Some Cleft Palate Info.... Under normal circumstances the hard palate closes completely before birth. A cleft palate is a birth deformity in which the palate (the roof of the mouth) fails to fuse along its midline. It can usually be corrected surgically, but it requires microsurgery by a specially trained and skilled veterinarian. It can just be the soft tissue, in which case it only presents as a cosmetic malformation, but if the hard palate is affected, it inevitably spells doom for the new born pup.
Often the condition leaves an open space through the roof of the mouth into the breathing passages. Food and other foreign material may pass from the oral cavity into the nasal cavity through this defect, leading to a chronic nasal inflammation and discharge. Excessive nasal secretion may be aspirated into the lungs. Affected puppies or newborns have difficulty eating and suckling and will not grow as quickly or as large as their littermates. Some pups with cleft palate that attempt to nurse, aspirate and die.
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.
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.
Certain breeds are most prone to cleft palate than others. The defect is more common in Cocker Spaniel, Dachshunds, German Shepherd Dogs, Labrador Retrievers, Schnauzer, Beagles and Shetland Sheepdogs. Dog breeds with short heads (brachycephalic breeds such as Pug, Shih Tzu and Boston terrier) can have up to a 30% risk of this disorder. In Brittany spaniels pedigree analysis indicates that cleft palate trait is inherited as an autosomal recessive.
Folic acid has been shown to prevent neural tube defects in humans. In a consistent breeding programme of Boston terrier dogs started in 1974, folic acid supplementation (5 mg/day) was introduced in 1981. The frequency of cleft palate fell from 17.6% without folic acid to 4.2% after its introduction, giving a reduction of 76%. |