Practitioner Issue 1, 2020

Page 1

Published by the Florida Association of Equine Practitioners, an Equine-Exclusive Division of the Florida Veterinary Medical Association Issue 1 • 2020

NEW INSIGHTS ABOUT DETECTING PREGNANT MARES AT RISK: WHAT WE HAVE LEARNED FROM A MODEL OF PLACENTITIS MARGO L. MACPHERSON, DVM, MS, DACT MALGORZATA A. POZOR, DVM, Ph.D., DACT

UPDATE ON DISEASES OF THE SINUSES AND GUTTURAL POUCHES DAVID E. FREEMAN, MVB, Ph.D., DACVS

TREATMENT OF SEPTIC SHOCK IN EQUINE PRACTICE

THOMAS J. DIVERS, DVM, ACVIM, ACVECC

NUTRITIONAL MANAGEMENT OF ENDOCRINE AND MUSCLE DISORDERS KELLY R. VINEYARD, MS, Ph.D.


EXECUTIVE COUNCIL RUTH-ANNE RICHTER

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

rrichter@surgi-carecenter.com

ADAM CAYOT DVM

adamcayot@hotmail.com

AMANDA M. HOUSE DVM, DACVIM

housea@ufl.edu

COREY MILLER DVM, MS, DACT

cmiller@emcocala.com

ANNE L. MORETTA VMD, MS, CVSMT, CVA

maroche1@aol.com

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

jackie@shellow.com

PHILIP J. HINKLE

The President's Line Dear Fellow Equine Practitioners, I hope this issue of The Practitioner finds you happy and busy despite the trying times. I’m always thankful that, as an equine practitioner, I get to enjoy the spring weather, even if I’m working instead of playing. This is a critical time to remember to take care of yourself, both physically and emotionally. The FVMA/FAEP is an excellent resource for veterinarians should we require anything, from emotional support to information on our profession, including how we are being affected by the COVID-19 pandemic. The FVMA/FAEP has recently put together a brochure about COVID-19, as it relates to animals. You are welcome to download and print the brochure the FVMA created (which can be found at FVMA.org) to share with your clients. While it is mostly mixed practice and small animal veterinarians who are facing virus-related questions, the brochure is an excellent resource to help calm clients and answer their questions. In addition to wellness resources, the FVMA/FAEP also keeps us informed and defends our profession against legal challenges. This enables us to concentrate on taking care of our patients. This issue of The Practitioner boasts timely topics, written by many of the speakers you may have heard at our 15th Annual Promoting Excellence Symposium (PES 2019) or our 57th Annual Ocala Equine Conference (OEC 2020). These articles are fantastic sources of new information on various equine-related topics. It was great seeing many of you at OEC 2020 this past January. The conference brought speakers, veterinarians, and industry professionals together in an informal and comfortable setting that was enriching for all who attended. PES 2020 will be held from October 8-11, 2020 at the Sawgrass Marriott Golf Resort & Spa in Ponte Vedra Beach. This part of Florida is filled with recreational options: golf, fishing, beaches, historical St. Augustine, shopping and much more! The speakers and their topics will be first-class. This is one veterinary conference you won’t want to miss! I want to express my deep gratitude to all our veterinary professionals who keep our industry running and our equines healthy. Thank you to all of those involved in making the FVMA/FAEP a leader in our profession. This includes the FVMA/ FAEP staff, our industry partners, the FAEP Executive council and all of you, our amazing members.

EXECUTIVE DIRECTOR

Best wishes,

phinkle@fvma.org

Armon Blair, DVM FAEP Council President

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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New Insights About Detecting Pregnant Mares at Risk: What We Have Learned from a Model of Placentitis MARGO L. MACPHERSON | DVM, MS, DACT MALGORZATA A. POZOR | DVM, Ph.D., DACT In the early 2000s, the late Dr. Michelle LeBlanc and her research team used ambitious methodology to establish a working model of induced placentitis in the mare. In this model, a clinicallyisolated inoculum of Steptococcus equi subspecies zooepidemicus was placed mid-way in the cervix, disrupting the critical cervical plug without fully breaching the cervix. Bacteria migrated, cranially, and inhabited the cervical pole of the chorioallantois.1 A second, more aggressive model of infection was developed by Dr. Sara K. Lyle and her co-workers by placing the bacterial inoculum directly on the chorioallantois.2 The rationale for this model was to develop a more consistent mode of chorioallantoic infection. Using either model, establishment of placental infection varies broadly between mares under experimental conditions, as do clinical signs. While some argue that a model does not realistically represent the clinical condition, the information gained has positively improved the outcome of many mares affected with placentitis and other conditions affecting the late term, pregnant of infection, but is frequently undetected if the mare’s perineal mare. region is not monitored daily.3 Premature mammary gland development can occur in mares with twin pregnancies as well The pathophysiology of equine placentitis as mares with placentitis, likely as a secondary response to the Initial studies by LeBlanc and her co-workers provided formative activation of the hypothalamic pituitary axis. Some mares have information regarding placentitis.1 Placentitis induced in 16 pony scant to no vulvar discharge present and/or minimal udder mares between 280-295 days of gestation resulted in 14 out of 16 development but have fulminant placental infection. These infected mares delivering dead or non-viable foals. Two foals born mares may suffer a subclinical infection that results in the death prematurely (days 311-313 of gestation) experienced accelerated of the fetus. Alternatively, some mares have extensive placental maturation and lived with minimal neonatal care. The duration separation due to infection but will deliver viable foals. Vigilant and intensity of uterine contractions were higher in infected monitoring of the perineal and mammary areas, particularly mares. Concentrations of prostaglandins E2 and F2α (PGE2 in mares “at risk,” is often the best line of defense for early and PGF2α) in allantoic fluid from mares with placentitis were detection of placentitis. Data from a clinical study4 showed that elevated. Concentrations of IL-6 and IL-8, cytokines involved in early detection of disease with physical and ultrasonographic inflammation, were elevated in the placentas of infected mares. monitoring allowed for early treatment of mares and a reduction All infected mares had gross thickening and purulent material of prematurely delivered foals by more than 30%. Daily at the cervical star of the placenta. Bacteria were located on the examination of the mammary gland and perineal area provides surface of the placenta, in the amniotic fluid and on the umbilical a simple, effective screening tool for early detection of placentitis. cord. Bacteria were isolated in fetal lungs from seven fetuses. The authors proposed that fetal infection occurred from the passage Mammary secretion electrolytes of bacteria through fetal membranes and into the amniotic fluid, Measurement of electrolyte values in mammary secretions is which the fetus inhaled or swallowed. Interestingly, not all fetuses a simple, semi-quantitative tool for determining imminent became infected from inoculated mares. This important data parturition as well as fetal readiness for birth.5, 6 Traditionally, showed that both infection and inflammation were involved in inversion of sodium and potassium concentrations, and a rise placentitis-induced preterm delivery, similar to other species. in calcium, signal impending parturition. These tools are widely Therefore, efforts for diagnosing placentitis have been directed at used in both laboratory measurements and in stall-side tests for identifying infection and/or inflammation. calcium (carbonate) concentrations. More recently, changes in mammary secretion pH have been used to predict imminent Physical examination findings parturition in both normal and abnormal equine pregnancies.7-9 Diagnosis of placentitis relies heavily on clinical changes, which While specific pH values predictive of impending delivery varied often lag behind the disease process. The most common clinical between studies, pH lower than 7.0 was predictive of foaling signs of placentitis include premature udder development and within 24 hours. This simple tool is easily applied to monitoring purulent vulvar discharge. Vulvar discharge is often the first sign both the normal and abnormal pregnant mare. 4  The Practitioner

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Ultrasonographic tools for diagnosis of placentitis

Transrectal ultrasonography in late gestation is useful for evaluating placental integrity (at the cervical star), fetal activity and fetal fluid character. The cervical star region of the placenta is the most frequently affected area in mares with placentitis due to the ascending route of infection. The combined uterine and placental unit is measured. Values of the combined thickness of the uterus and placenta (CTUP) for mares with normal pregnancies have been established.10 Mares with placental infection or inflammation will have an increase in CTUP measurements or a separation of the membranes with presence of purulent material.11 A caveat to this procedure is the inherent operator bias that occurs with two-dimensional ultrasound measurements. Repeat measurements performed by the same ultrasonographer allows for a more accurate diagnosis of disease.

measurement of progestagens requires sophisticated mass spectrometry equipment. However, many P4 immunoassays (radioimmunoassay and ELISA) cross-react with progestagens produced by the feto-placental unit. Cross-reactivity of assays must be determined for each commercial test used to measure progesterone. To aid in the detection of placental pathology and/ or response to therapy, it is recommended to monitor serial serum progesterone concentrations 3-4 times at 1-2 day intervals. These values can be assessed for trends, including a premature, gradual rise (prior to day 300 gestation) or a rapid drop (impending delivery) that may be useful for directing therapies.

Estrogens:

Estrogens are broadly produced in equine pregnancy by the fetoplacental unit. The fetal gonads produce estrogen precursors, which are aromatized by the placenta to produce a variety of estrogens including estrone, estradiol 17α and β, equilin and Transabdominal ultrasonography is an excellent tool for equilenin. Estrogen production increases from approximately evaluating fetal well-being and fetal fluid character as well as day 80 of gestation, peaks at 210 days of gestation, and gradually some areas of the placenta.12, 13 The technique has been well- decreases prior to delivery. High maternal serum estrogen described and is broadly used. Fetal health can be assessed concentrations (usually measured as estrone sulfate or total through transabdominal ultrasonographic measurements of fetal estrogens) indicate a functional feto-placental unit and are a heart rate, tone, activity and size. Transabdominal ultrasound strong indicator of fetal viability. The usefulness of this tool evaluation of the placenta provides the most accurate means of to detect and monitor pregnancy health has not been as welldiagnosing nocardioform placentitis. Similarly, a transabdominal defined as the measurement. Dr. R.H. Douglas reported that approach is the best and only method to identify late-term twins a total estrogen concentration greater than 1000 ng/mL was via ultrasound. consistent with a normal pregnancy between 150-280 days gestation.17 However, an association was made between mares More recently, Doppler ultrasonography has been investigated having total estrogen concentrations less than 500 ng/mL and as a tool for characterizing normal pregnancies14, 15 and for pregnancy loss. The value of measuring estrogens as predictors of identifying abnormal, late-term pregnancies, including mares placentitis was recently investigated by workers at the University with placentitis.15 Doppler ultrasonography allows assessment of of Kentucky.18 Estrone sulfate and 17β estradiol sulfate were fetal blood flow and perfusion, with a particular emphasis on the measured in normal pregnant mares and mares with ascending umbilical artery. placentitis. Estrone sulfate was not different between groups. 17β estradiol sulfate dropped rapidly after bacterial inoculation in mares, suggesting that this hormone might provide diagnostic Hormonal Assays and Biomarkers information from mares with placentitis. The authors postulated The limitations in sensitivity of clinical or ultrasonographic that hormonal changes in naturally occurring infections might parameters to aid in rapid diagnosis of equine placentitis have be more subtle, therefore accurate detection of 17β estradiol led to an investigation of laboratory-based tests to improve sulfate in mares with placentitis might be more difficult. diagnosis. Several hormonal assays and, more recently, bloodbased biomarkers contribute information that can improve the Time resolved fluoroimmunoassay technology was recently used diagnosis of placentitis. to assess steroid (progesterone and estrogen) hormones in plasma from a large number of pregnant mares. Samples were obtained Progesterone assays: from mares starting at 201 days gestation to foaling.19 Using this Several progestagens are synthesized by the feto-placental methodology, the authors measured progestin and estrogen unit to support pregnancy in the latter two-thirds of gestation. concentrations with anti-progesterone and anti-17β-estradiol These progestagens are metabolites of progesterone (P4) and antibodies. Mares were retrospectively assigned to two groups pregnenolone (P5). Dr. Jenny Ousey and her co-workers used based on the health and outcome of the foal (healthy foal group gas chromatography-mass spectrometry to measure serial and foal loss group). Between 240-320 days of gestation, mares concentrations of progestagens throughout pregnancy in mares with abnormal pregnancies had higher progestins and lower with both normal and abnormal pregnancies.16 All progestagens, estrogens than mares with normal pregnancies.19 Mares that except progesterone (P4), rose gradually in mare serum as were administered treatments for placentitis (ritodrine, synthetic pregnancy advanced. Mares with placentitis had higher levels progestins and trimethoprim sulfamethoxazole) that delivered of P4, P5 and metabolites when compared to normal, pregnant live foals showed changes in plasma steroid hormones that were mares. Mild increases in P4 were noted in mares with placental consistent with normal, foaling mares. Further, the authors pathology other than placentitis. Mares experiencing stress extrapolated cut-off values for progestins and estrogens at 20-day other than placentitis (such as colic or laminitis) showed normal, intervals from day 200 gestation forward that distinguished or slightly lower, levels of P4 and P5 metabolites. An accurate normal from abnormal pregnancies. The authors postulated that WWW.FAEP.NET |

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a one-time measurement of progestins and estrogens might be possible for predicting an abnormal pregnancy, particularly from day 241 to day 320 of gestation.19 This data suggests an alternative method for monitoring steroid hormones as predictors of abnormal pregnancy.

Relaxin:

Relaxin is a polypeptide hormone produced by the placenta. In mares, placental relaxin production begins around day 80 of pregnancy and continues until expulsion of the placenta. Relaxin concentrations have been advocated as a means of monitoring pregnancy health in mares and other species. Dr. Peter Ryan and his co-workers used a homologous radioimmunoassay to measure relaxin concentrations in mares with normal pregnancies and mares with placentitis.20 They showed a positive relationship between low maternal serum concentrations of relaxin and poor pregnancy outcome. The authors noted a high degree of variability in relaxin concentrations in pregnant mares, which they felt negatively affected accurate assessment with relaxin. To date, commercial assay of this hormone is not available.

Biomarkers:

Serum biomarkers, that reflect the health of the feto-placental unit, are an area of great interest in both human and equine pregnancies. The scope of biomarkers that have been identified in human pregnancy is broad, yet similarities between species are limited. Recently, acute phase proteins, such as serum amyloid A and haptoglobin (indicators of inflammation), have been examined in normal and abnormal equine pregnancies. Using ELISA technology, Dr. Coutinho da Silva and his co-workers measured serum amyloid A in normal pregnant mares and mares with experimentally induced placentitis.21 Serum amyloid A concentrations were shown to increase dramatically in the last 36 hours of normal pregnancy. Mares with placentitis demonstrated a premature rise in serum amyloid A. When serum amyloid A concentrations were monitored in mares that had been administered treatment for placentitis, concentrations were shown to decline in some mares, presumably as a response to treatment. In a similar study,22 SAA, haptoglobin, fibrinogen and white blood cell (WBC) counts were monitored in mares with normal pregnancies and mares with experimentally-induced placentitis. Similar to the prior study, SAA and haptoglobin increased rapidly after experimental infection and stayed elevated until abortion. However, in contrast to the previous study, SAA (and haptoglobin) did not rise prior to foaling in normal, pregnant mares. Fibrinogen and WBC counts were not affected by infection. Data from these studies demonstrate the usefulness of SAA as a screening tool for mares with placentitis. Serial measurements that can reveal trends in SAA concentrations as a result of infection, or in response to treatment, likely will yield the most useful information. As with previously validated tests for placentitis, changes in SAA concentrations are best used as an adjunct to ultrasonography and clinical signs. Alpha-fetoprotein, a protein member of the albuminoid superfamily, has recently been measured in fetal fluids and plasma from normal, pregnant mares and mares with experimentallyinduced placentitis.23 The protein is produced by the fetal liver and 6  The Practitioner

has been used as a predictor of abnormal pregnancy in humans.24 It has also been suggested that alpha-fetoprotein is predictive of placental abnormalities/insufficiencies, in addition to fetal anomalies such as neural tube defects. Plasma concentrations of alpha-fetoprotein from mares with experimentally-induced placentitis were elevated when compared to normal foaling mares.23 Increased concentrations were most evident in the immediate days preceding delivery, which limits the usefulness of the test as a diagnostic tool to initiate treatment for placentitis. There has been increased interest in the broad study of proteins in biologic and disease processes, termed proteomics. Kentucky workers recently performed protein analysis on fetal fuids (allantoic and amniotic fluid) from a population of normal mares and mares with experimentally-induced placentitis.25 One hundred thirty proteins were identified in either one or both fluids. Unique proteins were more consistently identified in amniotic fluid. Amniotic fluid from mares with placentitis contained three highly expressed proteins (haptoglobin, plasminogen isoform X2 and plasminogen-like isoform 1).25 Haptoglobin was also identified in allantoic fluid, but not as consistently.25 Some proteins were downregulated in amniotic fluid from mares with placentitis, including members of the keratin family, paraaminobenzoic acid biosynthesis pathway (folate synthesis) and extracellular matrix proteins.25 The significance of these findings has not been fully elucidated, but may lead to improved diagnosis of placentitis (upregulation of fetal fluid proteins) and/or a better understanding of the pathophysiology of the disease (up and down regulation of proteins).

Conclusions Diagnosis of pathologic conditions of the late term, pregnant mare, including placentitis, remains challenging. It is unlikely that a single, “silver bullet” test will accurately predict conditions that threaten pregnancies. Several exciting technologies are being explored that will aid in earlier, more accurate diagnosis of conditions, such as placentitis. Regular, thorough physical examinations, combined with pregnancy history and advanced diagnostic tools, will likely be the most effective means of identifying conditions that threaten pregnancy, allowing for prompt treatment.

References: 1. Leblanc MM, Giguère S, Lester GD, Brauer K, Paccamonti DL: Relationship between infection, inflammation and premature parturition in mares with experimentally induced placentitis. Equine Veterinary Journal 2012, 44:8-14. 2. Lyle S: The relationship between pro-inflammatory cytokines, prostaglandins and the fetal hypothalamic-pituitary-adrenal axis activation in mares with infective preterm delivery. PhD. Baton Rouge, LA: Louisiana State University; 2008. 3. Macpherson ML, Bailey CS: Treating the Mare with Placentitis: A Clinical Approach. Journal of Equine Veterinary Science 2008, 28(11):703-708. 4. Carrick JB, Begg AP, Perkins NR, O'Meira AO, O'Meara DO: Ultrasonographic monitoring and treatment of pregnant mares at risk for placentitis. Animal Reproduction Science 2010, 121(1-2, Supplement 1):331-333. Issue 1 • 2020


5. Ousey JC, Dudan F, Rossdale PD: Preliminary Studies of Mammary Secretions in the Mare to Assess Fetal Readiness for Birth. Equine Veterinary Journal 1984, 16(4):259-263. 6. Peaker M, Rossdale PD, Forsyth IA, Falk M: Changes in mammary development and composition of secretion during late pregnancy in the mare. JReprodFertilSuppl 1979(27):555-561. 7. Canisso IF, Ball BA, Troedsson MH, Silva ESM, Davolli GM: Decreasing pH of mammary gland secretions is associated with parturition and is correlated with electrolyte concentrations in prefoaling mares. Veterinary Record 2013, 173(9):218-218. 8. Korosue K, Murase H, Sato F, Ishimaru M, Kotoyori Y, Tsujimura K, Nambo Y: Comparison of pH and refractometry index with calcium concentrations in preparturient mammary gland secretions of mares. J Am Vet Med Assoc 2013, 242(2):242-248. 9. Hayna JT, Randell SR, Burden CA, Pozor MA, Benson SA, Kelleman AA, Giguère S, Macpherson ML: Mammary Gland Secretion pH and Impending Parturition in Ponies and Mares with and without Firocoxib. Journal of Equine Veterinary Science 2018, 66. 10. Renaudin CD, Troedsson MHT, Gillis CL, King VL, Bodena A: Ultrasonographic evaluation of the equine placenta by transrectal and transabdominal approach in the normal pregnant mare. Theriogenology 1997, 47(2):559-573. 11. Renaudin CD, Liu IKM, Troedsson MHT, Schrenzel MD: Transrectal ultrasonographic diagnosis of ascending placentitis in the mare: a report of two cases. Equine Veterinary Education 1999, 11(2):69-74. 12. Reef VB, Vaala WE, Worth LT, Sertich PL, Spencer PA: Ultrasonographic assessment of fetal well-being during late gestation: Development of an equine biophysical profile. Equine Veterinary Journal 1996, 28(3):200-208. 13. Reef VB, Vaala WE, Worth LT, Spencer PA, Hammett B: Ultrasonographic Evaluation of the Fetus and Intrauterine Environment in Healthy Mares During Late-Gestation. Veterinary Radiology & Ultrasound 1995, 36(6):533-541. 14. Ousey JC, KÖLLING M, Newton R, Wright M, Allen WR: Uterine haemodynamics in young and aged pregnant mares measured using Doppler ultrasonography. Equine Veterinary Journal 2012, 44:15-21. 15. Klewitz J, Struebing C, Rohn K, Goergens A, Martinsson G, Orgies F, Probst J, Hollinshead F, Bollwein H, Sieme H: Effects of age, parity, and pregnancy abnormalities on foal birth weight and uterine blood flow in the mare. Theriogenology 2015, 83(4):721-729. 16. Ousey JC, Houghton E, Grainger L, Rossdale PD, Fowden AL: Progestagen profiles during the last trimester of gestation in Thoroughbred mares with normal or compromised pregnancies. Theriogenology 2005, 63(7):1844-1856. 17. Douglas RH: Endocrine diagnostics in the broodmare: what you need to know about progestins and estrogens. . Proc Soc Theriogenology 2004:106-115. 18. Ball BA, Pease A, Sellon DC, White NA: AAEP/EVJ supplement 2013. Equine Veterinary Journal 2013, 45:1-1. 19. Shikichi M, Iwata K, Ito K, Miyakoshi D, Murase H, Sato F, Korosue K, Nagata S, Nambo Y: Abnormal pregnancies associated with deviation in progestin and estrogen profiles in late pregnant mares: A diagnostic aid. Theriogenology 2017, 98:75-81. 20. Ryan P, Bennet-Wimbush K, Vaala WE, Bagnell CA: Relaxin as a biochemical marker of placental insufficiency in the horse: a review. Pferdeheilkunde 1999, 15:622-626. 21. da Silva MAC, Canisso IF, Macpherson ML, Johnson AEM, Divers TJ: Serum amyloid A concentration in healthy periparturient mares and mares with ascending placentitis. Equine Veterinary Journal 2013, 45(5):619-624. 22. Canisso IF, Ball BA, Cray C, Williams NM, Scoggin KE, Davolli GM, Squires EL, Troedsson MH: Serum Amyloid A and Haptoglobin Concentrations are Increased in Plasma of Mares with Ascending Placentitis in the Absence of Changes in Peripheral Leukocyte Counts or Fibrinogen Concentration. American Journal of Reproductive Immunology 2014, 72(4):376-385.

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23. Canisso IF, Ball BA, Scoggin KE, Squires EL, Williams NM, Troedsson MH: Alpha-fetoprotein is present in the fetal fluids and is increased in plasma of mares with experimentally induced ascending placentitis. Animal Reproduction Science 2015, 154:48-55. 24. Goetzinger KR, Odibo AO: Screening for abnormal placentation and adverse pregnancy outcomes with maternal serum biomarkers in the second trimester. Prenatal Diagnosis 2014, 34(7):635-641. 25. Loux SC, Ball BA: The proteome of fetal fluids in mares with experimentally-induced placentitis. Placenta 2018, 64:71-78.

Margo L. Macpherson, DVM, MS, DACT Dr. Margo Macpherson received her DVM degree in 1990 from Michigan State University. She completed a residency and master’s degree in equine theriogenology at Texas A&M University. She spent time at the University of Pennsylvania and in private practice in central Kentucky, after leaving Texas. Dr. Macpherson is presently a professor and service chief in the section of reproduction at the University of Florida. She is interested in all aspects of equine reproduction, but has a special interest in problems affecting late pregnancy in the mare. For more than a decade, Dr. Macpherson has been unraveling strategies for treating mares with bacterial placentitis. She is a Diplomate and a past president of the American College of Theriogenologists, and she is currently on the Board of Directors of the American Association of Equine Practitioners.

Malgorzata A. Pozor, DVM, Ph.D., DACT Dr. Malgorzata A. Pozor is a clinical associate professor in the Department of Large Animal Clinical Sciences at UFCVM. She received her DVM and Ph.D. from the Academy of Agriculture in Poland. She is a diplomate of the American College of Theriogenologists (1996) and received the resident award from the Society for Theriogenology. Other awards include the Polish-American Agricultural Exchange Program Award (1988), the Superior Achievement Faculty Award from the Academy of Agriculture (1987) and the International Student Research Society Award (1984). Her clinical interests include reproductive behavior and endocrinology, veterinary andrology, and new modalities of imaging in diagnosis of reproductive disorders.

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UPDATE ON DISEASES OF THE SINUSES AND GUTTURAL POUCHES DAVID E. FREEMAN | MVB, Ph.D., DACVS Culture of S. equi equi from an abscess aspirate, nasal washes or swabs, or guttural pouch flush will confirm the diagnosis. Culture from a nasal wash is more sensitive in the detection of S. equi equi than a nasal swab, because a greater surface area of mucosa is sampled. Culture of a guttural pouch flush is more sensitive to the identification of chronic asymptomatic carriers than the culture of a nasopharyngeal swab/wash. New triplex qPCR techniques for rapid detection (2 h versus 48 h for culture) of S. equi equi DNA in nasal swabs or washes are considered approximately 10 times more sensitive than culture. PCR does Guttural Pouch Empyema not distinguish between live and dead bacteria. PCR testing Equine strangles is a purulent lymphadenitis of the upper is commercially available (e.g., Equine Diagnostic Solutions respiratory tract caused by the Lancefield Group C bacterium (http://www.equinediagnosticsolutions.com), UC Davis (direct Streptococcus equi subspecies equi. The organism is highly host- or via Antech and IDEXX)), and should be regarded as the gold adapted. It is a highly contagious disease that can occur at any standard diagnostic test for S. equi equi. Detection of antibodies age but is more common in young horses. The disease is usually against SeM-protein does not distinguish between an active sporadic in older animals. Morbidity is estimated between infection and a vaccination. It lacks the specificity to be used as a 30%-80% (it may be 100% in naïve populations of young animals). screening test for carrier horses. Mortality is reported between 0-10%. Diseases of the sinuses and guttural pouches are always challenging because of diagnostic limitations and complicated routes of access. This presentation will address current trends in managing these diseases and, especially, what we have learned from improved diagnostic techniques and treatments. Fitting the correct treatment to each case is rarely easy. Much of the discussion on guttural pouch empyema will cover strangles, because of the close relationship between this and the role of the guttural pouch in creating a carrier state.

Although the disease involves the upper airways and associated lymph nodes, dissemination to other locations may be hematogenous or via lymphatic vessels to cause abscesses in lymph nodes and other organs of the thorax and abdomen (or even the central nervous system). This is a form of the disease commonly referred to as “bastard strangles.” Nasal shedding of S. equi equi usually begins after a latent period of 2 to 3 days and persists for 2 to 3 weeks after the acute phase in most animals. The incubation period (exposure to clinical signs) is 3-14 days, this is the basis for the minimum 14-day quarantine period applied to new arrivals (ideally, the quarantine period is 3 to 4 weeks). After an outbreak, approximately 10% of recovering horses do not clear all infected material from guttural pouches or sinus tracts, and live bacteria can persist, in chondroids or on mucosal surfaces in a biofilm, for the rest of a horse’s life. The guttural pouches are the primary sites of carriage for more than 80% of horses, with the paranasal sinuses accounting for most of the remainder. These chronic carriers are important sources of contagion for other susceptible horses. Regional lymph nodes, such as submandibular and retropharyngeal nodes enlarge and become firm and painful 2-4 days after the onset of fever. The enlarged retropharyngeal lymph nodes can cause respiratory obstruction, but usually are, not always, externally evident. In most cases, affected lymph nodes rupture and drain 7 to 14 days after the onset of clinical signs and retropharyngeal nodes rupture into guttural pouches to produce a profuse mucopurulent nasal discharge. 8  The Practitioner

Treatment

Most cases of strangles are benign, and horses with few systemic signs may not need any treatment, other than nursing care. Approximately 98% of horses recover completely within weeks. The key principle of treatment is drainage with strict isolation. Penicillin remains the drug of choice for defense against the strangles organism and, to date, no resistance has been documented. It can be used in exposed animals with fever but without lymph node abscessation, or in animals that are at risk of asphyxiation, or that have “bastard” strangles. Rifampin can be added in difficult cases or in horses at risk of asphyxiation. Guttural pouch empyema is treated using local flushes through indwelling catheters or repeated endoscopy. Acetlycysteine (20%) into the pouches may aid in resolution of the empyema. A compounded penicillin gel, made from sodium (not potassium) penicillin G and gelatin, can be placed into the affected pouches. Chondroids must be removed either surgically or medically. Medically, this can be done using a memory-helical polyp retrieval basket. To prepare the penicillin gel (Waller), add 2 gm of gelatin to 40 mL of sterile water, heat or microwave to dissolve gelatin, then allow to cool to 45-50° C. Add 10 mL of sterile water to 10,000,000 units of Na penicillin G and then mix with gelatin to a final volume of 50 mL. Place in syringes and leave overnight at 4° C to set.

Complications of Strangles Infections

Complications have been reported in 19%-42% of strangles cases. Mortality associated with complication to infection may approach 40%. Enlarged retropharyngeal lymph nodes may compress the Issue 1 • 2020


pharynx, larynx or trachea resulting in upper respiratory tract Arterial Occlusion for Guttural Pouch Mycosis obstruction. This may occur even in the absence of overt external Methods for occluding the equine carotid arterial system include swelling. Retropharyngeal lymph nodes may rupture into the balloon catheters, microcoils and nitinol plugs. The transarterial guttural pouches, resulting in empyema. This complication is coil embolization (TACE) technique uses angiography to image common and may result in chronic shedding of S. equi equi by the affected vessels and identify any unusual branches and affected horses. sites of bleeding, and then places an embolization coil in the selected portion of the affected artery. Ultrasound (US) guided Although metastatic abscesses (bastard strangles) can occur transarterial coil placement can direct accurate occlusion of anywhere in the body, the most common sites include the lungs, carotid branches on the cardiac side of the guttural pouch and the mesentery, the liver, the spleen, the kidneys and the brain. can identify unusual branching. A combination of ultrasound Horses with intra-abdominal abscesses frequently present with and fluoroscopy can improve catheter guidance and reduce chronic weight loss and/or colic. Abdominal abscesses may be radiation exposure. palpable upon rectal examination. Transarterial occlusion with nitinol plugs is the method of choice Standing Surgical Removal of Inspissated Pus in the author’s hospital (Fig. 1). A nitinol vascular plug is a nickeland Chondroids titanium wire mesh that expands into a dumbbell configuration (Fig.1) when delivered to the target segment of artery to be occluded. The procedure is performed under fluoroscopic guidance using an approach and equipment similar to what is used for coil embolization. The nitinol plug has the advantage that only a single plug is required at each site whereas at least two transarterial coils are typically used at each site to stop blood flow. The nitinol plug can also be retracted into the delivery cable if placement is unsatisfactory, and migration or dislodgement from the target vessel is unlikely because the expanded plug is held securely by radial tension from the arterial wall. There is little difference in cost between the two methods and both require specialized equipment and expertise.

Ceratohyoidectomy

The ceratohyoid bone can be surgically removed in horses with Figure 1. This photo shows the removal of inspissated pus from the guttural pouch as a standing procedure. These horses have to be isolated from other hospital cases because they have strangles. A standing approach in isolation avoids surgery and anesthesia in the main hospital. Photo courtesy of Dr. David E. Freeman.

Many cases of guttural pouch empyema are caused by Streptococcus equi subspecies equi, and these cases can develop inspissated exudate and chondroids. Surgery, in such cases, should preferably be done as a standing procedure in an isolation facility, so the horse does not move through other parts of the hospital and contaminate surgery suites and anesthetic equipment with a highly contagious organism. Standing surgery also avoids the expense and risks of general anesthesia. A modified Whitehouse approach is used after sedation with detomidine HCl (0.01 mg/ kg IV) and butorphanol tartrate (0.03 mg/kg IV) and infiltration with ~30 ml of 2% mepivacaine HCl. If the guttural pouch is not distended, an assistant can insert a Chambers catheter through the nasopharyngeal ostium into the medial compartment, where the surgeon can help the assistant push it through the mucosal lining at this point. Once the catheter has penetrated, the tip of one’s hemostatic forceps can be placed in the open end of the catheter tip to guide the forceps into the guttural pouch, where it can then be used to expand the opening.

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Figure 2. A horse with temperohyoid osteoarthropathy (right side) with vestibular and facial nerve signs. Note its head tilt and ear/lip droop, which can develop acutely. Photo courtesy of Dr. David E. Freeman.

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temporohyoid osteoarthropathy (THO) to decrease forces on the ankylosed temporohyoid joint and, thereby, reduce recurrent fractures that exacerbate nerve compression. The ceratohyoid– basihyoid synovial joint is identified and disarticulated with cartilage scissors. The freed end of the ceratohyoid bone is grasped and the ceratohyoid bone is dissected from its attachments to the ceratohyoideus, the hyoideus transversus, and the genioglossus muscles. The hypoglossal nerve, lingual branches of the mandibular and glossopharyngeal nerves, and the lingual artery are lateral to the ceratohyoid bone and must be avoided. The ceratohyoid bone can be bluntly separated from its soft tissue attachments with a narrow osteotome or periosteal elevator. The cartilaginous articulation between the ceratohyoid bone and the stylohyoid bone is cut by cartilage scissors or continued elevation with the osteotome, taking care to avoid tension on the stylohyoid bone and temporohyoid joint. The standing procedure has been described, to date, in clinically affected horses. The results can vary, but some reports indicate recovery in 80% of treated horses with return to use. Treatment with analgesics and oral antimicrobial drugs can be considered if surgery is not an option.

Nasopharyngeal Obstruction Caused by Head Flexion

A recently described form of nasopharyngeal obstruction in adult horses has been attributed to impaired egress of air from one or both guttural pouches during poll flexion, possibly caused by an anatomic or functional defect in the salpingopharyngeal fold. The affected horses might have a form of guttural pouch tympany that is not manifested in the typical presentation in the foal. These horses have a history of respiratory noise and unwillingness to perform in a sport that requires head flexion. A standing laser fenestration of the median septum appears to be an effective treatment and can improve performance.

Ethmoid Hematoma

Ethmoid hematoma is a non-neoplastic, progressive and locally destructive growth in the paranasal sinuses that resembles a tumor in appearance and development. The largest hematomas arise from the ethmoidal labyrinth. Smaller, less common lesions originate from the floor and walls of the maxillary sinuses. As an ethmoid hematoma expands, the surface of its capsule ulcerates, and this causes epistaxis. The expanding hematoma also causes pressure necrosis of surrounding bone and spreads into the frontal sinus, the sphenopalatine sinus, the nasal passages, and the nasopharynx. An expanding hematoma rarely causes facial distortion, except possibly in foals. It is most commonly seen in horses older than six years but most often at 10-12 years of age. However, it has been described in a foal. The disease seems to be less common in Standardbreds than in other breeds. Bilateral disease is more common in females. Mild, persistent, spontaneous intermittent, and unilateral epistaxis is the most common clinical sign. The hematoma can be seen on radiographs as a smoothwalled, well-circumscribed density that contrasts well with air in the sinus cavity. However, CT is a far superior imaging modality and can identify sites and bilateral disease, so that surgery is better guided. A large frontonasal bone flap is the preferred approach. Horse 10  The Practitioner

Figure 3. Stylohyoid bones. The one on the left is affected by temperohyoid osteoarthropathy, with marked thickening on the bone at its articulation. Compare with the normal right side. Note: this can be a bilateral disease with clinical signs on the more severely affected side and then later develop similar changes and signs in the previously “unaffected” side. Photo courtesy of Dr. David E. Freeman.

temperament permitting, this should be a standing procedure with local anesthesia and sedation to improve access. This also reduces the chance of hemorrhage and the need for packing and hospitalization. Usually, a large opening from the sinus cavity into the nasal passage is created by surgical removal of the hematoma. The recurrence rate after a surgical removal of ethmoid hematomas has been estimated at 0%-44.4%, and longterm remission of clinical signs was reported as 33% in one study. A recurrence rate of 43% has been reported for bilateral lesions compared with 8% in unilateral lesions in one study. Recurrence may be recognized within the first 6-12 months after surgery and repeat endoscopic examination is recommended every 6 months. Improved methods of treatment, especially with improved access through large bone flaps, can facilitate the removal of the entire lesion and reduce recurrence. Recurrence should be documented by endoscopy and not by clinical signs, because remission of clinical signs does not rule out recurrence.

Wounds and Fractures

Blunt injuries to the frontal sinus and nasal bones caused by kicks from other horses or collisions with fixed objects cause open or closed wounds to the sinuses. Many can go unnoticed because the fracture fragments are forced into the sinus cavity and the overlying skin detaches from the bone to maintain a normal Issue 1 • 2020


facial contour. As healing progresses, the hematoma and fracture callous produce a firm, subcutaneous swelling along the fracture line and the depressed bone forms a facial concavity. Epistaxis and subcutaneous emphysema are common clinical signs of sinus trauma. Less common signs are dyspnea and epiphora. The fracture fragments can be exposed through a large curvilinear skin flap. Blood clots are removed and the sinus cavity is flushed liberally with saline solution. To facilitate elevation of the fracture fragments, holes can be drilled in the adjacent bone, and instruments can be passed through these to pry up depressed fragments. If the fragments wedge firmly together in their normal position and form a stable union, it may be unnecessary to wire them, but large fragments should be wired to the parent bone. All small fragments, without periosteal attachments, should be removed. The head should be bandaged to cover the wound, if possible, and the horse should recover from general anesthesia, either with assistance or by wearing a padded headguard. Healing after the repair of acute wounds is usually excellent, and cosmetically acceptable. In horses with long-standing, healed depression fractures, fluorocarbon polymer and carbon fiber can be used to restore facial contour, or the healed fracture fragments can be cut with a saw and elevated into position. However, a better cosmetic appearance can be obtained by a primary open reduction shortly after injury, rather than through facial reconstruction later. If severe fractures are not treated, complications, such as sinusitis, sequestra formation, facial deformity, abnormal bone growth in young horses and nasal obstruction, can be expected. If a sinus fistula forms to the outside after the sinus wound has healed, a mesh implant and sliding flaps can be used to cover the defects. Tissue expanders can produce sufficient skin to cover the defect, but skin alone is insufficient. Instead of mesh implants, muscle flaps can be used close to the defect.

Role of the Sphenopalatine Sinus in Sinusrelated Diseases Many sinus-related diseases in horses are well-advanced before they produce the outward signs that lead to a diagnosis. Because of this, these diseases can progress into the deeper recesses of the sinus cavities, where they become inaccessible by standard surgical approaches. In such locations, removal of the entire lesion becomes impossible and recurrence is likely. There is strong, recent evidence that the lesions that pose the most difficulty in treatment, and have the highest rate of recurrence, are those that invade the sphenopalatine sinuses (SPS). These sinuses are located at the base of the skull, positioned between the brain and ethmoid labyrinth dorsally and the pharynx ventrally. Various critical nerves pass around the outside of these sinuses (cranial nerves II-VI) so that any disease that destroys the wall of the SPS can also damage these nerves. Despite many improvements in access to the major sinuses in the horse’s head, an approach to the SPS has not been developed. A translaryngeal approach to the SPS has been developed to allow safe access to this important sinus cavity. The approach involves a clear endosocopic view to its interior and unrestricted access for long-handled instruments to remove lesions from within, without insult to vital nervous structures within the sinus. The surgical approach is composed of two parts. The first is to use a diode laser in a standing, transnasal, endoscopic approach to remove the pharyngeal mucosa over the bony floor of the sinus along the roof of the nasopharynx, 72 hours before sinusotomy to reduce intraoperative hemorrhage during sinusotomy. Additional laser debridement of the region is repeated, as needed, before the final sinusotomy to ensure complete mucosal ablation. The second part of the surgical approach is performed 72 hours after laser removal of mucosa. With horses placed under general anesthesia, a routine laryngotomy is performed. A special,

Figure 4. Approach to the sphenopalatine bone at the base of the skull (4). Note that this sinus is not always accessible through standard approaches and so can be the site from which an ethmoid hematoma can recur after surgical removal from the main sinuses. Photo courtesy of Dr. David E. Freeman.

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long-shanked burr is passed rostrally through the laryngotomy to the site of denuded mucosa to remove the bone from the floor of the sinus along the roof of the nasopharynx. Transnasal endoscopy is used to facilitate appropriate positioning of the burr and to monitor debridement. With this newfound access to the SPS, we may effectively treat, and prevent, the recurrence of some of the most devastating sinus lesions encountered in horses.

References: Boyle, AG, Timoney, JF, Newton, JR, Hines, MT, Waller, AS, Buchanan, BR. Streptococcus equi Infections in Horses: Guidelines for Treatment, Control, and Prevention of Strangles-Revised Consensus Statement. J Vet Intern Med. 2018;32:633-647.

CLASS-LEADING EQUINE WELLNESS SOLUTIONS Zoetis offers the vital products your practice needs from vaccines to dewormer products.

Lester, G. Strangles. SCAVMA Lecture notes, Course VEM 5335 2019; 15-24. Waller, AS. New perspectives for the diagnosis, control, treatment, and prevention of strangles in horses. Vet Clin North Am Equine Pract. 2014;30:591-607.

David E. Freeman, MVB, Ph.D., DACVS Dr. David Freeman graduated from the Veterinary College of Ireland in Dublin in 1972 and then worked in private practice in Ireland for 10 months. He did an equine internship at New Bolton Center of the University of Pennsylvania from 1974-1975, and he then did a residency in large animal surgery at New Bolton Center from 1975-1977. He was awarded a Ph.D. from the University of Pennsylvania in 1985. From 1981-1994, he was an equine surgeon at New Bolton Center, University of Pennsylvania. He became a board-certified surgeon with the American College of Veterinary Surgeons in 1989. He joined the faculty at the University of Illinois, College of Veterinary Medicine in 1994 and became head of equine medicine and surgery in 1998. In 2004, he joined the Department of Large Animal Clinical Sciences at the University of Florida, College of Veterinary Medicine as professor of equine surgery and associate chief of staff and, subsequently, as service chief in large animal surgery. He was also interim department chair in Large Animal Clinical Sciences at the at UFCVM from 2009-2012. He was invited to give the Sir Frederick Hobday Memorial Lecture by the British Equine Veterinary Association in 2004, and he was recognized by the Federal University of Minas Gerais, Brazil “in recognition of outstanding contributions to the development of equine surgery worldwide” in 2011. He is currently chief of large animal surgery at the University of Florida, a Martha and Arthur Appleton-endowed professor in equine studies and director of the Island Whirl Equine Colic Research Laboratory at UFCVM. Dr. Freeman has developed four widely used surgical procedures in horses and has described improvements and modifications in many others. His main areas of clinical interest are diseases and surgery of the equine gastrointestinal and upper respiratory tracts with special emphasis on improving survival after colic surgery. 12  The Practitioner

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TREATMENT OF SEPTIC SHOCK IN EQUINE PRACTICE THOMAS J. DIVERS | DVM, ACVIM, ACVECC The primary goals of septic shock management are to control or eliminate the initiating problem (bacterial infection, focal tissue injury) and to re-establish tissue blood flow and oxygen delivery to normal or above-normal values, without causing tissue edema or further oxidative injury.1 Hemodynamic targets should include some measure of the adequacy of cardiac preload (e.g. central venous pressure) and perfusion pressure (e.g. mean arterial pressure). These can be evaluated in the hospital by numerous methods. In field practice, these are mostly monitored through clinical exams, routine procedures and selected pointof-care testing.2 The treatment of septic shock is most successful during the early stage of shock, and when the initiating cause can be quickly controlled or eliminated.

VOLUME SUPPORT: THE BEST GENERAL TREATMENT

Expanding intravascular volume is generally the first priority when treating non-cardiogenic shock.3 This is best accomplished by administering crystalloids, hypertonic saline solution and balanced electrolyte fluids. Hypertonic saline solution has the advantage of causing a rapid increase in cardiac output and systemic arterial pressure with a decrease in pulmonary arterial pressure and only a brief reduction in vascular tone, all from a relatively small volume infusion. Therefore, hypertonic saline is the most practical fluid resuscitation treatment for field practice.4 Hypertonic saline may decrease polymorphonuclear adhesion molecules, which lessens the damage from marginating neutrophils. Additional effects from hypertonic saline may include enhanced phagocytic activity via enhanced toll-like receptor expression, decreased free radical formation, and diminished short-term tissue edema formation. Hypertonic saline should be used more cautiously in foals because of their inherent inability to regulate sodium.5 When it comes to the preferred polyionic, isotonic cystalloid, there is minimal to no evidence that lactated Ringer’s solution is better than Plasma-Lyte or other crystalloids. Neonatologists generally prefer a fluid with some magnesium and calcium, and in foals a lower-sodium fluid such as half-strength lactated Ringer’s solution (Na+ = 65.5 mEq/L) or Plasma-Lyte 56. These fluids should be rapidly administered while measuring systemic arterial pressure and central venous pressure (this can be estimated in the field by heart rate and mucus membrane color changes, speed of jugular vein distention after hand occlusion at the thoracic inlet, palpation of pulse pressure, volume of urine production and specific gravity of the urine). Colloidal pressure (most easily estimated by measuring total solids) should be monitored, as low colloidal pressure will decrease the benefit of crystalloids, and may result in tissue/ organ edema. If pulmonary or cerebral edema is a concern (most often a concern in recumbent neonatal foals or foals with sodium

16  The Practitioner

Photo courtesy of Dr. Corey Miller.

abnormalities), then small boluses of crystalloid fluids (2-3 mL/ kg) should be administered at a time, with reassessment between each fluid bolus. For horses of other ages experiencing septic shock, rapid administration of 10-20 mL/kg can be given initially, followed by assessments as previously described. Although more expensive, fluid therapy might include a combination of crystalloids and colloids. Colloids are theoretically important in treating septic shock and SIRS because of the vessel leakage that often occurs with sepsis and the inability of crystalloids to remain in the intravascular bed longer than 1 hour. Colloids help maintain colloidal intravascular pressure, thereby helping maintain crystalloids in the intravascular space for a longer time. Colloids may also plug some leaky capillary sites, although small molecule colloids may pass into the interstitial space and negatively influence intravascular homeostasis. Although there are potential benefits of colloids, such as reports of positive effects on mortality in septic humans, their value beyond what occurs with crystalloid therapy has been hard to confirm. Some recent reviews have even suggested they may increase mortality.6 Plasma and a synthetic colloid could be administered simultaneously, because each has separate and potentially beneficial effects in treating sepsis; they may also each have potentially harmful effects. The availability of commercial equine plasma, and the low adverse effects after its administration, has made it a very popular treatment for septic shock in foals and horses. From a physiologic standpoint, plasma might be considered a preferred colloid as it provides albumin, immunoglobulins, a balance of coagulation proteins, in addition to fluid volume and electrolytes. Issue 1 • 2020


PUMP SUPPORT

If fluid therapy alone is unsuccessful in normalizing blood pressure, cardiac output and perfusion, but CVP and intravascular volume is believed to be normal (indicating sufficient preload), the use of β1-adrenergic therapy to improve pump function is indicated. In field practice, jugular distention, following fluid therapy without improvements in urine production, may be an indication for treatment to improve pump (heart) function. Use Beta adrenergic drugs only if there is an adequate preload! Administration of dobutamine, 2-15 µg/kg per minute diluted in saline solution, for β1 activity, could improve microcirculatory perfusion independent of changes in cardiac output or blood pressure. If volume and pump support (e.g., dobutamine) are not successful in maintaining adequate blood pressure and improving urine output, dopamine (2-15 µg/kg per minute diluted in saline solution) can be administered. The lower dose stimulates renal dopaminergic receptors and increases renal blood flow. Aminophylline or norepinephrine could also be used to increase urine production. One of the best general indicators of successful perfusion is the production of a large volume of urine!

PRESSOR SUPPORT

Pressure support should only be used when the previous treatments (volume and pump support) have been attempted, and have been unsuccessful in satisfactorily providing adequate blood pressure and urine production! If fluid therapy and beta1agonist therapy are unsuccessful in improving blood pressure and the "forward flow" of blood with increased urine production, administration of norepinephrine (combined beta- and alphaagonist), 0.1-1.5 µg/kg/min can be attempted. Administering norepinephrine at the highest recommended dose with no

improvement in blood pressure and urine production in a volume replete/filled horse (normal CVP or near maximal intravascular volume expansion) suggests that the alpha receptors are no longer responsive. Vasopressin, 0.3-1.0 mU/kg/min (acting via the V1 receptors), could be administered to those patients that are refractory to the previously mentioned therapies. Short-term use of vasopressin (i.e., hours) could improve catecholaminerefractory hypotension, and increase urine production. In other species, vasopressin at this dose has a minimal effect on intestinal perfusion and heart rate. Vasopressin at higher dosages can decrease both heart rate and intestinal perfusion. Septic foals with “refractory hypotension” can be given hydrocortisone (0.20.4 mg/kg q 4h IV) as a treatment for relative adrenal insufficiency (hypothalamic-pituitary-adrenal axis dysfunction).7,8 Treatment with hydrocortisone may improve the efficacy of vasopressor therapy and may even help maintain intestinal perfusion during pressor (norepinephrine or vasopressin) therapy.

MAINTAINING ADEQUATE OXYGEN TO TISSUES

Hemoglobin (Hgb) levels should be kept within a normal range, as 98% of oxygen is transported in hemoglobin. Low levels of hemoglobin may indicate a need for transfusion, while too high levels may indicate a need for additional crystalloids. Oxygen treatment may be needed to maintain normal or above-normal free oxygen (PaO2). For most patients, the insertion of an intranasal tube in one or both nostrils (depending on the degree of hypoxia) can be used to administer humidified oxygen. Most adults, and even some foals, tolerate flow rates of 15 L/min, as long as there is not a noticeable noise in the nasopharynx caused by the oxygen flow. High nasopharyngeal oxygen flow rates may increase the end-expiratory lung volume, keeping airways open with the possibility of improving oxygenation and reducing respiratory rate. If the patient is comatose, oxygen is best administered via endotracheal tube, with or without positive pressure. For a septic foal with respiratory distress that requires mechanical ventilation, positive pressure ventilation with 50% oxygen concentration is generally recommended. PaO2 should be maintained at more than 70 mm Hg; PvO2 >35 mm Hg; SvO2 >60%; lactate, <2 mmol/L) and PvCO2:PaCO2 ratio close to one. Although oxygen therapy is difficult to perform in the field, small portable tanks can be effectively used in treating neonatal foals.

ANTIMICROBIAL SUPPORT

Adult Thoroughbred with Potomac horse fever (Neorickettsia risticii), septic shock and disseminated intravascular coagulation. Photo courtesy of Dr. Thomas J. Divers.

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Broad-spectrum coverage against life-threatening gram-positive and gram-negative aerobes might require intravenous penicillin and amikacin in foals, or penicillin and gentamicin in adult horses. Some additional treatment options are enrofloxacin combined with penicillin in adult horses or a higher generation cephalosporin, with or without amikacin, in foals. If anaerobic coverage is deemed important (e.g., intestinal, mouth, muscle, adult horse pneumonia or reproductive tract infections), metronidazole may need to be added to the treatment regimen. In adult horses, monotherapy (enrofloxacin or a cephalosporin) is commonly used as an initial therapy, if there is a concern about renal function. Imipenem or meropenem therapy is reserved mostly for foals with highly resistant organisms. The initial choice of antimicrobials depends on an understanding of which organisms are most likely present which can be based clinical signs, history of which organ systems are involved, sensitivity FLORIDAAEP |

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ADDITIONAL THERAPIES Most studies show little difference in septic shock outcome with corticosteroid administration, but corticosteroids inhibit arachidonic acid metabolism (prostanoids and leukotrienes) and are frequently used as a single dose (dexamethasone 0.25 mg/kg IV) early in severe septic shock when the condition is judged to be imminently life-threatening.

Treatment of neonatal foal with septic shock. Photo courtesy of Dr. Thomas J. Divers.

patterns in the practice area/farm, and potential toxicity.9 The earlier the antimicrobial therapy is started in septic, or even severe, hypotensive/hypoxemic shock, the better the prognosis; this is especially true in foals.

SURGICAL TREATMENT: SEPSIS-SOURCE CONTROL

When there is a localized septic area that can be safely drained, establishing drainage (e.g., septic uterus, etc.) or removing infarcted tissue (e.g., intestine, lung) and debriding necrotic tissue (e.g., septic myositis) is more important than antimicrobial therapy. In some colitis/enteritis cases, bacterial toxins can be bound in the intestinal tract by using activated charcoal or other binders (such as di-tri-octahedral (DTO) smectite).

COMPLIMENTARY TREATMENTS

Prostanoid Inhibitors

Flunixin meglumine, 0.3 mg/kg IV q8h, is generally administered if there is no primary gastrointestinal disease and urination has occurred. Flunixin meglumine, 1.0 mg/kg IV, can be given as an initial treatment particularly if colitis/enteritis is not the cause of the sepsis. Meloxicam (0.6 mg/kg IV), which is very expensive as a parenteral preparation in the United States, and firocoxib are the best available COX-2 specific inhibitors for the horse, and they might be best indicated for endotoxemia associated with severe gastrointestinal disease. Conversely, highly selective COX-2 inhibitors may not block thromboxane and prostaglandin F2-alpha (PGF-2 alpha), which are believed detrimental in equine sepsis. Flunixin meglumine, 0.3 mg/kg IV q8h, could be combined with firocoxib (0.1 mg/kg IV q24h).

Endotoxin Inhibitors

Hyperimmune plasma, 2 to 4 mL/kg IV, containing antibodies against the core lipopolysaccharide may be of some benefit in treating endotoxemia and Polymyxin B, 6,000 units/kg IV q8h (6,000 units = 1 mg), by slow intravenous administration may neutralize some circulating endotoxin. Polymyxin B is commonly used in treating septic horses, and adverse effects (renal toxicity and neuromuscular weakness) are uncommon. 18  The Practitioner

Pentoxifylline, 8.4-10 mg/kg PO or IV q12h, is commonly used to inhibit cytokines and may protect body organs from cytokine injury. Most studies on pentoxifylline suggest the drug needs to be administered before endotoxin challenge to be more effective.10 Inhibition of platelet aggregation may diminish microvascular thrombosis along with diminishing the inflammatory response associated with platelet aggregation. NSAIDs are not effective in inhibiting platelets in horses with sepsis, but heparin may be helpful. Dalteparin (low-molecular-weight heparin), 50 (adult) to 100 (foal) units/kg SQ q24h, has good activity against thrombin.11 The value of this drug treatment in horses with septic shock is unproven. Dalteparin has been reported to have an antiinflammatory effect in an ischemia-reperfusion rat model where an increased COX-1 activation, increased prostacyclin levels and a decrease in both tumor necrosis factor and interleukin-12 was noted.12 Lidocaine (1.3 mg/kg slowly IV followed by 0.05 mg/kg/ min continuous rate infusion [CRI]) administration, following correction of life-threatening fluid deficits, may have some benefits in treating septic shock.13 It may diminish leukocyte activation associated with endotoxemia, which may be helpful in preventing intestinal or other organ reperfusion injury. It may also provide analgesic effects, allowing less NSAID therapy in horses with damaged intestinal mucosa, and help maintain intestinal motility. Some recent studies in humans with early sepsis have shown outcome benefits following the intravenous administration of thiamine and vitamin C.14 Although these treatments have already been adapted to equine practice, as they are safe and relatively cheap, more research is needed to prove efficacy.

GLYCEMIC CONTROL

Glucose should ideally be maintained between 90-160 mg/dL in the foal. If the patient is hyperlipemic and hyperglycemic after correcting fluid deficits, controlling pain and/or anxiety, then regular insulin could be started at 0.05-0.1 units/kg per hour, while monitoring blood glucose and maintaining potassium therapy (unless hyperkalemia is present). Insulin may have direct, antiinflammatory/anti-apoptotic effects independent of glycemic control. The routine control of hyperglycemia with insulin in adult horses is not proven, and could have adverse effects. Foals that have a blood glucose <50 mg/dL can initially be given 1 mL/ kg 10-25% dextrose followed by continual administration of a lower concentration dextrose, if needed. Ulcer prophylaxis is common in foals with sepsis, although there is some belief that this therapy may predispose the foal to infectious diarrhea. Therefore, many veterinarians only use sucralfate for gastroprotective effects unless diarrhea is already present, in which case omeprazole, pantoprazole or ranitidine Issue 1 • 2020


are administered for gastroduodenal ulcer-prevention. If NSAIDs are expected to be used for several days, proton pump inhibitors (omeprazole) are preferred.

References: 1. Marino, PL. Septic shock. In: The ICU Book, 4th ed. Marino PL, ed. Wolters Kluwer Health Philadelphia, PA, 2014; 268-273. 2. Divers, TJ. Monitoring treatment of septic shock and SIRS. In: Equine Emergencies, 4th ed. Orsini JA and Divers TJ, eds. Elsevier, St. Louis MO, 2014; 570-572. 3. Fielding, CL, Magdesian, KG. Sepsis and septic shock in the equine neonate. Vet Clin N Am Equine Pract 2015; 31(3):483-496. 4. Schmall, LM, Muir, WW, Robertson, JT. Haemodynamic effects of small volume hypertonic saline in experimentally induced haemorrhagic shock. Equine Vet J 1990; 22(4):273-277. 5. Hollis, AR, Boston, RC, Corley, KT. Plasma aldosterone, vasopressin and atrial natriuretic peptide in hypovolaemia: a preliminary comparative study of neonatal and mature horses. Equine Vet J 2008; 40(1):64-69.

Thomas J. Divers, DVM, ACVIM, ACVECC

Dr. Thomas J. Divers earned his DVM from the University of Georgia and went to the University of California, Davis, School of Veterinary Medicine for an internship in equine medicine. He returned to the University of Georgia for his residency in large animal internal medicine. Currently, Dr. Divers is a professor of medicine and chief of the section of large animal medicine at the Cornell University College of Veterinary Medicine. He is a Diplomate of the American College of Veterinary Internal Medicine and the American College of Veterinary Emergency and Critical Care. Dr. Divers’ research interests include equine motor neuron disease, equine lyme disease, equine protozoal myelitis, and advances in internal medicine and critical care for horses and cows.

6. Bagshaw, SM, Chawla, LS. Hydroxyethyl starch for fluid resuscitation in critically ill patients. Can, J Anaesth 2013; 60(7):709-713. 7. Gold, JR, Divers, TJ, Barton, MH, Lamb SV, Place NJ, Mohammed HO, Bain FT. Plasma adrenocorticotropin, cortisol, and adrenocorticotropin/cortisol ratios in septic and normal-term foals. J Vet Intern Med 2007; 21(4):791-796. 8. Hart KA, Barton MH. Adrenocortical insufficiency in horses and foals. Vet Clin North Am Equine practice 2011; 27(1): 19-34. 9. Magdesian, KG. Antimicrobial pharmacology for the neonatal foal. Vet Clin N Am Equine Pract 2017; 33(2):47-65. 10. Barton, MH, Ferguson D, Davis PJ, Moore JN. The effects of pentoxifylline infusion on plasma 6-ketoprostaglandin F1 alpha and ex vivo endotoxininduced tumour necrosis factor activity in horses. J Vet Pharmacol Ther 1997; 20(6):487-492. 11. Armengou, L, Monreal, L,Delgado MÁ, Ríos J, Cesarini C, Jose-Cunilleras E. Low-molecular-weight heparin dosage in newborn foals. J Vet Intern Med 2010; 24(5):1190-1195. 12. Harada, N, Okajima K, Uchiba M. Dalteparin, a low molecular weight heparin, attenuates inflammatory responses and reduces ischemia-reperfusion-induced liver injury in rats. Crit Care Med 2006; 34(7):1883-1891. 13. Peiró, JR, Barnabé, PA, Cadioli FA, Cunha, FQ, Lima, VM, Mendonça, VH, Santana, AE, Malheiros, EB, Perri, SH, Valadão, CA. Effects of lidocaine infusion during experimental endotoxemia in horses. J Vet Intern Med 2010; 24(4):940-948. 14. Obi J, Pastores SM, Ramanathan LV, Yang J, Halpern NA Treating sepsis with vitamin C, thiamine, and hydrocortisone: Exploring the quest for the magic elixir. J Crit Care. 2020 Jan 8.

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NUTRITIONAL MANAGEMENT OF ENDOCRINE AND MUSCLE DISORDERS KELLY R. VINEYARD | MS, Ph.D.

Research and clinical experience suggest that horses with endocrine disorders such as Equine Metabolic Syndrome (EMS), Pituitary Pars Intermedia Dysfunction (PPID), Insulin Dysregulation (ID; defined abnormalities of insulin metabolism, i.e. hyperinsulinemia and insulin resistance), and muscle disorders, such as polysaccharide storage myopathies (PSSM) and recurrent exertional rhabdomyolysis (RER), may be better managed through certain dietary manipulations. These disorders are grouped together here because the dietary focus for horses with any of these conditions involves managing the amount and source of dietary carbohydrates and calories. The following article will discuss the practical application of nutritional principles to better manage horses diagnosed with these conditions. Additional informative and in-depth reviews are available on both endocrine1,2 and muscle disorders,3 covering related information on diagnostics and medical interventions.

Equine Metabolic Syndrome, Pituitary Pars Intermedia Dysfunction and Insulin Dysregulation

Although EMS, PPID and ID are unique medical conditions, they are somewhat interrelated and share commonalities when it comes to nutritional management. In many cases, horses diagnosed with these conditions are also obese (≥7 on the Henneke Body Condition Scoring System (BCS)). Obesity itself is a predisposing factor for EMS and insulin resistance (IR). It is important to recognize, however, that not all obese horses are insulin resistant, and not all insulin resistant horses are obese.4 If a horse is obese, weight loss should be induced by restricting the total number of calories offered to the horse. If a horse is both obese and insulin resistant, reducing bodyweight is sometimes all that is necessary to bring the horse back to normal glucose/ insulin homeostasis.5 A successful weight loss program involves reducing calories from both the concentrate and forage portion of the diet. A protein/vitamin/mineral supplement (ration balancer) designed to be fed at 0.1-0.2 lbs/100 lbs BW will provide nutrients missing in a forage-only diet, without the addition of unnecessary calories. Alternatively, a low-calorie concentrate (<1000 Cal/lb) designed for weight loss can be utilized for owners who prefer to feed a larger volume of concentrate. While on a weight loss program, pasture intake must be limited or eliminated. This can be accomplished by allowing only short (< 1 hour) grazing periods, utilizing a dry lot for turnout, utilizing electric fencing or a round pen in a larger pasture for confinement, or by using a grazing muzzle. Moderate quality grass hay should be fed at a restricted rate of 1.5-2% of the horse’s current BW/day. In some resistant cases, forage intake can be reduced to 1% BW, but anything less than that could compromise digestive function. 20  The Practitioner

The use of a grazing muzzle is an effective way to promote weight loss in horses housed on pasture. Photo courtesy of Dr. Kelly R. Vineyard.

When restricting hay, utilizing a small-hole hay net or slow feeder is a useful strategy to help prolong forage intake throughout the day. Initiating an exercise program that includes 30 minutes of forced physical activity 6 times per week is also recommended for obese horses. Not only will this facilitate more rapid weight loss, but exercise itself has been shown to improve insulin sensitivity in obese horses.6 For horses with EMS, horses diagnosed with ID or horses with a history of chronic laminitis, dietary non-structural carbohydrates should be limited in the ration. Commercial feed products should have the starch and sugar levels guaranteed on the tag, as claims of “low starch” or “low carb” without tag guarantees should not be relied upon for sensitive horses. Ideally, hays should be analyzed for soluble carbohydrates at a forage testing lab. Keeping the total ration ≤ 12% non-structural carbohydrate (starch + sugar) is recommended. Dividing the concentrate portion of the ration into three or more small meals per day will help manage insulin response to a meal, as will providing access to forages low in nonstructural carbohydrates on a continuous basis. In cases where testing hay is not practical, soaking hay in cold water for 1 hour or in warm water for 30 minutes may reduce starch and sugar content by 20-30%. Issue 1 • 2020


conditions can cause fructan accumulation, and seasonal influences result in the highest fructan concentration in spring grass, lowest levels during the mid-growing season, and moderate levels in the fall.7 Extra caution should be taken during these times, and grazing should be restricted to times when fructan content is lowest (late evening through early morning). In horses with severe and recurrent laminitis, allowing pasture access may never be an option. Mildly affected horses may be able to return to grazing under careful observation and if the above guidelines are adhered to. When managing a horse with PPID, it should not be assumed that the horse is also insulin dysregulated. In an epidemiological study, 43% of PPID positive horses were also hyperinsulinemic.8 Therefore, evaluating insulin status in PPID cases is recommended and will be helpful when developing a nutrition plan. For horses that are not hyperinsulinemic, any appropriate ration that meets their nutrient and caloric requirements is acceptable. Horses with PPID are more likely to experience muscle loss and are susceptible to immune suppression. Therefore, it is important to select feeds that provide high quality amino acids for muscle maintenance and adequate essential nutrients to support optimal immune function (especially trace minerals and antioxidants). For horses with concurrent PPID and ID, feeding recommendations for horses with EMS and/or ID can be followed based on the horse’s current body condition.

Recurrent Exercise Rhabdomyolysis and Polysaccharide Storage Myopathy

Dietary management strategies for RER and PSSM are similar and are based on reducing the soluble carbohydrate content of When selecting commercial feed products for horses with carbohydrate the ration, supplying additional energy with fat when necessary sensitivities, look for guaranteed levels of sugar and starch on the feed tag. and ensuring adequate vitamin E intake. RER is commonly seen Photo courtesy of Dr. Kelly R. Vineyard. in Thoroughbred racehorses in training, while PSSM1 is more commonly seen in Quarter Horses (with a higher prevalence in If a horse with ID is underweight (BCS <4), weight gain can halter horses), draft horse breeds and some warmbloods. PSSM2 be initiated by utilizing calorie-dense, controlled carbohydrate is recognized as a collection of different disorders that may have concentrates and forages. Selecting a concentrate that is ≤ 12% different recommendations for nutritional management, based non-structural carbohydrate is recommended, but if dividing on muscle biopsy results, and has been observed in Quarter the daily ration into multiple small meals per day (≤3 lbs), Horses (typically those bred for performance disciplines), concentrates with ≤ 20% non-structural carbohydrate may be Arabians, warmbloods and other light breeds. used safely. Fat supplementation with up to 3-4 cups of vegetable oil per day (depending on the size of the horse; introduce slowly) Horses with PSSM1 are more sensitive to dietary starch and will further increase the caloric density of the ration. Alfalfa hay, sugar levels because they accumulate more muscle glycogen which is more calorically dense than grass hay, is oftentimes lower than normal horses or horses with PSSM2. They also benefit in soluble carbohydrates; therefore, incorporating alfalfa hay is a from more calories supplied by dietary fat because they store good strategy to increase overall caloric intake. an amylase-resistant polysaccharide, which can’t be utilized as substrate for working muscle fibers. Diet and training adaptation Special considerations regarding the fructan content of forages to higher dietary fat levels can shift certain muscle fibers to must be made for horses with a history of, or those at risk for, utilizing fatty acids, relying less on glycogen, to fuel exercise. laminitis. Fructans are the primary form of stored carbohydrate “Easy-keepers” or less-active PSSM1 horses may not be able to in cool season grasses (e.g., orchardgrass, timothy), but they are consume higher fat levels without becoming overweight. In these not present in warm season grasses (e.g., Coastal bermudagrass, cases, significantly reducing dietary starch and sugar, by feeding bahiagrass) and legumes. Fructan content in cool-season pasture at least 1.5% BW of a low soluble carbohydrate hay (≤12% NSC) varies over the course of a 24-hour period and with changing and a ration balancer, can meet nutrient requirements without seasons and weather conditions. In general, fructan levels begin supplying significant starch and sugar, or additional calories. If to rise during the morning hours, peak in the afternoon, and a horse requires more calories, a controlled carbohydrate, fatare lowest overnight and in the early morning hours.7 Drought added concentrate feed should be incorporated into the ration. WWW.FAEP.NET |

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Specific amounts of soluble carbohydrate and fat to best manage each case tend to be variable depending on the individual horse and the total calorie demand. Horses with PSSM2 have abnormal muscle histology with glycogen aggregation, but do not accumulate excess glycogen or store an abnormal polysaccharide. The dietary recommendations for PSSM2 are not currently as well-defined, but these horses don’t seem to be as sensitive to dietary starch and sugar levels as PSSM1 horses. Current recommendations are to use low to moderate soluble carbohydrate concentrate feeds and utilize fat calories according to energy demands of the horse. Supporting muscle health and function with high-quality amino acids, specifically by using whey protein-based supplements, may be helpful in better managing symptoms in horses with PSSM2. Although a different condition driven by different mechanisms, horses with RER also benefit from a ration lower in dietary sugar and starch and higher in fat, but they can often tolerate more soluble carbohydrate in the diet than horses with PSSM1. Implementation of a regular exercise program is also important in the management of horses with both RER and PSSM, and efforts to reduce environmental stress may benefit horses with RER.9 Best results are reported when regular exercise is combined with dietary management, suggesting that the exercise component may be equally important as dietary alterations. Supplemental vitamin E, at a rate of 1000-2000 IU per day, should also be considered for horses with myopathies, and care should be taken to ensure that electrolyte requirements are being met according to sweat losses. In addition, feeding a large concentrate meal should be avoided in the 2-3 hours preceding exercise, as this may inhibit lipid oxidation in the muscle cell and exacerbate symptoms.9 The general guidelines of reducing dietary starch and sugar and increasing the fat content of the diet for horses with muscle disorders consistently proves beneficial, but the optimal diet seems to vary from case to case. This variation may be partially because horses with these conditions represent quite a range in age, activity level and genetic background, but it also may be due to a variation in individual starch and sugar sensitivity, and a need for fat to control symptoms based on the specific nature of the myopathy.

References: 1. Durham, A. E. 2017. Therapeutics for Equine Endocrine Disorders. Vet Clin North Am Equine Pract. 33(1):127-139. 2. Frank, N. and Tadros, E.M. 2014. Insulin Dysregulation. Equine Vet J. 46(1):103-12. 3. Valberg, S. J. 2018. Muscle Conditions Affecting Sport Horses. Vet Clin North Am Equine Pract. 34(2):253-276.

22  The Practitioner

4. Frank, N. 2010. Insulin resistance and equine metabolic syndrome. In: Equine Internal Medicine, 3rd Ed. Eds. S. M. Reed, W. M. Bayly, and D. C. Sellon. Saunders Elsevier, St. Louis, MO. 5. Gordon, M. E., M. L. Jerina, R. H. Raub, K. A. Davison, J. K. Young and K. K. Williamson. 2009. The effects of dietary manipulation and exercise on weight loss and related indices of health in horses. Comp. Ex. Phys. 6: 33-42. 6. Powell D., Reedy S., Sessions D. and Fitzgerald B. 2002. Effect of short-term exercise training on insulin sensitivity in obese and lean mares. EVJ Supp. 34: 81–84. 7. Longland, A. C. and B. C. Byrd. 2006. Pasture Nonstructural Carbohydrates and Equine Laminitis. J. Nutr. 136(7 Suppl):2099S-2102S. 8. Grubbs, S. T., Neal D.L., and T.J. Keefe. 2015. Epidemiological characteristics of horses at initial diagnosis. J Vet Intern Med 29:1231. 9. McKenzie, E. C. and A. M. Firshman. 2009. Optimal diet of horses with chronic exertional myopathies. Vet. Clin. Equine 25:120-135.

Kelly R. Vineyard, MS, Ph.D. Dr. Kelly Vineyard is a senior equine nutritionist with Purina Animal Nutrition where she is responsible for providing expert technical n u t r i t i o n a dv i c e a n d insights in a variety of areas, including new product innovation and research, veterinarian and customer support, sales and dealer training, and social media activity. Dr. Vineyard earned her Bachelor of Science in animal and dairy sciences from Auburn University and her Master of Science and Ph.D. in animal sciences, with a focus on equine nutrition, from the University of Florida. Her doctorate research focused on the effects of omega-3 fatty acid supplementation on immune function in horses, and she received the Innovative Research Award from the American Society of Animal Science for this work. Dr. Vineyard is a frequent publisher of and lecturer on equine nutrition with expertise in omega-3 fatty acids, immune function and performance horse nutrition. Her published work includes articles in the Journal of Animal Science and the Journal of Equine Veterinary Science. She also has a chapter in the textbook "Equine Applied and Clinical Nutrition." Dr. Vineyard has been involved with horses for most of her life. She is a USDF bronze and silver medalist in dressage, earning both with her beloved equine partner “The Roman Knows,” an off-the-track Thoroughbred.

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