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What are the physiological mechanisms involve in recrudescence from seasonal acyclicity in the mare? What management strategies are available for hastening recrudescence and what are the main reasons for doing so on TB stud farms?

*Light additional to ambient photoperiod at the end of the day e.g. turn lights on at 4:30pm and off at 11pm-- pineal gland signals the hypothalamus through secretion of melatonin. When the day length is shorter, melatonin released by the pineal gland suppresses GnRH synthesis and relase. When the day length is long, melatonin secretion is reduced and the inhibitory influence of melatonin on GnRH synthesis is removed

* Southern Hemisphere Aug 1 is the imposed official birth date of all TB horses. This avoids age changes during the racing season. Breeders try to have mares in foal as soon as possible after the official birth date-- 11 month gestation-- so start of the breeding season in the Southern Hemisphere is on Sept 1.  Only a quarter of the mares are already cycling regularly at this stage, the others are in a period of transitional oestrus.


Describe the potential abnormalities associated with the infertile "susceptible" mare, which may prevent her from conceiving or carrying a foal. What strategies would you employ to optimise fertility in a "susceptible" mare?

* Congenital abnormalities- conformational such as vulval seal- lips do not appose properly-- air may be aspirated can lead to inflammation--> infection--> transmitted to the uterus--> endometritis*** Management: Caslick operation removing thin strip of mucosa from each side of the vulva & suturing raw edges together

* Uterine tube abnormalities- PGE2 applied to the outside of the uterine tube via a flank incision restored tube patency

*Ovarian tumour- removal

* Endometritis- endometriosis- physical and chemical uterine curettage variable success; infectious endometritis- fungal or bacterial-- infusion of antifungal or antibacterial +/- systemic treatment

* AHF- PGF2alpha after 7 days

** Strategies to employ to optomize fertility in a susceptible mare

Special repro exam-- Physical exam e.g. vulva conformation, internal exam-- palpation and U/S, vaginal exam- manual & speculum.

U/S- assess uterus- diameter, tone, wall thickness, contents (air, fluid, cysts, pregnancy?)/ Ovaries- size and shape, presence of ovulation fossa (lost if ovarian tumor), presence, size, grade of fluctuation of follicles, CL

* Endometrial samples in dioestrous after day 7-- cytology and culture

* Uterine biopsy-- indicated in prepurchase exams, barren mares, and mares that require expensive repro surgery



Discuss the physiological control of parturition. Using your knowledge of the event, what drugs or techniques could be useful in correcting a dystocia in a mare?

* Uterine contractions start after the foetus releases cortisol-- the contractions force the placenta against the uterus and a release of oxytocin from the pituitary occurs (Ferguson's reflex)... this also stimulates the release of PGF2alpha which puts further pressure on the fetal membranes and results in the rupture of the chorio-allantois

* Oxytocin can induce labour

* PGF2alph can also induce parturition


Neuroendocrine control of spermatogenesis in the stallion

* LH effects spermatogenic tubules and Sertoli cells-- controls the rate at which they release formed spermatozoa into the lumen

* Testosterone and other androgens maintains spermatogenesis-- develop and maintain optimal male sexual behaviour as well

* LH, FSH, testosterone and inhibin exert a broad controlling influence over the process of spermatogenesis. Paracrine and autocrine factors within the testis exert a fine tuning influenceon spermatogenesis. Leydig cells produce opioid peptides and receptors for them are found in Sertoli cells.

** Oestrogens secreted by Sertoli cells or Leydig cells appear to play an important role in regulating the cyclic activity of spermatogenic epithelium.

The hormonal requirements for normal spermatogenesis have not been fully clarified. Androgens are

required for the development of the gonocytes to type A spermatogonia. Testosterone is

needed for the reduction division in the division of primary spermatocytes. FSH and

testosterone are needed for the maturation of the spermatid. Probably LH, FSH and

testosterone are all required in optimal balance for quantitative maintenance of normal



Maximizing fertility when inseminating mares with frozen semen

* Must be thawed properly

* Frozen sperm are fertile for a shorter period than fresh or chilled due to cell membrane damage suffered in the freezing/ thawing process.

* Mare will require 3 cycles to become pregnant

* Daily U/S exam to determine when the mare has oestrus folds and 3 cm follicle

* Mare is treated with ovuplant at this stage on the morning of Day 1, the mare will be expected to ovulate in the late afternoon of day 3

* Day 1 administer ovuplant (follicle no bigger than 30 mm) (3 cm = 30 mm)

* Day 2: scan to ensure she will not ovulate on her own-- check for soft follicle, disappearing oedema

* Day 3- scan to make sure has not ovulated if she has, inseminate anyway

* Day 3- 6 hours later inseminate

* Day 3- 6 hours later-- confirm ovulation

** In uterus, more semen


Managing twin conception in the mare

* Second scan carried out around Day 28- 30 to detect embryonic viability and to look for twins so they can be dealt with before endometrial cups are formed on day 35.

* Crush one of the twin vesicles manually-- best carried out during the mobility phase (prior to day 16). If unilateral twins are detected, it is easier to separate them prior to fixation.

* If found after 50 days-- you can try to abort one twin with injection of KCL or penicillin into the foetus thorax-- but often this kills both foetuses


You have been called to look at a very lethargic 12-year-old Thoroughbred gelding.
Owners indicate that the horse has lost considerable weight in the last few weeks. It
consumes about half a bale of lucerne hay daily. The horse has been wormed every 12
weeks with either “Equest plus” (moxidectin and praziqantal) or “Ivomec” (ivermectin).
When you examine the horse you notice it is in poor body condition (body score 2 of 5),
has a heart rate of 56 beats per minute, respiratory rate 24 breaths per minute and
temperature 38.6 oC. It passes normal manure and has normal gut sounds. A plaque of
ventral oedema is present between the front limbs. On auscultation of the chest there is
a grade 2 early systolic murmur audible on the left side only, loudest over the base of
the heart. Harsh lung sounds are evident in the dorsal lung fields, but no lung sounds are
evident below shoulder level on either side of the chest. A jugular pulse is seen
extending half way up the neck.

* Describe your approach to the investigation and management of this case. Interpretation of the history, clinical and laboratory findings already mentioned, potential DDX, how these could be rejected or confirmed, any treatment you might initiate.



ith t

he horse’

s head in neutral carriage, it is normal for a

jugular pulse to extend from the level of the thoracic inlet up to a point that is approximat

ely 1/3


the way up the neck. A jugular pul

se extending beyond this point is indicative of



(and cranial mediastinal masses)

. A normal jugular vein should fill within two to three

seconds after being occluded, and imm

ediately disappear o

nce that pressure is relieved. A non-

distended jugular vein i

s normally not palpable.

There is usually increased central venous pressure

in ho

rses with right sided heart failure, so there is venous engorgement and therefore an engorged

jugular vein.


An owner has asked you to look at her 8 yo eventing mare. For the last two weeks the mare has been spelled in a paddock and not observed bythe owner until today. The mare has a pink, fleshy, proliferating lesion approximately 5 cm in diameter protruding from the front of the fetlock area. The lesion is not painful to palpate and the horse is not lame. Describe your investigation and management of this case.

Your answer should include potential diagnoses and how you would distinguish between them as well as treatment options for two of the more likely diagnoses.

* Sarcoid- biopsy- removal-- destroy all tumour cells, miminize damage to healthy tissue

Eosinophilic granuloma- non-tumour nodular skin disease of horses-  not a common location however. Insect HS. Biopsy. Surgical excision.

Exuberant granulation tissue (proud flesh)- from a previous wound

* Pythiosis- fungus like organism in tropical/ sub-tropical areas... calcified necrotic tissue, exudate and protein, removed in their entirety from the fistulae. Intensely pruritic. Biopsy-- treatment is difficult and expensive

Cutaneous habronemiasis- Culicoides HS, Ivermectin + Corticosteroids to control rxn + removal

Viral papilloma- highly unlikely due to the age and presentation- no treatment usually indicated, resolve spontaneously

SCC- unlikely as usually unpigmented areas- surgical excision with wide margins- histopath first


** distinguish between them with a thorough history and look around the stable.


An owner has asked you to look at his yearling TB colt which is being prepared for the premium yearling sales. The horse has been noticed to stumble frequently while being lunged over the past 2 weeks and last night he was cast in his box and appeared to have considerable difficulty getting to his feet. The horse is well grown, in good body condition and has superficial skin grazes on the dorsal aspect of both hind pasterns. His heart rate is 32 BPM, RR 10 BPM and his temp is 37.4 C, he is eating well and there is normal fresh manure in his box.


Describe your approach to the investigation and mangement of this case. Interpret clinical data, possible DDX, details of those aspects of the clinical exam that are most likely to assist in establishing a diagnosis, any diagnostic aids you might consider and any recommendations you might make.

DDX: Osteochrondosis- osteochondral (bone and cartilage) fragmentation of articular surfaces in young, growing horses.

- Subchondral cystic lesions in young growing horses

Clinical exam:

- Swelling? Often bilateral if OCD, typical in the fetlock on sagittal ridge of MC/MT3.

Diagnostic aids:

- Radiographs flexed lateromedial view for sagittal ridge lesions, dorsopalmar/plantar views


- conservative-- restrict exercise, restrict diet, monitor radiographically... or if fragmentation present.. arthroscopic removal of osteochondral fragments, arthroscopic debridement of subchondral cystic lesions


You have been asked to examine a 3 yo TB colt in full work. Yesterday the horse can in a 1200 m race and came last by 15 lengths with a time of 1 minute 24 seconds. He had won his two starts prior to this, both over the same distance, in times of approximately 1 minute 8 seconds. the horse has a heart rate of 44 bpm, RR of 16 bpm and temperature of 37.6 C. The heart rhythm is irregular and very eratic and the heart sounds grade II systolic murmur audible loudest over the base of the heart. Vary in intensity from beat to beat. There is a grade II systolic murmur audible loudest over the base of the heart. Describe your investigation and management of this case.

Your answer should include an interpretation of the clinical data, any further investigation you might initiate, possible diagnoses, how these might be confirmed or rejected and any treatment you might consider.

Most horses with primary atrial fibrillation exhibit no clinical signs at rest or with moderate exercise/work; however, more strenuous exercise or work may result in evidence of reduced cardiac output. This can be seen in racehorses who are evaluated for a sudden reduction in race performance. In this setting, the clinical signs could also be due to paroxysmal atrial fibrillation, which can be identified only during the exercise period. In horses with primary atrial fibrillation, conversion to sinus rhythm with quinidine at a dosage of 22 mg/kg, PO, every 2 hr until conversion, is still the treatment of choice. The success rate for conversion is greatest in horses with atrial fibrillation of shorter duration. The chance for success is considered excellent if the duration is <4 mo and relatively good if >4 mo, although conversion may take longer and quinidine toxicity is more likely to develop. Horses with atrial fibrillation can also be successfully converted to sinus rhythm electrically (cardioversion). This requires the careful placement of electrode catheters in a pulmonary artery and the right atrium (via the jugular vein) of an awake horse followed by anesthesia. Electrical shocks of increasing intensity are then delivered through the catheters. This method is very successful but is time-consuming and expensive. Most horses can return to successful racing performance after conversion. However, some will revert to atrial fibrillation over time. Conversion to sinus rhythm is not indicated in horses with severe underlying cardiac disease, because the likelihood of conversion, or maintenance of sinus rhythm if converted, is very low.


a) factors predisposing to endometritis

b) induction of ovulation

c) retained foetal membranes

a) age, vulva abnormalities (improper apposition of lips), natural service, retained foetal membranes

b) GnRH can induce fertile ovulation in seasonally anoestrous mares but expensive and inefficient. Progestagens administered when a follicle is 20 to 25 mm in diameter. Dopamine antagonists administered to a mare in shallow anoestrous + hCG and deslorelin. LH-like hCG and Deslorelin (GnRH analogue) induce ovulation during oestrous.

c) RFM- should lose them within 3 hours of foaling. After 4-6 hours mare should be attended. Septic metritis can lead to laminitis, septicaemia and toxic shock. Penicillin + gentamycin+ oxytocin+ NSAID (flunixin)... fluids if kidney function is a concern.

Remove manually without forcing and flush with saline until clear.


You have been called to a TB filly foal which is recumbent and appears too weak to rise. It was born, unobserved approximately 3 days earlier. It had appeared normal to the owner for the first 2 days of life. Clinical examination reveals a heart rate of 140 bpm, a RR of 40 bpm and rectal temp of 38C. A soft systolic murmur is audible over the base of the heart. A weak suck reflex can be elicited. The MM are slightly jaundiced and dry. The cornea of the left eye is cloudy. There is no abdominal distension, no signs of abdominal pain and normal milk faeces are apparent on the end of the thermometer.

Sepsis is a clinical syndrome defined by the development of a systemic inflammatory response syndrome (SIRS) in response to proven or suspected infection. The condition implies an extensive, whole body insult after invasion of bacteria into tissue or a body fluid or cavity. The presence of viable bacteria in the bloodstream is termed bacteremia. Sepsis and SIRS are two of the most common problems of equine neonates, while bacterial infection accounts for nearly one-third of all foal mortality.

* Penicillin + amikacin sulfate+ Metronidazole (anaerobic)


* Sepsis, VSD, PDA, Tetralogy of Fallot but not the right clinic presentation


Write notes on:

a. PGF 2alpha

b. domperidone (Motilium)

c. Oxytocin

d. Altrenogest (Regumate)

e. human chorionic gonadotrophin

f. deslorelin (Ovuplant)

a. Uterus can produce prostaglandin, can cause uterine contraction at a slower rate than oxytocin lasting longer however (5 hours), regresses CLs-- can induce oestrous

b. Domperidone is a D2 dopamine receptor antagonist. Can induce ovulation in mares in shallow anoestrous. hCG and deslorelin (GnRH) are used in conjunction.

c. cause uterine contraction, remove fluids through the cercix, treatment of persistent endometritis causes contractions of the uterus, useful at the time of breeding for uterine clearance, enahnces uterine involution possibly

d. Altrenogest is an oral progestagen- can be used to delay oestrous or ovulation-- delaying the first post partum ovulation, can be given in an attempt to deliver one live foal even after aborting the other purposefully

e. hCG- ovulation inducing drug, usualling given with deslorelin (GnRH)

f. Deslorelin- used with hCG and Domperidone to induce ovulation


A client is adamant he wants his TB broodmare bred on foal heat because it is getting towards the end of the breeding season. What limitations would you put on foal heat breeding and hwat management procedures might you institute to maximize the mare's chances of conceiving? What alternatives could you suggest to the client?

Foal heat 5-12 days after foaling, average interval post foaling is 10-11 days

Seasonal variation

Decreased pregnancy rates and higher embryonic death-- possibly because of uterine involution, uterine infection, large uterine lumen

* Higher if they ovulate after day 10 post foaling versus before day 10

** Individual mare monitoring and selection by rectal and U/S and make sure normal foaling, no RFM, no evidence of metritis or endometritis, ovulation on or after day 10

**You can also shorten the luteal phase with PGF2alpha about 6 days after the first ovulation and breed on a shortened cycle to give more time for uterine involution

**You can give Altrenogest (Progesterone) to delay the first ovulation until after day 10 

** Can use oxytocin and/or PGF2alpha to possibly enhance uterine involution



Methods of breeding- natural, artificial insemination

Frequency of breeding- once per year due to gestation

Numbers of mares capable of being bred- one stallion 3 mares

Methods of transporting semen to other studs- raw (breed multiple mares from same ejaculate), cooled semen 75% first service conception


6 week old TB

Severe left hind limb lameness- sudden

LH swollen to the top of the fetlock

39.5 temp

** Septic arthritis- present with acute onset lameness, pyrexia, +/- joint swelling

**Synovial fluid analysis with arthrocentesiss ... Total WCC > 10 x 10^9/L, Protein > 25 g/L, neutrophils > 90%

** radiography-- often subchondral bone or physeal involvement

**U/S detect fibrin, swelling in deeper joints

** CT if you were going to do surgery

Treatment: Broad spectrum antibiotics, treat failure of passive transfer, lavage joint space, debride affected bone

Prognosis is guarded if bone is involved


a) Briefly discuss the diagnosis, prevention and treatment of endometritis

Diagnosis- Clitoral swabbing, endometrial culture and cytology > 5 neutrophils per field, inflammation is present, uterine biopsy, uterine luminal fluid on U/S

Prevention- oxytocin after foaling, oxytocin or prostaglandin if uterine fluid on U/S during oestrous as predisposed for PMIE

Treatment- Clitoral infections-- clitoral fossa packed with antibacterial cream, saline to flush uterine lumen, intra-uterine infusion of antibiotics based on culture and sensitivity, oxytocin to cause uterine contraction



b) Describe the behavioural and ultrasonographic signs of spring transition in mares
and indicate how you would advance the onset of cycling

Follicles that do not grow to a mature size

Mare does display heat but not enough oestradiol to induce LH receptor expression and endometrial oedema is weak or not present


c) List the indications for performing a Caslicks procedure

* Vulva lips that do not appose properly (endometritis risk)

* as mares age, abdominal muscles lose tone, reproductive tract becomes more pendulous and the dorsal vulva may be pulled forward

* Vaginal abnormalities-- downward sloping vagina

* Vulval shelf - severe abnormal conformation

* poor body condition- old, thin mares


6 week old TB filly, increasingly lethargic, cough, intermittent bilateral mucopurulent nasal discharge, food material in the nostrils. Suckling normally. 60 bpm HR, rr 48, temp 39.8, lung sounds are harsh, moist rattles on both sides

*DDX: EHV-1, Equine Influenza, Viral infection with secondary pneumonia, aspiration pneumonia, parasitic pneumonia (Dictyocaulus arnfieldi)

* Rhodococcus equi- cough and nasal discharge are inconsistent

- diagnosis: any young horse showing signs of respiratory disease

- clinical pathology- hyperfibrinogenaemia, leucocytosis, increased platelet count

- TTW or BAL

- thoracic radiographs

- Tx: macrolide AMs 4-10 weeks + supportive care

- Prevention- manure removal, prevent over crowding, reduce dust


TB yearling sternal recumbency, no evidence of colic, interested in eating and drinking, HR 36 and RR 12, temp 37.2 normal heart lung and gut sounds. Can get up but doesn’t remain standing. Fascicultation of limbs muscles is obvious. Horse taking short steps occasionally buckling at the knees.

* Exertional rhabdomyolysis- over exertion, high grain diets, concurrent illness, electrolyte imbalances, vit E and selenium deficiency

* Lameness exam + physical exam

* CBC and biochem- esp CK and AST and electrolytes, urinalysis (myoglobinuria?)

Muscle biopsy not likely necessary

Treatment: fluid therapy, relieve muscle pain with NSAIDs, sedation if necessary (ACE), Diet- goo quality hay with little or no grain, rested with light walking once stiffness has resolved

* If develops into chronic rhabdo: Blood samples-- baseline CK and AST and electrolytes-- exercise test 2 minutes wakling followed by 13 minutes trotting on a lunge line... post CK measurement at 4-6 hours after exercise.


a) The origin and physiological function of equine chorionic gonadotrophin (eCG).

Endometrial cups formed on Day 35-- leutotrophic properties leading to the formation of accessory/ supplementary/ secondary CL from ovarian follicles which develop during early pregnancy. This source of progesterone is aiding in the maintenance of pregnancy.


b) The elements and expected normal values of a breeding soundness examination in
a stallion.

1. general physical exam- observation of sexual mating and ability to mount, venereal disease? infectious disease?, serology, CEM hormonal assays

2. examination of external reproductive organs- normal penis, normal testicles and scrotum-- scrotal size 5-15 cm (scrotal calipers across their width and length)

3. examination of internal reproductive organs- pelvic urethra, body of prostate, seminal vesicles (size, consistency, lobulation, symmetry), bulbo-urethral glands, ampullae of vas deferens- diameter, consistency

4. semen collection and evaluation- 7 billion spermatozoa, >60% motility, bacterial cultures, pH of semen may indicate incomplete sperm release or infection, sperm morphology


d) The mechanism of action of Ovuplant™ in inducing ovulation in the mare. What
are possible reasons for prolonged inter-ovulatory intervals and occasional
acyclicity in Ovuplant™-treated mares?

* Ovuplant is a GnRH analogue

* Induction of ovulation is widely used because of the long and variable interval from the onset of oestrous to ovulation

* Persistent Mating Induced Endometritis with infection for more than 4 or 5 days, the embryo can be aborted with a premature release of PGF2alpha, with a decline in progesterone and shortened inter-ovulatory intervals. Susceptible mares.

* Acyclicity in Ovuplant treated mares (delay in return to oestrus)- treated mares had lower circulating LH and FSH after ovulation. Also causes down regulation of GnRH receptors, resulting in reduction of FSH and a delay in development of a follicle wave.


e) The origin of oestrogens during pregnancy in the mare and their relation to fetal

* Conceptus of the mare  has the enzyme systems capable of oestrogen production and day 12 and day 13 conceptus membranes have been shown to produce oestrogens in culture

* Oestrogens also come from the primary CL between days 35 and 40-- associated with onset of ecG

* Around day 60 the foetal placental unit graudally increases the oestrogen levels

* Gonads of teh fetus provide oestrogen precursors (DHA) converted to oestrogens by the placenta and conjugated in the liver of the mare

**estrone sulfate and total estrogens in blood, milk, urine or feces have been used for the diagnosis of pregnancy and as an indicator of fetal viability since some of the oestrogen comes from the foetus


f) The causes and treatment of endometritis in “susceptible” mares

* Natural service--> inflammation of endometrium due to organisms induced--> most mares resolves 24-48--> if infection persists 4 or 5 days embryo will enter unsuitable environment and will not survive--> in these mares premature release of PGF2alpha with a decline in progesterone and shortened inter-ovulatory intervals--> susceptible mares

** They are unable to elminate introduced microflora in time--reduced physical drainage from the uterus, inflamm modulators do not successfully suppress the physiological inflammation within 48 hours

Tx: clear the uterus of fluid and lavage with saline (catheter via the cervix), oxytocin to aid in clearance of the uterus, antibiotic infusion into the uterus


1.     What are some ways to induce oestrus in anoestrus mares?

* Termination of the luteal phase of the cycle using prostaglandins to induce oestrus

* Additional light treatment

* GnRH can induce fertile ovulation in seasonally anoestrous mares

* Progesterone if the mare is in transitional oestrous

*In responding mares, domperidone isgiven until ovulation occurs. Ovulation

-inducing drugs such as hCG (Chorulon™) and deslorelin

(Ovuplant™) are used in conjunction with domperidone.


1.     How does an autumn follicle (anovulatory haemorrhagic follicle) differ from a corpus haemorrhagicum?

Anovulatory haemorrhage follicles (AHF) are follicles which fill with blood but fail to ovulate. They eventually luteinize but may persist for several months if not treated with PGF2alpha and can therefore prolong the interoestrous interval significantly.

MOre than one PGF2alpha injection might be necessary 7 days after formation

They are more frequent towards the end of breeding season


1.     What are some of the differentials for functional infertility?

* Anoestrous

- GTC tumour

- retention of endometrial cups

- silent heated

- missed oestrus

- chromosomal abnormality

- negative energy balance

- seasonal

- drugs-- illegal anabolic tx, progesterone

* Abnormal cycle length

- ovarian cysts

- persistent CL


- endometritis resulting in early release of PGF2 alpha

* Regular cyclicity

- fertilization failure


- Ovarian haematoma


1.     List some differentials for early embryonic death in horses.

* Abnormal hormones-- luteal insufficiency

* Embryo quality--aged gametes or chromosomal abnormalities

* Uterine environment-- endometrial fibrosis, endometritis, uterine cysts