2018 Thoroughbred Breeders NSW Seminar Notes

2018

SEMINAR NOTES

THOROUGHBRED BREEDERS SEMINAR

Hunter Valley Equine Research Centre

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TABLE OF CONTENTS SCHEDULE OF LECTURES

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LECTURES Lecture 1: STALLION PHYSIOLOGY

5-14

Lecture 2: BROODMARE PHYSIOLOGY

15-20

Lecture 3: THE DIFFICULT BREEDER

21-22

Lecture 4: INTERNAL PARASITES

23-30

Lecture 5: NUTRITION & PASTURES - feeding in drought

31-67

Lecture 6: NEWBORN FOALS

68-78

Lecture 7: MANAGING PRE-TERM LOSSES IN MARES

79-95

Lecture 8: BIOSECURITY - Psittacosis from horses, what’s the risk?

96-98

Applying OneHealth surveillance to emerging zoonoses.

Lecture 9: FOAL FARRIERY - therapeutic

99-120

Lecture 10: SCOPING, X-RAYS & SURGERY

121-132

Lecture 11: NUTRITION - yearling preparation

133-134

© August 2018 Thoroughbred Breeders Seminar The Thoroughbred Breeders NSW, Hunter Thoroughbred Breeders and the Hunter Valley Equine Research Centre does not guarantee that this publication is without flaw and do not accept any liability whatsoever for any errors, defects or omissions in the information provided.

Hunter Valley Equine Research Centre

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Schedule of lectures

DAY 1: Monday 13th August 2018 Time

Session detail

8.30am

Arrival registration, coffee and introduction

9.30 – 10.30am

Lecture 1:

10.30 – 11.00am

Morning Tea Break – in front foyer

11.00 – 12.00pm

Lecture 2:

12.00 – 1.00pm

Lecture 3:

1.00 – 2.30pm

Lunch Break – in front foyer

Thanks to “The Hunted Gourmet”

2.30 – 3.30pm

Lecture 4:

Dr Peter Carrigan BVSc BVMS Mr Chris Lawlor Managing Director – International Animal Health Products

3.30 – 4.00pm

Afternoon Tea Break – in front foyer

4.00 – 5.00pm

Lecture 5:

STALLION PHYSIOLOGY

BROODMARE PHYSIOLOGY

THE DIFFICULT BREEDER

INTERNAL PARASITES (Including Bio Worma)

NUTRITION & PASTURES (Feeding in drought)

5.00pm

Lecture room closed

5.00 – 6.30pm

Light supper and drinks evening – in front foyer An opportunity for all to speak with lecturers and 'Special Guest Speaker'

Hunter Valley Equine Research Centre

Speaker

Dr Jim Rodger BVMs MRCVSc FACVSc

Dr Sean Finan MVB DACT Dr Wendy Perriam BSc.,BVMS(hons).,MANZCVSc (Eq.Med.),CMAVA.

Dr Peter Huntington BVSc MACVSc Mr Ross Watson Agronomist – Ross Watson Agriculture

Dinner thanks to our sponsors “The Hunted Gourmet” Dr Natasha Hamilton Racing Australia Equine Genetics Research Centre

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Schedule of lectures

DAY 2: Tuesday 14th August 2018 Time

Session detail

8.30am

Registration and coffee

9.00 – 10.00am

Lecture 6:

10.00 – 10.30am

NEWBORN FOALS Morning Tea Break – in front foyer

10.30 – 11.30am

Lecture 7:

11.30 – 12.30pm

Lecture 8:

12.30 – 2.00pm 2.00 – 3.00pm 3.00 – 3.30pm 3.00 – 4.00pm 4.00 – 4.30pm 4.30pm 5.00pm

MANAGING PRE-TERM LOSSES IN MARES BIOSECURITY Psittacosis from horses, what’s the risk?

Applying OneHealth surveillance to emerging zoonoses.

Lunch Break – in front foyer Lecture 9: FOAL FARRIERY - Therapeutic Afternoon Tea Break – in front foyer Lecture 10: SCOPING, X-RAYS & SURGERY Lecture 11: NUTRITION (Feeding for yearling preparation) Open discussion and feedback survey

Speaker

Dr Niamh Collins MVB MSc DipECEIM

Dr Joan Carrick BVSc MVSc PhD Dr Kathryn Taylor Public Health Physician – Hunter New England Population Health Thanks to “The Hunted Gourmet” Mr John Whiteley Master Farrier

Dr Angus Adkins BVSc FACVSc Dr Caroline Foote BSc.Agr. MSc. PhD

Seminar closed The Thoroughbred Breeders Assoc of NSW and Hunter Valley along with the Hunter Valley Equine Research Centre wish to thank all our Speakers, Special Guests and attendees.

Hunter Valley Equine Research Centre

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Lecture 1:

STALLION PHYSIOLOGY

Dr Jim Rodger BVMs MRCVSc FACVSc

Hunter Valley Equine Research Centre

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STALLION FACTS SPERMATOGENESIS • Cycle of seminiferous epithelium from primary cell division to spermatids with elongated nuclei takes 12 ¼ days • Spermatozoa enter caput epididymus after 35 days, can appear in ejaculate after 40 days • Total 40-49 days • OPTIMUM SPERM PRODUCTION • Total daily sperm output, depends on testicular size • Large variation between stallions • Seasonal variation (Peak June NH, Dec SH)

• Variation between fractions of sperm sample EJACULATION • 6-9 jets of semen • Most spermatozoa in first 3 jets • Sperm concentration varies between jets from about 5 million/ml in the first to less than 100 million in the last • Fewer sperm in the post ejaculate drops THE SPERM CELL • Single head + midpiece + tail • Plasma membrane over head • DNA in head • Double layered acrosome at tip of head • Cytoplasmic droplets, lost as sperm matures • Tail abnormalities affect motility • Size: – Approx 6.5-7 um long – Approx 3.5-4 um wide

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Lecture 2: BROODMARE PHYSIOLOGY Dr Sean Finan MVB DACT

Hunter Valley Equine Research Centre

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BROODMARE PHYSIOLOGY Sean Finan MVB Diplomate ACT Specialist in Equine Reproduction

Reproductive activity in the mare is seasonal; the natural breeding season in the horse extends from early spring until late summer which in the Southern Hemisphere is approximately October to March.

Horses are sometimes called ‘long day’ breeders; this refers to the link between increasing day length and reproductive cyclicity. There are secondary factors such as increasing temperature and increased dietary intake that also influence the onset of the breeding season. Due to the universal foaling date selected by many breed societies and the associated market forces it is desirable to produce a foal as early in the breeding season as possible, this means we breed mares earlier than they otherwise would under natural conditions.

This annual rhythm is controlled by the pineal gland at the base of the brain; the pineal gland releases melatonin in response to darkness and arrests melatonin release during periods of light. The action of the pineal gland influences the hypothalamus, also at the base of the brain, causing it to produce Gonadotrophin Releasing Hormone (GnRH). GnRH acts on the pituitary gland and results in the release of Follicle Stimulating Hormone (FSH) and Luteinising Hormone (LH) which act directly on the mare’s ovary to encourage follicular growth and subsequently ovulation respectively.

We can exploit the link between day length and reproductive cyclicity by artificially exposing mares to increased day length. This is a long-standing technique and was first described in 1947 by Burkhardt. Currently this is achieved by either maintaining mares under electric light in a stable or yard facility or by using a light mask that produces dim blue light into a single eye. Both methods have been shown to be equally successful in hastening the breeding season in non-cycling (anoestrus) mares. Both of these regimens should provide 16hrs of light followed by 8hrs of darkness. It has been industry tradition to provide light to a 12’ by 12’ stall with a 100W bulb which typically will produce approximately 100lux or ‘enough light to read a newspaper’.. More recent work published from University College Dublin in Ireland suggests that the amount of light needed may be even lower and they demonstrated that even 10lux of blue light was sufficient to suppress melatonin secretion.

The ‘equilume light mask’ that are now familiar to many provide 50lux of blue light. It takes 35 days to have any noticeable impact on the transition period so exposure to light therapy for a minimum of 60-70 days prior to intended breeding is recommended. With this in mind, Thoroughbred mares in the Southern Hemisphere typically begin light therapy on or before the 1st of July. It should be noted that light therapy does not hasten transition but merely starts the process earlier than it would otherwise happen, hence the importance of beginning light therapy in a timely manner.

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The onset of reproductive cyclicity is however not a sudden event, the hormonal changes are gradual occurring over a period of weeks called ‘transition’ or ‘vernal transition’. Mares in transition will have multiple follicles on their ovaries and experience multiple waves of follicular development, but do not ovulate. They experience periods of sexual receptivity and will ‘tease’ to a stallion but do not have a corresponding dominant follicle and do not ovulate, so these heat periods are not fertile. This phenomenon is known as ‘spring heating’. On average there are 3.7 follicular waves each lasting approximately 10 days each during the transition phase.

Once normal cyclicity has begun, the mare will typically cycle regularly every 21 days. During this time there is clear activity on the ovaries characterised by a follicular wave where multiple follicles grow until one in particular becomes dominant and ultimately ovulates releasing the oocyte (egg) for fertilisation in the oviduct. This cycle is made up of two distinct phases, the first phase, oestrus (56days), a period of sexual receptivity associated with a dominant follicle and the second phase, dioestrus (15 days), a period of non-receptivity associated with a structure known as a corpus luteum, the remnant the dominant follicle that has ovulated.

This 21 day cycle is controlled by a complex interaction of hormones. FSH (follicle stimulating hormone) is released by the pituitary gland at the base of the brain and stimulates growth of follicles on the ovaries. There are one or sometimes two waves of follicular growth before one follicle becomes dominant. The dominant follicle releases oestrogen (E2) at a rate relative to its size, (ie it secretes more E2 as it gets bigger). The dominant follicle concurrently secretes another hormone, inhibin. Inhibin negatively feeds back to the pituitary, signalling to reduce the amount of FSH being produced. Oestrogen is also feeding back centrally at the same time except it is signalling the follicles readiness to ovulate, when oestrogen levels reach a certain threshold, the pituitary releases a surge of LH (luteinising hormone) which results in ovulation.

During ovulation the dominant follicle collapses and subsequently fills up with blood. The cells that made up the wall of the follicle (Theca cells and Granulosa cells) now comingle and change their secretory activity, no longer producing oestrogen but now producing progesterone (P4). They now become large and small luteal cells, they form a structure on the ovary called a Corpus Haemorrhagicum which in a few days will organise and become a Corpus Luteum or CL. Progesterone is sometimes referred to as the hormone of pregnancy, its name is a combination of the latin terms pro meaning for and gestare meaning to bear or pregnancy. Progesterone is vital for the maintenance of pregnancy and the early pregnancy in the mare is reliant on the CL to produce the progesterone required for its survival. We have a synthetic analogue of progesterone called altrenogest popularly marketed initially as Regumate although it is sold under many different brand names now as both an oral and injectable preparation. Altrenogest has been shown to maintain pregnancy in mares without CLs and so were not producing any progesterone themselves, clinically however, low progesterone levels as a primary reason for pregnancy failure is quite rare.

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If a mare does not become pregnant, the CL continues to produce P4 until approximately day 14-16 when the endometrium or lining of the uterus releases prostaglandin (PGF2α). PGF2α acts on the CL causing luteolysis or destruction of the CL which then ceases progesterone production allowing the cycle to continue.

If the mare is bred at the appropriate time, the sperm and oocyte bind in the oviduct and if fertilisation is successful, the resulting embryo develops in the oviduct for 5-6 days before being released into the uterus proper. There follows a period of transit of the embryo around the uterus which appears to be important in signalling to the mare that she is pregnant (maternal recognition of pregnancy), this is a very complex interaction that in addition to the mobility of the embryo, involves chemical/hormonal signalling between the embryo and the mare that is not yet well understood.

During this time, the embryo continues to grow and at approximately day 17 becomes fixed in one location in the uterus; this is often at the junction of the body and the horns of the uterus, also called the corpus cornual junction. At this point the pregnancy is still being supported by progesterone from the initial CL, the ability of the CL to produce progesterone begins to decline slightly by day 35. In order to maintain progesterone levels necessary for pregnancy, the mare has developed a unique mechanism, between days 25-35, cells from the developing conceptus called trophoblastic cells begin to invade the lining of the uterus (endometrium) and form structures not seen in any other domestic animals, called endometrial cups. These cups produce large amounts of equine Chorionic Gonadotrophin (eCG) (previously called Pregnant Mare Serum Gonadotrophin (PMSG)). eCG, in combination with FSH from the pituitary stimulate the development of secondary and accessory CLs. The endometrial cups continue to secrete eCG until day 70 at which point the amount of eCG secreted begins to reduce as the endometrial cups start to degenerate, until day 110-120 at which point they are fully necrosed and detached from the endometrium. From 120 days to term Progesterone is produced by the foetoplacental unit. We use progesterone as a catch all term but in reality there are several different sub-types which work in concert to maintain the pregnancy (the main type produced by the fetoplacental unit is called 5α pregnanes), these different types make testing progesterone levels at this point in pregnancy difficult and results are generally unreliable on most commercially available machines. Fetoplacental progestin production is sufficient to maintain pregnancy as was demonstrated by studies that removed mares ovaries at approximately day 100 and the majority of mares continued their pregnancy to term without any supplemental progesterone.

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Gestational length in the mare is highly variable with the normal range suggested to be 330-360 days although there are reports of mares foaling later than this without complication for mare or foal.

Onset of foaling is heralded by yet another complex hormonal interplay. The foetus produces additional cortisol which aids in foetal maturation and signals a reduction in progesterone production.

Increases in Oestrogens, PGF2α, Relaxin and Oxytocin combine to facilitate relaxation of the cervix and expulsion of the foal. Parturition is divided into three stages: Stage 1 lasts 30mins to 4hrs. This is the period when the cervix relaxes and uterine contractions increase in intensity and the foal begins to rotate into position for delivery. During stage 1 the mare becomes restless, may appear mildly colicky and urinate small amounts frequently.

Stage 2 begins when the chorioallantois ruptures or the ‘waters break’. Once the foetus passes into pelvic canal additional oxytocin is released and abdominal contractions are elicited in what is called the ‘Ferguson reflex’. Stage two in the mare is explosive and typically lasts 20-30 minutes.

Stage 3 of parturition encompasses passing of the foetal membranes and uterine involution.

Membranes are typically passed within 3 hours of foaling and if not passed by this time may require treatment to hasten expulsion.

As the majority of mares foal at unsocial hours it would be beneficial to be able to confidently predict the time of foaling. Physical changes in the mare such as vulval laxity, relaxation of the pelvic ligaments, udder enlargement and ‘waxing’ of teat ends provide indications of imminent parturition.

Unfortunately we do not currently have a test that is 100% reliable. Along with the aforementioned physical cues there are some changes in the composition of mares’ milk prior to foaling that can be useful in monitoring readiness to foal. Calcium concentration in mares’ milk increases dramatically in the days prior to foaling and the levels of Potassium and Sodium invert typically within 24-36 hours before parturition. More recently, studies from Japan have identified milk pH as an indicator of readiness to foal which can be easily measured on certain readily available pH test strips. Both the milk electrolyte test and milk pH test appear to be better at predicting when the mare will not foal.

For example calcium concentrations can remain elevated for one day or for several days prior to foaling however mares are less likely to foal is calcium concentration is low. These tests are less reliable in maiden mares and mares with placentitis and other pathologies. They can be quite useful in planning the timing of surgery in cases where an elective caesarean section is required.

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The mare is also unique in that uterine involution and cyclicity occurs rapidly after foaling. 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). Careful selection of mares to be bred on this ‘foal heat’ can result in excellent pregnancy rates however conversely poor selection can result in poor pregnancy rates and an increased incidence of early embryonic loss. Studies have shown that the uterus is not histologically (microscopically) normal until 14-15 days in mares that have had an uncomplicated foaling.

Combining this information with the knowledge that it takes 5-6 days for the embryo to enter the uterus post ovulation allows us to formulate some rules to observe for maximum efficiency when using the foal heat. The rules are as follows: 1. Mare younger than 14 years old.

2. Uncomplicated foaling. (Including timely passing of placenta) 3. No evidence of any uterine abnormality. (the uterus is involuted to its normal size and there is no intraluminal fluid) 4. Ovulation occurs on day 10 or later.

As can be seen from this very brief synopsis, the physiology of the mare is complex and there is still much to be learned. Some suggestions for further reading are listed below:

1. Pathways to Pregnancy & Parturition (3rd edition). P.L. Senger Publisher: Current Conceptions This is not an equine specific book and covers the general principles of reproductive physiology in most domestic species with specific examples where applicable.

2. Manual of Equine Reproduction (3rd Edition). S. Brinsko, T. Blanchard, D. Varner and others Publisher: Mosby Elsevier

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Lecture 3:

THE DIFFICULT BREEDER

Dr Wendy Perriam BSc BVMS MANZCVSc CMAVA

Hunter Valley Equine Research Centre

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BROODMARES – THE DIFFICULT BREEDER NOTES………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… …………………………………………………………………………………………………………

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Lecture 4:

INTERNAL PARASITES

Dr Peter Carrigan BVSc BVMS

Mr Chris Lawlor Managing Director – International Animal Health Products

Pic Virbac

Hunter Valley Equine Research Centre

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Gastrointestinal Parasite Management on Stud Farms

Historically, gastrointestinal (GI) parasite management on stud farms has been based on whole-herd dosing at set 6 to 8 week intervals, with seasonal rotation of the drench class.

These protocols were very successful in controlling GI parasites, but have led to: 1. the development of SIGNIFICANT drench resistance in GI parasites, 2. a change in the disease-causing parasite population of the horse (move from large strongyles, to now small strongyles in adults and ascarids in juveniles), Further points to consider with regards to GI parasite management: a) Development of new drench classes is MINIMAL to NON-EXISTENT – with no new class having reached the equine market for over 25 years. Despite the wide selection of pastes and formulations on the market, there are only actually a small selection of drench classes available to us: b) CLASS RESISTANCE PATTERNS BZ’s

oxfenbendazole, fenbendazole

widespread small strongyle resistance

avermectins (ivermectin, abamectin) and milbemycins (moxidectin)

widespread ascarid resistance

(benzimidazoles) ML’s (macrocyclic lactones) THP’s

pyrantel and morantel salts

(tetrahydropyrimidines) HC’s

piperazine

(heterocyclic compounds) IP’s (isoquinoline-pyrozines)

praziquantel

effective against tapeworm

c) Our understanding of GI parasite spread in horse populations has evolved - around 20% of horses in a population shed 80% of the worm eggs on a pasture d) Parasite free horses are not possible NOR desirable - the goal should instead be to minimise parasite egg contamination of pasture e) We need to save REFUGIA – the subpopulation of GI parasites that escape exposure or challenge from a drench, and therefore by not exposing all GI parasites in the horse population to a drench, we maintain the drench susceptibility in the parasite population.

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It is important to note that the following recommendations only apply to horses 3 years of age or greater.

This brings us to strategic drenching – a concept that attempts to find a balance between minimising the risk of parasitic infections in horses, control parasite egg contamination of the environment, but also prevent the development of drench resistance.

It involves a targeted approach to GI parasites at an individual horse level, by identifying HIGH worm egg shedding horses through Faecal Egg Counting (FEC’s) and treating just those individuals.

This reduces our use of drenches by up to 80% - a financial saving, but also maintains REFUGIA, because by not drenching the LOW and MODERATE worm egg shedding horses, we are not exposing the GI parasites in these horses to a drench, thereby maintaining drench susceptibility in a parasite population.

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So let’s apply this knowledge. Drenching programs for adult horses should be designed with the

following principles in mind:

•

Two drench treatments per annum to all horses will be sufficient to control large stongyles, bots, and habronema. Focus drench treatments during seasons of peak transmission (i.e. SPRING [e.g.

Equest Plus Tape] and AUTUMN [ML+THP+IP – e.g. Equimax Elevation]).

•

All further treatments should be targeting HIGH shedding horses as identified through Faecal Egg Counts.

•

The old concept of “rotating” drenches is no longer recommended. Have your veterinarian regular evaluate the effectiveness of the drenches used on your farm every 2-3 years (using the FECRT).

•

Always use a DUAL-ACTIVE drench (i.e. 2+ drench classes): o Equimax Elevation – ivermectin, pyrantel & praziquantel

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o

AMMO Allwormer (red) – abamectin & morantel

o

Strategy-T – oxfenbendazole & pyrantel

o

MecWorma and Tape Allwormer – abamectin & morantel

o

Worma Paste – oxfenbendazole & piperazine

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Horses less than about 3 years of age require special attention as they are more susceptible to parasite infection and are more at risk for developing disease. During the first year of life foals should receive a minimum of four anthelmintic treatments.

• First: 8-10 weeks of age – Strategy-T • Consecutive: every 8-10 weeks – Strategy-T • Between 6 and 9 months of age and every 8-10 weeks after: swap to a dual-active drench with an ML base (e.g. Equimax Elevation, AMMO Allwormer, MecWorma & Tape Allwormer)

Environmental Management: • Rotate pasture with ruminants (i.e. cattle &/or sheep) – equine strongyle larvae are quite hostspecific and cannot infect cattle, sheep, goats or camelids • Faeces removal (every 3-5 days) – as much as is practical • Appropriate composting of manure and soiled bedding • Manage stocking densities such that there is always adequate pasture length • Don’t harrow (unless ambient temperatures exceeds 40.C) – as all this does is spread the parasite eggs across the pasture, so horses cannot pick in between faecal piles • Nematophagous fungi (BIOWORMA) looks as though it is going to be a game changer in controlling the free-living stages of parasites (i.e. pasture contamination). It will not replace the above-mentioned appropriate drenching protocols and environmental management, but it will certainly play a significant role in pasture parasite management. See over BioWorma International Animal Health.

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Biological Control of Horse Roundworms.

Feeding a natural fungus to horses can provide an effective alternative to chemical drenches to control worm parasites, by means of biological control. Rather than trying to cure round worm infestations with drugs, the aim is to break the worm life cycle by preventing livestock ingesting infective larvae when grazing.

Mode of action: Australian strains of the nematode-destroying fungus, Duddingtonia flagrans, were first discovered in a CSIRO farm survey during the early 1990s. When fed to horses, the fungal spores pass through the gut of the animal and are excreted with the worm eggs in the dung. The fungal spores then germinate and grow networks of traps which ensnare and kill the worm larvae soon after they emerge from the eggs. The adult worms living in the animals do not live forever, so this cycle of constant re-infection is required to maintain the worm infestation in the horses.

Results of Australian field studies in horses: Placebo controlled studies were conducted according to Good Clinical Practice standards by an independent contractor, in which the animals were fed the fungal spores dispersed in a nutritional supplement (placebo). The trials were undertaken in different seasons and climatic regions. In these trials efficacy was measured by direct counting of larval numbers on pasture over an 8 week period. A typical result is shown below. Over all five trials the reduction in larval numbers averaged 84 % (Healey, Lawlor et al., 2018).

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The main parasites encountered in the Australian horse trials included Small Strongyles (cyathostomes), Large Strongyles (Strongylus spp.), and Stomach Hair Worms (Trichostrongylus axei).

Safety: Long term safety studies were conducted in horses with the fungus fed at 10X dose over an 8 week period with no harm detected. Also, a suite of safety studies were conducted in laboratory animals, which showed the fungus is not infective or toxic, meaning it is safe for farmers to handle.

Residue studies: Laboratory studies by expert chemists showed that any residues produced by the fungus were below the appropriate European Union Safety guidelines. Further, investigation by specialist toxicologists showed freedom from undesirable characteristics such as genotoxicity.

Ease of use: The fungus is easy to use, by means of daily administration in a nutritional supplement or in rations. For best results, firstly perform a faecal egg count and if appropriate the horses should be treated with an effective chemical drench (avoiding total elimination of worms as young horses need to develop immunity), and then the fungus is fed to maintain their low-worm status. Ideally, the animals would also be moved at this stage onto pasture that had been rested to allow its burden of parasite larvae to die off (minimum 6 weeks). Alternately, a paddock that has been cross-grazed with another species of animal can be used. However, it is important to bear in mind the process of refugia management (see Wormboss guidelines for more about this) and to remember that the fungus will not affect worm larvae that have already emerged on the pasture.

Environmental impact of the fungus: CSIRO researchers also investigated the possible adverse effects of D. flagrans on beneficial soil organisms in a typical improved pasture (Knox et al., 2002). The presence of fungi in livestock faeces did not affect the abundance of beneficial soil nematodes and microarthropods. There were also no negative effects of fungal presence on the numbers of other nematode-trapping fungi. Over time, there was generally a decline in the presence of the fungi and the rate of decline appeared to depend on seasonal conditions. Drier conditions appeared to prolong the presence of the fungi in faecal matter.

Numerous other studies around the world have shown similar results and have demonstrated absence of impact on dung beetles and earthworms.

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Regulatory Approval: The APVMA granted registration of two products containing a CSIRO isolate of D. flagrans (IAH 1297) for control of gastrointestinal nematodes in grazing animal animals, namely BioWorma ® and Livamol® with BioWorma®. These products are made by Australian-owned International Animal Health Products Pty Ltd, who began collaboration with CSIRO in 1997.

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Lecture 5:

NUTRITION & PASTURES (feeding in drought)

Dr Peter Huntington BVSc MACVSc

Mr Ross Watson Agronomist – Ross Watson Agriculture

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Lecture 6:

NEWBORN FOALS

Dr Niamh Collins MVB MSc DipECEIM

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Common diseases of neonatal foals and when to refer 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 Laboured respiration

Respiration

Regular. 60-80 breaths/min at birth.

Decreases to 20 - 40 breaths/min within 1 hour of birth.

Exaggerated chest and abdominal movement Nostril flaring with breaths

Heart rate

Temperature

Activity

80-100 beats/min after birth. Can increase to 150 beats/min with struggling and attempts to stand.

Irregular Low >120 bpm

37.2- 38.5oC

> 38.5oC

Not reliable indicator of infection

< 37.2oC

Sitting sternal after few minutes

Not sitting sternal after birth

Standing and nursing within 2 hrs

Not standing/nursing within 3 hrs Bleeding

Umbilicus

White, moist in new born

Extremities

Warm

Cold

Urinate within 12hrs of birth

Straining to urinate

Urination

Leaking urine

Discoloured urine

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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 early neonatal period. The most common diseases which are encountered are Neonatal Syndrome, sepsis, prematurity, neonatal isoerythrolysis and diarrhoea. These diseases are outlined below.

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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.

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 period

Neonatal isoerythrolysis Bleeding into the chest or abdomen Severe bleeding from the umbilicus

Severe pneumonia Birth heart defects

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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 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 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 can tolerate any increase in milk volume.

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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 foal’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.

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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 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 unfavourable 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

Foetal Problems Maternal Problems

Twinning Placentitis Premature placental separation Sepsis (Infection) 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 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 foal’s intestinal tract can lead to poor tolerance of mare’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

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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.

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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 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

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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 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.

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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 due to the reduction in oxygen-carrying capacity of the foal’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.

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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 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) maybe 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.

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Lecture 7:

MANAGING PRE-TERM LOSSES IN MARES

Dr Joan Carrick BVSc MVSc PhD

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IMPORTANCE • Losses for Mare Owner • No return on investment • Feed • Farrier • Vet Fees • Vaccinations • Emotional Cost

Causes – Mare Factors • Mare General Health • Chronic infection • Chronic Pain • PPID or EMS • Obesity • Poor blood flow to the placenta • Poor musculoskeletal development

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CAUSES Perinatal

• Infectious/Inflammatory • Viral EHV

• EHV • EVA

• Bacterial/Fungal • • • • •

Ascending EAFL Chlamydia psittaci Focal Mucoid Other systemic • Leptospirosis

Placentitis Unknown

Other Blood flow

CAUSES

Perinatal

• Non-Infectious/Non-Inflammatory • • • •

Umbilical cord occlusion Poor placental perfusion Premature placental separation Congenital

Blood flow Unknown EHV

Placentitis

EHV

Unknown Placentitis

Blood flow

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CAUSES – INFECTIOUS/INFLAMMATORY • Placentitis • Ascending • Through the cervix

• Systemic • EAFL • Chlamydia psittaci

• Focal Mucoid

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PREVENTION • Vaccination • EHV • Keep mares in small groups • Biosecurity • Quarantine • Determine Risk • History • Lost 2 of the past 6 pregnancies • Ascending placentitis – slip more often

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TREATMENT • Monthly Antibiotics and Altrenogest • Cost for pregnancy • $4,000 - $6,000 • Is it useful?

• Antibiotic resistance

Placentitis EAFL Placentitis Unknown Placentitis EAFL Placentitis Unknown

Placentitis

Suspect

EAFL Placentitis Focal

HIGH RISK MARE • Monitor • Ultrasound examination • Blood samples • Serial progesterone and oestrogen • SAA

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Lecture 8:

BIOSECURITY

Dr. Kathryn Taylor Public Health Physician – Hunter New England Population Health

Psittacosis from horses, what’s the risk?

Applying OneHealth surveillance to emerging zoonoses

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Psittacosis from horses, what’s the risk? Applying OneHealth surveillance to emerging zoonoses.

Highlights: • Equine chlamydiosis is an emerging infectious disease of horses, with zoonotic potential in humans and implications for worker health and safety • Blood testing is unreliable for confirming the diagnosis in humans – if psittacosis is suspected, people are advised to have a nose/throat swab collected • Further understanding of the barriers and enablers to personal biosecurity practices among equine workers will assist in developing practical workplace risk minimisation strategies People who have close contact with animals, through occupation or hobby, are at an increased risk of contracting zoonotic diseases, such as psittacosis, a rare bacterial infection of humans which is endemic in Australian birds. In 2014, a cluster of respiratory illness among staff and students of a NSW veterinary school who had contact with Chlamydia psittaci-infected equine reproductive products prompted increased surveillance for the pathogen in both horses and humans in the Upper Hunter.

A multidisciplinary expert advisory group was formed in 2016. Enhanced surveillance was initiated for equine reproductive loss events, which were cross-notified to human health authorities. Contacts of confirmed equine cases were interviewed for exposure-prone procedures and symptoms of illness. This surveillance found C. psittaci was detected in ~20% of equine reproductive loss events submitted for laboratory diagnosis. However, only two thirds of people who came into contact with potentially infected material used personal protective equipment and only 18% used a face mask when working with equine reproductive materials or sick foals. Although 12 people reported symptoms of illness, none were laboratory-confirmed as having acute psittacosis through blood testing.

In 2017, further work was undertaken as the Longitudinal Equine-associated Psittacosis (LEAP) study, a seroprevalence study among a cohort of occupationally-exposed equine workers to determine exposure status both before and after foaling season. A total of 147 participants across 24 workplaces were enrolled. However, on baseline testing, although 12 people had a positive screening test (EIA antibodies), none were classified as having prior psittacosis exposure on subsequent confirmatory testing. Positive EIA antibodies were weakly associated with increasing age and number of foaling seasons worked. Those reporting a previous diagnosis of psittacosis were 3 times as likely to be EIA antibody positive as those that did not. During the 2017 foaling season, only 4% (6/129) reproductive losses/septic foals tested positive for C. psittaci. Due to a combination of low equine incidence, and poor performance of the human serological test, the second blood collection was suspended. Meanwhile, a subsequent cluster of respiratory illness in veterinary staff and students who cared for a septic foal with equine chlamydiosis at a NSW vet school resulted in one confirmed and three probable cases of human psittacosis.

In 2018, the LEAP study team will explore with people working in the thoroughbred breeding industry, factors associated with biosecurity and infection control measures when working with pregnant mares and their foals, to identify potential strategies that may reduce the risk of zoonotic infection.

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Lecture 10:

FOAL FARRIERY Therapeutic

Mr John Whiteley Specialist Master Farrier

Conformation and corrections

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ANGULAR LIMB DEFORMITIES IN FOALS 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.

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).

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Grading It is very important to closely monitor the foal’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 - 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 - a disaster case (weigh up options)

Angus Adkin’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).

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 physis (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 subluxation 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.

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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

The 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 abscess (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 (abscesses) 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 aid 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 be fitted firm but not tight, trying to allow some expansion toward the heel area. The heel area of the Dalric shoe should be modified so 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.

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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 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 rotatedin 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 causes 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:

SCOPING, X-RAYS & SURGERY

Dr Angus Adkins BVSc FACVSc

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Lecture 11:

NUTRITION (feeding for yearling preparation)

Dr Caroline Foote BSc.Agr.MSc. PhD

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2018 FEEDBACK SURVEY (Please complete and submit to the coordinators) Q1. Please rate each topic based on content & presentation (Low – Mid – High).

Please write beside each Lecture 1: STALLION PHYSIOLOGY Lecture 2: BROODMARE PHYSIOLOGY Lecture 3: THE DIFFICULT BREEDER Lecture 4: INTERNAL PARASITES Lecture 5: NUTRITION & PASTURES - feeding in drought Lecture 6: NEWBORN FOALS Lecture 7: MANAGING PRE-TERM LOSSES IN MARES Lecture 8: BIOSECURITY - Psittacosis from horses, what’s the risk?

Applying OneHealth surveillance to emerging zoonoses.

Lecture 9: FOAL FARRIERY - therapeutic Lecture 10: SCOPING, X-RAYS & SURGERY Lecture 11: NUTRITION - yearling preparation Q2. Do you think this seminar was aimed at your knowledge level? Y / N ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… …………………………………………………………………………………………………………

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Q3. Do you think there should be any practical content (hands on)?

Y/N

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Q4. Do you think any topics should be deleted from the seminar? Y/ N ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… …………………………………………………………………………………………………………

Q5. Do you think any topics should be added to the seminar?

Y/N

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Q6. Are there any other changes that could improve the seminar?

Y/N

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