It's a genetic disorder in dogs which manifests itself in puppies born with crippling deformities, eventually evident in the abnormal shape and length of their limbs. Chondrodysplasia is present in adult carriers as an auto-somal or simple recessive gene.
When chondrodysplasia occurs in dog breeds, however, it can be crippling and
can be found in association with other problems, such as deafness and shortened
lifespans. In the general dog population, chondrodysplasia can occur in
varying degrees. With the main focus being the front legs,
chondrodysplasia can range from appearing "nearly normal" to crippling
with all legs severely deformed.
We, as Malamute owners and prospective owners, have an opportunity to control the proliferation of chondrodysplasia in the Alaskan Malamute. And, with such control, there is also hope of its total elimination. Chondrodysplasia is a simple autosomal recessive gene. To produce a chodrodysplasitic offspring both parents must be carriers.
There are several steps in the elimination of the recessive gene from a
breed gene pool:
1) All chondrodysplastic animals are sterilized.
2) All animals producing a chondrodysplastic pup are sterilized.
3) Littermates of all known carriers either undergo a test breeding to determine if they are carriers or are sterilized.
History and Explanation For a number of years, breeders in both the United States and Canada were aware of occasional litters that contained deformed or "dwarfed" puppies, produced by parents who, themselves, showed no physical evidence of such deformity. It was not until the early 1970's that these puppies were conclusively proven to be the manifestation of a genetic disorder. At first, these affected dogs were known as "dwarves" because of their diminutive size. This term gave rise to considerable confusion. Veterinarians associated it with the dwarfism found in Hereford cattle, while owners associated it with any small Malamute. Since neither is correct, another name, chondrodysplasia (meaning "faulty cartilage"), was coined and brought into usage.
Chondrodysplasia in dogs was originally diagnosed as a form of rickets. Upon closer examination at various veterinary schools, it was determined that this diagnosis was incorrect. While it isn't known exactly what this crippling problem is, it has definitely been proven to be genetic, or inherited. A more technical description of this gene is "auto-somal," or "simple recessive." This simply means that the sire and dam must both carry this gene in order to produce an affected chondrodysplastic puppy.
In very young puppies, under six weeks of age, the deformity is often very difficult, if not impossible, to detect without x-rays, even to the practiced eye. But as the puppies grow older, the deformity becomes more evident in the shape and length of the front legs. However, not all chondrodysplastics are severely affected. In some adults, the front legs may appear "almost" normal.
It is not the chondrodysplastics themselves that are the major problem. The greatest concern is the use in breeding of the completely normal appearing dogs that possess or "carry" this gene. (A good parallel of this among humans is two brown-eyes parents producing a blue-eyed baby. In spite of their brown eyes, the parents both "carry" the gene for the blue eye.) While the breeding of two carriers can produce a chondrodysplastic, a litter from a breeding between a carrier and a "non carrier" (or clear) will contain only normal appearing dogs. Nevertheless, an undetermined number of puppies will themselves be carriers, having inherited the gene from their carrier parent. The continued whelping of such litters increase the number of carriers "at large" in the total canine population.
The eyelashes of a dog are made up of tiny hairs (D) called cilia. The cilia normally curve outward, away from the surface of the eyeball. Tiny glands at the base of the cilia help to make up the tear film that covers the eyeball (H) to provide it with moisture. Cilia that are in the normal position rarely cause ocular problems. When the cilia are in an abnormal position they can cause irritation to the eye.
Distichiasis is defined as "an extra cilia protruding from the meibomian glands at the eyelid margin." Distichiasis most commonly affects the dog, especially the American and English Cocker Spaniels, Miniature and Toy Poodles, English Bulldogs, and Golden Retreivers. Cats are usually not affected because they lack true cilia.
The meibomian glands are located along the inner eyelid margin and also contribute to the tear film. If cilia grow toward the eyeball they find an "easy way out" of the hair follicle by passing through the opening of the meibomian glands. When this occurs the cilia are in direct contact with the eyeball. The cilia that do this are termed distichia. The distichia are now able to cause keratitis (inflammation of the cornea), epiphora (excessive tearing), corneal ulceration by constantly rubbing on the surface of the eye. Blepharospasm (squinting ) may occur due to pain. All or some of these events may occur.
Distichiasis may be treated by removing the cilia that are causing the irritation. This can be done by cryotherapy, where the hair follicles are frozen at their base along the eyelid margin. This is the most effective method available, but recurrence is common. Electrolysis is another method that can be used. It involves placing a tiny needle in the hair follicle and sending an electrical pulse. This may be tedious if there are many distichia. Distichia can be plucked, but will return using this method of removal. Electrocautery, which is burning of the hair, is not recommended due to scarring.
Animals experiencing ocular problems should see a veterinarian as soon as possible. Rapid treatment is often necessary to maintain good vision.
Entropion is the inward rolling of the eyelid, most commonly the lower lid. This irritates the surface of the eye (the cornea) and may ultimately cause visual impairment.
Entropion is a common hereditary disorder in dogs. Selection for a particular conformation, of exaggerated facial features with prominent eyes and/or heavy facial folds, has created or worsened this problem in many breeds.
How is entropion inherited?
It is likely that ectropion is influenced by several genes (polygenic inheritance) that affect the skin and other structures that make up the eyelids, the way the skin covers the face and head, and the conformation of the skull.
What breeds are affected by entropion?
This problem occurs in many breeds. It is particularly severe in the mastiff, bullmastiff, Shar pei, and chow chow.
Entropion is seen in the Akita, American Staffordshire terrier, Pekingese, bulldog, pomeranian, pug, Japanese chin, Shih tzu, Yorkshire terrier, Staffordshire bull terrier, dalmatian, old English sheepdog, rottweiler, Siberian husky, vizsla, weimaraner, toy and miniature poodle. It is also seen in hounds ( basset hound, bloodhound), spaniels ( Clumber spaniel, English and American cocker spaniel, English springer spaniel, English toy spaniel, Tibetan spaniel), and sporting breeds (Chesapeake Bay retriever, flat-coated retriever, golden retriever, Gordon setter, Irish setter, Labrador retriever).
Entropion is common in giant breeds such as the Great Dane, Bernese mountain dog, mastiff, Saint Bernard, Newfoundland, and Great Pyrenees. In these breeds the central lower lid is often ectropic while the lid at the corners of the eye is entropic.
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. There are 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 entropion mean to your dog & you?
The problem is usually evident before a year of age. Discomfort from entropion will cause increased tearing and squinting. Your dog may be sensitive to light and may rub at its eyes. Chronic irritation by the turned-in eyelid may cause corneal ulceration and scarring which is painful and, if not corrected, can impair vision.
Dogs who have had surgical correction for a defect such as entropion may not be exhibited in the show ring.
How is entropion diagnosed?
The inrolling of the eyelid is readily apparent. Generally both eyes are affected. Depending on the degree of corneal irritation and the duration, there will be other signs such as those mentioned above. Your veterinarian will evaluate the degree of entropion and use flourescein dye to determine if there is any corneal ulceration.
FOR THE VETERINARIAN: The use of topical ophthalmic anaesthetic to anaesthetize the cornea and conjunctiva will enable eliminatation of the spastic component of the entropion in order to better evaluate the anatomic component. This is important before surgery is performed.
How is entropion treated?
Entropion is corrected surgically. If possible it is best to delay surgery until the dog is an adult since the involved facial structures are still growing and changing.
More than 1 operation may be required. It is better to correct the entropion conservatively and repeat the operation later if necessary, than to overcorrect causing ectropion. In breeds such as the chow chow that have particularly severe entropion related to heavy facial folds, several surgeries may be required.
Entropion is one of the eye conditions that is a result of selection by breeders and a demand by the public for such features as excessively prominent eyes and heavy facial folds. A responsible breeding programme will choose animals for breeding with a more normal head conformation, so as to select away from these exaggerated facial features and the problems associated with them.
The Vizsla Club of America has recognized entropion as an unacceptable problem in their breed, and advises breeders not to breed affected animals. Such leadership by breed clubs is important in discouraging this and other undesirable traits.
FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.
The lens is a unique living ocular tissue that is usually clear or transparent and is referred to as "the crystalline lens" by doctors. The normal lens focuses light on the the light sensitive nervous tissue located in the back of the eye which is known as the retina. The lens is an important link of the total visual system, yet the health of the entire eye should be evaluated before the lens develops a complete cataract.
What are cataracts: A cataract occurs when the lens in the eye turns opaque or white. The lens is the spherical body behind the pupil that focuses light rays. It is situated toward the front of the eye behind the cornea and iris. It normally is highly transparent. The lens can become totally or partially opaque due to the cataract. The cataract blocks the light rays, thereby impairing vision. Cataracts are common in dogs, representing one of the most important causes of vision loss. They are uncommon in cats.
What causes cataracts: Most cataracts are inherited. Hereditary cataracts affect many dog breeds. Breeds that are affected with hereditary cataracts that typically progress to blindness are the miniature poodle, American cocker spaniel, and miniature schnauzer. Other commonly affected breeds are the golden retriever, Boston terrier, and Siberian husky.
Other causes of cataracts include:
What are the signs of cataracts: If cataracts occupy less than 30% of the lens, or if they affect only one eye, they often go unnoticed. When cataracts occupy more than 60% of the lens, vision problems become obvious. The pet guardian probably will notice that the pet is having difficulty seeing. Vision impairment is noticed usually before any cloudiness in the eye is seen. If the cataract is caused by diabetes mellitus, the pet may have signs of diabetes, including excessive urination (polyuria), excessive thirst (polydipsia), and weight loss.
How are cataracts diagnosed: Cataracts are diagnosed by a good medical history and a thorough eye examination. Cataracts often are mistaken for sclerosis of the lens, a normal aging process. Sclerosis of the lens does not cause vision loss, and the veterinarian can distinguish the two easily on examination of the eye. Laboratory tests, except for determination of blood sugar, usually are not necessary because most are hereditary cataracts. Routine complete blood counts and serology (the study of antigen-antibody reactions) are used to screen for infectious diseases when cataracts are associated with anterior uveitis. Ultrasound imaging of the eye may be indicated when cataracts are advanced and surgery is anticipated, or to rule out other eye defects. Electroretinography (a graphic recording of the changes in the retina after stimulation by light) should be performed to evaluate the retina before surgery to rule out retinal degeneration or other retinal diseases.
How are cataracts treated: Animals with cataracts of all types should be monitored carefully for cataract progression. Hereditary cataracts in young dogs can progress quickly. Surgery is the treatment of choice for hereditary cataracts. Surgery may or may not be indicated to treat nonhereditary cataracts. Eye drops may be prescribed prior to surgery. Surgery normally can be done on any hereditary cataract that is causing or will cause vision loss. The prognosis for cataract surgery is better if surgery is done early in the course of cataract development. It is not advisable to delay surgery until the animal is blind in both eyes. Pets undergoing surgery may be hospitalized or may be cared for at home. Rarely is hospitalization required for longer than 48 hours.
What is the prognosis for animals with cataracts: Once a cataract develops, its rate of progression varies depending on its location within the lens and the age of the animal. As the normal lens ages, lens protein becomes insoluble and sclerotic, conditions which inhibit cataract progression. As a result, a small cataract in a one-year-old cocker spaniel may enlarge to cause blindness within several months, whereas a cataract of the same size in a 10-year-old poodle may require years to cause blindness. Cataracts caused by diabetes mellitus usually progress rapidly. With appropriate surgery, the prognosis (outcome) for good vision is excellent after removal of hereditary or diabetic cataracts. The prognosis after removal of other types of cataracts varies with the cause of the cataract.
Understanding the condition and its treatmentfor Hip Dysplasia
By Dr. Race Foster & Dr. Marty Smith
From Pet Pause, a Drs. Foster & Smith Inc. Publication, 2253 Air Park Road, Rhinelander, WI 54501, Spring 1996, Vol. 2 No. 2
Canine Hip Dysplasia is a relatively common disorder in veterinary medicine. The highest incidence occurs in larger, rapidly growing dogs. We find many people have misconceptions about dysplasia, considering it to be a form of arthritis affecting the hip joints. It is true that we see severe arthritis in dogs with this condition but this is the secondary result of dysplasia, not the primary problem. Once you understand the disease. you can easily understand its treatment. This article will explain what Hip Dysplasia is, its progression over the life of a dog, and the treatment of an affected pet. We will also consider its significance in breeding programs.
To better understand the condition, let's look first at the hip joint of the dog. It forms the attachment of the hind leg to the body with a "ball and socket" joint. The ball portion is the head of the femur, the long bone between hip and knee. The socket, called the acetabulum, is located on the pelvic bone. These two form the joint of a normal dog where the ball rotates freely within the socket. To facilitate movement, the bones are shaped to perfectly match each other with the socket surrounding the ball.
To strengthen the joint, the two bones are held together by a ligament going directly from the femoral head into and attaching to—the acetabulum. Also attaching to both bones and completely encircling the joint is the joint capsule. This thick band of connective tissue additionally acts to hold the bones together. The area where the bones actually touch each other is called the articular surface. It is perfectly smooth and cushioned with a layer of spongy cartilage. In the normal dog, all of these factors work together for smooth and stable joint function.
Hip Dysplasia is a disease that affects development of the hip joint in a young dog. It may or may not be bilateral (affecting both the right and left hip joints) . It is brought about by a laxity of the muscles, connective tissue, and ligaments that should support the joint. Even dysplastic dogs are born with normal hips but the soft tissues that surround the joint start to develop abnormally as the puppy grows. This is because of genetic factors in the individual dog. The most important result of the change is that the two bones are not held in place but actually move apart. The joint capsule and the ligament between the two bones also stretch, adding further instability to the joint. As this happens, the articular surfaces of the two bones lose contact with each other. The slight separation of the two bones of the joint is called subluxation; this—and this alone— causes all of the resulting problems we associate with this disease.
It is important to remember that if two bones within any joint lose their normal position in relationship to each other, their articular surfaces no longer correctly contact each other. The surrounding muscles of the dog's joint work to force the bones back together but they are never totally successful. Because of the dog's weight, the femoral head often rides up onto or over the rim of the socket. With every movement of the leg, there are now two abnormal areas of bone grinding against each other instead of contacting on a smooth articular surface. A disaster is about to occur.
Wherever these bones come in contact, new abnormally-shaped bone will grow. It is a vicious cycle; new bone growth causes further irritation which causes more abnormal bone growth. This is what we refer to as arthritis and it is usually a very painful condition. The femoral head that once looked like a smooth billiard ball now looks more like a head of cauliflower. The acetabulum (socket) that was once deep enough to enclose the femoral head is now shallow due to the grinding away of the rim. The edge is covered with bone spurs. As the condition progresses, more new abnormal bone forms and along with it comes further pain and distortion of the bone.
The puppy with Hip Dysplasia usually starts to show signs between five and 13 months of age. These range from mild discomfort to extreme pain when using the hind limbs. This will occasionally be seen following prolonged activity or when the dog gets up or lies down. Later in life the signs become more consistent, noted daily regardless of activity levels. Adult dogs that are in severe pain will usually decrease their activity. They are unwilling to run or climb stairs and, with decreased use, the muscles of their rear legs atrophy and become weakened. A few will learn to alter their gate and posture, often showing little or no signs of discomfort even though the bone changes are severe.
Signs of Hip Dysplasia in young dogs are generally thought to be from small irritations or even minor fractures occurring in the bone spurs that form around the socket. Fractures may be caused by the pup's increasing weight or exercise. Sudden periods of discomfort usually follow prolonged activity. In the adult, the discomfort is simply from arthritis of the deformed joints and chronic irritation.
How can Hip Dysplasia be diagnosed? The answer to that question also provides the hope for elimination of this debilitating disease. Only with x-rays can we truly diagnose dysplasia and hope to eliminate it. Regardless of what you have been told, you can never be positive that a dog showing rear leg lameness has dysplasia unless it is x-rayed. And you can never be sure that a dog showing no signs is disease-free without an x-ray You can be fooled either way.
The good news about Canine Hip Dysplasia is that most cases can be treated to help eliminate or decrease pain, allowing fairly normal levels of activity. Very few dogs today have to be put to sleep to alleviate suffering. There are always choices to be made, but the vast majority of affected animals can live quite comfortable lives.
Treatment is always directed at the stage of the disease. In the young suddenly showing discomfort, treatment is usually combined with rest. Bufferin combined with cage rest for five to seven days is usually adequate to "put out the fire" until the next flare-up. As the dog matures, surgery is the solution of outward signs of discomfort are consistent. Although a few patients can be maintained for long periods, even years, with pain medication and anti-inflammatory drugs, this is usually not the answer. There are three basic surgeries, all of which attempt to eliminate or reduce the pressure between the two arthritic surfaces.
The first surgery involves the cutting of the pectinious, which is one of the muscles that try to add stability to the joint by forcing the two bones back together. When it is cut or has a portion removed, the two bones move apart. We have had varied success with this procedure in our practice. It sometimes eliminates all pain and further surgery is not required.
The second type of surgery is the removal of the femoral head. No bony attachment between the leg and the rest of the body sounds radical, but the dog's body will compensate as the outer muscles in the area become stronger and hold the leg in place. This allows near-normal motion and use. Remember that the front leg of the dog is held to the body by muscles only; there is no bone-to-bone connection between the front legs and the rest of the skeleton. By removing the femoral head we eliminate the pain of the two bones coming in contact with each other. We have many active dogs in our practice that were able to continue their active lifestyles because of this surgery.
The final surgical technique available to a patient with dysplasia is total replacement with an artificial joint made of steel and high-impact plastic. This is very expensive and rarely necessary.
Throughout all of this, please remember that the individual dog affected with dysplasia can usually be helped to live a life that is generally free of pain. We would like to stress that fact. However, we cannot forget that some dogs do not respond well to medication or surgery.
Finally remember Hip Dysplasia is genetically spread from one generation of dog to the next. A veterinarian can certify that a dog is not dysplastic by having it x-rayed after 24 months of age. The x-rays are sent to the Orthopedic Foundation for Animals (OFA) for grading and certification. By breeding only those dogs certified as free of dysplasia, we continue our efforts to eliminate the disease. We want to point out that the system is working. It has been shown that in those breeds actively using OFA certification, the incidence of the disease is decreasing. If you are not x-raying your breeding animals, then you may contribute to the problem rather than the solution.
MONORCHIDISM & CRYPTORCHIDISM
Monorchidism literally means one descended testis, and is very rare. Cryptorchidism is the retention of one or both of the testes, usually in the abdomen. Cryptorchid testes can also be outside the body wall under the skin. The danger with cryptorchidism is that if the testis is in the abdomen, it is being exposed to a higher body temperature and is at great risk for Sertoli cell tumor (13 times more often than dogs with descended testes). Affected animals should be castrated (neutered). It is suspected to be a hereditary condition. Dogs which are unilateral cryptorchid (one testis is descended, one is not) can still be fertile and can pass the trait on to offspring. Cryptorchidism occurs most frequently in purebred dogs, in certain breeds, and within certain families of a breed.
TRICHIASISTrichiasis is an uncomfortable condition in which the eye lashes are misdirected toward the eye ball and scratch its surface, the cornea. The position of the lower lid is normal, but the lashes point in the wrong direction. This may cause infection and scarring of the cornea.
The most common cause is chronic inflammation with scarring in the lower lid. Such scarring can occur from lid infections, skin diseases, or from trauma and poor healing of the lid tissues.
Treatment by removal of the lashes is frustrating, because within a few weeks the lashes return to irritate the eye. Removal does provide temporary relief, however, permanent destruction of the lash follicle is the only sure way to prevent recurrences. This can be done by one of the following methods:
- The first is electrolysis. Here an electric current is passed through the base of the lash in hopes of killing the cells that produce the hair. Often about one-third of the lashes will regrow.
- A new method is now being used in which the offending lashes are treated with an Argon laser to destroy the hair follicle. The results are excellent, well tolerated and leave a good cosmetic appearance. Usually about one-third of the lashes regrow and often necessitate retreatment within six weeks.
Is a very common lid abnormality, is defined as the misdirection of eyelashes toward the globe. The misdirected lashes may be diffuse across the entire lid or in a small segmental distribution. Trichiasis has numerous causes, and the strategies to correct this problem are dictated by the anatomic abnormality causing the lash misdirection. The primary causes of trichiasis are involutional changes, posterior lamellae scarring (superior or inferior), epiblepharon, and distichiasis. Exact numbers on the frequency of trichiasis are unknown. Simple trichiasis involving only a few lashes is relatively common. Diffuse trichiasis involving the entire lid margin is much less common, and it is seen primarily in countries where trachoma is endemic. The primary morbidity associated with trichiasis is corneal abrasion, corneal scarring, and microbial keratitis. This condition can be vision threatening.
Race: No known racial predilection is evident.
Sex: No known sexual predilection is evident.
Age: Trichiasis can occur in all ages; however, this condition most commonly is seen in the adult years.
OVER & UNDERSHOT BITESAnatomy
Dogs normally have twenty-eight deciduous (primary or baby) teeth that erupt during the first six months of life. Most breeds have forty-two adult teeth. There are four types of teeth. Incisors are the smaller teeth located between the canines on the upper and lower jaws. They are used for grasping food and help keep the tongue within the mouth. Canines (also called cuspids or fang teeth) are located on the sides of the incisors and used to grasp food. Premolars (bicuspids) are for shearing or cutting food and are located behind the canines. The molars are the last teeth in the mouth. They are used for grinding nourishment for entry into the esophagus.
The way teeth align with each other is termed occlusion. Normal occlusion in most breeds consists of the upper (maxillary) incisors just overlapping the lower (mandibular) incisors (scissor bite). The lower canine should be located equidistant between the last (lateral) incisor and the upper canine tooth. Premolar tips of the lower jaw should point between the spaces of the upper jaw teeth. Flat faced breeds (Boxers, Shih-Tzu, and Lhasa Apso) normally do not have scissor bites.
Malocclusion refers to abnormal tooth alignment. Overbite (overshot, class two, overjet, mandibular brachygnathism) occurs when the lower jaw is shorter that the upper. There is a gap between the upper and lower incisors when the mouth is closed. The upper premolars are displaced at least twenty-five percent toward the front, when compared to the lower premolars. An underbite (undershot, reverse scissor bite, prognathism, class 3) occurs when the lower teeth protrude in front of the upper jaw teeth. If the upper and lower incisor teeth meet each other edge to edge, the occlusion is an even or level bite. When the upper and lower incisors do not overlap or even meet each other when the mouth is closed, the pet has an open bite. Anterior crossbite occurs when the canine and premolar teeth on both sides of the mouth occlude normally but one or more of the lower incisors are positioned in front of the upper incisors. Anterior crossbite is the most common malocclusion, is not considered genetic or hereditary, and is correctable. If there is an anterior crossbite there must be a condition termed posterior crossbite. Posterior crossbite occurs when one or more of the premolar lower jaw teeth overlap the upper jaw teeth. This is a rare condition that occurs in the larger-nosed dog breeds. A wry mouth or bite occurs when one side of the jaw grows longer than the other. It is considered hereditary and difficult to correct. Base narrow canines occur when the lower canine teeth protrude inward and can damage the upper palate. Often this condition is due to retained baby teeth and can usually be corrected through inclined planes used to push the teeth into normal occlusion.
For most breeds the scissors bite is ideal.
Scissors bite is one in which the upper incisors just overlap and touch the lower incisors.
(overbite, parrot mouth, class two, overjet, mandibular branchygnathism)
In this condition the upper jaw is longer than the lower jaw. There is a gap between the upper and lower incisors when the mouth is closed. Some puppies that are born with an overbite might
(underbite, reverse scissors bite, class 3, prognathism)
In this condition the lower jaw is longer than the upper jaw. If the upper and lower jaw meet each other edge to edge, the bite is referred to as an even or level bite. In some breeds of dog an underbite is the correct bite. Check your breed standard.
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