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2015

SEMINAR NOTES

STUD MIDDLE MANAGEMENT SEMINAR Hunter Valley Equine Research Centre


STUD MIDDLE MANAGEMENT SEMINAR

TABLE OF CONTENTS

Page

Schedule of lectures

2-5

LECTURES Lecture 1: The dry mare

6-15

Lecture 2: Pregnancy assessment and maintenance

16-23

Lecture 3: The wet mare

24-30

Lecture 4: Insights into the foaling mare

31-44

Lecture 5: Routine foal care

45-58

Lecture 6: Deworming and vaccinations in the horse

59-87

Lecture 7: Care of horses teeth

88-95

Lecture 8: Equine nutrition

96-103

Lecture 9: A Horses foot

104-115

Lecture 10: Foal confirmation and correction

116-137

Lecture 11: X-Rays and scoping

138-152

Lecture 12: Weanling to sale ring

153-156

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Hunter Valley Equine Research Centre Hunter Thoroughbred Breeders NSW Breeders

Schedule of lectures DAY 1: Tuesday 4th August 2015 Time

Session

8.30 –

 Registration and coffee

9.00am

 Introduction

9.00 – 10.00am

Speaker Derek Field

Lecture 1: The dry mare

Vet. Jim Rodger

 Basic Anatomy

BVMs MRCVSc FACVSc

 Cyclicity  Routine Pregnancy diagnosis

Morning Tea Break

Thanks to our sponsors

10.30 –

Lecture 2: Pregnancy assessment and

Dr Joan Carrick

11.30am

maintenance

BVSc MVSc PhD

10.00 – 10.30am

“Tartuca Espresso Bar”

 Why assess & maintain pregnancies?  What causes poor placentas?  How to assess the pregnant mare?

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11.30 – 12.30pm

Lecture 3: The wet mare  Foal heat

Vet. Sean Finan MVB

 Lactational Anoestrus  “Problem mares”

12.30 –

Lunch Break

1.30pm 1.30 – 2.30pm

Thanks to our sponsors “The Hunted Gourmet”

Lecture 4: Insights into the foaling mare

Vet. Wendy Perriam

 Stages of parturition

BSc BVMS MANZCVSc CMAVA

 Post foaling evaluation

Verna Metcalfe

 The placenta 2.30 – 3.30pm

Lecture 5: Routine foal care  The normal foal

Vet. Niamh Collins MVB MSc DipECEIM

 Common diseases in the first month  Neonatal syndrome

3.30 –

Afternoon Tea Break

4.00pm

Thanks to our sponsors “Tartuca Espresso Bar”

4.00 –

Lecture 6: Deworming and vaccinations in the

Dr Catherine Chicken

5.00pm

horse

BVSc MANZCVS PhD

 Internal parasite control (deworming)  Disease control & vaccination strategies 5.00pm

Lectures closed

John Sunderland

5.00 –

An opportunity for participants to speak with

“Mystery Guest”

7.00pm

lecturers and our 'Special Guest Speaker' over a light meal and drinks.

Hunter Valley Equine Research Centre

Dinner thanks to our sponsors “The Hunted Gourmet”

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DAY 2: Wednesday 5th August 2015 Time 8.15–

Session  Registration and coffee

Speaker David Merrick

8.30am 8.30 – 9.30am

Lecture 7: Care of horses teeth  Anatomy

Vet. Sam Nugent BVSc

 The importance of equine dentistry  Common dental abnormalities 9.30 – 10.30am

Lecture 8: Equine nutrition  Essential nutrients in broodmare & growing

Dr Caroline Foote BSc.Agr.MSc. PhD

foal rations  Nutrition & skeletal disease in foals  The value of Australian pastures

10.30 –

Morning Tea Break

Thanks to our sponsors

Lecture 9: A ‘Horses foot’

Vet. Luke Wells-Smith

11.00am 11.00 – 12.00pm

 Anatomy

“Tartuca Espresso Bar”

BVSc

 Maintenance  Common foot problems 12.00 – 1.00pm

Lecture 10: Foal conformation and correction  Angular limb deformities in foals

Michael ‘Spook’ Neville Master Farrier

 Common ALD conditions in foals  Corrective procedures

1.00 –

Lunch Break

2.00pm

Hunter Valley Equine Research Centre

Thanks to our sponsors “The Hunted Gourmet”

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2.00 –

Lecture 11: X-Rays and scoping

3.00pm

 Survey radiographs “How, Why & When?”

Vet. Angus Adkins BVSc FACVSc

 Scoping at the sales  Conditions which cancel sale 3.00 –

Lecture 12: Weanling to sale ring

4.00pm

Sam Fairgray

 Vendor  Sales Company  At the sales

4.00 –

 Open discussion (Tea & Coffee available)

4.30pm

 Collection of course critiques (Survey)

4.30pm

David Merrick

Close of Seminar

The Hunter Thoroughbred Breeders Assoc. and NSW Breeders along with the Hunter Valley Equine Research Centre wishes to thank all our Speakers and Special Guests.

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Lecture 1:

The dry mare

Jim Rodger BVMs MRCVSc FACVSc

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THE DRY MARE, OESTRUS, VERNAL TRANSITION, AND PREGNANCY DIAGNOSIS Dr Jim Rodger, Jerry’s Plains Veterinary Hospital We are going to start the sessions with a look at some basic functions of the brood mare by considering the dry mare. This includes the maiden mare and we will discuss very briefly the immature female. We shall look at the equine female, then the oestrus cycle. Understanding the breeding season requires a good understanding of the transition from winter anoestrus to the regular oestrus cycle, the vernal transition. At the end of the talk we will briefly discuss the various ways of diagnosing pregnancy, the measure of the success of the breeding season that leads to the ultimate goal- a new generation of foals. Horses have relatively few problems with congenital deformities. It appears that compared with other domestic species the mare has an ability to reject deformities very early in pregnancy, which this author feels may explain our difficulty in curtailing some levels of early foetal loss. The most common abnormality appearing in the literature is that of irregularities of sexual development at the chromosomal level. In affected foals there has been a mix up during cell division resulting in gains or losses of sex chromosomes. In normal mammals females have two x chromosomes, designated XX. In males there is one X chromosome and one Y, designated XY. In the abnormal population (which is small in number!), we have described XXY, XO and various other combinations all much rarer. These changes may not result in phenotypic or grossly visible changes but do frequently result in subfertility or infertility depending on the severity or extent of the abnormality. Individuals often have a high percentage of normal cells and can have a pregnancy. This pregnancy may have difficulty in being maintained.

Early embryos start with both male and female embryonic duct systems and one system develops under the influence of early hormonal changes while its opposite component fades away. Vestigial duct systems can occasionally be identified in adult horses. Development continues through pregnancy so that even early foetuses can be readily identified as male or female which is why early foetal sex testing can be carried out by ultrasonography by 60-70 days or earlier. However complete development of the sex organs particularly the ovaries and the hormonal system is not complete until the onset of puberty which normally occurs at around 12-15 months of age

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depending on the individual. By this time the brain, pituitary and reproductive tract start functioning in synchrony, we start getting early waves of follicle development and oestrus starts to occur.

Mare are seasonally polyoestrus which means oestrus cycles only occur at certain times of the year, notably spring and summer and during this time they have many regular oestrus cycles. Much of our work during the breeding season is aimed at managing the mares oestrus cycle or arranging for matings to be carried out at the optimal time to achieve pregnancy. Equine semen lasts a relatively short time, generally about two to three days in the mare depending largely on the stallion (some mares are great incubators!). Some stallions can have sperm which lasts much longer while others may have sperm which dies much earlier which results in reduced fertility and these stallions need much more management in the timing of their matings. The average mare has 17 days of dioestrus followed by five days of oestrus. To make life difficult she ovulates around 24 hours before the end of oestrus so an amount of prediction is required to breed her at the correct time. Breedings by natural service after ovulation infrequently result in pregnancy. During dioestrus waves of follicles develop some dying off, a process known as atresia, while some continue to develop. Eventually one or more follicles start to mature. Because of the extremely large size of the mares follicle and the fact it ovulates releasing the oocyte through a special part of the ovary called the ovulation fossa few ovulations occur in any oestrus period and it is mostly only one. This is in contrast with the cow with her small follicles that can ovulate from anywhere on the ovarian surface. During special breeding programmes a cow can produce 10, 20 or more oocytes in an ovulation episode. There is evidence of a number of external factors influencing the sexual behaviour of mares. Grazing on green grass has been observed by many workers as stimulating the onset of oestrus in spring. This may not just be a straight forward nutritional phenomenon and other factors may be involved. The social interaction between mares in a herd situation has also been seen to have an effect, not only on the onset of oestrus but also fertility. External and social factors also appear to play a role. Social bonds within a group, the presence of a male, and the nutritional state of the individuals and the group also play a part.

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After the primary follicle ovulates there are cellular changes in the empty follicle. Under the influence of luteinizing hormone a corpus luteum is formed. This is so called because the body of the follicle (the corpus) has a yellow appearance (luteum). The corpus luteum produces progesterone for the maintenance of the pregnancy. In most species including cows and humans this is adequate support throughout pregnancy. However the mare of course makes it much more complicated. The oocyte becomes fertilised in the oviduct (also called the Fallopian Tube). It is incubated there for around 5 days before entering the uterus. During this time the uterus has become prepared, cleaned out all the dead sperm and bacteria acquired during mating, and getting rid of any associated fluids or inflammation. If the uterus fails in this preparation infertility or early embryonic death may result. Further changes to the uterine environment continue while the uterus decides if this new arrival is for real until it finally fixes it in one place preferably at the base of one of the uterine horns. This occurs at 16 days, just in time to prevent the next oestrus.

Virginia Osborne many years ago in Sydney University showed on the basis of extensive abattoir studies, that the natural breeding season in the Southern Hemisphere is November to February. However led by the racing industry’s calendar most breed societies have moved their selected breeding season toward the 1st August foaling date and although the thoroughbred covering season goes on to the end of the calendar year coverings drop off rapidly by the end of November. This means we are breeding mares three to four months earlier than the natural period of maximum fertility. Also of interest are the changes due to length of day. As we get nearer the equator daylight length becomes less significant. A paper written in Mexico demonstrated or confirmed that close to the equator there is virtually no distinct breeding season and mares can be found cycling all year round. This is significant if planning breeding programmes in tropical or subtropical areas such as N. Australia or South East Asia.

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So vernal transition, or “spring heating” is an annual event. It is the transition from winter sexual inactivity to the sexual activity of spring and summer. The movement from oestrus and dioestrus gradually gains momentum like the swinging of a pendulum until distinct cycles are present. In that interim periodi follicle development is slow, oestrus periods are prolonged as they fail to reach their conclusion with a successful ovulation followed by luteinisation as the hormone levels are inadequate to finish that part of the cycle Vernal transition is characterized by prolonged oestrus, prolonged dioestrus, and haemorrhagic or anovulatory follicles. The main environmental factors stimulating the transition are increasing warmth, increasing nutrition and significantly increasing daylight length. Note this synchronization is necessary given that mares need to foal in spring time to provide ideal conditions for the foal. An eleven month pregnancy means that the foaling season and the breeding season have to be at the same time of the year.

So how does light affect the mares cycle. The pineal gland at the top of the brain, the “third eye” has long been known to be the starting point .This was dramatically demonstrated some years ago when Professor Dan Sharp in the USA surgically removed the pineal from some mares to demonstrate the changes. It appears in most animals this is associated with melatonin production and the association has been well established in mares. The signal then causes changes at the base of the brain which sends signals from the arcuate nucleus to the pituitary gland. There is a push-pull balance system in place between two hormones, prolactin and dopamine. Dopamine supresses the pituitary from producing gonadotrophin releasing hormones. We are able to use this knowledge by using dopamine antagonists such as sulpride or domperidone. Hence these drugs are available for use to hasten transition to follicle development and oestrus. Once dopamine production is suppressed prolactin production increases, Gn-RH production increrases and the pituitary starts to produce follicle stimulating hormone and luteinizing hormone.

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The body likes using balances of hormones, or sometimes pulsatile releases of hormones to different effects, so the balances between what appears to be conflicting hormones can produce different results. As daylight increases melatonin production decreases. In the hypothalamus Gn-RH production increases. Gn-RH, gonadotrophin releasing hormone, releases Follicle stimulating hormone (FSH) and luteinising hormone (LH) from the pituitary. These in turn affect follicle production and luteinization hence Corpus luteum formation. Leptins are a group of hormones playing a regulatory role in fat metabolism. Regulation of metabolism enables mares to be more successful breeders when they have good bodily condition Kisspeptin is released in the hypothalamus and stimulates Gn-RH release. Discovered in 1996 it has been shown to have a crucial role in the expression of Gn-RH release and hence a pivotal role in the release of the hormonal cascade. Experiments are therefore underway to investigate its potential use in modifying vernal transition. We have discussed temperature. It is obvious in the photograph here, taken in Newmarket, England in winter that mares will benefit from indoor housing which will keep them warm. It will also make food conversion more efficient as they will not need to burn energy to keep warm. There is also a probable benefit as artificial light is used for the workers to access the barn. How much light is needed? Basically if you can read the small print on a newspaper the light is adequate. For the more precise, 10-12 footcandles, or 107-129 Lux, which would require a 100 watt bulb.

Alternatives: 16 hrs daylight /8 hrs dark Or,

2.5 hrs extended light after sunset,

Or,

1.5-2 hrs light 9 hrs after sunset.

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BEWARE: 3 days interruption to the programme once started may reset the programme at start or even revert the mare to winter anoestrus!

As you can see latitude is all important. A mare on the equator is exposed to 12 hrs daylight/ 12 hrs dark all year round so there is not much advantage in increasing day length. However a mare in Scandinavia will see little daylight in winter so the artificial changes are profound. Hence we can expect greater results in Melbourne than in Townsville. I think it is fair to say on the basis of years of experience we can feel lucky in the Hunter Valley where at this latitude seasonal daylight variation is sufficiently small that many farms can rely heavily on nutrition and warmth. Don’t forget also the tradition of rugging and extra feeds to barren mares to get them on a “rising plane of nutrition” It is also important to manage fillies out of training so you don’t cause a “shutdown” when you bring them home and turn them out to pasture. We can also see differences in local geography. It has been observed that steep sided valleys running north to south in places like the Hunter Valley often experience shorter day lengths , later sunrise, earlier sunsets, than other places which requires special management considerations. A lot of work has gone over the years to try to adapt the mare to this abnormal timing or unnatural breeding season. Once mares start to develop follicles (greater than 2cm is generally accepted) it is possible to give the pendulum a push by holding the cycle in dioestrus by the use of a progesterone mimic, altrenogest. The discovery of this was a great step forward, More work has gone into moving further up the chain in the hormonal chain. Gn-RH can be used to initiate FSH or LH production. This has been effective but unfortunately is very expensive. It has been possible to influence the natural production of Gn-RH by the daily use of Domperidone or sulpride. This was described by Besognet in 1996 and other workers since. They work by suppressing dopamine production which in turn controls prolactin release. These actions end up by releasing Gn-RH. The use of these drugs has been refined by adding other hormones such as oestrogen to the regime.

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To further investigate the role of melatonin in the mare Guillaume & Palmer in France did some experiments on its use by oral administration. They found that giving it four hours before dusk mimicked prolongation of the night. However morning administration was not effective. But this regime would delay ovulation. In reverse, giving 1 hour of light 9.5 hours after sunset mimicked the shorter night we want to achieve to start vernal transition. So traditionally the use of lights in stables has been used. Recently a group in Ireland devised a different technique. This group put pretimed blue lights into a mask that would emit light automatically turning on every night at 4 pm. This was to have the same effect,as the traditional stable lights. After field trials in 2012 they published their results in 2013 and the masks are now commercially available.

We will briefly discuss signs of pregnancy and pregnancy diagnosis. There are obviously profound changes in the hormonal system when the mare becomes pregnant. These changes have since time immemorial been the basis of pregnancy diagnosis by animal handlers. Firstly the mare ceases to have an oestrus cycle. Secondly the anabolic effects particularly of progesterone result in changes to the mare’s appearance-she “blooms�, looks really well and may have temperament changes. As time goes on her abdomen will enlarge as the foetus grows and her physical appearance changes. This all takes too long in our commercial world so manual examination was developed. Skilled rectal examiners can palpate pregnancy reasonably confidently by 15-16 days with increasing accuracy to about 70 days after which the uterus becomes more relaxed and starts to disappear over the brim of the pelvis. However confident pregnancy diagnosis is still possible. Twin conceptions particularly in thoroughbreds is a problem and ultrasonography was developed in France to rapidly become the norm for early pregnancy diagnosis. Pregnancies can be diagnosed as early as 10 days and the presence of twins detected. For those with no access to ultrasound or even reliable manual palpation chemical tests are available.

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Chorionic gonadotrophin is produced from 40-90 days with a maximum reliability at around 60 days. A precipitation test can be used. Oestrone production is evident after 120 days and testing the urine is possible using the Cuboni test Detection of an early pregnancy factor has been predicted for many years, so far with no success. Apparently there is work currently being done in the University of Newcastle, NSW to revisit the idea.

SOME REFERENCES FOR FURTHER READING

Diagnosing Disorders of Sexual Development in Horses;Male or Female? The Horse Magazine Oct 16 2010,

Lear Age and Pasture Effects on Vernal Transition in mares. Theriogenology 199747(5) 1009-18. Carnenevale et

al. Social bonds between unrelated females increase reproductive success in feral horses Proceedings of the

National Academy of Sciences. Vol 106 No33, Cameron Influence of the dopamine antagonist domperidone on the vernal transition in seasonally anoestrus mares.

J.Reprod Fertil Suppl 2000 (56) Brendelmuehl, Cross. The Role of Kisspeptins in vernal transition management in mares Rural Industries publication May 2013 .

Scott Norman Effects if Pinealectomy and melatonin replacement on LH secretion in the anoestrus pony mare 1992, Proc

12th Int Cong Anim Reprod. 4 1882-1854 Cleaver, Davis, Sharp.

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NOTES…………

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Lecture 2:

Pregnancy assessment & maintenance

Dr Joan Carrick BVSc MVSc PhD

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Pregnancy Assessment and Maintenance Dr Joan Carrick, Specialist in Equine Medicine, Scone, NSW WHY ASSESS AND MAINTAIN PREGNANCIES?

Abortion and the delivery of sick weak or small foals is a significant source of loss for the thoroughbred breeding industry. The prevention of these losses by regular assessment and early treatment can save the industry a large amount of money each year. Costs to Stallion owners The majority of service fees in this region offer a free return, so although the stallion owners have been paid the service fee, any covering option for the next season that is used by a mare that has aborted is taking the place of a new fee paying mare. For stallions with high service fees this can result in the potential loss of millions of dollars a season. Costs to Mare Owners It costs each mare owner significant amounts of money to pay for feed, veterinary fees, farriers, worming and vaccination each year and this money is lost each year a mare fails to produce a foal. In addition, the growth of the foetus during pregnancy has an important role in its future health and performance potential. Human babies born prematurely or small rarely go on to become athletes and suffer increased risk of numerous chronic diseases. There has been little research into the effect of the health of the pregnancy on subsequently racing performance. A recent review of the foals that required intensive care at Clovelly showed that although they were just as likely to have a race as their siblings, they won fewer races and earned less money. In addition, the foals that were small or premature were less likely to be sold as yearling and less likely to race. Basically, if the mare has a poor placenta then she is less likely to produce a great athlete.

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WHAT CAUSES POOR PLACENTAS?

Mare General Health It is critically important that the mare is in good health and in optimal body weight. Malnutrition can have adverse effects on placental development and foetal growth but in this region obesity is more of a problem. Obesity can have several detrimental effects on pregnant women. There has been no research into whether similar effects occur in horses. Hormonal changes associated with pregnancy are designed to ensure adequate blood flow to the placenta and consistent high levels of nutrients are available. Obesity changes the hormonal profile of a mare and can make her more susceptible to Metabolic Syndrome which can cause increased blood pressure and predispose to laminitis. It is essential that optimal and not excessive nutrition is provided for each throughout pregnancy. Mares that have severe or chronic laminitis appear to be prone to delivering underweight poorly developed foals. Severe laminitis is associated with significant changes in blood pressure and blood flow which can limit the development of the placenta and lead to poor foetal growth. Once again good objective data through research is not available for horses. Poor dental health can have a detrimental effect on pregnant women. They are more likely to have stillbirth or deliver a premature baby. There has been no research into the association of poor dental health and its effect on pregnancy in horses. Any chronic infection has the potential to allow bacterial infection of a pregnancy which leads to a form of placentitis where the infection gets in through the blood stream rather than through the cervix, similar to EAFL. Mares that are suffering from any chronic infection should have their pregnancies regularly monitored. Similarly, mares that have recurrent hoof infections may be at increased risk of developing placentitis Specific Causes of Pregnancy Loss

EHV

Equine herpes virus infection remains a significant risk for pregnant mares. It is highly infectious and can spread rapidly through a group of pregnant mares causing very high losses. The losses in the Hunter Valley in the past 10 years have been < 10 % due to good

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vaccination and stringent biosecurity protocols. Ideally mare should be kept in the same small groups for their entire pregnancies and no horses should be introduced. This is not practical for stud farms so it is important to quarantine all arrivals, keep broodmares separate from weanling, yearlings and spellers and institute isolation protocols for all cases of abortion. BACTERIAL INFECTION Systemic placentitis – This occurs when the infection enters the placenta and the foetus through the blood stream. The infection appears first in the umbilical cord, amnion, foetus and then in the body of the placenta. There are several possible causes of this type of placentitis but in this region, EAFL associated with exposure to hirsuit (hairy) caterpillars is the most common. Other causes of this form of placentitis include leptospirosis, Q fever, Neospora and Salmonella. Determining whether a mare has this form of placentitis can be challenging as the regular transrectal scan does not always pick it up. The mare has to have a more detailed abdominal scan using a powerful scanner than can measure changes deep in the placenta and foetus. Ascending placentitis – This placentitis occurs when the infection enters through the cervix. The first region to be infected is the placenta close to the cervix. The infection spreads from there through to the rest of the placenta and into the foetus. The early changes with this form of placentitis can usually be seen when a transrectal scan is done. Focal Mucoid Placentitis – It is not really well understood how this placentitis starts. There is some evidence that it may be caused by the migration of the sharp spikes from the shell of hairy caterpillars. It normally occurs in the body of the placenta and causes a thick purulent exudate between the placenta and the uterus. Quite often the foetus does not get infected but its growth is limited and small under-weight foals are produced. Many of these foals are apparently healthy when they are born close to full term. BLOOD FLOW

Poor blood flow through the placenta or obstruction of blood flow through the umbilical cord is one of the major causes of abortion in this region. Typically most of these abortions occur before 270 days of gestation but can occur up to full term. Most commonly these problems are caused by the umbilical cord being longer than normal or when in inserts into the placenta in an unusual location. There may be a genetic component to the length of the

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umbilical cord but there has not been any research done in this field. It can be quite hard to detect these problems in the pregnant mares. Once again there are no easy blood tests available. Measurement of the blood flow through the uterine artery and the umbilical arteries is possible using advanced ultrasound techniques but there has been little research in this field and so information about the changes that occur is limited. There are some drugs that seem to be effective in reducing the problems associated with poor blood flow and there is quite active research into these medications for pregnant women HOW TO ASSESS THE PREGNANT MARE? Assessment

History – The mare’s breeding history will provide useful information about the risk of aborting this pregnancy. Mares that have failed to produce a foal twice in the past 6 years are at 4 times the risk of losing the pregnancy they are carrying than mares that have produced a foal every year or only missed once. Mares that slip due to ascending placentitis produce less foals in subsequent pregnancies than mares that slip due to EAFL or blood flow problems. They are also more likely to slip the pregnancy that they are carrying than mares that aborted due to other causes. Just because a mare aborted last year does not mean she is at higher risk. Physical Examination – The shape of a mare’s vulva and perineal region is important to protect mares from ascending infections. The Caslick surgery is critically important for mares with poor perineal anatomy and it is important to check that the surgery is adequate as the pregnancy progresses. Occasionally small regions of the Caslick surgery do not seal and it needs to be repaired. It is important to assess if the mare pools urine and how effective the cervix is. Without a good vulval and vaginal seal or a functioning cervix the mare is at very high risk for ascending infections. Blood work – The general health of the mare can be checked by blood work but there are few blood tests that are useful to indicate what may be going wrong during pregnancy. Testing the concentration of progesterone and oestrogen in the blood can indicate that there are problems with a pregnancy. Paradoxically during the last trimester of pregnancy (200 + days) the progesterone levels in the blood typically rise if there is a problem with the pregnancy. If the progesterone level is very low then the foetus is most likely dead or is going to die soon.

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A high progesterone level in late pregnancy indicates that the damaged placenta is not able to process the progesterone precursors that are coming to it from the foetus and the excess levels spill over into the blood stream. With sophisticated technology available in research laboratories the different types of progesterone in the blood can be detected and a better idea of what is going wrong with a pregnancy can be determined. Unfortunately this technology is not currently available in the field. Recently measuring serum amyloid A (SAA) in pregnant mares has been of interest to detect subtle inflammation. In experimental ascending placentitis, SAA rises sharply and it stays high in the pregnancies that the foals are aborted or are born dead but decreases in the pregnancies that respond to treatment. There has been very little work to determine whether SAA is useful to predict whether a mare is in the early stages of placentitis or is having problems with blood flow through the placenta. It would be very useful to have a blood test to detect whether mares have been exposed to hirsuit caterpillars and are developing EAFL but there is currently no way to do this. Ultrasound â&#x20AC;&#x201C; Ultrasound is used widely to monitor pregnancies in both mares and women. There are significant limitations to ultrasound. It is quite expensive, time consuming and only sections of the placenta can be successfully scanned. The trans rectal scan is good at detecting ascending placentitis once it has developed but we are not good at predicting whether it is likely to develop and so the scan would need to be repeated regularly in high risk mares. To evaluated EAFL and blood flow issues a trans-abdominal scan as well as the trans-rectal scan is needed and more expensive and technologically advanced machines are needed. It also takes quite a lot of time and training for veterinarians to gain the skills required to complete a good trans-abdominal scan.

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Treatment

Many mares that have slipped are treated with altrenogest and monthly antibiotics during subsequent pregnancies. This can be a very useful treatment if the mare has slipped due to ascending placentitis but will not prevent abortion due to blood flow problems. Monthly antibiotics may help to prevent mares from aborting due to EAFL but it is more important to prevent exposure to hirsuit caterpillars. The current research into how to control processionary caterpillars will be very useful to guide management of our mares in the future. There is a huge range of unusual bacteria associated with EAFL and many are resistant to common antibiotics, so blanket treatment of all mares can be completely ineffective. If there is a group of mares that may have been exposed to hirsuit caterpillars it is important to scan them to monitor how effective treatment is. It may be necessary to use different antibiotic regimes for different mares. Mares that have slipped due to poor blood flow can be very challenging for future pregnancies. There has been very little research into long cords and poor blood flow and until recently it was thought to be due to random chance and not likely to recur. However there are some mares that do repeatedly lose pregnancies due to poor blood flow and treatment with antibiotics will have no effect in preventing abortion. Monitoring high risk mares and treating problems early improves the chance that these mares will produce live healthy foals. This adds more costs for a mare that has failed to produce good returns and the cost needs to be balanced carefully against the potential earning of her progeny. Every year the mare fails to produce a foal adds further losses for the owner and reduces the value of the mare. Sum mary

Know the risks for each mare Review breeding history Investigate all losses Develop a breeding plan that balances Potential value of progeny Costs of monitoring and treatment

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NOTES…………

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Lecture 3:

The wet mare

Sean Finan MVB

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The Wet Mare Foal Heat Breeding, Lactational Anoestrus & The Problem Mare Dr Sean Finan

Foal heat breeding

The gestation of the mare is on average 340 days, although there is significant variation in pregnancy length. To maintain a yearly interval between foals the mare must conceive within 25 days of foaling down. The Thoroughbred markets appetite for early foals is justified by scientific studies that have shown that early foals are more successful in their racing careers than their counterparts that are born later in the season. The mare is unique in that the uterine involution and return of reproductive cyclicity occur rapidly after foaling. Breeding on this first post foaling heat, with careful case selection can result in excellent pregnancy rates and maintain a yearly foaling interval. Onset of oestrus is 5-12 days in 90% of mares with the average mare coming into season on day 10 post foaling (+/-2 days). In studies of a large number of mares:

43% of mares ovulated by day 9 93% ovulated by day 15 97% ovulated by day 21

As the season progresses foal heat and ovulation may occur earlier, a study in Texas found that mares who foaled in late Spring/early Summer ovulated 3 days earlier than mares that foaled early in the breeding season. In mares that have had an uncomplicated foaling the histological (microscopic) appearance of the uterus is back to normal by day 14-15 after foaling and by this time the uterus will be back to its normal size. There can be significant drawbacks associated with foal heat breeding and they need to be carefully considered when making breeding management decisions. These drawbacks

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include a 10-20% reduction in pregnancy rate and an increased rate of early embryonic death, particularly if the pregnancy inhabits the same uterine horn as the previous season. These negative aspects can be reduced and avoided by carefully selecting mares to breed on foal heat.

The four rules of foal heat breeding: 1. Mare younger than 14yo. 2. Uncomplicated foaling. (Including timely passing of the placenta) 3. No evidence any uterine abnormality. (the uterus is involuted to it normal size and there is no intraluminal fluid) 4. Ovulation occurs on day 10 or after.

Lactational Anestrus

Lactational anestrus describes mares that fail to cycle having recently foaled. Mares may have a normal foal heat and then stop cycling, while others may cease cyclicity even before having a foal heat. It occurs in about 3% of mares but can be as high as 16% in poor conditions. It is likely that lactation is only a minor factor in this condition and it appears that short day length is a much more significant contributor. Other risk factors include, inadequate nutrition, chronic pain or stress and potentially endometritis. It is more common in mares that foal earlier in the season and it is much less likely to happen in mares that foal after October 1st. Treatment options include GnRH agonists (Fertagyl & Receptal) and Dopamine agonists (Domperidone & Sulpiride). Treatment can be prolonged and frustrating so prevention is advised. Mares should be of adequate body condition score and enjoy adequate nutrition at the time of foaling and during the post foaling period. Keeping early foaling mares â&#x20AC;&#x2DC;under lightsâ&#x20AC;&#x2122; in late pregnancy and the post-partum period is a good preventative, there is the added benefit that light therapy in the early foaling mare can shorten pregnancy by an average of 10 days.

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The Problem Mare

The problem mare is a very broad topic with entire books dedicated to the cause, diagnosis and treatment of difficult breeders. In this presentation we will focus on the most common and most frustrating aspects of breeding the problem mare. Technically speaking a problem mare is any mare on a well-managed stud farm that is bred to a fertile stallion and failed to conceive on 3 or more cycles, in practice however the classification of a mare as being a problem breeder is a management decision and it may become clear much earlier than the 3 rd negative cycle that a mare may be a problem. There are a myriad of reasons that mares may become problem breeders but the most common issue confronted on breeding farms on a regular basis is endometritis characterized by excess uterine fluid. The presence of a small amount of fluid in the uterus after breeding is a normal finding and this fluid represents the mares normal response to the contamination of the uterus with debris and semen at breeding, this fluid should have dispersed by 48 to 72 hours. Fluid is evacuated by either being resorbed by the mare or for the majority of the fluid, draining through the open cervix. A percentage of mares mount an inappropriately intense response post breeding resulting in a large volume of uterine fluid and often this can be combined with bacterial infection and poor conformation which prevents the normal expulsion of fluid out of the uterus through the cervix.

Common diagnostic tools available when evaluating problem breeders include:

Visual appraisal: -

Body condition and perineal conformation

Rectal palpation: Ultrasonography: Culture and Cytology:

Combining these procedures dramatically increases the accuracy of the result. Low volume lavage culture and cytology allows an additional boost in accuracy as it provides a sample from a larger area of the uterus compared with a swab.

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Biopsy:

This involves the harvesting of a small portion of the uterine wall and evaluating it microscopically. Typically the result includes a grading of the sample with each grade corresponding with a probability of that mare successfully carrying a pregnancy.

Hysteroscopy:

This involves passing an endoscope into the uterus and visualizing its internal structure.

Treatment plans for these mares center around some key objectives: Correction of any conformational/ functional issues Poor perineal conformation should be addressed, this is most commonly done by performing a Caslick’s operation however some cases may need additional techniques such as perineal body reconstruction (Deep caslick or Gadd’s technique) or a perineal body transection (Pouret’s procedure). These techniques aim to improve the ability of the vulva to prevent aspiration of air and manure which will obviously reduce inflammation and decrease the risk of infection.

Promote uterine clearance This can be achieved by using ecbolic drugs the most common of which is oxytocin. These drugs work by stimulating the uterus to contract and expel any intrauterine fluid. Unfortunately oxytocin is quite short acting and so it must be administered several times daily to maintain its effect. Cloprostenol, a specific form of PGF2α is sometimes used to aid uterine clearance, it works in a similar way to oxytocin but the muscular contractions it causes are not as strong however they last much longer. A word of caution with Cloprostenol, as it is a synthetic form of PGF2α it causes luteolysis of the CL and so should not be used after ovulation. Although we know that PG does not work on the CL for the first 5-7 days after ovulation, recently it has been shown that prostaglandin injected anytime in the first 5 days after ovulation diminishes the ability of the CL to produce progesterone temporarily.

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Uterine clearance is also promoted by lavage of the uterus with saline. This technique dilutes and physically removes inflammatory fluids, bacteria and debris in an effort to break the cycle of inflammation. Typically lavage is achieved using one liter bags of saline and flushing is repeated until the returning fluid is clear.

Treat Infection Intrauterine antibiotics are the main stay of endometritis treatment. Intrauterine treatments are useful as they allow high antibiotic concentrations in the uterus, these concentrations would not be achievable with systemic antibiotics alone. Recently there has been quite a bit of discussion about the role of biofilm in bacterial endometritis. Bioflim is a substance produced by the bacteria that protects them from the actions of antibiotics. There are treatments that can disrupt the biofilm and allow antibiotics access to the bacteria, these treatments include N-acetylcysteine, tris EDTA and hydrogen peroxide. Biofilm is difficult to grow in the lab and so often we include these drugs in our treatments on the suspicion that there may be biofilm present.

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NOTES…………

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Lecture 4:

Insights in to the foaling mare

Wendy Perriam BSc BVMS MANZCVSc CMAVA

with

Verna Metcalfe

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Basics of Foaling - Care of the mare before, during and after, and of the foal at birth Dr Wendy Perriam

Monitoring and preparing the mare for parturition: Mares should be managed attentively during pregnancy to ensure the birth of a strong healthy foal. Maintaining the mare in good health, being familiar with the signs of impending parturition, and providing a suitable foaling environment will increase the likelihood of a healthy foal. Managerial programs will vary between properties and individuals and are often a reflection of prior experience, available expertise and financial considerations. The following discussion includes aspects of routine care for the mare and her foal in those crucial periods before, during and after foaling. It is advisable to move the mare to the area designated for foaling 4-6 weeks before her due date to allow the mare to become acclimated to the foaling premises and handling procedures. During this time period the mare is exposed to local pathogens enabling her to mount an immune response; antibodies to local pathogens may then be passed onto the foal via ingestion of colostrum. A month before foaling all mares should minimally receive a vaccination for tetanus. Individual stud farms may choose to vaccinate against other endemic diseases at this time (e.g. Rotavirus, salmonella, strangles). If the mare has had the vulva sutured (Caslicked) this may be opened approximately 2 weeks prior to her due date or when foaling appears imminent.

Gestational length: In mares the reported range of â&#x20AC;&#x153;normal gestational lengthâ&#x20AC;? is highly variable with a most frequently reported range of 320-360 days. The mean is 341 days however 1% of mares may carry for a year or more. It is therefore difficult to define what constitutes a pre or post term pregnancy on days of gestation. A mare that has foaled in previous seasons can serve as her own control with respect to expected gestational length- if her gestational length exceeds 2 weeks the pregnancy should be checked.1 Trans-rectal and or abdominal ultrasound can be used to assess foetal size and activity, foetal heart rate reactivity in response to foetal movement, placental thickness and integrity, and quality and quantity of foetal fluids.

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During the last week of gestation an unknown stimulus results in a hormonal change in the foetus resulting in elevation of foetal cortisol. This initiates a cascade of events to result in readiness of the foal for birth. The final stages of maturation are critical for the foal to ensure a viable outcome. Note that foals born before 320 days are typically premature and frequently nonviable2.

Predicting when foaling might occur: Throughout the last month the mare should be examined frequently for physical changes that indicate imminent foaling. Physical changes may include vulval laxity (elongation and softening), scant vulvar discharges, relaxation of the pelvic ligaments, udder enlargement and a change in the amount and character of mammary secretions. Mammary gland growth becomes quite apparent in the last month of gestation particularly in the last 2 weeks. Filling of the teats and changes in mammary secretion occur nearer to foaling. The udder typically becomes engorged in the last few days before foaling. Accumulation of waxy secretions on the teat ends from early colostrum formation usually occur 1-4 days before foaling- sometimes as early as 2 weeks before foaling â&#x20AC;&#x201C; and sometimes not at all. Occasionally milk leaks from the mammary glands for several days to weeks before foaling resulting in a loss of colostrum. Monitoring milk secretions is a valuable tool for predicting readiness to foal. Secretions change from straw coloured fluid to a milky white. Eventually a thick viscous fluid that is yellow to orange in colour becomes apparent as colostrum formation occurs2. Laboratory measures to predict foaling may be used. An increase in Calcium accompanied by inversion of Na+ and K+ concentration indicates readiness. Calcium concentration rises sharply 24-40 hours prior to parturition and Na+ and K+ invert (Na+ down and K+ up) within 3-5 days of parturition. These measures may be misleading in mares with precocious udder development and premature lactation as a result of placentitis .

Stages of Parturition (labour) Stage 1 â&#x20AC;&#x201C;This is the period of initial uterine contractions. Stage 1 is of variable length with subtle clinical signs; intervention is not required at this time. (Check she is no longer caslicked!)

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The mare may be restless, frequently urinate or defecate, sweat, have a reduced appetite and move away from the herd. This stage is associated with the critical but often under-appreciated period of foetal repositioning in preparation for delivery 3. A full term foetus undergoes purposeful movements to rotate the head and forelimbs into the dorsal position. This is followed by extension of the forelimbs and neck into the pelvic canal. The stimulation to initiate these movements is not known but regardless, given the low rate of dystocia, this is a remarkably efficient process. Stage 2-This stage begins when the mare breaks water -note the time this occurs. It is of short duration and is characterized by strong uterine contractions and delivery of the foal. Stage 2 is often described as an explosive event with delivery of the foal occurring within 20minutes. Several gallons of allantoic fluid are expelled when the chorioallantois breaks. If the placenta doesn’t rupture the red velvety surface of the chorioallantois appears (a condition referred to as ‘Red Bag’ delivery) – this membrane should be manually ruptured and the foal delivered expediently. A red bag delivery indicates the placenta is separating from the endometrium and fetal oxygenation will be impaired. Most mares deliver in lateral recumbency and will often get up and down between active contractions. Initially the foal’s forefeet should present at the vulva with the hooves facing down. One leg should be slightly in front of the other with the white amniotic membrane covering the feet (the amnion can look like a white balloon). The foal’s muzzle then appears resting on the carpi (knees) of the front legs. The most forceful contractions occur when the head and shoulders pass through the mare’s pelvis. The amnion usually ruptures at this point. If necessary, assistance can be provided at this time by gently pulling on the foal’s forelimb’s in synchrony with the mare’s abdominal press. Once the foal’s hips pass through the pelvis the mare usually rests for at least several minutes with the hind legs of the foal remaining inside the mare. If the foal has ruptured the amnion and cleared the fetal membranes from its nose, is breathing normally and is able to move into a sternal position, the foal and the mare do not need to be disturbed. Let the cord break naturally. If manual separation is deemed necessary the cord should be grasped with one hand on each side of the pre-determined break point about 3-5cm from the foal’s abdomen. Do not put tension on the abdominal wall and the cord should not be cut. Disinfect with 0.5% chlorhexidine (superior to iodine). Disinfect the navel several times per day during the first few days of life. If the mare has not risen the foal can be moved to near the mare’s

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head- this may reduce the likelihood of the mare accidentally stepping on the foal when she rises. Allow Dam-foal interaction to permit the development of a strong bond.

1

If after 10 minutes of second stage labor there is no progress, the position of the fetus should be checked. Use a clean and well lubricated arm. The vulva should be cleaned and a clean rectal sleeve is advised for this procedure. If the forelimbs and nose are present allow another 10 minutes of labour. If strenuous activity fails to advance the foal or the foal is not presenting as described, intervention is indicated. Walk the mare and obtain veterinary assistance. Intensively managed foaling units will routinely check the presentation of all foals at the outset of stage 2 labour. Maiden mares have tight birth canals and are at high risk for forcing the feet of the foal through the roof of the vagina and floor of the rectum. When safe to do so, maiden mares should be checked early in stage 2 labour to allow for foal repositioning when required. Stage 3- this stage is associated with mild post-partum uterine contractions and passage of the placenta. Expulsion of the foetal membranes should occur within 3 hours of birth. Immediate post foaling evaluation –normal foals2 Heart Rate Respiratory Rate

≥ 60 beats per minute first 5 minutes ≥ 60 breaths per minute and regular

Muscle Tone

Foal should be able to sit in sternal by 1-2 minutes

Responsiveness

Nasal or ear stimulation should induce active avoidance

Suck Reflex

Present between 2-20 minutes, most by 10 minutes

Time to Stand

Average 1 hour. Longer than 2 hours considered abnormal

Time to Nurse

Average 2 hours. Longer than 3-4 hours considered abnormal

Temperature

37.2-38.6C; non stressed value in mild weather

Nb. HR – 80-130 in first hour; day 1-5 80-120bpm.

RR – first 30 mins 60-80/min; 1-12 hours

of age 30-40 per minute

Care of the newborn foal on the stud Delivery of an alive foal not only provides a sense of relief but may also provide a misguided sense that all is now well – especially when the foal stands and nurses3. Many neonatal foals may appear to be completely normal and within a few hours can be severely compromised. Initial clinical signs of many disorders may be vague and go unnoticed 4.

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The immediate postpartum examination is extremely important as early detection of abnormalities and appropriate interventions are crucial to the outcome of compromised foals 3. Foaling attendants should be experienced in foal delivery and resuscitation and be able to recognize post foaling abnormalities. Immediately after delivery strong respiratory movements should start within 30 seconds, the mucus membranes should become pink within a minute and the heart rate should be between 60 and 120 bpm. A heart rate of less than 60 is considered abnormal. Many studs have intranasal oxygen available that can be administered to any potentially compromised foal. If in doubt administer intra-nasal oxygen. The umbilical cord should be allowed to break naturally; if there is excessive bleeding from the umbilicus firm digital pressure with a gloved hand or clamp should be applied. Apply antiseptic to the umbilical stump. At this stage it is pertinent to administer an enema to assist in passage of meconium. A phosphate enema such as Fleet® or mild warm soapy water may be administered very gently into the rectum. After 5 minutes the normal foal will respond to external stimuli and will have moved into sternal recumbency. A suck reflex should be present by 10 minutes after birth. Most stand within an hour and nurse within 2 hours. Thereafter remain bright, inquisitive when approached and be able to return to the udder and nurse consistently Foals that have not nursed from the dam by 3 hours should be supplemented with good quality colostrum either by bottle or nasogastric tube. Any deviation from the above behavioural timeline should initiate professional attendance.

Colostrum Colostrum ingestion is critical not only for passive transfer of IgG but also is a rich source of calories, Vitamin A and E, white cells, cytokines, growth factors, hormones and enzymes. Laxative properties have also been ascribed to its ingestion.5 Normal colostrum IgG concentration is >3000mg/dl and may exceed 9000mg/dl in some mares. This declines rapidly to negligible levels within 12 hours of delivery if nursed by healthy foals. The ability of the foal’s GI tract to absorb the large Immunoglobulin molecules decreases dramatically within the first 3-6 hours of life. Maternally derived antibodies can be detected in foal blood within 6 hours of colostrum ingestion 5 and routinely should be measured via blood test. Healthy foals consuming adequate amounts of good quality colostrum should have serum IgG concentrations of > 8g/L by 12-24 hours of age. Failure of passive transfer (FPT) is diagnosed when IgG ≤4g/L at 24 hours of age and supplementation with an oral or intravenous IgG source is indicated. Partial failure of passive

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transfer is diagnosed when Igg is 4-8g/L; supplementation may also be considered for these foals. Colostral quality can be evaluated immediately after delivery (before the foal nurses) using either a colostrometer or a Brix refractometer. The colostrometer measures specific gravity; good quality colostrum measures > 1.060. The brix refractometer measures refractive index with good quality colostrum measuring â&#x2030;Ľ23-25%. Poor quality colostrum occurs due to premature lactation, poor maternal immune or nutritional status, exposure to endophyte infected pasture, advancing maternal age and breed. If colostral quality is poor administer an alternate high quality source of colostrum by 12-18 hours of age. For example: If Brix refractometer < 15%= administer 1litre of a colostrum from a colostrum bank (over 4 feeds). If Brix 15-20% administer 500mls of colostrum from colostrum bank (over 2 feeds) If Brix 20-23% administer 250mls of colostrum from a colostrum bank If colostrum measures > 23% and the mare is not a maiden it is advisable to obtain and store 250mls of pre-suckle colostrum. Freeze and store in a well labelled and dated bottle. Storage in a domestic freezer is acceptable for 12 months (to retain IgG concentration.); storage at minus 70degrees C allows for permanent maintenance of all components 2. Do not use a microwave to thaw colostrum prior to use as it will denature the proteins.

Observations over the first few days of life Most foal deaths occur within the first week of life and particularly within the first 48 hours 2. It is important to realize that newborn foals with recently acquired infection look their best shortly following birth and may first show obvious signs of problems only after illness is well established. Unless problems are detected early these foals may die or require expensive long term therapy. Check the mammary glands of the mare to ensure the udder is soft and well nursed on both sides.

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Observation:

Considerations:

Mucus membranes

Should be moist and pink with swift refill time Jaundice (yellow membranes) – call vet immediately – NI or sepsis Dry- dehydrated Congestion or petechia (red dots)= sepsis

Eyes

Check for entropion (lid rolled in) ** most commonly the lower lid Check for cloudiness (opacities) – foals may show no discomfort with corneal ulcers Injection of sclera (reddening of white of eye)- may occur with dystocia or sepsis

Ribs

Fractures are common – notify vet if suspect foaling trauma, keep quiet & minimize handling

Umbilicus

Monitor size – rule out infection if large Bleeding Patent urachus (urine leaking) - often a nonspecific sign of concurrent disease. Umbilical hernia

Meconium

Passed in first few hours – routinely use a phosphate enema at birth to prevent retention Milky yellow faeces passed once meconium has cleared. Second enema if meconium retention – care with sensitive rectal mucosa. Do not repeat enema more than once. High retention can occur and requires veterinary intervention Foals nursing poorly are prone to meconium retention (cause and effect)

Urination

Within 12 hours of birth (later for fillies than colts) Should pass dilute pale yeallow urine – concentrated urine suggests dehydration

Abdominal size

Monitor for distention – urine or meconium retention

Milk at nostrils

Foal not nursing properly Cleft palate Pharyngeal incompetence

Limbs

Laxity – self resolves. If severe apply heel extensions to protect heel bulbs; do NOT bandage limb as this will cause further laxity. Flexural limb deformities – immediate support may be requiredbandage/splint/cast.

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The Placenta: The placenta should pass within 3 hours. Every placenta should be routinely weighed and examined thoroughly. The normal weight of the placenta is 10-11% of foal’s body weight. If the placenta is unusually heavy or light this should prompt veterinary intervention to examine the foal and assess the membranes. Foaling attendants should also routinely examine the placenta to check for potentially serious abnormalities- such as gross placentitis or partial retention of foetal membranes. Use hygiene when handling the placenta so as not to spread bacteria back to foals or mares. To examine the membranes lay the placenta out on a wet surface (non-stick) – often described as a “Reverse F”.

chorionic side Allantoic side

opening at cervical star.

Examine the surface that was adjacent the foetus- the allantoic side. It should have a smooth grey/white surface. Turn the placenta inside out and examine the red velvety surface (chorionic side)- a uniform red-brown appearance due to the presence of villi. Areas where villi were not present are smooth and pale as seen at the cervical star. The pregnant horn is usually longer and thicker and more oedematous than the non-pregnant horn. The non-pregnant horn is the most likely section to be retained – carefully assess that the tip of the horn is present in its entirety contact a veterinarian if there is any doubt. The amnion is white-mottled grey and semitranslucent. Changes in colour occur with meconium staining or haemorrhage. The hippomane is the soft rubbery usually brown/yellow oval -shaped mass that is a composite of minerals mainly from

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foetal urine and placental cells. It is of no clinical significance. The umbilical cord has 6-8 even twists along its length and the normal umbilical cord length is 36-83 cm with mean of 55cm.

Dystocia A difficult birth, which is referred to as a dystocia, is uncommon in the mare but when it does occur it represents a true emergency. Immediate intervention is indicated if a positive outcome is to be obtained. The short explosive nature of stage 2 labor in the horse allows little room for error and even small delays can lead to significant problems for the newborn foal and for the dam. The ultimate goal is to save life of the foal, save the life of the mare, and preserve future fertility7. The incidence of dystocia in thoroughbreds is approximately 4% and is usually associated with malposture of the head, neck or limbs. (Unlike cows, where foetal/maternal disproportions are common7). Mild dystocia is commonly managed on the breeding farm by foaling personnel. It is important to have a basic kit of suitable obstetrical equipment in addition to the routine foaling kit. * Sterile obstetrical lube (preferably with a sterile pump and tubing) ≥5litres, preferably warm * Obstetric ropes and/or chains and handles * A foal emergency resuscitation kit -“crash kit” * Ideally an oxygen tank with regulator attached to soft flexible tubing. Note calving jacks are not suitable for foaling mares and should not be used. Foaling mares can behave quite violently and in an unpredictable way. Stocks are generally not appropriate because many foaling mares will collapse without warning. Indications that there is a problem with stage 2 labor7: 

Failure of any foetal parts or amniotic membrane to appear at the vulval lips after ~ 5 minutes of waters breaking

Absence of strong contractions &/or no progression in the delivery process after~ 10 minutes of the start of stage 2 labour

Foals hooves upside down

Any abnormal combination of extremities appearing at the vulva (anything other than front feet & nose)

Any of these signs should prompt an examination of the foetus per vagina to determine if further intervention is required. Early intervention is important before the foal becomes wedged in the birth canal. Timing is critical.

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First rule of obstetrics = Cleanliness! Second rule =Lubrication! Third rule = Compassion! Wrap tail, clean the perineum, clean your hands and arms and apply clean lubricant +/obstetrical sleeve if desired. Vaginal examinations may be made using rectal sleeves and or surgical gloves however this may reduce sensation and this can hinder attempts at correction. Repeated vaginal examinations will traumatise the mare’s tissues and should be avoided.

Keep track of time – progress should be observed every 5 minutes or consider an alternative approach. It is recommended to call a vet for assistance in the following circumstances 8: If there has been no progress toward delivery after 10-15 minutes from rupture of CA If progress stops abruptly If mare becomes acutely painful or exhibits signs of shock If attendant is unsure if a problem exists If attendant is confident a problem is present If attendant does not have the knowledge training or ability to identify or correct the problem, Advice to the attendant whilst waiting for help could include keeping the mare walking to reduce straining and pain, and reduce the possibility of pelvic impaction of the foal. Allowing the mare to get up and down may help rotate a foal that is upside down and if a red bag is present the immediate rupture and delivery of the foal should be advised 9. Provide accurate information to the attending vet – how long has second stage labour been underway, when was the mare due, what manual intervention has been performed and what findings were determined. Has the foal shown any obvious movement to suggest it is still alive? In valuable breeding stock it is especially important not to risk major injury to the cervix through over enthusiastic vaginal delivery when caesarean section may be more appropriate. Short duration general anaesthesia may be indicated to enable hoisting of the mare’s hind quarters to allow repulsion of the foetus and repositioning for an assisted vaginal delivery. During delivery the force required to extract the foal should be no more than the strength of 2 reasonably strong persons. If extraction is ineffective consideration should be given to determine if the dystocia has been corrected. If caesarean is not an option and the foal is dead an experienced obstetrician can perform a fetotomy.

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Once the foal is delivered it at risk of a range of hypoxia induced disorders, as well as ruptured bladder, fractured ribs (or other trauma), failure of passive transfer, and it is common for the mare to retain her placenta. Even if the foal initially appears normal it is considered high risk for developing complications and should be managed attentively. Veterinary intervention may save the life of a foal in the event of a dystocia. However the undisputed key factors in foal survival are early recognition of a foaling difficulty by breeding farm personnel and an early call for assistance.

Post-partum problems in the mare Reproductive emergencies are relatively uncommon in the mare but the vast majority of those that do occur arise during late gestation, at foaling, or in the immediate post-partum period9. The most common post foaling complications are retained foetal membranes and acute septic metritis. Uterine prolapse or inversion of a uterine horn, uterine tears and severe hemorrhage or trauma are less common but important to recognize 9. Prolapsed bladder, prolapsed intestine, miscellaneous gastrointestinal conditions are rare post foaling complications. Urinary incontinence is often self-limiting however check the mare can actually void urine and the bladder is not overly distended. Mastitis is more frequently observed post weaning than immediately post foaling and may indicate the foal is not cross nursing. Retained Placenta: In the first instance a retained placenta is not an acute emergency, however if it is not dealt with properly and adequately it can rapidly result in progression to acute septic metritis (a severe infection of the uterus). The potential to cause septicaemia or endotoxaemia which can in turn result in laminitis and or death are very real consequences of inadequately managed retained foetal membranes. Normal passage of the placenta is within 1 hour; membranes are defined as retained after 3 hours. The general incidence varies from 2-10% of all deliveries, with RFMâ&#x20AC;&#x2122;s more common following dystocia, induced parturition or caesarean section. The most frequently retained section of the placenta is the tip of non-pregnant horn â&#x20AC;&#x201C; this area of the placenta should always be carefully evaluated to ensure the entire tip has been passed. Any retained tissue rapidly becomes devitalized and provides a perfect medium for bacterial proliferation â&#x20AC;&#x201C; a process that accelerates from around 6-8 hours post birth. Prevent infection by encouraging the timely passage of membranes. The initial approach commonly includes oxytocin from 3 hours post foaling 10-20i.u. Repeat 2 hours later. Manual

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removal is contraindicated. Veterinary intervention usually involves large volume lavage to encourage placental detachment and to dilute toxic products in the uterus. It is not uncommon for this process to take several attempts in order to avoid aggressive manual removal. In the interim the mare will require prescribed medication such as antibiotics and anti-inflammatories. She should be monitored very closely for fever, depression, inappetence, an increase in digital pulses, heat or lameness, and any other sign of systemic disease.

Conclusion Foaling is a natural and frequently efficient process, however when faced with any deviation from normal a â&#x20AC;&#x153;wait and seeâ&#x20AC;? approach is unlikely to result in a favourable outcome. Although much can be learnt from bitter experience the take home message is to pay close attention to detail and to call for professional assistance early. Foaling attendants are the key to ensuring the best result for the mare and her foal.

1. Manual of Equine Reproduction 3rd edition, Brinsko S. P., et al, 2011, Mosby Elsevier, Missouri USA. 2. Madigan J. E., The Manual of Equine Medicine, Publisher; The Manual of equine neonatal Medicine (www.equineneonatalmanual.com/). International Publisher: International Veterinary information Service, Ithaca NY, last updated 25FEB 2014 3. Govaere J et al., FoalinMare: Insights inside the Foaling Mare., Proceedings of the Annual Convention of the AAEP 2009 p266-267 4 McAuliffe S.B. & Slovis N, Colour Atlas of Disease and Disorders of the foal, 2008, Saunders Elsevier Philadelphia PA., pp 1-13 5 Vaala W., New Perspectives on the Late-Term Mare and Newborn Foal., Proceedings of the Annual Convention of the AAEP, Orlando, Florida 2007 pp 281-292 6 Obrien, P., Care of the neonatal foal on the stud, Proceedings of the 50th British Equine veterinary Association congress Liverpool, UK., 2011, pp162-163 7 Turner R.M., Lessons learned from Dystocia Dilemmas Proceedings of the AAEP Resort Symposium, Oranestad, Aruba, Netherlands Antilles. 2013 pp 125-132 8 McCue P., Approaches to dystocia in the field, Proceedings of the British Equine Veterinary Association Congress, Manchester UK., 2013 p19311 McGladdery A., How to manage a difficult foaling, Proceedings of the British Equine Veterinary Association Congress Liverpool UK., 2011, pp247-248 9 Stout Tom A.E., Post partum Problems in the Mare, Proceedings of the Annual Meeting of the Italian Association of Equine Veterinarians, Montesilvano Italy., 2011 pp 227-230

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NOTES………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ………………………………………………………………………………………………………………………

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Lecture 5:

Routine foal care

Niamh Collins MVB MSc DipECEIM

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Routine Foal Care- What Issues Can They Encounter In the First Month of Life Dr Niamh Collins MVB MSc DipECEIM Specialist in Equine Medicine Scone Equine Hospital The Normal Foal It is important to know the normal behaviour and parameters of a neonatal foal so the subtle abnormalities of a sick neonatal foal can be detected (Table 1). A normal foal after birth should be immediately active and trying to support its head and sit sternal. The foal should be responsive and touching the foal’s nostrils and ears should evoke a brisk response. The foal should develop a suckle reflex within 20 minutes of birth. This can be assessed by placing a clean finger in the foal’s mouth. Shortly after birth the foal should be attempting to stand and should be able to stand and nurse from the mare within 2 hours. The foal may need some guidance to find the teat and some mares may need to be restrained so the foal can nurse. This first nurse of colostrum is very important to the foal’s health as the foal is born without any immunoglobulins and relies on the absorption of immunoglobulins and other factors from the colostrum to help prevent disease. After nursing the foal should pass meconium and then lie down and sleep. The foal should subsequently get up readily and nurse about every 30 minutes.

When awoken the foal should get up, stretch and then go to nurse. It is very important to bend down and watch the foal nurse, ensure it has a good tongue seal, and no milk is coming out of its nostrils. A sick foal may stand under the mare and look as though it is nursing but not be sucking from the teat. Many of these foals have “milk staining” of the face which is an early sign of a sick foal. Foals which are not nursing can have failure of passive transfer, become dehydrated and hypoglycaemic. After nursing the foal should urinate (if it didn’t prior to nursing), be inquisitive, investigating the surrounding area and then lie down to sleep. Foals which do not do this are most likely to have a problem. Some sick foals forget how to lie down and fall asleep on their feet.

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Table 1: Parameters of a newborn foal. Normal newborn foal

Abnormal newborn foal Bright red

Mucous membranes

Pink and moist

Purple or yellow tinge Small haemorrhages

Regular. 60-80 breaths/min at Respiration

birth. Decreases to 20 - 40

Exaggerated chest and

breaths/min within 1 hour of

abdominal movement

birth. 80-100 beats/min after birth. Heart rate

Temperature

Activity

Laboured respiration

Can increase to 150 beats/min with struggling and attempts to

Nostril flaring with breaths Irregular Low

stand.

>120 bpm

37.2- 38.5oC

> 38.5oC

Not reliable indicator of infection

< 37.2oC

Sitting sternal after few minutes Standing and nursing within 2 hrs

Not sitting sternal after birth Not standing/nursing within 3 hrs Bleeding

Umbilicus

White, moist in new born

Extremities

Warm

Cold

Urinate within 12-18hrs of birth

Straining to urinate

Clear urine

Discoloured urine

Urination

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Common diseases of foals in the first month of life There are unfortunately many diseases that a young foal can succumb to in the first month of life. The most common diseases which are encountered are Neonatal Syndrome, sepsis, prematurity, neonatal isoerythrolysis and diarrhoea. These diseases are outlined below.

Neonatal Syndrome Over the years, many terms have been used to describe foals with Neonatal Syndrome including dummy foal syndrome, perinatal asphyxia syndrome (PAS), and hypoxic ischaemic encephalopathy. Most of these foals are initially normal at birth, but subsequently show abnormal clinical signs within the first 48 hours of life. Neonatal Syndrome is one of the most common reasons for referral of a foal to an intensive care unit. The exact cause of Neonatal Syndrome in foals is not known but multiple risk factors for the development of Neonatal Syndrome have been described and are summarised in Table 2. In some foals with Neonatal Syndrome, an uneventful foaling is observed and no risk factor can be recognised. It is thought that the foals experience a combination of hypoxia (inadequate oxygen supply) and ischaemia (insufficient blood supply) to the brain and other critical organ systems.

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Table 2: Risk factors associated with Neonatal Syndrome Predisposing factors:

Examples:

Severe maternal illness

Late term colic, severe pneumonia

Placental abnormalities

Placentitis Premature placental separation (â&#x20AC;&#x2DC;red bag deliveryâ&#x20AC;&#x2122;) Placental insufficiency (e.g. twinning)

Prolonged stage 2 labour

Dystocia

Induced delivery Caesarian section Rupture of the uterus Reduced umbilical blood flow

Umbilical cord compression or twisting

Failure to breath after delivery

Resuscitation after birth

Abnormal gestational length

Prematurity

Severe anaemia in neonatal

Neonatal isoerythrolysis

period Bleeding into the chest or abdomen Severe bleeding from the umbilicus Severe pneumonia Birth heart defects

The most common organs affected in foals with Neonatal Syndrome are the brain, kidneys and gastrointestinal tract, all organs with high blood supply and oxygen demand. Early signs of

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disease include a loss of affinity for the mare, aimless wandering, lethargy, and weakness. The foals can fall asleep while standing, forgetting to lie down. They also tend to spend longer periods of time sleeping than a normal foal. Loss of suckle reflex, tongue curl and difficulty swallowing milk are common clinical findings; the foals may persistently hang their tongue out of their mouth. The foals often have trouble locating the udder on their mare and try to suckle on walls, gates and handlers. The foals frequently are hyperexcitable and jittery in the early stages, particularly when restrained. Foals with Neonatal Syndromes can have seizures. If foals have repeated seizures, they are often comatosed or semi-comatosed between seizures.

The kidneys are the second most common target organ affected but clinical signs are often subtle. The foals can retain excess amounts of body water and consequently develop oedema. They may produce urine at an inappropriate concentration. Rarely, renal function continues to decline and renal failure ensues.

The gastrointestinal tract is the third most common target organ affected. Mild gastrointestinal dysfunction can be evident as mild indigestion, constipation with retention of meconium and failure to produce faeces for a prolonged time. The foals show failure of passive transfer (serum IgG<8g/l) as colostrum is either poorly ingested or not absorbed. Colic, diarrhoea and abdominal distension secondary to gas accumulation in the large intestine may also occur.

Diagnosis by your veterinarian will be based on the history [e.g. placentitis, dystocia, red bag delivery, meconium staining (indicating distress of the foetus), resuscitation at birth], a detailed neurological and clinical assessment, and exclusion of other potential conditions that would cause neurological disease in a neonatal foal. These foals need a full haematology, biochemistry and immunogobulin (IgG) determination as a minimum requirement.

Supportive therapy forms the mainstay of treatment for foals with Neonatal Syndrome and treatment of varying level of intensity will be required depending on the severity of the clinical signs and disease progression. In mildly affected foal, treatment may involve placement of a small diameter indwelling nasogastric tube and frequent (every 2 hours) milk feeding until the suckle

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reflex is strong and the foal is capable of nursing without milk aspiration. The introduction of small, gradual increases in milk amounts is important to ensure that the foal is capable of tolerating any increase in milk volume.

Moderately to severely affected foals require more intensive care and support and are usually managed at an intensive care unit facility. Treatment has the primary goal of supporting blood supply and oxygen delivery to the brain. The administration of intravenous fluids, intra-nasal oxygen, plasma, and drugs to maintain the foalâ&#x20AC;&#x2122;s blood pressure and adequate tissue perfusion may be necessary. Rapid control of seizure activity with intravenous medication is important to avoid any further deterioration in neurological status. Providing adequate nutritional support to maintain these foals in a positive energy balance is crucial to recovery and this is usually provided by enteral nutrition (milk administration by gravity flow using an indwelling stomach tube) or parenteral nutrition (intravenous nutrition consisting of glucose, amino acids and lipids). Foals with Neonatal Syndrome are very susceptible to secondary infections and need to be monitored closely for signs of infection. Early referral to an intensive care unit will increase the probability of successful treatment of these foals by ensuring appropriate and intensive treatment is provided as early in the disease process as possible.

The prognosis for foals with Neonatal Syndrome (with early and appropriate treatment) is generally good; the majority (>80%) with Neonatal Syndrome treated at our intensive care unit at Scone Equine Hospital are clinically normally within 10 days and no adverse effects on future athletic function are apparent. The prognosis is worse for foals with concurrent problems such as sepsis (infection), prematurity, and in those foals which fail to show neurological improvement within the first 5 days of intensive care and hospitalisation.

Prematurity The final development of the foal occurs very late in the pregnancy of the mare. Foals born even just 2-3 days too early may be unprepared for life outside the uterus and unable to survive without intensive supportive care. Factors associated with premature deliveries are listed in Table

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3. The cause of the foal’s early delivery can have important implications for the foal’s chance of survival, particularly in the determination of the foal’s ‘readiness for birth’. Premature foals exposed to an unfavorable intra-uterine environment (e.g. foals from mares with placentitis) may have early maturation of their organs and can have improved survival rates post foaling. In these foals, a history of a purulent vaginal discharge in the mare before foaling, early udder development and running milk several days or weeks prior to foaling or confirmation of placentitis by veterinary assessment of the placenta post foaling can be very useful. In contrast, foals prematurely removed from their intra-uterine environment (e.g. early induction of foaling with drugs due to severe illness of the mare or an emergency caesarian section) frequently adapt poorly to their extra-uterine environment and can be hard to save. Occasionally, late term colic or bleeding from uterine blood vessels in the mare pre-foaling can be misinterpreted as signs of first stage labour. Induction of foaling in these cases can have devastating consequences for the foal. The average gestational length of Thoroughbreds is 334 to 340 days and traditionally, a premature foal was one born prior to 320 days of gestation. However, the wide variation in normal gestational lengths in mares means that focusing on the gestational age of the foal may lead to inaccurate classification of foals as premature. A premature foal has a gestational length that is less than the normal gestational length for the dam and displays characteristics of prematurity. Table 3: Factors associated with premature deliveries Placental Problems

Twinning Placentitis Premature placental separation

Foetal Problems

Sepsis (Infection)

Maternal Problems

Severe maternal illness Early induction- inaccurate breeding dates Misinterpretation of late term colic as first stage labour Early caesarean section due to severe medical/surgical problem in mare

Physical findings characteristic of prematurity include: low birth weight and small body frame; a short silky hair coat, a domed forehead, and increased joint, ligament and tendon laxity (‘looseness’). Floppy ears due to incomplete ear cartilage development may be evident. General muscle weakness can lead to a delayed time to standing post foaling and a weak suckle reflex (a

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normal foal is expected to stand within an hour of birth and nurse from the mare within 2 hours of birth). Management of premature foals is often complicated and involves giving attention to multiple organ systems. Problems with the function of the premature foalâ&#x20AC;&#x2122;s intestinal tract can lead to poor tolerance of mareâ&#x20AC;&#x2122;s milk, gas accumulation in the intestine, and signs of colic. Intake and absorption of colostrum may be poor leading to failure of passive transfer. Failure of passive transfer predisposes foals to sepsis. Premature foals often have poor regulation of their own body temperature and need careful management to avoid becoming hypothermic (rectal temperature <37.2oC). They also may have problems with their kidney function in the initial few days of life. Breathing or respiratory problems are common in the premature foal. One of the most significant long-term consequences of prematurity is complications associated with incompletely ossified (not enough bone) in the small knee and hock bones; therefore radiographic assessment of premature foals is advisable. Mismanagement of foals with incomplete ossification of the knee and hock bones can lead to crushing injuries of these small bones and the development of angular limb deformities and secondary arthritis which can limit performance in later life. Treatment options for a premature foal range from supportive care to very intensive therapy of mechanical ventilation, intra-nasal oxygen, intravenous fluids and parenteral nutrition (intravenous nutrition). The foal will need to be confined until there is complete ossification of the cuboidal bones (as determined by repeat radiographic examinations). Their legs also need to be carefully monitored for the development of any angular limb deformities.

Sepsis Sepsis is the leading cause of death in neonatal foals. It is initiated by bacteria or their associated toxins and can trigger a serious inflammatory reaction in the foal which can affect multiple organ systems. Early recognition and appropriate treatment are critical to the successful management of foals with sepsis. Predisposing factors include: 1) Maternal factors- placentitis, maternal illness (e.g. colic), premature placental separation, dystocia

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2) Abnormal gestation length- prematurity 3) Failure of passive transfer, poor hygiene, over-crowding

If infection has occurred in utero (e.g. in foals from mares with placentitis), clinical signs of sepsis can be present directly after birth or appear within the first 24 hours of life. If infection is acquired after birth, clinical signs usually begin within two to four days of life. The clinical signs of early sepsis in the neonatal foal are often subtle but are frequently rapidly progressive. Depression, weakness, poor feeding, lethargy and excessive periods of recumbency or sleeping may be reported. The foal may have milk staining on its forehead as depressed foals often stand under the udder but fail to suckle. As time progresses, the lack of milk intake will result in dehydration and hypoglycaemia (low blood glucose levels). Mucous membranes are often bright red or injected. The coronary bands may develop a red line. Other common findings are tachycardia (heart rate>120 bpm) and tachypnoea (respiratory rate>40brpm). Body temperature abnormalities are variable in neonatal sepsis; the rectal temperature may be high (>38.5oC), low (<37.2oC) or normal (37.2-38.5oC). Petechiae (red spots) on the inside of the ears, sclera, vulva or oral mucous membranes suggest sepsis and/or clotting problems.

Other localising signs may be apparent such as distended joints or pain and swelling over a growth plate. The distended joints may or may not be associated with lameness and notably the absence of lameness does not rule out septic arthritis in a neonatal foal. Diarrhoea or enteritis is also a common early presenting sign of sepsis. Other gastrointestinal signs associated with sepsis include lack of gastrointestinal motility, abdominal distension, and colic. Infection of the umbilical structures may occur. Inflammation of the structures of the eye (uveitis), seizures, and respiratory distress may also be seen. If untreated, the foal may progress into septic shock where the mucous membranes become muddy, the heart rate elevates, the pulse becomes weak and the extremities become cold.

A low white blood cell count and low neutrophil count are common laboratory findings in sepsis. Elevated renal enzymes and low blood glucose may also be present. Immunoglobulin G (IgG) concentrations are frequently low (<8g/l) due to failure of passive transfer. Positive blood

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cultures are definitive proof of the presence of bacteria within the blood stream, but a minimum of 48 hours is usually required before these results are available from the laboratory.

Appropriate broad spectrum antibiotic therapy, intra-nasal oxygen, nutrition, intravenous fluids, hyperimmune plasma may be required depending on the needs of the individual foals. Early and aggressive treatment of joint infections, if present, is essential to optimise the chance of a successful outcome.

Ensuring the foal has an adequate immunoglobulin concentration (IgG) of > 8g/L at 12-18 hours of age, avoiding over-crowding and ensuring clean dry foaling areas are critical in trying to prevent sepsis. Unfortunately even if all these precautions are taken, a foal may still develop sepsis.

Neonatal isoerythrolysis In cases of neonatal isoerythrolysis, the foal inherits a specific red blood cell surface antigen from the stallion, which is incompatible with antibodies present in the mare’s colostrum. Following ingestion of colostrum, the antibodies are absorbed into the foal’s systemic circulation. The antibodies destroy the red blood cells which results in anaemia and an increase in bilirubin (a product of red blood cell break down) which causes the jaundiced or yellow appearance of the foal’s mucous membranes. The mare begins to produce antibody after exposure and sensitisation to incompatible red blood cell antigens. Sensitisation can occur when mares receive blood transfusions or when they get exposed to incompatible red blood cell antigens during pregnancy. Although mares can become exposed and generate antibody during any pregnancy, mares rarely give birth to foals with neonatal isoerythrolysis on their first pregnancy. However, once a mare has had a foal with neonatal isoerythrolysis, all future pregnancies are at risk.

Affected foals are normal at birth with clinical signs usually becoming apparent within 6 hours to 5 days of birth. Clinical signs vary in severity depending on the amount of antibody absorbed and the affinity of the antibody for the foal’s red blood cells. Many of the clinical signs observed are

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due to the reduction in oxygen-carrying capacity of the foalâ&#x20AC;&#x2122;s blood. Lethargy, weakness, high heart rate (heart rate >120 beats per minute), high respiratory rate (respiratory rate >40 breaths per minute), pale and icteric (yellow) mucous membranes are common clinical signs. Severely affected foals may be found collapsed due to shock and can also have seizures.

Anaemia will be confirmed on laboratory data. The serum bilirubin concentration (a breakdown product of red blood cells) will also be elevated.

Treatment consists of box rest, minimising stress, blood transfusions (if moderately to severely anaemic), providing an alternative milk source if the foal is less than 36 hours (to prevent further absorption of the offending antibody), intravenous fluids and antibiotics.

Prognosis is dependent on many factors including the amount of antibody ingested, the rapidity and severity of the red blood cell breakdown, the time course to detection, appropriate treatment of the foal and the presence of secondary complications. The disease can be prevented in mares which are known producers of foals with neonatal isoerythrolysis. The newborn foal should not be allowed any access to the mare and it should receive good quality colostrum from another mare. The mare should be milked out for 36 hours and all of this milk and colostrum discarded. The foal should be fed supplementary milk for 36 hours. After this period of time the foal can then safely nurse from the mare.

Diarrhoea Diarrhoea in foals is common. In foals less than 3 days of age, it is most commonly associated with sepsis. The episode of diarrhoea can be mild and self-limiting or life threatening with signs of severe sepsis as seen with clostridial infections. Common signs include fever, depression, dehydration and not nursing. Often signs of mild to moderate colic are present, even before the foal develops diarrhoea. Many therapies used in the treatment of diarrhoea are similar regardless of the cause of the diarrhoea. Restoring circulatory volume and correcting dehydration, electrolyte and metabolic

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abnormalities are essential. Intravenous fluids and electrolytes are used in moderately to severely affected cases. Oral fluids and electrolyte supplementation are used in mild dehydration where there is a functional GIT. Plasma is often used if low protein levels are found due to loss of protein through the inflamed gut lining.

Nutritional support is an important part of management of the foal with diarrhoea as many foals respond to milk restriction. Foals with abdominal distension and colic should be withheld from feeding until these signs resolve. They however need intravenous fluid and glucose supplementation whilst their access to the mare is restricted. Parenteral nutrition (TPN or intravenous nutrition) may be utilised if more prolonged gastrointestinal rest is needed. There are a variety of other therapies such as kaolin/pectin, bismuth subsalicylate, sucralfate and probiotics which are used in the treatment of diarrhoea in the foals. Their use will depend upon the clinical experience of the veterinarian and stud personnel. Supportive therapies such as regular cleaning and application of protective cream and fly repellants over the rump and vulva are important.

Strict hygiene and isolation protocols should be adhered to when treating foals with infectious diarrhoea. Often diarrhoea is part of a farm problem thus, where possible, control and preventative measures on the farm should be instigated.

Acknowledgement The author thanks Dr Jane Axon for providing assistance with the course notes.

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NOTES…………

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Lecture 6:

Deworming & Vaccinations in the horse

Dr Catherine Chicken BVSc PhD MACVSc DipVCS

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Deworming and vaccination of horses on stud farms Dr Catherine Chicken Internal Parasite Control (Deworming) on Horse Farms Introduction Historically, deworming protocols in horses have been based on seasonal rotation of different types of anthelmintics to target particular internal parasites at strategic times of the year. More recently, interval dosing has been the most commonly practised anthelmintic treatment method and is widely used. Most often, a macrocyclic lactone (ML) product (e.g. Ivermectin) is administered every 6-8 weeks (the observed egg reduction period or ERP) meaning horses are treated up to 8 times per year. We now know that frequent treatment of all horses in this way selects strongly for drug-resistant worms â&#x20AC;&#x201C; and once resistant, always resistant. Therefore, it is absolutely urgent that more sustainable approaches to worm control are adopted (7). There is emerging evidence of drug resistance in gastrointestinal worms on Australian horse farms, as is the case in many other countries (4).

Clinically significant gastrointestinal parasites in horses

The most clinically significant gastrointestinal parasites of the horse are the cyathostomins or small strongyles (small redworms), Parascaris equorum (ascarid or large roundworm),

Anoplocephala spp (tapeworm), Oxyuris spp (pinworm), Strongyloides westeri (threadworm), Strongylus vulgaris (large redworm), Gasterophilus spp (bots) and Habronema spp (table 1). Of these, the small strongyles, large roundworms (ascarids), and tapeworms are currently of most importance in the commercial horse breeding setting. In days of old, S vulgaris was the main clinical concern and was the target of parasite control strategies in horses. Interval dosing with anthelmintics was aimed at reduction of pasture contamination with eggs from this particular worm. Consequently, in recent years, S vulgaris has waned as a clinically significant internal parasite of the horse and small strongyles (cyathostomins), ascarids (Parascaris equorum) and tapeworms (A perfoliata) have taken over. The biology, life-cycles and host-parasite dynamics of the cyathostomins, A. perfoliata and P. equorum are very

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different from S. vulgaris, thus strategies designed for S. vulgaris will not be appropriate or very effective for controlling these parasites (10). Cyathostomins (small strongyles) reside in the large intestine of horses and can cause significant clinical problems when encysted larvae of this parasite are released en masse from the intestinal wall. An acute syndrome of sudden weight loss, often with severe diarrhea, is seen in temperate areas in late winter and spring, particularly in young ponies and horses (<5 yr old). This condition is known as larval cyathostominosis (5). The wormers effective against hypobiotic (encysted) larvae are moxidectin and 5 day fenbendazole (6).

Parascaris equorum (large roundworm) is most important for causing ill-thrift and poor growth in foals. It has a prepatent period (the period of time from ingestion of parasite infective stages until eggs are being shed in the faeces) of 10–12 weeks. Large numbers of infective eggs can remain viable for years in contaminated soil. Adult animals usually harbor very few, if any, worms. The main sources of infection for young foals are pastures, paddocks, or stalls contaminated with eggs from foals of the previous year. In heavy infections, the migrating larvae may produce respiratory signs (“summer colds”). In heavy intestinal infections, foals show unthriftiness, loss of energy, and occasionally colic. Intestinal obstruction and perforation have been reported. Diagnosis is based on demonstration of eggs in the faeces. If disease due to prepatent infection is suspected, diagnosis may be confirmed by administration of an anthelmintic, after which large numbers of immature worms may be seen in the faeces. On farms where the infection is common, most foals become infected soon after birth. As a result, most of the worms are maturing when the foals are around 4–5 months old. Treatment should be started when foals are approximately 8 weeks old (5).

Anoplocephala spp (tapeworm) infections have been associated with intestinal perforation, peritonitis, and subsequent colic. Colic from disturbances of the ileocecal area is more likely in horses with tapeworm (Anoplocephala perfoliata) infections than in those not infected. Colic associated with tapeworm infections often recurs. The site of attachment of tapeworms frequently becomes secondarily infected or abscessed. Mixtures of the macrocyclic lactones ivermectin or moxidectin with praziquantel are available and are highly effective against A perfoliata (5). Adult pinworms, Oxyuris equi, are more common in horses <18 months old and are found primarily in the terminal portion of the large intestine. Adult pinworms are of little significance in the intestine but cause perineal irritation after egg laying. Rubbing of the tail and anal regions,

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with resulting broken hairs and bare patches around the tail and buttocks, is characteristic and suggests the presence of pinworms. Application of cellophane tape to the skin of the perineum or scraping the area with a tongue depressor may recover ova for microscopic examination, but false-negative tests are common (5). The larvae of Strongylus spp (large strongyles) develop to the infective stage within 1â&#x20AC;&#x201C;2 weeks after the eggs are passed, under favourable conditions. Infection is by ingestion of infective larvae, which exsheath in the intestine and migrate extensively before developing to maturity in the large intestine. The prepatent period is 6â&#x20AC;&#x201C;11 months. The larvae of S vulgaris migrate extensively in the cranial mesenteric artery and its branches, where they may cause parasitic thrombosis and arteritis, potentially leading to gut damage and associated colic. Mixed infections of large and small strongyles are the rule in general (5).

Strongyloides westeri (threadworm) is found in the small intestine in foals. Adult horses rarely harbor patent infections, but mares often have larval stages within their tissues that are activated by parturition to move into the mammary tissue and, subsequently, are transmitted to foals in the milk. However, the relationship of S westeri infection with diarrhea in foals from 10 days of age has not been clearly established. Diagnosis can be made based on observation of eggs somewhat more oval and about one-third the length of strongyle eggs that contain larvae. Ivermectin and oxibendazole effectively remove S westeri. Transmission of larvae to foals via mare's milk may be prevented by routine treatment of mares with ivermectin within 24 hr after foaling (5). Horse bots, which are found in the stomach, are the larvae of botflies, Gasterophilus spp. In temperate areas, it is assumed that most animals are infected by the end of summer. Ivermectin is effective against oral and gastric stages of bots and, when used as part of a routine parasite control program, provides effective bot control throughout the season. Current recommendations for control include at least one treatment annually, at the end of the botfly season (5). The stomach worms Habronema muscae, H microstoma, and Draschia megastoma are widely distributed. Habronema spp eggs or larvae are ingested by larvae of house or stable flies, which serve as intermediate hosts. Horses are infected by ingesting flies that contain infective larvae or by free larvae that emerge from flies as they feed around the lips. Most anthelmintics have not been tested against Habronema spp or Draschia sp, although ivermectin is effective against their

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cutaneous larvae and against adults of H muscae. Moxidectin is also effective against adult H.

Muscae (5).

Table 1: Common clinically significant gastrointestinal parasites of the horse

Common name

Scientific name

Age affected

Effective drug classes*

Small redworms/small strongyles

Cyathostomins

< 3 years

ML’s (moxidectin), (+/- BZ’s, +/- Pyrantel).

Large roundworm/ascarid

Parascaris equorum

Foals > 8weeks and weanlings

ML’s and praziquantel in combination

Tapeworm

Anoplocephala spp

Any age but often yearlings

Praziquantel, double-dose pyrantel

Pinworm

Oxyuris spp

< 18months

ML’s, BZ’s, Pyrantel

Large redworms / blood worms/ large strongyles

Strongylus spp

> 6-11months

ML’s, BZ’s, Pyrantel

Threadworm

Strongyloides westeri

Foals (including young)

ML’s, BZ’s

Bots

Gasterophilus spp

All in mob by end Summer

ML’s

Habronema

Habronema spp, Draschia sp

All exposed to flies

ML’s

*effectiveness of drug classes subject to change as resistance develops, particularly with respect to Cyathostomins and Parascaris equorum.

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Anthelmintics for treating internal parasites in horses

There are three main classes of anthelmintics registered for control of nematodes in horses; benzimadazoles ([BZ’s] oxibendazole, oxfendazole, fenbendazole), macrocyclic lactones ([ML’s] ivermectin, moxidectin, abamectin) and tetrahydropyrimidines ([THP’s] pyrantel, morantel) (2). Praziquantel is used in the control of tapeworms .

Table 2: Classes of drugs available for treatment of horse worms Drug Class Benzimadazoles Tetrahydropyrimidines (THPs) Macrocyclic lactones

Active Ingredient Oxibendazole Oxfendazole Fenbendazole Morantel Pyrantel Abamectin Moxidectin Ivermectin

ERP 4 weeks 4 weeks 6-8 weeks 12 weeks

Table from: Anne Beasley, 2012. A new era in worm control, Horses and People magazine

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Many commercial wormers use combinations of 2 or more compounds from these classes of drugs to strategically target different types of gastrointestinal parasites in one product (table 3).

Table 3: Equine wormers and their ingredients

Brand

Benzimidazoles

Tetrahydro-

Macrocyclic

(BZ’s)

pyrimidines

Lactones

(THP’s)

(ML’s)

Morantel tartrate

Ammo Equest + Tape Equimax Equimax LV

Pyrantel

Equimax Elevation

Equimec + Tape Oxfendazole

Evolve iMax Gold

Morantel tartrate

MecWorma & Tape

Praziquantel

Abamectin

Praziquantel

Ivermectin

Praziquantel

Ivermectin

Praziquantel

Ivermectin

Praziquantel

Abamectin

Praziquantel

Ivermectin

Praziquantel

Ivermectin

Praziquantel

Abamectin Ivermectin

Noromectin Fenbendazole

Promectin Oxfendazole

Abamectin

Praziquantel

Ivermectin

Praziquantel

Pyrantel emboate

Ultramax Equine Worma Paste

Moxidectin

Abamectin

MecWorma & Bot

Strategy T

Abamectin

Ivermectin

Eraquell

Panacur 100

Other

Ivermectin

Equimec

Equitak Excel

Praziquantel

Oxfendazole

Razor Equine

Piperazine

Ivermectin

Praziquantel

Wormer

Table amended from AHIC paper on drug resistance in horses, 2015, Dr Anne Beasley, School of Veterinary Science, University of Queensland (3)

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Anthelmintic Resistance

Due to the emergence in many countries of resistance to most of the major classes of anthelmintics used in horses over the past two decades, there has had to be a rethink of the strategic approach to internal parasite control. Routine prophylactic treatments based on simple calendar-based schemes are no longer reliable and veterinary equine clinicians are increasingly seeking advice and guidance on more sustainable approaches to equine parasite control (1). As a result, treatment regimens utilising more frequent dosing, “interval dosing”, with anthelmintics have evolved which have likely enhanced the emergence of parasite resistance. Field studies published over the last decade indicate that BZ resistance is widespread globally in cyathostomins and there are also many reports of resistance to pyrantel in these worms. Cyathostomin resistance to ML compounds is emerging, principally measured as a reduction in strongyle egg reappearance time (ERT) observed after treatment. Ivermectin resistance is a further concern in the small intestinal nematode, Parascaris equorum, an important pathogen of foals (table 4).

Table 4: Current levels of resistance documented in major nematode parasites to 3 classes of anthelmintics in managed horse herds in the USA. Drug class BZ’s THP’s ML’s

Cyathostomins Widespread Common Early indications

Large strongyles None None None

Parascaris equorum Early indications Early indications Widespread

Table from: AAEP Parasite Control Guidelines, developed by the AAEP Parasite Control Subcommittee of the AAEP Infectious Disease Committee, Revised 2013.

These resistance issues indicate that horse gastrointestinal parasites must now be controlled using methods less dependent on anthelmintic use and more reliant on management practices designed to reduce the force of infection in the environment. Such strategies include improved grazing management integrated with targeted anthelmintic administration involving faecal egg count (FEC)-directed treatments (2). Careful consideration needs to be given when choosing wormers, especially for young horses. It is important to realise that every property is not the same. If you currently rely on ML wormers in your foals and weanlings, it would be wise to carry out faecal egg counts two weeks after

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treatment to check drug efficacy. If resistance has emerged (as shown by a <95% reduction in FEC), it is important to switch to a combination wormer that contains two active ingredients, one of which should be a non-ML (there are several on the market to choose from e.g. Equimax Elevation, Equitak Excel, Strategy-T) (3). Foals should first be treated at about eight weeks of age - no earlier - and then again around the time of weaning. For these first treatments, a wormer that targets P. equorum is essential, so a combination product is ideal. Another two treatments are recommended at nine months and 12 months of age when small strongyles are likely to have taken over as the main target parasite. For these treatments, the ML products should be sufficient. Ensure that one of those treatments contains Praziquantel, which is a narrow spectrum drug that specifically controls tapeworm (3). Until recently, there has been a distinct lack of research into internal parasite control on horse farms in Australia. This year, the results from an RIRDC funded study performed through the University of Queensland, involving horses from 42 farms from SE Qld, the Hunter Valley, tropical north Qld and Wagga Wagga, were published. The study investigated the resistance to ML drugs such as ivermectin (IVM) by 2 types of nematodes, the cyathastomins and Parascaris equorum.

Faecal egg count reduction tests (FECRTs) were utilised to determine whether there was evidence of ML resistance in either cyathostomins or Parascaris equorum. The FECRT is a simple comparison of faecal egg counts immediately before and two weeks after worming. When the drug being tested is fully effective against the target worm population, a 100% (or very close to 100%) reduction in faecal egg count is expected. Conversely, in cases where the worms have built up resistance to the drug, there would only be a reduction of 95% or less, indicating that some worms were able to survive the treatment and continue shedding eggs (3). The results from this study showed that the ML drugs (primarily ivermectin) remained effective against cyathostomins at 2 weeks post-treatment. In other words, this study provided no proof of ML-resistance among the study cyathostomin populations. However, additional data collected during the study period provided anecdotal evidence of a shortened egg reappearance period (ERP) on some properties, which can be interpreted as a shift in the sensitivity (towards resistance) of cyathostomins (4). A FECRT conducted on one group of foals in southeast QLD showed reduced efficacy (just 65%) of ivermectin against Parascaris

equorum, providing evidence for the presence of ML resistance in Australia (4).

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Since ML’s are the cornerstone of equine worm control and make up the bulk of registered anthelmintics, their continued efficacy is essential for the future of parasite management for horses. The broad survey of ML-resistance among cyathostomins yielding no evidence of reduced efficacy at 2 weeks post treatment, therefore, provides encouraging news for the horse industry. ML’s should continue to be utilised as part of an evidence-based, targeted, strategic worm control program (4). A reduction in the ERP of cyathostomins following treatment with ML’s, which has been documented overseas, appears to be occurring in Australia too. This finding has far-reaching implications, given that reduced ERPs often precede the emergence of drug resistance. This emphasizes the need for good product stewardship and also regular monitoring of drug efficacy (4). The poor efficacy of ivermectin against P. equorum reported in this study is of concern. ML drugs form the foundation for most worm control programs, and P. equorum is the most pathogenic of the nematodes infecting weanlings, impacting on growth rates and occasionally causing small intestinal obstructions. With continued use of ML’s in foals and weanlings, the prevalence of ML-resistance in populations of this worm can be expected to rise. This, combined with the additional observation of a shortened egg reappearance period for cyathostomins following ML treatment emphasises the need for prompt revision of the current worm control strategies of horse breeders, owners and managers (4).

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Summary for Parasite Control From: AAEP Parasite Control Guidelines,developed by the AAEP Parasite Control Subcommittee of the AAEP Infectious Disease Committee, Revised 2013.

What is a rational worm control program? Worm control programs are best viewed as a yearly cycle starting at the time of year when worm transmission to horses changes from negligible to probable. Furthermore, it is critical that all treatment recommendations be viewed in the proper context. All treatment and nontreatment recommendations are made within the context of a preventive program where FEC surveillance is being performed. These recommendations, which are based on epidemiological principles, may not apply to individual horses on farms. Thus, if presented with a horse showing evidence of parasitic disease during the times of the year when treatments are not recommended (e.g., summer in south, winter in north), then this horse should be treated â&#x20AC;&#x201C; and if the horse is showing overt symptoms of intestinal parasitic disease then moxidectin would be the treatment of choice since it is important to kill the encysted mucosal larvae in these animals. The larvicidal regimen of fenbendazole (10 mg/kg for five consecutive days) can be applied for this purpose, if a FECRT reveals full efficacy of this drug. It is important to keep in mind that these are just suggestions; thus, there are many variations of these suggested programs that would still meet the same goals and follow the same principles. Ultimately, each farm (with veterinary guidance) should develop its own program tailored to the specific needs of the farm and each animal. There is no such thing as a â&#x20AC;&#x153;one size fits allâ&#x20AC;? program. As outlined, all adult horses should benefit from a basic foundation of one or two treatments per year. Low egg shedding horses with naturally strong immunity to cyathostomins will need no other treatments because the two treatments have covered the needs of the other parasites and these horses are protected naturally from cyathostomins by their immune state. In traditional deworming programs, repeated treatment of low shedder horses every 2-3 months accomplishes little to improve their health, but it does promote drug resistance. Moderate and high egg shedders will need a third or fourth treatment for cyathostomins.

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Daily pyrantel tartrate or a moxidectin can be considered for suppression of egg shedding in consistent high strongyle shedders. Any additional treatments would be given on an â&#x20AC;&#x153;as neededâ&#x20AC;? basis depending on whether a specific parasitic infection or disease is diagnosed. For example, if Anoplocephala eggs are seen when performing FEC, a second tapeworm treatment during the year might be warranted. Likewise, if pinworms are diagnosed, any horse showing symptoms should be treated with an effective anthelmintic. Ivermectin and moxidectin remain the foundation for control of strongyle parasites, although signs of emerging resistance have been reported in Central Kentucky. In contrast, resistance to these drugs is common in P. equorum. Thus, efficacy should be proven with a FERCT before using these drugs to control P. equorum in foals. Strongyle resistance is well documented against pyrantel, fenbendazole, and oxibendazole, but these drugs are still effective against cyathostomins on some farms and can therefore be used if a FECRT has documented good efficacy. In addition, resistance in P. equorum is still uncommon for these drugs, thus these are often solid choices when targeting this parasite (10).

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Disease control and vaccination strategies on horse farms Introduction

When designing disease control strategies for farms it is important to remember the interaction between the host (in this case, the horse), the environment (the farm on which the horse is housed) and the pathogen (whatever causative agent you are concerned about) in any disease production. This host, environment, pathogen triad is central to production of any disease and must be considered in disease control on farms. Vaccination forms a vital part in disease control but is not, in all cases, a silver bullet. It should be viewed as forming an important part of a farm’s strategic disease control plan but must not be seen as a “fix all” in every situation for every disease.

From: Equine Infectious Diseases advisory board guidelines for vaccination, 2011

Risk of infectious disease is higher in the following conditions: 

frequent contact with horses from outside the property

the number of horses on the property (stocking rate)

management practices

the movement of horses to and from the facility

the presence of undiagnosed sub-clinical carriers or horses incubating disease (8)

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Principles of Vaccination

A vaccine is a biological preparation that improves immunity to a particular disease. A vaccine typically contains an agent that resembles a disease-causing microorganism, and is often made from modified, weakened or killed forms of the organism. The agent stimulates the body's immune system to recognize the agent as foreign, destroy it, and "remember" it, so that the immune system can more easily recognize and destroy any of these microorganisms that it later encounters. Vaccination Protocols

A “standard” vaccination program for all horses does not exist. Each individual situation requires evaluation based on the following criteria: 

Risk of disease (anticipated exposure, environmental factors, geographic factors, age, breed, use, and sex of the horse)

Consequences of the disease (morbidity/mortality, zoonotic potential)

Anticipated effectiveness of the selected product(s)

Potential for adverse reactions to a vaccine(s)

Cost of immunization (time, labor and vaccine costs) vs. potential cost of disease (time out of competition; impact of movement restrictions imposed in order to control an outbreak of contagious disease; labor and medication if, or when, horses develop clinical disease and require treatment, or loss of life.) (10)

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Recommended vaccination protocols – search “stud protocols” on the Scone Equine Hospital website homepage and follow the link to: stud_protocols_2014_ vaccination (pp 26-29)

FOAL VACCINATION First foal vaccination is advisable at 12 weeks 12 weeks

Equivac 2 in 1 (Tetanus/Strangles)

BROWN SYRINGE plus

Salmonella and Duvaxyn EHV (Herpes) 14 weeks

Equivac Strangles

PINK SYRINGE

16 weeks

Equivac 2 in 1 (Tetanus/Strangles)

BROWN SYRINGE plus

Salmonella, Duvaxyn EHV (Herpes) and Equivac HEV (Hendra virus) 22 weeks

Duvaxyn EHV (Herpes) and Equivac HEV (Hendra virus)

*Tetanus vaccination provides excellent immunity to disease and is highly effective in protecting against development of disease. *Strangles, Salmonella and Herpes vaccination will help prevent disease, and reduce the duration and severity of the disease. They do not provide total protection, and vaccinated horses may still develop the disease. *Hendra vaccination provides excellent immunity against disease.

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M are Vaccin ation Fully Vaccinated Mare 

Tetanus/Strangles: Previously vaccinated pregnant mares require a single Equivac 2 in 1 booster at least 4 weeks prior to foaling.

Salmonella: Previously vaccinated pregnant mares require a single Salmonella booster at least 4 weeks prior to foaling.

Equine Herpes Virus: Pregnant mares should be vaccinated with Duvaxyn EHV at 5th, 7th, and 9th month of pregnancy.

Equine Rotavirus: Pregnant mares should be vaccinated with Duvaxyn R at least 4 weeks before foaling due date.

Equine Hendra virus: Pregnant mares should be vaccinated with Equivac HeV at least 4 weeks prior to foaling.

Uncertain Vaccination History Mare 

Tetanus/Strangles: Previously unvaccinated pregnant mares require Equivac 2 in1 BROWN SYRINGE, repeated after 4-6 weeks, the 2nd vaccination at least 4 weeks prior to foaling.

Salmonella: Previously unvaccinated pregnant mares require a Salmonella vaccination, repeated after 4-6 weeks, the 2nd vaccination at least 4 weeks prior to foaling.

Equine Herpes Virus: Pregnant mares should be vaccinated with Duvaxyn EHV at the 5th, 7th, and 9th month of pregnancy.

Equine Rotavirus: Pregnant mares should be vaccinated with Duvaxyn R at the 8th, 9th and 10th month of pregnancy.

Equine Hendra virus: Previously unvaccinated mares require 2 initial vaccinations 3 to 6 weeks apart and boosters every 6 months.

*Tetanus vaccination provides excellent immunity to disease and is highly effective in protecting against development of disease.

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*Strangles, Salmonella, Rotavirus and Herpes vaccination will help prevent disease, and reduce the duration and severity of the disease. They do not provide total protection, and vaccinated horses may still develop the disease. *Hendra vaccination provides excellent immunity against disease. Booster Vaccinations 

Tetanus/Strangles: (Equivac 2 in 1 BROWN SYRINGE): annual boosters

Salmonella and Herpes (Duvaxyn EHV): every 6 months to provide maximum immunity. This is particularly important in foals and weanlings.

Hendra virus (Equivac HeV): at 6 months then annually.

Overview of diseases covered by routine vaccinations in horses Tetanus:

Tetanus is a disease caused by the bacterium Clostridium tetani. The organism is found in the intestinal tract and faeces, and is abundant in the soil. The spores of the organism can survive in the environment for many years. All horses are therefore at risk of this disease, even if they are relatively inactive.

Clostridium tetani gains access to the horse through infected wounds. The organism proliferates if there is low local tissue oxygen tension. The neurotoxin (tetanospasmin) reaches the central nervous system by passing up peripheral nerves and via the bloodstream, and binds irreversibly, thus treatment is difficult once clinical signs are evident (8). Clinical Signs Diagnosis of the disease is based on clinical signs, which include a spastic paralysis, with a classical “saw-horse” stance. Protrusion of the third eyelids, spastic paralysis of the muscles of mastication (“lockjaw”) and hypersensitivity to noise and light are also typically present. Death is due to asphyxia following paralysis of respiratory muscles (8). Horse showing clinical signs of tetanus : https://www.youtube.com/watch?v=wZS9_QTBhDk

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Vaccine The vaccine is a formalin-inactivated, adjuvanted toxoid that induces strong serological responses. EquivacÂŽ T vaccine is a tetanus vaccine manufactured by purifying and inactivating the toxin produced by the Clostridium tetani organism. It is a safe and very effective vaccine, and protective immunity is usually attained within 14 days of the second dose of the vaccine. It is indicated in the vaccination program of all horses (8). Clinical tetanus is rare in the commercial horse breeding setting due to high levels of vaccination and a highly effective vaccine. It is important to maintain high levels of vaccination to ensure on-going protection against this deadly disease. Tetanus Antitoxin Tetanus antitoxin is administered to horses that are at risk of tetanus, that are not vaccinated, and is prepared by immunising horses against the Cl. tetani toxin. It is then refined to be free of other serum proteins and concentrated. It neutralises the toxin and therefore provides short-term passive immunity. The antitoxin is administered subcutaneously on the opposite side of the neck to where the intramuscular toxoid (vaccine) is administered. Administration of the antitoxin carries with it the rare risk of Theilerâ&#x20AC;&#x2122;s Disease, an acute fatal hepatitis. This disease has been recorded four to ten weeks after the administration of an equine origin biologic, such as tetanus antitoxin. The risk of this disease should be assessed against the requirement for immediate tetanus prophylaxis, and is best evaluated by a veterinarian. Tetanus antitoxin is also used in the treatment of clinical cases of tetanus, administered either intravenously or into the subarachnoid space. Early administration in the course of the disease is important due to the irreversible binding of the toxin. (8)

Strangles

Streptococcus equi subspecies equi is a bacterium which causes the highly contagious disease strangles. Strangles commonly affects immunologically naive young horses (weanlings and yearlings), but horses of any age can be infected. While most horses recover,

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some individuals will die from the disease. Following natural infection a horse may become a carrier of the disease due to guttural pouch infection and as a result, intermittent/sub-clinical shedding may occur. The organism is transmitted through direct contact with infected or “carrier” horses or indirectly through contact with water troughs, equipment or personnel that have come into contact with affected horses. The greatest risk of infection comes from nasal discharge or pus draining from lymph nodes of infected horses (8). Clinical Signs Clinical signs may include fever (39-40°C); ample nasal discharge of pus and mucus; dysphagia (difficulty in swallowing) or anorexia; stridor (respiratory noise); enlarged or abscessed lymph nodes and in extreme cases asphyxia. Pneumonia, guttural pouch empyema (infection) and bastard strangles can be complications and in foals with a poor prognosis. The diagnostic sample of choice is an aseptically collected aspirate from an abscessed lymph node that has not drained or an infected guttural pouch, however this might not be possible in all cases. Strangles is no longer a notifiable disease in NSW. Please refer to the Department of Primary Industries for more information. Following natural or vaccination exposure to streptococcal antigens, certain individuals may unpredictably develop purpura haemorrhagica, an acute, non-contagious syndrome caused by immune-mediated, generalised vasculitis. Clinical signs develop within two to four weeks following exposure and may include hives with pitting oedema, or abnormal fluid retention of the limbs, ventral abdomen and head. Immediate medical attention should be sought for horses suspected of having purpura haemorrhagica. Following recovery from strangles, most horses develop a durable immunity that can persist for a number of years. Previous exposure does not provide life-long protection and these horses might show milder clinical signs of the infection. Horses that have recovered from infection can also develop a carrier state. These individuals carry the organism in the guttural pouch for several months and can only be detected by bacteriological sampling of the area. Managing an Outbreak Foals born of mares with strangles can be immune for the first two to three months due to colostral antibodies. It is recommended that mares and foals be separated into smaller

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groups in the first two to three months after birth, removing them from the herd with an active infection is also strongly advised.

Steps in managing an outbreak: 

the daily measurement of rectal temperature and immediate isolation of individuals with pyrexia

isolation of new arrivals

daily disinfection of water troughs

use of separate (labelled) feed and water buckets for stalled animals

pasture rotation and resting for one month prior to reintroduction of stock

segregation and culture of recently recovered animals until shedding/carrier status is known

identification and treatment of carriers with guttural pouch lavage and topical antibiotic application

vaccination may not protect against infection but can moderate severity

utilisation of new serum ELISA test to help management

Vaccine Vaccination is an important management tool in protecting against Strangles. Vaccination in the face of an outbreak should be carefully considered, as there is significantly increased risk of adverse reactions in exposed horses, including purpura haemorrhagica. Outbreak mitigation and the prevention of spread of S. equi infection are centred on management of horses, personnel, and facilities. A killed vaccine is the only option available for prophylaxis in Australia. Vaccination with this product may not provide complete protection. However, appropriate pre-exposure vaccination with this product appears to reduce the incidence and severity of clinical signs in affected horses (8). Equivac® S Strangles Vaccine is a cell free extract of the Streptococcus equi subspecies equi organism. Vaccination Schedules

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For adult horses that are unvaccinated or have unknown vaccination history, it is recommended that the horse to undergo the priming regimen

All foals should be vaccinated against Strangles

All Competitive/Pleasure and Breeding horses should be vaccinated against Strangles

New Developments in the Management of Strangles A new ELISA test has recently been developed that detects antibodies to the strangles organism. This may prove very useful in the management of strangles on horse properties – more information to come. Rotavirus

Rotavirus, a non-enveloped RNA virus, is a major infectious source of diarrhoea in foals, seen predominantly in horses aged one week to five months. While rotavirus diarrhoea morbidity can be high, mortality is low with veterinary intervention. Shedding can occur in recovered foals, however adults do not shed. Clinical Signs Equine rotavirus is transferred via the faecal-oral route and damages the small intestinal villi, resulting in cellular damage, maldigestion, malabsorption and diarrhoea. Most cases will resolve without treatment. Foals with the virus present symptoms quickly and will stop nursing and become depressed with diarrhoea within 12-24 hours of infection. The severity of a rotavirus infection depends on a horse’s immunity, inoculation dose and age, as it is generally more severe in younger foals. Horses are diagnosed with faecal antigen tests which are sensitive, rapid and specific. Treatment for the virus is generally supportive with fluid therapy to rehydrate foals, especially during hot environmental conditions.

Managing an Outbreak Outbreaks of rotavirus are related to poor hygiene and high stocking density. Mare owners need to be aware that strict biosecurity and disinfection during the foaling season lessens the morbidity associated with most types of infectious foal diarrhoeas and other contagious diseases. It is also advised that foals with diarrhoea be isolated from the herd to help in reducing the exposure of other young horses.

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Rotavirus is very stable and can survive for up to nine months in the environment. Farms with endemic rotavirus and high stocking rates should consider the use of the vaccine. Vaccination of mares results in a significant increase in foals‟ rotavirus antibody titers. Field trials of rotavirus vaccination in pregnant mares have shown a decrease in incidence and severity of foal diarrhoea on farms that historically had annual rotaviral diarrhoea cases. Other studies have shown increased rotavirus antibodies in vaccinated mares‟ colostrum. Vaccine The only vaccine available in Australia contains inactivated rotavirus Group A and is indicated for administration to pregnant mares to enhance concentrations of colostral immunoglobulins against equine rotavirus (Group A). The vaccine has been used in mares since 1996 in the USA and is considered to be safe (8). Vaccination Schedules

Please refer to the Equine Infectious Diseases Vaccination Protocol for more information. Salmonella Salmonella infection can cause serious diarrhoea in both adults and foals. It is also the cause of septicaemia and polyarthritis in foals. There are a number of serovars of Salmonella that are capable of causing disease in horses and humans alike. It is important to recognise the zoonotic risk of Salmonella (infection can pass between animals and humans). People working with infected animals should practice strict hygiene. Clinical manifestations range from no abnormal clinical signs (subclinical carrier) to acute, severe diarrhoea and even death. The disease is seen sporadically but may become an epidemic, depending on the virulence of the organism, level of exposure, and host factors. Infection can occur via contamination of the environment, feed, or water or by contact with animals actively shedding the bacteria. Stress appears to play an important role in the pathogenesis—a history of surgery, transportation, or change in feed; concurrent disease, particularly GI disorders (colic); or treatment with broad-spectrum antimicrobial drugs often precedes the diarrhoea.

Salmonella enterica of the serogroup B includes S enterica serovar typhimurium and S enterica agona, two of the most frequently isolated serovars from horses with clinical disease. Knowing the serovar and antibiogram can help track or monitor the type of serovar of salmonellae affecting any given group or population of horses. The emergence of multidrug-resistant S

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enterica isolates is concerning both in dealing with nosocomial infections and zoonosis (infections that can pass between animals and humans) (12).

Clinical Findings Three forms of salmonellosis have been recognized in adult horses. One is the subclinical carrier, which may or may not be actively shedding the organism but has the potential to transmit the bacteria to susceptible animals either by direct contact or by contamination of the environment, water, or feed sources. Multiple faecal cultures may be necessary to identify carriers, because the organism is shed in the faeces intermittently and in small numbers. If stressed, the carrier may develop clinical disease. The second form of the disease is characterized by a mild clinical course, with signs of depression, fever, anorexia, and soft but not watery faeces. Affected horses may have an absolute neutropenia. Clinical disease may last 4â&#x20AC;&#x201C;5 days and usually is self-limiting, and S enterica can be isolated from the feces. Recovered horses may continue to excrete the organism in their faeces for days to months; therefore, isolation of the shedding horse and thorough cleaning and subsequent disinfection of the contaminated area are recommended. The third form of salmonellosis is characterized by an acute onset of severe depression, anorexia, profound neutropenia, and frequently abdominal pain. Diarrhoea develops 6â&#x20AC;&#x201C;24 hr after the onset of fever; feces are fluid and foul smelling. Affected horses dehydrate rapidly, and metabolic acidosis and electrolyte losses occur as the horse deteriorates. Clinical signs of sepsis and hypovolemic shock can progress rapidly. There may be signs of abdominal discomfort, straining, or severe colic secondary to ileus, gas distension, and colonic inflammation and possible infarction. Protein-losing enterocolopathy can occur with plasma protein concentrations becoming dangerously low (albumin <2 g/dL) after a few days of diarrhea. These horses can become bacteremic due to bacterial translocation of enteric organisms, and coagulation abnormalities resulting in disseminated intravascular coagulation can occur. If untreated, this form of salmonellosis is often fatal. Salmonella bacteremia can occur in neonatal foals, especially from farms with endemic salmonellosis. Prevention of salmonellosis is difficult, because the organism is present in the environment as well as in the faeces of some healthy animals. In a hospital environment where horses are stressed, may be off feed, and are often receiving antimicrobial treatment, aggressive

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identification and strict isolation of salmonellae-infected horses is indicated. Biosecurity practices to minimize cross-contamination between hospitalized horses are also advisable. People working with infected animals should practice strict hygiene (12). Vaccination An inactivated bacterin adjuvanted vaccine that provides protection against diarrhoea, septicaemia and polyarthritis caused by Salmonella typhimurium infection in horses is available. This vaccine is not wholly effective in protecting against salmonellosis, due to it being derived from one serovar only, but is a useful part of disease control on farms. For vaccination recommendations please see the SEH website and follow link to:

stud_protocols_2014_ vaccination (pp 26-29). Equine Herpes Virus

Equine herpesvirus 1 (EHV-1) is a double stranded DNA virus, which is endemic in horse populations worldwide. EHV-1 is a respiratory pathogen that rapidly establishes a systemic infection and spreads throughout the body via a cell associated viraemia. EHV-1 causes a mild respiratory disease, but the most serious disease manifestations are EHV-1 abortion and neurological disease (equine herpesvirus myeloencephalopathy). EHV-1 is closely related to EHV-4 which is also primarily a respiratory pathogen. EHV-4 respiratory disease is most commonly reported in young horses, often associated with weaning. Both EHV-1 and EHV-4 establish lifelong latent infections in recovered horses. Previously exposed horses may reactivate these latent infections, which may subsequently become a source of infection for new outbreaks. Clinical Signs Both EHV-1 and EHV-4 circulate on breeding farms in a silent cycle of infection, where foals are infected early in life. This early infection is often associated with respiratory disease, especially in weaned foals. Most cases of evident respiratory disease in young horses are associated with EHV-4 infection. Clinical signs include mild serous, or pale yellow, nasal discharge, which becomes mucopurulent with secondary bacterial involvement. Infection will

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occasionally present as enlargement of the lymph nodes that drain the upper respiratory tract and occasional episodes of coughing. EHV-1 neurological disease (EHM) occurs following infection of the endothelial cells of the blood vessels of the central nervous system (CNS). Vasculitis results in reduced blood supply to the CNS and the clinical signs are directly related to the site of the vasculitis. Clinical manifestations range from mild signs, such as bladder atony (inability to urinate properly) and ataxia, through to tetraparesis (a weakness of the limbs) and recumbency. EHM is rare in Australia, although the neuropathic strain of EHV-1 associated with EHM overseas has been isolated in Australia. EHV-1 Abortion EHV-1 abortion is the most serious manifestation of EHV-1 infection. Abortions typically occur in late gestation, but have been reported as early as five months gestation. Cell associated viraemia is central to the pathogenesis of EHV-1 abortion. EHV-1 abortion occurs following infection of the endothelial cells of the blood vessels of the placenta. Vasculitis results in reduced blood supply to the placenta and subsequently rapid abortion occurs with very few warning signs. This disease process is very rapid and abortion occurs quickly after foetal death, so that the aborted foetus is fresh looking and minimally autolysed or decomposed. In late gestation some affected foetuses may even be born alive. Most EHV-1 abortions occur as single sporadic cases, although if large numbers of pregnant mares are exposed to the index (first) case, large abortion storms can occur.

Managing an Outbreak All equine abortions should be considered as EHV-1 abortions until proven otherwise. Immediate management of the site and affected animal is critical to minimising exposure of other, in-contact, horses. Outbreak management strategies include:

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Securing the area and ensuring appropriate biosecurity measures for in contact personnel.

Removing the affected mare (housed separately or with non-susceptible horses such as non-pregnant mares)

Careful collection and containment of foetus and membranes for laboratory testing

Management of in contact pregnant mares to minimise stress and spread from further abortions

Vaccine Currently, an EHV-1/EHV-4 inactivated whole virus vaccine is available in Australia. This vaccine has been shown in challenge trials to reduce the severity of respiratory disease and reduce the likelihood of EHV-1 abortion. This vaccine is widely used in the breeding industry as an aid to control losses associated with EHV-1 abortion (8) Suggested Vaccination Schedule Herpesvirusstud_protocols_2014_ vaccination (pp 26-29)

SUGGESTED VACCINATION SCHEDULE Foals

1st Dose 9-12 weeks old (January) 2nd Dose 5 months old (March) 3rd Dose 7 months old (June)

Yearlings and Racehorses

1st Dose at any time 2nd Dose 4 - 6 weeks later

All Stock

Booster vaccination every 6 months

For Control of Abortions Initial vaccination for unvaccinated mares

Two doses at 4-6 week intervals

Routine vaccination for pregnant mares

5th, 7th, 9th, month of pregnancy (February, April, June)

Hendra

Hendra virus is a virus carried by flying foxes that inhabit Australia, Papua New Guinea, and surrounding islands. So far, clinical disease due to Hendra virus infection has only been recognised in Australia. Flying foxes appear to be unaffected by the virus. Rarely, Hendra

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virus spreads from flying foxes to horses, (spillover events) causing severe disease, and may then spread to people or animals in close contact with infected horses (9). There is yet to be a case of Hendra virus in the Hunter. However, given the high level of horse movement between the Hunter and areas known to have had Hendra cases previously it is not inconceivable that it may occur. Horses with Hendra infection can shed virus prior to showing clinical signs therefore it is up to all of us to remain vigilant in looking out for potential Hendra cases, particularly in horses that have been transported from Queensland or the North Coast of NSW into our district. Cases appear to occur more frequently in the cooler months of the year - two cases have been confirmed in horses recently in FNQ & the North coast of NSW

- so the timing of movement of horses into the Valley for the breeding season coincides with the time of the year when Hendra cases are most likely to occur. Clinical Signs

Any sick horse â&#x20AC;&#x201C; many and varied! Initial outbreak at Hendra.... respiratory signs/sudden death. Then over the years..... neurological signs. Then in recent years...... colic signs, weight shifting, general discomfort. Vaccination Vaccination for Hendra virus is the single most effective means of protecting horses, and therefore humans, from disease development. The vaccine is an adjuvanted subunit vaccine containing soluble sG protein which allows for identification of infected vs vaccinated horses. It is for use in healthy horses from 4 months of age and is for the active immunisation of horses against Hendra Virus as an aid in the prevention of clinical disease caused by Hendra virus. The course of vaccine administration involves two intramuscular (IM) doses 21 days apart and then periodic boosters. The onset of immunity is 21 days following the second dose.

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Acknowledgements: Much of the information in these notes has been collated from other sources as outlined in the reference list. I would like to acknowledge the assistance of Anne Beasley, James Gilkerson and Cecilia Gavin for providing valuable help in gathering information.

References: 1. Nielsen, M.K. Fritzen, B. Duncan, J. L. Guillot, J . Eysker,M Dorchies, P. Laugier, C. Beugnet, F. Meana, A. Lussot-Kervern, I. And Von Samson-Himmelstjerna, G., 2010. Practical aspects of equine parasite control: A review based upon a workshop discussion consensus, EVJ 42 (5) 460-468. 2. Matthews, J., 2014, Anthelmintic resistance in equine nematodes. International Journal for Parasitology: Drugs and Drug Resistance 4, 310-315. 3. http://www.horsecouncil.org.au/ahic/index.cfm/news/drug-resistance-in-horse-worms-an-australian-study/ 4. Beasely, A. 2015 Macrocyclic Lactone Resistance on Australian Horse Farms. RIRDC Project Summary PRJ-008135, Pub. No. 15/066. 5.http://www.merckvetmanual.com/mvm/digestive_system/gastrointestinal_parasites_of_horses/ 6. http://www.medicanimal.com/A-Complete-Guide-to-the-Types-of-Worms-Affecting-Horses-and-the-Drugs-Effective-Againstthem/a/ART111545 7. Beasley, A., 2012, A new era in worm control of horses. Horses and People, p 12-16. 8. Gilkerson, JR., Begg, L., Chopin, J. Equine Infectious Diseases Advisory Board Vaccination Guidelines, 2011, Pfizer Animal Health. 9. Hendra_virus_primefact_970 NSW DPI. Released/ reviewed 1 June 2014 http://www.dpi.nsw.gov.au/agriculture/livestock/horses/health/general/hendra-virus/hendra 10. AAEP Parasite Control Guidelines, developed by the AAEP Parasite Control Subcommittee of the AAEP Infectious Disease Committee, revised 2013. http://www.aaep.org/custdocs/ParasiteControlGuidelinesFinal.pdf 11. AAEP Principles of vaccination http://www.aaep.org/info/principles-of-vaccination?osCsid=p5v0q9gabqcimrlf01ou98n9v7 12. Salmonellosis in horses http://www.merckvetmanual.com/mvm/digestive_system/intestinal_diseases_in_horses_and_foals/salmonellosis_in_horses.html

Reference material for further Hendra virus information: 

Hendra_virus_primefact_970 NSW DPI. Released/ reviewed 1 June 2014 http://www.dpi.nsw.gov.au/agriculture/livestock/horses/health/general/hendra-virus/hendra -wealth of information regarding all aspects of Hendra virus.

DPI fact sheet showing correct use of PPE – November 2013 http://www.dpi.nsw.gov.au/__data/assets/pdf_file/0003/494202/Hendra-virus- ppe-procedures.pdf

Dr Deb Middleton, CSIRO, AAHL discussing the development of the vaccine http://www.hendrafacts.info/the-vaccine.html

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NOTES………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ………………………………………………………………………………………………………………………

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Lecture 7:

Care of horses teeth

Sam Nugent BVSc. (Hon 1). MANZCVS

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EQUINE DENTISTRY Dr Sam Nugent BVSc.(Hon 1).MANZCVS. Scone Equine Hospital, Scone, NSW.

The horse has evolved to graze for long hours on abrasive herbivorous food material. Unlike ruminants horses do not regurgitate their food so have only one opportunity to grind their foodstuff. The horse’s teeth play an important role in grinding the food down to a small particle size to allow for more efficient digestion. A horse will eat 13-16hr/day, chewing 60-100 chews /min. This causes a high degree of wear to the horse’s teeth. Anatomy Horses have hypsodont teeth. That is in order to cope with the high degree of wear the horses teeth have a high crown above the gum line and they erupt over much to its life. This rate or eruption (2-3mm/year) is similar to the wear of the teeth by a horse on a paddock based diet. Concentrated diets or lush pasture will result in a decrease of wear but the teeth still erupt at the same rate, hence overgrowths occur. The horse’s teeth have a high degree of hard enamel folded around softer but stronger dentine. This makes the teeth stronger for wear and tear, but attributes to the sharp enamel points that develop on the teeth. In the horse the lower dental arcade is straighter and 20-30% narrower than that of the upper arcade. The dental surface of the teeth is also angled at 12-15 degrees. This further contributes to the sites of dental overgrowths. This is also related to the hard enamel that is infolded through the teeth. The adult horse has 12 incisor teeth at the front of its mouth (6 upper and 6 lower). The purpose of these teeth is to bite off grass or hay. When the teeth are held at eye level the incisors should touch and be parallel to the ground. If the incisors do not meet or are not parallel then this is a sign not that there is an incisor problem but that there is a problem with molar occlusion further back in the mouth. The adult horse has 24 cheek teeth (3 premolars and 3 molars in each of the 4 arcades). The role of these teeth is to grind food to aid digestion. A foal has 3 deciduous premolars in each arcade, these are replaced by adult teeth and also the 3 adult molars erupt. The teeth will grow from a

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tooth bud until they erupt into wear (the tooth root develops). The teeth will continue to erupt until it is worn down to the root, this will take 20-30 years. Dental eruption proceeds throughout the life of the tooth. The cheek teeth are tightly compressed together to form a solid occlussal surface, which forms a solid single chewing unit. Also the occlusal surface is ridged to allow for more effective grinding of feed.

The Chewing Cycle Chewing is a repetitive cyclical motion resulting from the contracture of musculature. Horses have a chewing cycle consisting of 3 phases: the opening stroke, the closing stroke, and the power stroke. This gives the chewing cycle a 3 dimensional action. The mandible articulates with the maxilla at the temporomandibular joint (TMJ). When eating, the horse uses its lips to prehend food material and pull it between the incisor teeth. The incisors cut or grasp the food material. The passage of food across the occlusal surfaces of the cheek teeth and its subsequent movement caudally within the oral cavity can be likened to that of an auger. It is important to remember at this stage that all 6 cheek teeth function as a single unit and feed material is processed by each portion of each tooth only once, as the bolus is moved caudally. The cheeks keep the ingested, partially masticated feed within the oral cavity. As the feed material is crushed it is directed in the oral cavity by the occlusal surface of the cheek teeth and the function of the tongue. . The food works its way to the back of the mouth where swallowing is initiated by the presence of a food bolus in the oropharynx. Subsequently the motion of chewing must be considered as a 3D motion, not just a simple up and down motion. An important part of this motion is that the lower jaw moves forward and back in relation to the upper jaw (rostro-caudal motion). This action becomes very important when explaining many abnormalities that occur with the horses teeth. Painful oral disorders or TMJ pain can cause changes in direction and forces of mastication and thus affect the wear pattern of cheek teeth. The horse being a herd animal has developed so as to not outwardly show any signs of dental disease. By the time many of the signs of dental disease become apparent the deterioration is severe. Research has shown a high prevalence (up to 80%) of dental disorders in populations of horses. Signs of dental disease are many and non-specific. They include dropping partially chewed food (quidding), packing food into cheeks, poorly digested food present in faeces, bitting

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or head carriage problems, head tilt when eating, foul smelling breath, excess salivation, and weight loss.

Common examples of dental abnormalities There are a vast range of examples of problems with horseâ&#x20AC;&#x2122;s teeth. For this presentation only the common problems of grazing animals will be mentioned and not the problems of ridden animals. These disorders can either be developmental (congenital) or acquired (develops during lifetime). Incisor problems are usually a sign of cheek teeth abnormalities. Before any correction of the incisors it is important to accurately diagnose and treat any cheek teeth abnormalities. Sharp enamel points on the cheek teeth and ulceration of associated soft tissue structures. Any asymmetry in the positions of the jaws or teeth result in uneven dental wear. The fact that maxillary cheek teeth are wider than mandibular cheek teeth contributes to the development of enamel overgrowths on the outside of the upper cheek teeth and the inside of the lower cheek teeth. These sharp points may lead to gum and tongue ulceration resulting in dental pain. This can be corrected by routine dental floating. Rostral and caudal hooks. This is often the result of the upper cheek teeth arcades being positioned further forward than the lower cheek teeth arcades. Rostral hooks on the front upper cheek teeth are easy to see and develop early in the horseâ&#x20AC;&#x2122;s life as this tooth erupts at about 2.5 years of age. Caudal hooks on the back lower teeth are harder to detect without thorough examination and develop later in the horses life as this tooth erupts at about 4 years of age. Caudal hooks should not be confused with the Curve of Spee (rising slope of the mandible at the back of the mouth). Hooks can affect the motion of chewing, especially rostro-caudal motion, as well as causing soft tissue ulceration. Small hooks can be simply corrected by rasping however larger hooks may require more extensive correction. Parrot mouth (overshot jaw). The upper jaw extends past the lower jaw. This results in incisor and cheek tooth surfaces not aligning so overgrowths become a problem. The upper incisors can grow past the lowers restricting mandibular movement. . Cheek teeth overgrowth occur as rostral and caudal hooks. The parrot mouth cannot be corrected, however routine dental maintenance can prevent the condition worsening.

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Caps. This is where the deciduous teeth are retained over the erupting permanent tooth. This occurs in horses 2-4.5 years of age. These can cause oral discomfort while being displaced as well as eruption bumps on the jaw. If the caps are ready to be removed then this is an easy procedure. Remember that premature removal of caps can damage the underlying teeth. Overgrowths (step mouth) +/- missing teeth). This occurs when there is a lack of occlusion by opposing teeth (tooth lost or missing). Overgrowths can be managed by routine maintenance, but once again large overgrowths will require more extensive correction. Ramps. Exaggeration of the upward slope of the front lower cheek teeth. This can be corrected by dental maintenance. Excessive transverse ridges (ETRâ&#x20AC;&#x2122;s). All cheek teeth have 2 ridges running across there occlusal surface, each ridge has corresponding groove on opposite arcade. These ridges are important for grinding of food and the passage of food through the mouth, however if they become exaggerated they can affect chewing motion as well as causing overgrowths and diastemas. These are corrected by dental maintenance, however often more extensive correction is required. Wave mouth. Presence of an undulating or wave like appearance to the occlusal surface of the cheek teeth arcades. This can be due to the age of horse or due to acquired dental abnormalities. The condition can be corrected in younger horses, however it is not advisable to correct the condition in the older horse. Displacements of cheek teeth. These can be developmental or acquired and are displaced sideways into the gum or tongue. These not only disrupt the chewing cycle but also cause extensive ulceration and pain. Mild displacements can be manage by removing offending edges however many displacements will require cheek tooth removal. Extra (supernumerary) teeth. An extra tooth in an arcade result on loss of alignment of the arcade and so overgrowths and diastemas occur. Extra teeth will require removal. Fractures of cheek teeth. Trauma (often unknown origin) results in fracture of the cheek tooth and often displacement of a fragment of the tooth can occur. The offending fragment can be removed, however often the internal structure are exposed and a tooth root infection will necessitate removal of the tooth.

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Diastemes A cheek tooth diastema is a detectable space between adjacent teeth. As mentioned the rows of CT are compressed tightly together to act as a single grinding unit. However if spaces develop between the teeth then food material can become impacted into the space and lead to periodontal disease These can be acquired (loss of CT or displacements) or developmental (common in older horses due to consequence of continual dental eruption). These can often be resolved by cleaning out the pocket and resolving the underlying cause. If this fails then widening of the diastema is advised.

The dental examination The frequency of routine dental examination will depend upon; -

the age of the horse; younger horses that are replacing teeth will need more frequent examinations and older horses may developed problems that need more frequent examinations.

-

role of the horse; horses in training will need more frequent attention than horse in a paddock

-

Diet; concentrates vs paddock

-

and the presence of any predisposing problems.

Ideally younger horses should be checked every 6 months where older horses should be checked every 12 months. Corrective dental procedures such as routine floating (reduction of sharp enamel points) are the corner stone of routine dental work. However as the above examples indicate many horses require more extensive dental management than just routine floating. Corrective floating procedures are often performed to; 1) relieve pain associated with overgrowths, 2)reduce dental overgrowths,3)improve mastication and digestion of feed,4) prevent discomfort and improve the horses performance. A careful and complete oral examination is critical in the diagnosis of dental pathology and the planning of dental corrective procedures. Simply removing the enamel overgrowths may only be treating the result of the problem not the cause of the problem. Teeth should be examined

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visually and palpated for any abnormality. This is impossible to do without a good quality gag, a good light source and adequate restraint of the horse. A complete set of good quality dental equipment will allow corrective procedures to be performed in an efficient precise manner.

Periodontal disease Periodontal disease describes inflammation of the supporting structures of the tooth (the gum, periodontal ligaments and bone). This is a very significant disorder in horses, however usually secondary to other disorders, such as diastemas. Impaction of food material into periodontal pockets results in inflammation and infection that can result in the loss of the toothâ&#x20AC;&#x2122;s supporting structures and the eventual loss of the tooth. This condition affects all age groups and studies have shown the disease to be present in about a third of horses. The condition once developed is very difficult to treat in the horse and as a result prevention is the best cure. This demonstrates the importance of dental prophylaxis (the examination of the oral cavity and the use of corrective procedures to arrest disease processes before clinical signs are seen).

Is there a relationship between periodontal disease and fertility? In humans it is well documented that women with severe periodontal disease are up to 7 times more likely to abort their pregnancy or have a low birth weight child. Research has demonstrated that up to 60% of horses over 15 years of age will have periodontal disease. There has been no research in horses on the link of periodontal disease and infertility, so my question is can we help the fertility of many older mares by performing accurate and effective dental examinations and procedures?

sam.nugent@sconeequine.com.au

.

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NOTES………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ………………………………………………………………………………………………………………………

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Lecture 8:

Equine nutrition

Dr Caroline Foote BSc.Agr.MSc. PhD

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Feeding the pregnant mare and foal to sale ring Dr Caroline Foote

Feeding broodmares and growing foals is one of the most important and challenging areas of equine nutrition. Nutrient requirements increase markedly as the mare gets closer to foaling, and it is the correct intake and balance of these nutrients that will assist in producing a strong and healthy foal. Optimum fertility and proper balanced nutrition are inter-related. An adequate energy intake, matched to the mare's requirements to achieve and maintain optimum condition, is paramount to success in horse breeding.

Energy For the pregnant broodmare, energy will be used for not only maintenance of bodily functions, but will also be used for the developing foetus and associated mammary and placental tissues. Additional energy in the form of concentrate feed may be required to meet the demands of the unborn foal and provide reserves to prepare the mare for lactation.

160

140

120

MJ/Day

100

80

60

40

20

0 Early gestation

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Late gestation

Early lactation

Late lactation

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Energy requirement of broodmares before and after foaling. Growing foals have a certain energy requirement for growth. The amount of energy required by the individual foal will be dependent on its age, weight, rate of growth, environment and any natural exercise. If too much energy is provided in the ration, the risk of skeletal disease is greatly increased. If not enough energy is provided, growth rate will be reduced.

To provide sufficient dietary energy and protein for optimal growth and often for maximum mature size, grain will most likely be required.

This is particularly the case for rapidly growing

thoroughbreds intended to be sold as yearlings. Oats is often used as the primary energy source in growing horse diets. Compared to other grains, oats is a relatively safe feed, being higher in fibre and having less indigestible starch compared to barley and corn. For growing horses requiring improved body condition (particularly as yearlings) other energy sources such as rolled barley and rice bran may be useful as these feeds tend to be “cooler” and more “conditioning”.

Protein Protein provides the amino acid building blocks for the development of the unborn foal. Good quality protein with adequate lysine and other amino acids is essential for foetal development, with the requirement increasing by 30% during the last three months of pregnancy.

It is important to ensure that the broodmare and growing foal’s diet not only contains adequate protein but that the protein is of “high quality”. Proteins composed of a high proportion of the “essential amino acids” are referred to as high-quality proteins. Those containing a high proportion of “nonessential amino acids” are low- or poor-quality proteins. Protein feeds that contain high levels of essential amino acids include soybean meal, canola meal and lupins. Copra and sunflower contain relatively low levels of essential amino acids, and are therefore generally unsuitable as the sole protein source in growing foal rations.

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Minerals and Vitamins

Dietarily, minerals and vitamins should be regarded as a group rather than individually. As the intake of a mineral increases above that needed, the amount absorbed and/or excreted in the urine and/or faeces also increases. An excess amount absorbed may be harmful. That not absorbed may bind other minerals, decreasing their absorption and possibly resulting in a deficiency of these minerals.

It is therefore the balanced amount of all minerals in the diet that is important. Indiscriminately adding one or even several minerals to the diet is likely to be more harmful than beneficial. Therefore, minerals should not be added to the diet unless it is known which ones and how much are needed.

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Importance of minerals and vitamins in stud farm nutrition Nutrient

Deficiency symptoms

Excess symptoms

Calcium

Bone deformities/skeletal weakness, problems and rickets in young horses

Phosphorus

Inadequate bone formation, retarded growth, infertility and poor conception, lowered milk production

Bone weakness, decreased uptake of calcium

Copper

Reduced cartilage formation in foals

Horses can tolerate high levels of copper in the diet, maximum tolerable level 250mg/kg

Zinc

Reduced appetite, retarded growth, thickened skin and hair loss

Enlarged joints and lameness in foals

Iron

Anaemia

Excess iron toxic to young foals

Manganese

Irregular ‘season’ cycles in mares, joint cartilage and bone formation reduced

Anaemia and infertility

Selenium

Lower fertility in mares, poor muscle development and pale, weak muscles in foals (White Muscle Disease)

Loss of hair of mane and tail, bent legs in foals, lameness and hoof separation

Iodine

Deficiency in late gestation can result in foals born dead or weak, goitre in mature horses

Infertility and abortion in mares (most commonly due to excess seaweed meal as a natural supplement). Foals can develop enlarged joints and contracted tendons if excess is fed

Vitamin A

Loss of appetite, poor growth, infertility in mares

Ill-thrift, rough coat, weakness, anaemia

Vitamin D

Depression of calcium uptake, weak bones, swollen joints, slow closure of growth plates in bone and reduced growth rate in young foals

Promotes increased uptake of calcium, especially when phosphorus is in excess, increased calcification in tissues

Vitamin E

Weight-loss, subcutaneous swellings, rough coat, decrease in the animal’s immune response to infectious diseases, impairs reproduction in both males and females of many species of animals

joint

May reduce uptake of trace minerals iron, zinc, magnesium and manganese

Adapted from: Kohnke et al. (1999)

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Developmental Orthopaedic Disease and Nutrition Developmental Orthopaedic Disease (DOD) encompasses a range of skeletal problems associated with growth and development in the foal. DOD is a multifactorial condition, but nutrition has been shown to play a key role: 

Feed imbalance and high energy intake are stronger DOD inducing factors than a high but balanced feeding level;

Feeding diets high in soluble carbohydrates to growing horses has been implicated in the development of orthopaedic diseases however several studies have failed to show a correlation between the type of feed offered to growing foals and the incidence of DOD;

While likely to be rare on the larger commercial stud farms in Australia, it has been suggested that inadequate protein intake may result in the inhibition of bone remodelling, which may contribute to DOD. Foals reared on mature grass hay or pasture forage, and a cereal grain mix containing minimal protein may be at risk of a protein deficiency which may be exacerbated under drought conditions;

Studies have shown a correlation between the occurrence of skeletal disease in horses and reduced and imbalanced amounts of calcium, phosphorus, copper and zinc. The incidence of these diseases decreased significantly when these minerals, particularly copper were increased in the diet.

It is well known that the diet of the pregnant mare can influence the “soundness” of her future foal. Recent research has shown that pregnant mares on an “enhanced” nutritional plane (i.e. more energy in the feed than required) were more likely to have foals that subsequently developed skeletal disease compared to mares kept in an average body condition during gestation. This phenomenon is referred to as “foetal programming”.

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University of Qld study: Radiograph results of foals born from mares fed higher versus lower energy diets during gestation (NA = no abnormalities) Foal Number Mare Diet Group 1 High Energy 2 High Energy 3 High Energy 4 High Energy 5 High Energy 6 Low Energy 7 Low Energy 8 Low Energy 9 Low Energy 10 Low Energy

Radiograph Comments OCD - Bone cyst left hind lateral condoyle OC left hind lateral condoyle & splint bone right fore MCIII OC - septic tendon sheath NA No Radiograph available NA NA NA NA NA

Mare body weight during gestation is therefore of critical importance. Pregnant mares should be maintained in moderate body condition (condition score 2.5-3) which can be particularly challenging when faced with good seasons (i.e. plenty of grass). Feed and supplement choices then become even more important to ensure an adequate supply of critical nutrients while minimising unnecessary body weight gain. Australian Pastures Australian pastures, particularly improved pastures for stud farms are good sources of energy and protein for mares and foals. However, mineral intake (particularly calcium, copper and zinc) may be inadequate from pasture alone. Providing free-choice supplementation, such as a salt/mineral block will provide a source of added nutrients, but it is difficult to know whether the mare or foal is consuming the proper amount each day. In these situations, a low energy but highly concentrated mineral supplement (such as a farm balancer pellet) is advised.

Summary 

Biggest challenge for stud farm nutrition: creating a balance between energy intake, pasture availability and mare and foal bodyweight

Improved pastures offer a good source of energy and protein but are nearly always lacking in critical trace minerals

The broodmare appears to play a key role in the future skeletal health of her foal

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NOTES………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… …………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………

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Lecture 9:

A ‘Horses Foot’

Luke Wells-Smith BVSc

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The Equine Hoof: Management on a Thoroughbred Stud Farm Dr Luke Wells-Smith BVSc The management of the horses foot is an essential part of the Thoroughbred industry, from foals to yearlings, to racehorses and eventually to the breeding population; broodmares and stallions. This presentation aims to describe the basic anatomy, the growth process of the foot, maintenance and common foot problems seen on Thoroughbred stud farms. Anatomy The equine foot is made up of bone, soft tissue, keratinised hoof structures and growth centres. The major bones within the foot are the pedal bone and navicular bone, and to a certain extent the short pastern bone (second phalanx). The collateral cartilages originate on the wings of the pedal bone and are attached to the coronary band. Soft tissue structures include the Deep Digital Flexor Tendon (DDFT), navicular bursa, collateral ligaments of the coffin joint and the suspensory apparatus of the navicular bone. The keratinised structures of the equine hoof include the hoof wall, sole and frog. The growth centres include the coronary band and the solar and frog corium. Growth of the Hoof The growth centres; coronary band and the solar and frog corium are responsible for the regeneration of the equine hoof as the foot starts to wear due to everyday movement and subsequent abrasion due to environmental conditions. If the foot does not regenerate or abrasion occurs at a higher rate than growth, the soft tissue and bone structures may be damaged causing lameness. The hoof wall grows down from the coronary band as small tubules, microscopically similar to strands of hair. The hoof tubules are joined together side by side and attached to the pedal bone through the lamellar attachment. The lamellar attachment is similar to that of Velcro and forms a tight interdigitating junction between the hoof wall and pedal bone. If the lamellar attachment is damaged, new lamellar tissue needs to grow down from the coronary band as the hoof tubules move towards the ground surface. The sole and frog corium grow in a similar fashion, growing from the solar surface of the pedal bone to the ground surface. Maintenance Maintaining the equine hoof is of particular importance. There are many different factors that affect how the hooves are managed, these include the age group and discipline of the horse, the

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type of ground surface, the environment moisture content, individual conformation of the horse and any hoof pathologies that may be identified. Age group Foals and weanlings require frequent farriery examinations and trimming to manage conformation through the growing phase. In the young horse the growth plates are susceptible to any changes in load, this load is transferred from the ground surface to the hoof and up the limb. Changes in hoof growth patterns and hoof conformation can affect the growth plates, particularly the distal metacarpus/metatarsus (above the fetlock) and to a smaller extent, the distal radius/tibia (above the knee and hock). Not only are the growth plates affected, so to are tendons and ligaments that interact with the hoof capsule. The hoof conformation can be affected by a disparity between the long bone length and deep digital and superficial digital flexor muscletendon unit lengths. As the long bones lengthen during a rapid growth phase, the tendons and ligaments do not grow at the same rate. This disparity in length affects the hoof wall angle and heel height, and can cause flexion of the coffin joint and possibly flexion of the pastern and fetlock joints (severe case with superficial flexor tendon involvement). Spelling and horses returning to work require particular farriery practices dependent upon multiple factors; length of time in preparation/number of starts, length of time of the spell, any medical/musculoskeletal problems sustained during track work, trainers expectations/requirements etc. The majority of horses arriving on the farm after a lengthy time at the race track have a long toe-low heel conformation. There are many variables that likely contribute to this foot conformation; length of time at the track/number of starts, type/regime of training practices, training surface, stall bedding, farrier and trainer expectations of farriery practices. Many times the horses arrive on the farm in racing plates, usually information surrounding when the horse was last shod is difficult to obtain. Based on the condition of the horseâ&#x20AC;&#x2122;s hooves, any pre-existing conditions and the length of time the horse will be spelling for, determines which farriery practices will be performed. In some cases, particularly in a short spelling time (less than 4 weeks), it is best that the horse is re-shod to reduce the length of toe and to improve heel quality and mass. This may mean that the horse is shod in a heartbar or sole pack, applied to shift load to the frog and digital cushion. Spelling periods greater than 4 weeks and if the hoof structure is adequate, removing the shoes and rounding the edges off the hooves is important. This allows the nail holes to grow out and to load the frog and digital cushion. Many times, the removal of shoes will cause a transient lameness. In many cases this is due to that fact that when

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a horse is training in a rim shoe (open heel shoe), the load over the frog and digital cushion is reduced as they are elevated from the ground surface. When we remove the shoes on arrival at the spelling farm, the frog and digital cushion can now come in contact with the ground surface, causing a transient lameness. If the lameness persists or is severe, there is likely another cause of the lameness which requires both veterinary and farrier investigations. Dependent on the trainers requirements will determine whether the horses need to be re-shod prior to leaving the farm and arriving at the training stables.

Type of ground surface Depending on what surface the horse is living on will have an affect on what hoof maintenance strategies are chosen. When horses are maintained on surfaces with a high moisture content such as on improved, irrigated pastures or after rainfall, there is a reduction on the wear of the hoof. This reduction in wear may require more regular trimming to ensure the hoof does not become too long, predisposing to white line separation, hoof wall crack and abscess formation. Depending on the soil type in combination with a high moisture content can also alter management strategies. Black soil after rain becomes sticky and will become impacted underneath the sole. The impaction of mud in the sole can cause excessive pressure on the solar corium, causing abscess formation and lameness. To prevent the impaction of mud on these soil types, regular cleaning out of the sole is important. Although the horse may live in a high moisture, low abrasive environment for the majority of the time, when moving from paddock to paddock or from paddock to the crush, the horse may encounter areas of high abrasion, such as gravel or bitumen roads. The highly abrasive environment along with higher speeds (trotting or cantering) and a soft hoof capsule can cause excessive wear on the hoof capsule and results in lameness. On rocky and sandy surfaces particularly when the moisture content is low can cause excessive abrasion. This is particularly important during the summer months. Limb conformation The way the hoof interacts with the ground surface is determined by the conformation of the limb. Horses maintained barefoot will wear according to the conformation, this is amplified when the horse is maintained on an abrasive surface. In the horse with a fetlock varus and a â&#x20AC;&#x2DC;pigeon

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toedâ&#x20AC;&#x2122; appearance will wear the lateral (outside) aspect of the hoof wall and the medial (inside) aspect will wear less, causing a discrepancy between the medial and lateral wall length. The greater the discrepancy in wall length, the more likely a lameness will develop associated with lack of wall mass. Similarly, a club foot tends to wear the toe more frequently, allowing the heel to grow longer and worsening the club foot appearance. Limb conformation and hoof wear are very important in the growing horse, particularly if wear is excessive from being maintained on a highly abrasive surface.

Common Foot Problems

Club foot The club foot can cause a problem in all age groups. It is particular importance in the growing horse if the horse is destined for the sale ring or race track. Club feet are most likely heritable (i.e. passed down from the dam or sire) and are present at birth to a certain extent. We believe that the club foot occurs as a discrepancy between the length of the bony column and the musculotendon unit, as described early. As the horse goes through different grow phases the club foot may appear worse. Couple a rapid period of growth with a highly abrasive surface, where the toe wears away and the heel grows long, the club foot can increase in severity very rapidly. Radiographs of both front feet are important in deciding the degree of club foot and to see if there is any damage to the tip of the pedal bone. The mainstays for managing the club foot in the growing horse are; 1. Reduce the tension on the deep digital flexor tendon 2. Reduce wear at the toe 3. Limit rapid growth periods By trimming the heels back to the widest part of the frog and elevating the heels with a shoe, we shift weight away from the toe and to the heels, and reduce the tension on the deep digital flexor tendon. Now it seems counterintuitive to take off heel then replace it with a wedge. The reason we do this is because the heels do not grow at a right angle to the ground surface, instead they tend to ground forward towards the toe. As the heels grow forward, the centre of pressure of the foot moves towards the toe which further increases pressure and wear at the toe. Once a shoe is in place, we reduce the wear of the hoof wall at the toe and a lot of the time we improve the comfort level of the horse which allows for the horse to use the limb correctly.

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To ensure we limit rapid growth phases diet and exercise needs to be controlled. This can be difficult with horses on pasture and with changes in weather, and horses that are still nursing from the mare. A small yard with minimal pasture is probably the best option for a growing horse with a club foot. The small yard allows for controlled exercise and for any pasture to remain relatively poor in quality. Additionally, complete feeds with a consistent hay source will provide the majority of the nutrition for the horse. It is best to involve an equine nutritionist when considering changing the diet of the growing horse. If the horse is nursing from the mare, ensure that the foal does not have access to the mares feed, either by feeding separate to each other or feeding up high so that the foal cannot reach. Also the use of a muzzle on the nursing foal can also reduce the intake of high energy milk. If the horse does not respond to the above conservative management, surgery of the check ligament of the deep digital flexor is an important treatment option in the growing horse. The check ligament helps to anchor the deep digital flexor tendon to the leg, by cutting this ligament, it releases tension on the tendon, allowing the hoof to grow in a more normal conformation. Check ligament surgeries are best performed before the age of 12 months for a good cosmetic result. The club foot is also important to consider in the adult horse. High grade club feet can impact on performance and management in the race horse, and also can be a cause of lameness in the breeding population. The reason for the cause of lameness in the breeding population is likely due to a lack of sole under the tip of the pedal bone. If the sole depth is minimal for a long period of time, the pedal bone will become irreversibly damaged causing a chronic lameness. Once damage to the pedal bone occurs, the lamellar attachment is also weaken, which predisposes the horse to laminitis. By shoeing club footed breeding stock, particularly through periods of high abrasion will reduce wear and improve sole depth, further protecting the tip of the pedal bone.

Hoof avulsions and coronary band injuries Horses tend to injure themselves and one of the more common areas of injury is the foot. Lacerations to the coronary band and damage to the hoof wall occur in all age groups and are usually associated with a high impact against a hard surface such as a fence. Injuries to the foot may vary in severity depending on what structures are involved. Injuries involving the hoof wall and coronary band are relatively uncomplicated to treat and have a good prognosis for return to racing if treated correctly. Once the hoof wall has detached from the coronary band and lamellar junction, as we learnt earlier, it needs to grow down from the coronary band. This means that any

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detached hoof wall needs to be removed as it will impinge on the new growth of hoof wall and lamellar attachment. Depending on the size of the hoof wall that needs to be removed, a hoof capsule or lower limb cast may need to be applied for four weeks. The cast keeps the area clean and provides stability, allowing the optimal environment for healing. Once the cast is removed at four weeks, a decision is made as to whether or not the horse goes back into a cast or if a shoe may be used. Lacerations involving other structures such as the pedal and navicular bones, the deep digital flexor tendon and synovial structures such as the coffin joint and navicular bursa, require a more advanced and intensive treatment plan. It is important to involve both your vet and farrier in the assessment of these injuries to ensure other soft or bony structures are not involved.

Laminitis Laminitis is typically a disease of the adult horse, however there are a small number of foals and yearlings that develop laminitis every year. Laminitis is the inflammation and subsequent damage to the lamellar attachment between the hoof wall and the pedal bone. There are three categories of the causes of laminitis that we typically describe; 1. Endocrine/Hormonal Associated Laminitis 2. Sepsis Associated Laminitis 3. Supporting Limb/Mechanical Laminitis Endocrine/Hormonal Associated Laminitis Hormone associated laminitis accounts for approximately 90% of all cases of laminitis. Two hormonal conditions of the horse that are associated with laminitis are Equine Metabolic Syndrome (EMS) and Equine Cushings Disease (PPID). EMS is associated with insulin resistance (similar to type 2 diabetes in humans), obesity and laminitis. We are still investigating exactly how insulin fits the laminitis picture, however we do know if we inject the horse experimentally with high levels of insulin, that laminitis ensues. Insulin is responsible for transporting glucose from the blood stream into the cells, along with other important hormone cascades. Insulin is produced by the body after a meal high in glucose is consumed. We think that horses that are consistently fed diets high in non-structural carbohydrates (i.e. sugar) produce spikes of insulin. These continual spikes of insulin eventually cause insulin resistance and predisposes the horse to laminitis. The best way to diagnose a horse with EMS is to perform a baseline, fasted insulin test

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and to perform a glucose feeding trial. Horses, with the exception of ponies, even with EMS, typically have a normal fasted insulin. By feeding a glucose meal based on the horses weight, we can monitor the response to glucose. Horses with insulin resistance will have a sustained high insulin level 2 hours after feeding. The interesting thing about EMS and the Thoroughbred horse population, is that insulin resistance may be transient. In the Thoroughbred broodmare in third trimester, insulin resistance may increase, similar to pregnancy diabetes in humans. This further predisposes the mare to laminitis. Equine Cushings Disease occurs in all breeds of horses, from as young as 6 years of age in ponies. Equine Cushings Disease in the Thoroughbred typically occurs at an age greater than 12 years of age. Equine Cushings Disease is the increase in size of the pituitary gland, an area of the brain responsible for hormone regulation. This results in an increase production in pre-cursor hormones, most importantly Adrenocorticotropic Hormone (ACTH). Equine Cushings Disease horses can have a long coat (in and out of winter), drink and urinate more frequently than most horses and are predisposed to laminitis. Equine Cushings Disease horses with active laminitis tend to also have insulin resistance. Sepsis Associated Laminitis Typically sepsis associated laminitis is seen in cases of systemic illness such as pneumonia, diarrhoea, severe vasculitis/cellulitis and retained placenta etc. With any of these above disease processes there is a septic focus whereby inflammatory mediators, toxins and micro-organisms are absorbed into the blood stream. These products then lodge in the microvasculature around the body causing further infection and disease. As the equine foot has an intricate microvascular bed, micro-organisms and toxins tend to lodge there. This sets up a massive inflammatory response within the hoof capsule, causing damage and eventually detachment of the lamellar apparatus and potentially sinking of the pedal bone. Sinking is the severest form of laminitis due to the massive amount of inflammation and instability of the lamellar attachment.

Supporting Limb/Mechanical Laminitis This form of laminitis is identified in horses that have had a severe lameness in one leg that results in the overloading of the supporting limb. Depending upon the initial severity of lameness and the time in which the horse was overloading the supporting limb will determine the likelihood and severity of supporting limb laminitis. The most common scenario where we see supporting

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limb laminitis in the hospital scenario is in cases of limb fracture or synovial infection (joint or bursa infection) where the horse is loading the opposite limb constantly for a long period of time. Another scenario is mechanical overload of the lamellar attachment after fast work on a hard surface. This is known as ‘road founder’ and is relatively uncommon in modern times. ‘Road founder’ was identified frequently when horses were working for long periods of time on bitumen/dirt roads. We do see some cases of ‘road founder’ particularly if horses escape their paddock and gallop along a bitumen/dirt road. Diagnosis Diagnosis of laminitis is not as straight forward as you would think. Horses can be ‘foot sore’ for a multitude of different reasons, however laminitis always needs to be ruled out in cases of lameness localised to the foot. When diagnosing laminitis it is important to take a thorough history, in particular the age and breed of the horse, pregnancy status, history of previous lameness and any systemic illness recently. The clinical signs of laminitis range in severity and depend upon whether it is an acute (recent) or chronic (ongoing) episode of laminitis. Typical clinical signs of laminitis include increased digital pulses, lameness at the walk and trot, reluctance to walk, reluctance to lift up feet, ‘saw horse stance’, divergent growth rings on the hoof capsule etc. Horses with laminitis may be positive to hoof testers, however in the dry months where the hoof capsule is hard and the horse has reasonable sole depth, the horse may not react to hoof testers. Foot x-rays are a great way to diagnose laminitis. It gives us a wide range of measurements that we can monitor as the case progresses. Some of these measurements include the sole depth under the pedal bone, width of the hoof wall, signs of pedal bone rotation etc. Radiographs can also identify areas of potential abscessation, pedal bone infection and damage, and hoof wall separation. To obtain further information on the current episode of laminitis, a venogram can be performed. The venogram is where special contrast solution is injected into the palmar digital vein and the foot is x-rayed. The contrast can be seen on the x-ray and it helps us to identify areas of poor blood supply. Blood supply is thought to be essential for foot growth and regeneration of the lamellar attachment, therefore improving areas of poor blood supply is important in cases of laminitis. X-rays and venograms are also useful to monitor the progress of a case over time. As the foot grows both the x-ray measurements and venogram findings should start to improve if we have

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applied the correct mechanics to the foot. The measurements and findings are not improving, perhaps we need to change our treatment regime. Also x-rays are useful in positioning the shoe on a laminitic foot to make sure we are in the correct position. Treatment The treatment of laminitis has varied greatly throughout history. This section will focus on the mainstays of treatment and how the Equine Podiatry and Lameness Centre manages many horses with laminitis Australia wide. Identification of the cause of laminitis As mentioned previously, there are three categories of laminitis; hormone associated, sepsis associated and supporting limb laminitis. The underlying cause of laminitis needs to be identified and managed to ensure that the laminitic episode is stabilised. Cryotherapy Applying ice to the foot and lower limb is an effective way to reduce the development of laminitis, particularly in cases of sepsis associated laminitis. The ice needs to be applied continuously and changed on a regular basis (every 2 hours in summer) to ensure a hoof wall temperature of less than 10 degrees. This form of therapy is less useful in horses that have chronic, stable laminitis and are not systemically ill. Anti-inflammatories The use of anti-inflammatories such as phenylbutazone (Bute) are important in the management of cases of laminitis. Laminitis is an inflammatory condition, therefore anti-inflammatories are essential to stop the inflammatory cascade and reduce pain. The dose of anti-inflammatories is very important. Very high doses over long periods of time can have detrimental affects of the gastro-intestinal tract and kidneys. There is minimal evidence to support the thought that antiinflammatories affect foetal growth. Mares that have had chronic, severe laminitis tend to produce small foals, however this is likely due to pain associated with the laminitic episode, not the administration of anti-inflammatories. Therapeutic shoes Depending on whether the horse is in the acute phase of laminitis or has a chronic form will depend on the type of therapeutic shoe used. The surface the horses lives on and the availability of a stable/small yard will also determine which type of shoe is recommended. The main goals for therapeutic shoeing the laminitic horse include:

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1. Reduce the tension on the deep digital flexor tendon 2. Shift the load to the back half of the foot 3. Ease break-over 4. Apply shoe parallel to the solar surface of the pedal bone By elevating the heels, as mentioned previously, will reduce the tension on the deep digital flexor tendon and shift load to the back half of the foot. Using a shoe with a rolled toe or a rocker will ease the break-over. Applying a shoe parallel to the solar surface of the pedal bone is probably one of the most important concepts, but is frequently forgotten when treating a case of laminitis. This is particularly important in cases of laminitis with pedal bone rotation. If the shoe is not applied parallel to the solar surface of the pedal bone it can cause pressure under the tip of the pedal bone and further damage will occur. In horses with pedal bone rotation, to apply the shoe parallel to the solar surface of the pedal bone requires glues and potentially cast material. This technique also requires the use of an x-ray machine to ensure the shoe is applied correctly. Cutting the deep digital flexor tendon in severe forms of laminitis can improve the outcome of many cases. By cutting the tendon we remove all of the deep digital flexor tendon pull and load the back part of the foot. Over a period of 3 months, the ends of the deep digital flexor tendon heel back together and the horse can typically walk around the paddock comfortably if the laminitic episode has been controlled. Horses with damage to the tip of the pedal bone are not good candidates for deep digital flexor tendon surgeries. Once the pedal bone is damaged it is a source of pain. If the deep digital flexor tendon is cut in cases with pedal bone damage, they tend to contract their deep digital flexor tendon over 3-6 months, requiring further surgery. Horses with pedal bone damage and pedal bone rotation require a wedged heel shoe to be applied parallel to the solar surface of the pedal bone for long periods, as described above to improve sole depth and to encourage hoof wall growth. Prognosis The long term prognosis for horses with laminitis depends on the severity of the case and the intended use of the horse. In the breeding population the horse does not need to undergo work under saddle, therefore more severe forms of chronic laminitis can be managed. If the case of laminitis is not monitored on a regular basis, damage to the pedal bone can occur. Once the pedal bone is damaged it cannot repair and a chronic lameness can occur. It is important to monitor cases of laminitis regularly both clinically and with x-rays to ensure that the pedal bone is healthy. If the pedal bone begins to deteriorate, further more intensive therapeutic shoeing practices may be required and the longevity of the case is severely affected.

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Lecture 10:

Foal confirmation & correction

Michael ‘Spook’ Neville Master Farrier

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ANGULAR LIMB DEFORMITIES IN FOALS Michael ‘Spook’ Neville Goals

Angular limb deformities (ALDs) are becoming more commonly observed in foals of all breeds for a number of reasons including over-nutrition of mares, intra-uterine malposition, ingestion of toxins by pregnant mares, and other metabolic imbalances such as defective ossification. The treatment of such foals has become more critical, especially for breeds of foals intended for high level competition. The level of treatment can range from regular therapeutic trimming, to a number of other methods, including extensions and surgery, (being mindful of the goals of the client) in considering if the foal is to become a sale prospect, a pleasure riding horse, or an athlete. Remembering that even sale prospects should have a balance between making a sale, and the horse continuing on to become a performance athlete.

Initial Observation

It is recommended to have an initial observation of all foals between 7 - 10 days of age. In many cases foals born with mild (G1) deviations can be corrected at this age with a lesser effort, due partly to improving muscle tone and strengthening ossification. It is also highly important as the new hoof is still in a pliable state. The hoof hardens considerably over several days (depending on conditions) and can harden into an imbalanced or broken away state, causing stress on growth plates etc. You should try to envision the foal’s growth development. This can take some experience, but is a very important step towards an end result. Firstly, take notice of the conformation and characteristics of the dam (mother) and also of any genetic traits of the sire.

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Consideration should then be given to muscle, height, and the environment, and lastly, whether the foal was premature or not. It is always very important to take note of the foaling date (eg: tag on the mare).

Grading

It is very important to closely monitor the foalâ&#x20AC;&#x2122;s progress right from the first consult through to yearling stage if possible. Keeping a consistent grading technique is vital for further consultations. Good grading can assist in deciding if the ALD is improving or not, which can in turn indicate whether or not to be more aggressive with further treatment. It is also very important to synchronise your grading system to others you work with (i.e. vet, farrier, stud groom, owner etc.) in order to liaise competently together. A grading system from 1 to 4 is widely used: Grade 1 being a mild deviation (etc) which is noticeable Grade 2 - an obvious deviation which is easily recognised and warrants extra treatment. Grade 3 - a major deviation requiring immediate attention plus stall rest in most cases. Grade 4 being a disaster case (weigh up options)

Angus Adkinâ&#x20AC;&#x2122;s Grading System example. +1V = Grade 1 valgus knee (+ means valgus) -1V = Grade 1 varus fetlock (- means varus)

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COMMON ALD CONDITIONS IN FOALS

Offset or Benched Knees and Varus (Deviating in) Fetlocks It is becoming more common in most breeds for foals to be born with an offset knee and varus fetlock conformation. These cases require constant monitoring using a grading system as the condition worsens with most foals, due to weight gain and muscle development through to yearling stage. Even at 7 -10 days, foals with o/s dev in will have excess medial toe growth due to load gain on the lateral side (especially the heel) which can cause uneven growth plate load (compression on the medial side) creating a worsening effect.

Grade 1 cases can be corrected successfully with balanced trimming on a regular basis, using grading to ensure progress. Grade 2 cases at 7 – 10 days should be trimmed down to level and re-examined in 7 days, depending on the result whether to push a further 7 days if improved, or a decision made for lateral extension and/or periosteal elevation (strip). Grade 3 cases generally require stall rest – knee is often bowed as well. A lateral Dalric extension (or equivalent) can be taped on for support even earlier than 7 days and glued on afterwards if no improvement. Most will require medial p.e. and possibly cannon or medial knee p.e. with extensions. Some cases can also have flexor tendon misalignment, medially. These cases can be difficult and require regulated exercise. It is important to note that fetlock growth plate (distal cannon) ossifies at 6 – 8 weeks, so p.e. results are gained from 3 – 5 weeks.

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Narrow Chest Base Wide, Rotate in with Varus fetlock Quite common in lighter breeds (t/bred, light performance horses) and also in some foals born early or first foalings. Most of these foals can be difficult to re-align, but can carry this confirmation into high level competition as most rotate in (heel out) deformities commonly land flat during flight, although will have a wing out (paddling) action. Most will have an off-set knee with a slight valgus. I have noted that over correction of varus fetlock (with strip or bridge) can aggravate valgus knee as an early yearling. Dalric extensions do not have the normal effect due to even load on landing flat. Small Equithane extensions with weekly monitoring can be effective, or strips (p.e.) with no extension. We use very few bridges on these cases.

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Rotate Out Another of the more common limb deformities - also one of the hardest to correct. It is important to note whether the foal has a narrow chest and whether the foal has a varus fetlock or hangs in, in flight – as rotate-out horses will always wing in, in flight. If the foal has a varus fetlock as well, the flight will be over-emphasised and can cause brushing during performance. A rotation can be detected during assessment by landing on the lateral heel first. Patience is the key to rotate-out deformities – being aware of varus fetlock as there is limited time to correct fetlocks. Chest muscle development helps to correct. Rotate out cases with off-set knees will often bow in flight. The bowing action should decrease as chest development increases.

Grade 1 – 2 Level trim at 7 – 10 days. RX 10 – 14 days. Level trim, again dressing medial toe (if hang in)

Grade 3 If there is no indication of varus fetlocks, stall rest with shallow bedding, and medial Dalrics taped on or glued with close monitoring of fetlocks. Never use medial Equithane, as it tends to pull hoof capsule in rapidly. Patience is the key. Be aware of possible pain related issues and chest muscle tears. Chiropractic – even low grade hoof pain can cause rotational deformity (watch for dragging in flight).

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As long weaners or yearlings, exercise to develop chest muscles can help (aquatread, ponying).Lunging in heavy conditions is not recommended as interference in flight can occur especially when tiring.

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Forward Knees – Down in Pasterns - Bowing in Flight

Each year I have noted 2 – 3 foals in this condition – generally heavy shouldered foals. If there are no major deviational faults, possibly treat with Cu-algesic or bute (low doses). Restrict exercise, slow down growth rate and look for early weaning if lacking improvement.

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Windswept

Foals born with a windswept conformation (front limbs aiming left/ hind limbs aiming right), often have a slight curvature of the spine. These foals will often respond more readily to treatment as muscle tone improves and spinal column straightens. More attention to treatment of the varus affected limbs with extensions to support load forces generally improves curvature.

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Upright (Ballerina syndrome) â&#x20AC;&#x201C;Contracted Tendons

Many foals are born with or acquire many variables of tendon contraction â&#x20AC;&#x201C; in many cases due to growth spurts (tendons not growing at same rate as bones). Foals born with deep flexor contractions (DFC) should be stall rested immediately. Support or 3 day casts are recommended in most severe cases of DFC. Foals heel(s) will be off the ground, resulting in excessive load on toe area, which can cause sole compression or bruising to the extent of small fractures of (distal) P3. Raised heel (wedged) Dalrics can be taped on and monitored daily, with use of oxytetracycline (oxytet) and/or Cu-algesic -dosage recommended by veterinarian. Do not give oxytet before foal is 24 hours old. Ulcergard is also recommended with use of bute or Cu-algesic

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If a wedged Dalric is glued, the wedge can be rasped down into a rocker shape as the foal progresses. The wedges are important tools in these situations, as they help distribute weight evenly (heel – toe), easing toe compression and also aiding in “resting” DDF, allowing the tendon to stretch (lengthen) when the heel is adjusted. If wedges are used in older foals (up to yearlings) the height of the wedge should be twice the angle (or height of heel to ground) after de-rotation when the affected leg is half a step behind normal position. The 4-point or rocker trim is recommended thereafter. In a lot of tendon contracture cases, mechanical forces can cause bowing or toeing in conformation. Lateral Dalrics with wedges can be used with the wedges alternated (on – off) as required or lateral Dalrics used in soft, deep bedding.

In severe cases where little response to treatment results in a club, surgery can be used. Either check ligament cut, or deep flexor above attachments of check (refer Dr Redden) De-rotation of P3 plus slight toe extension and raised heel putty can be applied, shortening the heel over 24 hours. Some post-surgery scarring is to be expected. One of the main goals is to maintain blood flow to circumflex arteries to promote sole growth and keep hoof quality by keeping even load pressures similar to laminitic cases. Knuckling forward of the fetlock is generally an indication of the contracture of the superficial flexor tendon, which can be very difficult to treat mechanically. Stall rest and light exercise is recommended. Also, can be pain related, so use of Cu-algesic is an option.

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Valgus Knee (Carpus) or Medial Deviation

The valgus knee conformation is very common in young foals â&#x20AC;&#x201C; especially weak or premature foals. The valgus deformity can be caused by poor ossification of the carpal bones (carpal bones can appear rounded with spaces between, indicating a lack of mineralized cartilage). Early diagnosis, restricted exercise and treatment can prevent further compression to carpal bones and compression to lateral side of the growth plate. It is very important when evaluating valgus knees (especially bi-lateral) to note whether the foal has a narrow chest, as most will improve as the chest develops, load forces shift and muscle tone develops.

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Grade 1 valgus knee cases are generally self-corrected – a level trim, RX 10 – 14 days. Grade 2 cases require a level trim at 7 – 10 days, but need constant monitoring and restricted exercise. It is also important to watch for hang in (wing in, in flight), which is a compensation for load forces Grade 3 cases need stall rest. Often the foal will need figure-8 support wraps and/or medial Dalrics taped on – closely monitored to ensure no over-correction of fetlock. We have had many cases of Grade 3 valgus where over-correction of the fetlock was apparent and lateral p.e. was necessary. Medial fetlock p.e. was performed at the same time. Growth plate above the knee ossifies at 8 – 12 weeks – therefore, allow time for other treatments before performing a p.e., as over-correction can be common. Also, note pinching or shortening of lateral physys (has a scalloped look) this can be an indication that a p.e. is warranted at this stage.

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Flaccid tendons

Many foals are born with flaccid tendons (down in pastern) more common in hind limbs. Premature foals are especially prone. Stall rest is recommended and the application a couch heel made of vetwrap and support bandages for the first 24 hours. Dalric heel extensions can be taped on for the first 2 â&#x20AC;&#x201C; 5 days. After noticing a strengthening of muscle tone, heel extension can be alternated (on â&#x20AC;&#x201C; off) in 24 hour intervals to allow strengthening to continue. (If heels are left on they become reliant). It is important to trim affected feet flat from toe to heel (sometimes lowering the heel) to alleviate a fulcrum (point of balance) to rock back behind. By pushing the point of balance back it promotes a rock forward to the toe. In severe (Grade 3) cases, a sublaxation of pastern joints can occur. Restricted exercise is essential, and a rocker shoe can be applied in older foals after muscle tone improves. Often flaccid tendons can be associated with bowed hock and/or varus fetlock. A Dalric extension shoe - modified to include heel/lateral support by use of an aluminium plate riveted on (see sickle hocks).

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Hind Limb Varus Deformities

There are a remarkable percentage of newborn foals with varus fetlocks. Noticeably in Australian thoroughbreds, there is a higher percentage in near hinds (left rear), possibly due to intra-uterine malposition. Bowing hocks can also be very common. Grade 1 cases can be easily corrected by level trim at 7 – 10 days. RX 10 days - monitor. Grade 2 cases require trim at 7 days. RX 7 - 10 days for possible lateral extension (use Dalric if hock is bowed). Grade 3 cases require stall rest and lateral Dalric taped on as early as possible. RX 7 days (possibly glue on Dalrics will be needed). It is noted that p.e. on hind limbs do not respond as well as fore limbs, therefore more emphasis is needed on mechanics.

Sickle Hocks (Curved hocks)

Sickle or curved hocks can be associated with flaccid hind tendons and can be the result of premature foaling. Most require restricted exercise and should be monitored weekly for signs of crushed or collapsed tarsal bones. An early indication of crushed tarsal bones can be a “bunny hop” action when breaking into a trot or canter. Hocks should then be radiographed to confirm. Hocks can be treated with minimal Bute or Cu-algesic (with Ulcergard) with complete stall rest with RX -14 re-assessment.

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Long Pointy Hind Toes

He untrimmed foal, even at 10 â&#x20AC;&#x201C; 12 days, can produce a long pointy toe. Many of which develop a deep stress bruise at the centre of the toe area, due to the stress on the laminae. Often these bruises can develop into an abcess (infection) which can travel up the laminae towards the coronary band. These foals should be trimmed in a 4-point fashion or squared off to relieve laminae stress, and monitored for infection. All infections (abcesses) should be poulticed in a fashion to draw infections to the distal hoof â&#x20AC;&#x201C; not encouraged to break out at the coronary band, which can leave a scarring or weakness in the laminae, which in turn can possibly lead to problems during performance years such as toe cracks.

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Applying Dalric Extensions Dalric extensions are a great aide in the treatment of many (ALDs). They can be used medially or laterally depending on whether the deformity is valgus or varus. The main aim of the Dalric Extension is to support the load forces of affected leg and to provide support for stressed sesamoids and carpal or tarsal bones as they continue to ossify. They also prevent breaking away of hoof wall which is likely due to weight bearing forces. I prefer to only use Dalric Extensions on foals up to 14 days as they support the hoof completely medial/lateral and should only be taped on up to 5-7 days. After 14 days a decision can be made whether to utilise Equithane Extensions or continue with Dalrics. In most cases where a knee or hock is bowing Dalric use should be extended. In the case of a foal rotating in the Dalric has less mechanics (see notes) therefore other treatment is necessary. The Dalric Extension has an adjustable wall which should e fitted firm but not tight, trying to allow some expansion toward the heel area. The heel area of the Dalric shoe should be modified as to not affect the coronary band. The shoe can then be either taped on (for short periods on young foals) or glued on with either Dalric Glue (provided) or with Equithane. With the aid of Elastoplast to hold shoe in place until glue sets. When a Dalric is taped on one wrap around the hoof capsule then continued around the Dalric helps prevent shoe twisting on the hoof.

It is recommended in young foals (up to 30 days) that the Dalric be removed before 7 days, after that they should be removed before 10-12 days. A close daily monitor of Dalrics several days after application is essential. Watching for signs of over correction (if used medially) also in severe

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cases a bulging of the coronary band can occur which is an actual expansion of the coronary band not a contraction of the hoof, which many people are lead to believe. If this occurs beware of slight vertical cracks below coronary band, which left unnoticed can become infected and be very painful. If this occurs remove shoe immediately and reassess for reapplication or possible Equithane. I have noted some cases where lateral extensions are used on hind limbs with bowed hocks, where there is a lot of hock action, that the shoe can grip on ground surface which can cause an aggravation of the coronary band, resulting in a horizontal crack. Softer bedding is recommended for these applications. Most Dalrics have best results in softer bedding where available.

Applying Equithane Extensions Equithane extensions are predominately utilised laterally in cases of varus fetlock deformities and rotated in deformities and are used often in conjunction with periostal elevation surgeries. It is not recommended for use on foals less than 14 days old or until hoof structure is capable of supporting an extension. Equithane should not be used on foals with any hoof wall weaknesses or cracks, etc, as the high temperature during setting time can result in a scorching of the laminate, causing infections. Also try to avoid applying Equithane to young foals in very hot conditions as rapid setting of the Equithane cases extreme heat and may cause laminate aggravation. Try to avoid foals being subject to hard surface conditions, as there have been a number of cases of lameness associated with foals galloping on hard conditions possibly causing slight P3 fractures. The amount of extension required depends on the severity of the deviation being aware of cases where there is a valgus knee involved with varus fetlocks, especially in some narrow chest base wide foals (see notes).

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Lecture 11:

X-Rays and Scoping

Angus Adkins BVSc FACVSc

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NOTES………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ………………………………………………………………………………………………………………………

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Lecture 12:

Weanling to Sale ring

Sam Fairgray

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YEARLINGS SALE ENTRY AND SELECTION VENDOR 

Choosing a sale for your yearling  Sale companies  Entry fees  Commission charges  X-Rays  Yearling conformation issues

Horse Conformation  Size/Length  Muscle mass  Leg conformation  Movement  Head  Overall appearance

Pedigree  Stallion  Dam  Foal number  Depth of pedigree ie stakes winners in first three dams  Current form of pedigree  Sex of your yearling

Buyer bench  Previous buyer history  International verse Local Market

Placement in sale catalogue  Starting letting of each sale  Market trends

Valuing your yearling  Expected price  Market valuation  Average sale price of sale

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SALES COMPANY 

When to enter your yearling  Sale entries open  Catalogues finalised and going to print

Pedigree scoring  Stallion  Mare  Understanding the scale 1-12

Physical/Type scoring  Time of sale  Physique of yearling

Stallion numbers in catalogue  Keeping your yearling at the upper end of the sale

On farm inspections  Sales company representative  Comparing your yearling to other farms

AT THE SALES 

Presentation of your yearling

Marketing

Buyer communication

CHOOSING A SALE FOR YOUR YEARLING Selecting the sale that your yearling will maximise its value takes a lot of thought and research. There is several options to sell your yearling but placement is the key to gaining the highest financial return.

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NOTES………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ……………………………………………………………………………………………………………………… ………………………………………………………………………………………………………………………

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2015 Thoroughbred Breeders Seminar Notes  

"The Dry Mare - Basic anatomy, Spring transition, Cyclicity and routine pregnancy diagnosis" "Pregnancy Assessment and Maintenance" "The Wet...

2015 Thoroughbred Breeders Seminar Notes  

"The Dry Mare - Basic anatomy, Spring transition, Cyclicity and routine pregnancy diagnosis" "Pregnancy Assessment and Maintenance" "The Wet...

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