|
 Hope that you never have a litter with cleft palates. But if you do, this may explain the cause of at least some cases.
Let’s start at the beginning, with a short review of the birds and the bees. The sperm cell, with half the chromosomes needed for a new pup (and a little less than half the DNA it will get) penetrates the ovum (egg) and triggers cell division, with the multiplying cells having the right number of chromosomes, and characteristics from both families. After a while, these cells are seen to start segregating some in groups that will later form intestines, some groups that will become heart tissues, others destined to end up as reproductive organs, etc. It takes a while, so part of the way through the process, you might have a club whose members act alike for a time, but then, like Southern Baptists, split into splinter groups that become increasingly different from the cells whose division formed them. Some chromosomes in any one group go dormant, while others take over the job of activating the DNA and RNA that determine whether the cells are skin or hair cells, whether they express pigment, and a multitude of other inherited things. Chromosomes that deal with how a dog barks do not function in cells that make up the skin, even though all the chromosomes with their genes are in all the somatic body cells. After the first few divisions of the fertilized egg, the mass is called an embryo. Like a seed or acorn that contains all the leaves, bark, roots, growth patterns, disease resistance, and more, the animal embryo can be thought of as the grown dog and its descendants in future tense.
In some lower animals, the segregation of tissues in the embryonic urogenital tract never is completed, the way we understand it in mammals, where the genitals are near but distinct from the urinary organs. You can think of them as having an interrupted or halted development compared to the higher animals. However, the closer to the time of conception and early division, the less the differences in embryos of worms, frogs, Chihuahuas, water buffalos, and pterodactyls. The differences become apparent as the cell groups continue to specialize, which is an ongoing process up to and even after birth.
Sometimes something goes wrong during the embryonic development of structures on their way to completion. If development is halted or damaged, the part of the body that should be normal later, just isn’t. The example we are looking at here is the development of the central dorsal line of the body. Early embryos in that area look a little like flat worms or pancakes, and as they (we, too) grow, the edges curl or fold up and are supposed to unite along the top. Ever make raviolis or apple tarts? You fold the edges of the pastry so that the filling is enclosed, and you pinch the dough together in order to fuse it and keep the contents from falling or leaking out, until you can bake it. The spinal cord is the ravioli filling, and the finished vertebral column is the baked shell. If the phone rings before you pinch the dough, and your darling toddler daughter puts the half-completed job into the oven and cooks them before you get back, the contents are exposed. A similar thing can happen in the molding of the body if embryonic development is interrupted. Premature babies are at higher risk because some of them haven’t finished the process of closure before they are popped into the oven known as the world outside of the womb. Incomplete frontal skull bones, spina bifida, and hemivertebra are examples of the defects that can occur along the dorsal midline.
Midline closure defects are expressed in a variety of ways; in German Shepherd Dogs, I have seen incomplete closure to the midline of the scalp, incompletely formed tails, skull defects, spina bifida, and cleft palates. I believe them to be related in most cases. Sometimes other midline abnormalities are found; some would include umbilical hernias, and although they may be an embryo defect of another sort, I doubt those are related to the others. Cleft lip (harelip) is probably caused at a different time during gestation than cleft palate or the other disorders named above. As we say in good obedience training and many other things, Timing is everything.
Cleft palate is a condition in which, for genetic and/or environmental reasons, the hard surface of the roof of the mouth and the softer palate behind it fail to close completely. The first sign something is wrong (if you don't examine your pups immediately after delivery) is usually milk bubbling out the nose when the newborn attempts to nurse. In addition to strictly genetic cause, there are numerous other cases of environmentally-mediated cleft palate. It is a frequent defect found in offspring of diabetics. It has been produced experimentally by vitamin A imbalance whether too much or too little, and is often a result of poisons and steroids taken or produced by bitches in the first three weeks of gestation. Such corticosteroid production increase frequently can be associated with unsound character and/or a severe scare (fright). In canines, a deficiency of vitamin B-12 has also been identified as a cause. Antihistamines given early in pregnancy, at least in some doses, are also suspect. Viral infections at that stage, or certain other chemicals have also been determined to cause cleft palate. I believe natural or synthetic hormones and steroids are potentially very dangerous if given to bitches during pregnancy; most of the time, cleft palate is a steroid caused birth defect. Cortisone and similar steroids can also facilitate spontaneous bleeding, which is more perilous during whelping and surgical convalescence than at other times.
|
Possible Problems In The First Three Weeks
|
While some deaths and other difficulties are genetically controlled or otherwise out of the breeder's power to prevent, many are avoidable if the midwife/pediatrician is knowledgeable and careful. Generally speaking, if you pay heed to the subjects of genetics, nutrition, sanitation, disease prevention, and management, you'll increase your chances for a normal, healthy, successful litter growing to adulthood.
Start with the bitch, for a healthy female will make for a healthy litter in most instances. Some drugs or excessive vitamin A administered during pregnancy have been identified as causing cleft palate, reduced litter size, mummified fetuses, and nervous system disorders, as well as eye, ear, and heart defects in the pups. Exposure to too much carbaryl (Sevin is the most common tradename) insecticide may produce deformities in intestines and abdominal-thoracic fissures; other insecticides may cause skeletal deformities in pups if the pregnant bitch has been exposed to very high levels. Be sensible in your use of these, and your dam will likely be safe. A friend of mine tragically dosed his bitch with 10% Sevin dust (the concentration used for garden pests) instead of far less of the 5% dust used for fleas and ticks, when she was newly delivered of a litter of pups. It killed both her and all of the puppies. It was the wrong time to use it, and he used far too much.
During the first week, the combination of the dam's carelessness and failure to lactate account for the greatest losses in neonatal deaths, and the latter may be partly due to the breeder's carelessness in the area of sanitation and prevention of infection. Statistically speaking, the less common causes of death in that first week include cleft palates, which are probably found in less than 3 percent. Such pups either are euthanized on the second day or die soon after from aspiration pneumonia due to the milk they suck going through the nasal passages into the lungs.
Harelip is a split in the front portion of the palate, extending up the center of the front lip between where the middle incisors would later come in, and as far as the nose bulb in most cases. It is caused by a disruption in the embryo development at a slightly different time than cleft palate is. Sometimes, if the psycho-biochemical disruption has continued for a longer period of time than an instantaneous trauma, you may find both conditions in the same pups. You may have met people with both. Although it is surgically treatable in humans, it is not, or at least is not worth the effort, in dogs.
Brief Selections from Case Histories
Several years ago an Ohio dog club member had a small litter of puppies born with cleft palates. One puppy had the cleft palate alone, another had the malformed lip/mouth, and another puppy was born with all its internal organs outside its body. This is an instance of where midline closure defect is expressed on the ventral portion of the dog as well. All pups in the litter died.
|
|
She found out, through some detective work, that it was due to a chemical ingested or inhaled. Nothing in her house or yard would have caused this and she asked around the neighborhood if anyone sprayed any yard chemicals (pesticides, insecticides, herbicides). Nobody did, or at least in her neighborhood. She finally figured out that when she was visiting her son at a new neighborhood and park that her dog had been exposed to chemicals sprayed on the grass, and then found out that a neighbor of his across the street had in fact had the famous-name company spray their yard, but took the flags down as soon as they were finished. So her dog was exposed to the lawn chemicals by absorption through the very porous pads as well as possibly by inhaling for a day or two. This was at the critical point in her pregnancy and pups’ embryo development when this exposure would most likely cause this problem. The first trimester is the time of greatest risk.
I once bred a bitch who was hard as nails to a great show dog named Hein, noted for pigment and hips, and my litter had one somewhat flighty, spooky bitch pup whose temperament characteristics did not immediately show themselves. When that bitch grew up, the owners bred her. During the first trimester, this bitch had a sudden and traumatic fright. Even though it lasted only a few minutes, and her nervousness was at a peak for a few hours or more, the repercussions followed at parturition. Her litter all were born with cleft palates. A couple had harelip as well. All were euthanized. She never had any pups with cleft palate afterwards. The male that I bred my bitch to was of normal temperament, but produced more than his share of nervous offspring. One all-black son of his, bred by the owners and named Phantom, produced many spooky pups and a great deal more were produced by his offspring, in turn.
Such changes from the norm of midline closure are possible through that psychophysical route, such as a bitch in that stage of pregnancy being badly frightened or startled. Her own hormonal chemicals act the same way that administered steroids could. Of course, the always-flighty or nervous bitch is far more susceptible to such an unusual event than a stable bitch is.
When I had mentioned that observation in a magazine article, someone wrote to me, How could that theory account for the marked association of facial cleft with brachycephaly? Short-faced bitches are more nervous and flighty perhaps? Or could it be genetic, I wonder! No, as I had written, there are more causes than this one. Nervous temperament can be and usually is very strongly genetic, as would be any unusual or "touchy" reaction to steroidal imbalance. Plus, brachycephalic dogs, however lovely in the eyes of owners, are short-faced because of abnormal pituitary/hypophysis glands. This "master gland" affects all other endocrine glands and all hormones, directly or indirectly. Including those that affect cleft palate. Perhaps the defect that causes a Bulldog face with pushed-in nose and undershot jaw is side-by-side with the defect that directly or indirectly interferes with normal midline closure in the embryo just before birth or earlier in gestation.
Although kennel-blind fanciers of Lhasa Apsos and other short-faced breeds have claimed that this opinion is not supported by anything we know about endocrinology or genetics, I have studied enough biology and genetics to disagree. It is generally assumed that the growth patterns such as shape of head (some breeds such as Saints, Newfies, etc. retaining "juvenile" looks) are related to the function of the pituitary/hypophysis, and growth hormones interacting with other hormones. I learned a long time ago that the pituitary/hypophysis of breeds with Pug/Peke/Bulldog-type faces are physically different than those in breeds with "ancestral" type heads (GSDs, wolves, Malamutes, Spitz, etc.) I leave it up to the naysayers to come up with a better explanation as to why these brachycephalic breeds have the look of a dog that ran 35 mph into a brick wall.
A Westie breeder wrote to me: We also one time had a whole litter of clefts. There was no history of clefts in either the line of the dog or the bitch. In fact, we had bred both sire and dam previously with no clefts at all. We spoke to various veterinarians about this. And they determined it was from a viral infection that I had when the puppies were in the critical period of gestation. Could be. Environmental irregularities can make for somatic irregularities. That same correspondent later wrote, Thank you! This explains the cleft palate puppy we had last year after our two bitches got into a fight. Dusty was at the critical time for palate development. And my other bitch lost her whole litter! Hormones! Ugh!
To avoid midline closure defects, there are several steps you should take. Naturally, the first is to be careful about your choice of breeding pairs. After insuring the genetic component as much as feasible, make sure that the environment is one that promotes good health and avoids toxins and psychological traumas. Don’t let your bitch roam, especially during the first 3 weeks of pregnancy. Make sure you do everything to favor full-term gestation. If you have brachycephalic (especially toy) breeds such as Pekes, Pugs, Bulldogs, Bostons, and the like, research the ancestors and siblings for any problems before you breed your own dog.
And, since it is not all that common, Don’t worry; be happy.
Fred Lanting is an internationally respected show judge, approved by many registries as an all-breed judge, has judged numerous countries’ Sieger Shows and Landesgruppen events, and has many years experience with SV. He presents seminars and consults worldwide on such topics as Gait-&ucture, HD and Other Orthopedic Disorders, Anatomy, Training Techniques, and The GSD. He conducts annual non-profit sightseeing tours of Europe, centered on the Sieger Show (biggest breed show in the world) and BSP. Check out his website: www.MrGSD.com
|
|
|
|
|
CAUSES OF CONGENITAL CLEFT PALATE |
|
|
There are several possible causes for congenital cleft palate:
-
Genetic cause
An hereditary basis for the disease is suspected for congenital clefts but the mechanism has not yet been determined. Any such genetic trait is thought to be multifactorial recessive, polygenic and dominant with partial penetration.
-
Excess vitamin A intake during pregnancy
In 1967 Wiersig and Swenson reported that 125,000 IU of Vitamin A per kilogram body weight given to Beagle bitches on days 17-22 of gestation resulted in cleft palate developing in their puppies.
Vitamin A is an essential nutrient for normal growth and defects in bone growth are seen with insufficient as well as excessive dietary intake. Vitamin A has a controlling influence over both the osteoblasts and osteoclasts in epithelial cartilage and so there is a rational explanation as to why excessive vitamin A intake might result in cleft palate.
In addition, commercially prepared complete pet foods contain more than sufficient available vitamin A yet breeders and owners frequently supplement their pet's ration with vitamin supplements. High vitamin A content is also a feature of many natural food sources including liver and fish oils. Cod liver oil is a very popular nutritional supplement with pet owners and it contains 18000mg per 100ml (4000 IU per gram). Some vitamin injections contain as much as 500,000 IU of vitamin A per ml.
-
Cortisone
Administration of cortisone during pregnancy can lead to the development of cleft palate in the fetus
-
Hydroxyurea
Administration of the cytotoxic drug hydroxyurea (hydroxycarbamide) is reported to cause cleft palate.
Acquired cleft palate is common following falls from a height, and less commonly following road traffic accidents. |
|
|
|
Cleft Palate or Cleft Lip Complex,
Occlusal Anomalies, Tongue Anomalies |
|
Cleft Palate or Cleft Lip (Harelip) Complex: This is due to a disturbance of the processes that form the jaw and face during embryonic development. Cleft of the lower lip is rare and usually occurs on the midline. Clefts of the upper lip, usually at the junction of the premaxilla and maxilla, may be unilateral or bilateral, complete or incomplete, and often are associated with clefts of the alveolar process and palate. The defect may also involve the palate alone. Developmental anomalies affecting other organ systems can occur in ~8% of affected dogs and cats. The defect commonly occurs with other defects in large animals as well, such as arthrogryposis, which is inherited in a simple autosomal recessive manner in Charolais cattle. In small animals, incidence is higher in the Beagle, Cocker Spaniel, Dachshund, German Shepherd Dog, Labrador Retriever, Schnauzer, Shetland Sheepdog, and Siamese cats. Brachycephalic breeds can have up to a 30% risk factor. In large animals, cleft palate/lip complex has been reported in cattle, sheep, goats, and horses. The primary etiology is hereditary, although maternal nutritional deficiencies, drug or chemical exposure, mechanical interferences with the fetus, and some viral infections during pregnancy have also been implicated. Ingestion of toxic agents may also play a role; for example, ingestion of lupines ( Lupinus sericeus and L caudatus ) during the second and third months of gestation in cattle can potentially result in “crooked calf disease,” of which cleft abnormalities may be a component.
Initial signs include difficulty suckling, dysphagia, and evidence of milk dripping from the nostrils when the newborn attempts to nurse. Respiratory infection due to aspiration of food is common and a grave consequence with a poor prognosis. Examination of the oral cavity generally readily reveals the defect, except in foals having only a cleft of the soft palate that may be difficult to see.
Initial management requires intensive nursing care, including hand or tube feeding to ensure daily nutritional and caloric requirements are met, as well as the occasional need for appropriate antimicrobial therapy to treat for secondary infections of the rhinarium or lower respiratory tract. Surgical correction is effective only if the defect is small and is usually done at ~6-8 wk of age in small animals, before their general health is compromised. Various surgical techniques, ranging from simple closure to the need for sliding grafts or prosthetic implants, are used, depending on the severity and location of the defect. More severely affected animals may require multiple surgeries for successful correction. Surgical repair should be attempted only after ethical questions have been addressed, and the affected animal should be surgically sterilized or removed from breeding stock to prevent reproducing the anomaly in future offspring.
Occlusal Anomalies: Brachygnathia (overshot, short lower jaw, or parrot mouth in horses) is manifest when the mandible is shorter relative to the maxilla. It can be found to varying severity and incidence in all species of animals. In cattle, it is inherited as a polygenetic factor and can be associated with other anomalies such as impacted molar teeth and osteopetrosis ( Osteopetrosis) in Angus calves and Simmental cattle, or with chromosomal aberrations such as trisomy, which is lethal. In small animals, mild forms may be of no clinical significance; however, more severe forms may result in trauma to the hard palate or the restriction of normal mandibular growth secondary to erupting adult mandibular canine teeth. Diagnosis is through careful oral examination. Treatment varies from none to various orthodontic or endodontic procedures, depending on severity. In small animals, the mandibular canine teeth are often removed or shortened, with concurrent pulpotomy or root canal. A range of occlusal defects in sheep, from brachygnathia to mandibular aplasia and agnathia, is reportedly inherited as a simple autosomal recessive. Craniofacial dysplasia of Limousin cattle is characterized by a convex profile of the nose, short lower jaw, deficient ossification of frontal sutures, exophthalmus, and a large tongue; it is thought to be due to homozygosity of a simple autosomal recessive gene.
Prognathia (undershot, or monkey or sow mouth in horses) is found when the mandible is longer relative to the maxilla. It is identified on oral examination by finding the mandibular incisors in contact with or rostra to the maxillary incisors. In brachycephalic dogs and Persian cats, it is considered a normal breed characteristic. Despite being seen to varying degrees, it rarely requires any specific treatment.
Tongue Anomalies: Ankyloglossia or microglossia refers to incomplete or abnormal development of the tongue. It is often referred to as “bird tongue” in dogs and may be a component of the fading puppy syndrome. Affected puppies have difficulty nursing and do poorly. Oral examination reveals missing or underdeveloped lateral and rostral thin portions of the tongue that result in prehensile and motility disturbances. It is generally lethal.
|
| |
| LINKS TO ARTICLES ON OTHER SITES |
|
|
|
|
| |
|
|
E-mail to a friend
Print