2010 Thoroughbred Breeders Seminar Notes

HTBA & HVERC MIDDLE MANAGEMENT Stud Course 2010

Course Program - Day One

9.00-9.30

Registration / Introduction / Coffee

9.30 -10.30

Lecture 1

John Chopin PhD, FACVSc Mare – basic reproduction / follicular cycle Some ultrasound findings associated with the cycle

10.30 – 11.00

Coffee

11.00 – 12.00

Lecture 2

Allan Gunn, DACT Mare – Revision of the cycle Hormones involved Methods of altering and assisting cycle management Spring transition Autumn transition – shuttle mares Foal Heat ‘Lactation anoestrus’ Ultrasound finding associated with the cycle

12.00 – 13.00

Lecture 3

Jane Axon, DACVIM Neonatal Foals

13.00 – 14.00

Lunch

14.00 – 15.00

Lecture 4

Catherine Russell, FACVSc Equine Gastric Ulcer Syndrome (EGUS) EGUS on stud farms – stallions, mares, spellers, weanlings, older foals and neonates

15.00 – 15.30

Afternoon Tea

15.30 – 16.30

Lecture 5

Joan Carrick, PhD, DACVIM An update on Hendra Virus Biosecurity for known and emerging diseases Sample collection and submission to a laboratory – what stud staff can do to improve biosecurity and diagnostic outcomes.

17.00 – 17.30

Evening Drinks

17.30 – 18.00

Presentation by Kirsten Todhunter Caterpillar Abortion Status

18.00 – 20.00

BBQ and Speeches

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Course Program - Day Two 8.30 – 9.00

Breakfast

9.00 – 10.00

Lecture 6

Jim Rodger, FACVSc Stallion assessment: Libido Fertility Analysis of records Sperm analysis and the reasons for it

10.00 – 11.00

Lecture 7

Troy Butt, DACVS Laminitis: Causes, especially on stud farms How to deal with the laminitc mare Acute Chronic and associated welfare aspects

11.00 – 11.30

Coffee

11.30 – 12.30

Lecture 8

Chris O’Sullivan, DACVS Yearling radiography What do we know now?

How to optimize the procedure as vendors

12.30 – 13.30

Lunch

13.30 – 14.30

Lecture 9

John Maxwell – Alpha Horse Yearlings How to handle and deal with yearlings to assist in optimizing showing for sales

14.30 – 15.00 15.00 – 15.30

Afternoon Tea End of course discussion

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Mare Reproduction Lecture One Dr John Chopin, PhD, FACVSc Registered Specialist in Equine Reproduction Resident Veterinarian Coolmore Australia

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Anatomy Summary There are 2 ovaries in the mare (right and left). The ovaries play a critical role in reproduction to produce the oocyte (egg) for fertilisation and the hormones that help reproduction. Ovarian size can depend on activity. Small ovaries are found in anoestrus, whereas maximal size and activity is found during the breeding season. Once the follicle has released the oocyte, it collapses and forms the next important structure of the ovary – the corpus luteum. Corpora lutea (the plural of corpus luteum) form after ovulation and can start with a blood clot. The clot then shrinks and is replaced by yellow luteinised tissue which will undergo luteolysis (destruction of the corpus luteum) and form the corpus albicans. During pregnancy extra corpora lutea can form under the influence of endometrial cups between days 40 to 160. The uterine tube joins the ovary to the uterus and is the site of fertilisation and early embryonic life. The uterus is bipartite with 2 horns and a body. The endometrium has conspicuous folds with a cell cycle related to the stage of the oestrous cycle.

UTERUS

BLADDER

EXTERNAL GENITALIA

OVARY

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Ovary The basic functional unit of the ovary is the follicle. The follicle contains the oocyte (egg) and also the cells that produce the hormones important for sexual behavior and mating. The size of the ovaries depends on follicular activity. The smallest ovaries are found during anoestrus (no sexual activity), dioestrus (when the mare has “cycled off” and is not teasing) and at the end of pregnancy Once the follicle has released the oocyte, it collapses and forms the next important structure of the ovary – the corpus luteum. The mature corpus luteum is 2 to 3 cm in diameter. A mature corpus luteum is not normally seen with a large number of ovarian follicles. A large number of ovarian follicles are seen with no or a regressing corpus luteum. The largest ovarian follicles are 3 to 7 cm in diameter; however larger follicles can sometimes be present. When the ovarian follicle ovulates to release the oocyte, a corpus luteum forms. The corpus luteum starts as a blood clot in about 50% of ovulations (corpus haemorrhagicum). The clot shrinks, and the lining of the crater becomes luteinised (grayish brown in colour).

Luteolysis is the process of destroying the corpus luteum. The luteal gland is now called the corpus albicans as it regresses due to its white colour During pregnancy numerous secondary corpora lutea may form beginning on approximately day 40.

These are gone after day 160, along with the primary corpus luteum. Not all pregnancies form accessory corpora lutea and there does not appear to be any adverse effect on foetal survival.

SMALL FOLLICLE

CORPUS HAEMORRHAGICUM

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Uterine Tube The uterine tube joins the ovary to the uterus. The uterine tube has the amazing capability of transporting male and female gametes, providing the site of fertilisation, and supporting the young conceptus up to day 5.5 to 6 post ovulation, when the embryo emerges from the utero-tubal junction into the uterus.

Uterus Uterine type in the mare is bipartite, meaning that it has 2 horns as well as the main body. The surface lining of endometrium is conspicuous with longitudinal folds. The endometrial mucosa has longitudinal folds or mosaic-like folds. The uterus is responsible for receiving semen from mating, sorting good sperm from the semen and ejecting the rubbish, and then supporting the pregnancy from a young embryo to term.

Cervix The cervix is an important structure as it forms a valve from the external world into the uterus. It has to dilate enough to allow semen to enter the uterus (mating) to allow fertilization. The cervix has to stay open long enough to allow inflammatory debris to exit the uterus but close in time to stop loss

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of the very small early embryo. The cervix has to stay shut for the entire pregnancy to prevent contamination and infection. The last job is to dilate enough to allow the birth of a foal and then recover without injury.

Vagina The vagina forms the passage from the outside world to the uterus. It has to accommodate the penis of the stallion, allow urine to be dispelled without contaminating the uterus, and form the birth canal.

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External Genetalia The external genitalia provide the last of the barriers to contamination and infection to the uterus. They are responsible for sexual display, mating and also the birth of the foal. The external genitalia is delineated by the anus dorsally then the perineum between the anus and dorsal commissure of the vulva. The ventral commissure of the vulva houses the clitoris.

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Placenta The placenta is produced by the embryo/foetus and is vital for support of pregnancy. Not only does it allow the transfer of oxygen and other nutrients to the foal, it also is responsible for the removal of waste products including carbon dioxide. The placenta also has to provide a (fluid) environment for the foetus to develop inside, protect it and prepare it for life outside the uterus.

ALLANTOIS

UMBILICAL CORD

AMNION

YOLK SAC REMNANT

HIPPOMANE

CHORION AT CERVICAL STAR

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Physiology Summary Mares are seasonally polyoestrous, mediated by changing photoperiod, temperature and nutrition.

There is a breeding season and an anovulatory season separated by transitional periods. The reproductive physiology of mares is controlled by hormones including melatonin from the pineal gland, GnRH from the hypothalamus, FSH and LH from the pituitary gland, and ovarian hormones including oestradiol, progesterone, inhibin and androstenedione.

Ovulation Prediction Follicles increased in size during oestrus and were tense to touch. In the 24 hours prior to ovulation the follicles felt much softer. Ovulation prediction is difficult. There are several aspects to predicting ovulation.

1. The degree of softness is the most useful criteria for predicting ovulation. The follicle should reach an adequate size along with the definite softening on palpation. This occurs in 40% of mares in the 12 hours before ovulation. The average size of a preovulatory follicle in a Thoroughbred mare 72, 48 and 24 hours before ovulation are 40, 45 and 50 mm respectively. Individual mares are consistent in their range of ovulatory diameters between cycles.

2. The shape of the follicle changes from spherical to pear shaped in 85% of mares in the 24 hours or more consistently in the 12 hours before ovulation.

3. The follicular wall thickens, although this may happen too early to be useful.

4. The fluid in the follicle becomes slightly echogenic using ultrasonography as granulosa cells are shed. This may also occur in large degenerate follicles.

5. The follicle stops growing in the 24 hours prior to ovulation. The ovulating follicle was the largest follicle 6 days before ovulation; the second largest had stopped growing during this time.

Cervical appearance can also be used to predict ovulation. In maiden mares the preovulatory appearance of the cervix is a deep pink colour with some secretion. The cervix is uniform in shape and flattened due to it being limp with oedema. The cervical opens to 2 fingers in diameter. In

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mares that have foaled, the cervix is hard to feel during rectal palpation. It is deep pink in colour with a shiny appearance and is flaccid with oedema. The opening is 4 to 8 cm in diameter.

Luteolysis The endometrial clock for prostaglandin release is thought to be set when there is a rising level of plasma progesterone following a fresh ovulation. Hence an ovulation during dioestrus is more likely to become a persistent corpus luteum. When prostaglandin is released, luteolysis occurs and progesterone levels drop. This is the signal for FSH release and follicular growth develops.

Female Physiology and Endocrinology The mare is a seasonal breeder with the peak of breeding in late spring/summer. A transitional period follows when the mare moves from anoestrus to full cyclicity. Shedding of winter hair usually occurs as the mare comes out of anoestrus. Transition is marked by waves of emergent ovarian follicles that usually regress. One follicle eventually emerges and ovulates. This ovulation marks the start of full cyclicity. Oestrous cycles have 2 stages – oestrus and dioestrus. Oestrus is the period of oestrogen dominance; ovarian follicle dominance, maturation and ovulation; and sexual receptivity.

Dioestrus is the period of corpora luteal activity; progesterone dominance; and no sexual receptivity.

Pineal Gland The equine pineal gland is a reddish, brown ovoid projection from the epithalamus between the rostral colliculi and thalami at the base of the brain. Its short stalk contains the pineal recess of the third ventricle and a suprapineal recess covers the gland dorsally. The pineal gland is homologous to the third eye in lower vertebrates, and is responsible for interpreting environmental stimuli relating to light-dark cycle and season, with horses being long day-length breeders.

Hypothalamus Contralateral hypothalami face each other across the third ventricle of the brain. They are joined at the base, which continues into the pituitary gland. Gonadotrophin releasing hormone (GnRH), a decapeptide, is produced in the parvicellular neurosecretory cells in the preoptic nuclei. It is produced as part of a larger molecule and separated at secretion. GnRH travels to the anterior pituitary through the hypothalamic-hypophysial portal system. The hypothalamus releases GnRH to control the pituitary gland release of both follicle stimulating hormone (FSH) and luteinising hormone (LH).

During dioestrus GnRH secretion is pulsatile with small pulses interspersed with periodic large pulses. This pattern causes secretion of mainly FSH. GnRH pulses occur every 60-120 minutes in early

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oestrus and accelerate to every 20-30 minutes as ovulation approaches, leading to a change from FSH to LH dominance. Oestrogen in small amounts and progesterone in large amounts also inhibit the release of GnRH. In the early half of the oestrous cycle, however, oestrogen has a positive feedback control on the release of GnRH.

Pituitary Gland Most of the pituitary gland lies in the hypophysial fossa of the basisphenoid bone below the brain.

There are 2 parts to the pituitary gland – the neurohypophysis and the adenohypophysis. The neurohypophysis releases oxytocin into the blood stream. The oxytocin originates from the hypothalamus, in the magnocellular cells of the paraventricular nuclei, which project down into the neurohypophysis of the pituitary gland. The bulk of the adenohypophysis is the pars distalis, which produces reproductive hormones such as prolactin, FSH and LH. FSH and LH are glycoprotein hormones. Glycoprotein hormones consist of 2 dissimilar subunits, called  and . The  subunit is species specific and identical between glycoprotein hormones. The  subunit gives each glycoprotein its biological activity.

The anterior pituitary gland produces FSH in response to GnRH release. FSH then travels in the blood to the target organ, the gonads. In the female FSH stimulates ovarian follicular growth. FSH is released in a bimodal pattern with peaks in early and late dioestrus. There are 2 major waves of follicular growth coincident with the 2 surges of FSH. FSH starts to rise 4 to 5 days before an ovarian follicular wave. The peak of FSH is 3 days before the emergence of the wave, which then plateaus for 5 days. The release of FSH is driven by GnRH. Divergence of the dominant ovarian follicle coincides with the decline in FSH 2 days following wave emergence. Oestrogen and inhibin produced from the ovarian follicles act as negative feedback to FSH secretion, while activin increases FSH secretion.

LH has a similar structure and chemistry to FSH. GnRH release from the hypothalamus stimulates LH release from the pituitary gland, although there is an association between releases of oxytocin in oestrous mares and LH release so that repeated sexual stimulation might also increase LH and advance ovulation.

LH concentrations are low during the midluteal phase, but rise a few days before oestrus after progesterone decreases due to luteolysis. LH peaks during oestrus at ovulation, and returns to midluteal levels over a few days. LH is thought to be the gonadotroph responsible for luteal support.

Ovulation can occur in some mares with a low LH level, indicating that ovulation will occur without a detectable LH surge. The inverse relationship with progesterone suggests a negative feedback by progesterone.

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Ovary The ovaries are the female gonads that are responsible for production of steroid hormones and the oocyte and provide the endocrinological environment necessary to support the early stages of pregnancy. The ovaries of the mare hang from the roof of the abdominal cavity at the level of the fourth or fifth lumbar vertebrae. The left ovary is caudal to the right, but there is a lot of movement and variation in position. The equine ovary has an external collagenous zone around a central parenchyma containing follicles and corpora lutea. The parenchyma surfaces at the ovulation fossa, where oocytes are released at ovulation.

The ovary is most active in summer during the physiological breeding season and least active in winter depending on latitude. During winter anoestrus no ovarian activity is present due to inhibition of GnRH by melatonin. Late winter and early spring is the period of anovulatory receptivity called transition. Follicles produce oestrogen for prolonged periods and follicles undergo atresia rather than ovulate. In the normal oestrous cycle, there are two major waves of follicular growth coinciding with the two FSH surges. One follicle is selected to mature, while the other follicles undergo atresia. The dominant follicle ovulates and forms initially a corpus haemorrhagicum (CH) which becomes the corpus luteum (CL) under the influence of LH. The corpus luteum is derived from granulosa cells and is compelled to produce progesterone because it is incapable of converting progesterone to other hormones. Granulosa cells in the ovarian follicle luteinise before ovulation.

FOLLICLE CL

Diagram representing the hormonal interplay of the female physiology.

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OVULATING

CH

CL

FOLLICL

FOLLICE

E

Diagram representing the oestrous cycle of the mare with hormones in the graph and diagrams of the ovarian structures on the bottom. The red band represents behavioral oestrus.

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Seasonal Effects on Endocrinology Mares are seasonally polyoestrous. This is in response to changing photoperiod, temperature and nutrition. There is a breeding season and an anovulatory season separated by transitional periods.

Many mares will remain sexually receptive although the ovaries are in quiescence. Some mares continue to cycle during winter: 16 to 63%.

Season can affect the length of the oestrous cycle, through an alteration in the length of the follicular phase. Oestrus was longest in late autumn to early spring and consistently short during late spring and summer. There was a difference in the length of oestrus during summer and autumn compared with winter (6.6 days and 6.6 days vs. 9.3 days), but no difference in the length of dioestrus. In spring ovulation took longer (14 days) compared with summer (10.4 days) and autumn (10.2 days). In spring LH levels were lower and ovarian follicular growth was delayed.

Seasonal effects are controlled by the pineal gland. The use of lights and temperature in controlled chambers designed to simulate spring and summer during autumn and winter, hastened the onset of seasonal activity. Other signals are probably involved in the seasonal effect of cyclicity in mares.

Thyroxine levels were significantly higher in the cycling mares compared with mares in anoestrus during winter but no causal relationship has been established. Mares in very poor body condition entered acyclicity early, whereas most mares in very good body condition continued cycling during winter. Plasma leptin, insulin-like growth factor and prolactin were greater in mares with good body condition scores.

Seasonal effects were mediated through changing levels of GnRH secretion. One study found that total hypothalamic GnRH content was not affected by season. However, the distribution within the hypothalamus was significantly affected by season. Immunoreactive GnRH is present throughout all of the hypothalamus, with the highest concentrations in the most ventral, rostral and medial areas.

In summer GnRH accumulated in the most rostral and ventral areas of the hypothalamus. Another study examining the preoptic-suprachiasmatic area, the body of the hypothalamus and the stalk median eminence found that season affected the GnRH content of the hypothalamus, but not the concentration or total number of GnRH receptors on the anterior pituitary.

Increased photoperiod hastened the response to exogenous GnRH as measured by LH levels. The use of a dopamine antagonist, perphenazine, advanced the first ovulation after spring transition.

This may have been through the action of the pituitary hormone, prolactin.

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LH is low in winter and high in summer with no seasonal pattern to FSH fluctuations. FSH and/or LH concentrations and pulse frequency increased during spring and summer compared with winter and LH decreased in autumn. The decrease in FSH lags behind LH going into winter, so follicles can continue to develop. Season did affect the content of LH in the anterior pituitary, but not the FSH content. LH content of the anterior pituitary increased from the anoestrous to the oestrous period and LH release in response to exogenous GnRH followed a similar pattern.

Transition The breeding season is broken into 4 parts: seasonal breeding season, autumn transition, seasonal anoestrous, vernal or spring transition. The breeding season is the period of polyoestrous fertility associated with late spring and summer. Anoestrus is the period of sexual inactivity and sexual indifference during the winter months. The 2 transition periods are the periods of adaption between summer and winter.

The proposed series of inter-related steps involved in vernal transition are: 1. Increasing photoperiod acts on the pineal gland to decrease the secretion of melatonin, and this increases GnRH secretion.

2. GnRH secretion stimulates FSH release, but not LH, because of their respective pituitary gland stores.

3. Ovarian follicular development begins in response to FSH, but follicles are not steroidogenically competent, so low levels of oestrogen are secreted.

4. With time a steroidogenically competent ovarian follicle develops and high levels of oestrogen are secreted.

5. In response to oestrogen, pituitary LH synthesis and secretion occurs. The first ovulation of the year takes place.

Ovulation Ovulation occurs through the ovulatory fossa and 23 of 25 observed ovulations occurred during the night. Ovulation requires tissue remodeling to release the oocyte. Remodelling occurs through the action of matrix metalloproteinases such as colleganases, gelatinases and proteoglycans. The

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intrafollicular rise in progesterone plays an important role in the activation of these enzymes.

Ovulation occurs within 48 hours of the end of oestrus, but ovulation can occur anytime (even dioestrus) and the length of oestrus varies from 3 to 40 days.

Ovulation Prediction All the information gathered including teasing, examination of the cervix, rectal palpation and ultrasonography, aims to increase the efficiency of the stud farm by trying to minimise the number of services or inseminations per mare per oestrous cycle. This ensures that the stallion or semen is not wasted in a mare that is unlikely to ovulate within a reasonable time after insemination. This increases the efficiency of stallion usage and maximises the number of mares that the stallion can breed or inseminate in a season. The end point of the examination is a prediction of when the mare is most likely to ovulate.

Teasing The use of a trained teaser to determine which mares are in oestrus will limit the number of rectal examinations required. The teasing process is not exact and some flexibility might be required with mares that are unwillingly to show behavioural oestrus. Adequate exposure time for each mare is necessarily to induce oestrous behaviour. This will be facilitated by yard design to allow all mares’ access to the teaser with minimal competition or dominance from mares higher in the pecking order. The teaser needs to be gentle but determined, and “shy� mares might need individual attention from the teaser. This will necessitate facilities designed to minimise injury, but allow the teaser close contact with the mare.

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STALLION

MARE

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Cervical Examination

Rectal palpation of the cervix can help determine the stage of the oestrous cycle. The cervix is small, closed and firm to palpate under the influence of progesterone during dioestrus. During oestrus the cervix is relaxed, open and softer under the influence of oestrogen. The cervix is small, relaxed, but closed during anoestrus. The oedema and relaxation of the cervix increased as the time of ovulation approached. The secretions in the vagina were very stringy and clear at the time of ovulation.

FORNIX

EXTERNAL OS

Cervix in early oestrus, still slightly pale but moist and starting to open.

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Rectal Palpation Rectal palpation of the uterus and ovaries help determine the stage of the oestrous cycle. Palpation of the uterus can provide information, as the tone, the diameter and position are influenced by the stage of the oestrous cycle. Ovarian palpation can determine the activity of the ovaries and individual structures such as ovarian follicles and corpora lutea. Ovarian palpation has its pitfalls; however, as a corpus haemorrhagicum can be mistaken for an unovulated follicle.

Rectal Ultrasonography The use of ultrasound technology has greatly increased the accuracy of assessing ovarian and uterine activity. The ultrasonographic characteristics of the follicular wall were examined to identify the optimal breeding day for mares. The roughness of the follicular wall and the characteristics of follicular fluid on ultrasonography were not useful to predict ovulation. The increasing echogenicity of the granulosa layer and the appearance and development of an anechoic layer underneath the granulosa layer indicated impending ovulation. The appearance of the anechoic layer was more prominent early in the season compared with late season ovulations. The appearance of the anechoic layer was also useful to distinguish which ovarian follicle was likely to become the dominant follicle.

The changes in uterine oedema as assessed by ultrasonography have been used to predict ovulation. A score from 0 to 5 was given for the degree of uterine oedema from mil to maximal. The start of behavioural oestrus was synchronous with an endometrial oedema score of 2.

When the administration of an

Post mortem specimen showing technique of rectal ultrasonography

ovulating agent (hCG) was timed with maximal oedema rather than

given when the ovarian follicle reached 35mm in diameter, the ovulation occurred within 48 hours in 80-98% of mares. Endometrial oedema decreases before ovulation, to an average score of 1.3 at ovulation. The most dynamic change in uterine oedema is in the uterine body and this should be used instead of the uterine horns to assess impending ovulation.

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Persistent anovulatory follicles occurred in about 8% of oestrous cycles. These persistent anovulatory follicles decrease reproductive efficiency since affected mares do not ovulate and fertilization and pregnancy do not occur. Ovulation failure prolongs the interovulatory period and treatment options are limited, as the anovulatory follicles do not respond to ovulating agents. See section following for further discussion.

ULTRASOUND

UTERUS

TRANSDUCER

OVARIAN FOLLICLE

Ultrasonograph of a medium sized ovarian follicle.

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THICK WALL OF FOLLICLE

Ultrasonograph of a mature follicle with slight shape change and slightly thickened wall.

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FOLLICLE SHAPE CHANGING

Ultrasonograph of mature follicle with early shape change.

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LUTEINISING THICK WALL

REDUCED FOLLICULAR FLUID

Ultasonograph of 2 follicle in the stage of ovulating with ovarian fluid disappearing and very thickened follicular wall.

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CORPUS LUTEUM

Ultrasonograph of previous ovulating follicles that have now formed 2 corpus luteums with central blood clots.

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Combination of management tools to predict ovulation No reliable ultrasonographical predictor of ovulation could be found by. In general the combination of softening of a large follicle, particularly when painful on palpation per rectum, and a substantial change in follicular shape can be used to predict ovulation within a 24 hour period. Ovulation prediction is difficult but there are several criteria available to help predict the timing of ovulation.

1. The dominant follicle increases in size during oestrus and becomes tense to touch. In the 24 hours prior to ovulation the follicle feels much softer. The degree of softening is the most useful criteria for predicting ovulation. The follicle should reach an adequate size (ď‚ł 35mm) and a definite softening should be palpated. Softening of the follicle occurs in 40% of mares in the 12 hours before ovulation. The sizes of a preovulatory follicle in a Thoroughbred mare 72, 48 and 24 hours before ovulation are 40, 45 and 50 mm respectively. There is little variation in the range of ovulatory follicle diameter between cycles in an individual mare.

The ovulating follicle is the largest follicle 6 days before ovulation in 82% of mares, and by this time the second largest follicle stops growing. The follicle stops enlarging in the 24 hours prior to ovulation. Forty one minutes prior to ovulation a break or protrusion of the follicle wall at the ovulation fossa is a consistent feature. Thirty minutes prior to ovulation the follicle diameter decreases by 13%. The collapse and extrusion of follicle contents (or ovulation) occurs in about 42 seconds.

2. Follicle shape may also indicate impending ovulation. The shape of the follicle changes from spherical to pear shaped in 85% of mares in the 24 hours before ovulation. The mare’s ovary is unusual in that there is a collagenous zone around the ovary with the germinal parenchyma in the centre of the ovary. This limits ovulation and release of the oocyte through an ovulation fossa on the ventral border. The change in shape of the ovarian follicle prior to ovulation is the follicle forming a channel to the ovulation fossa.

3. The follicular wall thickens prior to ovulation. This may occur too early in the process to be used as an indicator for the timing of ovulation.

4. The echogenicity of the follicular wall increases (100% of mares) and echogenic spots appear within the follicle prior to ovulation (54% of mares). The fluid in the follicle becomes slightly echogenic as granulosa cells are shed. This may also occur in large degenerate follicles.

These changes are not consistent enough or close enough to ovulation to be useful in predicting the timing of ovulation.

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5. The appearance of the cervix using a speculum can be used to predict ovulation. This method is less accurate for predicting ovulation than ovarian palpation, as the cervix changes in relation to circulating steroid levels, and not in relation to ovulation. In maiden mares, the preovulatory cervix is a deep pink colour with some mucous secretion present.

The cervix is uniform in shape and flattened as it is limp with oedema. The cervix is dilated enough to insert 2 fingers (3 - 4cm). In mares that have foaled, the preovulatory cervix is difficult to feel by rectal palpation. It is deep pink in colour, has a shiny mucous appearance and is flaccid and oedematous. The external os is 4 to 8 cm in diameter.

Persistent Anovulatory Follicle (PAF) Summary Failure of ovarian follicles to ovulate can occur in spring or autumn transition but also during the season. The follicles appear large and can appear filled with blood. Anovulatory follicles can luteinise but generally fail to ovulate and are infertile. The incidence can vary from 4.5 to 8% but is more common in the late ovulatory season but is associated with age, the use of luteolytic agents and some individual mares. There are a few endocrinological studies that indicate an endocrinological defect as a possible aetiology.

Ovulation failure has been seen as a normal event during spring and autumn transition. These follicles might contain blood and fibrous bands. Thickening of the follicular wall is thought to be associated with luteinisation and the administration of prostaglandin can induce luteolysis. The majority of anovulatory follicles last 1-4 weeks, appear resistant to ovulating drugs and pregnancy is unlikely if ovulation does occur. Pregnancy rate for 71 PAF cycles inseminated was 0%. The latest paper on the incidence and appearance suggested some risk factors but did exclude large persistent anovulatory follicles that did not appear to have luteinised.

Incidence The incidence of PAFs varies from 4.5% (8 of 182 oestrous cycles) to 8.2% (151 of 1694 oestrous cycles). The incidence of PAFs might be lower in the early ovulatory season (5%) and higher in the late ovulatory season (20%) but are likely to occur early or late rather than in the middle of the season. There was a significant association with age (4.4% incidence with mares 6-10 yrs, 13.1% incidence with mares 16-20 yrs). Recurrence of PAF within the same season was high (43.5%) with the likelihood of having consecutive PAFs was 31.5%. In 6 mares that had a history of PAFs in the

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previous season, the occurrence of PAFs was 54% of all oestrous cycles. Individual mares had a lot higher incidence of PAFs (25%) than other mares (3% and none).

Ultrasonography Normal uterine oedema was seen in 78.3% of PAF cycles. Endometrial score was not different between PAFs and normal follicles for the 3 days before ovulation.

The indicators of impending ovulation (decreased turgidity, loss of spherical shape, echoic specks in antrum, serration of granulosum, and an apical area) did not differentiate viable follicles from PAFs up until the day of expected ovulation. PAF become haemorrhagic by apparent entry of blood into the follicle. There was increased blood flow in the PAF follicles 24 hours before expected ovulation but due to overlap this was not a reliable indicator. The increased blood flow of the PAFs was in the apical area where rupture should occur and in an ovulating follicle, there is minimal blood flow prior to ovulation.

Endocrinology In autumn transition, FSH surges in early

Large haemorrhagic

dioestrus reduce from

follicle

2 to 1 surge per cycle before cessation of cyclicity. LH production

Ultrasonograph of a persistent haemorrhagic follicle.

was also reduced but this was thought to be linked with reduced FSH production. These authors thought that the absence of the FSH surge in early dioestrus lead to sub-optimal follicular development.

The plasma levels of progesterone and LH were not different between PAFs and normal follicles.

PAFs can also form during dioestrus. There was elevated plasma oestradiol in the PAF group in the late follicular stage, just before the oestradiol peak (2 days before ovulation) but no difference up until expected ovulation. On the day when mares with a mature follicle where administered an ovulating drug, there was significantly lower plasma inhibin and plasma androstenedione in those mares that had non-viable follicles.

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Plasma progesterone was measured in 42 mares with PAFs and found to be greater than 1ng/ml in 85.7% of mares. The administration of PG reduced plasma progesterone in these mares. There was an association between the use of hCG or GnRH and the luteinisation of the PAF.

Aetiology Individuals appear to be more prone to the condition. It appears to increase with age and more likely to occur early or late in the season. There are endocrinological aberrations that point to this being involved. The failure of FSH priming in early dioestrus, the increased level of plasma oestradiol and low plasma inhibin and low plasma androstrostenedione in the late follicular stage.

The use of cloprostenol to short cycle dioestrus might induce some individuals to produce PAFs and it appears to be dose dependent. The premature stimulation of a young follicle with LH/hCG could induce premature luteinisation without follicle rupture as seen in pregnant mares under constant stimulation with eCG. The use of PG can release LH and this might be the mechanism of the effect of cloprostenol on PAFs.

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From (Ginther, Gastal et al. 2006).

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From (Ginther, Gastal et al. 2006).

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From (Ginther, Gastal et al. 2006).

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Pharmacological Manipulation Summary Human Chorionic Gonadotropin (hCG – Chorulon) is used to induce ovulation when there is a mature ovarian follicle (35mm). Ovulation should occur 36 hours post injection (2500 IU, IV), but this depends on the time of the season, the maturity of the ovarian follicle and possibly previous exposure to this large antigenic molecule. Mares early or late in the season tend to act unpredictably with delayed response early or late in season or early ovulation in the late part of the season. One typical protocol is the use of hCG on a mature follicle with mating or insemination planned 24 hours after injection.

Gonadotropin releasing hormone (GnRH – Ovuplant) is a pellet injected under the skin designed to induce ovulation when given on a mature ovarian follicle. Ovulation should occur around 44 hours post injection. Response is a little more dependable with mares that may have developed antibodies to hCG and are showing a subsequent delayed response. This drug is more expensive and the main use is for frozen semen insemination, because the ovulation timing is in a smaller, tighter time period than with hCG. This hopefully requires less palpations and therefore less work than with the use of hCG. Cloprostenol (Estrumate) is used to induce luteolysis, however, has a high rate of side effects. This drug has uterine contraction/spasm inducing properties. In cases with excessive uterine oedema, mucoid luminal fluid or were prolonged contraction for 5 hours is desired, cloprostenol might be useful.

Altrenogest (Regumate) is most commonly used in nonpregnant mares to help shift from transition to full cyclicity. The use of Regumate should be restricted to mares that some ovarian follicles 25mm in diameter. With smaller or less ovarian activity Regumate is unlikely to work. The mare is kept on Regumate for a period of 10 days and examined. If therapy has worked there will be a large mature follicle or a fresh corpus luteum. The mare should continue to cycle normally.

Progesterone Releasing Intravaginal Device (PRID) is seen as a cheaper way of administering progestagen for 10 days. There are some limitations to their use. The first is that the response is not as dependable as Regumate, so ovarian follicles of at least 30mm should be present before a response to therapy is expected. Another limitation is the induction of a vaginitis, which will delay mating or insemination for 2-3 days until the vaginitis resolves post removal of the PRID. Problematic mares, especially with a history of endometritis should not be considered for PRID therapy because of the development of vaginitis.

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Oxytocin is used as a uterine contractility drug. Doses of 10-20 IU are used, any higher will abolish rhythmic contractions that expel fluid and induce spasm. The effect lasts 1 hour, so a frequency of up to every 2 hours can be used. Although work has been done to confirm oxytocin benefits, none has been done to investigate ideal dosing rates and intervals.

Propantheline (Propan B) is used as a parasympatholytic to relax the rectum for rectal palpation. The most common indication we use propantheline for is to induce rectal relaxation for multiple pregnancy reduction (twin squeeze). The dose is 100mg given IV, the desired effect is within 30-60 seconds with the rectum relaxing, after several minutes the uterus loses tone and is hard to locate by palpation. So the window for the desired effect is immediately after rectal relaxation and before the uterus loses its tonicity.

There are 3 stages to consider with pharmacological manipulation of the mare – anoestrous, transition, and cycling mares.

Anoestrus The manipulation of mares in deep winter anoestrus can be useful for breeding mares out of season or assisting mares that are not cycling normally during the breeding season. GnRH has been used to induce follicular activity but a single injection of 1-4mg of GnRH produced no effect. Three to 4 injections of GnRH at 10 day intervals plus concomitant progesterone treatment induced follicular development but failed to produce ovulations. The administration of GnRH in a pulsatile manner induced ovulation in 4 of 4 mares. The use of slow release GnRH caused ovulation in 13 of 18 ponies (76%) and 120 of 136 Thoroughbred mares (88%). Ovulation was induced in a dose dependent manner with an osmotic minipump delivering GnRH. Ovulation was achieved in 7 of 10 mares with 100ng GnRH/kg/hr. GnRH has also been used as a SC depot injection and at the high dose rate (90 ď ­g/day) the ovulation rate was 58.8% and this took 12.9 days to induce ovulation. A protocol for using GnRH was applied to acyclic mares during the breeding season and 86 of 108 mares (80%) ovulated. The fertility of these ovulations during the breeding season ranged from 43-48%.

Transitional The induction of ovulation in transitional mares is useful with the pressure to breed late in the transitional or early in the ovulatory season. A single injection of GnRH (2-4mg) induced ovulation in 20 of 30 transitional mares, 12 to 96 hours after injection. The use of GnRH analogue busrelin given as a twice daily IM injection induced ovulation in 7 of 15 mares. A subcutaneous implant induced ovulation in 9 of 15 mares whereas none of the controls ovulated. The repeated use of a GnRH implant in late transition could accurately induce ovulation.

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The use of allyl trenbolone – Regumate is a popular pharmacological method to shift mares through transition. Thirty two of 33 ovulated in response to the use of oral progestagen (30mg allyl trenbolone – Regumate). Clinical experience suggests that mares in late transition are more likely to respond to Regumate than mares in earlier stages of transition.

Cycling Mares are either in oestrus or diestrus during the ovulatory season. Pharmacological manipulations are either aimed at inducing predictable ovulation in oestrus or changing mares from dioestrus to oestrus. Although there is a small need to delay ovulation in oestrus when delayed inseminations are required.

The inability to accurately predict ovulation makes timed matings and timed insemination (such as with frozen semen) a labour intensive process. Ovulating agents, such as gonadotropin releasing hormone (GnRH) analogues or human chorionic gonadotrophin, narrow the window of ovulation timing, assist in synchronising and predicting the timing of mating/insemination with respect to ovulation and can hasten ovulation if administered when a mature follicle ( 35 mm) is present.

These greatly decreases the work needed to monitor mares that require timed mating or insemination.

Human Chorionic Gonadotrophin (hCG) hCG is a glycoprotein hormone with an  and a  subunit that is produced by cytotrophoblasts of the chorionic villi of the human placenta. It appears in the urine a few weeks after conception and reaches a peak at approximately 50 days of pregnancy and then decreases. hCG is used to reduce variation in the time from onset of oestrus to ovulation, and reduce the length of oestrus. hCG has a LH like action on ovarian follicles and is administered when there is a large (35 mm in diameter) mature ovarian follicle. Administration of hCG (2500IU) should cause ovulation between 24 to 48 hours after injection.

The use of hCG does not adversely affect fertility, and breeding efficiency is improved with less services by the stallion required. There is some suggestion that the use of hCG might improve fertility, as the pregnancy rate per cycle and pregnancy rate per mating was higher in the hCG group (74%, 74%) compared with the control group (40%, 31%).

Repeated use has the potential to develop refractoriness or anaphylaxis. Although 100% of treated mares produce anti-hCG antibodies with one to four injections of hCG, there is not a strong correlation between antibody titre levels and the failure to respond to hCG, or cross-reactivity with LH. It is currently recommended that hCG be not used more than twice a year in the one mare.

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Gonadotrophin Releasing Hormone (GnRH) GnRH is a decapeptide produced on ribosomes of the rough endoplasmic reticulum as a prohormone in the hypothalamus. It is then cleaved when it passes through the plasma membrane. Negative feedback to the hypothalamus is from steroid hormones. Protein hormones are not soluble so their receptors are on the outside of the plasma membrane. They modify the secondary messenger system. Peptide hormones are inactivated and degraded by elements in the blood, liver and kidney and then excreted. The administration of GnRH to mares during anoestrus and transition stimulates ovarian follicular development and ovulation by increasing FSH.

Deslorelin Deslorelin (Ovuplant TM, Peptech Animal Health Pty Ltd, NSW) is a synthetic GnRH analogue, which is presented in the form of a biocompatible slow-release pellet, which stimulates the release of LH and FSH from the pituitary gland. Each implant contains 2.1mg deslorelin (as deslorelin acetate). The chemical structure for deslorelin is {(6-D-tryptophan-9-(N-ethyl-L-prolinamide)-10deglycinamide)}GnRH. The product is a biocompatible pellet, which causes no systemic side effects and minimal local reaction. Deslorelin stimulates the release of luteinising hormone (LH) from the anterior pituitary, thus the administration of a deslorelin pellet induces ovulation within 48 hours in 80 – 96% of mares with a mature follicle. The efficacy of deslorelin inducing ovulation is equal to hCG. There is no evidence of refractoriness with repeated use, although recent work suggests there might be an increase in interovulatory period with repeated use of deslorelin in a small number of mares. The interovulatory period was significantly lengthened when control ovulations (22.0 days) were compared to those after the administration of 3 deslorelin implants at once, or one deslorelin implant administered daily for 3 days (36.8 days). Gonadotrophs were lower in the subsequent dioestrus when deslorelin was used to induce ovulation, with FSH and LH suppressed for at least 14 days after deslorelin administration. Despite early work to suggest that deslorelin does not have any negative side effects, the body of new work suggests a hypothalamic and/or a pituitary suppression in most mares for up to 2 weeks post administration.

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The Cycle Lecture Two Dr Allan Gunn BSc.Agric; BVM&S; MACVSc (horse medicine; reproduction); MRCVS; Diplomate ACT Veterinary Director (Reproduction), The Barn Veterinary Services

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Cycle Definitions In the mare, it is easier to define the beginning of the cycle as the day of ovulation.

The mare is in oestrus for approximately 4-8 days. Shows signs of heat/ in season/horsing.

Also known as the follicular phase.

The cycle length is approximately 23 days, leaving approximately 17 days of dioestrus. No obvious signs associated with this period. The non follicular, or luteal, phase.

CL

Oestrus 6 days

Unresponsive.

Dioestrus 17 days (13 days PG Response.)

4 Days

Oestrus Cycle The oestrous cycle is controlled by hormones. Hormones are produced in various parts of the body.

These hormones have effects on various tissues or organs within the body.

It is the link between the production of hormones, the inter-related effects of these hormones, and their effects on organs in the body that is known as the oestrus cycle.

It is important to realise that it is a cycle, and that the phases move from one to another in a methodical and co-ordinated manner.

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Organs, Hormones and the Links: Organs Brain

Higher centres



Hypothalamus



Surge and Tonic Centres



Pituitary

Reproductive Organs 

Ovary



Uterus



Cervix



Vestibulo-vagina and vulva

Hormones This review will be examining and discussing SIX of the main hormones involved in the reproductive cycle of the mare.

Gonadotrophin Releasing Hormone GnRH (‘The Driver’) This hormone is produced in the hypothalamus, and is a small peptide (not big enough to be a protein). Effectively this is the ‘Driver’ of the reproductive cycle. It is released in pulses and in minute quantities. It is secreted into a portal blood system, that takes it directly to the pituitary.

Follicle Stimulating Hormone - FSH (‘The Stimulator’) This hormone is produced in the pituitary and is a glycoprotein that is formed in two subunits, alpha and beta. This hormone ‘recruits’ follicles from the ovary, stimulating them to grow.

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Luteinising Hormone - LH (‘The Ovulator’) Also produced by the pituitary, a glycoprotein in two subunits. This hormone induces final growth of large follicles, and induces ovulation.

Oestrogen - E2 (‘The Receptor’) This hormone is produced by a developing follicle, so produced in the OVARY. It is a steroid hormone, that is relatively big, fat soluble and transported around the blood with carrier proteins. This hormone is important is preparing the reproductive organs, and the brain for copulation. Oestrogen controls signs of Oestrus.

Progesterone - P4 (‘The Regulator’) This hormone is produced by the ovulated follicle, or corpus luteum (CL), ie the OVARY. This is also a steroid hormone. This is the hormone that is responsible for the maintenance of pregnancy, and for the outwardly quiet behavioural signs. In the mare, it is mainly the lack of P4 that is responsible for oestrus-like behaviour. This hormone is the ‘Regulator’ of the cycle.

Prostaglandin - PGF2alpha (PG) (‘The Terminator’) Under the influence of P4 (so a CL is present), the Hypothalamic tonic centre produces low levels of GnRH. This induces release of FSH, which recruits follicles from the ovary. These follicles start to get larger. They produce E2.

The uterus does not detect a pregnancy, so there is NO Maternal Recognition of Pregnancy (MRP).

The uterus then produces PGF2a. This lyses the CL, so the production of P4 ceases. Now that there is no P4, negative feedback on the surge centre is removed.

The follicles continue to get bigger under the FSH effect. More E2 is produced by the growing follicle.

E2 has a NEGATIVE feedback effect on the FSH, so FSH production begins to decline.

E2 has a POSITIVE feedback effect on the SURGE centre, and LH production is increased. This allows the follicle to mature, and to produce more E2.

The E2 has effects on the reproductive system and brain. This induces the changes we recognise as Oestrus: Behavioural signs of looking for a male, squatting, urinating, winking and finally standing to be mounted (‘breaking down’).

Ultrasonographically we see a large follicle, and uterine oedema. Visually, an open cervix, and relaxed vulva.

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Ultimately, the hypothalamic surge centre produces a surge in GnRH production. This induces a LH surge, and the mature or ripened follicle ruptures. The oocyte, or egg, is released from the ovulation fossa which is unique to equids, and travels down the uterine tube to meet the sperm waiting for it, hopefully to unite and form an embryo. Formation of an early embryo is typically very successful, usually in the region of 90%. The embryo enters the uterus after about 5-6 days from ovulation.

The ruptured follicle then fills up with blood. Initially this is called a corpus haemorrhgicum (CH). This matures into a CL, which starts producing P4. And the cycle goes around again.

Follicular Dynamics Illustration

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Hormonal Feedback Loops

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Ultrasonographic Detection of Cyclical Changes Per rectum palpation and ultrasonography are the cornerstones of stud farm reproduction. That is not to say that other parts of the management of brood mares is not important, in fact to the contrary. Having as much information as possible, such as history, teasing, age, foal age and mare idiosyncrasies enhances breeding success. That makes it so important for you to be part of the whole breeding system.

Effectively the cycle can be followed by palpation and ultrasonographically by scanning the ovaries, uterus and cervix. The cervix and vagina/vestibule can be palpated and scanned, but are more effectively monitored visually, using a speculum, or direct palpation.

Ultrasound Ultrasound involves the use of very high frequency sound waves that are emitted from, and recorded by a transducer. Fluid looks black, dense tissues such as a CL look white. In between density of tissues are variable shades of grey. Air and bone reflect all the ultrasound waves, and shows up as a white line. It is a very safe diagnostic procedure.

Ovary The normally functional ovary is about 5-10cm in diameter. This varies with follicular sizes. Follicles grow from microscopic size, to about 50 mm in size at ovulation in the early season. Ovulation size tends to decrease as the season progresses.

The size of the follicles is detected by ultrasound, typically being noted from about 25mm in diameter. Deviation occurs at approximately 20-25mm. They grow at about 3 mm/day, and ovulate at approximately 40-45mm.

Uterus The uterus is an approximately T-shaped tubular structure. At the back of the uterus is the cervix, which is a muscular and fibrous structure. The uterus consists of the body, which runs towards the head from the cervix, forming the lower part of the T. The uterine horns, of which there are two, branch out to the left and right forming the upper part of the T. Each of those portions of the T are attached to the ovary by the uterine tubes (sometimes called oviducts).

As the cycle progresses, and the follicles grow producing more E2, the uterus appears to be more oedematous, ie. has more fluid within the tissues. This is seen on ultrasound as a slightly larger tubular diameter, with increasing visibility of ‘folds’. On the screen this has an obvious ‘cart wheel’, or ‘cut orange’ effect. The oedema and follicular size tend to increase simultaneously.

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Cervix This is an important barrier to the uterus, and consists of smooth muscle and fibrous-like tissue. It also contains mucus secreting cells. The cervix undergoes changes during the reproductive cycle reflecting this importance in allowing the entrance of sperm in oestrus, and preventing entrance of contaminants when not in oestrus- dioestrus or pregnancy.

During oestrus, the cervix is relaxed, ‘floppy, pink and open. This allows sperm to be ejaculated directly into the uterus. Being open also allows the Uterine Defence Mechanisms to clear the uterus of contaminants after copulation. When in di-oestrus, the cervix is tightly closed, contains varying amounts of mucus, and is white or pale in colour.

Vulva Although not examined ultrasonographically, it is readily examined visually. During oestrus the lips are flaccid and relaxed, similar to that noticed at foaling. When not in oestrus, they are tightly closed and firm.

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Altering the Oestrus Cycle There are two phases of the cycle

Luteal Phase Long; CL present; Dominated by Progesterone.

Follicular Phase Relatively short; Follicles present; Dominated by Oestrogen.

From this, it can be seen that the most effective way of altering the cycle is to alter the length of the luteal phase.

Increasing Luteal Phase Primary Reason: Sychronisation.

Done by substituting P4 for longer than ‘normal’. This does not always work effectively in horses, as it does in other species such as ruminants, as mares may ovulate under the influence of P4. So called ‘Dioestrus ovulation’.

Method:

Altrenogest (Regumate ®)

Daily P4 injections Intravaginal devices (CIDR®; Prid ®; Cue Mate®) Implants (not licensed for use in horses, eg Crestar®)

Decreasing the Luteal Phase: This is a relatively common practice in theriogenology. It is typically by administration of PGF2a. and is required to be administered once CL is susceptible. Doses used can be as low as 0.1 ml cloprostenol (Estrumate® or similar). Thus susceptibility depends on dose, and age of CL. Usually after 4-5 days.

It is important to note that when the mare actually shows signs of oestrus, will depend on the follicular dynamics- presence of follicles that are growing, or grown. Hence the importance of understanding the effects of growing follicles.

In the thoroughbred industry, if there is a large follicle present at the time of PG administration, it is possible that the mare will ovulate before she will stand to be served by the stallion. Typically this requires about 48 hours.

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Increasing the follicular phase In the mare this is not easy or practical, as the mare may ovulate under the influence of P4.

Decreasing the follicular phase This is commonly done in the TB industry. Using ‘ovulating’ drugs such as hCG (Chorulon®); deslorelin implants (Ovuplant®) or the ‘new’ deslorelin injection. It is important to note that this is not always successful, but has a success rate of approximately 85%. If the follicle ovulates within about 36 hours, it implies the follicle has probably ovulated on its own. The follicle needs to be mature enough to respond, and is typically more than 30mm in diameter.

Spring, or Vernal, Transition Approximately 80% of non pregnant mares outside of the tropics, will cease cycling in Winter, known as Winter Anoestrus. That means there are two transition periods; one from cycling to not cycling, in autumn. The other from not cycling to cycling, in the Spring time.

The initiation of cyclicity is effectively the same for all periods from non cycling to cycling, these are at puberty, in Spring, and after foaling.

It is important to be aware that transition does not happen overnight. It is a long slow process that takes from 45days, usually about 60-90 days to occur. The full stimuli to initiate transition are still not fully understood, nor is it understood why some mares do not stop cycling.

Undoubtedly, this is one of the most frustrating periods to deal with in the thoroughbred industry.

Transition starts with an increase in GnRH release from the hypothalamus. This is most likely from the tonic centre. The effects on the hypothalamus are probably integrated by ‘higher’ centres in the brain, and involve a series of complex inputs to the hypothalamus. Recent work has shown that the final pathway is by chemicals known as Kisspeptin, which encourages GnRH release, and RFamide related peptides (RFRP’s) which discourages GnRH release.

The tonic release of GnRH encourages the release of gonadotropins- FSH and LH- from the pituitary.

FSH appears to present within the pituitary, whereas it appears that a part (Beta subunit) of the LH requires to be made (synthesised) by the pituitary. This is the final activity prior to ovulation in vernal transition.

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The release of FSH encourages the growth of follicles within the ovary. These follicles produce oestrogen. The oestrogen feeds back on the tonic centre to produce more GnRH, so more FSH. The oestrogen prepares the mares reproductive organs, and brain for oestrus. However, it is reported to take about 3.7 waves of follicles, at about 14 day intervals to occur before ovulation will occur. (3.7 * 12= 45 days).

Once a mature follicle develops, known as steroidogenically competent, LH is manufactured, then released by the pituitary. It appears that it is the concentration of oestrogen that induces the final production of LH. A follicle that produces enough oestrogen, and has enough LH receptors (LHR’s), can now exert positive feedback on the surge centre of the hypothalamus. This GnRH surge induces an LH surge, which induces ovulation.

Once ovulation has occurred vernal transition is COMPLETED.

In summary 

Higher centre input to hypothalamus.(LIGHT)



Increased hypothalamus GnRH



Pituitary FSH release.



Follicles grow



Oestrus behaviour- variable.



Steroidogenically competent follicle



LH synthesis and release from GnRH surge

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Ovulation and the end of transition It is also important to realise, that during this time, the uterus requires to be ‘activated’ by the P4 and E2 produced in transition, as it has also been dormant during the anoestrus period.

‘Higher Centre’ Input There are many parts of the brain that detect body and environmental changes, and produce chemicals and transmitters that ultimately act on the hypothalamus.

These include Leptins (nutrition), corticosteroids and adrenaline (stress), opioids and MELATONIN. Melatonin is produced from the pineal gland, which is affected by light detected by the eye.

Increased periods of darkness relative to light, induces the production of an enzyme that is involved in the final pathway in the production of melatonin. So increased light means less enzyme, and less melatonin produced.

Melatonin in long day breeders, such as the mare, inhibits the release of GnRH from the hypothalamus. So by increasing light- day length- less melatonin is produced, and GnRH secretion is encouraged. That is thought to be one of the main mechanisms for synchronising vernal transition.

Prolactin, a short protein, is also produced by the anterior pituitary. This increases with increasing daylight, and its release is decreased by the presence of dopamine. Domperidone blocks the action of dopamine, thereby increasing prolactin.

Management of Vernal Transition Light From the discussion on the initiation of vernal transition, it can be deduced that LIGHT is probably the single most important factor in starting vernal transition. Giving barren mares access to increased day length around the time of the winter solstice (shortest day) is the most reliable method of enhancing vernal transition.

There are at least two important points: 1. Vernal transition cannot be shortened with the addition of light. It takes about 60 days (2 months) for transition to occur. The aim of lights is to bring the whole period sooner in the year. So placing mares under lights needs to be started at least by 01 July in the Southern hemisphere breeding of thoroughbreds. Ready for 01 September breeding date.

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2. Light needs to be added at the end of the day, and needs to be bright enough so that a newspaper can be read in that light. Making at least 14.5 hours of light in total for the day.

The lights should not be left on all night.

Nutrition Mares in good condition, not too thin or too fat, tend to cycle more readily earlier in the season.

There have been more than one report of the ‘green grass’ effect encouraging the end of transition.

Nutrition is obviously an important part in the reproductive cycle.

Other Management Factors: Mares should not be stressed, as corticosteroid, opioid and adrenaline release decrease GnRH release.

Temperature has an added effect, if animals are warm and comfortable, they are more likely to cycle sooner. It is interesting to note that light is also the main factor governing coat length, not temperature.

Pharmacological (Drug) Assistance in Vernal Transition There are many drugs used with varying success in manipulating vernal transition. Typically they are not very successful, and that is why there are many and varied treatments. Light is undoubtedly the most important single factor in inducing vernal transition.

GnRH or analogues Deslorelin implant (Ovuplant ®); Goserelin implant (Zoladex®); Buserelin injections (Receptal®); Gonadorelin (Fertagyl®- licensed for use in cattle and rabbits only).

Caution needs to be exercised for a number of reasons: Implants can also ‘downregulate’ the pituitary (FSH/LH), so may end up prolonging the transition period.

The doses of injectables tends to be relatively high, and often need to be given frequently.

This is costly, often with a poor response.

Some of the drugs are not licensed for use in horses, and have no proven efficacy.

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Dopamine Receptor antagonists Typically in Australia this is Domperidone. Other drugs include sulpiride and metoclopramide.

The efficacy of this drug is variable, and it appears that sulpiride may be the most effective in this family.

FSH A synthetic equine FSH (reFSH) has been used in the USA, although it is once again not available. It’s main use has been to try and superovulate mares for ET programmes. It has shown promise in enhancing the vernal transition.

Other crude extracts of the pituitary of the horse have been used with minimal success.

Porcine FSH (Folltropin ®) has been used with limited success in the mare.

LH hCG (Chorulon®) has FSH and LH effects in most species, but mainly LH effects in the mare.

The transition period may be shortened slightly by administering hCG to mares with a large steroidogenically competent follicle that is taking time to ovulate.

Oestrogen In theory, the use of oestrogen may be possible. Practically it tends to increase the length of transition due to its negative feedback on the tonic centre.

Prostaglandin Theoretically administration of PG has resulted in an increase of FSH in the brain. Practically it is not used.

Progestagens Typically this involves the use of Regumate ®, or use of an intravaginal device such as CIDR®, PRID®, or Cue Mate®.

The theory behind the use of progestagens to enhance the progression of vernal transition, is to allow the buildup of LH in the pituitary whilst under the influence of the progestagen.

This treatment meets with variable success. Mostly, the use of true progesterone, as is found in the intravaginal implants, appears to be more effective in hastening vernal transition than does the synthetic regumate. However, they all appear to be useful in synchronising the end of oestrus.

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Importantly, most drug treatments should be considered as an adjunct to management options, especially LIGHT. They are usually more effective as the mare is nearing the end of transition.

Transition is one of the most frustrating conditions to deal with as a stud worker, veterinarian, owner, and stallion manager.

Kisspeptin The possible use of Kisspeptin to induce ovarian activity in anoestrus may be the next exciting option in the quest to ‘conquer’ vernal transition frustrations.

Foal Heat After foaling, the mare quickly starts to cycle once again. It takes between 8-20 days before the mare will ovulate. It is the same sequence of events that occurs at puberty, and vernal transition, as occurs post foaling.

GnRH is produced in response to the decrease in progesterone after foaling. This leads to a pituitary release of FSH. Follicles start to grow, such that they are about 35mm at approximately 10 days post foaling. They produce oestrogen, that initially feeds back negatively on the tonic centre. LH continues to be produced to ensure the follicles mature, and produce higher concentrations of oestrogen. There is no progesterone after the end of pregnancy, and the increased oestrogen induces a surge of GnRH from the hypothalamic surge centre, and ovulation occurs. The cycle continues as normal after this. Sometimes it does not, see lactational anoestrus below.

On this subject, it is pertinent to broach the subject of foal heat mating. There are strong schools of thought, that the horse (mare) has been evolutionarily designed for this rapid return to oestrus, so that she can continue to be pregnant every 12 months. In young mares, typically below 12 and certainly below 10 years old, this is usually the case. Within certain criteria, foaling rates have reportedly been the same as those bred to later cycles. A subject which, in my opinion, should not be ignored.

‘Lactational Anoestrus’ This is a term used to describe mares that have foaled, and are lactating, that do not show signs of oestrus. Typically there are two presentations:

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1. The mare that does not show any signs of oestrus or follicular development of more than 30mm diameter for about 30 days post foaling.

2. The mare that ovulates between 10-20 days post foaling, but then does not show any signs of oestrus or follicular development for approximately 20 days after ovulation.

Although, lactational anoestrus describes the condition, it is unlikely that it is the production of milk that is causing the lack of cyclicity. Lactation does not tend to induce anoestrus in the mare, unlike other species such as the beef cow, and the pig.

There appear to be some mares that are predisposed to this condition, and will do it repeatedly.

Often they will ovulate and then ‘shut down’ for variable periods of time. Foal heat service is one option in mares with this history.

The most likely reason for the lack of cyclicity in these mares is due to a nutritional imbalance or deficit. Fortunately they are not that common, which probably explains why there is no known reason for this occurrence.

As would be expected, treatment options are many and varied, and include: 

Foal Heat mating



Increased feeding of the mare



Fostering the foal to a surrogate dam



Removing the foal from the mare for varying periods of time



Drug administration such as GnRH, FSH, Domperidone, Regumate ®, and intravaginal progesterone implants (especially where the mare has had an ovulation, this has been very successful).

Summary The ovarian cycle is just that, a cycle. Imposed on that cycle in the mare, are the periods of cyclicity, transition, and acyclicity.

Knowledge of the hormonal status during cycling allows modification of the cycle lengths to enhance productivity of reproduction in the mare.

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Common Diseases in the first three days Lecture Three Jane Axon BVSc MACVSc DACVIM Registered Specialist in Equine Medicine Clovelly Intensive Care Unit, Scone Veterinary Hospital

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Introduction Over the last 20 years there have been large developments in the treatment and management of a sick foal so that the old belief of a “sick foal is a dead foal” is no longer true. Many studies have highlighted that the quick early recognition of the sick foal and subsequent early aggressive treatment is critical to a successful outcome. Recognising the “high-risk pregnancy” and being prepared for the birth of a compromised foal is also essential.

The following article outlines problems that may indicate the birth of a potentially compromised foal, how to detect an abnormal foal and some of the more common neonatal diseases.

Careful monitoring of the pregnant mare is essential to detect any problems which may be occurring with the pregnancy. Any systemic illness the mare has during her pregnancy such as colic, diarrhoea or laminitis may have an impact on the foetus and result in the birth of a weak, compromised foal.

Mares showing clinical signs of an abnormal pregnancy may also produce a potentially compromised foal. The most common abnormal clinical signs seen during pregnancy are a purulent vaginal discharge and premature lactation or udder development, which are clinical signs of placentitis. The infection in the placenta can spread and cause an infection in the foetus. The placenta may also be compromised and therefore not provide adequate nutrition and oxygen to the foetus. A mare with a previous history of an abnormal delivery or problem pregnancy should also be monitored closely as she has an increased likelihood of producing another compromised foal. The identification of a potential problem with the pregnancy and the high possibility of a compromised foal being born should alert stud personnel and the veterinarian so there is closer monitoring of parturition and the newborn foal and there is potentially earlier detection of neonatal illness… the key to a successful outcome.

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

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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 (Figure 1) 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.

Limb abnormalities such as tendon laxity or contracture limit the foals’ ability to stand, nurse or walk and will need further veterinary attention.

Common neonatal diseases There are unfortunately many diseases the newborn foal can succumb to. The most common diseases which are seen are septicaemia, Hypoxic Ischaemic Syndrome and prematurity. Many of the diseases of the neonatal foal can occur together and are often a result of placentitis. The more common diseases encountered are outlined below.

Hypoxic Ischaemic Syndrome (“Dummy” foal) Neonatal Maladjustment Syndrome, dummy foal, wanderer, barker foal, perinatal asphyxial syndrome are all other names for Hypoxic Ischaemic Syndrome (HIS). This disease is currently thought to be caused by the lack of oxygen supply (hypoxia) and poor blood perfusion of tissues (ischaemia) of the foal which can occur either during pregnancy, during parturition or shortly after birth. Our current knowledge on the disease has been extrapolated from human medicine and experiments in other species. The severity and types of clinical signs depends on what organs are affected and on the length of time and severity of the oxygen deprivation and poor tissue perfusion.

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The most common organ systems involved are the brain, kidney and gastrointestinal tract, although any organ can be affected.

Placentitis, placental insufficiency, general anaesthetic of the pregnant mare, dystocia, C-section and premature placental separation (red-bag delivery) are all potential causes of HIS. The disease can also occur from apparently uncomplicated pregnancies and deliveries, so there is still more to learn about the different causes of this disease. After the foal is born problems such as neonatal isoerythrolysis, fractured ribs, pneumonia and prolonged recumbency from contracted tendons can lead to the development of HIS. The clinical signs may be present at birth or develop over the next 3 days and will depend on the organs involved. The clinical signs of brain involvement vary from milder clinical signs such as lack of affinity for the mare, lack of suckle reflex, inability to find the udder or hyper-responsiveness to more severe signs: irregular respiratory rate with periods of not breathing and convulsions. Foals may have abnormal vocalisation (barkers), although this is not common. If the kidneys are affected, foals may show signs of renal failure (development of oedema, produce urine at an inappropriate concentration). Gastrointestinal tract involvement may be seen as mild colic or in more severe cases the foal may display signs of septic shock, severe colic with blood discoloured diarrhoea. Treatment depends on the organ systems involved and severity of the clinical signs and is aimed at supporting the foal until the damaged tissue heals. The treatment may range from placing an indwelling stomach tube so the foal can be fed until a suckle reflex develops, to intensive therapy of intranasal oxygen (Figure 2), intravenous fluids, parenteral feeding (providing intravenous nutrition) and anticonvulsant therapy. The majority of foals (>90%) with neurological signs recover and are normal adults and athletes. If other organs are affected the recovery depends on the severity of the damage and the organs that are affected.

Prematurity The reported gestational length of the mare is from 320-365 days, however there are reports of mares which produce a normal foal at 305 or 410 days of gestation. This highlights that all mares have their own gestational length. So if a foal is born from a mare at 305 days, the foal is “normal” for the mare that has a normal gestational length of 305 days, but 4 weeks premature for a mare whose normal gestational length is 335 days. So a “premature foal” is one which is delivered before the due date of the mare. A dysmature foal is born on time for the mare however the foal hasn’t received the nutrition it needs to

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grow and is born looking like a premature foal. These foals have similar clinical problems as premature foals.

The most common cause of a premature foal is placentitis. Other causes include early removal of a foal due to severe maternal illness, twins and induction of parturition based on calendar dates rather than the foal’s maturity.

Premature foals have a classic soft silky hair coat, are small, have floppy ears, domed forehead and increased tendon and joint laxity (Figure 3). The internal organs of the foal are also “premature� so often the lungs, gastrointestinal tract, kidneys and glucose regulating systems are not functional.

These foals also have incomplete ossification of their cuboidal bones (Figure 4a & b). The immature bones are easily crushed and damaged if the foal has too much exercise or gains too much weight.

Treatment options for a premature foal range from supportive care to very intensive therapy of mechanical ventilation, intravenous fluids and parenteral nutrition. The foal will also need to be confined until there is complete ossification of the cuboidal bones (as determined by radiographs).

Their legs also need to be carefully monitored for any angular limb deformities.

The unborn foal that has been subjected to in utero stresses, which occur with a chronic illness of the mare or a placentitis, have had their maturation hastened and are often born with mature lungs and hormone regulation. These foals have a better chance of survival and thus it is possible for foals to be born as early as 280 days of gestation and survive. A foal which has been removed from the in utero environment before final maturation of the organ systems has occurred (such as with a terminal C-section in a mare with a broken leg) has an extremely poor to hopeless prognosis for life.

Septicaemia Septicaemia is a term used to describe a generalised systemic infection within the blood stream and may involve multiple organs. The infection may then localise into an area and cause an infection in the lung (pneumonia), gastrointestinal tract (enteritis), joint (septic arthritis), bone (osteomyelitis) or other area. Septicaemia is the leading cause of death in neonates. The foal can become infected before it is born (via a placentitis) or after it is born. This occurs most commonly by the foal ingesting bacteria in the first few hours of life when it is finding the udder to nurse or investigating its environment.

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Infection by bacteria can cause mild clinical signs such as dullness and decreased nursing, or can set off a cascade of reactions in the foal which can result in shock and death. It is thus imperative the infection is detected early and appropriate aggressive treatment begun. In some cases however even this is not enough to save the foal.

Treatment of these foals depends on the severity and location of the infection. Bacterial septicaemia is treated with antibiotics. Intravenous plasma may be used to improve the foal’s immunity and other therapies such as intranasal oxygen, intravenous fluids and drugs which improve the blood pressure and tissue perfusion may be utilised.

Ensuring the foal has an adequate immunoglobulin concentration (IgG) of > 8g/L, avoiding overcrowding and ensuring clean dry foaling and newborn areas are critical in trying to prevent septicaemia. Unfortunately even if all these precautions are taken, a foal may still develop septicaemia.

Diarrhoea Diarrhoea in the neonate is common and in the foal less than 3 days of age it is most commonly associated with septicaemia. The episode of diarrhoea can be mild and self limiting or life threatening with severe sepsis as seen with clostridial infections. Common signs include fever, depression, dehydration and not nursing. Often signs of colic are present, even before the foal develops diarrhoea.

Many therapies used in the treatment of diarrhoea are similar regardless of the cause. Restoring circulatory volume and correcting dehydration, electrolyte and metabolic abnormalities are essential. Intravenous fluids and electrolytes are used in more severe cases. Oral fluids and electrolyte supplementation is used in mild to moderate dehydration where there is a functional GIT. Plasma is often used if hypoproteinemia is present and it also provides immune factors.

Antibiotics should be used in foals < 7days old due to the infectious aetiologies and high risk of translocation of bacteria.

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) 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

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diarrhoea in the young foal. Their use will depend upon the clinical experience of the veterinarian and stud personnel. The use of antiulcer medications is debatable, however use is recommended in older (> 7 day old) foals. 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.

Meconium impaction Meconium is the first manure a foal will pass. It consists of amniotic fluid and cellular debris that is swallowed during the foalâ&#x20AC;&#x2122;s development in the uterus. The meconium is brown olive green in colour, firm to hard consistency and is usually passed within the first 24 â&#x20AC;&#x201C; 36 hours after birth. The meconium may become impacted in the rectum, or small or large colon. The foal may have already passed some meconium prior to signs of an impaction developing. The foal may show clinical signs of colic (rolling, kicking at belly, lying on back), straining to defaecate, wander around aimlessly or go to the udder but not nurse. The signs of colic usually occur just after the foal has just nursed.

Treatment involves administration of an enema, oral drench of paraffin oil, administer intravenous fluids and/or pain relief. Some impactions may need to be treated surgically; however this is extremely rare if the impactions are treated early.

Ruptured bladder A ruptured bladder or uroperitoneum (urine in the abdominal cavity) can occur in both colts and fillies. The defect in the urinary tract not only occurs in the bladder but can occur anywhere from the urachus (tube connecting the bladder to the amniotic sac while the foal is in utero) to the ureters (tubes from the kidney to the bladder). It has traditionally been thought to occur more commonly in colts and occur during the foaling process however recent reports have highlighted the condition is just as common in fillies and may also occur after parturition.

Foals with uroperitoneum are usually normal at birth and may urinate normally. Classically the foals strain to urinate and produce small amounts of urine; it should be noted however that foals with colic can also display these symptoms. The foalâ&#x20AC;&#x2122;s abdomen will also begin to increase in size with the increasing accumulation of urine. As the foal can not get rid of the urine out of its body, it begins to absorb the waste products from the urine and develop abnormal electrolyte abnormalities, in

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particular high potassium concentrations (an electrolyte which is high in urine). The abnormal electrolyte concentrations can become life threatening.

The foal needs surgery to repair the defect in the urinary tract. However the foal’s electrolyte levels need be stabilised first with intravenous fluids and drainage of urine from the abdomen. Once the defect is repaired the foal has a good prognosis.

Neonatal isoerythrolysis Neonatal isoerythrolysis (NI), also referred to as “jaundiced foal or haemolytic foal” occurs when the foal ingests colostrum from the mare which contains antibodies against its own red blood cells. 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 gums (Figure 5).

The mare develops antibodies by being exposed to the blood of a previous foal (such as during foaling or with a placentitis) or having a previous blood transfusion. The foal is affected if it has inherited the blood type from the stallion which the mare has produced antibodies against. There are many different blood types of horses, unfortunately the 2 most common types are the most common involved in NI. The clinical signs vary depending on the severity of the destruction of the red blood cells (haemolysis). The foal is normal at birth and then can develop symptoms within 6 hours or until around 7 days of age. The longer the clinical signs take to develop the less severe the haemolysis and clinical signs. The clinical signs range from an increased respiratory rate and jaundiced (yellow) mucous membranes to recumbency and seizures.

The treatment depends on the severity of the clinical signs, and some foals with the most severe form of the disease can die despite intensive therapy. Some foals may require intranasal oxygen therapy and a blood transfusion; other foals may just need careful monitoring.

The disease can be prevented in mares which are known producers of foals with NI. The newborn foal should not be allowed any access to the mare and receive its colostrum from another source.

The mare should be milked out for 36 hours and the milk and colostrum discarded. The foal should be fed supplementary milk for 36 hours. After this period of time the foal can then nurse from the mare.

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Umbilical problems The umbilicus or navel needs to be closely monitored for the first few weeks of life. Shortly after birth the umbilicus should be moist but have no excessive bleeding. The umbilicus should be carefully disinfected shortly after it breaks and twice daily for the first 2-3 days after birth. Dilute disinfectants such as 2.5% iodine are recommended, anything stronger may be caustic and lead to tissue damage and necrosis. The solution is best applied with a small spray bottle, spraying the umbilicus but avoiding the surrounding skin.

The umbilicus may become infected which is usually seen as moistness, tenderness to touch, presence of swelling and purulent discharge. Sometimes the internal part of the umbilicus may become infected and there is no obvious external sign of swelling or infection. Ultrasound examination will be able to visualise the infected remnants. The umbilicus may also leak urine (patent urachus) as it contains the urachus.

The majority of foals with a patent urachus or infected umbilicus will respond to medical management of antibiotic therapy and keeping the foal in a clean dry yard or small paddock.

Previously surgery was recommended however now it has been found that the majority of these conditions resolve with medical treatment alone.

Entropion This occurs when the eyelid, most commonly the lower, rolls in. It can be present at birth or occur after birth and is usually associated with prematurity, dehydration, or generalised muscle weakness.

The hair from the eyelid then rubs on the cornea and, if left untreated, results in a corneal ulcer. This can be a very serious condition and can result in loss of the foalâ&#x20AC;&#x2122;s eye. If an entropion is seen, the eyelid can be manually rolled out or temporarily sutured out, and the eye examined to assess if an ulcer has formed. Corneas are less sensitive in foals, thus ulceration can be present without evidence of pain and fluorescein staining is needed to highlight the ulcer. Treatment may involve topical broad-spectrum antibiotic therapy, though severe deep ulcers may require surgical treatment.

As highlighted above the key to a successful outcome is careful monitoring of the newborn foal so there is early detection of any illness. This will allow the instigation of early and aggressive treatment. Treatment of the critically-ill neonate is time and labour intensive thus referring your foal to an intensive care unit which will have the nursing, veterinary staff and expertise to provide 24 hour intensive care for the foal should be considered.

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Normal newborn foal

Abnormal newborn foal Dark reddish pink

Mucous membranes

Pink and moist

Purple or yellow tinge Small haemorrhages Laboured respiration

Regular. 60-80 breaths/min at birth.

Respiration

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

Exaggerated chest and abdominal movement Nostril flaring with breaths

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

Irregular

increase to 150 beats/min with struggling and attempts to stand.

Low

37.5 - 38.5oC

> 38.6oC

Not reliable indicator of infection

< 37.4oC

Sitting sternal after few minutes

Not sitting sternal after birth

Standing and nursing within 2 hrs

Not standing/nursing within 3 hrs

Temperature

Activity

Bleeding Umbilicus

White, moist in new born Leaking urine

Extremities

Warm

Cold

Urinate within 12hrs of birth

Straining to urinate

Clear

Discoloured

Urination

Table 1: Parameters of a new born foal

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Figure 1. Foal nursing showing good tongue seal on teat. Foal also has an indwelling nasogastric tube through which it had been fed until it developed the good suckle.

Figure 2. Intranasal oxygen therapy utilised on a recumbent foal with lack of tongue control, a common finding in foals with HIS.

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Figure 3. Premature foal highlighting domed forehead, floppy ears, small size, and thin silky coat.

b.

a.

Figure 4a and b. Radiographs of a hock and carpus from a premature foal with incomplete ossification.

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Figure 5. Foal with pale yellow mucous membranes from neonatal isoerythrolysis

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Equine Gastric Ulcer Syndrome (EGUS) Lecture Four Dr Catherine Russell, FACVSc Scone Equine Hospital

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Equine Gastric Ulcer Syndrome(EGUS) Anatomy and Physiology Horses are grazing animals and their digestive system is designed for constant consumption of plant food. The stomach continuously secretes acid which is important in breaking down protein. The acid secreted by the stomach is hydrochloric acid, a highly corrosive chemical, and the stomach has evolved very effective methods to counter damage to the stomach lining. The stomach can be divided into two main sections defined by the internal lining, the squamous mucosa and the glandular mucosa. These two sections are separated by the margo plicatus.

Squamous mucosa The squamous mucosa lines the oesophagus and upper half of the stomach. It has no protection from the mucous layer except for a thick layer of keratin on the surface of the cells that acts like armour reducing the risk of acid damage to the cells from contact of acid. Like all cells in the stomach they have a remarkable ability to heal.

Glandular mucosa The glandular mucosa lines the lower half of the stomach and comprises many cells that produce the various chemicals and hormones of the stomach. The parietal cells produce acid which is released into the stomach via a proton pump and this secretion is regulated by histamine, prostaglandins, and various hormones.

The glandular mucosa has many defences against acid which include buffering (bicarbonate), physical barrier (mucous) and a high blood flow to assist in rapid healing and to supply high levels of oxygen and nutrients for optimal cell health. Prostaglandins are a hormone that acts on the stomach to increase blood flow, increase mucous and bicarbonate secretion and inhibits acid release. A side effect of the family of non steroidal anti-inflammatory drugs (NSAID) (eg finadyne or phenylbutazone ie bute) is that they inhibit the production of prostaglandins in the stomach.

When these defences are overwhelmed small ulcers form and with constant exposure to acid the cells are unable to migrate and reproduce and deeper ulcers are formed. This develops a vicious cycle where damage to deeper layers releases hormones that stimulates vasoconstriction (reduced blood flow) and parietal cells to release more acid thus causing more damage to occur.

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EGUS This syndrome comprises 4 distinct conditions that affect different ages of horses and areas of the stomach, oesophagus and duodenum.

Foals 1. Neonatal Gastric Ulceration This condition is confined to newborn foals and most frequently occurs in the squamous mucosa above the margo plicatus. These ulcers are associated with poor blood flow to the stomach as is seen with hypoxic ischemic syndrome (dummy foals, red bag delivery) and septicaemia. This condition is occasionally associated with rupture of the stomach. There is a reported prevalence of 25-57% in neonates. Clinical signs are usually not shown and may not be apparent until the stomach ruptures. Recumbent neonates are more likely to have an alkaline pH whilst ambulatory foals will produce acid by 2 days of age. A retrospective study from the Neonatal Intensive Care Unit at New Bolton Center showed no difference in the survival outcome of neonates that were treated prophylactically with antiulcer medication and those that were not treated. Treatment relies on aggressive supportive care to the foal including intravenous fluids, intranasal oxygen therapy and blood pressure support.

2. Gastro-duodenal ulcer disease (GDUD) This condition is mainly seen in foals at foot and most likely starts as inflammation of the duodenum.

The thickened walls and reduced motility of the duodenum causes delayed gastric emptying and thus prolonged exposure of the stomach to acid. Severe cases can involve the lower oesophagus, stomach and duodenum. As the duodenum heals strictures (narrowing) may form that further delay gastric emptying and worsens the clinical signs. This form is likely to have an infectious cause as it can be seen in outbreaks and often following diarrhoea. Clinical signs can vary from none to diarrhoea to teeth grinding, weight loss, increased salivation, foals lying on their backs, to catastrophic signs of colic, depression and collapse with a ruptured stomach or duodenum. Acid suppression is vital in the management and treatment of these foals however has little impact on preventing the disease. Severe cases with strictures and reflux may respond to radical surgical treatment however this is currently not recommended due to their poor long term prognosis after surgery.

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Adults 3. Glandular and pyloric ulceration.

This condition is reproduced with large doses of NSAIDs such as phenylbutazone. These drugs reduce the prostaglandins delivered to the stomach which interfere with the stomach defences by reducing blood flow, bicarbonate and mucous production. This condition has clinical signs ranging from none to inappetance and colic after eating. This condition is more likely to be seen following an overdose of NSAID but may also be seen in brood mares and stallions with chronic lameness and long term treatment with phenylbutazone.

4. Squamous ulceration This well known condition is reported in 40 to 87% of performance horses particularly race horses.

Risk factors include stress, transport, high-energy feed, confinement in stalls, lack of contact with other horses, crib biting, wind sucking, playing a radio in the barn, intermittent feeding and exercise.

The number and grade of ulcer detected increases with time and intensity of training. This condition remains poorly understood as two recent studies show high levels of ulcers in brood mares (70%) and race horses (100%) housed exclusively in paddocks. The condition is performance limiting and is associated with a reduced appetite, weight loss or failure to thrive.

In the stud situation it is seen with sale preparation of weanlings and yearlings, pretraining and training of race horses, ie any condition associated with stress and boxing. This condition may also be seen in stabled stallions with a high work load, high concentrate feed and little turn out.

Treatment and prevention is dependent upon acid suppression and management changes including turnout, smaller more frequent feeding, increased roughage in the diet and reduction of stress.

Diagnosis Clinical signs in at risk horses can be highly suggestive of gastric ulcers particularly if the horseâ&#x20AC;&#x2122;s signs improve with treatment. Anti-ulcer medication is costly and so definitive diagnosis is important and is obtained by passing an endoscope into the stomach to visualise the ulcers. Horses have feed and water withheld for a minimum of 6 hours to ensure the stomach is empty and can thus be adequately visualised. Various grading systems have been developed that allow comparison between operators and between examinations to show response to treatment.

Novel techniques for diagnosing ulcers are being investigated and include breath tests and feeding a known amount of sucrose and testing the concentration in blood or urine after a set time. Sucrose can only be absorbed across damaged gastric wall.

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Treatment Treatment is reliant upon reducing risk factors and acid suppression.

Acid Supression There are many products that are marketed for sale for the treatment of EGUS. Stopping work and turning a horse out to a paddock has been reported as a highly effective treatment for gastric ulcers however this is not practical in the performance horse so we will discuss the following main antiulcer medications.

1. Histamine H2 Receptor Antagonists These drugs work directly on the histamine receptor of the gastric cell to prevent secretion of acid via the proton pump. It is worth noting that there are other receptors of lesser importance that can also stimulate the proton pump to secrete acid. This drug must be given every 8 hours for maximum effect. Ranitidine (Ulcerguard速) is the most well known of this class of drugs.

Recent claims from the company that a double and triple dose once a day are effective at preventing ulcers in racehorses are interesting however the numbers were low and there were no controls in the experiment. It should also be noted that there is significant horse to horse variation in the oral bioavailability (ability to absorb the drug) and thus the higher dose is recommended. It has been shown to resolve clinical signs of EGUS in horses in training but does not cause resolution of ulcers.

2. Proton pump inhibitors The proton pump is found on the luminal surface (interior of the stomach) of the gastric cell and is the only pump that controls release of acid into the stomach. The most well known is Omprazole (Gastrozol速, Omoguard速, Gastroguard速 etc). These drugs are given once a day and once ulcers are healed can be given at a quarter of the dose to prevent recurrence of ulcers.

Experiments in horses in training have shown a complete resolution of ulcers with these drugs.

The optimal timing of treatment is 4 -8 hours before training. The maximal response to omeprazole occurs at 3-5 days however young foals show a rapid response after the first dose.

Treatment duration Most ulcers will resolve after 2-4 weeks of treatment. Due to the variation between horses treatment times should be tailored to individual horses.

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Equine Biosecurity Hendra Virus and Other Infectious Diseases Lecture Six Dr Joan Carrick, PhD, DACVIM Scone Equine Hospital

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Purpose of Biosecurity To prevent, respond to, and recover from diseases that threaten the health and welfare of horses and the people who care for them.

Introduction The recent occurrence of Equine Influenza and Hendra virus in horses in Australia has highlighted the national importance of biosecurity however thoroughbred farms in the Hunter Valley are reminded of the importance of biosecurity every year when mares abort. An increased awareness and excellent biosecurity protocols has resulted in a very low incidence of EHV-1 infection in the mares in the region and limits the spread of the disease on affected farms so that typically only 1-3 mares are affected in any one outbreak.

The most effective way to prevent the spread of any infectious disease is effective hand hygiene â&#x20AC;&#x201C; providing hand-washing facilities and applying hand disinfectants is the single most important technique to reduce the spread of infectious disease. Most diseases are spread by contact between infected horse and susceptible horse or through contact with infectious organism on the hands and clothes of the people who care for the horses or on the equipment used on the horses.

Hendra Virus The disease is caused by a virus that is carried by flying foxes and only intermittently infects horses.

The disease has only been recorded to occur east of the Dividing Range in Queensland and Northern NSW, however could theoretically infect horses in any region where flying foxes occur.

The first outbreak of Hendra virus was in a racing stable in Brisbane in 1994 and since then more than 30 cases have been recorded. Seven people have been infected with Hendra virus and four have died, hence the disease poses a significant risk to people who care for horses. In addition, most cases in horses are fatal with over 70% of known infected horse dying rapidly from the disease.

The clinical signs of the disease a fairly nonspecific, and includes fever, depression, respiratory or neurological disease with rapid progression to death. Many horses with colic, pleuropneumonia and severe colitis may also present with these signs.

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The purpose of this presentation is to describe the tools required to design an appropriate protocol to protect horses and staff from a very rare but potentially fatal disease. Other important infectious diseases which require effective biosecurity protocols will also be discussed, including, EHV-1 Strangles, Salmonella, Rotavirus, and Rattles.

Risk The key to designing an appropriate biosecurity protocol is to assess all the risks thoroughly.

There are risks to people and risks to the horse, each of which can be divided into two aspects a) the risk of mortality â&#x20AC;&#x201C; that is the risk of a person or horse dying from the disease b) the risk of morbidity â&#x20AC;&#x201C; that is the risk of a person or horse actually getting the disease.

Control of a disease with both a high morbidity and high mortality is enormously difficult and requires extreme biosecurity measures â&#x20AC;&#x201C; an example is SARS or a human adapted form of avian influenza. Fortunately no equine disease which currently threatens Australian horses fits into this category.

Mortality (Risk of Death): Hendra virus: Human mortality

High

> 50%

Equine mortality

High

>70%

When designing biosecurity protocols it is essential to ensure the possibility of human and horse infection is stringently controlled.

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EHV-1/4:

Human Mortality

- None

Equine Mortality

- Very High â&#x20AC;&#x201C; all infected fetusesâ&#x20AC;&#x2122; are aborted or die shortly after birth

When designing Biosecurity protocols is important to prevent horse to horse infection but human infection is of no concern.

Salmonellosis:

Human Mortality

Low to Moderate

Equine Mortality

Moderate

Biosecurity protocols need to aim to minimize the chance of infection of both horses and humans, however the consequences of infection are not as dire as for Hendra virus.

Rotavirus:

Human Mortality

None to low

Equine Mortality

Low to Moderate

The consequence of infection for an individual is not severe and the protocols should be aimed at preventing the spread of the disease horse to horseâ&#x20AC;&#x201C; it requires a more herd/population based approach than individual protection.

Strangles:

Human Mortality

None to Low

Equine Mortality

Low to Moderate

Similar to the control of rotavirus, a Biosecurity program for strangles needs to be primarily aimed at preventing the spread of the disease.

Rattles:

Human Mortality

Low (normal people) High (immune-suppressed)

Equine Mortality

Low to High

The mortality of Rattles is low if the disease is detected early in the clinical course but can be very high if detected late. The primary aim of a Biosecurity protocol for Rattles is to detect the infection early so it can be treated effectively and this will prevent spread of the disease to susceptible foals.

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Morbidity (Risk of spread of the disease):

Hendra:

Human Morbidity

Low

Equine Morbidity

Low

Hendra virus requires close contact with the bodily fluids of an infected horse. It does not spread rapidly from horse to horse or from horse to human. Good barrier protection (face mask, goggles, gloves and hand hygiene) should minimize the risk of infection, however the consequences of infection are so serious that the number of people in contact with a possibly infected must be kept to a minimum.

EHV-1/4

Human Morbidity

None

Equine Morbidity

High

EHV-1 spreads very rapidly through the secretions of an infected horse; both the nasal secretions and the vaginal secretions post abortion. Isolation of the infected mare and the in-contact mares is essential to prevent spread of the disease.

Salmonellosis

Human Morbidity

Moderate

Equine Morbidity

Moderate

Salmonella spreads through contact with infected faecal material â&#x20AC;&#x201C; horses with diarrhoea shed vast amounts of the bacteria in huge volumes of diarrhea. All equipment and material that are in-contact with the infected horse rapidly become covered in the bacteria and are potential mechanisms for the spread of the disease. Good barrier protection and extremely good hygiene (hand washing and disposal of soiled materials) after contact with the infected horse is absolutely essential to control the spread of this disease.

Rotavirus

Human morbidity

none to low

Equine morbidity

high

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Foals are susceptible to this virus and develop diarrhea, whereas adult horses can carry the virus without ill effects. Control of this disease requires very strict isolation of infected and in-contact horses, but is rarely undertaken because the disease has such a low mortality.

Strangles

Human morbidity

none

Equine morbidity

high

All horses are susceptible to Strangles and the disease spreads rapidly through a population of horses. The disease is spread by contact with infected material from an abscess or the nasal secretions of an infected horse. Isolation of all infected and in-contact horses is essential to control the disease. In addition the identification of carrier horses is required to prevent the re-introduction of the disease onto a farm.

Rattles

Human mortality

low (normal) to high (immunosuppressed)

Equine mortality

low to moderate

There is continuing investigation and controversy about the spread of R equi â&#x20AC;&#x201C; infected foals are a good source of large numbers of the organism, however the bacteria can live in the soil and can be shed by adult horses in their faeces. Early identification and then isolation of infected foals from other foals are very important criteria in controlling the spread of this disease. Isolation of in-contact horses is not effective is not required to prevent the transmission of the disease.

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Biosecurity Protocols Because there are differences in the risk of certain disease in horses newly arrived on a property, there should be different protocols for the new arrivals and resident horses.

New Arrivals All new arrivals should be kept isolated for 2 weeks, preferably in the group they arrived in.

Horse that have recently arrived from coastal QLD or Nth NSW pose the greatest risk of Hendra virus and should be placed in their own arrivals facility so that if a horse gets ill, appropriate protection can be instituted easily and inadvertent exposure to Hendra virus is prevented.

Any horse the arrives from coastal Queensland or Northern NSW that develops a fever, neurological disease or a respiratory disease within 2 weeks of arrival MUST be considered a very high risk of Hendra virus infection. A veterinarian should examine the horse as soon as possible and obtain samples to test for Hendra virus â&#x20AC;&#x201C; the NSW DPI at Menangle have set up an excellent PCR system and results are available normally in 48 hrs. A mask, goggles, gloves and disposable overalls should be worn when attending the horse until appropriate testing is completed (approximately 48 hrs).

The most effective way to prevent spread of disease from new arrivals is to test for the major infectious diseases and only release horses from quarantine that have tested negative. Overseas there are PCR diagnostic tests for Strangles, Salmonella, and EHV-1 readily available and routinue testing of all arriving horses is frequently conducted so that freedom from disease can be determined 48 â&#x20AC;&#x201C; 72 hrs after arrival. The NSW DPI has a state of the art PCR facility as a result of the EI epidemic and they are now rapidly conducting PCR testing for Hendra virus and EHV-1; demand for Salmonella and Strangles testing could rapidly result in the development of the tests.

Isolation of the new arrivals means that the horses should be kept at least 1 meter from all resident horses and contact with the new arrival horses, their faeces or any equipment used on the horses does not occur. It is most effective if there is a team of staff whose only responsibility is the care of these horses. If staffing does not allow for a separate team, then the new arrivals should be fed and

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handled after all the resident horses. Any new arrivals that become ill should be treated as though they are carrying an infectious disease until proved otherwise. If the horse is from coastal Queensland or Northern NSW then it should be assumed to be at high risk of Hendra virus and protective overalls, gloves, goggles and mask worn to examine the horse and a veterinarian should be consulted immediately.

Biosecurity for Sick Horses Whether the horse is a new arrival or a resident horse, the principles of controlling infectious diseases are the same. To control Salmonella, Strangles and EHV-1and most other infectious diseases, the affected horse should be removed from the group and placed in isolation so that the horse, all excretions and all equipment used on the horse does not come in contact with any other horse. The in-contact horses (horses in the same paddock or that have been in direct contact in the past week) need to be kept isolated for all other horses for at least 2 weeks and monitored carefully for signs of the disease. These horses should be treated as though they also have the infectious disease until proven otherwise, either by testing or by completion of the quarantine period. The people who care for and monitor these horses should not handle other horses until they have disinfected â&#x20AC;&#x201C; removed overalls, gloves, boots and washed hands. Contact with and movement of this group of horses should be avoided until the quarantine period (2 wks) is completed â&#x20AC;&#x201C; ie worming, dental work, vaccinations and farrier work should be delayed unless urgent. For diseases that have a low mortality but high morbidity, such as Strangles and Rotavirus, the affected horse could be kept in the group of horses it is found with a strict isolation procedure applied to the group. The primary difficulty in controlled highly infectious diseases such as Equine Influenza and rotavirus is that the disease has already spread to new horses and possibly new groups before the first case shows clinical signs. To control further spread of the disease the groups of horses closest to the infected group should also be quarantined.

Effective control of infectious diseases requires vigilance and awareness of the possibility of the disease, appropriate rapid diagnostic testing and effective quarantine and hygiene.

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Stallion Assessment Lecture Seven Dr Jim Rodger, FACVSc Jerryâ&#x20AC;&#x2122;s Plains Veterinary Hospital

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Selection of the Stallion Select Carefully For What You Need 

Ability



Appearance (quality control)

Good limbs 

Able to stand up to work



Laminitis is a common killer of stallions

No evidence of congenital disease 

Hernia, parrot mouth, spavin, ringbone, sidebone

No evidence of neoplasia 

Testicular tumours are rare

A masculine appearance with well developed genitalia is often a good indication of a stallion libido.

The stallion should have sound limbs and be kept fit. Stallions that are overfed and under worked may develop problems, particularly laminitis.

There should be no sign of an abnormal or inguinal hernia. Monorchid or hypoplastic testicles not likely to produce adequate sperm. Pickett(1977) maintains that semen production is related to testicular size and that the combined width should be no less than 70mm to achieve satisfactory production. There are indications that testicle size and development may be impaired under the influence of anabolic steroids (Blanchard, 1983; W.P. Howey, personal communication) and we certainly see sires with poor first season performances that later improve, although no accurate correlation has been made in these sires.

Testicular neoplasms fortunately are rare. Size differences may be associated with post orchitis fibrosis. (Caron, Barber & Bailey, 1985) The penis should be a normal size and shape with no injuries. The glans penis should be examined for ulceration or habronema infection. We have had several stallions affected in this way and they need careful management. A case of penile paralysis associated with malnutrition has been described (Carr & Hughes, 1984).

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Insurance Criteria Masculine Appearance 

Mature

Well developed genetalia 

Testicular size



Sperm production

Physiological parameters 

Blood profiles

The Maiden Stallion 

Patience required in starting stallion off



May take 2 weeks for first covering



Mismanagement may lead to behavioral abnormalities



Major changes from previous pre-stud environment

The introduction of the maiden stallion to his first mares is probably the most important step of all and may influence his whole stud career. It may take up to two weeks to have a first successful covering and a great deal of patience is necessary. Once covering normally the young stallion should continue to do so. Mismanagement at this stage may result in unruly behavior and the development vices such as biting and kicking, or loss of libido or importance. It is also the time when injury is most likely. Most of these horses have been stabled next to fillies and have often been reprimanded for behaving in a natural way and trying to mate. The stallion may therefore arrive suffering from a degree of psychological importance and refuse or be unable to serve. One now famous stallion arrived at this stud and refused to work despite all attempts and variations in procedure. Eventually he was ridden and used to round up the mares. Immediately after that he began to serve normally.

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Impotency 

Hormonal



Ejaculation failure



Abnormal behavior



Hypothyroidism

Impotency has been generally associated with low luteinizing hormone and low oestradiol 17-B, but serum testosterone does not appear to be lowered (Wallach, Pickett and Nett, 1983). Others find these lowered levels inconsistent (Irvine, Alexander & Hughes, 1985).

Some horses may mount, maintain an erection, make good pelvic thrusts but still fail to ejaculate.

Care must be taken to ensure that ejaculation occurs and this may require an extra person in addition to the mare and stallion handlers.

The environment in which the horse works may adversely affect his performance. Rasbech (1975) described eleven cases of ejaculatory disorders in normal healthy stallions of which three revealed after simple correction of environmental factors. A second group (4) has poor libido and inadequate erection or intromission and a third group (4) appeared to have a functional disturbance of the neural mechanism controlling ejaculation.

Complete isolation and excessive use as a teaser a long with rough and overuse as two or three year old stallion have all been recorded (Pickett & Voss, 1975) as contributing to abnormal sexual behaviour.

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Vices 

Vicious or antisocial behavior



Results of Isolation



Self Mutilation



Mastibation

Some stallions that have had reputation of being vicious or hard to handle have become placid after being taken out of isolation. One such stallion that could not be caught abs had to serve mares at the end of a race is now quiet enough to stomach tube without a twitch after being moved to a dairy farm and being ridden around his mares.

It is not is a scope of this paper to extensively describe semen disorders, except to introduce a stallion that produced small volumes of watery semen, with resulting low fertility. It was suspected that the stallion was masturbating. Services by this stallion were then spread out so that he was used daily when possible and mares were all served twice. This resulted in improved semen and a return to normal fertility. The stallion was also moved to a yard where he could see more mares and cattle.

Injuries 

Physical trauma



Haemospermia associated with ulceration



Testicular injuries



Testicular fibrosis



Testicular adhesion



Penile injury

An over enthusiastic server can also be a problem. One result of over vigorous mating can be penetration of the roof of the vagina of the mare, particularly in younger mares (Held & Blackford, 1984). These mares should be treated with tetanus toxoid and parental antibiotics. They can become pregnant from that service but I am reluctant to examine them at the time of the next oestrus and leave them for six weeks. No suturing of the injury is normally required.

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A serving roll can be used to prevent this accident, putting the roll between the mare and the stallion, placed under the mares tail and above the stallions penis. This most satisfactory roll I have used in simply a roll of Johnson and Johnson cotton wool still in its plastic bag, holding it to the neck of the bag.

The same device has been used for a stallion with ulceration of the glans penis involving the fossa glandis and urethral fossa. These ulcers may be initiated and made worse by trauma during copulation before being attacked by flies and habronema. The use of a rool keeps the stallion back from the anterior vagina and will reduce the trauma. Ulcers are best treated with topical antibiotic cream and fly repellant.

Haemospermia may be the result of urethral ulceration , or of ulceration of the glans area.

Pseudomonas has occasionally been isolated fro these ulcers and topical gentamycin has been used satisfactorily. Sexual rest is of extreme importance to allow healing to take place. Pickett and Voss (1975) have described techniques for making radiographic and ultrascopic examinations in cases of haemospermia. A case of haemospermia associated with a migrating stronylus edentatus has been described (Pickett & Voss, 1975).

Scrotal Heat Stress Includes Altered Sperm Chromatin Structure Associated with a Disease in Protamine Disulfide Bonding in the Stallion Charles C. Love and Robert M. Kenny Hofman Centre for reproductive Studies, University of Pennsylvania School of Veterinary Medicine, Kennett Square, Pennsylvania 19348

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Abstract A variety of testicle insults can induce changes in the structure of spermatozoal chromatin, resulting in spermatozoal DNA that more susceptible to acid-induced denaturation. The degree of change in the DNA can be measured using sperm chromatin structure assay (SCSA). The SCSA measures the relative amounts of single and double stranded DNA after staining with the metachromatic dye, acridine orange.

Here we used a stallion model (n=4) to study the effects of scrotal heat stress on spermatozoal DNA. This model was created by insulting stallions tests for 48 h and collecting sperm daily thereafter for 60 days. Changes in the SCSA were then correlated with protamine disulfide content and proatmine types and levels.

Results of SCSA indicated that the susceptibility of spermatozoal DNA to denaturation was dependant on the spermatogenic cell stage that the ejaculated sperm was in at the time of the heat stress. Spermatozoa with altered DNA had a decrease in the extent of disulfide bonding that was associated with an increase in the susceptibility of spermatozoal DNA to denaturation in the absence of protamine changes.

Reproductive Tract Abnormalities ď&#x201A;ˇ

Infected Accessory Glands (Bacterial)

ď&#x201A;ˇ

Antisperm Antibodies (Injury)

Short term infection may be associated with streptococcal infections venereally transmitted. Stallion will normally overcome the infection himself.

Pseudomonas may be venereally transmitted but may be transmitted in contaminated washing water. Pseudomonas and some other infections may become established following destruction of normal flora by overuse of disinfectants.

Urinary tract infections may cause inflammatory changes resulting in ulceration with haemospermia, blocked ampullae, urospermia etc Sheath infections may be associated with poor hygiene or excessive attention Some viral infections such as eva may be transmitted by the respiratory route

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Genetics

Epididymal Dysfunction 

Cytoplasmic droplets



Low sperm motility

Developmental Abnormalities 

Cryptorchidism



Intersex

Cytogenetics Some stallions may appear normal, behave normally and produce what appears to be a normal ejaculate.

Cytogenetics studies have led to descriptions of chromosomes abnormalities that may be associated with impaired reproductive performance (Halnan, 2985). It is possible that such infertility problems be associated with abnormalities in the chromosomes, in particular deletions in a paired banding.

(Halnan, personal communication). This may become one of the most interesting developments on the study of infertility in the next few years.

Infertility in stallions associated with low sperm motility, cytoplasmic droplets.possibly epididymal dysfunction of genetic origin.galloway J.reprod. Fert.,suppl35(1987) 655-656.

Copyright:

J.A.Rodger Centre for Equine Reproductive Medicine Jerry’s Plains, NSW

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Laminitis Lecture Seven Dr Troy Butt, DACVS Scone Equine Hospital

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Introduction Laminitis, or founder, is one of the more common causes of lameness and production loss on breeding farms. In many cases, founder can be a crippling disease that results in the death of the horse. Quick diagnosis and emergency therapy is essential in the early stages of founder in order to stop the disease process and help stabilize the feet. Once the feet are stabilized, they must be rebalanced and supported with shoes in order to (hopefully!) return the horse to its previous function.

Anatomy and Physiology The main structures of the foot that concern us in regards to founder are: 

Hoof wall, sole, and frog



Coffin bone



Lamina - structure that holds the hoof wall, sole, and frog onto the coffin bone



Deep digital flexor tendon – attaches to the back of the coffin bone and is responsible for flexing the foot.

The hoof wall, sole, and frog are attached to the coffin bone by the lamina.

There are 2 types of lamina: 

“Sensitive” lamina (attaches to the coffin bone)



“Insensitive” lamina (attaches to the hoof wall).

The sensitive and insensitive laminae are made up of many overlapping folds. These folds create a very large surface area for attachment and are responsible for holding the hoof wall onto the coffin bone.

The sensitive and insensitive laminae are connected together by microscopic attachments.

When the hoof wall grows, these microscopic attachments release and then reform, allowing the hoof wall to move downward.

When founder occurs, the attachments between the lamina are destroyed, which allows the sensitive and insensitive lamina to separate.

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Which horses are affected? 

Overweight or pregnant broodmares



Increase in weight



Metabolic derangements



Hormonal changes



Insulin resistance

Sick horses 

Post-operative colic, diarrhea, uterine infections (metritis), retained placenta, uterine rupture.



Bacterial toxins



Horses on hot feed rations or unlimited access to grass



Feeds high in complex sugars and starches



The trigger is not known

Clinical Signs 

Front feet are usually more affected than the hind



Single limb lameness (if only one foot affected).



Bounding digital pulses



Decreased willingness to pick up feet



Pain on hoof testers



Reluctance to move



Presence and frequency of “foot pumping”



“Half rearing” and bringing hind legs well under when forced to walk (severe)



Recumbancy (severe)



Puffy coronary bands (severe)



“Ringed” hoof wall (chronic)



Domed sole at the toe (chronic)



Exposed sensitive tissue at sole (chronic)

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Three Clinical Syndromes No rotation or sinking of coffin bone 

Best case scenario



No change in position of coffin bone



Good prognosis for soundness and athleticism

Rotation of coffin bone Lamellar attachments release at front of foot and tip of coffin bone rotates downward. If rotation is mild, reasonable prognosis for soundness with diligent foot care and shoeing.

If rotation is severe and tip of coffin bone has NOT penetrated sole, guarded prognosis for soundness, reasonable prognosis for salvage with diligent foot care and shoeing.

If rotation is severe and tip of coffin bone penetrates sole, prognosis for salvage is poor

“Fatal sinker syndrome” – sinking of coffin bone All lamellar attachments release and coffin bone “sinks” into hoof capsule.

Grave prognosis for survival – Euthanasia usually recommended

Emergency Treatment for Acute Founder Treatment is aimed at supporting the foot and preventing further rotation of the coffin bone. Please note that the damage to the lamella has started well before clinical signs of founder occur.

Step One: 

The basis of initial treatment is:



Offload the hoof wall



Helps prevent ongoing separation of lamina



Reduce tension of the deep digital flexor tendon on the back of the coffin bone.



Decreases leverage on the coffin bone. This is accomplished by one of 3 methods:

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1. Placing horse in a sand yard 2. Placing sole support systems on the feet such as “Lilly pads” (thick Styrofoam insulating board), sole putty or placing heel wedges on the feet.

3. “Ultimate” shoes

Step Two Contact BOTH your veterinarian and your farrier. Both must work together in order to achieve the desired outcome: stabilization and support of the feet AND elimination of the inciting cause of the founder.

Icing the feet is often recommended as emergency treatment; however, the lamellar damage has occurred by the time that clinical signs are noted. Although icing will not hurt the horse, it will not be as beneficial as providing heel wedges and sole support.

Therapeutic Treatment for Chronic Founder Chronic cases are the “repeat offenders” that have ongoing founder episodes OR horses that have gone through the acute phase of founder and have now stabilized. X-rays of the foot before shoeing are crucial for evaluation of coffin bone positioning and foot balance.

No coffin bone rotation or sinking 

Straight bar shoes +/- 3 degree heel wedge and sole pack



Regular shoes at the next reset

Rotation of coffin bone (mild) Re-align hoof wall and coffin bone by rasping toe and cutting heels. Straight bar shoes +/- 3 degree heel wedges and sole pack OR rocker shoes with sole pack.

These shoes are required for at least 6 months.

Rotation of coffin bone (severe) 

Re-align hoof wall and coffin bone by rasping toe and cutting heels.



Hoof wall resection may be necessary to re-align foot.



Deep digital flexor tendon tenotomy is often necessary to reduce leverage on coffin bone.



Straight bar shoes with heel wedges and sole pack OR rocker shoes with sole pack

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

Shoes are required for an extended period

If the coffin bone is exposed through the sole, there is a very complicated and poor prognosis. Reversed shoes and sole pack at heels only, surgical debridement of exposed coffin bone, regional antibiotic limb perfusions, etc may be required.

“Fatal sinker syndrome” 

Grave prognosis for survival



Little can be done with shoeing to help this condition



Radical surgery (complete hoof wall resection and “T-casting”) has been reported but, in my opinion, is inhumane.



Usually results in euthanasia

Conclusion Early recognition of clinical signs and early emergency measures to support the foot are critical.

Best results are achieved when Farriers and Veterinarians work together.

Most founder cases are labor intensive and require ongoing foot care.

Horses with “Fatal Sinker Syndrome” have a grave prognosis for survival.

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Yearling Radiography Lecture Eight Dr Chris Oâ&#x20AC;&#x2122;Sullivan BVSc DipVCS MS Diplomate ACVS

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What do we know now?

Veterinarians who view films for purchasers at sales are predominately experienced (>10yrs practice) veterinarians. The majority have either experience on the racetrack or are surgical specialists. In interpreting yearling sales films they make a judgement call on the clinical significance of lesions that are identified. The risk they may develop into a clinical problem and the impact that may have on a horses’ ability to race and subsequent performance. Their opinions are based on: 

Experience: obviously veterinarians with experience treating and managing horses in race training will be biased by their individual experiences with specific problems. Also some experience regarding the purchaser or trainer will also influence the decision making.



Scientific Data: there are numerous studies which look at the impact that lesions seen in the repository have on thoroughbred race performance. There are weaknesses in this data which is inherent when looking at performance. While many of the studies look at large numbers of yearlings (n=1162 – 2773) applying the findings of these studies to specific cases is difficult.

The level of agreement on specific lesions among veterinarians is variable and dependant on the type of lesion seen or joint involved. Veterinarians seem to have better agreement on lesions of the hock particularly ‘OCD’.

What else would we like to know?

Ideally we should seek as an industry data on individual lesion types over large numbers of horses with an aim to develop more standardised method of reporting. This should be based on the likelihood of a specific lesion to becoming clinical, and its subsequent impact on the horses racing career.

How to optimise the procedure as vendors?

Horse preparation Well handled quiet horses will provide better quality films and improve the occupational health and safety of the radiographers. Horses should also have their feet well trimmed and be cleaned of all mud. Small balls of mud in the coat can closely resemble bone fragments on radiographs.

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The Veterinarian Insist on quality radiographs and quality interpretation of the films. Both the horse and the skill and equipment of the veterinarian will determine the quality of the films. Ideally nothing is missed and no surprises occur when arriving at the sales or worse in the ring. In the repository quality is essential (no movement, correct angles and exposures), since when veterinarians are reporting on poor quality or non-diagnostic films they can only report to potential purchasers on what they can see. In cases where a clear decision cannot be made it will often lead to a potential purchaser scratching the horse off their list. Purchasers are often reluctant to approach vendors regarding film quality. Unfortunately for vendors the loss of potential purchasers under such conditions is typically a silent attrition.

Survey radiographs Surveys are aimed at identifying potential problems early and managing them appropriately.

Obviously the cost benefits of the films need to be considered on an individual yearling basis.

Surveys are generally performed around the month of August. However it should be noted that some OCD lesions may not become radiographically apparent until 12 months of age or in some rare cases later. The information gained on surveys allows assessment of a whole draft of yearlings and tailored treatment of individuals. The information also allows an analysis of management/environmental changes and their potential impact on lesion formation. Survey information can also often assist in deciding the sale destination of the yearling.

Treatment is generally divided into either medical or surgical therapy dependant on the lesion.

Medical therapy includes exercise restriction, drugs (DMOADâ&#x20AC;&#x2122;s, Cartrophen, Tildren, corticosteroids), shock wave therapy, IRAP, nutrition and weight control. Surgical therapy is predominately arthroscopic surgery.

Sales Radiographs Need to be taken within 42 days of the sale and need to be presented to the sales company in the appropriate format by the deadline (typically 4 days prior to sale). Ideally as a vendor you will have an accurate and well constructed veterinary report on each of your lots. I would advise against using the reports to attract prospective purchasers. Most genuine purchasers will have the films assessed by a veterinarian representing them.

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Terminology used is not well defined with most describing horses as Low, Moderate and High risk.

The key is to ask; â&#x20AC;&#x2DC;risk for what?â&#x20AC;&#x2122; Veterinarians seem to evaluate the risk as either the risk of the specific finding manifesting as a clinical problem and requiring treatment, or its affect on the horses likelihood to race. I use this terminology to describe the risk of the horse developing a clinical problem associated with the identified pathology on the radiographs. I then describe the treatment scenarios of the specific pathology and likelihood of it to impact on the horses racing career. Not all pathology that is high risk is an indication that the horse is unlikely to race. Veterinarians will often also recommend a period of time or other treatments. Some lesions will improve with time and often at the sale there are lesions identified that may still worsen, particularly if the horse was to enter work. Often its advised to delay the break in of such horses up to 6 months to minimise the likelihood of the pathology progressing.

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Yearling Preparation Lecture Nine John Maxwell & Ross Lindemann Alphahorse

Page | 98

The Yearling Preparation Creating a plan for productivity, safety and results.

1. The beginning of prep and typical traps a) Green horses b) Green staff c) The plan 2. The roles and responsibilities of everyone in prep and at the sale a) Grooms b) Showers c) Horses d) Management 3. The problems are the same world over a) Handling of the horse b) Focusing on the wrong issues c) Management pressures and the negative outcome d) Knowing your role e) Environment 4. The Horse a) The horse is the Product, investment, Hobby or the Livelihood b) Aids c) Matching the horse to the staff d) Position in sale e) The only industry

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Notes

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Notes

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Notes

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