HEALTH ISSUES

Dwarfism in the Friesian and Warmblood Friesian Horse

Since the Friesian horses first arrival in Australia in the late 1970's, there has been a rather limited gene pool, with until recent years, only two imported stallions, Lyckle B (Ulrik 168), Maurits Friso (Dagho 247) and a handful of related mares sired by Ysbrand producing the majority of breeding stock.

Since the publication of this article in the Australasian Warmblood Friesian Association newsletter in 2001 more references to cases of dwarfism have been reported, with in total five alleged cases in Australia since the arrival of the first purebred Friesians.

What is common, is that all of the alleged horses are said to carry the same bloodlines. Two dwarf foals are alive at the time of writing this article, the owners choosing not to euthanase. One was a purebred named Coobydale Silhouette sired by Lyckle B. The other dwarf, a 75% Warmblood Friesian was sired by Lyckle B's son - Othello S. Other noticeable similarities appear in the bloodlines of both cases with the mare lines carrying the blood of the stallion Maurits Friso and one of the four original mares sired by Yjsbrand 238.

Editors note: Silhouette died in June 2003 at 14 years of age. She was the oldest recorded living Friesian dwarf with the University of Utrecht records showing six years longevity.

In the case of the latest Warmblood Friesian dwarf foal, there is the possibility that the outside component of the Thoroughbred blood may be the contributing factor in that instance.

As seen in the following reports taken from the early days of the Friesian revival in Holland, when dwarfism in the Friesian was first noted, the veterinarians at this time (early 20th century) suggested that "Every stallion, even if only sired one dwarf foal, is a heterozygote and can therefore with a heterozygote mare produce a dwarf foal". This is probably where some could go into panic, as many of the breeding horses in Australia carry these lines! From this same report the veterinarians point out that "There are several stallions, that delivered dwarf foals, then there are many that served many mares that never sired a dwarf foal. The latter do not have the dwarfism factor, indeed had they had this factor, they would have - after serving a heterozygote mare, who certainly occurred within the served material - sometimes sired a dwarf foal. As long as a stallion has not sired a dwarf foal, we have no proof that he possesses the factor". Several AWFA Inc breeders have tested out this theory by breeding their stallions to the known dwarf producing lines as well as close relationship breeding, with thankfully only positive results, so it must be pointed out that not every horse within the same bloodline will produce dwarf foals.

The following reports lead to a number of questions, such as, does inbreeding play a part in the scenario and is it genetic? Should stallions or mares that have bred dwarf foals continue to be bred with?

As to the mode of transport of the dwarfism factor, the AWFA Inc does not suggest that any of the horses mentioned, carry a factor to pass on dwarfism. The association however does encourage members to thoroughly investigate their breeding options, with direct questions asked of purebred breeders. If in doubt seek veterinary advice. It would seem that the best approach is one of common sense, as adopted by the FPS in the early 20th century which was to err on the side of caution and not use animals who have already shown that they produce this undesirable factor.

"Friesian Studbook Stallions, vol.1-early 20th century 'The stallion station Nijtap came into being in 1902 when the 9 year old Frits 95 was bought by the stallion association in Beetsterzwaag.In 1915 this station ceased as in present form and was reopened in Nijtap in 1926. The second stallion purchased was Cremer 136 in 1928. He stayed at Nijtap until his rejection for the Studbook in 1935. Mrs. van der Vlugt remembered the commotion about this rejection very well. According to former secretary Huijing the main reason was the large number of "midget" foals in his offspring. Another reason was the fact that Cremer showed a certain amount of "roan" in his colour which he passed on to his offspring as well.

Cremer was sold after his rejection, but would breed many more (un-registered) mares in the surroundings of Drogeham. Many of his offspring could be identified by the white hairs all over their bodies.' 'Us Heit 126 was born in 1917. He bred at De Oorsprong from 1920 to 1931, when he was rejected. He became the father of the registerd sons Cremer 136 and Elius 138, and 34 daughters. We see many of his daughters back in well known lines.' Some stallions fathered by daughters or granddaughters of Us Heit are: Knjilles 141, Evert 179, Mengelberg 145, Orleans 148, Petrus 152, Peter 153, Plutus 156, and Ynse 164. 'The fact that this stallion line did not get more wide-spread is probably also due to the dwarf foal factor, a frequent problem in the Friesian horse breeding, that was - and still is - passed on quite often. This was considered to be a serious problem at the judgings in the 1920's and would be reported in the stallion's information. Later on the stallion keepers came to the conclusion that this information would decrease the number of breeding services of their stallions, and they did their utmost to prevent the information from becoming public.'

Via the male line, Prins 109 could only be found in Cremer 136 and Elius 138. But the Studbook wasn't very knowledgable about the problem of inbreeding yet, and - for obscure reasons - would reject both stallions within a short time. In Cremer's pedigree the name Friso 117 is absent, and that is why the Breeding Committee later tried to bring stallions from the Cremer-line back to the foreground. These attempts didn't have much result, on one side because of too much quality loss, on the other side because of the pre-potency of the dwarf-factor and the roan-factor.'

'It was a striking detail that Cremer passed on his "roan" to Plutus 156, who passed it on to many of his descendants. The stallion Wytze 163, a Plutus son, bred from 1943 to 1944. In 1945 the male Cremer line had disappeared from the Studbook. But the female Cremer line is especially known via the well known mares Gepke 1463, mother of the preferent stallion Aizee 170, and Klavervrouw 1505, mother of the stallion Eelke 183.' Us Heit's other son, Elius 138 was owned by Jan Bouwstra, who, when he heard that Elius would be rejected from the breeding, let his emotions cloud his attachment to the stallion and he sold him to a broker who sold Elius to England. He is attributed to having said "I have done many stupid things in my life, but the most stupid thing was when I sold Elius." The stallion Nammele 147P was out of the mare Aafke 1380, who was also the other of Elius 138. Nammele bred until he was 23 years old and stood at several breeding stations. Of his four approved sons, Jabik 187 was rejected in 1958 after six disappointing breeding seasons, and Lutse 192 was exported to South Africa. 'We know that Nammele gave very small foals, but we do not know how many. A closed front of stallion keepers and horse traders would get rid of these foals as soon as possible.' So the accepted "line" for the dwarf factor is Cremer. This male line died out, but the mares, as mentioned, could have played a role in further instances of dwarfism since 1945. Cremer is also attributed to passing on the white hairs scattered on the body and today, this is ocassionally seen in some foals on certain parts of their bodies and is cause for retention in the foal book.

A veterinarian report on dwarfism in the Friesian horse in the early 20th Century It was mainly Wriedt and Mohr from Sweden and Wilson and Crew from Scotland who drew the attention to the meaning of letaal and sub- or semiletaal factors in breeding of pets.

Letaal factors are factors that, if found homozygote are the cause of infertility. Morgan divided the letaal factors in gametic, that is those that cause the eggs of spermacides to die before reaching full fertility and homozygote, that stunt the development of fertilised eggs of embryos and cause them to die too.

These letaal factors cause infertility which shows when in crossing we get a strong difference between the expected amount of various forms and the amount actually produced. Since these letaal factors are as a rule recessive, they only have this result if found homozygote. If in a family one or more letal factors occur, then with inbreeding they will often be the cause of the sometimes occurring infertility.

In pets so far we only know zygotic factors. Sub or semiletaal factors are factors that if homozygote, they cause young that are born to live but have little life expectancy, or have abnormalities which prevent them from growing up to useful pets. We know of two categories within the letaal and subletaal factors; recessive and dominant factors. In the horse a recessive subletaal factor is found which causes atresia coli often combined with gliomen in the brains.

The Friesian horse, that in past centuries was found in the whole of Holland, later with only little variation in some provinces, has been exclusively bred for the past fifty years in the province of Friesland and then only in small numbers so that few years ago there were but 3 or 4 studs (stallions) of which the number has now increased. Inbreeding was therefore one of the results even though one has tried to avoid this.

From the family trees of foals one can conclude that they are the product of brothers or sisters, in nearly all pedigrees of almost all generations one frequently finds the same horse. So inbreeding, in some form or another, seems to be a rule. It has now become apparent that in Friesland now and then dwarf foals are born, always from a mare and stallion of the Friesian breed. These dwarf foals are in color build and conformation like the Friesian but are much smaller. They are black, with a nice sheen, have strongly developed mane and tail, a noble head, a high neck, quite a lot of temperament, but the legs and mainly the hind legs are very weak in the joints so that some slightly bend and give way and the foals' gait is uneven - this causing many breeders to have them put down.

We have here at the institute a 2 year old dwarf that shows all these characteristics and has a height of 11.7 hands. For a normal Friesian horse of this age one may expect a height of 15.5. The cause for dwarfism in humans is often an abnormality of the hypophysis cerebri. We were in the position to do a clinical section on a dwarf foal. The hypophyse turned out to be smaller than that of normal foals of the same age.

My colleagues Schultze and Ten Thije did tests that showed that the gland was affected with atrophy and many eosinephile cells were there, yet colloid was missing. Apparently there is a connection between the abnormalities in the hypophysis and dwarfism.

We have further investigated these dwarf foals in Friesland. The FPS and foremost the inspector of this stud book, Mr Jos Plet, has assisted us with that. We have found more than 30 cases in recent years and of 26 of these we more or less had all the background information to make up family trees. From the studbook it became clear that there are stallions that never sired dwarf foals, yet several did and do. Of the 26 foals we have info on, 7 are out of Paulus 121f, 7 out of Us Heit 126f., 3 out of President 123f, 2 out of Alva 113f, 2 out of Theunis 125f, 1 out of Prins 109f, 1 out of Friso 117f, and 1 out of Stefanus 124f.

The stallions, as far as we could find out, that never sired dwarf foals are Vredestichter 127 f, Vitello 128f, Ynte 130f, Arend 131 f. Several breeders excluded mares that gave birth to dwarf foals from breeding or refrained from having their mares served by stallions that had sired dwarf foals. However, in many cases the same mare that had delivered a dwarf foal, would in years to come - sometimes served by the same stallion, other times by different stallions - have normal foals.

As far as we could trace we can say that never has a Friesian thrown a dwarf foal out of an Oldenburger stallion. Among the stallions that are in the 4th or 5th pre-generation of nearly all foals we shall first name Nemo 51f. From all pedigrees inbreeding is clear. We can conclude that we are again dealing with a 'sub letaal factor, that if occurring as 'homozygoot causes the growth of a dwarf foal, and if occurring as 'heterozygoot' ends up in nothing. The sub letaal factor is therefore recessive. When this factor that is rather widespread, entered into the Friesian studbook, is not known and can not be traced. Stallions such as Nemo and Frits, had this factor already, though from their pedigree we have little knowledge. Neither do we know whether such dwarf foals were born in further in the past and if so, whether they were rare. The dwarfism factor in foals can therefore be categorized with the group of recessive sub letaal factors.

The Friesian horse breeders will of course ask for ways to prevent the birth of these foals to eliminate the Friesian breed of the unwanted dwarfism factor. This is not easy, but may be possible. These following precautions will be necessary: Every stallion, that possesses the dwarfism factor, must be excluded from breeding. By looking at the stallion itself, this will not be evident, it will only be concluded from this stallion siring a dwarf foal with a hetero zygote mare. In breeding with heterozygotes there is a 1/4 chance of a dwarf foal. Every stallion, even if only sired one dwarf foal, is a heterozygote and can therefore with a heterozygote mare produce a dwarf foal. There are several stallions, that delivered dwarf foals, then there are many that served many mares that never sired a dwarf foal. The latter do not have the dwarfism factor, indeed had they had this factor, they would have - after serving a heterozygote mare, who certainly occurred within the served material - sometimes sired a dwarf foal. As long as a stallion has not sired a dwarf foal, we have no proof that he possesses the factor. If we were to use only those stallions that do not have the factor, then they could serve as many heterozygote mares possible and never sire a dwarf foal. If such a stallion serves many mares, the mares who do not possess the factor, will only deliver foals without this factor; if such a stallion serves heterozygote mares, then half of the foals will not have the factor, half will but only heterozygote. If we only allow stallions without the factor then with every next generation the number of foals without the factor will increase substantially and the number of heterozygotes will decrease equally. We shall therefore exclude the heterozygote stallions from breeding and with that decrease the chance of producing dwarf foals. So would it be possible to only raise foals as stallions that do not have the dwarfism factor? To do that, one should select mares without the factor. If a mare was served for a subsequent amount of years by a stallion which we know to be heterozygote and never sired a dwarf foal before then chances are ample that she will not have the factor. If we were to put this mare to a stallion proven to be free of this factor, then we can say with great certainty that the foals produced do not possess the factor. The colts can be raised to become studs who will never deliver dwarf foals and the fillies will be kept for breeding mares.

Now one can exclude also each and every mare from breeding that has ever thrown a dwarf foal as we can be sure she is heterozygote. As far as this is practically possible it is recommended. The question whether inbreeding enhances the chance of dwarfism and the question whether it should be avoided is therefore no issue for Friesland. We are dealing here with a breeding practice in a relatively small area and since only a few years ago there were only 3 or 4 stallions at stud there will be the same stallions in every pre-generation of these horses. From the family trees it is obvious that this is ever the case so that we can avoid the smallest yet not all inbreeding from now on. If it were possible to cross horses from families where the factor does appear with those from families who do not have the factor, then dwarf foals would no longer be born yet this is practically not possible. The inbreeding here can not be avoided. In conclusion the Friesian breeders must do the following: Exclude all stallions from breeding that have ever sired a dwarf foal, as much as possible exclude mares that have ever thrown a dwarf and breed as many as possible stallions and brood mares by older mares that, when served by a heterozygote stallion never threw a dwarf foal, and serve these mare by a stallion proven not to possess the factor. If these measures are taken then the number of dwarf foals born will strongly decrease and after several generations no longer exist.

Whilst all information contained in this report is believed to be correct and complete, no responsibility is accepted for errors or omissions, however caused. The association carrying on business under the name Australasian Warmblood Friesian Association Inc and affiliate bodies, its members and clients expressly disclaim all and any liability to any person in respect of anything, done or omitted to be done by any person in reliance, whether whole or partial, upon the whole or any part of this report. All interested persons should make their own enquiries to verify information as well any additional or supporting information supplied and it is the responsibility of interested persons to satisfy themselves in all respects.

"This article is kindly reproduced with the permission of the World Register - Australasian Warmblood Friesian Ass Inc (1995)"  www.awfa.org/