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The Practitioner Published by the Florida Association of Equine Practitioners, an Equine-Exclusive Division of the Florida Veterinary Medical Association Issue 1 • 2013

IN THIS ISSUE 6 | Treating 'Dummy' Foals in the Field

13 | Preparing the

Mare for the Breeding Season

17 | Equine Protozoal

Myeloencephalitis


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Letter from the President Dear Fellow FAEP Members, Exactly one year ago I sat down to write my first president’s letter and I shared with each of you what we, as an organization, had accomplished. The FAEP merged with the FVMA in February of 2011 and much has happened during the course of the last 21 months. We have conducted six continuing education conferences, three wet labs and a student appreciation day that were all extremely well received. Our two most recent conferences experienced record attendance and the dentistry wet lab that Dr. Jack Easley facilitated in Ocala (on November 16 as part of the 50th Ocala Equine Conference, November 16-18) was sold out a month before it was held. Almost two years after our merger and in the spirit of the recent national election, I can confidently report in my final letter to you, before passing the gavel to incoming president Dr. Anne Moretta, that the state of our FVMA/ FAEP union is strong. Both of our most recent conferences, the 8th Annual Promoting Excellence Symposium in the Southeast at the Waldorf Astoria Naples and the 50th Annual Ocala Equine Conference, went very well. Our speakers did a great job and the plan is to include some of their material in upcoming editions of the Practitioner. The FVMA staff and our Executive Director Phil Hinkle were organized and efficient (as usual). Thanks also to our industry council members whose support makes these events possible. The fishing tournament was a big success and will allow us to continue funding our annual scholarship to a deserving University of Florida senior veterinary student. The FAEP Council is in the process of reviewing all of the attendee comments and, as we work to prepare next year’s schedule, we will adjust accordingly. Our conferences for 2013 will include (but are not limited to) the 4th Annual Promoting Excellence Equine Foot Symposium at the DoubleTree by Hilton in Orlando from June 28-29, the 9th Annual Promoting Excellence Symposium in the Southeast at the Boca Raton Resort and Club from October 17-20, and the 51st Annual Ocala Equine Conference from November 15-18. It has been my honor to serve as your 2012 FAEP council president. Thanks for your support and I look forward to seeing you at some (or all!) of our upcoming events in the next year. Sincerely, Ann L. Moretta, VMD, MS 2013 FAEP Council President

EXECUTIVE COUNCIL Anne L. Moretta, VMD, MS FAEP Council President

maroche1@aol.com Suzan C. Oakley, DVM, Diplomate ABVP (Equine) FAEP Council Vice President

oakleyequine@gmail.com Gregory D. BonenClark, DVM, Diplomate ACVS FAEP Council Past President

gbonenclark@fevaocala.com Mr. Philip J. Hinkle Executive Director

phinkle@fvma.org

COUNCIL REPRESENTATIVES Amanda M. House, DVM, Diplomate ACVIM

housea@ufl.edu

Liane D. Puccia, DVM

pucciavet@aol.com

Ruth-Anne Richter, BSc (Hon), DVM, MS

rrichter@surgi-carecenter.com

Corey Miller, DVM, MS, Diplomate ACT FAEP Council Representative to the FVMA Executive Board

cmiller@emcocala.com

Continuing Education Of ferings in 2013! FOOT SYMPOSIUM Orlando, FL June 28-29, 2013

9TH ANNUAL PROMOTING

EXCELLENCE SYMPOSIUM, Boca Raton, FL October 17-20, 2013

The Practitioner is an official publication of the Florida Association of Equine Practitioners, an Equine-Exclusive Division of the Florida Veterinary Medical Association.

4  The Practitioner 

OCALA EQUINE CONFERENCE Ocala, FL November 15-18, 2013

Issue 1 • 2013


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The Practitioner  5


TREATING 'DUMMY' FOALS IN THE FIELD

The success rate for treating ‘Dummy’ foals has increased tremendously since the early 1980s from a little over 60% to a greater than 80% rate of survival to discharge in most hospitals. We have also been able to translate many treatments from the referral hospital to the field with good success for the practitioner. The management of ‘dummy' foals is labor intensive, can be expensive and is often emotionally stressful for the owner, particularly if managed in the field. This article reviews the processes contributing to development of the syndrome of ‘dummy foals’ and provides information on how to translate many specific and supportive treatments to the field situation.

P E R I N ATA L A S P H Y X I A S Y N D R O M E : THE ‘DUMMY’ FOAL Neonatal encephalopathy (NE) is one of the most common diseases of the equine neonate and is also described as dummy foal syndrome and neonatal maladjustment syndrome (NMS). There are a wide spectrum of clinical signs associated with NE ranging from mild depression with loss of the suck reflex to grand mal seizure activity. The majority of affected foals are normal at birth but show signs of central nervous system (CNS) abnormalities within a few hours following birth although some will not show signs until 24 hours of age. Management of foals presenting with signs consistent with a diagnosis of NE requires complete examination of other body systems and provision of specific and supportive therapies 6  The Practitioner 

by  PAMELA A. WILKINS DVM, MS, PhD, Diplomate ACVIM-LA; ACVECC

of all affected body systems. Although Perinatal Asphyxial Syndrome (PAS, NMS, HIE, ‘dummy foal) is most clinically obvious as NE, the gastrointestinal tract and kidneys are very frequently affected; complications associated with these systems should be anticipated, in addition to cardiovascular, respiratory, and endocrine disorders.

Pathophysiology The underlying pathophysiologic details of PAS and NE in the foal are unknown and likely multifactorial and equine neonatologists have long looked to human studies and models of the human disease for understanding of the syndrome in the equine neonate. NE is commonly associated with adverse peripartum events, including dystocia and premature placental separation, but a fair number of foals have no known peripartum period of hypoxia, suggesting that these foals result from unrecognized in utero hypoxia. There is increasing evidence that cytokinemia, resulting from placental infection or insult, is a major contributor to NE in infants, and probably foals, with incidence of NE increased with the presence of maternal fever, something veterinarians have suspected for the last decade or so. Perinatal brain damage in the mature fetus usually results from severe uterine asphyxia due to an acute reduction of uterine or umbilical circulation. Calcium overload of neurons secondary to the insult leads to cell damage by activation of calcium dependent proteases, lipases and endonucleases. Issue 1 • 2013


Protein biosynthesis is halted. Calcium also enters the cells by glutamate-regulated ion channels as glutamate, an excitatory neurotransmitter, is released from pre-synaptic vesicles following anoxic cellular depolarization. Once the insulting event is over, protein synthesis remains inhibited in specific areas of the brain and returns to normal in less vulnerable areas of the brain. Loss of protein synthesis appears to be an early indicator of cell death due to the primary hypoxic/ anoxic event. A second wave of neuronal cell death occurs during the ‘reperfusion’ phase and is thought to be similar to classically described ‘post-ischemic reperfusion injury’ in that damage is due to production of and release of oxygen radicals, synthesis of nitric oxide (NO) and inflammatory reactions and is thought be associated with the neurotoxicity of glutamate and aspartate excitatory neurotransmitters. There is some evidence that this excitotoxic cascade extends over several days from the time of insult and is modifiable. The activation of the Nmethyl-D-aspartate (NMDA) subtype of glutamate receptors is implicated in the pathophysiology of traumatic brain injury and is suspected to play a role in NE/PAS. Magnesium and many drugs that control seizures have been demonstrated to block these receptors.

Treatment Therapy for the various manifestations of PAS involves: ƒƒ Control of seizures ƒƒ General cerebral support ƒƒ Correction of metabolic abnormalities ƒƒ Maintenance of normal arterial blood gas values ƒƒ Maintenance of tissue perfusion ƒƒ Maintenance of renal function ƒƒ Treatment of gastrointestinal dysfunction ƒƒ Prevention/recognition/early treatment of secondary infections ƒƒ General supportive care It is important that seizures be controlled as cerebral oxygen consumption increases five-fold during seizures. Diazepam and midazolam can be used for emergency control of seizures. If seizures are not readily stopped with diazepam or midazolam, or more than two seizures are recognized, then www.faep.net 

diazepam should be replaced with either phenobarbital given to effect or a midazolam constant rate infusion (CRI). In cases of HIE, ketamine and xylazine should be avoided because of their association with increased intracranial pressure. It is important to protect the foal from injury during a seizure and also to ensure the patency of their airway to prevent the onset of negative pressure pulmonary edema or aspiration pneumonia. The most important therapeutic interventions are aimed at maintaining cerebral perfusion. Cerebral interstitial edema is only truly present in the most severe cases and, if suspected, can be treated with mannitol administration. Both mannitol and hypertonic saline infusions are minimally effective treating cellular edema. Thiamine supplementation in the intravenous fluids can be administered to support metabolic processes. Only if cellular necrosis and vasogenic edema are present are drugs such as mannitol and dimethylsulfoxide (DMSO) indicated. The author rarely uses DMSO, has not used it at for the last decade and has not recognized any change in outcome by discontinuing its use. There is evidence suggesting that naloxone increases ischemic injury in neonatal rats, making use of this compound controversial. GABAergic agonists (gabapentin) are being used by some practitioners in the managements of PAS/NE in foals, based on evidence showing neuroprotection when used in ischemia, both alone and in combination with NMDA antagonists like magnesium. There is no good quality evidence for the use of allopurinol, a xanthine oxidase inhibitor. Foals with PAS often have a variety of metabolic problems. The normal period of hypoglycemia that occurs postpartum should not be forgotten and should not be treated aggressively for fear of worsening the neurologic injury due to transient hyperglycemia. Foals suffering from PAS will also have frequent recurrent bouts of hypoxemia and occasional bouts of hypercapnia. INO2 is generally needed in these cases both as a preventative therapy and as direct treatment. Additional respiratory support, particularly in those foals with centrally mediated hypoventilation and periods of apnea or abnormal breathing patterns, include caffeine (per os or per rectum) or doxapram CRI. Foals requiring positive pressure ventilation or with severe respiratory disorders should be referred to a hospital. When evaluating these cases and considering alternatives for treatment, pH is important. If the respiratory acidosis is not so severe as to adversely affect the patient (generally > 70 mmHg), and the pH is within normal limits, hypercapnia may be tolerated. Maintaining tissue perfusion and oxygen delivery to tissues is a cornerstone of therapy. Oxygen carrying capacity of the blood should be maintained; some foals will require transfusions to maintain a PCV >20%. Adequate vascular volume is important, but care should be taken to avoid fluid or sodium overloading. Early evidence of fluid overload is subtle accumulation of ventral edema between the front legs and over the distal limbs. The kidney is a target for injury in these patients and it is not unusual for renal compromise to play a significant role in the demise of these foals. These foals present with signs of fluid overload and generalized edema. It is important that The Practitioner  7


urine output and fluid therapy be balanced in these cases to prevent additional organ dysfunction associated with edema. Overzealous use of diuretics and pressors in these cases can result in diuresis requiring increased intravenous fluid support and can be counterproductive. Low doses of dopamine, administered as a constant rate infusion (CRI) of 2-5 μg/kg/ min, are usually effective in establishing diuresis by natriuresis. Bolus (0.25-1.0 mg/kg) or CRI (0.25-2.0 mg/kg/hr) furosemide can be administered but once diuresis is established electrolyte concentrations and blood gas tensions must be followed. Many antimicrobial agents used in the management of these cases, most notably the aminoglycosides, depend on renal clearance. Aminoglycoside toxicity occurs in the equine neonate and will exacerbate or, at the least, complicate the management of renal failure originally due to primary hemodynamic causes. Foals with PAS commonly present with ileus, recurrent excessive gastric reflux and gas distention. These problems are exacerbated by constant feeding in the face of continued dysfunction and continued hypoxia. Frequently, enteral feeding cannot meet their nutritional requirements and partial (PPN) or total parenteral nutrition (TPN) is required. Special attention should be paid to the passive transfer of immunity status and glucose homeostasis in these cases. Clinical signs of injury to the gastrointestinal tract can be subtle and lag behind other abnormalities for days to weeks. Foals with PAS are susceptible to secondary infection. Treatment of recognized infection is required and antimicrobial treatment is almost always required and should be broad-spectrum. Repeat determination of IgG concentration should be made and additional intravenous plasma therapy may be required. Any acute deterioration in the condition of a foal with PAS indicates a need for further evaluation for possible sepsis.

PRACTICAL SOLUTIONS TO COMMON PROBLEMS OF THE FOAL Long-term Intravenous Access:

Long-term intravenous access for fluid administration or antimicrobial administration may be necessary in some cases. In these cases, placement of ‘over the wire catheters’ provides the best solution. Placement of these catheters is more challenging than over the needle catheters, but with practice placement becomes straightforward. Having sufficient help available is important, as good restraint of the patient is necessary. If help is not readily available, small doses of diazepam (2-5 mg per foal, IV) can make the process easier. Xylazine should be avoided in very young foals as it can cause transient hypertension. Acepromazine should not be used in foals with potential for seizure activity. Small doses of butorphanol (~3 mg/foal) are tolerated fairly well. Catheterization should be performed under sterile conditions. The site should be clipped and surgically prepped. Placing a rolled towel under the foal’s neck in the mid-cervical region elevates the neck and makes catheter placement easier. Catheters should be sutured in place. Large volumes of flush are not required for these catheters and the catheter patency can usually be maintained by flushing with 5 ml heparinized saline after each use. These catheters should be flushed 8  The Practitioner 

at least 4 times daily. There is generally no need to place a bandage or any other type of protection over the catheters.

Tube Feeding:

Never feed a cold foal! Foals able to tolerate enteral feeding but too weak to suck properly from the mare, or any foal without the ability to suck, may benefit from placement of a long-term enteral feeding tube. The tubes are well tolerated by foals and they can learn to suck from a bottle or from the dam around them. They are small diameter tubes that are placed as nasoesophogeal tubes. They can be purchased with enteral feeding bags that attach to them and they have small, attached caps to prevent air aspiration into the esophagus. Feeding should always be performed under gravity flow only. It is ideal to pass a large bore nasogastric tube to check for reflux before placing these tubes, as a foal with significant gastric fluid accumulation, or blood tinged gastric fluid, should not be fed enterally until this is resolved. Once the feed is administered the tube should be flushed with a small volume of water ad recapped. Foals should be standing or in sternal recumbency during the feeding and should remain in that position for at least 5 minutes once feeding is completed. In general a foal with a healthy gastrointestinal tract will tolerate 10% of it body weight in milk or milk replacer divided into every 2 hour feedings (12 times per day). For a 100 pound foal, this would be: 100lb x .10= 10 lb 10 lb / 12 = 0.83 lb per feeding (~13-14 ounces) If the foal tolerates this well, it can be gradually increased to 15 to 20 percent of its body weight over a few days if the foal continues to not nurse or drink from a bucket. If the foal shows evidence of colic or abdominal distention, feeding should be discontinued for a few hours and reinstated slowly. All enteral fluids should be administered under gravity flow only and the foal should be kept standing or in sternal recumbency for 5-10 minutes once the feeding is completed to prevent aspiration.

Arterial Blood Gas Analysis:

Arterial blood gas analysis has traditionally been performed primarily at large referral institutions. However, the advent of stable and durable portable blood gas analysis units has expanded this ability to the private practitioner. Units are available as either new units or refurbished units. Two popular units are the IRMA and the I-STAT units.

Fluid Therapy in the Field:

Fluid therapy in foals can be undertaken in the field, keeping in mind some differences between the neonate and the adult. The intravenous route should be used for initial resuscitation and administration of glucose and plasma. Oral fluid supplementation is possible, but should only be done under gravity flow. Fluid therapy should be conservative during postpartum resuscitation, as the newborn foal is generally not volume depleted unless excessive bleeding has occurred. If intravenous fluids are required for resuscitation, administration of 20 ml/kg of a non–glucose-containing polyionic isotonic fluid Issue 1 • 2013


over 20 minutes (about 1 L for a 50-kg foal), known commonly as a ‘shock bolus’, can be effective. Non–glucose-containing polyionic intravenous fluids should be used because hyperglycemia, but not hypoglycemia, immediately after fetal or neonatal asphyxia has been shown to interfere with the recovery of brain cell membrane function and energy metabolism in neonatal piglets. These findings suggest that post–hypoxicischemic hyperglycemia is not beneficial and might even be harmful in neonatal hypoxic-ischemic encephalopathy. The foal should be reassessed after the initial bolus and additional boluses administered as necessary. These same indications should be used when administering ‘shock bolus’ treatment to neonates with other conditions requiring fluid resuscitation, such as sepsis. Failure to respond well to bolus therapy probably indicates a need for referral to a hospital. Glucose-containing fluids can be administered as a constant rate infusion (CRI) both after resuscitation and for energy support in the sick neonatal foal at a rate of 4 to 8 mg/kg/min, particularly in the obviously compromised foal. If the foal requires glucose during resuscitation, dextrose can be added to the bolus liters as 0.25-1% dextrose (5-20 ml 50% dextrose) per liter. This will approximate 4-8 mg/kg/min. A rapid method of calculating an appropriate rate in the field for administering 5% dextrose in water at 4 mg/kg/min is as follows: [(Body weight in pounds) x 2] + [(Body weight in pounds) x 20%] = #mls/hour For a 100 lb foal, this becomes: [(100) x 2] + [(100) x 10%] = 200 + 40 = 240 mls 5% dextrose in water/hour * This can be “ballparked” at 250 mls per hour to most average (50 kg) foals! If this rate is not sufficient to keep blood glucose concentration within a normal range (60-140 mg/dl) then the rate can be doubled, or the same rate can be used with a greater dextrose concentration, such as 10% dextrose. A fluid pump is a good idea to use for this and many can be found on the secondhand market for very reasonable cost. Most pumps will require specific administration sets. Hand-held glucometry units are commonly used to monitor glucose concentrations in the blood or plasma, but should be assessed for their accuracy in the specific conditions they are used in, as they can be quite inaccurate. Fluid management of the ill neonate, particularly over the first few days of life, must take into consideration that the neonate is undergoing a large transition from the fetal to the neonatal state and that important physiologic changes are taking place. The newborn kidney has a limited ability to excrete excess free water and sodium, and the barrier between the vascular and interstitial space is more porous than that of adults. The approach taken has been one of fluid restriction, in particular sodium restriction but also free water restriction, and has resulted in improved outcome and fewer complications,. The calculations used for ‘dry’ maintenance intravenous fluid support takes into consideration the ratio of surface area to volume and partially compensates for insensible water losses. The majority of maintenance fluids are then provided as 5% dextrose to limit sodium overload www.faep.net 

and provide sufficient free water to restore intracellular andinterstitial requirements. The calculation for maintenance fluid administration is as follows: First 10 kg body mass 100 ml/kg/day Second 10 kg body mass 50 ml/kg/day All additional kilograms 25 ml/kg/day As an example, the average 50-kg foal would receive 1000 ml/day for the first 10 kg of body mass, 500 ml/day for the next 10 kg of body mass, and 750 ml/day for the remaining 30 kg of body mass for a total of 2250 ml/day. This translates to an hourly fluid rate of about 94 ml/hr for maintenance. Most foals will generally receive 1.5 to 2 times maintenance but the rate must be adjusted higher if there are large ongoing losses. Potassium is generally supplied to the foal at 20 mEq/L of fluids administered, and then adjusted as needed. Fluid and sodium requirements can be adjusted for ongoing losses exceeding the maintenance requirements. Remember that the first urine produced by foals is generally quite concentrated, with a specific gravity in some cases of 1.050 or more. In the critically ill foal the sodium requirement can be met with as little as 140 mEq of sodium per day (1-3 mEq per kg/day for growth), about that administered in a single liter of isotonic crystalloid fluids. One liter of commercially available equine plasma will have a sodium concentration of ~170 mEq/L due to aniticoagulation with sodium citrate. A normal neonatal foal will gain 1-3 kg/day. Any larger than anticipated weight gains or losses should result in closer evaluation of the foal. If possible, urine specific gravity should be measured several times daily (and should be hyposthenuric after 24 hours, specific gravity < 1.010 ), and fractional excretion of sodium measured if renal injury or dysfunction is suspected. In practice, fluid boluses frequently used, as maintenance of intravenous lines can be challenging, particularly if the foal remains in a stall with the mare and is active. The total amount of fluids needed should be calculated for the day and then divided in to bolus administrations ranging from every 2 to every 6 hours, depending on the condition of the foal; ideally bolus administration should be limited to 1-2 liters per bolus. The sodium load administered with this route will be greater than that of constant rate infusion as dextrose should not be administered by bolus at large concentration, ie more The Practitioner  9


than 1-2.5%. Potassium should not be added to fluids being administered as a bolus. If the oral route is available for hydration, this can be used in foals that are not nursing but are able to tolerate enteral feeding via indwelling nasoesophogeal tube.

Prognosis: The prognosis for foals with PAS is good to excellent when it is recognized early and aggressively treated in term foals. Up to 80% of these neonates survive and go on to lead productive and useful athletic lives. Prognosis decreases with delayed or insufficient treatment. Concurrent problems such as prematurity and sepsis, and failure to resolve hyperlactatemia within 48 hours of presentation in foals with PAS (as accumulating evidence suggests); indicates a poorer prognosis for ultimate survival.

Table 1: Drugs and dosages used in the treatment of perinatal asphyxial syndrome/ neonatal encephalopthy. Not all neonatal doses have been generated using pharmacokinetic analyses and are based on experience only. DRUG

INDICATION

DOSE

POTENTIAL COMPLICATIONS

Diazepam

Single or short term seizure control

0.1-0.2 mg/kg (5-10 mg to a 50 kg foal IM or IV)

Rapid administration IV may result in respiratory depression

Midazolam

Single or short term seizure control

0.1-0.2 mg/kg (5-10 mg to a 50 kg foal IM or IV) NOT water soluble.

Rapid administration IV may result in respiratory depression

Midazolam CRI

Longer term control for repetitive seizures. Mild sedation for hyperresponsive or ‘jittery’ foals.

3-6 mg/hr. Midazolam is water soluble and CRI is administered in isotonic crystalloid fluid using a 0.5 mg/ml concentration.

Rapid administration IV may result in respiratory depression Higher doses may be used if necessary. Advantage is ability to titrate to effect and reversibility if needed.

Phenobarbital

Longer term seizure control

2-5 mg/kg IV slowly over 20 minutes. Start with lower dose and monitor to effect. Maximal effect expected after 45 minutes.

Respiratory depression, hypothermia, hypotension and haryngeal collapse particularly at higher doses or in more severely affected foals.

Thiamine

Metabolic support

1-20 mg/kg q12 hr added to IV fluids (protect from light)

None

Mannitol

Intercellular edema: osmotic diuretic

0.25-1.0 g/kg IV as a 20% solution rapidly over 15-20 minutes

Dehydration. May result in significant hyperosmolarity with repeated administration. May exacerbate cerebral bleeding.

Dimethylsulfoxide

Anti-inflammatory, Intercellular edema: osmotic agent

0.1-1 gm/kg IV as a 10%solution

Odor; OSHA restrictions in some areas, hemolysis; dehydration

Gabapentin

Neuroprotection: GABA receptor agonist.

10-15 mg/kg/day divided equally and given orally 3 to 4 times a day

None described: an uninvestigated drug in equine neonates

Magnesium CRI

Neuroprotection: NMDA receptor antagonist.

*See below. Can precipitate other infusates, test compatibility or discontinue when administering intravenous antimicrobial drugs.

In very high doses (>10x) muscular weakness can occur as can hypotension

CRI: constant rate infusion *Magnesium CRI: Remove 20 ml from 100 ml bag sterile isotonic saline (0.9%). Add 20 ml 50% MgSO4 for a final volume of 100 ml. Administer loading dose at 25 ml/hr for a 50 kg foal for 1 hour, decrease infusion to 12.5 ml/hr thereafter. This is approximately 50 mg/kg loading dose followed by 25 mg/kg maintenance dose. Infusion can be maintained for 24-48 hours.

Table 2: Commonly used antimicrobials in neonatal foals and their dosages. It is important to recognize that many antimicrobials have different dosages and interval in the foal, especially the neonate, than those used in adults. Not all neonatal doses have been generated using pharmacokinetic analyses and are based on experience only. 10  The Practitioner 

TABLE 2

Issue 1 • 2013


DRUG

DOSE, ROUTE, FREQUENCY

COMMENTS

Acyclovir

16-20 mg/kg PO TID

Amikacin sulfate

< 1wk old: 25-30 mg/kg IV SID 2-4wk old: 20 – 25 mg/kg IV SID

Ampicillin sodium

50-100 mg/kg IV QID

Azithromycin

10 mg/kg PO SID for 5 days then EOD

Hyperthermia, diarrhea in foal and mare

Cefazolin

25 mg/kg IM TID/QID

1st generation cephalosporin

Cephalexin

30 mg/kg PO TID

1st generation cephalosporin

Cefuroxime

30 mg/kg/day PO BID/QID 50-100 mg/kg/day IV TID/QID

2nd generation cephalosporin

Cefotaxime

50-100 mg/kg IV QID

3rd generation cephalosporin

Ceftazidime

40 mg/kg IV TID/QID

3rd generation cephalosporin

Ceftiofur

5 mg/kg IV BID 10 mg/kg IV QID CRI: 1.5 mg/kg/hr Nebulized: 1 mg/kg as 25 mg/ml solution TID/BID

3rd generation cephalosporin No CNS penetration Ideally given over 20 mins Higher doses: broader gram-ve spectrum

Cefpodoxime

10 mg/kg PO BID/QID

3rd generation cephalosporin

Ceftriaxone

25 mg/kg IV BID

3rd generation cephalosporin

Cefepime

11 mg/kg IV/IM TID

4th generation cephalosporin

Chloramphenicol

50 mg/kg PO QID

Public health/OHS concerns

Clarithromycin

7.5 mg/kg PO BID

Hyperthermia, diarrhea in foal

Doxycycline

10 mg/kg PO BID

Enrofloxacin

5 mg/kg PO SID

Chondropathy and arthropathy

Erythromycin stearate

25 mg/kg PO TID

Hyperthermia, diarrhea in foal and mare

Fluconazole

8 mg/kg loading then 4 mg/kg PO BID

Gentamicin sulfate

< 7do: 11-13 mg/kg IV SID Older foals: 6.6 mg/kg IV SID Nebulized: 2.2 mg/kg as 50 mg/ml solution SID

Imipenem

10-20 mg/kg IV QID

Metronidazole

10-15 mg/kg PO or IV TID

10 mg/kg BID if increased GIT absorption may occur.

Oxytetracycline

10 mg/kg IV BID

Nephrotoxic, give slowly

Na or K Penicillin

20,000 – 50,000 IU/kg IV QID

Use upper dose in severe infections

Procaine penicillin

20,000 – 50,000 IU/kg IM BID

Rifampin

5 mg/kg PO BID

Ticarcillin and clavulonic acid

50 – 100 mg/kg IV QID CRI: 2-4 mg/kg/hr

Trimethoprim -sulfonamide

30 mg/kg PO/IM/IV BID

www.faep.net 

Nephrotoxic TDM: 30 min peak > 45 μg/ml 8 hr trough: < 15 μg/ml 12 hr trough: < 5 μg/ml

Nephrotoxic TDM: 30 min peak > 25 μg/ml 8 hr trough: < 5 μg/ml 12 hr trough: < 2 μg/ml

Use with other antimicrobials

Dose/kg is combined trimethoprim and sulfonamide

The Practitioner  11


Suggested Reading:

Goldberg RN, Bara R, Das A, Finer NN, Sanchez PJ, Poindexter BB, Van Meurs KP, Carlo WA, Stoll BJ, Duara S, Guillet R, Higgins RD; Brain injury following trial of hypothermia for neonatal hypoxic-ischaemic encephalopathy. for the Eunice Kennedy Shriver National Institute of Child Health and Human Development Neonatal Research Network. Arch Dis Child. 2012 Jul 17.

Pathophysiology:

Kempski O. 2001. Cerebral edema. Seminars in Nephrology 21(3): 303-307.

Martin-Ancel A, Garcia-Alix A, Gaya F et al. 1995. Multiple organ involvement in perinatal asphyxia. Journal of Pediatrics 127(5): 786-793.

Tagin MA, Woolcott CG, Vincer MJ, Whyte RK, Stinson DA. Hypothermia for neonatal hypoxic ischemic encephalopathy: an updated systematic review and meta-analysis. Arch Pediatr Adolesc Med. 2012 Jun 1;166(6):558-66.

Nelson KB, Willoughby RE. 2000.Infection, inflammation and the risk of cerebral palsy. Current Opinion in Neurology 13(2): 133-139. Vexler ZS and Ferriero DM. 2001. Molecular and biochemical mechanisms of perinatal brain injury. Seminars in Neonatology 6(2):99-108.

Treatments:

Giguère S, Sanchez LC, Shih A, et al. 2007. Comparison of the effects of caffeine and doxapram on respiratory and cardiovascular function in foals with induced respiratory acidosis. American Journal of Veterinary Research 68(12):1407-16. Maroszynska I, Sobolewska B, Gulczynska E et al. 1999.Can magnesium sulfate reduce the risk of cerebral injury after perinatal asphyxia? Acta poloniae pharmaceutica 56(6):469-473.

Pamela A. Wilkins DVM, MS, PhD, Diplomate ACVIM-LA; ACVECC

Greenwood K, Cox P, Mehmet H et al. 2000. Magnesium sulfate treatment after transient hypoxiaischemia in the newborn piglet does not protect against cerebral damage. Pediatric Research 48(3):346-345.

++ Pamela Wilkins received her DVM from Cornell University in 1986, performed her internship at Cornell in Equine Medicine and Surgery from 1986-1987, and completed a Master’s of Science Degree from Cornell in 1991. Between 1986 and 1989, she served as the main clinician for the Neonatal Intensive Care Unit at Cornell.

Whitelaw A. 2000. Systematic review of therapy after hypoxicischaemic brain injury in the perinatal period, Seminars in Neonatology 5(1):33-40.

Fluid Therapy:

Bell EF, Acarregui MJ: Restricted versus liberal water intake for preventing morbidity and mortality in preterm infants. Cochrane Database Syst Rev 2:CD000503, 2000, and 3:CD000503, 2001 (update). Palmer JE. Fluid therapy in the neonate: not your mother's fluid space.Vet Clin North Am Equine Pract.2004;20:63-75.

++

++

Park WS, Chang YS, Lee M: Effects of hyperglycemia or hypoglycemia on brain cell membrane function and energy metabolism during the immediate reoxygenation-reperfusion period after acute transient global hypoxia-ischemia in the newborn piglet, Brain Res 2001;901:102-108.

In 1995, she returned to Cornell, completed both board certification in Veterinary Internal Medicine (1995) and a PhD in Cardiovascular and Respiratory Physiology (1998). In 1998, Dr. Wilkins returned to New Bolton Center as a faculty member spending part of the year in the neonatal intensive care and part in large animal internal medicine, and completed the requirement for board certification in Veterinary Emergency and Critical Care.

Prognosis:

++

Axon J, Palmer J, Wilkins PA. 1999. Short-term and long-term athletic outcome of neonatal intensive care unit survivors. Proceedings of the American Association of Equine Practitioners 45:224-225. Baker SM, Drummond WH, Lane TJ et al. 1986.Follow-up evaluation of horses after neonatal intensive care. Journal of the American Veterinary Medical Association 189(11):1454- 1457.Freeman L, Paradis MR. 1992. Evaluating the effectiveness of equine neonatal intensive care. Veterinary Medicine 87:921-926.

In 2008 she was a full professor in Equine Internal Medicine and Emergency and Critical Care at the University of Illinois, where she continues to serve as Section and Service Chief for Equine Medicine and Surgery. ++

Borchers A, Wilkins PA, Marsh PM, Axon JE, Read J, Castagnetti C, Pantaleon L, Clark C, Qura'n L, Belgrave R, Trachsel D, Levy M, Bedenice D, Saulez MN, Boston RC. Association of admission Llactate concentration in hospitalised equine neonates with presenting complaint, periparturient events, clinical diagnosis and outcome: a prospective multicentre study. Equine Vet J Suppl. 2012 Feb;44 Suppl 41:57-63.

++

The Future:

Massaro AN, Chang T, Kadom N, Tsuchida T, Scafidi J, Glass P, McCarter R, Baumgart S, Vezina G, Nelson. KB Biomarkers of Brain Injury in Neonatal Encephalopathy Treated with Hypothermia. J Pediatr. 2012 Apr 10. [Epub ahead of print]

In 1991, she began residency training in large animal internal medicine at the University of Pennsylvania’s New Bolton Center.

++

Wilkins PA. Advantages and potential pitfalls of point of care (POC) glucose and lactate monitoring. In Proceedings American Association of Equine Practitioners Meeting, 2007;53:356-359.

Guillet R, Edwards AD, Thoresen M, Ferriero DM, Gluckman PD, Whitelaw A, Gunn AJ; CoolCap Trial Group. Seven- to eight-year follow-up of the CoolCap trial of head cooling for neonatal encephalopathy. Pediatr Res. 2012 Feb;71(2):205-9.

In 1989, Dr. Wilkins entered private equine practice employed by the Equine Clinic at Oaken Croft.

++

Dr. Wilkins has published more than 300 manuscripts, abstracts and book chapters during her career and has presented at more than 50 veterinary meetings, local, national and international professional meetings.

Her current research interest is in metabolic markers of clinical outcome in both neonatal and adult critically ill horses, although she continues to pursue her interests in cardiovascular physiology, coagulation, sepsis and respiratory diseases.

Shankaran S, Barnes PD, Hintz SR, Laptook AR, Zaterka-Baxter KM, McDonald SA, Ehrenkranz RA, Walsh MC, Tyson JE, Donovan EF,

12  The Practitioner 

Issue 1 • 2013


PREPARING FOR THE MARE BREEDING SEASON

by  STEVEN P. BRINSKO, DVM, MS, PhD, DACT

The seasonal breeding pattern of mares combined with registry derived time constraints, results in a narrowly confined breeding season. For most equine practitioners in the northern hemisphere, the operational breeding season extends from midFebruary through the first week in July. However, preparing the mare for the upcoming breeding season actually begins in the fall. This includes ensuring that all broodmares are maintaining good body condition and are on an adequate preventative health care program. In addition, all barren and slipped mares should be evaluated and treated as necessary in the fall. In order to facilitate the birth of foals as soon after January 1 as possible, the veterinarian is often called on to assist in breeding mares early in operational breeding season, the beginning of which precedes the natural breeding season by more than a month. To this end, artificial lighting programs and hormone administration are used to 1) hasten the onset of the breeding season, 2) induce ovulation in cycling mares being bred, 3) synchronize estrus and ovulation in individual mares or groups of mares, and 4) increase the opportunity for establishment of pregnancy in foaling mares bred early in the postpartum period.

of the year. Dopamine D2 receptor antagonists (sulpride, domperidone) have been investigated for their potential to advance the ovulatory season in mares. In controlled studies, their success when used by themselves has been equivocal except in mares in mid- to latetransition. However, results from the use of D2 receptor antagonists in combination with a lighting program have been more encouraging. Subjecting anestrous mares to 14.5 hours of light on January 10, with administration of sulpride (1 mg/kg I.M. twice daily) beginning two weeks later, resulted in a 17 day advancement of the first ovulation of the season in 86% of mares compared to lighted mares not given sulpride. This program has also been used in central Kentucky for non-cyclic race-trained maiden mares arriving at the breeding farm in February or March. For one group of 16 maiden mares treated in this manner, 10 responded (64% response rate) to treatment and ovulated 13.4 ± 4.2 days after beginning sulpride administration. In the mares that responded to treatment the pregnancy rate was 50% (5/10), and all of the mares that responded but failed to become pregnant continued to have regular estrous cycles thereafter.

Artificial Lighting

Shortening the late transition period with progestogens

The physiologic breeding season can be successfully manipulated to fit into the operational breeding season by artificially increasing the photoperiod. The minimum length of light exposure required is generally considered to be providing 14-16 hours of light stimulus (artificial plus natural) per day. Lighting programs have traditionally been thought to require a minimum of 8-10 weeks for response. Therefore, mares in the northern hemisphere are exposed to the lighting system by December 1 to establish normal cyclic activity by mid-February. Timed appropriately, lighting essentially shortens the period of anestrus and brings mares into transitional estrus earlier so that normal cyclicity is established by the time the breeding sheds open. Maiden and barren mares should be placed under lights to increase breeding efficiency. By doing so, these mares can be bred and hopefully become pregnant early in the season before stallion books get heavy with later foaling mares. Early foaling mares should also be exposed to lights. This is because early-foaling mares, which are not exposed to lights, can be at risk for entering seasonal anestrus if they do not become pregnant on foal heat breeding, especially in northern latitudes where ambient conditions can be quite harsh early in the year. In addition, mares with foals born near the first of the year tend to have a longer gestation length than mares with foals born late in the season. Early foaling mares placed under lights, tend to foal about 10 days earlier than their non-lighted counterparts.

Dopamine antagonists The exact mechanism of ovarian stimulation remains unclear. However, there is evidence that inhibition of dopamine activity in late anestrus mares can shorten the interval to first ovulation www.faep.net 

Variations of progestogen treatment of mares in transitional estrus are commonplace in the equine industry. Rationale for the use of progestogen/progesterone treatment to hasten the onset of ovulatory estrus is based on mares in transitional estrus having an insufficient storage/release of LH from the pituitary to promote maturation and ovulation of a dominant follicle. Progestogen treatment, generally suppresses LH release during administration, and has been postulated to provide storage and subsequent release of sufficient LH to induce follicular maturation and ovulation once progestogen supplementation ceases. Progesterone in oil (150 mg each day; i.m.) or altrenogest (0.044 mg/kg each day; p.o.) for 10-15 days are common treatment regimes for this purpose. If mares are in early transitional estrus (i.e., only follicles < 20 mm are present), they are unlikely to respond. For best results, ensure multiple follicles ≥ 25 mm diameter are present on the mare’s ovaries prior to instituting therapy. Estradiol, in combination with progesterone, can also be used to shorten (or synchronize) the late transition period. As with altrenogest treatment, mares should be in mid- to latetransition for treatment to be successful in initiating regular estrous cycles. The dose for estradiol/progesterone is 150 mg progesterone and 10 mg estradiol-17βintramuscularly once daily for 10 days. Some practitioners also administer 10 mg PGF2α on the last day of steroid treatment just in case some mares in the group have ovulated and formed a corpus luteum. An ovulation-inducing drug is administered to mares once a dominant follicle (≥ 35 mm diameter) is achieved. With this regimen, mares typically ovulate 18-23 days after the beginning of steroid treatment. The Practitioner  13


No commercial preparation containing both progesterone and estradiol is currently licensed and available for use in mares, but practitioners can obtain the formulation from veterinary pharmaceutical compounding companies. Progestogen treatment, with or without estradiol, has also been used beginning about 60 days after initiation of artificial lighting programs and appears to have an additive effect on inducing estrous cycles. Known as “programing”, this method of synchronization is used to get groups of non-lactating (maiden, barren, not-bred) mares bred during the first week of the season when breeding sheds open. Progestogen treatment is generally begun in late January (28-30), with ovulations expected February 14-22 (approximately three weeks after starting treatment). Breeding Soundness Examination

HISTORY Since a variety of ailments exist which may reduce or abolish a mare's reproductive potential, a breeding soundness examination should begin by gathering all pertinent medical and reproductive history regarding the mare. Reproductive information that should be part of the history includes: Age of the mare, previous breedings, number of live foals produced, date of last foaling, pregnancy losses (number and stage of gestation), breeding management, stallion(s) to which the mare was bred, genital infections and treatments. Since a variety of ailments exist which may reduce or abolish a mare's reproductive potential, a breeding soundness examination should begin by gathering of all pertinent medical and reproductive history regarding the mare. Reproductive information that should be part of the history includes: Age of the mare, previous breedings, number of live foals produced, date of last foaling, pregnancy losses (number and stage of gestation), breeding management, stallion(s) to which the mare was bred, genital infections and treatments. Information regarding the mare's estrous cycle should also be obtained. Whether or not the mare has normal estrous cycles, and exhibits strong outward signs of heat (i.e., is sexually receptive) when exposed to a stallion during estrus is especially important for Thoroughbred mares and others that are to be bred via natural cover. GENERAL PHYSICAL EXAMINATION Good general health extends the longevity of broodmares, and favors the ability of a mare to support a pregnancy to term and provide sufficient high quality colostrum and milk for optimal foal development. All body systems (e.g., digestive, respiratory, urinary, cardiovascular and nervous systems, and special senses) should receive at least a cursory examination to prevent overlooking conspicuous problems (this includes the mammary glands). It is also prudent to evaluate conformation for defective traits that are potentially heritable. The mare’s body condition score is an important part of the physical examination and should not be ignored. Using a body condition scoring system of 1-9, mares with body condition scores of 5 or more have higher pregnancy rates and fewer cycles per pregnancy than mares with lower body condition scores. Mares entering the breeding season in high body condition, and maintained in high body condition during the season, 14  The Practitioner 

have earlier onset of regular estrous cycles, higher pregnancy rates, and are less likely to lose pregnancies than mares either entering the breeding season in poor body condition, or losing body condition during the breeding season. EXAMINATION OF THE EXTERNAL GENITALIA The reproductive examination should be initiated by a thorough inspection of the external genitalia, with the conformation of the vulva, perineum, and anus being closely evaluated. Any conformational abnormalities or vulvar discharge are noted. The long axis of the vulva should be vertical, with the vulvar labia well apposed to produce an intact vulvar seal against contamination. The labia of the vulva can be parted gently, in order to document that the mare has an intact vestibulo-vaginal seal. This seal is important to deter ascending uterine infection. If the vestibulo-vaginal seal is incompetent, parting the vulvar lips will result in aspiration of air, which is heard as a "sucking" noise. TRANSRECTAL EXAMINATION After examining the external genitalia, the internal genitalia (the cervix uterus, and ovaries) are evaluated for normalcy via palpation per rectum using a systematic approach. After determining the length, width and consistency of the cervix, the uterus should be examined for evidence of pregnancy prior to proceeding with more thorough palpation. The uterus should be palpated in its entirety for size, symmetry between uterine horns, and evidence of luminal contents. The ovaries of the mare are generally "bean-shaped", and range in size from that of a golf ball to a tennis ball. The ovulation fossa can be readily palpated in the normal ovary. This is important to identify because mares can develop ovarian tumors (e.g. granulosa cell tumors; GCT) that result in substantial increase in ovarian size and loss of the ovulation fossa. Ovarian size can also be markedly increased with hematoma formation, which occurs when excessive bleeding follows ovulation and formation of the corpus hemorrhagicum. The ovaries are examined for the presence of follicles and the size of the follicles should be noted. Unlike in the cow, corpora lutea are not as readily palpable in the mare, to suggest that she is having normal estrous cycles. However, corpora lutea can be identified on the mare’s ovaries via transrectal ultrasonography. Very small (1-2 cm diameter) hypoplastic ovaries are sometimes found bilaterally, in which case gonadal dysgenesis as a result of sex chromosome abnormalities should be suspected. If one ovary is enlarged and the other is small and inactive, a granulosa cell tumor involving the enlarged ovary should be suspected especially if the ovulation fossa cannot be detected on the enlarged ovary. Sometimes, one or both ovaries may be absent. If only one ovary is missing, it was likely removed previously because of an ovarian tumor. After a thorough palpation, the reproductive tract should be examined via ultrasonography. The uterus should be scanned in its entirety making note of the endometrial echotexture and presence or absence of luminal contents, especially the amount and character of any fluid present. The ovaries are examined for follicular activity (taking note of the number, and size of follicles present on either ovary) as well as for the presence or

continued on p. 16 Issue 1 • 2013


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The Practitioner  15


absence of corpora lutea. Significant ovarian asymmetry or abnormal texture detected by palpation may indicate neoplasia. Early in the season, if it is not known if the mare has become cyclic, it can be difficult to determine if the asymmetry is due to suppressive effects of elevated inhibin from a GCT or if one ovary is still relatively inactive and the larger ovary has an ovarian hematoma. The ultrasonographic appearance of granulosa cell tumors is so variable, depending on their structure and composition, that their definitive identification via ultrasound can be problematic. However, demonstration of high inhibin, testosterone or antimullerian hormone (AMH) concentrations in hormonal assays from a mare with an enlarged, firm ovary and a small contralateral ovary will usually confirm the diagnosis of granulosa-thecal cell tumor. VAGINAL SPECULUM EXAMINATION After thoroughly cleansing the vulva and surrounding areas to avoid contamination, a sterile vaginal speculum can be inserted into the vaginal cavity to allow examination of this area. Abnormalities detected via vaginal speculum examination include persistent hymen, vaginitis/cervicitis, vaginal varicosities, adhesions (scarring of the cervical opening or vaginal vault), lacerations or tears of the posterior cervix or vaginal walls, and accumulation or purulent material or urine in the vaginal cavity. Most abnormalities of the cervix affect its lumen and cannot be readily identified by palpation per rectum. For this reason, the cervix is more thoroughly evaluated by visual inspection and digital palpation per vaginum. For digital palpation, using a sterile glove, the index finger is inserted into the cervical lumen, the thumb is apposed on the outside of the protruding cervix, and the entire circumference of the cervix is palpated between the thumb and forefinger to determine if muscle separations or lacerations are evident. Luminal adhesions can also be detected by advancing the index finger along the entire length of the cervical lumen. In some cases, particularly older maiden mares, the cervix may be difficult to dilate. Such mares tend to accumulate fluid within the uterus due to insufficient ability of the cervix to properly dilate when in estrus.

ENDOMETRIAL CYTOLOGY Cells can be retrieved from the endometrial surface to examine for the presence of an active inflammatory process using a swab in a similar manner as when obtaining the culture. Both endometrial cultures and cytologies can also be obtained via a low volume lavage method. Stained cytology preparations are examined under a microscope for the presence of neutrophils, microorganisms, and healthy or unhealthy luminal epithelial cells. Since the cytology can be examined the same day, the presence or absence of acute endometritis can be determined immediately, whereas the culture results can take several days. ENDOMETRIAL CYTOLOGY Providing the gross physical condition of the mare and reproductive tract are within normal limits, evaluation of an endometrial biopsy is probably the single most important means of assessing the mare's potential as a broodmare. Aseptic procedure is the same as that for procuring an endometrial swabbing for culture, except that it is important to pass the closed biopsy punch far enough into the uterus to ensure a representative specimen of endometrium is obtained. Biopsy specimens should be obtained at the base of one of the uterine horns where, after cessation of the mobility phase, early development of the embryo occurs. Endometrial specimens obtained too near the cervix have reduced glandular density and shallow gland penetration into the lamina propria, which prevents accurate assessment of glandular normalcy or pathology. After acquisition, the endometrial specimen is placed in a suitable fixative, such as Bouin’s solution, Davidson’s solution or 10% buffered formalin, and transported to a reference laboratory for interpretation.

Written Summary for Client/Owner As with any type of soundness examination, a written report should be given to the client/owner that summarizes findings, including any definitive diagnosis, recommended treatment, and prognosis for future fertility. This document is also useful for review in determining response to treatments and in assessing breeding outcome

ENDOMETRIAL (UTERINE) CULTURE The objective of an endometrial culture is to determine if any microorganisms (i.e., bacteria or fungi) are present within the cavity of the uterus and are causing endometritis. It must be remembered that it is easy to contaminate the swab smple with microorganisms originating from the outside environment, perineum, vulva, vagina, or cervix. Therefore, a positive culture alone, in the absence of signs of inflammation does not indicate that the mare is infected. Contamination often leads to the false impression that a mare has an endometrial infection particularly when an endometrial cytology or biopsy is not performed in conjunction with the endometrial culture. As a result, the mare may be treated unnecessarily and/or miss an opportunity to be bred. Hence, it is imperative to thoroughly cleanse and dry the mare's hindquarters, and to use a guarded swab and sterile equipment when swabbing the endometrium for bacteriologic culture. Ideally, an endometrial cytology should be obtained with every culture to confirm the presence or absence of acute inflammation. 16  The Practitioner 

Steven P. Brinsko DVM, MS, PhD, Dipl ACT ++

Received his DVM Degree from the University of Florida in 1985. ++ Completed a combined Residency and Master’s Degree program in Theriogenology at Texas A&M University in 1990. ++ ++

PhD from Cornell University, Cornell, NY, in 1995.

Four years on faculty at Colorado State University College of Veterinary Medicine and Biomedical Sciences ++

++

++

Professor and Section Chief of Theriogenology at Texas A&M University responsible for Teaching, Evaluation and Treatment of Mares and Stallions Performs Research in Multiple Facets of Equine ReproductionAuthor and Co-Author of more than 100 manuscripts related to Reproduction Current President of the American College of Theriogenologists Issue 1 • 2013


Equine Protozoal Myeloencephalitis

E

quine protozoal myeloencephalitis (EPM) is a common neurological disease of horses that have spent time in the Americas. Horses with EPM most commonly have abnormalities of gait but also may present with signs of brain disease. The disease ranges in severity from mild lameness to sudden recumbency and clinical signs usually are progressive. Two causative agents have been isolated from affected horses: Sarcocystis neurona is the cause of enzootic EPM and Neospora hughesi is the cause of sporadic EPM. Serologic surveys suggest that up to 50% of horses in the U.S. have been infected with S neurona. Serologic surveys of horses have suggested an exposure rate to Neospora spp. of 10-25% in certain regions of the U.S. (particularly the Sacramento Valley of California). EPM is considered a treatable disease although often the response is incomplete.

HISTORY AND DISTRIBUTION The disease was first recognized in the U.S. in 1964 (reported in 1970), and possibly earlier in Brazil. Since 1970, EPM has been reported in horses from most of the contiguous 48 states, Canada, and Panama, Brazil and Argentina. There also have been unpublished reports of the occurrence of the disease elsewhere in Latin America. The majority of affected horses are 1 to 5 years old, but older horses commonly also are affected. Although EPM has been diagnosed presumptively in a 2-month-old, the disease is almost unknown in suckling foals. Prevalence of EPM by breed and gender is close to that in the general horse population; however, Standardbreds and males were over-represented in two published surveys. EPM also has been reported in several ponies.

CAUSATIVE AGENT(S) Protozoa may be found in any part of the CNS, usually in association with mixed inflammatory cellular response and neuronal destruction. Schizonts (a proliferating form of the organism also known as meronts), in various stages of maturation, or free merozoites are seen commonly in the cytoplasm of neurons or mononuclear phagocytes and rarely in other inflammatory or CNS cells. The parasite is in the order Apicomplexa, that includes the family Sarcocystidae. In 1991, protozoa from the spinal cord of a horse from New York state were isolated in continuous culture in a bovine monocyte cell line and named S. neurona. Since then, many additional isolates have been obtained in monocyte or other cell culture lines from horses throughout the country (including UF). A few cases of EPM, both in the U.S. and in Canada, have been associated with Neospora hughesi.

LIFE CYCLE Species of Sarcocystis have an obligatory prey-predator twohost life cycle. The genus is named for the terminal developmental stage (sarcocyst) found in the intermediate host. The sarcocyst is the only developmental stage that is infectious for the definitive host. Because S. neurona sarcocysts have been found in only one horse (a foal), it is assumed that the horse is www.faep.net 

by  ROBERT MACKAY, BVSc, PhD, DACVIM usually an aberrant dead-end host. Ingestion of sarcocysts by the appropriate flesh-eating (i.e., predator or scavenger) definitive host results in invasion of the small intestinal epithelium and sexual proliferation and differentiation to produce oocysts. The oocysts of Sarcocystis each contain two sporocysts which usually are released before they are passed with feces. Sporocysts are immediately infectious for the intermediate host. They are quite persistent in the environment and may survive for months, even during extremes of heat and cold. Intermediate hosts are infected by ingestion of contaminated feed or water. The Virginia opossum (Didelphis virginiana) has been identified as the only definitive host in the U.S.. Several intermediate hosts including the nine-banded armadillo (Dasypus novemcinctus), the striped skunk (Mephitis mephitis), and the raccoon (Prylon locor) have been identified. Their combined geographic range covers the area where EPM occurs. Several Pacific marine mammals are naturally infected by the organism. The domestic cat also can support the life cycle but the significance of cats in maintaining S neurona in the environment is unknown. The hosts for N. hughesi are not known.

DIAGNOSIS AND EPIDEMIOLOGY Definitive ante-mortem diagnosis of EPM is very seldom possible. Proof of diagnosis post-mortem is demonstration of protozoa in CNS lesions, often done with immunohistochemical staining. The diagnosis frequently is made presumptively, even when the organism is not seen, if characteristic inflammatory changes are found. 1. Antibody tests a. ELISA tests against S neurona surface antigens (snSAGs). A newly offered ELISA that detects equine IgG directed against the surface antigens snSAG2,4/3 (Equine Diagnostic Solutions, Lexington, KY) shows considerable promise. To increase the specificity of the test, it is performed on CSF and serum and rendered as a serum:CSF ratio. A ratio of <100 is consistent with EPM whereas a ratio of >100 makes diagnosis unlikely. In certain cases (usually when there is a high concentration of CSF albumin), the lab calculates a C-value to compensate for damage to the blood-brain barrier. C-values significantly greater than 1.0 are consistent with the diagnosis of EPM. Another ELISA directed against snSAGI (Antech), which has been offered commercially for several years, is unlikely to be useful. Approximately half the S neurona isolates, thus far examined, do not express this antigen. This conceptual and practical problem with snSAGI testing likely has now been rectified by the addition of reagents that detect antibodies against snSAG5 and 6. The creator of this test (Dr. S. Ellison, Pathogenes, Ocala, FL) claims that serum titers for snSAG1,5,6 alone (i.e., without the need for serum: CSF ratios) are highly sensitive and specific for the diagnosis of EPM. The Practitioner  17


b. Immunofluorescent antibody test (IFAT) An I FAT test on whole organism targets for use with serum and CSF samples is offered by the University of California, Davis. The IFAT shows good sensitivity and specificity when tested against a small panel of "gold standard" negatives and positives, but its accuracy in typical cases encountered in the field is unknown. In our experience, the test is unreliable. It also is known to crossreact in horses infected with Sarcocystis fayeh, a common horseadapted protozoan. c. The Western Blot assay for S. neurona antibody is the original diagnostic test for EPM. Large serologic surveys from many states generally have shown overall seropositive rates of 2565% of horses tested by Western Blot. Once horses seroconvert, they probably remain seropositive for months to years. Sensitivity is high (>90%) but specificity is low (i.e. many false positives.) Western Blot CSF has somewhat better specificity for EPM although there remains a problem with false-positive results. A proportion of plasma IgG is normally filtered into the CSF so western blots may become falsely positive in horses with high titered plasma. Blood contamination during CSF collection is another important cause for false-positive Western Blot results. 2. Polymerase Chain Reaction (PCR) Experience with the test indicates that, when used alone as a test for EPM, it has low sensitivity and high specificity (close to 100%). This test has fallen into disuse because of technical concerns about the way the test is run. Ancillary Aids to Diagnosis: There are abnormalities upon CSF analysis in some horses with EPM. It has been reported that as many as 35% of horses at a referral hospital have increased protein concentration (>77 mg/dL) or nucleated cell count (>6 cells/uL). My experience is that, among horses with mild clinical signs of EPM (i.e., those that typically are encountered in practice), a very low percentage have any abnormality on routine analysis. Creatine kinase (CK) activity may be high in CSF, reflecting diffusion of BB isoenzyme from damaged CNS gray matter. Unfortunately, inadvertent inclusion of a small plug of epidural fat or dura during CSF collection can dramatically elevate CK activity, thus reducing the specificity of the test. Clinical Signs: Because protozoa may infect any part of the CNS, almost any neurologic sign is possible. Importantly, however, horses with EPM do not have a fever. The disease usually begins insidiously, but also may present acutely and be severe at onset. Signs of spinal cord involvement are seen more commonly than signs of brain disease. Horses with EPM involving the spinal cord have asymmetric (occasionally symmetric) truncal and limb weakness and ataxia. When the spinal cord behind the second sacral segment (S2) is involved, there are signs of cauda equina syndrome, which may include degrees of rectal, anal, bladder, and penile paralysis and hypalgesia of the skin of the tail and perineum. If gray matter is damaged for more than one to two weeks, there may be obvious skeletal muscle atrophy (usually asymmetric) and electromyographic evidence of denervation. Common locations for atrophy in horses with EPM are gluteals, biceps femoris, triceps, infraspinatus/supraspinatus, and serratus ventralis. EPM lesions in the spinal cord also may result in demarcated areas of spontaneous 18  The Practitioner 

sweating or loss of reflexes and cutaneous sensation. Signs noticed at the walk or during neurologic exam include any to all of the following: Pelvic sway, asymmetric stride length, toe-dragging, and circumduction of hindlimbs. Other signs may only be noted during breaking and/or training. There may be frequent bucking, headtossing, excessively high head carriage, difficulty maintaining a specific lead, and difficulty negotiating turns. Some signs which usually are attributed to primary musculoskeletal disease, such as back soreness or upward fixation of the patella(s) can be caused by weak or asymmetric use of muscle groups in horses with EPM that are in training. The most common manifestation of brain disease in horses with EPM is a brainstem syndrome with obtundation and asymmetric vestibular (VIII) nerve dysfunction. There also may be facial paralysis (VII), dysphagia (IX, X), tongue paralysis (XII), laryngeal paralysis (X), strabismus (III, IV, VI), diminished eye retraction reflex (VI), and weak jaw tone (V). With involvement of the rostral brainstem and/or cerebrum, EPM may manifest as seizures, visual deficit/abnormal menace response, and behavioral abnormality. Without treatment, EPM tends to progress but this is not always the case. Progression to recumbency occurs over hours to years and may occur steadily or in a stop-start manner. Treatment: The conventional protocols for antiprotozoal therapy involve a combination of sulfonamide (usually sulfadiazine or sulfamethoxazole) and pyrimethamine given orally. These agents act synergistically to inhibit protozoal folate synthesis. Because pyrimethamine also has slight inhibitory activity for mammalian dihydrofolate reductase, there is potential for inhibition of hematopoiesis and other toxic side-effects in treated horses. An affordable FDA-approved sulfadiazine/pyrimethamine suspension (ReBalance™; Phoenix Scientific, St. Louis, MO) became available early this decade, was withdrawn, and is now back on the market with a new label, produced by Pegasus Laboratories, and marketed by PRN Pharmacal. Compounded suspensions and pastes are offered by numerous compounding pharmacies usually at highly discounted rates. Because of the renewed availability of the FDA-approved version, the compounded drug should not now be prescribed. A single oral dose is given once daily by syringe. Because feeding, especially of alfalfa hay, has been shown to reduce absorption of pyrimethamine (or trimethoprim) by up to 50%, it is suggested that treatment is given at least an hour after and before hay is fed. Currently, it is recommended that horses with EPM are treated with sulfonamide/pyrimethamine for 3-6 months. An anti-coccidial of the triazineone family, ponazuril (Marquis®) was the first drug to win FDA approval for use in EPM. The drug is given as a dial-by-weight paste at 5 mg/kg for 28 days. In November 2003, the 5-nitrothiazole drug, nitazoxanide (Navigator®) also was approved by the FDA but was withdrawn from the market in 2008. A triazinedione, diclazuril, also has won FDA approval and a product, Protazil® (Schering) was introduced in 2011. A quinolone anticoccidial, decoquinate, in combination with the immunostimulant levamisole, is being tested and marketed in Ocala (Dr. S. Ellison, Pathogenes). Initial reports of its efficacy are promising; however, the efficacy of this treatment needs to be studied more rigorously before the results can be compared

continued on p. 20 Issue 4 • 2012


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with the multi-center studies performed for other drugs. Approximately 55-70% of horses improve with any of the above regimens, and an estimated 10-20% can be considered complete recoveries. It is rare for severely affected horses (grades 3 or 4) to completely recover and such horses may be more susceptible to relapses after the initial period of treatment. Relapses may occur over several years in at least 10% of treated horses. Treatment of horses that relapse usually is less successful than treatment of initial disease. Mild to moderate anemia (PCV 20%) is occasionally seen in horses given SDZ/PYR for 6 months. Anemia resolves within several weeks after drugs are discontinued. Rarely, neutropenia and thrombocytopenia also have been observed in treated horses. There have been isolated instances of abortions and neonatal disorders after treatment of pregnant mares, although a causal relation has not been established. Despite a theoretical concern about the fertility of stallions treated with EPM, no adverse effect has been documented. In human beings, folinic acid (5-formyl-THF), a form of bioactive tetrahydrofolate, is given to prevent or treat toxic effects of pyrimethamine. Preformed folate cannot be used by protozoa, so this practice has no effect on antimicrobial efficacy. Folic acid (the substrate of DHFR) is sometimes given to horses in an effort to prevent toxicity but on theoretical grounds probably has no positive effect and may actually be deleterious. Of far greater value is the provision of good quality folate-rich pasture or alfalfa hay. If the PCV drops below 20% or there is severe neutropenia or thrombocytopenia, antimicrobial treatment may be discontinued for 1-2 weeks until hematologic values return to an acceptable range. If signs are severe or rapidly progressive, it may be wise to give a loading dose of ponazuril or diclazuril to achieve effective CNS concentrations of drug more quickly than the usual 10-12 or 3-4 days, respectively, that are required. I usually give a full tube of Marquis (35 mg/kg in a 500-kg horse) followed by a regular course of ponazuril. Anti-inflammatory/antioxidant therapy can be used for several days during the initial period of antimicrobial therapy or during any period of exacerbation. A reasonable protocol is flunixin meglumine (1.1 mg/kg IV) twice daily for three days, then once daily for four days. Some clinicians like to give DMSO during the initial three days of treatment. When signs of brain disease are severe or the horse is in danger of becoming recumbent at onset of therapy, one to several doses of corticosteroid (e.g., dexamethasone, 0.050.1 mg/kg) is/are sometimes used. In an effort to minimize inflammatory damage and promote healing in the CNS, the antioxidant environment can be maintained throughout the treatment period by oral vitamin E supplementation (10-20 lU/kg/d), preferably as the natural form of a tocopherol (e.g., Elevate, Kentucky Performance Products). Signs of toxicity are very rare with ponazuril or diclazuril treatment; however, severe colitis, fevers, and depression have been seen in horses treated with nitazoxanide. It is widely assumed that these signs occur secondary to clostridial overgrowth in the large intestine. Some clinicians attempt to promote cell-mediated immunity by use of immunostimulants such as killed Propionibacterium acne (Eqstim), killed Parapox ovis virus (Zylexis), mycobacterial cell wall extract (Equimune IV), levamisole, alpha interferon, or 20â&#x20AC;&#x201A; The Practitionerâ&#x20AC;

transfer factor (4Life Transfer Factor). In persistent protozoal diseases of human beings, such as leishmaniasis, the efficacy of such approaches is established. Prevention: Horses ingest infective opossum sporocysts with feed or water. Opossums are omnivores, and are attracted to grains, moist or dry cat or dog food, fruit or garbage. Therefore, horse and pet food should not be left out and open feed bags and garbage should be kept in closed galvanized metal containers, bird-feeders should be eliminated, and fallen fruit should be removed. Opossums can be trapped and relocated or scared off by a patrolling big black dog. Less practically, paddocks can be opossum-proofed by placing a partially buried 2- inch x 4-inch mesh fence and electric wire on the outside of existing horse fence. It is probable that sporocysts are distributed from the point of deposition by birds and/or insects, so it may be prudent to control populations of these potential vectors, at least within horse barns. Steam cleaning has been shown to kill sporocysts, so feed and water containers could be cleaned by this technique. An issue which hasn't been addressed is the possibility of contamination of commercially-prepared feeds with S. neurona sporocysts. Because they have been heated (60 - 166 C) during preparation, "hot-processed" feeds (e.g., steam flaked, pelleted, or extruded feeds) are unlikely to harbor viable sporocysts. Because intermediate hosts do not directly infect horses, control of intermediate host populations is unlikely to be effective. An EPM vaccine was sold under limited license by Fort Dodge Animal Health. The notably simplistic approach to vaccine development, i.e., use of killed cultured whole organisms, was criticized and the vaccine was withdrawn in 2007 without having shown evidence of protection. Any of the drugs used as treatment can be used as preventatives, although there are no reliable data to support this practice. In the harness horse industry, it is common to give several high doses of toltrazuril, and low-dose decoquinate also is being marketed for this purpose.

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