Mike McHardy’s Rathmor Stud is in sizzling form, one of the leading KZN-based farms currently on the national log sporting a winners to runners percentage of 39.1%, with Average Earnings Per Runner of R37,977 and season earnings of just over R1,7-million.

Producing winners weekly around the country and in particular for owner Mr Mario Ferreira, their pairing and vision to acquire well bred mares has paid off over the past few years, and seen the likes of Group winners such as Mississippi Burning (Gr1) and Nexus (Gr2) as well as Copper Mountain and Hasta Manana come through the ranks.

They enjoyed three winners in four days – two coming from KZN with newly licensed trainer Lorenzo Karriem (who recently enjoyed his first double), and Mogok colt Ntabazondi breaking his maiden in the care of Gavin Van Zyl in Johannesburg.

The McHardy’s stand a son of War Front, a half-brother to Gr1 winner Honor Code and Gr2 winner Noble Tune, Declarationofpeace covering his first book of mares in 2021 and receiving a full book.

They also stand Linngari, a stallion whose progeny are a pleasure to own with regular visits to the winners enclosure – 9 wins from 20 runners and 36 places to date.

A fantastic story and update about Flying The Flag’s second dam, Cassandra Go. Flying The Flag stands at Bush Hill Stud and his first crop will be yearlings in August 2018. 

By Daithi Harvey

As foundation mares go they don’t come much better than Cassandra Go (Ire) (Indian Ridge {Ire}). When her owner Trevor Stewart bought her as a foal over 20 years ago, he could only dare dream of the journey that she would bring him on or indeed of the racing dynasty that she would spawn. News that her granddaughter, dual Group 1 winner Rhododendron (Ire) (Galileo {Ire}), is nearing a return to action brought the mare back into focus and now 22 years of age, Cassandra Go is reported to be in fine fettle by Stewart having only recently given birth to her 13th foal.

“She delivered a lovely filly by Gleneagles (Ire) on Mar. 18 and as usual she had an easy foaling, everything was straightforward and we are very lucky,” Stewart told the TDN a few days ago. “She is quite predictable. She goes a minimum of a month overdue, this time she went a bit longer, perhaps it was something to do with the weather or getting older but she is very healthy and looks considerably younger than she is. I must add that she has been wonderfully managed by James Hanly and his team at Ballyhimikin Stud.”

Such is the mare’s wellbeing, Stewart has her booked to be covered by another dual Guineas-winning son of Galileo in Coolmore’s Churchill (Ire). “I think it makes a lot of sense. Churchill is out of a very fast mare, he’s inbred to Mr. Prospector and even more significantly it represents a double cross with Indian Ridge, which is quite rare these days, so I think it is a very exciting cover. Obviously the Galileo line has also worked brilliantly with the family but as he is slightly out of reach, I’m hoping Churchill represents the next best thing.”

The Cassandra Go story could have taken a number of different routes. Stewart originally bought her as a foal to pinhook, but famously got a rush of blood to the head and bought her back as a yearling for 200,000gns. “It was one of those moments you regret immediately after the event but it has turned out to be the most wonderful story,” he says.

Training was the next step for Cassandra Go and she was dispatched to Geoff Wragg in Newmarket. While success wasn’t immediate, she improved with age. She beat Musical Treat (Ire), subsequently the dam of dual Classic winner Finsceal Beo (Ire) (Mr. Greeley), in a 3-year-old maiden but it wasn’t until a year later that she made her stakes breakthrough when winning a listed race over the minimum trip at Bath in May of 2000 before following up in the G3 King George S. at Goodwood a few months later. She continued to flourish as a 5-year-old, winning the G2 Temple S. at Sandown and the then G2 King’s Stand S. at Royal Ascot before finishing up her racing career with a fine second to the brilliant Mozart (Danehill) in the G1 Darley July Cup.

“It’s rare enough that a top-class race filly breeds one better than herself and even more rare that her daughter then does something similar,” he says.

Of course Stewart is alluding to Cassandra Go’s highest achieving daughter Halfway To Heaven (Ire) (Pivotal {GB}), the triple Group 1 and Classic-winning filly who has passed on those rare genes to her own daughter, last year’s G1 Longines Prix de l’Opera winner Rhododendron.

He adds, “A big factor in the whole equation has been Galileo and I am lucky in that I have sold three daughters of Cassandra Go and all three have gone to Coolmore.”

While the exploits of Halfway To Heaven, a €450,000 yearling purchase by Demi O’Byrne at Goffs, have been well documented, it was the purchase a year earlier of Cassandra Go’s third foal Theann (GB) (Rock of Gibraltar {Ire}), in 2005 at Goffs by John Magnier that planted the initial seeds. Theann would go on to achieve stakes success on the track when carrying Evie Stockwell’s colours to victory in the G3 Summer S. at York in 2007 before ultimately leaving a more lasting legacy through her own daughter Photo Call (Ire) (Galileo {Ire}), who struck at the highest level in the GI First Lady S. in 2016 and the GI Rodeo Drive S. in 2015.

The Coolmore team  returned to this illustrious family when MV Magnier bid 1,600,000gns for Cassandra Go’s yearling filly by Invincible Spirit (Ire), consigned by Ballyhimikin Stud at Tattersalls Book 1 last October. The now 2-year-old is in training with Aidan O’Brien and has been named Fantasy (Ire). “It’s a lovely name so it will be exciting hopefully to see her make her debut sometime this year,” Stewart says.

“While luck plays a major part in the development of these great families, human input is equally important and I have reaped the benefit of having some amazing people involved, from the team at Ballyhimikin dealing with the mares and foals to the trainers that have been involved with the progeny in their racing careers. Geoff Wragg did a wonderful job with Cassandra Go, Aidan O’Brien is obviously a genius and I was also lucky enough to have had an association with Henry Cecil.”

The nurturing early years that Stewart’s bloodstock receives is paramount for their future development and to that end he has nothing but praise for the farms that he partners with. “I keep the majority of my mares with James Hanly in Ballyhimikin, but I also keep some with the Donworths in Round Hill Stud. Both farms are run by superb people and the attention to detail is second to none, which is so important when dealing with this kind of livestock.”

The above mentioned link with the late Sir Henry Cecil came through Cassandra Go’s seventh produce Tickled Pink (Ire). On the track, Tickled Pink carried Stewart’s silks to success on three occasions with two of those wins coming in the G3 Abernant S. at Newmarket and the G3 Coral Charge, beating colts on both occasions. Tickled Pink then took the obvious route back to Ireland to join the broodmare band at Ballyhimikin and her first produce to go through the sales ring fetched 500,000gns when bought by Shadwell at Tattersalls in 2016. Subsequently named Eraad (Ire) (Dark Angel {Ire}), he made a pleasing debut last winter for Charlie Hills and hopes are high that he can make his mark this year.

Recalling Tickled Pink’s stint in training at Warren Hill Stewart says, “It was a very poignant time with Henry’s illness and when she was a 2-year-old, he told me she was a group-class filly. It took her until she was four to achieve that though and before the Abernant S. I had wanted to target a listed race for fillies at Bath but Henry rang me and pleaded with me to allow him to run her against the colts in the Abernant. He was adamant she would win and I relented and thankfully he was right. I think that was his second-last visit to a racecourse.”

Tickled Pink also has a Shamardal 2-year-old in pre-training and a yearling filly by Gleneagles that will be retained. Stewart can also look forward to her delivering a foal by Frankel (GB) in the coming weeks before the mare travels to Newmarket for a date with Dubawi (Ire). “We’re certainly giving her every chance but I suppose with her pedigree and race performance she deserves it.”

As well as Tickled Pink, Stewart has also retained an unraced full-sister to Halfway To Heaven called Allez Alaia (Ire) (Pivotal {GB}) and, with the recent arrival of the newborn Gleneagles filly, already given the moniker of Holly Golightly, he has some exciting young stock coming through.

“It was always my idea to have three fillies [out of Cassandra Go] to breed from and that is the main reason I sold the yearling at Tattersalls last year as I knew then that Cassandra was carrying a filly. In the end she went to the best home one could hope for,” he says.

Allez Alaia is also not being spared sire power and has a yearling filly by Kingman (GB), who will be retained, and a filly foal by Dark Angel (Ire). She visits Churchill imminently. This season’s cover is one Stewart is really looking forward to, as he says, “The mare is by Pivotal and with the Pivotal/Galileo cross having been so successful it sort of feels like I am digging deep where the gold is.”

As an owner, Stewart’s colours have been carried to success in Ireland, England and France, and it is the latter country where his silks are most likely to be seen this summer.

He explains, “Most of my racehorses are in training in France at the moment, the prizemoney and premiums are certainly attractive. The way I look at it is, in Ireland it is so competitive, you are taking on Aidan O’Brien and the rest every day of the week. In England the prizemoney isn’t great but the racing is fantastic, while in France you have a bit of everything and if you have a very good horse you can travel. Obviously things can change but that’s where they are at the moment, but it is a moveable feast.”

Stewart enjoyed a nice winner recently at Chantilly when Hunaina (Ire) (Tamayuz {GB}), trained by Henri-Francois Devin, beat some smart types in a conditions race at Chantilly on Mar. 6. The ex-Aga Khan filly was bought by Stroud Coleman Bloodstock at Goffs last November for €140,000 and gained a valuable bit of black-type on her first start for her new owners when third in the Listed Prix Miss Satamixa at Deauville in January. Stewart is hopeful of increasing that black-type to capital letters in the coming weeks.

He says, “I bought Hunaina in partnership with James Hanly and Anthony Stroud and she now goes for the Listed Snowdrop S. at Kempton in a few weeks’ time. She won quite nicely last time and we think highly of her so hopefully the listed race is a stepping stone to even better things throughout the season.”

Being the custodian of a family replete with such speed, Stewart is obviously keen to maintain that element but also to breed horses that will stretch that bit further, though the eighth furlong is far enough for him. “One’s dream is to have pure speed and one’s dream is still to produce a Guineas winner,” he mused.

Having already achieved that when Halfway To Heaven won the G1 Irish 1000 Guineas in 2008, Stewart has now upgraded that original dream to include winning a 1000 Guineas as an owner-breeder. Given the quality of his mares, that is no far-fetched fantasy and Stewart rightly is of the opinion that he could not afford to go to the market and buy some of the fillies that he is producing himself, thus retaining his homebred fillies gives him a better than sporting chance of realising that dream in the coming years.

The breeder puts a lot of thought into his coverings, delving deep into the pedigrees of his mares and the stallions he is considering using, and while ultimately he tries to keep it simple, he does, as he puts it, go ‘off piste’ now and again. One thing is certain, whatever decisions he has made over the past two decades concerning Cassandra Go and her daughters has reaped huge dividends and it has all the hallmarks of a pedigree that will prosper for generations to come.

Peter Gibson will be giving an informative feedback presentation at the KZN Breeders AGM on Thursday 11 February, regarding the recent Asian Racing Conference that took place in India which also addressed the movement of our horses internationally out of South Africa.

The slides below cover the main points of discussion for Thursday:

·         Overview

·         Outbreak History

·         Risk Analysis + Conclusion

Also see the link with the presentation given by Mick Goss at the Asian Racing Conference on the Sporting Post website.

AHS Update for ARC 2016 – OVERVIEW

AHS Update for ARC 2016 – OUTBREAK HISTORY

AHS Update for ARC 2016 – RISK ANALYSIS + CONCLUSION

The KZN Breeders Club AGM will take place at the Nottingham Road Hotel at 11am.

This condition is more formally known as neonatal hypoxic ischaemic encephalopathy (HIE) and is seen as abnormal behaviour during the first few days of life. Other common names for the disease are ‘wanderer foals’ and ‘barker foals’.

The exact cause of the condition is unknown but appears to involve asphyxia (lack of oxygen) and ischemia (poor blood supply) to the brain or other organs during late gestation, delivery or the early neonatal period.

Some of the common causes are:

• Foaling problems such as red bag deliveries, dystocias, caesarean sections, foals that need to be resuscitated at birth and induction of labour
• Placental abnormalities such as placentitis and premature placental separation
• Maternal problems include anaemia, endotoxaemia secondary to colic, cardiovascular disease or hypotension (low blood pressure)
• Thoracic trauma such as fractured ribs or prolonged thoracic compression during difficult delivery has also been implicated.

Clinical signs:

There are two major types of this condition:

1. The foal appears normal at birth and has often suckled normally. These foals deteriorate within 6-24 hours with rapid progression of the condition over the first 24 hours.

2. The foal is abnormal from the outset and is often clumsy and confused. These foals don’t have a suck reflex and are disinterested in feeding.

Neurological signs are the most evident clinical signs including poor teat seeking behaviour, tongue hanging out, head pressing, loss of suck reflex, ‘barking’, hyperesthesia on handling, seizures, weakness and abnormal posture.

Respiratory signs are also seen including dyspnoea, abnormal breathing patterns, shallow breathing and breath holding.

These foals are far more susceptible to secondary conditions such as septicaemia.

Diagnosis:

This can be difficult in the early stages as the signs are often subtle unless the history indicates towards a foal at a high risk of developing this disease. Concurrent disease processes in other body organs and generalised depression can obscure clinical signs of HIE.

The placenta can be useful in the diagnosis and early recognition of a high risk foal. If there is any indication of placentitis, thickening of the placenta or premature placental separation these foals need to be monitored closely for development of this condition.

Treatment:

Often in the early stages it is difficult to differentiate this condition with septicaemia and it is therefore common practice to provide combined treatment in all cases. Even if these foals don’t start off with septicaemia, they are at a far higher risk of developing it than normal healthy foals.

The treatment is often very intensive and can become very expensive.

Treatment is aimed at:

• Reducing any cerebral oedema (brain swelling)
• Improving cerebral perfusion and oxygenation
• Controlling any seizures if present
• Preventing /controlling/treating concurrent sepsis with necessary antibiotics
• Ensuring adequate transfer of immunity, it is very important to check all foals IgG levels.

Nursing treatment:

1. Regular turning of the foal to prevent trauma and bed sores.
2. Feeding via a naso-gastric tube. Some foals require total or partial parental nutrition if they have concurrent diarrhoea, gastric ulcers or colic.
3. If the foal is born with HIE ensure it gets adequate good quality colostrum.

Prognosis:

Foals that develop HIE after birth have a much better prognosis and complete recovery is possible provided they get the appropriate treatment. Those foals that are born with HIE have a poor prognosis for survival without intensive and expensive treatment. Concurrent sepsis (or other complicating disorders) reduces the prognosis to almost hopeless.

The rate at which the foal improves is also important. If there is no improvement after 4 days of treatment the prognosis becomes far poorer.

Bosch Hoek Equine Hospital is a state of the art Equine hospital situated in the beautiful Kwa-Zulu Natal Midlands of South Africa. Our primary goal is to offer clients and their horses world class care and expertise for both surgical and medical conditions with a rehabilitation centre to match.

If you require our services or would like to discuss anything please call one of us on the numbers below:

Dr Helen Tiffin 082 966 9324
Dr Jenny Lawrence 082 836 9897
Dr Anna Bowker 082 849 3456
Dr John Hodsdon 072 165 7122

Dr Jenny Lawrence Equine Veterinarian BVSc Jenny qualified in 2005 after which she worked as a small animal veterinarian in the United Kingdom for 3 years. In 2008 she returned to South Africa to begin equine work with the late Dr Dave Mullins before joining the Bosch Hoek Equine Hospital where she has become an important part of our team and has a special interest in foal medicine. Jenny recently returned to the UK for a short period where she worked with renowned breeding expert, Dr Jonothan Pycock as well as spending time at various equine hospitals and AI centres in the UK.

Physitis is a developmental condition seen in young, rapidly growing horses, leading to visible enlargement of the growth plates, often accompanied by heat and pain over the swelling as well as varying degrees of lameness. (“Physis”=growth plate + “itis”= inflammation). Growth plates are the areas on the ends of long bones of young horses from where the bones grow or lengthen.

Basics of bone formation:

The growth of long bones occurs at a highly specialised region at one or both ends of the bone, called the physis. When a foal is born, most of the skeleton has ossified (turned to bone) with cartilage remaining at the site of the growth plates to allow for further growth in length.

Gradually the bone matures and replaces the cartilage in a process known as endochondral ossification. This leads to lengthening of the bone and so the horse grows in height and is able to carry its increasing weight. The growth plates mature and close sequentially from the ground up, with the most active, the distal cannon bone (just above the fetlock) closing at approximately 4 months, and the distal radius and tibia (just above the knee and hock) closing at 18 to 20 months.

Most long bone growth is complete by 2 years of age. The rate of ossification is dependent on the load placed onto the limb (physical activity and weight) as well as nutritional factors. A fine balance must be maintained to ensure the correct rate of bone formation.

Decreased activity causes weaker bone to be deposited and increased activity will cause stronger bone to be formed, unless the increased stress occurs too abruptly. Abrupt increases in weight or activity will find the physis unprepared and the bone will be overloaded, leading to micro-instability and pain. The physis reacts by laying down secondary bone (“callus”) in an attempt to strengthen the bone, resulting in the typical bony swellings. An understanding of the process of bone formation greatly helps us to understand how and why physitis occurs.

What causes physitis?

Physitis is a multifactorial syndrome with managemental, physical and infectious causes.

• Overnutrition (rich young pasture or high grain feeds) leads to rapid weight gain which overloads

the newly maturing physis. This is the most common cause of physitis. Undernutrition

means that the building blocks needed to create new bone are not available (especially calcium).

• Physical causes include direct trauma to the growth plate, excessive exercise, or secondary

trauma from unbalanced weightbearing or poor conformation. For example, a foal with a

contracted tendon or other lameness in one front limb may present with physitis in the opposite

limb due to the increased weight load on the “good” limb.

• Infectious physitis occurs when there is a bacterial infection present in the growth plate, either

directly from a penetrating wound or via the bloodstream in a septicaemic foal. The physis is

predisposed to bacterial infection due its very convoluted blood supply; bacteria tend to “sludge”

in the blood vessels and subsequently infect the surrounding bone.

What are the signs?

The most common sites for physitis are the distal cannon (just above the fetlock), the distal radius (just above the knee) and less commonly the distal tibia (just above the hock). Due to the stage at which these physes mature, signs are typically seen in the fetlock region from 3-6 months and the knee from 8 months to 2 years.

How is it treated?

The treatment consists of addressing the primary cause and preventing any secondary damage or permanent angular limb deformity. The length of treatment required varies with the severity of the physitis but is generally between 2 weeks and 2 months.

Treatment includes:

• Exercise restriction (but not total box confinement as some stimulation is needed to mature the

growth plates). For example: either small paddock rest, or box confinement with short periods of

paddock exercise (1-2 hours at a time).

• Reduction of body weight and particularly a reduction in the energy content of the diet should be

made. The diet should have the correct calcium/phosphorus balance as well as adequate copper

and zinc.

• Regular (2 weekly) balancing by a farrier – very slight rasping is adequate.
• Non-steroidal inflammatories (Metacam, Bute)
• Correction of any underlying angular limb deformities
• Infectious physitis requires intensive antibiotic treatment systemically and locally.
• Firm, warm, and sometimes painful

enlargement of the growth plate, most often

medially (on the inside of the limb),

sometimes giving joints an “hourglass”

appearance.

• Varying degrees of lameness, from mild

stiffness to overt lameness.

• Flexion of the affected joint may be resented
• The fetlock conformation may become more

upright and the fetlocks and knees may

deviate outwards, as the foal tries to bear

weight on the outside of the hoof (to alleviate

pain coming the inside of the limb). If a foal

starts to “go bandy” after having previously

normal conformation, consider subclinical

physitis and treat it accordingly.

• Radiographs/X-rays show thickening of the

physeal cartilage and callus formation.

The typical hard

swellings in a recent

physitis weanling

An X-ray showing

physitis of the distal

radius (Just above

the knee joint)

What is the prognosis?

Physitis is a self-limiting disease which resolves when the growth plates close. Provided that no secondary limb deformities have occurred, the prognosis is good.

Bosch Hoek Equine Hospital is a state of the art Equine hospital situated in the beautiful Kwa-Zulu Natal Midlands of South Africa. Our primary goal is to offer clients and their horses world class care and expertise for both surgical and medical conditions with a rehabilitation centre to match.

If you require our services or would like to discuss anything please call one of us on the numbers below:

Dr Helen Tiffin 082 966 9324
Dr Jenny Lawrence 082 836 9897
Dr Anna Bowker 082 849 3456
Dr John Hodsdon 072 165 7122

A boarding mare owned in a partnership at Rathmor Stud named War Echo (Complete Warrior – Distant Echoes by Prince Sao) has now had two “extended” gestation periods with both her foals and we discussed this unusual behaviour with Dr Allen Bechard of Almiray Veterinary Practice.

The mare was sent to stud at the age of 13 after spending her younger years as a show-jumper after a brief racing career.
She is a half-sister to Harry’s Echo and Champion Broodmare Stormsvlei – the dam of the mighty Pocket Power and River Jetez who is currently campaigning overseas.

Due to her purchase date, she was covered late in the season on the 20 November 2008. She foaled her Carpocrates filly (now named Athena’s Echo) on the 24 November 2009 – and because of her extended gestation period she was rushed back to Ravishing before the closing of breeding season, but unfortunately she re-absorbed the foetus which left her barren the next year.

She was subsequently covered by Ravishing on 2 September 2010, just the day after breeding season opened. Another interesting note about this mare is that she only visited Ravishing once – yet only conceived almost 10 days later – a testament to Ravishing’s exceptional fertility.

She was brought into the foaling barn early, the 12 July, to settle into her stable and new routine as her foal was expected early August 2011. She kept Mike and Tanya McHardy waiting, and she eventually foaled a beautiful Ravishing filly – now named by her owners Quest For Glory – at 11:08 pm on 11 September 2011. Mike McHardy was heard to say that War Echo had broken all gestation records at his farm!

Dr Allen Bechard says “the normal gestation for a mare is very variable but between 310 and 370 days is considered normal, with 340 days being usual. Mares tend to be consistently early or maybe consistently late. If we take 340 days as average, we have specific mares that usually foal 3 weeks early and other mares that are consistently late.
The foal gets its nourishment from the placenta which is attached to the inner lining of the uterus. The area of attachment plays an important role in the rate of growth of the foal. If a mare has some scar tissue affecting the uterine wall, or endometrial cysts or any other factors that reduces the area of placental attachment, the rate of growth of the foal is affected. The foaling process is largely dependent on the foal deciding its mature enough to be born. A late foal is not necessarily negatively affected.
There are not necessarily any dangers with a mare having a long pregnancy. The most important factor there being enough time to get her back in foal. I would expect all breeds to show a variance in gestation time, and gestation time would be partially hereditary.”

When discussing the possibility of mares being induced, Dr Allen Bechard says “mares can be induced, but there has to be an extremely good reason, such as another life threatening condition. The reason for this is that one is inducing a foal to be born that is not mature enough. The time from conception to maturation varies from mare to mare.”

War Echo has been sent to A.P. Answer this season.

Dr Allen Béchard B.V.Sc. (Pret) runs his veterinary practice from Nottingham Road. If you would like to contact his practice please see the details below:

ALMIRAY Veterinary Practice cc
CK 2009/067088/23
Telephone: 033-2666198
Fax: 033-2666861
Office Cell: 0828413601
Email: almiray@bundunet.com

If you would like to contact Rathmor Stud, please phone Mike or Tanya 033 – 266 6853 or alternatively email rathmor@bundunet.com.

]]> https://kznbreeders.co.za/guest-column/vet-news-and-info/extended-pregnancy-gestation-in-mares/feed/ 2 https://kznbreeders.co.za/guest-column/vet-news-and-info/how-the-great-white-came-to-be/ https://kznbreeders.co.za/guest-column/vet-news-and-info/how-the-great-white-came-to-be/#respond Sat, 19 Sep 2015 08:00:00 +0000 http://kznbreeders.co.za/guest-column/vet-news-and-info/how-the-great-white-came-to-be/

How “The Great White” Came To Be

Natalia Banasiak (B.Sc Zoology) has kindly provided us with an insight into how Rathmor Stud’s white Thoroughbred colt with the brown ears came to be.

Traits are passed down from the parents down to the offspring: half a foal’s genetic make up comes from the dam and the other half from the sire. When the egg and sperm fuse to create the zygote, it results in a genetically unique foal. Mendel’s famous experiments with pea plants showed the principles of trait inheritance and they helped him develop the concept of recessive and dominant genes (though, of course, he didn’t know about genes at the time – that only came after the discovery of DNA around 90 years later). What he showed, basically, was that an individual has two copies of the allele responsible for each gene. Individuals can be either homozygous if the two alleles are the same or heterozygous if the two alleles are different and these alleles can have either recessive, complete dominant or partial dominant effects on each other.

We also need to differentiate between genotype and phenotype. The genotype of the individual is the genetic code (ie. the sequence of alleles present in an individual) while the physical manifestation of the genotype is the phenotype – basically what the horse looks like (in this case, the foal’s colour). How the horse looks is entirely dependant on its genotype – you can’t have a grey horse without the grey gene, or a coloured horse without one of the coloured genes – and how the genotype is expressed depends on the nature of the individual genes and alleles.

Recessiveness and Dominance

In most cases of heterozygous individuals, one gene will be dominant over the other (recessive) gene and so the individual will display the phenotype of the dominant gene. The recessive phenotype will only be displayed if the individual is homozygous for the recessive gene. In a few select cases, the genes will compete for dominance and will therefore appear as an in-between state of the two genes.

To demonstrate, let’s look at the base colours of horses: chestnut, black and bay. First we look at the Extension locus that determines if the horse will be ‘black’ (eumelanin is expressed) or ‘red’ (phaeomelanin is expressed). The alleles for this are E, which is the dominant extension allele for black pigmentation, and e, which is the recessive extension allele responsible for red pigmentation. So, the EE and Ee genotypes result in a black base phenotype and only the ee genotype will result in a red base phenotype, ie. a chestnut.

Next we look at the Agouti locus that ‘creates’ a bay by affecting the dilution of eumelanin and results in black remaining only at the horse’s points. The expression of Agouti (A) is dominant so both Aa and AA will result in a bay, while aa will leave a black. It has no effect on chestnuts as they have no eumelanin expression for the gene to work on.

So, in summary:

EE/aa or Ee/aa = black
EE/AA, EE/Aa, Ee/AA or Ee/Aa = bay
ee/AA, ee/Aa or ee/aa = chestnut

All other colours work in essentially the same way. The cream dilutions are the best example of a case of incomplete dominance as the heterozygous and homozygous expressions of the genotype result in different phenotypes – think of the differences between a palomino (heterozygous, nCr) and a cremello (homozygous, CrCr).

Now that we’ve gone through the basics, I can get onto the complicated stuff relating to the KIT locus and hopefully make sense. The KIT locus determines all the paint patterns including rabicano and dominant white. For a horse to show the phenotype of these patterns it must have at least one copy of the gene as it is a dominant gene and multiple patterns can be present on the same horse.

At this juncture it is important to address the issue of mutation. Mutation in the genomic sequence is the basis of changes in all living things and this is inescapably linked to the process of evolution as selection (both natural and artificial) acts on the variation within a species. Even in the simplest case of two alleles at one locus, those two alleles must have arisen somehow. Mutations are especially important in creating variation within a closed population such as the Thoroughbred gene pool. There are many ways in which a mutation can occur and there are different types of mutations too. Since the KIT locus is long, this makes point mutations (the change of one base into another) occur relatively easily. Dominant White is caused by missense or nonsense mutations in the KIT locus which will become dominant. Missense mutations result in the production of an altered amino acid in the protein product and a nonsense mutation will create a ‘stop codon’ which will cause the transcription process to be truncated prematurely.

Once the mutated gene is created it is hereditary so the horse’s offspring have a 50% chance of inheriting the colour mutation.

I’m going to go through all the patterns to show the differences in patterns and I’ll put in brackets which do occur in the *TB gene pool.

Tobiano – not present in Thoroughbreds
Tobiano is the most dominant of the KIT mutations and is characterised by white markings that are smooth edged and cross the horse’s topline. Tobianos also often have white legs, two-toned tails and the white tends to be kept away from the eyes and face. The colour on a tobiano often radiates from source points on the horse that include the face, ears, chest, genitals and the tail tip. The medicine hat pattern is an extreme for of tobiano – so despite what many people have said about the Rathmor colt he is NOT a medicine hat even though the pattern is similar phenotypically.

Frame/Frame Overo – present in Thoroughbreds, spontaneous mutation
Here the white markings are restricted to the body and neck (ie. no white over the topline) and have jagged edges. There may be white on the legs but it is not a ‘requirement’ and there is often extensive white over the face but typically over the eyes.

Splash – present in two Thoroughbred families (Hey What The and Mata Biru), spontaneous mutation
Horses with the splash gene typically have extensive white on the legs that can extend up the belly but rarely crosses the topline. Splash horses also have extensive white over the face that extends over the eyes and often results in blue eyes.

Sabino – present in Thoroughbreds, carried from Arabian ancestry
Probably the easiest of the paint patterns to overlook as it can often be mistaken for ‘normal’ markings like blazes and white stockings. In more characteristically marked horses, the pattern is irregular and jagged, gravitating upwards and on the face but avoiding the eyes. White lip markings and belly spots are also common. The edges of the markings may also take on a roan-like appearance. A homozygous sabino genotype (SbSb) is assumed to result in maximum expression of white. The edges get more and more roan-like as expression increases to the point where they can’t really be described as edges at all!

Rabicano – present in Thoroughbreds, carried from Arabian ancestry
Usually thought to be linked to roan, this is actually also a KIT mutation and is closer to sabino. It is characterised by white hair on the flank and dock; when maximally expressed it can be very dense but when minimally expressed it may only be expressed by sparse white hairs at the top of the tail (commonly called a skunk tail) or white hair occurring at the base of the tail. The roaning effects often spreads with age.

Dominant White – present in Thoroughbreds, spontaneous mutation
This is the pattern I predict the white colt is! So far, 11 mutations of the KIT locus have been identified, labelled W1 through W11; each of which is separately heritable and has a slightly different phenotypic expression. I stress, the phenotype of maximum sabinos and dominant whites can be almost indistinguishable but the genotypes are different so they are not the same thing. Dominant White horses are born with unpigmented pink skin, white hair and dark eyes however horses can also have patches of colour. These patches of colour tend to be located along the topline especially at the ears and mane. This is also not a form of albinism – something that has never been documented in horses.

In the Thoroughbred gene pool spontaneous DW mutations have occurred in the following cases – to name a few:

Click here onto Rathmor Stud’s Facebook page to post your suggested name for the colt.

*TB – abreviation for Thoroughbred

We discuss the breeding lifespan of mares with Dr Allen Bechard of Almiray Vet Practice who gives some enlightening insights into the effects of age on a broodmare with regards to productivity, fertility and conception.

Mares are individuals and can differ greatly from one horse to the next, but a point to bear in mind is that fertility is fairly heritable and historically, mares have not necessarily been selected for fertility reasons.

A mare’s productivity will be affected by the age she starts breeding. If a mare does begin her breeding career as early as a 3 or 4 year old, there is no reason she should not continue into her late teens or early twenties. This is providing she is sound and well in herself and her reproductive system is not adversely compromised along the way.

With a mare that might be bred later in life, say as an 8-10 year old, her breeding career might not necessarily be prolonged because many reasons for reducing fertility later in life are age-related and not necessarily due to the number of foals.

“Old maiden mare syndrome” which is classically seen in a well-performed sport mares such as a polo, show jumping or eventing mares which are bred at the end of their sporting careers may be in their mid-teen years and are often difficult breeders due to post breeding endometritis susceptibility and degenerative changes to the endometrium.

For those considering the option of purchasing a well-bred ageing mare at a disposal sale or auction on the basis of a well-bred pedigree, it is always better to purchase one in foal. As far as buying an old empty well bred mare is concerned – one would have to consider the following: How well-bred is she? How long has she been barren for? What stallions did she last visit? Was she treated to assist her to conceive? Was a specific reason found for her lack of conception? How old is she?

Take into account the fact that the average brood mare usually produces regular foals until late teens, although cases of mares as old as 26 are not unknown.

The ideal age for a mare to begin her stud career from a physical perspective would be four years old. However, early-maturing, well-grown fillies have been bred at 3 with no complications.

There is a relationship between a mare’s breeding age and the size of foals, the first is generally smallish, the second is bigger and from about the third foal on, until the mare is in her late teens, the foals are optimally sized. Old mares generally produce smaller foals, due to reduced effectivity of the uterine wall.

In terms of the length of breeding life of a mare, the viability for breeding purposes varies depending on the value of the mare. A recent study on 20 000 American brood mares showed the following results, which indicates clearly how fertility is closely related to age.

Mares Age:                         3-8yrs      9-13yrs      14-18yrs       >18yrs

Mares producing live foals:    84%         82%            67%             56%

In conclusion, a mare’s breeding lifespan depends on a number of factors, but can start from as young as three (optimally four) and continue into the mid-teens in optimal conditions. However, fertility issues associated with age can affect the viability of the older mare, although in the right conditions, there is no reason to stop breeding a well-bred mare if she is still producing quality foals.

Dr Allen Béchard B.V.Sc. (Pret) runs his veterinary practice from Nottingham Road. If you would like to contact his practice please see the details below:

ALMIRAY Veterinary Practice cc
CK 2009/067088/23
Telephone: 033-2666198
Fax: 033-2666861
Office Cell: 0828413601
Email: almiray@bundunet.com

We have all heard the shocking news about our recently crowned Champion stallion, for the 5th year in a row, Jet Master suffering from this virus.

Here are some facts, with the assistance of Dr Sarah Seitz (Bsc DVM) about what the virus is. West Nile Virus or WNV is a mosquito borne RNA virus that affects the central nervous system and can cause severe neurological disease (meningitis & encephalitis).

The disease is naturally transmitted between birds via mosquitoes. Humans and horses are “dead end hosts”. This means that humans and horses can get the disease if bitten by a mosquito that previously bit an infected bird, however, the levels of virus in the blood of humans and horses does not reach high enough levels to be able to be transmitted by mosquitoes. In other words, if a mosquito bites an infected horse or human, the mosquito cannot transmit the disease. It can only transmit the disease if it bites an infected BIRD. Person to person or horse to horse transmission through contact does NOT occur. (Need a mosquito that has bitten an infected bird).

WNV was first discovered in a febrile woman in the West Nile district of Uganda in 1937, and was first discovered in the western hemisphere in 1999 in the Bronx zoo in New York.

99% of infections caused by WNV are asymptomatic – the body’s immune system quickly clears the virus. Only in 1% of cases, does neurologic disease occur. WNV is found throughout most of the world including Africa, Asia, Europe, the Mediterranean, the Middle East, Australia and the Americas. The disease is carried by migratory birds who in turn carry WNV into new areas.

WNV can be destroyed by many disinfectants including sodium hypochlorite solutions (bleach dilutions), 3% hydrogen peroxide, and 8% formaldehyde. It is also inactivated by UV light, gamma irradiation and heat. Reducing the risk of exposure to the mosquitoes that may carry the virus is also an important part of prevention. It involves eliminating mosquito breeding sites to reduce the number of hatching mosquitoes, and to reduce exposure to adult mosquitoes. Mosquitoes breed in stagnant water, so reduction of breeding sites involves eliminating stagnant water sources.

Human illness can be classified into 2 forms: West Nile Fever (mild and flu-like) and West Nile Neuroinvasive disease (severe neurologic disease).

The incubation period in horses is 3-15 days (time from infection to manifestation of signs). Infection with West Nile Virus does not always lead to signs of illness in people or animals. Horses appear to be a species that is susceptible to infection with the virus. In horses that do become clinically ill, the virus infects the central nervous system and may cause symptoms of encephalitis. Clinical signs of encephalitis in horses may include a general loss of appetite and depression. Most infection in horses is subclinical (asymptomatic). In symptomatic cases, horses may display anorexia, & neurologic signs.

West Nile encephalitis describes an inflammation of the central nervous system. Neurologic signs include ataxia (stumbling, falling), weakness, paralysis of one or more limbs, impaired vision, inability to swallow, teeth grinding, aimless wandering, circling, facial paralysis and convulsions. Horses may have one or more of these signs of varying severity.

Fever may be present but not in all cases. If a stallion does develop fever, fertility for the following 60 days may be compromised.

It is important to note that not all horses with clinical signs of encephalitis have West Nile encephalitis. Certain other diseases can cause a horse to have symptoms similar to those resulting from infection with West Nile Virus. If you are concerned that your horse may be exhibiting signs of encephalitis, please contact your veterinarian. Laboratory tests are necessary to confirm a diagnosis. It is important to diagnose WNV because infection is an indication that mosquitoes carrying the virus are in the area and need to be eliminated.

Some horses do not survive, but horses that do recover may not necessarily return to full function. 10-20% may have residual defects such as weakness, exercise intolerance, muscle atrophy or behavioral changes. There is no cure for WNV, and treatment consists of supportive care.

A WNV vaccine for horses is available, whilst vaccination of horses is not a guarantee of protection against infection it is the best method of prevention.

What Is It?

West Nile Virus is a viral disease that causes neurological signs. It is transmitted by mosquitoes and is carried by wild birds, crows are known to die from the disease. Like Horsesickness, it is not a contagious disease. Humans can be infected by the disease if bitten by infected mosquitoes but cannot be infected by horses with the disease, unless they are performing a post mortem. This disease generally occurs in the warmer months of the year when mosquitoes are most prevalent.

Clinical Signs:

Not all horses become clinically ill. The virus attacks the central nervous system and causes encephalitis. The clinical signs can vary from very mild to coma and death. The horses with the mild form of the disease have a fever, are listless and have a loss in appetite. The more severe cases show ataxia, circling, depression, weakness and in the most extreme cases convulsions, coma and death. The severe clinical signs can be confused with Neurological Herpes, Botulism and Rabies and the mild cases can be confused with any disease that causes listlessness and a fever.

Diagnosis:

Blood samples taken in EDTA tubes and samples of brain and spinal cord from post mortem are used to diagnose the disease. As this disease can look like many other diseases it is advisable to also do a complete blood count.

Treatment:

There is no specific treatment for this disease, only symptomatic and supportive care. This is aimed to reduce the discomfort, pain and inflammation and to reduce secondary bacterial infections and keep the horse hydrated. The more severe cases can become costly to treat as they are often recumbent and need intensive nursing care to minimise secondary muscle damage and ‘bed sores’. These horses often need to be put in a sling which can be costly to erect. It is important to keep stress to a minimum and protect the patient from adverse weather conditions.

Prognosis:

Majority of horses with WNV show mild symptoms and recover rapidly. Neurological signs are infrequent and if well supported these horses recover well. Coma and death from the disease is rare.

Prevention:

As with the midges, preventing the mosquitoes from biting the horse is the best form of prevention. This includes using insecticides on the horse and in the stables, stabling between dust and dawn, removing stagnant water and turning lights off in the stables at night. Drug companies are looking at importing a vaccine in the near future.

Bosch Hoek Equine Hospital is a state of the art Equine hospital situated in the beautiful Kwa-Zulu Natal Midlands of South Africa. Our primary goal is to offer clients and their horses world class care and expertise for both surgical and medical conditions with a rehabilitation centre to match.

If you require our services or would like to discuss anything please call one of us on the numbers below:

Dr Helen Tiffin 082 966 9324
Dr Jenny Lawrence 082 836 9897
Dr Anna Bowker 082 849 3456 (away until August)
Dr John Hodsdon 072 165 7122

Dr Jenny Lawrence Equine Veterinarian BVSc Jenny qualified in 2005 after which she worked as a small animal veterinarian in the United Kingdom for 3 years. In 2008 she returned to South Africa to begin equine work with the late Dr Dave Mullins before joining the Bosch Hoek Equine Hospital where she has become an important part of our team and has a special interest in foal medicine. Jenny recently returned to the UK for a short period where she worked with renowned breeding expert, Dr Jonothan Pycock as well as spending time at various equine hospitals and AI centres in the UK.