Genetic Diseases Are Unique to Three Varieties of Poodle
Genetic diseases that occur in Poodles are as unique as the three varieties. In fact, size has a lot to do with the diseases seen in Toy, Miniature and Standard Poodles.
Among the genetic disorders that occur in Toy Poodles are luxated patella and Legg-Calve-Perthes. Both can be extremely painful and cause lameness. Miniature Poodles may suffer from optic nerve hypoplasia in which they are born partly or completely blind. Standard Poodles are among the breeds prone to chronic hepatitis and eventual liver failure.
Breeders are encouraged to stay informed about diseases that occur commonly in their varieties and to take steps whenever possible to reduce their occurrence in their bloodlines. Here is an overview of these genetic diseases.
LCP & Luxating Patella in Toys
Janet Reed of Ypsilanti, Mich., has bred Foxmore Toy Poodles for more than 40 years and produced more than 150 champions. "To breed quality dogs you have to be aware of potential problems," she says. "Luxated patella and Legg-Calve-Perthes are two diseases that Toy breeders should be aware of."
Because both diseases are considered genetic, Reed is adamant about not breeding dogs that develop the disorders. In fact, she will not breed any dog diagnosed with bad hips or stifles. That philosophy is applauded by veterinarians and other experts.
Legg-Calve-Perthes (LCP) is technically defined as avascular necrosis of the femoral head. LCP occurs when an abnormal supply of blood to the femoral head of the hip joint causes the cartilage to wear away. The bone then starts to die, thus becoming irregularly shaped and no longer fitting properly into the socket. Fortunately, a surgical process called femoral head ostectomy (FHO) can alleviate the pain and correct the problem.
"LCP ends up turning into a degenerative joint disease of the hip, which is what you often seen in larger breeds that develop hip dysplasia, but it's not caused by the same thing," explains Christine Scruggs, V.M.D., of Waterford, Conn., a breeder of Standard Poodles. "I have diagnosed LCP in puppies as young as 6 months and adult dogs as old as 3 years."
The disorder almost always begins in dogs less than 8 months of age, thus it is considered a disease of growing puppies. It typically occurs in toy and miniature breeds that weigh less than 25 pounds as adults. Miniature Poodles may also develop LCP.
The most common clinical sign of LCP is lameness due to pain in the hip joint. Owners sometimes notice some degree of lameness, but disregard it or attribute it to excessive exercise. A dog may also present with acute signs, such as suddenly carrying a hind leg. In mild cases, dogs exhibit periodic lameness, and in more severe cases, permanent limping is seen on the affected leg.
Radiographs, or X-rays, are taken of puppies suspected of having LCP to detect radiographic changes. Veterinarians look for indications such as a widening of the joint space, a decrease in bone density, sclerosis, and thickening of the femoral head.
The FHO surgical process involves removing the femoral head and neck, which obliterates the bony joint. A dog will then form a functional scar tissue joint. Though this could result in a shortened stride, or slight limp, on the operated leg, the pain is gone. Full recovery usually takes about six weeks. Lifetime care includes keeping a dog active and avoiding obesity.
The Orthopedic Foundation for Animals (OFA) maintains an LCP registry that helps breeders to identify dogs that test normal for LCP. Owners should submit one standard radiograph taken of the dog in the standard hip-extended ventrodorsal view. A board-certified veterinary radiologist will review the radiograph to determine whether a dog is normal and thus qualifies for the registry. A dog must be a minimum of 12 months of age to be eligible for an LCP number. For information, breeders and owners may visit the OFA Web site at www.offa.org.
Luxating patella is another painful genetic disease affecting Toy Poodles. This condition occurs when the kneecap in one or both rear legs pops out of place, causing permanent or temporary lameness. A normal knee, or stifle as it is called in dogs, moves smoothly up and down in a groove at the lower end of the thighbone. A displaced kneecap can occur inside or outside the joint, can be temporary or permanent, and can be partial or complete.
Experts believe dogs that have a luxating patella are born with a shallow groove and weak ligaments that fail to hold the kneecap in place. Other causes include ligaments that are too tight to allow for sufficient flexibility, and a lag between the time it takes for a dog's legs to grow to maturity and for cartilage to mineralize. All these structures and processes are affected at least to some extent by genetics.
Scruggs routinely screens susceptible breeds, including Toy Poodles, for luxating patella. During an examination, she can diagnose the problem in puppies as young as 8 weeks of age by putting the knee through normal range of motion exercises to feel whether it tracks properly when the joint is flexed and extended. A popping sound confirms a luxated patella.
Treatment depends on the severity of the condition. Owners of mildly affected dogs should monitor the condition to be sure it doesn't get worse, Scruggs advises. Limiting activities that stress the affected joint can also help to slow progression of the disease, she says.
Surgery is recommended if the kneecap pops out of place more frequently or if the patella is permanently luxated. Puppies generally recover from surgery in two to three weeks, and adult dogs in four to six weeks. Surgical treatment averages around $1,200, depending on the geographical location and availability of veterinarians trained to perform the procedure.
Experts generally advise against breeding dogs with the condition because of the strong genetic component of luxated patella. They also agree much remains to be learned about the condition, including a better understanding of genetics, physiological causes, disease prevalence, and more effective treatment options. Meanwhile, OFA maintains a patellar luxation registry. Information is available at www.offa.org.
Optic Nerve Hypoplasia in Miniatures
Optic nerve hypoplasia is an inherited disorder in Miniature Poodles that results in varying degrees of blindness in one or both eyes from birth. Though the specific gene mutation has yet to be identified in dogs, several genes have been identified as causing the eye disorder in humans.
No treatment corrects the problem, but dogs that have limited vision or are blind are able to adjust for their handicap by relying on their acute senses of smell and hearing. In fact, some dogs function so well that their owners are unaware of the abnormality.
Jessie and Jane Burrow of Burline Poodles in Austin, Texas, were unaware their finished champion "Hunter," a black male Miniature Poodle, had optic nerve hypoplasia until CERF (Canine Eye Registration Foundation) testing was conducted in preparation for breeding. The testing confirmed he was blind in one eye.
"I raised and showed Hunter and never realized there was a problem," Jessie Burrow says. "Several people wanted to breed to him as soon as he finished. Lo and behold, we discovered he had optic nerve hypoplasia."
The Burrows hadn't noticed Hunter showing any signs of visual loss, such as bumping into walls or running sideways. "In hindsight, the only thing that should have given us an indication of a problem was Hunter's fear of heights," recalls Jessie Burrows. "He would not go up or down steps, and when we put him on a grooming table, he would stay exactly the way he was put, even if it was a couple of hours."
Ultimately, Hunter was neutered and placed in a loving pet home.
In a normal dog's eye, the optic nerve head, which carries signals from the retina to the brain, is from 2 ½ to 3 millimeters in diameter, says Greg Acland, BVSc., DACVO, professor of medical genetics at The Baker Institute for Animal Health of Cornell University.
"In a true optic nerve hypoplasia case, when you look into the eye, it's much smaller than that and the dog has, to some extent, severe loss of vision in the affected eye," Acland explains. "In really severe cases, the optic nerve can be tiny or essentially absent, and the dog will be completely blind in that eye."
Veterinary opthalmologists, such as Acland, are able to detect the disorder during a routine eye examination in puppies as young as 6 weeks by using a magnifying instrument, an ophthalmoscope, and a light source to see inside the back of the eye. Even with modern advancements in veterinary medicine, determining whether a dog is visually impaired is still fairly crude. Additionally, optic nerve hypoplasia may be difficult to differentiate from micropapilla, a similar eye disorder in which there also is a small optic nerve, but dogs show no evidence of visual impairment.
"It has been argued for many years whether the two conditions — optic nerve hypoplasia and micropapilla — are related," says Acland. "Some experts have a belief, or gut feeling, that if you look at lines of poodles in which breeders have bred dogs with micropapilla, then you can end up with dogs with true, absolute blinding optic nerve hypoplasia. But, not everybody agrees with that, not all ophthalmologists and certainly not all breeders."
The disorder appears to be autosomal recessive, Acland says. If so, dogs that carry the mutated gene do not have optic nerve hypoplasia themselves, but when bred to another carrier will produce affected offspring, as well as healthy and carrier offspring. Several generations down the line as dogs are bred together that share a common ancestor, or carriers, some offspring wind up with the eye disorder.
Since the genetic mutation causing the eye disorder has not been discovered, experts recommend not breeding dogs with optic nerve hypoplasia or their close relatives. To help breeders identify dogs free of eye disease, the Canine Eye Registration Foundation maintains a registry of dogs certified free of heritable eye disease. For information, visit www.vmdb.org/cerf.html.
Chronic Hepatitis in Standards
A slow but progressive disease, chronic hepatitis eventually causes liver failure. Though the underlying cause is not known, the higher incident rate in Standard Poodles leads experts to believe the disease is inherited.
Margaret Thornton of Denver recently lost her black Standard Poodle, "Renata," to chronic hepatitis after a seven-year battle with the disease. "It's just a horrible, horrible thing to have to go through," she says. "Managing the disease was a full-time job. I had to feed and medicate Renata on a tight schedule or else she would become sick and start vomiting."
Renata first started showing signs of the liver disease at 5 years of age. She became wobbly and wouldn't eat. Originally, the condition was thought to be Addison's disease, a disorder in which dogs cannot produce sufficient amounts of the hormones cortisol and aldosterone. Unsure about the diagnosis, the veterinarian did not treat Renata for Addison's, and the dog's condition improved.
Two years later, Renata's signs returned, and Thornton took the Standard Poodle to the veterinary teaching hospital at Colorado State University. David Twedt, D.V.M., DACVIM, professor of small animal medicine, performed a liver biopsy that confirmed chronic hepatitis.
Elevated liver enzymes, detected through a blood test, may suggest chronic hepatitis, which is then confirmed via liver biopsy. Though the elevated liver enzymes could be determined in dogs as early as 2 to 3 years of age, seldom do owners recognize a potential problem. A biopsy is performed surgically, via laparoscopy or by a needle biopsy using ultrasound guidance.
As the inflammation progresses, clinical signs of hepatitis begin to appear around 7 to 10 years of age. Signs include vomiting, lethargy, lack of appetite, and fluid in the abdomen. By this point, 60 percent or more of the liver is already damaged, Twedt says.
Though no cure is available, early diagnosis and intervention can help dogs live comfortably for many years. Drug therapy treatment helps to stop the inflammation and progression of ongoing liver damage. To help identify affected dogs early, Twedt recommends that owners and breeders of Standard Poodles have annual blood screening tests for dogs starting at 3 years of age. Blood work taken when a dog is young provides a base line for normal function.
"Those early tests, even if a dog doesn't show clinical signs, are important and might help identify early on if a dog has chronic hepatitis," Twedt says.
Twedt, along with researchers at the University of California-Davis, is collecting DNA blood samples from Standard Poodles in an effort to learn more about the genetic implications of chronic hepatitis. The goal is to identify the gene mutation and potentially develop a screening test for the disease. Owners or breeders interested in participating in the study should contact Twedt at (970) 297-1274 or by e-mail at David.Twedt@ColoState.edu.
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