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Past research has reported a high statistical correlation between blue eyes and deafness in Whites. Not all white cats have blue eyes nor are all white cats deaf, but an independant factor may give rise to both blue eyes and deafness in Whites. A common factor may mean that blue eyes could be a pointer to cats carrying a higher risk of deafness.
The term "E-factor" is used to denote those polygenes which contribute to raising the risk of both deafness and blue eyes in white cats.
There is no reason to suppose that these polygenes should not be carried by coloured cats as well as Whites, but only have an effect in Whites. This could be the reason that hereditary patterns of white deafness have been very difficult to find, leading to claims that the incidence of white deafness is purely random.
|Deaf kittens are visually more active|
It is well known that white cats can suffer from deafness, but there are many misconceptions about the frequency of occurrence and the causes. Attitudes vary from regarding white deafness as "inevitable" or even, with some breeders, desirable with show cats, or "regrettable" but impossible to eliminate, to "curable" if only the cause was known.
Theories include the associated blue eyes, head markings in kittens, absence of "cat's eyes" shine, and the carrying of the white spotting gene. These all appear to have been derived from the study of a breeding colony of white cats by Bergsma and Brown, published by the Journal of Heredity in 1971.
This study extended over a number of years and is the only known detailed study made of white deafness although there have been many other papers published on histological investigations and other details. It is inevitable therefore that the Bergsma and Brown paper is widely quoted on the subject. Unfortunately a number of misconceptions have arisen over the years and it was thought worth while to make a reassessment of the paper from the point of view of a pedigree white cat breeder.
The most widely repeated misconception is the frequency of deafness in whites. Various percentages of defective hearing can be derived from Bergsma and Brown, from 52 % from white to white crosses to 11% from white to coloured cats. All of these are much higher than is found in randomly selected populations as their original 21 cats were selected with a bias towards deafness and blue eyes.
The reason for this is quite simple. The Bergsma and Brown paper was primarily a study of the Waardenburg syndrome in humans, using cats as a model, as test mating followed by sacrifice is a procedure not approved for the Human Species. A number of coloured cats were included in the original breeding stock as controls, but for the study, deaf whites were what was needed.
It is important to say that in some parts of the Bergsma and Brown study, the sample size is very low. Only four white cats ref 1 were thought to be homozygous ref 2 and of these only one was fully tested with white and coloured mates. Only one all-white cat was bred from high grade white spotted parents. This proves that a white cat does not necessarily have to carry a full white W gene, but interestingly it was half deaf, so deafness can be associated with high grade white spotting. However, with such low samples, any statistics will have a high error rate.
The gene pool of the Bergsma and Brown foundation breeding stock was comparatively small ref 3 - only 7 male and 14 female white mongrels, most with at least one blue eye. Their definition of "white" ref 4 was a cat with over 90% of white fur. An unstated number of coloured cats were brought in as controls and mates. All this means that the test group were probably not representative of any pedigree cat populations, nor was there any requirement for them so to be, given the purpose of the paper.
The 1995 White Deafness Survey is being undertaken to establish the frequency of occurrence of hearing loss in pedigree and pet cats, and to test the association of eye colour, eye shine, head markings and parental colouring. A survey was conducted some years ago under the auspices of a Breed Club, including the collection of a large number of pedigrees, but no results were ever published nor is this data available hence the call for this Survey.
The purpose of this Preliminary Report and Assessment is to derive ideas and principles from available papers and studies in order to test these from the collected data and to determine what directions to pursue. Care must be taken not to fall into the temptation to adapt the data to a theory rather than the theory to the data.
2 Papers and Sources
The starting point was of course the cat breeder's Bible, Genetics for Cat Breeders by Roy Robinson, who has offered his personal help in addition. The Bergsma and Brown paper, as above, is the only other major source and a short paper by Pat Turner has given valuable information about the Siamese blue eyes.
A bibliography is not given, but footnotes follow references to scientific terms and papers. Anglicisations will be used frequently. Abbreviations used are Bergsma and Brown, (B&B) ref 5. Genetics for Cat Breeders (GCB) ref 6, and Blue Eyes, White Fur and Deafness, by Patricia Turner (PT) ref 7. A copy of the Elversland and Mair 1980 paper was obtained, which gives histological details of aural degeneration but not a great deal of help with live animals. An excellent account of the genetics of white spotting is given in The Pigment Parade by Lorraine Shelton.
Some early data is available from the Survey which is not statistically significant yet, but it does illustrate that there is not a firm linkage between the factors under study and deafness. B&B indicate, ref 8 for instance that cats unilateral ref 9 for both blue eyes and deafness do not show a relationship between the side of occurrence of the two conditions. If there is a common factor or factors, it looks as if these act independently, in other words, the deafness is not caused by blue eyes, nor blue eyes caused by deafness.
3 An Hypothesis
The purpose of this Survey is to try to determine what is causing white linked deafness in order to eliminate it or at least to reduce it to a low proportion of cats. What is clear from all of the available literature is that little is in fact known about the underlying genetics which is causing a number of phenotypic ref 10 conditions such as blue eyes or deaf ears. It may be useful to list what is derived so far.
|3 a)||Deafness mainly occurs in all-white or nearly white cats.|
|3 b)||There is some association between blue eyes and deafness.|
|3 c)||There are two forms of blue eye, one not associated with deafness.|
|3 d)||The deaf-associated blue eyes have no tapetum lucidum ref 11.|
|3 e)||There may be an association between hearing and head marks on kittens.|
|3 f)||There is no firm link between any of the above conditions, for instance orange eyed cats can be deaf and blue eyed cats can be fully hearing ref 12.|
|3 g)||Odd eyed cats are more prone to deafness and blue eyed cats are even more prone. The degree of deafness is also dependant on the dosage of white genes, highest in homozygous whites
ref 18. This may, however, be due to an accumulation of additive polygenes in high risk cats.
I am proposing, for the time being, that the gene or group of polygenes responsible for causing both blue eyes and defective ears in white or near white cats is provisionally given the letter "E" for 'Eyes and Ears'. This may be an oversimplification unless it is shown to lie on a single locus ref 15 and have the simple segregation ratios ref 16 that a single gene would follow. It is possibly not a simple dominant or recessive ref 17 but at least we will have an entity we can characterise.
Assuming the existence of an 'E-factor' consisting of a gene or cluster of polygenes, how can we describe its effect?
|3 h)||First of all, it has a zero or negligible effect on coloured cats. It requires at least one "W" gene or high grade spotting "S" gene to be present to take effect.|
|3 i)||It appears to have more effect with a higher "dose" of white genes, ref 18 in other words with genotypes 'WW', 'WS' or 'SS'.|
|3 j)||It is variable in expression, in other words varies in the degree to which it affects an individual cat. It also shows incomplete penetrance ref 19 which means that sometimes it has no effect at all.|
|3 k)||Its variability is in the number of organs, eyes or ears, affected rather than the degree of blueness or deafness. An individual eye is usually either blue or not; an affected inner ear is often totally degenerate and deaf or not. One eye can be blue and the other orange; similarly only one ear can be deaf.|
|3 l)||If deafness and blue eyes were caused by the W gene acting alone, then there would be no pattern of inheritance in the incidence of either. However, the tendency to both blue eyes and deafness is clearly inherited. In addition PT ref 20 describes blue eyed white cats with the genotype cscsW_ which do not exhibit deafness.|
|3 m)||There is no immediate link ref 12 between blue eyes and deafness, either with unilateral or bilateral ref 9 eye colour or deafness. What is clear, however ref 21 is that a higher incidence of blue eyes is associated with a higher incidence of deaf ears. In other words, blue eyes do not cause deafness or deafness cause blue eyes, but both are caused by another factor, the suggested "E" gene.|
|3 n)||An independent factor causing blue eyes in whites is carried ref 22 by coloured cats with no effect on eyes or ears as it is only switched on by a 'W' or 'S' gene. This is strong evidence of the existence of an 'E-factor'.|
4 The Nature of Whiteness
There are strong parallels between the white spotting gene "S" and the deaf ear/blue eye "E-factor" effect. Both are highly variable and random in pattern. For any particular area of the skin, it is either pigmented or not and the variability of the spotting is in the total area of affected surface and in the number and placement of spots, but not the degree of pigmentation. GCB describes ref 23 how the colour of various areas of the coat is established at an early stage in the development of the foetus.
When a fertilised egg first develops, it starts dividing into 2, 4, 8, 16 cells and so on. When there are hundreds of cells, they begin to differentiate into head and legs and organs. A cell which is going to be a leg divides and redivides and the cells further differentiate into a foot and toes and so on. At one stage there are about 34 cells which are going to colour skin and fur and, as they differentiate, they also establish what colour they are going to form. With spotted animals, the "S" gene either becomes active in each cell or not.
The pattern of each of the resulting areas often recurs, for instance there are distinct areas on the head which can produce a crisscross pattern or square margins on the forehead, with or without an inverted "V" over the nose. These and other spotted areas vary in size, of course, but don't move about very far, giving rise to gloves, boots, bibs and lockets.
The sporadic nature of the 'E-factor' may be not unlike the white spotting gene which is popularly held to be the single but variably dominant ref 17 'S' gene. B&B state ref 24 that the white gene "W" and the main spotting gene "S" lie on the same locus ref 15, in other words are variations of the same gene.
An interesting corroboration for this common locus has occurred following the recent import of a native Turkish cat from Van, which is white as all native Vans should be according to the people who live in Van. Two of its kittens were test mated brother to sister and the result was a preponderance of over-coloured kittens which do not seem to be heterozygous for spotting. Further tests will be very interesting. Another confirmation of a B&B result is the birth of an all-white Turkish Van kitten to Van pattern parents, showing that this is possible as in the 1971 paper.
On the other hand it has also been shown that a white cat masking white spotting can have coloured kittens without white when crossed with an unspotted coloured cat. This contradicts Bergsma and Brown unless there is more than one locus for white spotting. The range of white or white spotting genes suggested by B&B need not necessarily all be on the same locus. If there is a "locket gene" on a different locus, for instance, this may well explain some of the results reported by breeders trying to eliminate persistent lockets and bikini marks.
To clear up a possible confusion, some Registeries insist that a white kitten born to a Turkish Van is a Turkish Angora, but others accept a large range of colours of Turkish Vans and Turkish Angoras, including white. In Europe at least, the body and head type of Turkish Vans is quite distinct from Turkish Angoras. Personally I include as Turkish Vans white cats which look like Turkish Vans and have come from Van in Turkey, and am prepared to argue the point.
Both 'W' and 'S' genes contribute to deafness to a greater or lesser extent and probably act additively ref 18. A cat homozygous for white spotting 'SS' normally has more white than heterozygous 'S-' cats with the same genes and is thought to be more likely to show deafness. This need not be true, however. If two white and/or white spotted cats both bear a risk of deafness from a polygenic factor, it may be this third factor which is doubling up. This needs to be tested by examining white x white matings between cats with a low incidence of deafness..
Assuming that there is an inherited independant 'E-factor' which is turned on by whiteness, the number of organs it affects is variable. If it is turned on at a similar stage of differentiation as the fur colour cells, then it could be affecting a single cell which is later going to develop into an eye or ear. This part of the mechanism is random. One or both eyes or ears may be affected with no relationship between them.
B&B ref 14 describe the genes which give rise to blue eyes in the presence of white, and if these genes are also responsible for deafness, then this description also applies to the 'E-factor'. In this section it is probably not useful to be too rigorous as we are discussing the nature of the white and white spotting genes but if, as seems likely, both the gene or genes for all-white and white spotting are control genes for both deafness and blue eyes, then the variability of these effects may be due to the variable natures of the "E" and 'S' genes respectively.
Not only is white spotting variable but there are different types of white spotting patterns so there may be other distinct alleles on the "W" locus or independent genes involved. Patterns include:
|4 a)||Head smudges on otherwise all-white kittens. These do not persist into the adult coat and the cause may be nothing to do with the usual white spotting.|
|4 b)||The Van pattern. It is not known if it is a distinct spotting gene or whether it is due to a stabilisation of polygenes caused by breeding Van to Van. Turkish Vans are said to be largely free of deafness.|
|4 c)||The Harlequin. This has random and irregular patches on a white background.|
|4 d)||Piebald or irregular white on black and black on white patches.|
|4 e)||Medium grade patterns such as jackets.|
|4 f)||Lower grade patterns such as gloves and bib as seen on bicolour Birmans, Ragdolls and Maine Coons. This commonly also shows an inverted "V" on the face.|
|4 g)||Mitts only as on Birmans and Snowshoes. K J Clark ref 25 has suggested this is due to a recessive "g" gene.|
|4 h)||The persistent medallion and abdomen spot. Kühn and Kröning, 1928, ref 26 suspected a recessive or semi-dominant gene acting alone or interacting with the "S" gene.|
There are various ways of describing the variability of genes, such as penetrance, incomplete dominance or expressivity and these are defined in the footnote below ref 19. In addition, a variable genetic effect may be caused by polygenes ref 13.
Polygenes are clusters of genes all having the same general effect but each one only partially contributing to that effect. Each of these individual polygenes are passed on according to the usual rules of inheritance with the result that their cumulative effect does not follow simple rules and tends to vary, sometimes from full to no appearance.
It does not take many polygenes to produce a wide range, for instance there are eight combinations of three genes. If the polygenes are incompletely dominant, partially penetrant or with variable expressivity, then the result is impossible to predict. One can forgive the temptation to use the term 'polygene' as shorthand for 'unpredictable' or 'we don't know the cause'.
It is not surprising that any gene or genes interacting with white spotting of whatever origin is also variable in effect and difficult to analyse. This does not mean that it is not worth pursuing. In the guise of the 'E-factor', the cause of blue eyes and deafness has a certain degree of predictability and it may well be possible to breed it or them out of white cats.
5 The Nature of Deafness
Before moving on to a very promising clue about blue eyes and a breed of white cats which is largely free of deafness, it is worth discussing a little-publicised theory.
As can be seen from B&B ref 4 white induced deafness is seen in not only all-white but also in high grade white spotted cats. It was also suggested that a doubling of the white "W" gene or the addition of the probably related "S" gene increased the chances of both blue eyes and deafness per eye or ear. This is probably the source of the rumour current amongst cat breeders that white spotting causes deafness. It may have a marginal effect on the incidence of deafness, but a prime cause it is not.
The widely disseminated "white spotting" theory also quotes a correlation between white spotting in parents or parents 'carrying' white spotting and deaf white kittens of 75%. With the incidence of deafness in whites of the order of 8% of the all-white population, and the incidence of white spotting estimated at around 50%, the latter well swamps the former. If the active sample of deaf cats is less than 100, sampling error "noise" is very high. Deafness affects about 8% of each 50% with or without white, so if data could be obtained from 300 white cats which would be pretty difficult, we would only have samples of about 12 with white and 12 without.
When attempting to separate a minor component from a major, it is not sufficient to do this by subtraction, especially in the presence of "noise", but the data have to be deconvolved with a known template. In the case of genetic effects, there are mathematical rules governing probable incidences which must be taken into consideration in the deconvolution. Sheer coincidence may easily be the major factor.
Deconvolution in the presence of noise can give unpredictable results, making a statistical analysis of a small sample of animals potentially meaningless. This is useful if one wants to use statistics to prove a preconceived theory. As above, there may be a small increase in the incidence of white deafness in cats with high grade white spotting, but this is not going to prove to be the main cause.
The most serious flaw in the "white spotting theory" is the inclusion of "carriers" of the dominant white spotting gene. On the face of it this appears to be an inconsistency, but it may be possible for the gene to be present and either not fully expressed or lying hidden in a tabby pattern. If the 75% correlation quoted above included non white spotted cats with a white spotting in their parentage, this would include a much greater number of cats. In some breeds like Maine Coons this can be the majority of cats giving a demographic correlation with deafness.
In other words, a deaf kitten is automatically more likely to have white spotted ancestors simply because there are more of them. Only if virtually no cats with no white spotting in their parentage were deaf could a correlation be established. No data on this has even been seen so the theory must be regarded as unproved.
The actual process of degeneration of the inner ear is fairly irrelevant to the process of eliminating deafness unless a detectable genetic basis can be found. what breeders need is a way to predict high risk matings in order to avoid them.
Hearing loss is caused by degeneration of the organ in the cochlea which acts like a microphone turning vibrations into electrical nerve impulses. A study of dissected kittens has shown that this is progressive in the first weeks after birth.
6 Two Types of Blue
The Foreigns have a different form of "oriental' ref 27 blue eye which has been called "Turner blue" and is common in colourpointed cats, variously known as Himalayan, Siamese or Oriental with a capital "O". As with the paler "occidental' ref 27 blue eyes, it is caused by a lack of pigment in the irises, but the genotype is different, being based on the Siamese or Himalayan "cs" gene. There appears to be a good marker here as the tapetum is normally present in these eyes, but this will have to be tested in the Survey.
Early Survey results have revealed an odd eyed cat missing a tapetum in the orange eye and a bright yellow one in the occidental type blue eye. The norm is the other way around and an occasional anomaly by now should not cause surprise. There are degrees of deficient tapetums, from one case of an eye with practically no reflection at all which may be caused by a degeneration of the retina as well, but a missing tapetum as illustrated by B&B shows a dull red reflection in which the tapetum is transparent to the choroid which lies behind the retina and which shows a maze of blood vessels. Sometimes small flecks of normal tapetum are visible and occasionally small patches are missing within an otherwise normal tapetum layer.
Occasionally, however, a Foreign White is found with pale blue eyes, missing tapetums and a tendency to deafness ref 28. It is suggested that these genes were carried in from occidental whites used to introduce the white genes to the Foreigns, so all outcrosses are now made to yellow eyed whites. Deafness has largely been bred out of Foreign Whites which shows that this is possible in a white breed and also shows that the white gene is not inherently responsible for deafness.
If it is indeed possible to breed out white deafness in Foreign Whites carrying the usual "W" gene, then this suggests that an independent vector like the 'E-factor' is at work. If we can identify which animals have the 'E-factor' on board and, more importantly, identify some which do not, then it may be possible to eliminate white deafness from other white breeds.
It is worth noting here that the success in at least reducing the incidence of deafness to a low level in both Turkish Vans and Foreign Whites has come about by mating white with white. While homozygous whites which carry the propensity for deafness may or may not be more likely to suffer from deafness, It will be impossible to trace and eliminate the gene or genes responsible for causing deafness without breeding white with white.
If the proposition in section 3n above is accepted, then reintroducing coloured cats into a white breeding programme is very likely to bring back 'E-factor' genes as apparently happened with Foreigns when crossbred to occidental breeds. This would mean that white with white mating is not only essential for eliminating the 'E-factor' genes and deafness, but is also essential to maintain good hearing in whites.
It has been claimed ref 29 that the increase in the incidence of deafness in present populations of white cats brought about by mating white with white would give rise to that increase in deafness being passed on to future generations. This is conjecture and is not shown within breeds where white or near white is interbred such as Persians, Turkish Vans and Foreign Whites. A further and possibly even more unproved argument made during discussions of the proposed European Convention for the Protection of Animals is that such an increased incidence of deafness can be passed on to coloured cats. It is believed that this argument has been used in favour of the legal restrictions on the breeding of white cats in parts of Germany.
7 Head Markings
As has been mentioned in section 1, the Bergsma and Brown paper was primarily a study of Waardenburg"s syndrome in humans. There are six signs in Human beings suffering from this syndrome, but three do not show up in cats - folded eyelids, thick base to nose and eyebrows meeting in the middle. Two which do are odd eyes and deafness, and the other one, a white quiff of hair, is possibly comparable.
Waardenburg's syndrome does not get much of a look in in B&B, however, and the cats have taken over as they tend to do. It is not explained why parallels are being drawn between the human and feline syndromes when the human hair is normally pigmented apart from the quiff, but the cats are white. However the aural degeneration is similar and the link to blue eyes is there, and we have Waardenburg to thank for the best survey of deafness in cats ever done.
The quiff remains a problem in that it does not readily show up in white cats and would have no effect on the hearing of coloured cats. The only parallel is in the presence or absence of temporary dark markings on the heads of some otherwise all-white kittens. If a central quiff is involved, this may remove any central mark, but frequently markings are multiple and offset. Markings may be absent for reasons other than the Waardenburg quiff and present if they do not happen to coincide with it exactly. There is statistical evidence in B&B of a correlation between head markings and good hearing, but this is not explained or defined and it is possible that this is not the action of the Waardenburg quiff.
Preliminary Survey results have identified a unilaterally deaf, odd eyed cat which had a prominent head marking as a kitten. The deaf ear was on the side of the orange eye. Also found was an unmarked kitten which was stone deaf. Head markings seem to be an unreliable guide to deafness or the 'E-factor' but may point to heterozygosity of the 'W' gene or absence of an 'S' gene or a 'W' variant with a slightly reduced expressivity ref 19 and with a consequent reduction in consequent deafness. The only certain use of the dark markings may be to show the presence of blue carried under the white after microscopic examination of the hairs.
The ultimate objective of the White Deafness Survey and of this Discussion Paper is to eliminate deafness from white cats. This may have to involve closing the breeding group and by maximising the risk of deafness by mating white to white and creating homozygous white cats or mating whites only to coloured cats with a proven low E-factor. Only when this produces an acceptably low incidence of deafness can the group be considered to be free of deafness. This is an extreme solution and if the necessary testing procedures produced many deaf kittens, then it would not be justified.
In the meantime, a hypothesis needs testing and tests are needed to justify some of the assumptions made by B&B and the conclusions drawn in this paper. The survey is designed to give appropriate data for tests. In particular we need to examine the following:
|8 a)||The incidences of deafness in coloured, non-blue eyed whites and occidental blue eyed whites.|
|8 b)||The incidences of deafness in oriental blue eyed whites.|
|8 c)||The incidence of deafness in high grade spotted cats such as Turkish Vans.|
|8 d)||The involvement of a gene or cluster of polygenes referred to as the 'E-factor' in causing both occidental blue eyes and deafness.|
|8 g)||The incidence of the hidden 'E-factor' in coloured cats.|
|8 e)||The relevance of the temporary dark mark on white kittens to deafness.|
|8 f)||The relevance of the tapetum in blue eyed white cats to deafness.|
|8 h)||The relevance of carrying more than one white type gene to deafness, either heterozygous white 'WW' or white with spotted 'WS', or heterozygous spotting 'SS'.|
It is probably unnecessary to analyse the 'E-factor' or to discuss how the deaf ear degenerates in order to eliminate or greatly reduce deafness. Pedigree cat breeders are horrified at the thought of sacrificing kittens in order to do histological examinations and the value of a diagnosis, however accurate, in a dead cat has to be more than questioned.
What is permissible is experiments in breeding provided distress in not caused to individual cats. Deaf cats are at a disadvantage but usually compensate with increased visual and tactile awareness and usually live a happy life when cared for by cat lovers. However, any animal in chronic distress should be euthanised and deliberately producing distressed kittens is not desirable so this must be the overriding principle in any test breeding programme.
Wherever possible, statistics from current breeding programmes should be used to track down the existence of an independent 'E-factor' and to make plans for eliminating it in white cats. The main hypothesis of this discussion paper is that this independent factor exists, rather than a direct link between blue eyes and white fur. This is a bit of a 'chicken and egg' dilemma, in that whiteness is certainly the major factor in triggering both blue eyes and deafness, but it is unlikely that blue eyes directly causes deafness or vice versa. Logically these would track each other in frequency in group statistics without being directly interconnected in individuals if they were both caused by a common factor. Most literature suggests such an independent factor or factors which this paper is calling the 'E-factor'.
While it is too early to draw any firm conclusions from the survey, reading of the various available papers and verbal evidence from various breed groups would indicate that the tendency to deafness can be greatly reduced in white cats. The general incidence of deafness in occidental white breeds is said to be about 8% and this is consistent with early Survey results. B&B tables suggest that blue eyed cats are about three times as likely to be deaf as pigmented eyed animals and Turkish Van breeders quote about 4% for their breed where odd eyed cats are much more common than blue eyed. Foreign Whites are stated ref 28 to be free of deafness if showing yellow eyes or oriental blue eyes.
To throw totally unsubstantiated figures into the argument, considering the entire population of occidental type white cats, probably about 5% to 10% of the most common orange or green eyed cats are deaf; about 10% to 20% of the less common odd-eyed are deaf; and about 20% to 40% of the rarer blue-eyed whites are deaf. I am more than open to correction of these figures, and this is after all a discussion paper. They do provide a starting point to the main purpose of the White Deafness Survey which is to suggest a way to reduce the incidence of deafness in white cats to a figure which is acceptable compared with other unwanted genetic abnormalities. GCB suggests ref 31 that 1% or below is a target to aim for with severe abnormalities, and 5% for the less severe. How severe deafness should be considered compared with abnormalities causing chronic pain like hip dysplasia is a moot point. Breeders and owners with experience of deaf cats and kittens generally find that they are capable of leading normal healthy and happy lives as indoor domestic pets, and some can even adapt safely to life out of doors. It is arguable that a single figure percentage of deaf kittens as is experienced in coloured eyed white cats is acceptable.
If indeed white deafness is associated with occidental blue eyes, and this is a major item to be investigated by the Survey, then eliminating deafness will also largely eliminate blue eyed and odd eyed white cats but, and this is a big but, this does not mean that eliminating blue eyed and odd eyed white cats will eliminate deafness. for one thing as stated elsewhere, there are strong indications that a high E-factor can be carried by coloured cats.
The target of 5% if applied to occidental blue eyed whites may involve a reduction of the 'E-factor' genes of the order of one eighth, which might also reduce the incidence of deafness in associated orange and green eyed cats to near 1%. This may well be a feasible step to take if we can establish where the 'E-factor's are coming from, which is probably the general population of coloured cats. A permanent reduction would involve principally breeding white with white, of course taking great care following any outcrossing to coloured cats.
If a target of 5% is applied to white cats in general, everything gets much easier, as odd eyed and blue eyed cats are much less frequent than orange eyed or green eyed. Quoting actual figures is impossible as the data is not available, but it may only need a reduction in E-factors of two to three times. Please don't quote this figure as it is pure speculation - it may be safer to say that the required reduction is much less.
Instead of extensive testing which if successful will inevitably produce many deaf kittens, it may be possible to watch for markers. Another purpose of this Survey is to establish usable markers out of the various factors listed in section 3 such as head smudges and blue eyes without tapetums. If breeders and exhibitors felt they could not do without blue eyed whites, one solution would be to introduce the cs gene and the associated oriental blue eyes into the breed if this is permitted for that breed.
This section is very prone to misquoting and attention is drawn to the copyright claimed for the whole document. While I wish this document to be widely discussed, I must emphasise that this final section is pure conjecture, hopefully to be verified or not by the Survey. Therefore the figures in this section must not be quoted out of context. They are given as an encouragement that, provided the 'E-factor' hypothesis is upheld, it should be quite feasible to greatly reduce or virtually eliminate deafness in all-white cats.
If it is possible to sharply reduce the incidence of deafness in Turkish Vans and almost eliminate it in Foreign Whites then, with a little applied knowledge, the deaf occidental type white cat could be an animal of the past.
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Updated 25 September 97
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