Knee joint problems with cats

Three years ago the veterinarian section of Felikat Magazine issued an article on congenital defects of the knee joint (Ottenschot, 1986). In this article attention was paid to a problem that was then only spotted in sporadic instances with cats. Ottenschot refers to a number of only eight cats with patellar luxation (= loose knee joint) he received in his practice till then. The eight cats were: three Devon Rexes, one domestic cat, two Abyssinians and two British Blues. By now many readers will know that recently in Holland the number of cases of affected British Shorthairs increased substantially. The way this defect has increased with this breed is to be regarded really alarming. For me it is reason to go further into the genetic backgrounds. I would also like to show how cat breeders could do something about it. First of all I will, not as a veterinarian but as an interested cat breeder, briefly explain what exactly the defect is, how it can be diagnosed and what remedies there are.

Usually the knee joints of cats are fairly strong. On cats suffering from patellar luxation the kneecap (patellar) can, when the leg is stretched, be pushed inwards. With healthy cats this requires quite some force and the kneecap (patellar) will immediately pull back into its normal position as soon as the pressure is released. When the patellar is loose, it won't return immediately to normal position and it may be necessary to bend the leg before the knee repositions to regular. Sometimes the patellar even remains next to the joint if the leg is completely bent. With cats suffering from this defect in an even worse degree, the kneecap (patellar) may even jump spontaneously out of place and the cat will stretch its leg and "shake" it in a somewhat peculiar but characteristic way until the kneecap (patellar) returns. Cats with a serious form of patellar luxation find difficulty in walking and especially in jumping. When they get older (and heavier) this often converts to lameness or paralysis of one or both rear legs. It can be diagnosed best by means of an X-ray, whereas a veterinarian who is specialised in osteopathy may also be able to make a diagnosis by feeling whether or not the knees are all right (Ottenschot, 1986). In the latter method it is very important that a standardised method is used and that the test is not performed by a vet who is absolutely not experienced in it. If this test is performed by an "non-experienced" vet the results will be untrustworthy and not mutually comparable. In light cases surgical action will not be necessary and measures to prevent the cat from getting overweight will suffice. In more serious cases (always consult your veterinarian) there are various options, of which I would like to mention two. The first one is the "tightening" of the capsule around the knee joint, but there is also the possibility to deepen the groove in which the kneecap (patellar) usually is. Both methods have been implemented successfully.

Patellar luxation with cats can also occur as a result of a (serious) accident. Yet, in the majority of the cases there is a hereditary cause. Ten years ago the experts didn't dare to do any specific statements on the way the defect is passed on to offspring and it was suggested that one or more recessive genes were involved. Others have since then claimed that various genes are responsible and that we are dealing with polygenetic inheritance (Scholden, 1984, Robinson, 198x). As I am convinced of the correctness of the last described point of view, I will try and justify this statement.

As to the inheritance there are in fact four possibilities, i.e.:

I will try to prove the first three options can be eliminated. Possibility a. and b. both give an indication to one dominant gene. Possibility a. is excluded because there are quite a lot of cases in which both parents have good knees but do get kittens that dont. With possibility b. we have three different genotypes (AA, Aa and aa: AA the cripple cat, Aa the cat with poor knees and aa the cat with perfect knees). Here too it counts that it cannot be explained how two cats with perfectly normal knees are reproducing luxating kittens (aa x aa will never result in Aa or AA). So that option is also eliminated. This leaves us with the options c. and d. Inheritance by one single recessive gene is impossible, because then the result would be solely cats with and without this defect. In reality, however, there is always a continuous variation in the seriousness of the defect in cases of patellar luxation. There are cats with normal kneecaps that absolutely have no defect at all. Then there are the cats with loose kneecaps that can be moved fairly easy but get back to their regular position themselves. The third group consists of the cats of which the patellar gets back in position by gentle bending and in the fourth category the patellar remains next to the joint even if the leg is bent. In case the defect is even more serious, the kneecap will occasionally luxate spontaneously. Lameness and paralysis of the rear leg are symptoms of the serious form.

Between all these degrees of seriousness intermediate forms may occur which shows that there clearly is a gradual change from a perfect to a seriously defective knee joint. This is a clear clue that more than one gene is involved. In the course of the years I have been collecting quite some breeding data, in particular about English Devon Rexes, a breed that had this defect, especially during the late seventies and the early eighties. From these data it appears that in one nest often more than one kitten luxates. These and other details contradict with what would happen if only one (recessive, dominant or not entirely dominant) gene were involved but can be explained if we take the polygenetic inheritance as a starting point, a way in which quite a lot of characteristics are inherited that are growthrelated. Whether or not a threshold character is involved in patellar luxation is not clear yet. If that were the case, a minimum number of plus-genes (those responsible for patellar luxation) would have to be active before an actual defect of the knees would occur.

This requires some explanation on polygenetic inheritance. When a characteristic is inherited through more than one gene, it can best be visualised as follows. The more plus-genes a certain cat has, the more it will show that characteristic in its appearance; the more minus-genes, the less. Is the length of the nose involved, then the plus-genes are the genes that give the cat a long nose, and the minus-genes give the cat a short nose. The more "plus", the longer the nose. Are two average-nosed cats mated, the majority of the offspring will have average-length noses, but the extremes (very long nose and extremely short nose) also occur, though sporadic.

With this image in mind we return to the patellar luxation. To make things easier comprehensible I pretend to know exactly how many genes are involved (5 pairs) and in addition I assume that cats with more than two plus-genes have loose kneecaps. If two cats with knees that are not perfect (both five plus-genes) are mated, but lack any sign of lameness ("average"; that would be called with regard to the length of the nose, though not in this case), much of the offspring will have knees resembling those of both parents. One or two kittens will have perfect knees in spite of all, but just as much there will be cripple kittens.

Interbreeding two cats with miserable knees will predominantly result in offspring with patellar luxation. Are two cats with apparently good knees (both with two genes but just below the threshold character) mated, it is yet possible that those cats reproduce kittens with slightly loose kneecaps; in this case some thirty percent. So for each born kitten the odds are one in three. Do we take another case as a starting point, the odds are going to be different. For example: a cat with two plus-genes x a cat with one plus-gene results in a chance of more than 12 percent per kitten (one in eight) to have patellar luxation. And so on. Of course we are not certain whether or not it will go exactly like this, but it is certain that the defect is inherited this way more or less, which is important if we want to eliminate this defect from the breed.

Elimination of a congenital defect that is caused by more than one gene by means of breeding, is always a fatiguing and time-consuming activity. Think for example of a hip dysplasia with a dog, which defect is also inherited polygenetically. Yet there are good results to be achieved; I will try to explain that by means of patellar luxation with the Devon Rex. It has been some ten years ago that patellar luxation occurred at large scale in a number of English Devon catteries. Animals from these catteries were exported, mainly to Germany. Regularly luxating kittens were born in Germany and in Holland too the defect sometimes occurred. On the initiative of a German breeder the case was tackled seriously and catteries that regularly had kittens with the defect, had X-rays made of all cats that were born in their catteries. Most breeders (in Holland) have all kittens checked at the age of three months. In order to eliminate the defect, the following line of conduct is kept up with by the German and Dutch breeders, i.e.: do not breed with any animal that shows only the slightest trace of patellar luxation symptoms!

In ten years time this line of conduct had positive results and during the past two years the defect has, as far as I know, occurred neither in Holland nor in Germany. At the same time many breeders in England had other opinions. They didn't think that negatively of the defect and didn't have their animals checked. The result is not hard to be guessed: in cases like these it cannot be excluded that from time to time a breeder mated animals suffering from the defect, thus not reducing the number of cases. The result is a rather frequent occurance of patellar luxation with English Devons, this contrary to the "continental"; Devons. When the defect was made known at first on the continent, fortunatelllly there were only few imports from English catteries suffering heavily from the defect. At the time the breeding program was started, the situation was not very bad yet, as a result of which good results could be achieved in a relatively short period of time.

In general it can be said that the fight against the defect should be focused on reducing as many plus-genes as possible from the population. The degree, in which this is supposed to be done, is a choice one has to make. When following a strict approach one doesn't breed at all with cats that only got the slightest defect on the knees, nor with their parents, brothers and sisters. A less severe approach only excludes cats from breeding that haven't got perfect kneecaps.

Although the latter approach makes things easier for the breeders, it does take longer to achieve the same result in the end. If, for instance, all British Shorthair breeders were to decide to combine their efforts to eliminate the problem as soon as possible, the strict approach is to be preferred of course. In practice it will be often so, that this is an idealistic point of view, but that in the hard reality of the cat world the less rigid approach appears to be the maximum achievable. Less than that will lead to it that in future the Dutch British Shorthairs will be talked about in the same way as about the English Devons. Burying ones head in the sand is always the easiest way, but it doesn't solve a thing. To determine what animals are suffering of patellar luxation, we need to have all animals checked, e.g. when you are at the vet's to have them vaccinated, when attending a meeting of the breedersassociation, and preferably before actually breeding with the animals (e.g.) when they have their first IF-test.

Although patellar luxation is not a mortal disease, it is a serious defect. It is therefore obvious that cats suffering from the defect (no matter in what ligth a degree) should be excluded from the breeding program. I would think it is also clear to each well-thinking human being that breeding with animals that had successful surgery on their knees is to be considered irresponsible. For the cat itself such an operation may (if successful) be fine, but the genes are not changed through this surgery, and the cat may spread the defect on the breed via his/her offspring. A Felikat breeder has his sire operated on his kink-tail. Why not, do you think, possibly right. To enlist this animal, however, after his surgery, for shows, intervenes with the rules of Felikat and Mundikat and of the FiFe and therefore it should be possible to have such conduct reprimanded. It is to be morally reprehensible and irresponsible to have this sire filed in the studlist and to have him mate without informing the owners of the queens.

I am not familiar of such practices with cats with patellar luxation, but there are breeders and owners of studs who do not hesitate to use cats with poor knees for breeding. When their attention is pointed to this, they come up with the argument that the cat is walking properly though the patellar is a bit loose.

The past few years I have, unfortunately, been dealing with quite some cases of congenital defects with cats. A serious thing for the cat, but with a proper breeding program a lot can be done about it. Much worse is the way the breeder is tackling this problem. I understand perfectly well that many breeders are ashamed when one or more of their cats appear to be suffering from or to be the carrier of a congenital disease/defect. But there is absolutely no reason to be ashamed of that, for it simply is a matter of a lot of bad luck. The only thing to be ashamed of, is when the fact is concealed and nothing is done about it. What=s more, one is selling kittens of which the new owner B as a future breeder B is going to be ashamed about (undeservedly) for he was not aware of it. To tackle issues like these properly, one does not only need to work with a program for the elimination of the defect from the breed. It requires joint efforts of preferably all breeders. The attitude and co-operation of the respective breedersassociations may be of major importance with regard to this. The associations often know the problems at first hand and in case of conflicts that will undoubtedly occur in an early stage, they can act as mediators and guides. They can also provide their members with detailed information on the existence of and possible remedies for the defect. Stimulation of a research program (what cats are affected by the defect) and filing of the data seems to be one of the tasks for the breedersassociation.

Also for the Aumbrella@ association (in the Netherlands: Felikat or Mundikat) there is an important task. Many genetic defects (one of them being patellar luxation) occur in different breeds. If a particular breed is encountering a problem, this association can be of assistance to the breeders and the respective breeders= association through the experience that was gained earlier in other breeds in the own country and abroad. This way solving the problem can be started much more efficiently. The association can also mediate in cases of disputes or arguments on the approach of the problem. Finally the association, after careful consideration, can decide to take countermeasures in order to force the breeders to co-operate in a fixed breeding program. This was not the case yet until now, but I don't consider it impossible for the future.

By now it should be clear to all of you that a genetic problem is not something only the cat is affected by. The breeder, the breedersassociation and the cat fanciersassociation have a task ahead which is quite clear to me. The past practice unfortunately taught me that not everyone agrees on this. It will, however, benefit the cats once you decide to stop escaping your responsibilities or stop breeding.