Published by the Florida Association of Equine Practitioners, an Equine-Exclusive Division of the Florida Veterinary Medical Association Issue 3 â€¢ 2019
JANUARY 24-26, 2020 | OCALA, FLORIDA
GENETIC TESTING: WHAT TESTS ARE AVAILABLE AND WHEN TO USE THEM
STEPHANIE J. VALBERG DVM, Ph.D., DACVIM, DACVSMR
UPDATE ON EQUINE CORONAVIRUS
SALLY DeNOTTA DVM, Ph.D., DACVIM LINDA MITTEL MSPH, DVM
CREEPING INDIGO: A CLOSER LOOK AT THE PLANT AND ITS TOXINS ROB MACKAY BVSC (Dist), Ph.D., DACVIM
MANAGEMENT OF EQUINE STRANGLES
AMANDA M. HOUSE DVM, DACVIM
The President's Line EXECUTIVE COUNCIL RUTH-ANNE RICHTER
BSc(Hon), DVM, MS FAEP COUNCIL PAST PRESIDENT
ADAM CAYOT DVM
AMANDA M. HOUSE DVM, DACVIM
COREY MILLER DVM, MS, DACT
ANNE L. MORETTA VMD, MS, CVSMT
JACQUELINE S. SHELLOW DVM, MS REPRESENTATIVE TO FVMA EXECUTIVE BOARD
Dear Fellow Equine Practitioners, Fall has quickly arrived — and with it so does the announcement of FAEP 2020 programs! The Council, program planning committee and FAEP staff are very excited to announce that Ocala Equine Conference (OEC) 2020 will be January 24-26, 2020, at the Hilton Ocala. The program is anticipated to be another exciting and educational opportunity for equine practitioners across Florida and the United States. Registration for the conference will open November 1. Details about the program can be found in this issue of The Practitioner, highlighting the ever-popular Ultrasound Wet Lab and a packed CE schedule. As this issue of The Practitioner reaches you, some of you may be returning from the 15th Annual Promoting Excellence Symposium (PES). This year’s program theme was “Comprehensive Management of the Equine Athlete,” and topics — such as lameness, imaging, rehabilitation and medicine — were covered by an incredible group of distinguished speakers. Thank you to the Council, symposium planning committee, FAEP staff and resort staff for going above and beyond to put on a wonderful program this year. Couldn’t make it to the 15th Annual PES? Save the date for the 16th Annual PES, which will be October 8-11, 2020, at the Sawgrass Marriott Golf Resort & Spa in Ponte Verde Beach, Florida. We’re already excited about PES 2020 and hope to see you there! The 2020 Florida Legislative Session begins early this year, and the FVMA/FAEP will be visiting Tallahassee for our 2020 Legislative Actions Days on January 22-23, 2020, to advocate for veterinary medicine, the profession, and our organization and members. We invite our members to reach out to any Council members or the FVMA/FAEP for more information on how you can become involved in our 2020 Legislative Actions Days and advocating for your profession. As we head into the end of 2019, we look back at everything we’ve accomplished as an organization and for equine veterinary medicine — and it really has been a lot and very beneficial to our members. We take those positives as we start planning for 2020 to ensure we continue to provide world-class, equine-exclusive educational opportunities at our premier conferences and beyond!
PHILIP J. HINKLE
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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Issue 3 • 2019
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DEDICATION. EQ UINE D I V I S I O N
GENETIC TESTING: WHAT TESTS ARE AVAILABLE AND WHEN TO USE THEM STEPHANIE J. VALBERG | DVM, Ph.D., DACVIM, DACVSMR
The selective breeding of animal populations usually gives rise to a common founder, and one stallion can disseminate a genetic trait to many thousands of related offspring within a few decades. Traits can be controlled by one gene or influenced by many different genes (polygenic). This paper will present single-gene diseases for which there are (July 2019) validated genetic traits affecting the Quarter Horse and Arabian Breeds. Single-gene diseases in horses are primarily inherited as either autosomal dominant or autosomal recessive.
Autosomal dominant traits: Require only one copy of the
on websites like Google Scholar, and by consulting veterinarians and experts in the field.
What is a scientifically validated genetic test?
Peer-reviewed scientific publications are the traditional means by which a genetic test is validated to provide concrete evidence of the involvement of a genetic variant in a specific trait. In the age of social media, some genetic tests are being popularized on Facebook or other media outlets in the absence of validation and verification by scientific publication and peer review.
mutant gene to cause disease. Breeding of an affected heterozygous horse (one copy of the defective gene) to a normal horse results in a 50 percent chance of producing an affected horse. Breeding two heterozygous affected horses has a 50 percent chance of producing a heterozygous affected, 25 percent chance of a homozygous affected (two copies of the defective gene) and a 25 percent chance of a homozygous normal being born.
When veterinary genetic testing has been scientifically validated it means the following steps have been taken: 1. A diagnosis of disease has been carefully established in a group of “affected” horses and confirmed to be absent in a group of “unaffected” (i.e. non-diseased) horses. This diagnosis should be based on the highest standard for testing for a particular disease (i.e. blood test, tissue biopsy, etc.). 2. A change in the genetic sequence — called a genetic variant Autosomal recessive traits: Requires two copies of the — has been identified in the diseased horses that passes mutant gene to cause disease. Breeding two affected horses results statistical tests, showing it is significantly associated with the in a 100 percent chance of producing an affected horse. Breeding presence of the disease. two carriers results in a 25 percent chance of producing an affected 3. The test of association between the variant and the disease is horse, a 25 percent chance of a normal horse and a 50 percent replicated in additional, separate populations of diseased and chance of a carrier. Breeding an affected and a carrier results in a healthy horses to ensure the accuracy of the association. The 50 percent chance of producing an affected horse and a 50 percent frequency of the variant across breeds is reported. chance of producing a carrier. 4. The genetic variant is examined to establish that it changes the function or regulation of a protein or at the very least Genetic penetrance: Some genetic mutations have variable carefully modeled to show how it alters molecular biology to penetrance. This means that a horse may inherit the disease but, create the specific disease. in some individuals or in some breeds, it does not result in clinical signs of disease. Most importantly, as part of the publication process, a careful peer review is conducted by scientists. Peer review allows the results to Genetic tests: Genetic testing in horses is not regulated in be evaluated by other scientists who examine the methods used, the U.S.; therefore, it is up to animal owners and veterinarians to results produced and conclusions reached by the investigators. If determine if a genetic test does in fact identify susceptibility to accepted for publication, the article identifies and describes the a clinical disease or a specific trait. Not all genetic tests that are genetic mutation, including the location of the sequence change commercially offered have been proven to be associated with the and gene involved. Publication also allows other scientists to disease they purportedly are testing for. In other words, users of the attempt to replicate the findings. True, disease-causing variants test need to critically question if the existence of the genetic variant will stand up to this scrutiny. being tested for has been shown to truly indicate the presence or susceptibility to a disease. This determination should be informed by asking genetic testing laboratories for the peer-reviewed publications relating to the genetic test, looking for publications
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Table 1: Equine genetic diseases that have scientifically validated tests
Mode of inheritance
QH, Paint, Appaloosa
Hyperkalemic Periodic Paralysis
Glycogen Branching Enzyme Deficiency
Hereditary Dermal Asthenia
20 breeds: QH, Paints, Continental European drafts, Warmbloods……
Polysaccharide Storage Myopathy
Overo Lethal White Syndrome
QH, Paint, Appaloosa
Immune-mediated Myositis, Nonexertional Rhabdomyolysis
Lavender foal syndrome
Ocipitoatlantal axial malformation
Junctional Epidermolysis bullosa
Junctional Epidermolysis bullosa
Homozygotes 5X risk
Ocular squamous cell carcinoma
Hoof Wall Separation Disease
Fell Pony Syndrome
Fragile foal syndrome
GENETIC DISORDERS OF QUARTER HORSE-RELATED BREEDS Six genetic diseases have been found in Quarter Horses that have genetic tests commercially available. The six known genetic mutations in Quarter Horses include: Hyperkalemic Periodic Paralysis (HYPP), Glycogen Branching Enzyme Deficiency (GBED), Hereditary Equine Regional Dermal Asthenia (HERDA), Type 1 Polysaccharide Storage Myopathy (PSSM1), Malignant Hyperthermia (MH) and Nonexertional Rhabdomyolysis/IMM WWW.FAEP.NET |
(MYHM). Information is available on our website: https://cvm.msu.edu/research/faculty-research/valberg-laboratory. In my opinion, this breed distribution reflects the larger number of Quarter Horses in the U.S. relative to other breeds, a tendency to line breed, and the openness and dedication of the Quarter Horse Association to finance and support investigation into equine genetics. As of February 1, 2012, the AQHA began offering a panel test that includes HYPP, HERDA, MH, GBED and PSSM1.
@FLORIDA_VMA | The Practitioner 5
HYPERKALEMIC PERIODIC PARALYSIS (HyPP) Breeds affected: Quarter Horse-related bloodlines. Bloodlines: Horses descendant from Impressive. Prevalence: 3 percent of the Quarter Horse breed is affected. 60 percent of halter horses. Age affected: Signs usually begin by 2 to 3 years of age. Clinical signs: Range from asymptomatic to intermittent muscle tremors and weakness. Horses homozygous for HyPP may present with difficulty swallowing or respiratory distress. Inheritance: Autosomal dominant. Mutation: A point mutation that results in a phenylalanine/ leucine substitution in a key part of the voltage-dependent skeletal muscle sodium channel alpha subunit that controls channel activity (SCN4A). GLYCOGEN BRANCHING ENZYME DEFICIENCY (GBED) Breeds affected: Quarter Horse-related bloodlines. Bloodlines: Horses descendant from Zantanon and King. Prevalence: 8 percent of the Quarter Horse breed. 28 percent of Western pleasure are carriers. Age affected: Signs usually present in utero or at birth. Clinical signs: Abortion or stillbirth, may be born alive and are weak at birth. With supportive care, may live to up to 18 weeks of age. Death may be sudden when exercised on pasture, associated with weak respiratory muscles or the result of euthanasia due to persistent recumbency. Treatable flexural deformities of all limbs and recurrent hypoglycemia (low blood sugar) and seizures occur in some affected foals. Inheritance: Autosomal recessive. Mutation: A point mutation in exon 1 changes a tyrosine to a premature stop codon in the glycogen branching enzyme gene (GBE1) that is expressed in numerous tissues. HEREDITARY EQUINE REGIONAL DERMAL ASTHENIA (HERDA) Breeds affected: Quarter Horses. Bloodlines: Working cow and cutting horses. Prevalence: 3.5 percent of the Quarter Horse breed and 28 percent of cutting horses are carriers. Age affected: Signs usually begin by 1.5 years of age. Clinical signs: Wounds or sloughing skin, loose easily tented skin that does not return to its original position, scars, and white hairs at areas of hair re-growth found along the back and saddle area or areas with trauma. Healing is slow. Inheritance: Autosomal recessive. Mutation: Point mutation that results in a glycine to arginine
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substitution in the equine cyclophilin B gene (PPIB) that plays a role in the processing of collagen for the anchoring of the skin to underlying tissue. Type 1 POLYSACCHARIDE STORAGE MYOPATHY Two forms of PSSM appear to exist: Type 1 and Type 2 PSSM. The mutation for Type 1PSSM is in the GYS1 gene. The cause or causes of Type 2 PSSM are not yet known. Breeds affected: More than 20 breeds including Quarter Horserelated bloodlines, Belgians, Percherons, Morgans, Mustangs and some Warmblood breeds. Bloodlines: Present in founders of Quarter Horses and therefore widespread in all types of Quarter Horses with highest prevalence in halter and pleasure horses. Prevalence: 36 to 50 percent of Belgians and Percherons, 8 percent of the Quarter Horse related breeds, 30 percent of halter horses. Penetrance is variable with many draft horses not showing clinical signs. Age affected: Signs usually begin by 2 to 3 years of age but may occur in Weanlings. Some horses are subclinical. Clinical signs: Firm painful muscles, stiffness, skin twitching, sweating, weakness and reluctance to move with light exercise. Sometimes gait abnormalities, mild colic and muscle wasting. Serum CK and AST activity are elevated, except in Drafts. Inheritance: Autosomal dominant. Mutation: Point mutation that results in an arginine to histidine substitution in the GYS1 gene that codes for the skeletal muscle form of the glycogen synthase enzyme. MALIGNANT HYPERTHERMIA Breeds affected: Quarter Horse-related bloodlines. Bloodlines: High frequency in one or two QH families, often co-exists with PSSM. Prevalence: <1 percent of the Quarter Horse breed is affected. Age affected: Adults. Clinical signs: High temperature, metabolic failure and death under anesthesia. Tying up and fever. Signs of PSSM are more severe when both mutations are present. Sudden death. Inheritance: Autosomal dominant. Mutation: Point mutation that results in an arginine to glycine substitution in the RYR1 gene. MYOSIN HEAVY CHAIN 1 MYOPATHY Breeds affected: Quarter Horse-related bloodlines. Bloodlines: High frequency in reining horses, working cow horses, halter horses. Prevalence: 8 percent of the Quarter Horse breed is affected.
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Age affected: Weanlings to adults. Clinical signs: Either severe nonexertional rhabdomyolysis with very high CK and AST or rapid onset muscle atrophy, especially involving the epaxial and gluteal muscles causing immunemediated myositis. Inheritance: Autosomal Codominant with homozygotes more severely affected. Mutation: Point mutation that results in a glutamic acid to glycine substitution in the MYH1 gene.
GENETIC DISORDERS OF ARABIANS SEVERE COMBINED IMMUNODEFICIENCY (SCID) Breeds affected: Arabian. Prevalence: 8 percent in U.S. carriers. Age affected:< 6 months of age. Clinical signs: Recurrent infections, respiratory disease, eventual death.
OCCIPITAL - ATLANTO - AXIAL MALFORMATION (OAAM) Breeds affected: Arabian Horses Prevalence: 19 percent carriers. Age affected: Signs usually between 1 to 6 months of age. Clinical signs: Ataxia, abnormal head posture, clicking noise when head is flexed, visible asymmetry malformation of headneck junction. Inheritance: Autosomal recessive. Mutation: 2.7 kb deletion of highly conserved sequence within the homeobox D3/4 region. This is not the only mutation that causes OAAM in Arabian horses. Conflict of interest statement: Dr. Valberg and colleagues own the license for PSSM1 testing, and she receives sales income from its use. Dr. Valberg, Michigan State University, Dr. Finno and the University of California, Davis have a patent pending for the genetic test for MYHM. Their financial and business interests have been reviewed and managed by the universities in accordance with its conflict of interest policies.
Inheritance: Autosomal recessive. Mutation: 5 base pair deletion in the gene coding for DNAdependent protein kinase (DNA-PK) catalytic subunit. LAVENDER FOAL SYNDROME (LFS) Breeds affected: Arabian, higher prevalence in Egyptian Arabians. Prevalence: 8 – 17 percent carriers. Age affected: Signs present at birth. Clinical signs: A dilute coat color and a range of neurological signs, including recumbency, opisthotonous, paddling movements and extensor rigidity leading to euthanasia. Inheritance: Autosomal recessive. Mutation: A single base pair deletion in the MYO5A gene that codes for the protein myosin-Va. CEREBELLAR ABIOTROPHY (CA) Breeds affected: Arabian Horses. Prevalence: Rare. Age affected: Birth. Clinical signs: Ataxia, hypermetria and intention head tremors. Inheritance: Autosomal recessive. Mutation: A single nucleotide polymorphism located adjacent to a potential binding site for GATA-2. GATA-2 is a transcription factor involved in expression of MUTYH, a post replication DNA glycosylase.
Stephanie Valberg, DVM, Ph.D., DACVIM, DACVSMR Stephanie Valberg is a professor in large animal medicine, College of Ve t e r i n a r y M e d i c i n e , Michigan State University and the Mary Anne McPhail Dressage Chair Equine Sports Medicine. She received her DVM from the Ontario Veterinary College and completed a Ph.D. in equine exercise physiology at the Swedish University of Animal Science. Dr. Valberg’s research centers on neuromuscular diseases in horses with a special focus on genetic diseases of skeletal muscle and their nutritional management. Dr. Valberg was inducted into the Equine Research Hall of Fame in 2012. She has received several awards including British Equine Veterinary Association Clinical Award 2014, University of Minnesota’s Postdoctoral Mentor 2013, MVMA Outstanding Faculty Award 2013, 2012 Milne Lecturer at AAEP, the 2001 and 2010 Pfizer Award for Research Excellence, and the 1999 EquiSci International Award. Dr. Valberg has more than 136 scientific publications and is a frequent speaker at national and international veterinary, nutrition and genetic conferences. She is an avid three-day eventer with her 5-year-old Warmblood Cajun.
@FLORIDA_VMA | The Practitioner 7
UPDATE ON EQUINE CORONAVIRUS SALLY DeNOTTA | DVM, Ph.D., DACVIM LINDA MITTEL | MSPH, DVM The first outbreaks of Equine Coronavirus (ECoV) were reported in Japan, Europe and the U.S. from 2009-2011. Since that time, ECoV has emerged as an increasingly prevalent cause of enteric disease in adult horses. Currently reported worldwide with increasing incidence, this single-stranded RNA virus in the beta coronavirus family has established itself as an emerging infectious disease of importance in this country and across the globe. Primarily a gastrointestinal pathogen in horses, ECoV causes lethargy, fever, anorexia, and occasionally colic and diarrhea. The role of ECoV as a cause of enteric disease in foals is still unclear as the virus can be detected in both healthy and sick foals. This article highlights current knowledge regarding the transmission, clinical signs and management of ECoV in horses.
Improved awareness and availability of diagnostic testing has led to steadily increasing numbers of confirmed ECoV cases reported by diagnostic laboratories since 2010, and positive cases of ECoV have been identified in all states except Hawaii and Alaska. In a recent study, 9.6 percent of adult healthy horses from the United States tested seropositive to ECoV.1 In one study, the geographic region (Mid-West), breed (Draft horses) and specific uses of horses (ranch/farm and breeding use) were all statistically significant risk factors for seropositivity. While seropositive horses appear to be relatively common, those actually shedding ECoV in their feces appear to be rare, and in a recent prospective study of horses presenting to a veterinary hospital for gastrointestinal disease, ECoV was isolated from less than 1 percent (1 out of 258) of fecal samples.2 ECoV cases occur year round with a large proportion diagnosed during the winter months.
Transmission of ECoV is fecal-oral and occurs when horses come into contact with horses shedding ECoV in their feces or exposure to contaminated surfaces and fomites. Stalls, muck forks, manure spreaders, thermometers, hands and clothing can also contribute to the spread of ECoV. Risk factors for infection include exposure to clinical and subclinical horses shedding ECoV in feces and co-mingling with horses of unknown infection status. A small percentage of horses infected with ECoV will have PCR positive nasal secretions; however, it is not known whether this represents viral tropism for respiratory epithelium or fecal contamination.3,4 During farm outbreaks, horses that appear clinically unaffected may shed the virus and serve as reservoirs for infection and spread within the herd. Environmental persistence is not currently known; however, greater survival and viability of ECoV is to be expected in colder weather and is one possible explanation for the apparent higher prevalence of virus positive fecal samples and clinical disease during cooler weather. Another possible explanation is that horses are often stabled together in the cold weather and their close proximity increases the risk of transmission.
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Figure 1: A 6-year-old Quarter Horse gelding presented for lethargy and inappetence. A diagnosis of ECoV was confirmed via fecal PCR. Photo courtesy of Dr. DeNotta
Equine infection with ECoV manifests as enteric disease in adult horses (Figure 1). The incubation time following exposure is relatively short with horses developing clinical signs of disease within two to three days following experimental infection.5 The clinical severity of presenting signs is generally mild, although more severe disease and mortality have been reported. Cases may occur in individual horses or as herd outbreaks. Morbidity rates in outbreaks have been reported to be between 10 to 83 percent.6 Clinical signs are largely attributable to intestinal inflammation, and indicators of concurrent endotoxemia (hyperemic or toxic mucous membranes, tachycardia, tachypnea) may be present (Figure 2). A consistent hematological abnormality observed
Figure 2: Toxic mucous membranes in a 3-year-old Thoroughbred with ECoV. Hematologic findings included severe leukopenia (<2000 cells/ uL) characterized by neutropenia with left shift (band neutrophils) and toxic changes. Photo courtesy of Dr. DeNotta
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in horses infected with ECoV is leukopenia due to neutropenia and/or lymphopenia. Neutrophil left shift (band neutrophils) and toxic changes are variably present. Biochemical profiles are often normal but may reflect alterations secondary to anorexia (hyperbilirubinemia) and/or dehydration (pre-renal azotemia). Some infected horses remain completely asymptomatic but will shed ECoV in their feces, and these silent shedders likely contribute to the spread of ECoV within populations. Clinical signs of ECoV as reported from 20 outbreaks6,7 • Anorexia (97%) • Lethargy (88%) • Fever (83%) • Leukopenia (73%) characterized by neutropenia (65%) and lymphopenia (83%) • Soft manure and/or diarrhea is an inconsistent finding (23%) • Colic (19%)
Figure 3: A 12-year-old miniature horse presented for inappetence, lethargy and 103oF fever. Feces was PCR positive for ECoV. Hyperammonemia was confirmed after the mare was observed head pressing (shown above). Miniature horses appear to be at increased risk for developing hyperammonemia when infected with ECoV. Photo courtesy of Dr. DeNotta
Hematological analysis frequently reveals leukopenia (73 percent) characterized by neutropenia (65 percent) and lymphopenia (83 percent). Biochemical profiles are often normal but may reflect reported to range from three to 25 days, although the authors have alterations secondary to anorexia (hyperbilirubinemia) and/or followed horses that continue to shed virus for >30 days following outbreaks including horses that remained asymptomatic the entire dehydration (pre-renal azotemia). time they were shedding virus. In a small experimental infection 5 Recently, mortality from ECoV-associated necrotizing enteritis study, horses shed from days three to 15 following infection. has been reported.6,8 In these cases, severe intestinal inflammation Carrier status is currently unknown, but subclinical horses have and disruption of mucosal barriers leads to hypoproteinemia, been found to shed the virus in feces and likely serve as silent electrolyte derangements, septicemia, and, rarely, systemic reservoirs for infection. In a recent outbreak in Florida, horses deterioration and death. The mechanisms for this severe form of in stalls adjacent to a clinical ECoV case never developed fever ECoV have not yet been elucidated; however, severity of clinical or clinical signs but were leukopenic on hematologic profiles and signs have been associated with viral load in horses and other PCR positive for ECoV on feces. At least one of the horses involved in this outbreak never showed clinical signs but remained PCR species affected by coronavirus. positive on feces for 6+ weeks (DeNotta, unpublished data). Additionally, hyperammonemic encephalopathy is a rare but reported complication of ECoV infection. Excessive ammonia production is attributed to an increase in ammonia-producing enteric bacteria secondary to disruption of normal intestinal A diagnosis of ECoV infection relies on the presence of clinical microbiome; thus, blood ammonia concentrations should be signs compatible with ECoV infection, hematological changes determined for any horse displaying neurologic signs with ECoV (neutropenia and/or lymphopenia), exclusion of other infectious (lethargy, obtundation, wandering, ataxia, seizures). Miniature agents (Salmonella, Potomac Horse Fever, Clostridial enterocolitis, horses appear to be at higher risk of complications from ECoV etc.) and the detection of ECoV in feces. In experimental infection infection, the reason for which is unknown (Figure 3). studies, horses began shedding ECoV in their feces three to four
Diagnostic Sampling, Testing and Handling
Under natural conditions, fecal shedding of ECoV has been Laboratory/website
Real-time PCR Research and Diagnostics Core Facility, University of California, Davis, CA https://pcrlab.vetmed.ucdavis.edu/veterinary-diagnostics/ veterinary-submission-formsdiagnostic-tests-and-panels Animal Health Diagnostic Center, Cornell University, Ithaca, NY https://www.vet.cornell.edu/animal-health-diagnostic-center IDEXX Laboratories, West Sacramento, CA https://www.idexx.com/en/equine/ equine-reference-laboratories/test-menu/
days following infection, and peak viral shedding occurred three to four days after the development of clinical signs.5 Laboratory
Fresh feces. Refrigerate and ship with ice packs. 1. Fresh feces. Approximately 1 gram or 1 ml. 2. Fresh intestinal necropsy tissue. A minimum of 0.5 cm x 0.5 cm. 3. Fecal swab. If horse has diarrhea and firm stool is not available, allow swab to absorb liquid feces or roll the swab in fecal material and cover cotton swab. Ship in an insulated container with ice packs. 5-10 grams fresh feces in container (preferably sterile) with ice packs.
Table 1: Laboratories offering PCR testing for Equine Coronavirus
@FLORIDA_VMA | The Practitioner 9
support of ECoV infection should be based on the molecular detection of ECoV in feces via PCR (Table 1). Post-mortem diagnosis of ECoV can be achieved by PCR on feces, small intestinal contents or tissue from the small intestine collected at post-mortem examination. Positive ECoV cases have been confirmed in all states of the U.S. except for Hawaii and Alaska.
Treatment and Prognosis
and ideally handle infected horses last and as infrequently as possible. Diligent hand washing is also important, and a 70 percent ethanol hand sanitizer should be used when moving between horses. Horses should remain in strict quarantine until confirmed to be fecal PCR negative. Typically shedding periods range for two to 21 days but may last longer in some cases. Therefore, isolating infected horses for a predetermined period of time and then presuming the horse to be no longer shedding is not recommended.
Treatment for ECoV involves supportive care based on the clinical signs, and most cases will resolve with minimal or no intervention within a few days to one week. Non-steroidal anti-inflammatories Although coronaviruses affect a multitude of species, including (NSAIDs) can be helpful for reducing fever and mitigating humans, ECoV has not demonstrated any zoonotic potential inappetance. Accurate weights should be obtained on miniature at this time; however, standard hygiene precautions and use horses to prevent NSAID overdose. More severe cases and those of personal protective equipment should be utilized with any with evidence of necrotizing enterocolitis (hypoproteinemia, diarrheic patient due to risk of coinfection with zoonotic agents. endotoxemia, septicemia) may require hospitalization for enteral Transmission between horses and cattle has not been documented. or parenteral fluid therapy, colloid support, antimicrobials, and correction of electrolyte and metabolic derangements. Horses For detailed guidelines regarding general biosecurity on equine with hyperammonemic encephalopathy have been successfully facilities and events, along with instructions for handling managed with treatments targeted at reducing the production and outbreaks of infectious disease within equine population, the absorption of ammonia within the intestinal tract — including reader is referred to guidelines set forth by the American neomycin (10 mg/kg PO q8-12h) and lactulose (150-200 mL PO Association of Equine Practitioners (AAEP). The guidelines q6-12h) — in addition to the aforementioned supportive therapies. are available to AAEP members at: https://aaep.org/sites/default/ Fecal transfaunation has not been specifically evaluated for the files/Documents/BiosecurityGuidelines_Sept2018.pdf. Up-to-date treatment of ECoV but may be beneficial for horses with diarrhea. reports of ECoV by county and state, and further information regarding infectious disease, is available open-access through The prognosis for ECoV is generally good, with most infections the Equine Disease Communication Center at http://www. being mild and self-limiting. Exposure to the virus can result in up equinediseasecc.org/. to 85 percent infection rate, but most animals do not show clinical signs. Mortality is generally low with 96 percent of horses surviving References to discharge in a recent report of hospitalized cases of ECoV.9 1. Kooijman LJ, James K, Mapes SM, Theelan MJ, Pusturla Horses more severely affected with intestinal mucosal barrier N. Seroprevalence and risk factors for infection with disruption or hyperammonemic encephalopathy have reduced equine coronavirus in healthy horses in the USA. Vet J prognosis and require more intensive medicine intervention. 2017;220:91-94.
Prevention and Biosecurity Prevention of ECoV infection involves minimizing contact between horses of unknown infection status and maintaining high standards of sanitation in all equine facilities and carefully disposing of manure where it cannot contaminate pastures, paddocks or drinking water. New horses in equine facilities should be quarantined for three weeks before integration into resident population. There are currently no vaccines for ECoV. Vaccines have been used successfully to prevent bovine coronavirus (BoCV) in herds, a closely related beta coronavirus; however, these vaccines have not yet been evaluated in horses. Any horse with fever and no evidence of respiratory illness should be considered suspect for ECoV and isolated from other horses immediately. Horses found to be positive for ECoV via fecal PCR should remain in isolation and strict biosecurity measures and manure management instituted to prevent the spread of infection to other horses in the vicinity. Other horses on the property should be monitored for fevers (assess temperature at least twice daily) and/or leukopenia. Farm personnel working with horses shedding ECoV should wear disposable gloves and personal protective equipment (gowns or dedicated coveralls, boot covers) 10 The Practitioner
2. Sanz MG, Kwon S, Pusturla N, Gold JR, Bain F, Evermann J. Evaluation of equine coronavirus fecal shedding among hospitalized horses. J Vet Intern Med 2019; 33(2):918-922. 3. Pusturla N, Holzenkaempfer N, Mapes S, Kass P. Prevalence of equine coronavirus in nasal secretions form horses with fever and upper respiratory tract infection. Vet Rec 2015; 177:289. 4. Pusturla N, James K, Mapes S, Bain F. Frequency of molecular detection of equine coronavirus in faeces and nasal secretions in 277 horses with acute onset of fever. Vet Rec 2019; 184(12):385. 5. Schaefer E, Harms C, Viner M, Barnum S, Pusturla N. Investigation of an experimental infection model of equine coronavirus in adult horses. J Vet Intern Med 2018; 32(6):2099-2104. 6. Pusturla N, Mapes S, Wademan C, White A, Ball R, Sapp K, Burns P, Ormond C, Butterworth K, Bartol J, et al., Emerging outbreaks associated with equine coronavirus in adult horses. Vet Micro 2013; 162:228-231. 7. Pusturla N, Vin R, Leutenegger C, Mittel L, Divers T. Enteric coronavirus infection in adult horses. Vet J 2018; 231:13-18.
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8. Fielding C, Higgins J, Higgins J, McIntosh S, Scott E, Giannitti F, Mete A, Pusturla N. Disease associated with equine coronavirus infection and high case fatality rate. J Vet Intern Med 2015; 29:307-310. 9. Berryhill E, Magdesian K, Aleman M, Pusturla N. Clinical presention, diagnostic findings, and outcome of adult horses with equine coronavirus infection at a veterinary teaching hospital: 33 cases (2012-2018). Vet J 2019; 248:95-100.
Sally DeNotta, DVM, Ph.D., DACVIM Sally DeNotta is board certified by the American College of Veterinary Internal Medicine and serves on the clinical faculty at the University of Florida College of Veterinary Medicine. She is also the UF Equine Veterinary Extension coordinator. Dr. DeNotta grew up on the rural Oregon coast and received her veterinary degree from Oregon State University. She spent time in private practice in both Colorado and Oregon before heading to upstate New York where she completed an internal medicine residency at Cornell University. Following residency, she joined the clinical faculty at Cornell while obtaining a Ph.D. developing optical techniques for in-vivo imaging of the central nervous system. She joined the UF faculty in 2018, where her clinical interests include infectious disease, neurologic disorders, colic, coagulation and neonatology.
Linda D. Mittel, MSPH, DVM Dr. Linda D. Mittel is an equine veterinarian that practiced more than 25 years before taking a position at the New York State Veterinary Diagnostic Laboratory at Cornell University. She owned her equine practice for more than 20 years, caring for horses in New York and Connecticut. Before arriving in the New England area, she practiced in Kentucky, Arkansas, Texas and Florida as a resident veterinarian on large breeding farms. She also owned a private veterinary laboratory in Connecticut for many years. She is a faculty member at Cornell University College of Veterinary Medicine in the Department of Population and Medicine. She works in the New York State Veterinary Diagnostic Laboratory as a diagnostic intelligence officer with the Veterinary Support Services group (VSS), consulting with the laboratory clients on diagnostic sampling, testing and interpretations of lab results. She also provides continuing education to New York state practices on diagnostic sampling and updates on disease detections and new test developments. As part of VSS, she teaches veterinary students diagnostic medicine and students in the MPS program. She was a Cornell consultant to the ARK Import Export Center at JFK for the design, development and operations of the USDAapproved private quarantine facility at JFK Airport. She has a special interest in equine infectious diseases, particularly tick-borne diseases, parasitology and fevers of unknown origins. She and Dr. DeNotta diagnosed the first case of Equine Coronavirus in a miniature at the Cornell University Hospital for Animals.
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CREEPING INDIGO: A CLOSER LOOK AT THE PLANT AND ITS TOXINS ROB MACKAY | BVSC (Dist), Ph.D., DACVIM
IMPORTANCE AND IMPACT
Creeping indigo (CI; Indigofera spicata, Forsk) toxicosis is an emerging problem among horses in Florida and neighboring southeastern states. The plant likely entered Florida prior to 1940 as a result of separate inadvertent introductions in Alachua and Dade counties. It has subsequently naturalized and spread throughout Florida and into neighboring states. Individual cases and small outbreaks of CI-associated toxicity in equids have been recognized from about 1980 in Dade Country and 2000 along the I-4 corridor with sporadic additional cases in north Florida.1 The signs are those of severe generalized neurologic dysfunction with dementia, obtundation, blindness, ataxia and seizures. Treatment is supportive only and generally unsuccessful. At least 300 horses had died in Dade County alone by 1988, when the syndrome was first associated with CI.2 Florida has more than 500,000 horses, ranking third in the U.S.3 Horses in Florida are used in approximately equal numbers for racing, showing and recreation. The state's horse industry annually contributes about $3 billion in direct and $5.1 billion in total economic impact. The magnitude of the threat posed by CI toxicosis to the equine industries of Florida is difficult to quantify. The plant tends to advance surreptitiously across pastureland to be consumed in toxic amounts by grazing horses before owners are even aware of the problem. Because it is a prostrate plant that
Figure 1: Figure 1a: Indigofera spicata showing characteristic pods, a single pink flower and ovate clover-like leaves. 1b: An area of pasture heavily grazed by horses with >40 percent I. spicata in Marion County, Florida. Inset 1b: Individual I. spicata plant removed from this pasture. 1c: Typical lingual and buccal ulcerations in a horse that was grazing in a pasture similar to that shown in Figure 1b.
12 The Practitioner
expands radially as ground-hugging runners from a submerged central crown, CI is difficult to spot under the leaves of pasture grasses.2 The plant is highly palatable to all herbivores, and horses may graze it in preference to pasture.2 Conditions inimical to pasture health, including overgrazing and drought, favor CI growth and eventual dominance of pasture foliage.4 It has been suggested that clinical signs are likely when toxic Indigofera spp. are > 20 percent of pasture.5 Well-maintained pastures at professionally run operations thus would seem inhospitable to CI; however, we recently found > 40 percent CI in pastures at a sizeable sport horse farm in Marion County that was experiencing numerous cases of suspected CI toxicosis. Anecdotal reports suggest that CI-associated deaths occur predominantly in recreational horses from small operations and annual deaths likely are considerably higher than the ~20 logged on a horse owner's website.6
Creeping indigo is native to Africa, Madagascar, most of Asia, the near East and Brazil.4 In the early 20th century, it was thought to have potential as livestock forage and ground cover.2 Specimens were imported for study at the Agricultural Experiment Stations of the universities of Hawaii and Florida.7,8 Although the plant was highly palatable and nutritious when fed as a dietary supplement, CI caused weight loss, abortion, corneal edema and liver cirrhosis in cattle, sheep, rabbits and guinea pigs when fed as the principal diet. Signs occurred after one to three weeks consumption and led to death if feeding was continued. Although research was stopped in the mid-1930s, the plant apparently escaped containment at both sites, and there was presumed contiguous spread from Gainesville in the following decades.2 There is evidence for a separate introduction (unknown source) into Miami-Dade County that had established in the Homestead area by 1940.9 With continued spread from both sites (and perhaps others) for more than 80 years, the now thoroughly naturalized herb has been found and vouchered in herbaria as I. spicata in 49 of the 67 Florida counties10 and adjacent counties of Georgia and Alabama. Beginning in the early 1980s, horses in the Homestead area of Dade County began dying with signs of what is now recognized as CI toxicosis.2 These horses had lingual, oral and corneal ulcers; corneal edema and photophobia; and progressive neurologic dysfunction characterized by dementia, obtundation, blindness, seizures and ataxia. Despite the severity of neurologic signs, histology of CNS tissues was usually normal. By 1988 when the cause was recognized, more than 300 horses may have died in Dade County alone.2 For a decade thereafter, cases of CI toxicosis Issue 3 • 2019
were restricted to a small area of southern Dade County, and the condition was unknown elsewhere in the state. Starting in 2000, however, I began to see individual cases and small outbreaks in horses from Hillsborough and Pinellas counties in central Florida, and cases have since continued unabated along the I-4 corridor and more recently in Marion County and north Florida.1 Some of these cases have been logged by a Florida horse owner who maintains a CI website and at least two additional cases have been reported in Alabama and Georgia.6
microscopy.12 Obtundation and pelvic limb ataxia were terminal signs noted in rabbits fed I. spicata leaflets.7 Hydrocephalus and cerebral atrophy were found at necropsy. The toxin is incorporated into plant glycosides and accounts for up to 0.27 percent of dry weight of toxic indigo species.5 Although this putative role of 3-NPA in CI toxicosis of horses is highly plausible, it should be noted that the toxin was detected in only trace amounts or was absent from I. lespedezioides specimens analyzed in Brazil.12 The plants studied were not from the scene of a toxic episode; however, 3-NPA concentration peaked in Indigofera spicata is also naturalized in northeastern Australia, blood at about 1 μg/mL after intra-abomasal administration of and fatal toxicosis in ponies in Queensland was recently 10 mg/kg to cattle and sheep.18,19 Elimination half-life was only reported.5 Similar clinical signs of plant toxicosis have been about 60 minutes, so 3-NPA is unlikely to be detectable in the known for many years in horses eating I. linnaei in northern blood of naturally occurring cases after they stop eating and was Australia11 and I. lespedezioides in northern Brazil.12 not found in three ponies eating I. spicata that was 0.27 percent 3-NPA (dry weight).5 The injurious effects of the various toxic indigo plants are reputed to reside in two potent toxins: l-indospicine (IND) and 3- Still unknown and unstudied are the results of CI consumption nitropropionic acid (3-NPA) (Figure 2).2,5 Indospicine is a non- in amounts less than those causing neurologic signs. Camels fed protein amino acid analog of arginine that is thought to induce < 10 percent dietary dry matter as CI lost 8 percent bodyweight non-neurologic toxic effects, at least partly by competitive over 20 days despite appearing healthy throughout.16 Camels inhibition of nitric oxide synthase. Free IND typically is 0.05- and horses butchered for pet food and/or human consumption 0.15 percent of the dry weight of toxic indigo plants5,13 and presumably were clinically normal prior to slaughter but causes liver damage and corneal edema when given in pure form levels of IND in pet food were high enough to cause liver to experimental animals.13,14 Interestingly, horses apparently are injury in dogs.13,16 Indospicine at “subclinical” doses also is resistant to its hepatotoxic actions.5 Indospicine can readily be known to be an abortifacient and teratogen in experimental detected in the blood at ppm concentrations in animals grazing settings.13,20 Whether or not these or other insidious problems I. spicata or I. linnaei and accumulates and persists at high levels are occasioned by subchronic CI ingestion by Florida horses in tissues.5,13,15 Meat from animals grazing CI is a documented remains to be determined. threat to humans and pets consuming it, and indospicinecontaminated camel and horse meat has fatally poisoned dogs in Australia.16,17 Although indospicine is not reported to be directly neurotoxic, an argument has been made that it may potentiate Rationale for Selected Toxin Dose the toxicity of 3-NPA.13 The nitrotoxin 3-NPA is a potent and There is only minimal data relating clinical signs, serum toxin irreversible inhibitor of mitochondrial succinate dehydrogenase, concentrations and amount of CI consumed. Two ponies a key enzyme in both the citric acid cycle and complex II of the euthanized because of severe I. spicata-associated clinical electron transport chain.18 Neurons lack energy stores, so they signs had plasma IND concentrations of 28.1 and 28.3 μg/mL, are extremely vulnerable to ATP depletion thus accounting for and 3- NPA was not detected.5 Concentrations for IND and the prominent neurologic signs of experimental 3-NPA toxicity. 3-NPA in pasture CI plants were 1.5 and 2.7 mg/g dry weight, Although histologic CNS changes usually are not seen by light respectively, and I. spicata averaged 24 percent of pasture microscopy, distorted mitochondrial morphology in neurons biomass. If it is assumed that healthy equids consume pasture of horses poisoned by Indigofera may be detected by electron equivalent to 6.75 percent of bodyweight/day, and pasture
EXPERIMENTAL FEEDING STUDY
grass and CI are 20 percent and 33 percent DM,5 respectively, it can be calculated that healthy ponies grazing CI as 24 percent of their pasture intake would daily be ingesting about 8 mg/kg IND and 14 mg/kg 3-NPA. Horses eating 10 pounds of I. linnaei (Birdsville indigo) daily began showing signs of toxicity (i.e., Birdsville Disease) after 25 days.21,22 On the basis of the average IND concentration of 0.5 mg/g DM reported for I. linnaei,23 these horses would have been consuming about 5 mg/ kg IND daily (and unknown 3-NPA dose). Horses fed the same dose for only one week remained normal.22 Camels eating 337 μg/kg IND daily as dried chopped I. spicata remained healthy during the 32-day feeding period although they lost weight.15 On the basis of these reports, it seems very unlikely that CI fed for five days at a daily rate of 1 mg/kg IND and a similar dose of
Figure 2: Molecular structures of IND and 3-NPA.
Continued on page 20 WWW.FAEP.NET |
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Improving Practice Profitability Amy Grice, VMD, MBA
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The Reality of Equine Practice in 2019
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Amy Grice, VMD, MBA
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Figure 3: Plasma protein concentrations during and after feeding of CI containing 1 mg IND/kg/day.
3-NPA would have adverse clinical effect.
Materials and Methods The aerial parts of CI plants were collected from 37 sites within 50 miles of the University of Florida (Gainesville, Florida). Approximately 100 kg of fresh CI were collected. After collection, the plants were air dried on mesh racks. Dried CI plants averaged 24 percent of the mass of fresh CI. Dried CI was assayed for IND and 3-NPA by liquid chromatography/tandem mass spectrometry.24,25 This experimental study used five mixed breed pony mares ranging from 19 to 22 years old and weighing between 311- 457 kg with body condition scores of at least 4/9. During CI feeding, ponies were housed in stalls and fed 15 g/ kg of a combination of CI, alfalfa hay and coastal Bermuda hay. This amount of CI provided IND and 3-NPA at 1 mg/kg and 0.005 mg/kg bodyweight/day, respectively. Ponies were fed CI for five days then turned out on grass for 28 additional days with access to coastal Bermuda hay and free-choice water. Clinical and clinicopathologic evaluations were performed during CI feeding and for four weeks thereafter. Blood was collected and plasma was analyzed by LC/tandem MS for IND and 3-NPA.24,25 The study was approved by the Institutional Animal Care and Use Committee of the University of Florida.
Figure 4: Plasma l-indospicine concentrations in ponies fed CI from Days 1 to 5.
20 The Practitioner
Results and Discussion
CI mixed with chopped alfalfa was eaten enthusiastically by all ponies for the five days it was offered. No abnormal clinical signs were observed during the experiment; however, there was a significant increase in plasma protein concentration during the feeding period (Figure 3). Concentrations increased from (x" ± sd) 7.3 ± 0.21 g/dL before feeding to 8.8 ± 0.72 g/dL 24 h after beginning CI, then gradually decreased to 7.9 ± 0.33 g/dL 12 h after the last feeding and declined further to baseline values after turnout on grass. Parallel changes in plasma concentration were found for both globulin and albumin. The rise in plasma protein concentration was consistent with a 17 percent reduction in plasma volume and suggests that even short-term ingestion of modest amounts of IND-rich CI has potentially adverse effects. IND and 3-NPA in dried CI were 2296 ± 777 µg/g dry matter (range 1520 to 3500) and 14 ± 10 µg/g (range 6 to 30), respectively. IND concentration was comparable to those reported previously (500 to 1500 µg/g5,13), but 3-NPA was much lower than the 2700 µg/g reported for CI associated with fatal toxicosis in ponies in Queensland, Australia.5 Plasma IND increased from 0.04 ± 0.03 µg/mL to 3.6 ± 0.52 µg/mL after five days of CI ingestion (Figure 4). Twenty eight days after CI feeding was stopped, plasma IND was 1.3 ± 0.33 µg/mL. Elimination was first order with t½ of 25.2 days which is comparable to the 18 days calculated for camels fed I. linnaei.15 Two-compartment pharmacokinetic modeling predicted a steady state concentration of 22 µg/mL at Day 126 of CI ingestion (Figure 6). Trace increases (0.01 to 0.05 µg/mL) of plasma 3-NPA occurred two hours after CI feedings and days one and six (Figure 5). IND can be detected in the blood of horses during and for > four weeks following consumption of modest amounts of CI. Because 3-NPA concentration in CI was very low, the role of this toxin in CI poisoning is called into question. This toxin also was detected in only trace amounts or was absent from another toxic indigo plant, I. lespedezioides, in Brazil.12 An important limitation of both the current and Brazilian studies, however, is that indigo
Figure 5: Plasma 3-nitropropionic acid concentrations in ponies fed CI.
Issue 3 • 2019
testing and came back positive for S. neurona antibody. On routine blood testing, there was mild leukopenia (5.7 k/µL), thrombocytopenia (139 k/µL) slightly high bilirubin (2.4 mg/ dL), alkaline phosphatase (202 U/L) and creatine kinase (589 U/L). Treatment was continued, and signs were fluctuant but three days later the mare was repeatedly falling to the ground and struggling to get to her feet. On one occasion, she fell against a fence. Creeping indigo was found on the farm this day, and CI toxicosis was suspected from this point forward. The signs progressed, including marked weight loss, and the mare was euthanized on Day Five of the illness.
Figure 6: Simulated CI feeding for 250 days.
plants were collected from locations in which outbreaks were not occurring. It will be important to analyze CI plants from the sites of active outbreaks to address this issue. Techniques and results from this study can be used to quantify IND and 3-NPA in: 1.) CI from varying locations and environmental conditions and 2.) plasma (and CSF) in affected and unaffected horses eating CI.
FIELD INVESTIGATION History
On March 26, 2018, owner brought six horses from her property in Maryland to her new farm in Marion County. The new property hadn’t had horses for the previous four years. Horse 1, a 29-year-old Mini gelding, became ill on May 8 (40 days after arrival) and was attended by local veterinarian. The horse was lethargic, reluctant to walk, ataxic in the hindlimbs, inappetent and not drinking much water. There was bilateral blepharospasm and tearing. Treatment was IV fluids, DMSO and oxytetracycline. Bloodwork was submitted and showed mild leukopenia (5.8 k/µL), high triglycerides (355 mg/dL) and CK (918 CK U/L), and low calcium (8.9 mg/dL). The horse declined rapidly and two days after onset there was obvious weight loss, prolonged periods of recumbency and he could only rise with assistance. Temperature remained normal; HR was 58/minute. Because of continued rapid decline, the horse was euthanized later in the day. On May 16 (48 days after arrival), Horse 2, an 18-year-old Thoroughbred cross mare, suddenly began tearing and had “bulging, swollen, wild eyes” but was still eating and alert. A local veterinarian called. She noted normal temperature and mentation. The left conjunctiva was hyperemic and edematous, but there was no corneal uptake of fluorescein. The mare was thin and tucked up in the abdomen. She was moderately ataxic and weak, worse in the hindlimbs. Cranial nerve examination was normal. The mare was given flunixin, IV fluids, DMSO, dexamethasone and NeoPolyDex for the left eye. Blood was submitted for EPM
On May 26 (58 days after arrival*), Horse 3, a 17-year-old Thoroughbred mare, was noted to be losing weight and was found with her head in a corner with profuse ocular tearing, blepharospasm and photophobia. There were large ulcers on the tongue and gums. Over five days, the horse continued to lose weight, stopped eating, and appeared weak and ataxic. The mare was given ozone treatments daily during this period. She continued to drink but had diarrhea by the fifth day, at which time she was euthanized. The paddocks were again inspected, and large patches of CI were found, especially around the shelters. The owner estimates, however, that less than an eighth of the pasture sward was CI. The three surviving horses were removed from paddocks (on approximately May 20) then turned out on sprayed, rented paddocks. A team from University of Florida College of Veterinary Medicine visited on June 7, 2018. The property had been sprayed for CI (for the second time) two weeks before the visit. Pastures were walked and were largely free of CI. A few of the surviving plants were harvested for analysis. Several strong stands of CI were found in alleys and adjacent to outbuildings. These also were sampled. Three horses were living on the property and had been present during the exposure to CI. These were examined and found to be clinically normal.
Toxin Analysis The results of toxin analyses of plants and blood samples are shown in Tables 1 and 2. IND concentration of CI plants collected several weeks after the cases in Marion County were like those from CI collected around Gainesville and in Queensland5 (Table 1). As was the case in plants from locations around Gainesville that were not associated with CI toxicosis cases, 3-NPA concentrations at the outbreak property were very low in comparison with those from paddocks grazed by ponies in Queensland. This finding further challenges the notion that 3-NPA is responsible for the neurologic signs of CI toxicosis. It can be seen that plasma IND concentrations in the two terminally ill horses (~2.5 µg/mL) are similar to those from clinically normal experimental horses after three days of subtoxic amounts of CI, but higher than the adjusted plasma IND found in the three surviving horses from the Marion county outbreak (1 – 2 µg/mL). Surprisingly, plasma IND in
*Dates of illness for this horse may not be accurate. WWW.FAEP.NET |
@FLORIDA_VMA | The Practitioner 21
the Marion County horses were < 10 percent of those in Queensland ponies with CI toxicosis.5 It is clear from these findings that there is not a linear relationship between plasma IND concentrations and signs of CI toxicosis. The reason for this is not known, but possible causes include differences in tissue saturation by IND that are not reflected in plasma concentrations, role of unknown (and unmeasured) toxins in pathogenesis of clinical signs and differences in measurement techniques in different locations. It will be important to continue to gather evidence from CI outbreaks to further explore these possibilities.
References: 1. MacKay RJ, Jennings E, Sellers B., Ferrell J, House A. 2015: Creeping indigo, a poisonous plant of concern in Florida pastures. SS-AGR-395. University of Florida Institute of Food and Agricultural Sciences, Gainesville. http://edis. ifas.ufl.edu/ag399. Accessed August 30, 2016 2. Morton JF. Creeping indigo (Indiigofera spicata Forsk) (Fabaceae) – A hazard to herbivores in Florida. Econ Bot 1989;43:314-327. 3. American Horse Council Foundation. 2005: The Economic Impact of the Horse Industry in the United States. The American Horse Council 4. Datasheet - Indigofera spicata (creeping indigo). 2016. In: Invasive species compendium. CABI, Wallingford, UK, http://www.cabI.org/isc/datasheet/79262. Accessed August 31, 2016 5. Ossedryver SM, Baldwin GI, Stone BM, et al. Indigofera spicata (creeping indigo) poisoning of three ponies. Aust Vet J 2013;91:143-149. 6. Nina's warriors (creeping indigo resource). 2016. http://www. ninaswarriors.com/. Accessed August 25, 2016 7. Nordfeldt SH, L.A.Morita, K., Matsumoto H, Takahashi M, et al. Feeding tests with Indigofera endecaphylla Jacq. (creeping indigo) and some observations on its poisonous effects on domestic animals. Univ Hawaii Agric Exp. Sta Techn Bull 15;1- 33:1952 8. Emmel MW, Ritchey GE. The toxicity of Indigoferae endecaphylla Jacq. for rabbits. J Amer Soc Agron 1941;33:675-677 9. Accession #33246. Florida Museum of Natural History. University of Florida Herbarium - Collections Catalog. 2016. http://www.flmnh.ufl.edu/herbarium/cat/search. asp?accno=33246. University of Florida. Accessed August 25, 2016 10. Wunderlin RP, Hanse BF, Franck AR, et al. Atlas of Florida plants. Institute for Systematic Botany, University of South Florida, Tampa, 2016. 11. Carroll AG, Swain BJ. Birdsville disease in the central highlands area of Queensland. Aust Vet J 1983;60:316-317. 12. Lima EF, Riet-Correa F, Gardner DR, et al. Poisoning by Indigofera lespedezioides in horses. Toxicon 2012;60:324-328. 13. Fletcher MT, Al Jassim RAM, Cawdell-Smith AJ. The occurrence and toxicity of indospicine to grazing animals. Agriculture- Basel 2015;5:427-440. 14. Hegarty MP. Toxic amino acids of plant origin. In: Effects of poisonous plants on livestock. (Keeler RF, van Kampen KR, James LF, eds.), 1978. Academic Press, New York, NY, pp. 575-585.
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Issue 3 • 2019
15. Tan ET, Al Jassim R, Cawdell-Smith AJ, et al. Accumulation, persistence, and effects of indospicine residues in camels fed Indigofera plant. J Agric Food Chem 2016. 16. FitzGerald LM, Fletcher MT, Paul AEH, et al. Hepatotoxicosis in dogs consuming a diet of camel meat contaminated with indospicine. Aust Vet J 2011;89:95-100. 17. Hegarty MP, Kelly WR, McEwan D, et al. Hepatotoxicity to dogs of horse meat contaminated with indospicine. Aust Vet J1988;65:337-340. 18. Majak W, Pass MA, Muir AD, et al. Absorption of 3-nitropropanol (miserotoxin aglycone) from the compound stomach of cattle. Toxicol Lett 1984;23:9-15. 19. Pass MA, Majak W, Muir AD, et al. Absorption of 3-nitropropanol and 3-nitropropionic acid from the digestive system of sheep. Toxicol Lett 1984;23:1-7. 20. Pearn JH. Studies on a site-specific cleft palate teratogen – toxic extract from Indigofera spicata Forssk. Brit J Exp Path 1967;48:620-626. 21. Hopper PT, Hart B, Smith GW. PREVENTION AND TREATMENT OF BIRDSVILLE DISEASE OF HORSES. Australian Veterinary Journal 1971;47:326-&. 21. Hopper PT, Hart B, Smith GW. Prevention and treatment of Birdsville disease of horses. Aust Vet J 1971;47:326-328. 22. Rose AL, Banks AW, McConnell JD. Birdsville disease in the Northern Territory. Aust Vet J 1951;27:189-196. 23. Tan ET, Materne CM, Silcock RG, et al. Seasonal and species variation of the hepatotoxin indospicine in Australian Indigofera legumes as measured by UPLC-MS/MS. J Agric Food Chem 2016;64:6613-6621. 24. Gardner DR, Riet-Correa F. Analysis of the toxic amino acid indospicine by liquid chromatography-tandem mass spectrometry. Int J Poisonous Plant Res 2011;1:20-27. 25. Liu H, Liu G, Kang L, et al. Determination of 3-nitropropionic acid in poisoning samples by ultra-performance liquid chromatography-tandem mass spectrometry. Wei Sheng Yan Jiu 2016;45:56-60.
Rob MacKay, BVSc (Dist), Ph.D., DACVIM Rob MacKay is from New Zealand and completed his BVSc at Massey University. Af ter several years in dairy cattle practice, he moved to the U.S. and did an internship in equine medicine at the University of California, Davis and a residency in large animal medicine at the University of Florida, where he has remained. He was board certified by the ACVIM in 1981 and received his Ph.D. in the field of tumor immunology in 1987. Dr. MacKay has been on the faculty at the University of Florida College of Veterinary Medicine since 1987 and holds the rank of professor of large animal medicine. His clinical interests are equine internal medicine with a focus on neurologic diseases of large animals. His current research focuses on anhidrosis in horses and toxic plants of local importance.
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MANAGEMENT OF EQUINE STRANGLES AMANDA M. HOUSE | DVM, DACVIM
Strangles is caused by bacterial infection with Streptococcus equi subspecies equi (referred to as S. equi). The bacteria typically infect the upper airway and lymph nodes of the head and neck. The disease has been in the equine population for centuries and was first reported in 1251. The infection is highly contagious in horse populations and can recur on farms with previous outbreaks of the disease. It is one of the most commonly diagnosed contagious diseases of the horse worldwide. The persistence of this infection on farms is multifactorial. The bacteria can survive on water sources (buckets and troughs) for over a month, but the primary source of recurrent infections is most likely asymptomatic carrier horses that can shed the bacteria to other horses for months to years. Historically, strangles got its name because affected horses were sometimes suffocated from large, infected lymph nodes that obstructed their upper airway or trachea. The hallmark clinical signs of infection are fever (temperature >101.5ºF), nasal discharge and enlarged submandibular lymph nodes (in the space between the lower jaw bones) which ultimately abscess. Purulent nasal discharge is typically present, although it may initially be clear. The retropharyngeal lymph nodes, which are behind the throatlatch, may also become enlarged and abscess. These will sometimes drain into the guttural pouches which are air-filled spaces within the head that are an expansion of the Eustachian tubes. Guttural pouch infection and pus accumulation (empyema) are often the result of retrophayngeal lymph nodes that abscess and rupture into the guttural pouches. Guttural pouch infection may also occur from bacterial entrance through the pharynx (throat). Anorexia, depression and difficulty swallowing may also accompany signs of infection. Fortunately, although strangles is highly contagious and can affect many horses on a farm, most horses with infection recover without complication. The occurrence of complications will increase the likelihood of death from the infection (from 8 to 40 percent of cases). Complications from infection with S. equi include spread of the infection to lymph nodes other than the head and neck (also known as metastatic infection or bastard strangles), immunemediated disease (such as purpura hemorrhagica), muscle disease and pain, and lack of milk production. Studies report complications to occur in approximately 20 percent of strangles cases. Horses that develop complicated infection typically require antibiotic and additional therapies based on veterinary examination. Clinical signs of strangles are highly suggestive of the diagnosis; however, definitive diagnosis is made by culture of the bacteria from a sample of purulent discharge (from the nose or guttural
26 The Practitioner
Endoscopy picture of a horse with strangles. Photo courtesy of Dr. Martha Mallicote at UF
Endoscopy picture of a horse with strangles. Photo courtesy of Dr. Martha Mallicote at UF
pouch), a lymph node abscess or a nasal-pharyngeal wash. Polymerase chair reaction (PCR) is a very sensitive test that is also available and detects bacterial DNA. PCR cannot tell the difference between live and dead bacteria, so it’s typically used in conjunction with culture. However, if consecutive PCRs are negative, the horse is unlikely to have strangles. The real challenge is diagnosing horses that are asymptomatic carriers, which this author likes to evaluate with guttural pouch endoscopy, lavage
Issue 3 • 2019
Management of an Outbreak Strangles is a reportable disease in some states, and the state veterinarian may need to be notified as well. Movement of any horses on or off the farm should be stopped, and new horses should not be introduced. Take the temperature of all horses on the farm twice daily. Normal rectal temperature is 99 to 101.5°F. Monitoring the rectal temperature and isolating horses at the first sign of fever is one of the most effective ways to stop the spread of infection. Infected horses can transmit the bacteria to healthy horses one to two days after they develop a fever. An isolated area should be set up for horses with fever and any other signs of illness (nasal discharge, etc.). Extreme care should be taken not to mix horses with infection and horses exposed to horses with strangles to unexposed horses. Ideally, three groups of horses should be created: 1.) infected horses 2.) horses that have been exposed to or in contact with infected horses and 3.) clean horses with no exposure. No nose-to-nose contact or shared water buckets should occur among the groups. Unexposed horses should be kept in a “clean” area and, ideally, should have separate caretakers, cleaning equipment, grooming equipment, water troughs and pasture. People and equipment can transfer the infection from horse to horse. Extreme care, handwashing and disinfection of supplies must be observed by everyone involved. If different individuals cannot care for infected and healthy horses, then healthy horses should always be dealt with first. Dedicated protective clothing, such as boots, gowns or coveralls, and gloves, should be utilized when dealing with infected horses. Thorough cleaning and disinfection are critical when dealing with any infectious disease. All water troughs should be thoroughly cleaned and disinfected daily during an outbreak. Read the label instructions on disinfectants to be sure they are used at the correct dilution and are active against S. equi. All surfaces and stalls
Strangles. Photo courtesy of Dr. Sally DeNotta
and PCR. Anywhere from 4 to 50 percent of the horses on farms with recurring strangles are carriers of the infection. Most horses will begin shedding (bacteria can be transmitted from nasal secretions to other horses) the bacteria from their nasal passages a couple of days after the onset of fever. Bacterial shedding occurs intermittently for several weeks. Some horses may continue to shed the bacteria for months to even years, serving a continual source of new infections on the farm. All diagnostic tests and treatment of affected cases should be done under veterinary supervision. Antibiotic therapy remains controversial for the treatment of strangles. Uncomplicated cases of submandibular lymph node abscessation do not require antibiotic therapy in this author’s opinion. Complicated cases and those requiring tracheostomy for management of respiratory distress generally do require antibiotic and other supportive therapies. There is some evidence that treatment with antibiotics — such as penicillin — at the first sign of fever and in horses with no lymph node enlargement may prevent infection; however, early antibiotic treatment will also prevent these cases from developing immunity to the infection and subsequently makes them susceptible to reinfection sooner.
Purulent drainage from guttural pouch with strangles. Photo courtesy of Dr. Sally DeNotta
@FLORIDA_VMA | The Practitioner 27
had the disease within the previous year also do not need to be vaccinated. Once recovered from an active infection, 75 percent of horses have immunity for one to two years. Vaccination of horses recently exposed to strangles, that have high antibody levels, may result in purpura hemorrhagica. Vaccination is only recommended in healthy horses with no fever or nasal discharge.
References: 1. ACVIM Revised Consensus Statement: https://onlinelibrary. wiley.com/doi/full/10.1111/jvim.15043
Chondroids. Photo courtesy of Dr. Fairfield Bain
should be disinfected following removal of manure and organic material. Manure will inactivate bleach and iodine-type solutions. Manure and waste feed from infected horses should be composted in an isolated location and not spread on the pastures. Pastures that were utilized for sick horses should be rested for a minimum of four weeks. A serious challenge when dealing with an outbreak of strangles is identifying the horses that are carriers of the bacteria but are not showing any signs of illness. These horses can shed the bacteria for weeks, months or even years, and serve as a continual source of reinfection for your farm. Ideally, all horses on the farm should be tested for strangles. Use of the bacterial culture and PCR combined identifies carriers with a 90-percent success rate. Nasal pharyngeal swabs or washes can be done to sample the horses for infection. The washes improve the chance of identifying carrier horses. Additionally, all sick horses should be tested three consecutive times and be negative all three times before being put back with healthy horses. Previously infected horses can shed the bacteria for weeks to months or even years in rare cases. That is the reason that three negative test samples are recommended prior to reintroduction to the healthy herd. For the most accurate diagnosis of carriers and horses without obvious clinical signs, upper airway and guttural pouch endoscopy can be performed. This procedure allows for identification of infections that can develop in the guttural pouch and culture of that area. Although disinfection, isolation procedures and diagnosis can be costly, they are certainly cheaper than additional outbreaks on a farm. Vaccination is one method for prevention and control of infection with S. equi. With strangles, vaccination will likely reduce the severity of disease in the majority of horses that are infected. Available vaccines can be administered by intramuscular and intranasal routes. Improper administration of the vaccination can result in poor protection against infection and/or complications at the site of injection; therefore, administration by a veterinarian is recommended. The intranasal vaccination results in the best local immunity.
2. ht t p s : //a a e p. o r g /s i t e s /d e f au l t /f i l e s / D o c u m e nt s / DiseaseFactsheetStrepequi.pdf
Amanda M. House DVM, DACVIM (Large Animal) Amanda M. Hou se , DVM, DAC V I M (L a rg e Anim a l) is a clinical professor in the Department of Large Animal Clinical Sciences at the University of Florida College of Veterinary Medicine. Dr. House is the director of the Practice-based Equine Clerkship program, which enables veterinary students at UF to have a clinical ambulatory rotation with private practitioners, and she has served as the director of student affairs since September 2015. She completed her Bachelor of Science in animal science from Cornell University. After graduating from Tufts University School of Veterinary Medicine in 2001, Dr. House completed an internship and large animal internal medicine residency at the University of Georgia’s Veterinary Teaching Hospital. Dr. House became board certified in large animal internal medicine in 2005. Her professional interests include neonatology, communication training, infectious disease and preventative health care. Dr. House became a faculty trainer for the Bayer Communication Project/Institute for Healthcare Communication modules for veterinary medicine in 2012. Dr. House is active on committees for the American Association of Equine Practitioners and the Florida Association of Equine Practitioners. She was president of the Florida Association of Equine Practitioners in 2010 and is currently a council member of the FAEP.
Vaccination is generally not recommended during an outbreak of strangles. If there are horses on the farm with no clinical signs of infection (fever, nasal discharge, etc.) and no known contact with sick horses, vaccination may be considered. Horses that have 28 The Practitioner
Issue 3 • 2019
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