Flat Chested Kittens – from Aurora Burmese Cattery
Updated 2004
“Working together for the benefit of our cats”

NB: I am not a veterinarian or a geneticist – just passionate about Burmese and all pedigreed breeding cats. The following data contains some of the results and my conclusions of 12 years voluntary research into birth defects and nutritional needs of pregnant and lactating queens.
I started this research before I bred my first litter and found it so interesting that I am still doing this voluntary work with the helpful input of dedicated breeders.  
Because of the fact that there are many breeders who do not understand the complexities of the science of animal husbandry and others who know a hell of a lot more than I do, I have tried to simplify my findings to a level that the majority will comprehend without being derogatory to anyone. There is always something new to learn, even for the professionals!
Always discuss your problems with your vet! Don’t be afraid to ask for a second opinion.

Worldwide, birth defects are occurring in all breeds of pedigreed cats and also in domestic cats. Some behaving erratically which makes the mode of inheritance (or if inherited at all) difficult to establish. Most Universities and research teams are of the opinion that birth defects are under-reported. I know for a fact that this is very true. Many breeders do not discuss their problems for obvious reasons. Don’t blame each other when things go wrong; just be diligent in selecting and caring for your breeding animals. Somebody recently said to me “wherever you have livestock you will also have dead stock”. This is sad but so true –  as all farmers will tell you.

 Just some of the problems reported in cats are:

1.    Flat chests.
2.    Funnel chests.
3.    SpinaBifida
4.    Cranial deformities.
5.    Hypokalaemia
6.    Cutaneous Asthenia (stretchy skin disease)
7.    Renal diseases including PKD.
8.    Heart defects.
9.    Eye diseases.
10.    Tail defects – common (Congenital and Recessive and accidental- also may be linked to Copper deficiency – see Winn Foundation update)
11.    Hernias – often an accident of birthing.
12.    Cleft palates.
13.    Diabetes.
14.    Testicular anomalies.
15.    Paw and limb defects.
16.    Allergies.
17.    Bowel disease.
18.    Spasticity
19.    Hind limb paralysis.
20.    Loss of colour pigmentation.
21.    Polymyopathy.
23.    HD
24.    Blood group incompatibility.

Definition of Teratogenicity
<pharmacology> The ability to cause defects in a developing foetus. This is distinct from mutagenicity, which causes genetic mutations in sperms, eggs or other cells. Teratogenicity is a potential side effect of many drugs, such as thalidomide.

The main topic here is Flat Chested Kittens Syndrome.

Breeds that are presently documented to be afflicted with flat chests. There may be more now. Some go back decades.
1)    Abyssinians
2)    Bengals
3)    Birmans
4)    Bobtails
5)    Bombays
6)    British    
7)    Burmese
8)    Burmillas    
9)    Domestics.
10)    Exotcs
11)    Maine Coons
12)    Norwegian Forest Cats
13)    Ocicats
14)    Orientals
15)    Persians
16)    Ragdolls
17)    Russians
18)    Siamese
19)    Singapuras
20)    Spotted Mists    
21)    Tonkinese
(Prof.Niels Pedersen told me he has seen it in domestics and others in UC Davis’ 1000 cat breeding colony many years ago now.) It might be connected to the Siamese albino gene. The beginning of the Burmese had far too small a genepool.

Other species with the same or very similar problems:
    Dogs – very common Flat chests in puppies treated with Vit E by some breeders.
    Humans – (We don’t marry relatives and our gene pool is trillions- in humans it is a dominant gene)
There are probably many more, but I don’t have sufficient time to check everything out.

Some Dog Breeders are treating Flat Chests successfully with Vit.E….DIETARY MANAGEMENT and reverting the diet back to the “old fashion” bones and raw meat. This BARF diet is promoted by Dr Ian Billinghurst of Bathurst NSW and he has written 2-3 books on this subject.

Many cat breeders have “gut feelings” about some dietary imbalance being a large part of their problems, and have had improved results by dietary changes. A lot more research still needs to be done and accurate records kept by as many breeders as possible. Most recent data suggests bacterial infections in the dam might be a big part of the problem.

Some experienced and successful Burmese breeders are equally adamant that the problem is- Congenital. (Not genetic – but environmental – like German Measles in humans) and it is known that flu affects foetus, as will any virus in early pregnancy. Recent 2004 data suggests that bacterial infections in the dam and poor diet leads to FCK kittens being born. 5 breeders in Qld recently had a gut/bowel infection in their dams and all had FCKs in those litters where Mum was infected. All these aspects need to be considered as the way in which it turns up is very erratic.

Researchers believe it is most likely to be in the DNA. Some have suggested a mutant gene is assorting in the cat population as a whole. I have been told that it is in wild cats too. When white tigers are mated to white tigers they get birth defects, but no specific information was volunteered. Whites have to go to goldens. Tigers will not mate close relatives! Their gene pool is also too small and food supplies insufficient as their habitats are being destroyed. Cheetahs, in particular, suffer when kept in captivity with many succumbing to F.I.P. The diets for wild cats in captivity do not meet the normal requirements of these animals. Many wild animals, of several species, fail to breed successfully in captivity. Their fertility suffers and their babies often die. There is a documented colony of Lions living in a valley in SA and they never leave this valley surrounded by steep rocky cliffs. They have bred amongst themselves for a very long time (complete details elude me for the moment) and they are the healthiest colony ever studied. (Just trying to open up the big picture and make the topic more interesting.) I have found via research that outcrossing doesn’t necessarily fix the problem for the queen, which could indicate that it has a dominant mode of transmission that is also incomplete and erratic. It also suggests that it could simply be a developmental problem with some kittens. If one breeds from an affected kitten, this could also explain total disasters in some litters.

An American breeder of Singapuras believes that only deep-sea fish, not estuary fish, should be fed as she thinks Potassium Iodine deficiency is the cause of FCKs. She conversed with a university research team and was very thorough in her studies. This breeder got FCKs in her first litters and altered the diets, and learned how to detect carriers. (You can feel a slight ridge or angle anywhere in the ribcage… these kittens carry the defect. It can be very minimal, easily missed and transient – lasting only a day or so.)

Well, I can see how all of these opinions can be justified and so I will try to explain what I have found to date.

I do not believe that this is caused by a recessive gene. (For those who don’t understand this point I will try to simplify what this means. Recessive faults are passed to offspring when BOTH PARENTS carry the fault, or for that matter it could be a good thing, which you wish to breed into your line, such as a preferred coat colour (for want of a better example.) You get approximately 25% of progeny affected in this manner. But beware, you also get another 50% carriers!

There are breeders in the program that have had FCKs 50-100% of the litter affected regardless of which stud they have used.(I know one who used 5 different studs). Many breeders have seen whole litters affected and that is not what a recessive gene normally does. UK research teams say that 66% of Burmese worldwide are suspected carriers of FCKs, and about 4-5 years ago a new cattery per week was being added to their data bank of FCKs in England.

(Prof.Pedersen, not a geneticist – but extremely highly qualified teaching and research veterinarian of USA and a person whom I hold in high regard, states that when he has seen FCKs, even in domestics, and it does not fit any genetic pattern that he is aware of and believes the environment is involved. This was a long time ago now and professional opinions might be different today.)

One genetic researcher dismissed the 50-100% of affected kittens in any one litter, saying that the breeder has bred from a flat chested kitten to be getting these results. I do not think that this is always true because some bloodlines are more affected than others. (ie: Familial) But I do know breeders who choose to breed from kittens that were “only a little bit flat” and their problems are still ongoing. Some mildly affected kittens might sneak through when breeders are trying to assess litters, as these mild cases can be difficult to pick up if you are not taught how to identify them.

Any type of Dominant Gene needs only to be carried by one parent to show up in the kittens. An Incomplete Dominant Gene will occur erratically causing confusion to the breeder when trying to assess their breeding programs, especially if they have been told that a recessive gene is the cause of their woes. Some breeders have desexed stock on this theory only to find that the problem is still there sometimes in worse numbers that before. Dominant genes cause higher numbers of progeny to be affected than recessive genes. Many of you have had or know of someone who has had whole litters severely flat chested. This should not occur if a recessive gene is involved. The other thing to be considered is that if all FCK producers were desexed, would we just breed in other, perhaps worse, problems ie Hypokalaemia and stretchy skin disease. I consider these to be worse because they affect the health of your kittens for the rest of their lives. Don’t forget that desexing reduces the size of the gene pool. I guess it depends on how serious you perceive your problem to be? And, what if, the defect is dietary/environmental, like extreme heat during pregnancy?

POLYGENES are to be suspected when the incidence occurs a great deal more in one family of cats than in the general population. This also fits the bill more accurately than the recessive theory. THRESHOLD CHARACTERS   “set the point at which development goes past a certain threshold and mutation occurs” Perhaps you can imagine line breeding to set the length of fur in a long-haired cat and when you achieve results then continue to breed and in-breed with these animals until all your progeny appears with the desired coat length. These animals have reached a desired threshold regarding your goal of coat length and you have “locked” it in so you always get what you want. This is a simplified way of describing what “threshold” means. Once it is there it can take many years to reverse the process. Picture a little graph with short coats being at one end and long coats being at the other end. Somewhere between is the point (threshold) at which the coat changes from short-medium to long. This is your threshold character and any cats above or beyond this point will always produce long coats when mated to any cat with average length of hair. It can also be the point at which mutation occurs and when a gene mutates it remembers how it did it and will do it over and over again. The late Roy Robinson was writing a paper for me on how to breed out threshold characters when he died. He was extremely interested in data from my research and felt that breeders in the past had not given him accurate data and had, in fact, under-reported their FCKs. When breeders do this, it makes it impossible for geneticists to come to a correct decision as maths play an important part in their calculations. Roy and I were corresponding after his 3rd edition of Genetics for Cat Breeders went to press.

The CONGENITAL THEORY … I can see why some breeders are convinced that this is the case and it makes a lot of sense. If I hadn’t been told by several experienced breeders about when and how FCKs got into our Australian stock, then this theory would make the most sense of all, especially since other breeds and species have the defect. Congenital means that something happens in the environment during pregnancy causing birth defects. A good example is human babies being born deaf as a result of their mothers coming into contact with German Measles during their pregnancy, and also what happened to babies whose Mothers had taken Thalidomide. It can also be a problem relating to diet. Don’t forget the problem in dogs. They are also fed largely commercial diets and, these days, a lot of dried food.

The gene causing rib cage deformities in man is a dominant gene, which affects mainly males.

So, what do I think is happening? I believe what is being inherited is a possible metabolic hiccup of a familial nature  causing a developmental anomaly that is manageable by good husbandry and that all kittens can be at risk. Kittens are not born completely developed (can’t see, don’t immediately get up and run like a foal for example, need some stimulation to pee etc. and various little “triggers” in their brain start to “switch on” after birth.) I think that some of the problems breeders have told me about points to a dietary imbalance and possible infections in the dam during pregnancy and that a good balanced supplement several times a week after the first trimester of pregnancy along with vitamin A (5000 iu) once a week only in the last three weeks of pregnancy and twice in the first week of lactation at the same time using a vitamin E (200mg) supplement can be helpful in decreasing the risk factors for most queens. Vitamin A doesn’t work well by itself, but is better given with Vit E. Plus give all newborn kittens from queens who have produced FCKs 2 drops of calcium syrup 3 times a day in the first week of their lives or give them 2 drops of Nutridrops vitamin syrup several times a day until they are mobile. (usually around 10 days).

Cats have a high requirement for Vitamin A normally…1500iu daily, and if they don’t eat raw meat, liver etc then they may not be getting all they need. Also, the pregnant queen needs even more attention to her diet because she is trying to support life. If she is “at risk” then it is foolhardy to ignore her diet.  Of course there are “tough” little girls who do well throughout their pregnancies and lactation without needing any intervention from you, but I believe there are significant numbers of queens (especially Burmese) that do not fit into that bracket. Australia’s leading cat specialist has told me that if any cat is going to be adversely affected by drugs, anaesthetic or chemicals applied to the skin you can bet your bottom dollar that it will be a Burmese every time! Vitamin E is a good antioxidant and one can get all the information on these Vitamins and their benefits from any health food shop. We must not forget that our pets are not living a normal life, are subjected to high stress levels and certainly are not eating what God intended them to eat. ie: what cat can go out hunting and come home with “bikkies” and a tin opener? They are not vegetarians but would naturally get their plant matter from the digested contents of their prey’s stomachs. We do our very best for them and some commercial foods are as good as one could expect them to be, but not what the cat would first choose. Older textbooks connected FCKs to a deficiency of Vitamin A and nutritionists believe that quality commercial foods adequately cover all needs. But don’t forget that nobody knows what is normal for Burmese because nobody is doing the amount of research that is required to build data banks of what NORMAL is! Also I have been informed that the standards to which the pet food industry conforms allow a large range to qualify as satisfactory. The differences in the range are so wide that it is possible that they are erring on the low side of acceptable. One fully qualified professional person working in the pet food industry said it may be an enzyme problem – we were talking about dried food at the time because most of the queens reported to me were big bikkie eaters.

Another interesting point is one breeder who has been around for a long time said that she got FCKs in the first two litters of a mother and her daughter about 28 years ago or more now – but never had it again until she worked with new outcrossed stock. I asked her what she did about it at the time and she said “nothing – same girls, same stud and no changes in the environment (including food). These cats bred on for years without another hiccup. On thinking about this – it was about 25-30 or so years ago that significant changes were made to the food industry standards – and that change was an addition of Taurine which scientists had proved to be causing birth defects and which was not in the diet in sufficient quantities at the time. (Ref; Feline Husbandry – Diseases and Management in the Multiple Cat Environment. N.Pedersen. USA)

Prof.C.J.Wilkinson has been quoted as saying cats store Vit A in their liver and every time they are stressed they deplete the stores. It is quickly used by calling, mating, showing, birthing, lactating, illness and so on. It does not take long to be all gone if the diet does not contain enough to keep topping up supplies ahead of demand. Calling induces stress especially if not being mated. So it does not necessarily mean that one litter a year is the answer. It depends on the cat involved.

Cats cannot properly process Vit A that comes from plant material. It is better in the natural diet. Raw meat supplies a lot of Vit A and Taurine, but not enough calcium. Older breeders used to give one Cod Liver Oil capsule once a week to their breeding cats.

TAURINE may also be involved,( or at least the way a cat’s metabolism processes it) and a team in England was investigating this quite a long time ago now.

Taurine: Many breeds are troubled by defects connected to Taurine deficiencies. Recorded Taurine blood levels in Burmese FCKs and their littermates are extremely high but still nobody knows if these levels are “normal” or not. Burmese FCKs and their littermates have the highest ever-recorded blood taurine levels. Apparently it should be in tissue not blood, which I believe is pointing once again to metabolic errors in the breed or a deficiency of something else that is needed to “balance” the diet and process it more efficiently.

You might find it interesting that it appears to be known that the same cat that brought FCKs into Australian bloodlines is thought to have introduced Hypokalaemia (Potassium deficiency). Many breeders were asking for help with Potassium deficiencies and I declined at this stage because of an already heavy workload, but my curiosity was wetted and I started to look into this problem whilst working on the diet and found that Potassium is needed in certain levels for cats to make the best use of their available Taurine and Calcium. An English Nutritionist, who phoned me re my research, was interested in a possible connection between Potassium and FCKs as it is possible that stress during birthing might be causing a drop in Potassium which, in turn, is affecting the metabolism creating a much higher than normal demand for other significant vitamins, ie Vit A, E etc.  

It is often noted by breeders that queens with the problem are not always good “doers”, picky eaters, often not prolific callers, more often than not, do not eat placentas or give much attention to the newborns during labour, also don’t seem to like liver in their diet, often prefer dried food and crave for the attention & contact with their owners as a desexed pet would do. Some experienced breeders think it is basically a problem in the dam, but can’t figure out what is wrong. A reasonable amount of data suggests that either parent can pass on the fault. It does not seem to be sex linked (like haemophilia in people) but more often than not the typiest kittens are the ones affected and also the biggest kittens. (Threshold character effect?) For a long time in England they thought that Lilacs were clear of the defect, but my research proved exactly the opposite in Australia. Hundreds of lilacs and chocolates a year appearing as FCKs. The hotter the weather, the more frequent this and multiple other gross abnormalities presented. About 4-5 Summers ago when bush fires raged across NSW, Vic, and SA, birth defects of kittens born as blobs sent a message of concern from many catteries. Other observant breeders have noticed kittens on heat pads in Winter suddenly “start going flat” only to recover quickly when the heat pad is removed. Post mortems performed at Qld Uni. found nothing wrong with bones but something definitely not right about rib cartilage. One kitten had a “floating rib cage”. Other breeders who have not participated in the program have said that when they get the problem they just increase the vitamin supplements to the queen. A few breeders have told me that they have had a couple of FCKs in a litter and at some later stage admitted that the problem was not just FCKs but some kittens had SpinaBifida, tail defects and a “monster” as well. Sometimes, well-meaning friends will say that there wasn’t 1 FCK but 50% of the kittens were deformed. This is why we know that defects are under-reported and incomplete data is just a nuisance to researchers. Nobody can help you if you fail to report accurately. Also, with medical teams working on spina bifida in humans and treating with folates, then when litters arrive with Fcks and spina bifida in the same litter, if diet is causing one problem, then it may be causing the other also.

Vets involved in canine research express some concern that processed food may be “too good” and promote growth faster than the bones can support body weight. One Labrador breeder I know has returned her breeding animals to an all-fresh and natural diet, heavily supplemented with a wide range of vitamins and minerals with excellent results and no more skeletal problems since. This diet is explained in Dr Ian Billinghurst’s books and it is referred to as The BARF diet (Bones and fresh raw food) Be aware that dog food is not just what cats should eat as their metabolism is different but the basics are the same, except that dogs will eat things that are “off” where cats are fussier.

Another point I wish to bring up is that many of the meat industry are using more and more growth promoting hormones and special supplements to chooks and cattle to get better meat. So you can see that nutrition is an extremely complex subject and common sense should prevail. Experiment by all means, but make sure that the diet is overall good for cats. One dog breeder is raising two of my pet kittens on BARF and they are thriving, healthy, sturdy and good muscular development. They devour the food with great excitement, have no bowel or gut problems, or mouth problems either. And the litter tray smells better. NB: Keep the calcium/phosphorous ratio about 1:1.

Some truth may be in all of the above and that is why I choose to give good balanced supplements to all my pregnant queens as often as I remember and Vit A & E twice after birthing. Every one of my queens consume large amounts of Nutrigel (or Nutripet/Energel) during labour and it helps restore energy and combats sudden drops in nutrients whilst under stress. Yet other breeders say that by giving supplements you are simply masking the problem. Well, my reply is, what about the breeders who have always, as part of their normal husbandry routine, done exactly this or fed differently, and never had the defect. They don’t know or think that they are masking any problem. How many untroubled breeders doing this might be out there? Would you say, change your habits to see if you get faults in your lines? I can imagine their reactions. They simple say that breeders with defects don’t know what they are doing, don’t know how to handle kittens, and don’t have the background knowledge of pedigrees. They might be right, but most breeders are really trying to do their best with a fairly small gene pool.(PS: a large number of cats doesn’t necessarily mean a huge genepool if they all came from the same “pack of cards”.) I have noticed that for a while (about 20 years ago) breeders would cross FCK and Hypokalaemic lines and get some very good results, but that doesn’t seem to always work these days and the defect of potassium deficiency is on the increase now. Most of the books I have read suggest that a 3-5% defect rate is acceptable when practising any animal husbandry. Each person must decide for themselves what they are prepared to work with. There are far worst things than FCKs. If you have many cats and only have problems with one or two, then desex those and rebuild with the “safer” ones. This includes males as well as females. But if you have had all queens and studs produce the occasional FCK, then work harder on the diet and the environment, especially stress levels. Any queen which has several FCKs in multiple litters is not worth continuing with as she was most likely affected at birth and it has been missed during the selection process. Because most bloodlines are fairly closely related, sometimes outcrossing makes no difference at all. Better results with father/daughter matings than with someone else’s stud have been recorded. I do not advise new breeders to inbreed, because they often do not have the background knowledge of bloodlines and it is usually safer to outcross than inbreed.

Probably, one of the important things about all of the above is the occurrence in other breeds and species. At first it seemed to occur in all cats with any connection to Siamese. I know of one breeder who had it in his Burmese litters, desexed his stock and then got it in his Siamese queen. What did they have in common? Diet and environment. She was on lease and the previous owner claimed to not have had problems with her. She had been mated to the same stud as before. More recently I have been told of other breeders who have had FCK kittens in different breeds of cats in the same time frame. Definitely suggests that something other than genetics is going on.

I would like as much feedback from as many breeders as possible about diet and environment. Give Vitamins A & E as above and carefully monitor your results. Vit A = 5000 iu a week (and even up to 10000 iu a week has been used successfully by Persian breeders) in the last trimester of pregnancy if some but not a complete improvement is shown. For those brave enough, then repeat troubled matings try the above and document the results for me, please. .NB TOO MUCH VIT A IS TOXIC AND WILL CAUSE BIRTH DEFECTS – IT WAS TO BE WITHDRAWN FROM SHELVES BECAUSE OF THE RISK FOR PREGNANT WOMEN. LIKE SOME ALTERNATE REMEDIES THE AMOUNT AND TIMING IS CRITICAL. Always give Vit E at the same time as Vit A. Older breeders used to feed more fresh foods, cod liver oil, bones, cheese, eggs and some tin food. Their diets were similar to Dr. Ian Billinghurst books. (one being Grow Your Pups With Bones). Canine Control Bodies appear to be far more helpful to dog breeders than Feline Control Bodies are to cat breeders. Also I have found dog breeders to be far more open and helpful to each other than cat breeders in general. Most cat breeders blame the stud if they own the dam and vice versa. Also, many supplements designed for cats and kittens do not contain Taurine. Mavlab (Qld) used to manufacture a taurine supplement but it was taken off the market due to low demand. Taurine is a very necessary and very important dietary need of cats.

Flat chested kittens can be saved, especially if detected early enough, and the vast majority of the “recoveries” go on to lead normal, healthy and active lives. I am currently trying to ascertain a safe level of potassium supplement for breeding cats. Potassium gluconate is safer than other forms of Potassium, but at this stage I would suggest that minimal dose be supplemented in the latter stage of pregnancy. In UK, a scientist who has written to me, has used:

Treatment of FCK, as suggested by Bristol:

Dissolve 1 ‘Sandos K’ tablet in 100 ml warm water
Give 0.025 ml to affected kitten (about 2 drops) x 2 daily
(no rapid improvement until the kitten is 2 weeks old, then gradual improvement)

FCK seems to be affected by the environmental condition of the queen: any adverse situation during pregnancy seems to render the queen liable to produce FCKs.

Since Sandos K is unavailable in Australia, I am waiting on a reply regarding a suitable alternative.

The next paragraph is well worth noting because I have seen it give great results, not only by using Calcium syrup but breeders have had great success with Nutridrops (good balanced supplement for cats and kittens).
A vet in WA reported that he has successfully treated FCK Persians with 0.25 mil of Calcium syrup every 6 hours (night too) until the condition corrects. These Persian kittens have been taken home by the nurse for treatment, so that means that they have also been fed a milk formula. Good formulas like Troy Animalac don’t cause scouring and contain all the vital ingredients. I always use this one for any routine feeding of kittens born into very large litters. It is normal for my females to have 7-9 kittens in a litter (have had 12) and I choose to help the Mum feed them. It gives me great pleasure and the Mums like me being with them.

When a kitten is badly affected some vets will do a surgical correction, but this, so I am told, is very traumatic for the kitten. Also they are reluctant to do this because they believe it will lead to FCKs being kept or sold for breeding.  A very clever new breeder saved a kitten by making a cast out of the cardboard centre of a toilet roll. You cut it about 1”– 1.5” long, slit it down the length, place a thin layer of wadding under the front legs and sticky tape the cardboard around the chest. Put a small thick elastic band on the kitten as a collar and then tape the front and back of the cast to it to stop the cardboard from slipping down over the back legs. This helps the kitten to take the weight off its chest. It can then lay on its back and sides, is less stressed, breathes easier, then gains strength and suckles better. Feed the kitten yourself but leave it with Mum for comfort and warmth and soon the kitten will be back on Mum and suckling off her again. I saw her kitten, almost dead, laboured breathing, going cold, make a miraculous recovery and almost back to normal within a week. Of course you need to have the kitten’s heart and lungs checked by a vet before placing it in a pet home. Never be tempted to breed from a FCK. All cats can produce this but if you breed from one you will get more FCKs in higher numbers in subsequent generations.

Some information via Internet about Vit E:

 Vitamin E and selenium are closely related in their nutritional biochemistry, and we see a similar close relationship in the diseases associated with their deficiency.  

Deficiency states of vitamin E and/or selenium place young growing animals at risk of acute severe diseases, which in Australasia are commonest and best recognized in sheep, cattle, pigs and horses, and less commonly in chickens. In this situation, the most vulnerable organs are the skeletal muscles and the heart, with the liver also a recognized target in the pig. In chickens the vascular endothelium is the prime target site, with secondary complications developing in the nervous tissue of the hindbrain.
 In the young, rapidly-growing, post-natal mammal, the enlarging cells of type1 (oxidative) fibers of skeletal muscle are at highest risk of this kind of injury. Similarly in the neonate, the growing fibers of cardiac muscle are in the same category.


Read as much as you can about genetics and nutrition and consult your vet when in doubt.

Recommended basics;

1    Feed fresh raw meats every day. Some cooked meat for variety. Cooking does destroy nutrients.
2    Cooked deep-sea fish is rich in nutrients including potassium iodine and copper as is shellfish.
3    Cheese or a calcium supplement. Bal Cal is good as the calcium/phosphorous ratio is maintained. Bones are good too, and chicken necks but be careful of bacteria in chicken and hormones. This bacteria can cause bowel bacteria in cats to flourish out of control. I like to feed lamb spare ribs in preference to chicken necks or wings.
4    Yoghurt to maintain good gut and bowel flora balance. Acidophilous capsules can be sprinkled on food. Always give these capsules after illness or medications.
5    Brewers Supa Yeast Supplement (contains Potassium and minerals including copper) sprinkled like salt on meals 2-3 times a week. Most of the B group vitamins here.
6    General vitamin supplement for queens considered at risk.
7    Quality dried food in minimal quantity. Preferrable those without chemical preservatives and no chicken by-products. My queens who don’t eat dried food and those who only have a little dried food have not had FCK kittens. On the other hand I once had a queen who would not eat anything else but dried food and she had an ongoing problem. Her daughter was the same and even an outcrossed stud did not solve the problem. Both were desexed.
8    Feed queens in labour large quantities of Nutrigel paste which boosts energy and supplies heaps of vitamins. Give a calcium supplement after birthing.
    Give newborn kittens calcium/vitamins as above.
9    Sprinkle Iodised Table Salt on main meal sometimes (source of potassium iodine.)
10    Offer a good feed of raw calf or lamb liver about every 10 days to those that love it. Sauté some for those who won’t eat it raw. Nutrient rich Liver is very important part of the diet and a good source of copper, taurine, Vit A etc.
11    Cooked lamb/beef hearts occasionally.
12    A little tinned food for those who are picky. Tinned food may be causing renal potassium loss and over activity of the bowel. You don’t want the nutrients in the litter tray. Snappy tom tinned fish doesn’t contain chicken by-products, cereals, vegetables or chemical preservatives either.
13    Give Vit A and E together as soon as birthing is over and again 2-3 days later.
14    Last trimester Vit A & E for girls that don’t eat liver or very much raw meat. Not before mating or in the first trimester.
15    Don’t use heat pads very much at all. Prefer covered hot water bottles placed in a corner of the kitten box where mum and babies can move away if they wish. All of room heating set low is better than direct heat.
16    Provide fans for cooling but be aware that newborn kittens cannot adjust their body temperature like we do and die quickly of hypothermia.
17    Handle newborns a lot and stop them from lying on their stomachs all the time.
18    Have a “rough and lumpy” bed for mum and babies. Slippery surfaces in kittening pens or boxes do not give kittens the traction they need to get up and off their chests.
19    Supplement all kittens if they are hungry and always those that are not gaining much weight.
20    Keep stress levels in all breeding animals as low as possible. Simply providing cattery cats with their own accommodation and grassed and sunny exercise runs often helps in this area. Cats do get Vit K from grass and D3 from the sun. Try to keep their lives as natural as possible with safety of course. Fresh air and exercise is very important.
21    I prefer not to worm or apply flea treatment to pregnant girls.
22    I also do not vaccinate pregnant females.
23    Flu kills in utero.
24    Treatment for ringworm causes birth defects if given to pregnant queens and currently working studs.
25    Many drugs cause birth defects.
26    Burmese are allergic to many things.
27    Keep catteries clean and scrubbed. Don’t use chemicals like round-up in the area.
28    Cuddle every cat each day.
29    Make an effort to be with queens in labour.
30    Fresh clean water daily.
31    Litter trays done at least once a day, more if needed.
32    Disinfect with AviSafe, (or similar), pool chlorine, and ammonia – but not at the same time of course. Hot water and detergent kills most bugs on utensils. Different cleaning products work for different things.
33    Protect your stud by not allowing queens to use his litter tray, food or water bowls. Keep contact to a minimum. This reduces the risk of infection with virus or bacteria. Studs need fresh air, sun and grass too.
34    Wash your cats after a show before they have contact with other cats in the house.
35    Bacterial infections cause bowel disease in kittens and it is not genetic, and is triggered by feeding weanlings tinned food or food too rich for them.
36    Inbreeding can set problems in lines. Health & vigour & temperament should not be sacrificed for Best in Show awards.
37    If your pregnant girl has diarrhoea or vomiting she may suffer some potassium loss as well as other vital nutrients, which can lead to problems with the kittens.

If any breeder wants more help they may contact me.
Contact your vet if you are not sure of anything in this letter.


Hoping you found this document interesting and helpful.