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Canine Cleft Palate
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This article will help
you better understand cleft palate in puppies and kittens. If your
pet is showing any symptoms or signs of disease, please contact your
veterinarian. We want you and your pet to be happy and
healthy.
Cleft palate is a skeletal disorder occasionally seen in puppies
and kittens of all breeds. A cleft palate results when the bones forming
the roof of the mouth do not grow normally. This results in an opening
in the roof of the mouth that communicates into the nasal cavity.
What are the symptoms?
Puppies and kittens as young as one day old will often have milk
come out their noses as they nurse. They may also inhale milk into their
lungs, causing a difficulty in breathing or even pneumonia. When the
pet's mouth is examined, a slit will be seen in the roof of the mouth.
What are the risks?
The milk tends to enter the nasal passages and lungs. Most patients
will die at an early age from pneumonia and/or malnourishment.
What is the management?
Mild openings in the mouth roof can be surgically corrected.
More severe instances cannot. Frequently if the cleft palate cannot
be surgically closed, euthanasia is advised.
click on photos to see larger image
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What is Cleft lip/palate?
This is an opening in the lip or the roof of the mouth that occurs
due to failure of normal fusion processes during embryonic development.
Cleft palate and cleft lip may result from either hereditary or environmental
causes (such as the use of certain drugs during pregnancy).
How is cleft lip/palate inherited?
Cleft palate is believed to be an autosomal recessive trait in
the Brittany spaniel. In the English and French bulldog, pointer,
and shih tzu, the trait may be autosomal dominant with incomplete penetrance.
What breeds are affected by cleft lip/palate?
English and French bulldog, pointer, shih tzu, Boston terrier,
Brittany spaniel, cocker spaniel, dachshund, German shepherd, Labrador
retriever, miniature schnauzer, and Pekingese.
For many breeds and many disorders, the studies to determine
the mode of inheritance or the frequency in the breed have not been
carried out, or are inconclusive. We have listed breeds for which there
is a consensus among those investigating in this field and among veterinary
practitioners, that the condition is significant in this breed.
What does cleft lip/palate mean to your dog & you?
Affected pups are born with the condition. A minor defect will
cause little or no problem, while a more severe defect will cause signs
such as a chronic nasal discharge (that may include food), poor growth,
aspiration pneumonia (from inhalation of food), or even death.
How is cleft lip/palate diagnosed?
Your veterinarian will diagnose these conditions on physical
examination.
How is cleft lip/palate treated?
Mild problems may not require any treatment, but more serious
defects will require surgical repair to prevent complications such as
aspiration pneumonia.
Breeding advice
Affected animals should not be used for breeding, and it is prudent
to avoid breeding their parents and siblings as well.
FOR MORE
INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.
Copyright © 1998 Canine Inherited Disorders Database. All rights
reserved.
Revised: April
03, 2001.
This database
is a joint initiative of the Sir James Dunn Animal Welfare Centre at
the Atlantic Veterinary College, University of Prince Edward Island, and
the Canadian Veterinary Medical Association.
reprinted with kind
permission from:-
Alice Crook, DVM,Coordinator, Sir James Dunn Animal
Welfare Centre, Atlantic Veterinary College,University of Prince Edward
Island, 550 University Ave.Charlottetown, PEI C1A 4P3
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BIRTH DEFECTS: CLEFT PALATE WHY AND WHEN
Fred
Lanting
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-&-Structure, 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: http://www.MrGSD.com
Reprinted with kind permission of Fred Lanting
Author of The Total German Shepherd Dog
This is the expanded and enlarged second edition, a "must" for
every true GSD lover. It is an excellent alternative to the "genetic history"
by Willis, but less technical and therefore suitable for the novice, yet
very detailed to be indispensable for the reputable GSD breeder. Chapters
include: History and Origins, Modern Bloodlines, The Standard, Anatomy,
The German Shepherd in Motion, Shows, Showing, and Training, The Winners,
Nutrition and Feeding, General Care and Information, Health and First Aid,
Parasites and Immunity, Diseases and Disorders, The Geriatric German Shepherd,
Breeding, Basics of Genetics, Reproduction, Whelping, The First Three Weeks,
Four to Twelve Weeks, Trouble-shooting Guide
Permission to reprint this article may only be given by the author
Fred Lanting mailto:mrgsd@hiwaay.net
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