in Lexington, Kentucky. He is a native of Annapolis, Maryland. He received his bachelor of science from Radford University, Doctor of Veterinary Medicine from Purdue University, interned at Arizona Equine Center, and completed his residency in Internal Medicine at the University of California, Davis. Dr. Slovis has published over 60 manuscripts in both national and international peer-reviewed veterinary journals. He is the editor of both the Atlas of Equine Endoscopy and The Atlas of Diseases/Disorders of the Foal, both distributed by Elsevier. He implemented the current infectious disease and equine emergency response programs at Hagyard Equine Medical Institute and holds the position of infectious disease officer. He is also a certified hyperbaric technologist for humans and animals.

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24  The Practitioner 

Issue 1 • 2021


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@FLORIDA_VMA | The Practitioner  25


TOOLS OF REHABILITATION ~ Part Two ~

SARAH PLEVIN | BVMS, MRCVS, CVA, DABVP, DACVSMR, RCVS SPECIALIST

PULSED ELECTROMAGNETIC FIELD THERAPY (PEMF)

SCIENCE

Pulsed electromagnetic field (PEMF) therapy is a non-invasive, nonthermal treatment that involves pulsing electromagnetic fields in tissue to promote healing. Implementation of PEMF therapy in veterinary medicine is increasing. Pathologies that are often treated include bone fractures, inflammation, arthritis, pain, edema, and chronic wounds. As with most adjunct ‘modalities,’ the science is conflicting. For every testimonial and study on one side of the argument, there appears to be a counter, and most work has studied the effect of magnets on bone.

Most research into PEMF is in humans and is primarily focused on bone, so there is limited evidence of its efficacy in horses. The strongest evidence for PEMF efficacy lies with non-union or slow-to-heal fractures.

MECHANISM OF ACTION

EQUINE-SPECIFIC SCIENCE

HUMAN RESEARCH

In humans, PEMF has been found in in vitro and in vivo studies to be highly influential in the fracture repair process. It has been shown to be clinically beneficial in the treatment of fractures and especially non-union fractures. Additionally, in vitro PEMF has Despite only a few good equine scientific studies being available, been shown to directly stimulate mesenchymal stem cells and there are plenty of anecdotal testimonials. Owners and trainers promote osteogenesis.46 Notably, PEMF therapy is approved by use this modality in the form of MagnaWave, magnetic blankets, the FDA for use in humans for treatment of long bone fracture and boots. nonunion and following lumbar/cervical spine fusion surgery. A pulsating magnetic field or PEMF is said to produce one main result: stimulation of cell metabolism.

There is conflicting evidence in equine medicine regarding its ability to aid in fracture repair with one prominent 1987 study describing its beneficial effects for incorporation of autogenous Increased calcium ion (Ca2+) signaling has been identified cancellous bone grafts into osseous defects, whilst another 1989 as a critical factor underlying the observed biological and study reported no significant differences in bone healing for acute clinical effects of PEMF treatment. Release of intracellular fractures. In the latter study, surgically induced cortical lesions Ca2+, driven by PEMF exposure, is thought to lead to increased of the third metacarpal/tarsal bone were created and PEMF and binding of Ca2+ to calmodulin (CaM) and activation of a control horses were compared.47,48 variety of subsequent downstream signaling pathways related to metabolism, inflammation, apoptosis, vascular tone, and A couple of additional equine studies that are clinically relevant increased nitric oxide production. In addition, the small currents involve the use of PEMF in the form of magnetic blankets. produced within tissues create electrical signals which are thought Although such blankets are extremely popular with clients, to stimulate osteogenesis.45 Introduction of an electromagnetic the science is not encouraging. A 2013 study in polo ponies field at a fracture site is thought to stimulate bone and osteoblasts determined no beneficial effects of using a PEMF blanket for in a way similar to mechanical loading. Wolff ’s law states that back pain as did a 2014 study in the Equine Veterinary Journal, mechanical stress on bone produces electrical potentials which which documented, that in healthy horses, a magnetic blanket control bone growth. PEMF is thought to replace the naturally did not induce additional significant effects on muscle blood flow, occurring electrical impulses exerted upon bone by movement. skin temperature, mean nociceptor thresholds, or behavior when There is still ongoing debate, however, regarding the mechanism compared to nonmagnetic blankets.49,50 of action of PEMF at the cellular and molecular level.

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SCIENCE: SOFT TISSUE

Whilst there is not a significant amount of evidence to support its use in soft tissues in humans or horses, it is worth mentioning a couple of studies. The first is an in vitro 2020 human study demonstrating the ability of PEMF to modulate human tendon cells response to an inflammatory environment, with the inference that a therapeutic potential for tendon regeneration may exist.51 A second equine study from 1985, however, cautioned against the use of PEMF for tendon healing, suggesting it may delay the healing process. Clearly more research is needed.52

HOW WE USE IT

We primarily use PEMF for its proposed ability to aid bone healing and for its suggested pain-reducing and anti-inflammatory properties. Many of our clients own a MagnaWave™ and, if they do, we will incorporate this into our rehabilitation protocol. Treatment takes between approximately five to 15 minutes and can be started in the acute phase of injury. We do not advise its use in tendon rehabilitation due to the lack of supporting evidence and the suggested potential negative effects (Figure 5).

WHOLE-BODY VIBRATION THERAPY (WBVT)

WBVT is an ‘above ground’ or ‘in ground’ vibrating plate that horses stand on. It has recently gained popularity with many large equine facilities now owning a ‘vibrating plate.’ Manufacturers propose that WBVT increases muscle strength, postural stability, and power, presumably by stimulating motor neurons, skin receptors, muscle cells, and joint mechanoreceptors. Human research suggests that acute vibration exercise elicits a warmup effect, and that vibration training seems to improve muscular power. WBVT has also been suggested to improve balance in older humans.53 Optimal vibration parameters to achieve maximum benefits in the horse, such as frequency, amplitude, acceleration, and duration, are currently unreported (Figure 6).

MECHANISM OF ACTION

It is known that vibration is a mechanical oscillation. A periodic alteration of force, acceleration, and displacement over time and that energy is transferred from the vibration device to the horse; however, the mechanism of action for WBVT is still not fully understood. Human research suggests that vibration induces specific responses of the body that could be exploited for therapeutic purposes. Vibrations generated by the vibrating platform are transmitted throughout the body and have been shown in human research to stimulate all sensory receptors within the epidermis, dermis, joint capsules, and muscle spindles.54 Vibration plates with both horizontal and/or vertical oscillation exist both in the veterinary and human fields. Vertical vibration is thought

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Figure 5. Magnawave. Image courtesy of Dr. Sarah Plevin.

to mimic, most closely, the natural movement of the horse and most equine studies use vertical vibration plates. A 2018 human study, however, evaluating the effect of both horizontal and vertical whole-body vibration exercise in patients with chronic back pain detailed no difference between the two.54

EFFECT ON MUSCLE/TENDONS

Vibration exercise is characterized by cyclic transition between eccentric and concentric muscle contractions. Vibration has been shown to cause a discharge from muscle spindle ends which elicits an excitatory effect on alpha motor neurons leading to muscular contraction. Muscle activation due to vibration was shown in a 2013 human study to be due to something called the tonic vibration reflex. This reflex represents the sustained contraction of a muscle subjected to vibration. Other studies have suggested that motor firing is synchronized to the frequency of vibration.55

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EFFECTS ON BONES

Numerous human studies have shown WBVT enhances bone strength. The specific mechanism of action is not proven for this yet, but it is theorized that vibration signals are osteogenic.

PAIN

Human studies have shown vibration-induced pain relief. It is thought to work via the gate control theory, where fastconducting somatosensory afferent nerves block poorly myelinated nociceptive afferents at the spinal level. Additionally, Rittweger reported relief from pain and improved function in human patients with chronic lower back pain after 12 weeks of WBV therapy. In this study, these positive effects were attributed to improved proprioception and improved muscular coordination of the lumbar pelvic region.53,54

EQUINE-SPECIFIC SCIENCE

This is an area where equine-specific research is sparse, but a 2013 study measured general clinical parameters on seven horses following 10 minutes of whole-body vibration exercise (performed independently both in horizontal and vertical planes) at a frequency of 25-21 Hz. The study found no ill effects on the horses or discomfort measured via their serum cortisol and creatinine kinase (CK) levels, which were found to be significantly lower following treatment. Additionally, in this study, bone markers were not altered, suggesting no measurable osteoblastic effect from vibration therapy in this population of horses.56 Conversely, a 2015 equine study involving 12 horses reported the ability of WBVT to maintain bone density in horses confined to their stalls.57 A 2009 human study reported significant osteogenesis and increased fluid flow through the extracellular spaces in bone thought to be the result of the loading forces from vibration therapy.58 A 2017 study looking at eight horses demonstrated a short term (30 days) positive effect in horses with chronic musculoskeletal pathology. However, it warned of the possibility for adaptation or negative effects on certain musculoskeletal injuries if used for extended periods. The study cited the need for more research.59 Importantly, a second 2017 study demonstrated the ability of a vertical WBVT plate to increase the mass of the equine multifidus muscle as efficiently as baited stretches. In this study, nine horses underwent vertical WBVT two times per day five days per week for a period of 60 days.60

HOW WE USE IT

Figure 6. Whole-body vibrating plate. Image courtesy of Dr. Sarah Plevin.

28  The Practitioner 

Currently, if a farm has a vibration plate, we will include its use into our rehabilitation program. Horses start using this modality at around two to four weeks post injury approximately three to five times per week for 15-30 min. WBVT is also often part of a standard maintenance program for many of the horses under

Issue 1 • 2021


our care. Not only do most horses find it relaxing, but its proven ability to increase the mass of the multifidus muscle means it has a place as part of a horse’s daily routine, especially at barns where baited stretches are unlikely to be performed.

EXERCISE

Exercise-based rehabilitation techniques do not involve a piece of specialized equipment and are, therefore, sometimes forgotten. However, they probably represent one of the most important aspects of athletic rehabilitation from injury.

MECHANISM OF ACTION

In humans it has been shown that the central nervous system (CNS) pre-programs activity in certain trunk muscles, e.g. transversus abdominus and multifidus muscles have been shown to activate prior to limb movement. Human patients with back pain display delayed activation of these muscles, which ultimately deprives the painful and injured spinal segments of timely support.61 Findings to date suggest the same to be true for horses. The multifidus muscle provides intersegmental stabilization and contributes two-thirds of the total increase in spinal stiffness imparted by muscular action. Consequently, it has a central role in spinal stability, and, for that reason, we will focus on this specific group of muscles. Unlike, the larger visible muscles such as the longissimus dorsi and the iliocostalis muscles, which improve with time when injured, the multifidus muscle does not automatically resume its normal function following recovery from injury. This concept is fundamental in understanding how to rehabilitate a horse with back pain or injury. In humans, specific physiologic interventions are needed to restore the size and function of the multifidus muscle once injured. In people, specific exercises have been shown to reduce the rate of recurrence from 84% in untreated controls to 30%.62 Similarly in horses, hypertrophy of the multifidus muscle has been shown in response to certain exercises. While there are many different exercises that can be performed in the hopes of achieving the goals of improving strength and balance, enhancing range of motion, and aiding rehabilitation from injury, baited stretch exercises or carrot stretch exercises are the most commonly performed and researched and have been shown to aid rehabilitation of the back.

HOW TO PERFORM BAITED-STRETCH EXERCISES

Using bait, usually a carrot, the handler encourages the horse to move its chin to various anatomical locations. The movement must be active and not passive i.e. the handler cannot position the horse or push its head into position. The horse must perform the stretches and hold them.

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Figure 7. Baited stretch: chin to carpi. Image courtesy of Dr. Sarah Plevin.

STRETCHES: 1. Chin to chest 2. Chin to knees 3. Chin to feet 4. Lateral bending: • Chin to girth • Chin to hock • Chin to hip All movements are performed with the horse against a wall to stop it cheating. Stretches are repeated three to five times and held optimally for 10-20 seconds, although to start with most horses will only manage to hold the stretch for a couple of seconds. Stretches should be performed three to five times per week (Figure 7).

EQUINE-SPECIFIC SCIENCE

The research validating these stretching exercises was published in 2011 by Stubbs et al.62 In the study, eight horses performed the exercises bilaterally with five repetitions for four to five days per week for three months. Between the initial evaluation and final evaluation, the multifidus cross-sectional area (CSA) was shown to increase significantly for all spinal levels measured on both left and right sides. Additionally, asymmetries in the muscles CSA between left and right sides were shown to decrease significantly, indicating the effectiveness of dynamic mobilization exercises in activating the equine multifidus muscle. The performance of these exercises several times per week was recommended to maintain or improve the function of deep spinal stabilizer muscles.

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HOW WE USE IT

We encourage willing trainers/owners of any athletic sport horse to perform these stretches as part of their daily exercise routine. Our show horse clients are very accepting of these exercises but generally in a large TB training barn, it is quite hard to make sure every groom is performing these exercises regularly and appropriately. For this reason, in most of our TB training barns, the horse will go on a vibrating plate a couple of times a week as part of their routine. As already mentioned in terms of maintaining multifidus muscle symmetry and activating these muscles, the vibrating plate has been documented to have similar effects as performing baited-stretching exercises.

Figure 8. Position of probe for ultrasound examination of the multifidus muscle. Image courtesy of Dr. Sarah Plevin.

Because changes in the multifidus cross sectional area (CSA) have been associated with ipsilateral osseous pathology in the horse, ultrasound evaluation of the multifidus muscle is an integral component to our comprehensive back pathology and pain workup.63 Ultrasound has been shown to be an accurate and repeatable way to monitor and measure the CSA of the multifidus muscle at each spinal level. It is suggested that three images be acquired at each spinal level to account for slight variations in position or angulation of the probe.

FACILITATION-BASED EXERCISE Facilitation-based exercise includes a range of modified exercise techniques using training aids to enhance specific areas of the musculoskeletal or neuromusculoskeletal systems. The aim of these techniques is to alter mechanoreceptive and proprioceptive feedback which alters motor control. There is a vast body of scientific literature to support the application of these techniques in humans but not as much in the veterinary field.

MECHANISM OF ACTION

Figure 9. Ultrasound image of the multifidus muscle. Image courtesy of Dr. Sarah Plevin.

30  The Practitioner 

Peripheral sensors include cutaneous mechanoreceptors, Golgi tendon organs, and muscle spindles. They all relay information to the central nervous system (CNS) via (type 1a and type 2) afferent fibers to modulate and coordinate locomotion. The mechanism of action for most of these facilitation-based exercises utilizes to some extent ‘reflexes,’ specifically the stretch reflex and the inverse stretch reflex. For example, when the muscle spindle in the center of the muscle is stretched—the sensory nerve is activated and there is a reflex muscle contraction. Similarly, stretching of the Golgi tendon organ—during muscle contraction—causes reflex inhibition and muscle relaxation.

Issue 1 • 2021


EQUINE-SPECIFIC SCIENCE (1) TACTILE STIMULATORS OR WEIGHTED BOOTS A series of studies in the equine literature determined that the type and weight of tactile stimulator was able to alter the magnitude of the kinematic and kinetic variables during the swing phase of a stride. Studies by Clayton et al. have demonstrated the ability of hindlimb stimulators to increase hindlimb joint flexions and increase the positive work performed by the tarsal musculature. Joints that seem to have increased flexion when wearing stimulators include the stifle, tarsal, metatarsophalangeal, and distal interphalangeal joints.64 Studies looking into the specifics of tactile stimulators suggest that rehabilitation after an orthopedic injury should progress from light weight tactile stimulation, which restores range of motion by facilitating stifle and tarsal musculature, to weighted stimulators that also strengthen hip musculature.

How They Are Used

Clinical use of weighted boots is not common in our demographic of TB training horses, but their use can be common in the show jumping world. A 2009 study looking at six show jumpers demonstrated that horses wearing weighted boots achieved significantly greater hindlimb flexion/elevation, achieving 30 cm more clearance over jumps than when not wearing them.65 This same study warned of the potential

Figure 10. Stretch reflex and inverse stretch reflex arc. Image courtesy of acefitness.org.

negative effects of continued or sustained use of such weighted boots, citing the potential for damage or hyperextension and injury of the equine lumbar musculature. Aligned with the conclusions of this study, the FEI states the maximum weight of a boot allowed is 500g. FEI cited welfare concerns as the reason for the rule.

How We Use It

Because of these concerns, we only advise their use during rehabilitation and not for routine or competition use. Currently, we do not use them for any purpose in our practice. If the goal is to increase the ROM of joints, we prefer to use trotting poles or the underwater treadmill

(2) TROTTING POLES Exercises such as hand walking, walking over poles, and hill work all aim to return the soft tissues and bones to normal physical capacity.

Mechanism of Action

In the context of rehabilitation, poles are thought to be beneficial for training proprioceptive skills, improving or restoring ranges of joint motion, and strengthening the propulsive muscles (flexors during swing phase and the extensor muscles during stance). Stepping over an obstacle is a complex motor skill. It requires visual perception of the position and size of the obstacle, an intact neuromotor control system to make decisions and relay commands to the peripheral nervous system, and an appropriate muscular response to ensure obstacle clearance by the limbs during their swing phase. The therapeutic effects of trotting over poles are likely to include improvements in the horse’s balance, stability, and precision of movement.66

Figure 11. Ground trotting poles. Image courtesy of Dr. Sarah Plevin.

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Figure 12. Pessoa training aid. Image courtesy of Dr. Sarah Plevin.

Science

Two important studies performed in 2015 involving eight horses supported the use of trotting poles for rehabilitation in horses that could move symmetrically (non-lame horses): in both studies, horses were evaluated trotting on level ground (over no poles), and over poles placed at 11cm and 20 cm height. The first study showed that peak vertical forces and extension of the metacarpophalangeal joints (MCPJ) and metatarsophalangeal joints (MTPJ) were not increased when horses trotted over ground or low poles with the suggestion that such activity does not impose additional risk to a rehabilitating horse.67 The second study determined the use of trotting poles to be effective for activating and strengthening the flexor musculature. Hoof position was raised, and limb joint flexion was increased as ground poles were placed higher off the ground. The greatest amount of flexion and hoof raise was identified with poles placed 20 cm above the ground surface. Additionally, unlike with proprioceptive devices such as tactile stimulators, or weighted boots, the effects did not decrease over time due to habituation.68

(3) ELASTIC RESISTANCE BANDS Mechanism of Action

A system of elastic resistance bands has been suggested to provide proprioceptive feedback during motion to encourage recruitment of core abdominal and hindquarter musculature for improved dynamic stability. The theory being that neural pathways need to be stimulated for muscles to be functional. The stimulus needs to be repeated until the motor control portion of that movement becomes a normal neural response.

Equine-specific Science

Two sensory facilitation elastic band aids have been studied. The first is the ‘Equi Band’ system. This system comprises a hindquarter band intended to increase proprioception through stimulating a neuromuscular response, resulting in greater pelvic limb muscle activation and an abdominal band that fits around the middle third of the abdomen, with the intention of increasing recruitment of abdominal musculature during locomotion. In a 2017 study, involving seven riding horses, a gradual increased use of the ‘Equi Band’ system over a four-week training program was instituted. Motion-detection equipment with inertial sensors was used to evaluate the back’s three-dimensional movements before 32  The Practitioner 

and after the four-week program. Evaluations on six areas of the back during unridden trot, both in-hand on hard surfaces and on the lunge on soft surfaces, were performed. At the end of the program, horses showed less side-to-side and rotational vertebrae movement compared to the initial evaluation.69 Another system marketed as an aid to strengthen the back and engage the hind quarters, but which has limited scientific evaluation, is the pessoa training aid. It consists of one rope that goes behind the horse’s hindquarters and two side ropes which fold back on themselves around a pulley. The first section attaches to a bit and the second to a roller. A 2013 study looked at 12 horses lunged with and without a pessoa training aid and found the system to have potential benefits for general training and rehabilitation as a method for improving posture and stimulating core muscle activation without increasing load on either forelimbs or hindlimbs (Figure 12).70

CONCLUSION Although many rehabilitation modalities show promise, good scientific studies are few and far between. Confusion exists over which modalities are most effective and how to appropriately use them in the horse. Anecdotal reports are numerous for almost all rehabilitation modalities, and while this may encourage optimism, it should not be the yardstick by which we determine if a tool is efficacious. It is certainly not appropriate to rely solely on the manufacturer to validate the use of equipment. Specific and detailed information regarding correct protocols for the species under question is needed and high-quality research is the only way to achieve this. Without more focused and definitive equine research, many rehabilitation tools will be sub-optimally or inappropriately used based on non-species-specific manufacturer’s instructions with the possibility of undermining their true potential.

References 45. Pilla, A., Fitzsimmons, R., Muehsam, D., Wu, J., Rohde, C., & Casper, D. (2011). Electromagnetic fields as first messenger in biological signaling: application to calmodulin-dependent signaling in tissue repair. Biochimica et Biophysica Acta (BBA)-General Subjects, 1810(12), 1236-1245. 46. Huegel, J., Choi, D. S., Nuss, C. A., Minnig, M. C., Tucker, J. J., Kuntz, A. F., ... & Soslowsky, L. J. (2018). Effects of pulsed electromagnetic field therapy at different frequencies and durations on rotator cuff tendon-to-bone healing in a rat model. Journal of shoulder and elbow surgery, 27(3), 553-560. 47. Kold, S. E., Hickman, J., & Melsen, F. (1987). Preliminary study of quantitative aspects and the effect of pulsed electromagnetic field treatment on the incorporation of equine cancellous bone grafts. Equine veterinary journal, 19(2), 120-124. 48. Sanders-shamis, M. A. R. L. E. N. E., Bramlage, L. R., Weisbrode, S. E., & Gabel, A. A. (1989). A preliminary investigation of the effect of selected electromagnetic field devices on healing of cannon bone osteotomies in horses. Equine veterinary journal, 21(3), 201-205. 49. Biermann, N. M., Rindler, N., & Buchner, H. H. F. (2014). The Effect of Pulsed Electromagnetic Fields on Back Pain Issue 1 • 2021


in Polo Ponies Evaluated by Pressure Algometry and Flexion Testing—A Randomized, Double-blind, Placebocontrolled Trial. Journal of Equine Veterinary Science, 34(4), 500-507. 50. Edner, A., Lindberg, L. G., Broström, H., & Bergh, A. (2015). Does a magnetic blanket induce changes in muscular blood flow, skin temperature and muscular tension in horses? Equine Veterinary Journal, 47(3), 302-307. 51. Vinhas, A., Rodrigues, M. T., Gonçalves, A. I., Reis, R. L., & Gomes, M. E. (2020). Pulsed Electromagnetic Field Modulates Tendon Cells Response in IL‐1β‐Conditioned Environment. Journal of Orthopaedic Research®, 38(1), 160-172. 52. Watkins, J. P., Auer, J. A., Morgan, S. J., & Gay, S. (1985). Healing of surgically created defects in the equine superficial digital flexor tendon: effects of pulsing electromagnetic field therapy on collagen-type transformation and tissue morphologic reorganization. American Journal of Veterinary Research, 46(10), 2097-2103. 53. Rittweger, J. (2010). Vibration as an exercise modality: how it may work, and what its potential might be. European journal of applied physiology, 108(5), 877-904. 54. Kim, H., Kwon, B. S., Park, J. W., Lee, H., Nam, K., Park, T., ... & Kim, T. (2018). Effect of whole-body horizontal vibration exercise in chronic low back pain patients: vertical versus horizontal vibration exercise. Annals of rehabilitation medicine, 42(6), 804. 55. Zaidell, L. N., Mileva, K. N., Sumners, D. P., & Bowtell, J. L. (2013). Experimental evidence of the tonic vibration reflex during whole-body vibration of the loaded and unloaded leg. PloS one, 8(12), e85247. 56. Carstanjen, B., Balali, M., Gajewski, Z., Furmanczyk, K., Bondzio, A., Remy, B., & Hartmann, H. (2013). Shortterm whole-body vibration exercise in adult healthy horses. Polish journal of veterinary sciences, 16(2). 57. Hulak, E. S. (2015). Influence of whole-body vibration on bone density in the stalled horse (Doctoral dissertation, Middle Tennessee State University). 58. de Zepetnek, J. O. T., Giangregorio, L. M., & Craven, B. C. (2009). Whole-body vibration as potential intervention for people with low bone mineral density and osteoporosis: a review. Journal of Rehabilitation Research & Development, 46(4). 59. Halsberghe, B. T. (2017). Long-term and immediate effects of whole-body vibration on chronic lameness in the horse: a pilot study. Journal of Equine Veterinary Science, 48, 121-128. 60. Halsberghe, B. T., Gordon‐Ross, P., & Peterson, R. (2017). Whole body vibration affects the cross‐sectional area and symmetry of the m. multifidus of the thoracolumbar spine in the horse. Equine Veterinary Education, 29(9), 493-499. 61. Stubbs, N. C., Hodges, P. W., Jeffcott, L. B., Cowin, G., Hodgson, D. R., & McGowan, C. M. (2006). Functional anatomy of the caudal thoracolumbar and lumbosacral spine in the horse. Equine Veterinary Journal, 38(S36), 393-399. 62. Stubbs, N. C., Kaiser, L. J., Hauptman, J., & Clayton, H. M. (2011). Dynamic mobilisation exercises increase cross WWW.FAEP.NET |

sectional area of musculus multifidus. Equine veterinary journal, 43(5), 522-529. 63. Stubbs, N. C., Riggs, C. M., Hodges, P. W., Jeffcott, L. B., Hodgson, D. R., Clayton, H. M., & Mc Gowan, C. M. (2010). Osseous spinal pathology and epaxial muscle ultrasonography in Thoroughbred racehorses. Equine Veterinary Journal, 42, 654-661. 64. Clayton, H. M., White, A. D., Kaiser, L. J., Nauwelaerts, S., Lavagnino, M., & Stubbs, N. C. (2010). Hindlimb response to tactile stimulation of the pastern and coronet. Equine veterinary journal, 42(3), 227-233. 65. Murphy, J. (2009). Weighted boots influence performance in show-jumping horses. The Veterinary Journal, 181(1), 74-76. 66. Paulekas, R., & Haussler, K. K. (2009). Principles and practice of therapeutic exercise for horses. Journal of equine veterinary science, 29(12), 870-893. 67. layton, H. M., Stubbs, N. C., & Lavagnino, M. (2015). Stance phase kinematics and kinetics of horses trotting over poles. Equine veterinary journal, 47(1), 113-118. 68. Brown, S., Stubbs, N. C., Kaiser, L. J., Lavagnino, M., & Clayton, H. M. (2015). Swing phase kinematics of horses trotting over poles. Equine veterinary journal, 47(1), 107-112. 69. Pfau, T., Simons, V., Rombach, N., Stubbs, N., & Weller, R. (2017). Effect of a 4‐week elastic resistance band training regimen on back kinematics in horses trotting in‐hand and on the lunge. Equine veterinary journal, 49(6), 829-835. 70. Walker, V. A., Dyson, S. J., & Murray, R. C. (2013). Effect of a Pessoa training aid on temporal, linear and angular variables of the working trot. The Veterinary Journal, 198(2), 404-411. Sarah Plevin, BVMS, MRCVS, CVA, DABVP, DACVSMR, RCVS Specialist Dr. Sarah Plevin is a sports medicine specialist and partner at Florida Equine Veterinary Associates. Originally from the United Kingdom, she graduated from Glasgow Veterinary School in Scotland. After, completing a surgical internship in Ocala, Florida, she went into general practice for a couple of years before undertaking a lameness fellowship and then pursing specialist qualifications. She is double boarded with the American Association of Veterinary Practitioners and the American College of Veterinary Sports Medicine and Rehabilitation. Dr. Plevin has also attained status as an equine sports medicine specialist from the Royal College of Veterinary Surgeons and is certified in veterinary acupuncture. Currently, Dr. Plevin devotes most of her time to clinical research and leads the research department at FEVA, where her focus is on preventing injuries in the juvenile TB racehorse. She has presented her work both nationally and internationally. Outside of work, Dr. Plevin is a keen swimmer and enjoys all outdoor activities. She is married with four young children and enjoys traveling extensively throughout the world with her family.

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MSK Ultrasound:

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The Practitioner Issue 1, 2021  

Published by the Florida Association of Equine Practitioners, an equine-exclusive division of the FVMA. Save the Date - PES 2021 (October 21...

The Practitioner Issue 1, 2021  

Published by the Florida Association of Equine Practitioners, an equine-exclusive division of the FVMA. Save the Date - PES 2021 (October 21...

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