Many different types of testing can be used to determine if your dog has a congenital illness. This is very important if you intend to breed your dog. Here are some of the types of testing used to determine if your dog has a congenital illness:
*According to OFA guidelines Hips, Eyes, Patella (knee cap), Thyroid, and Cardiac disease are the types of testing that are specific to french bulldogs. It however does not hurt to have more testing, in fact it will only give you a better sense of releif that you have a healty dog. The following were taken directly from the offa.org website.
Hip Dysplasia
- OFA Evaluation - OR
- OVC Evaluation - OR
- PennHIP Evaluation
Eye Examination by a boarded ACVO Ophthalmologist- Annual recertification recommended
Patellar Luxation
- OFA Evaluation
Autoimmune thyroiditis (Optional)
- OFA evaluation from an approved laboratory
Congenital Cardiac Database (Optional)
- OFA Evaluation
Eye Examination
Any board certified Veterinary Opthalmologist can perform annual eye testing for congenital blindness and this is a test that should be done annually according to the offa.org webpage. If you go to this site it will direct you to another site were you can pick from a list of Veterinary Opthalmologists that a licensed to perform this testing.
The Dysplastic Hip Joint
Hip Dysplasia is a terrible genetic disease because of the various degrees of arthritis (also called degenerative joint disease, arthrosis, osteoarthrosis) it can eventually produce, leading to pain and debilitation.
The very first step in the development of arthritis is articular cartilage (the type of cartilage lining the joint) damage due to the inherited bad biomechanics of an abnormally developed hip joint. Traumatic articular fracture through the joint surface is another way cartilage is damaged. With cartilage damage, lots of degradative enzymes are released into the joint. These enzymes degrade and decrease the synthesis of important constituent molecules that form hyaline cartilage called proteoglycans. This causes the cartilage to lose its thickness and elasticity, which are important in absorbing mechanical loads placed across the joint during movement. Eventually, more debris and enzymes spill into the joint fluid and destroy molecules called glycosaminoglycan and hyaluronate which are important precursors that form the cartilage proteoglycans. The joint's lubrication and ability to block inflammatory cells are lost and the debris-tainted joint fluid loses its ability to properly nourish the cartilage through impairment of nutrient-waste exchange across the joint cartilage cells. The damage then spreads to the synovial membrane lining the joint capsule and more degradative enzymes and inflammatory cells stream into the joint. Full thickness loss of cartilage allows the synovial fluid to contact nerve endings in the subchondral bone, resulting in pain. In an attempt to stabilize the joint to decrease the pain, the animal's body produces new bone at the edges of the joint surface, joint capsule, ligament and muscle attachments (bone spurs). The joint capsule also eventually thickens and the joint's range of motion decreases.
No one can predict when or even if a dysplastic dog will start showing clinical signs of lameness due to pain. There are multiple environmental factors such as caloric intake, level of exercise, and weather that can affect the severity of clinical signs and phenotypic expression (radiographic changes). There is no rhyme or reason to the severity of radiographic changes correlated with the clinical findings. There are a number of dysplastic dogs with severe arthritis that run, jump, and play as if nothing is wrong and some dogs with barely any arthritic radiographic changes that are severely lame.
(offa.org)
The Luxating Knee
What is Patellar Luxation?
The patella, or kneecap, is part of the stifle joint (knee). In patellar luxation, the kneecap luxates, or pops out of place, either in a medial or lateral position.
Bilateral involvement is most common, but unilateral is not uncommon. Animals can be affected by the time they are 8 weeks of age. The most notable finding is a knock-knee (genu valgum) stance. The patella is usually reducible, and laxity of the medial collateral ligament may be evident. The medial retinacular tissues of the stifle joint are often thickened, and the foot can be seen to twist laterally as weight is placed on the limb.
Patellar Luxation Categories
Patellar luxations fall into several categories:
- Medial luxation; toy, miniature, and large breeds
- Lateral luxation; toy and miniature breeds
- Lateral luxation; large and giant breeds.
- Luxation resulting from trauma; various breeds, of no importance to the certification process.
Numbers 1, 2 and 3 are either known to be heritable or strongly suspected.
Medial Luxation in Toy, Miniature, and Large Breeds
Although the luxation may not be present at birth, the anatomical deformities that cause these luxations are present at that time and are responsible for subsequent recurrent patellar luxation. Patellar luxation should be considered an inherited disease.
Clinical Signs
Three classes of patients are identifiable:
- Neonates and older puppies often show clinical signs of abnormal hind-leg carriage and function from the time they start walking; these present grades 3 and 4 generally.
- Young to mature animals with grade 2 to 3 luxations usually have exhibited abnormal or intermittently abnormal gaits all their lives but are presented when the problem symptomatically worsens.
- Older animals with grade 1 and 2 luxations may exhibit sudden signs of lameness because of further breakdown of soft tissues as result of minor trauma or because of worsening of degenerative joint disease pain.
Signs vary dramatically with the degree of luxation. In grades 1 and 2, lameness is evident only when the patella is in the luxated position. The leg is carried with the stifle joint flexed but may be touched to the ground every third or fourth step at fast gaits. Grade 3 and 4 animals exhibit a crouching, bowlegged stance (genu varum) with the feet turned inward and with most of the weight transferred to the front legs.
Permanent luxation renders the quadriceps ineffective in extending the stifle. Extension of the stifle will allow reduction of the luxation in grades 1 and 2. Pain is present in some cases, especially when chondromalacia of the patella and femoral condyle is present. Most animals; however, seem to show little irritation upon palpation.
Lateral Luxation in Toy and Miniature Breeds
Lateral luxation in small breeds is most often seen late in the animal's life, from 5 to 8 years of age. The heritability is unknown. Skeletal abnormalities are relatively minor in this syndrome, which seems to represent a breakdown in soft tissue in response to, as yet, obscure skeletal derangement. Thus, most lateral luxations are grades 1 and 2, and the bony changes are similar, but opposite, to those described for medial luxation. The dog has more functional disability with lateral luxation than with medial luxation.
Clinical Signs
In mature animals, signs may develop rapidly and may be associated with minor trauma or strenuous activity. A knock-knee or genu valgum stance, sometimes described as seal-like, is characteristic.
Sudden bilateral luxation may render the animal unable to stand and so simulate neurological disease. Physical examination is as described for medial luxation.
(offa.org)
| Here is an example of BAER ear testing on a puppy. This is used to detect congenital hearing loss in dogs. |
| Brain Auditory Evoked Response (BAER), Auditory Brainstem Response (ABR) Testing | ||||||
Puppies of many breeds of dogs may be born with deafness of one or both ears (congenital deafness):
Akita, American-Canadian Shepherd, American Eskimo, American Staffordshire Terrier, Australian Cattle Dog, Australian Shepherd, Beagle, Bichon Frise, Border Collie, Borzoi, Boston Terrier, Boxer, Bulldog, Bull Terrier, Cardigan Welsh Corgi, Catahoula Leopard Dog, Cavalier King Charles Spaniel, Chihuahua, Chow Chow, Cocker Spaniel, Collie, Dalmatian, Dappled Dachshund, Doberman Pinscher, Dogo Argentino, English Bulldog, English Cocker Spaniel, English Setter, Foxhound, Fox Terrier, French Bulldog, German Shepherd, Great Dane, Great Pyrenees, Ibizan Hound, Italian Greyhound, Jack Russel Terrier, Kuvacz, Labrador Retriever, Maltese, Miniature Pinscher, Miniature Poodle, Mongrel, Norwegian Dunkerhound, Nova Scotia Duch Tolling Retriever, Old English Sheepdog, Papillon, Pit Bull Terrier, Pointer, Puli, Rhodesian Ridgeback, Rottweiler, Saint Bernard, Schnauzer, Scottish Terrier, Sealyham Terrier, Shetland Sheepdog, Shropshire Terrier, Siberian Husky, Soft Coated Wheaten Terrier, Springer Spaniel, Sussex Spaniel, Tibetan Spaniel, Tibetan Terrier, Toy Poodle, Walker American Foxhound, West Highland White Terrier, Whippet, Yorkshire Terrier.
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| Causes of congenital deafness | ||||||
In dogs the merle and piebald genes have been associated with congenital deafness.
In cats deafness is associated with white hair color and studies indicate that white cats with a blue irises have a higher incidence of congenital deafness than white cats with non-blue irises.
For further information on deafness in dogs please visit Professor Strain’s website: www.lsu.edu/deafness/deaf.htm
Objective electrophysiological testing of hearing function has been performed on dogs and cats routinely since the 1980’ies. The BAER test evaluates the animals response to stimulation with loud sound. Sound is delivered directly into the ear-canal and the response to sound is “captured” with sophisticated equipment that shows the electrical response (cochlear and brain) (in milli volts). In some patients bone-conduction BAER may be used to differentiate between conductive vs cochlear dysfunction.The BAER test protocol approved by the Orthopaedic Foundation for Animals (www.offa.org) is used.
(baertest.org)
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Approved OFA Thyroid Laboratories
The laboratory certification process will include quality control, quality assurance and reagent certification. Laboratories may apply and, if successful, will be approved to perform analysis for OFA thyroid certification. A site visit by a qualified veterinary endocrinologist chosen by the OFA will be required and continued quality assurance and quality control will be necessary to maintain certification. Fully certified status can be obtained by passing the site visit and passing the results of the first OFA quality assurance assay result test. The approved laboratory must be contacted for the appropriate submission forms, sample handling procedures, and laboratory service fee before collecting the sample.
See the offa.org website for a list of approved laboratories.
(offa.org)
Congenital Cardiac Disease and the OFA
Congenital heart diseases in dogs are malformations of the heart or great vessels. The lesions characterizing congenital heart defects are present at birth and may develop more fully during perinatal and growth periods. Many congenital heart defects are thought to be genetically transmitted from parents to offspring; however, the exact modes of inheritance have not been precisely determined for all cardiovascular malformations.
Developmental Inherited Cardiac Diseases (SAS and Cardiomyopathy)
At this time inherited, developmental cardiac diseases like subaortic stenosis and cardiomyopathies are difficult to monitor since there is no clear cut distinction between normal and abnormal. The OFA will modify the congenital cardiac database when a proven diagnostic modality and normal parameters by breed are established.
However at this time, the OFA cardiac database should not be considered as a screening tool for these diseases.
Purpose of the OFA Cardiac Database
To gather data regarding congenital heart diseases in dogs and to identify dogs which are phenotypically normal prior to use in a breeding program. For the purposes of the database, a phenotypically normal dog is defined as:
- One without a cardiac murmur -or-
- One with an innocent heart murmur that is found to be otherwise normal by virtue of an echocardiographic examination which includes Doppler echocardiography.
(offa.org)
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