American Akita – strong, unpretentious dogs.  

But unfortunately,  the situation in breed doesn't improve every year.  

In our country there aren't a lot of opportunities, in comparison, for example, with the USA for to check genetic diseases of dogs.  

RKF doesn't demand obligatory checks of health before the breeding.

 

But befor you have a puppy, you need to learn about some of the problem of the breed.

 

 

Dysplasia.

 

The reasons of emergence of this disease still precisely aren't studied. It can be both heredity, and wrong cultivation of a puppy, and poor diet mothers during pregnancy and still a heap of other factors of "letters" influencing emergence in the father-in-law.

 

Elbow Dysplasia

 

Elbow dysplasia is a general term used to identify an inherited polygenic disease in the elbow of dogs. Three specific etiologies make up this disease and they can occur independently or in conjunction with one another. These etiologies include:

1. Pathology involving the medial coronoid of the ulna (FCP)

2. Osteochondritis of the medial humeral condyle in the elbow joint (OCD)

3. Ununited anconeal process (UAP)

Studies have shown the inherited polygenic traits causing these etiologies are independent of one another. Clinical signs involve lameness which may remain subtle for long periods of time. No one can predict at what age lameness will occur in a dog due to a large number of genetic and environmental factors such as degree of severity of changes, rate of weight gain, amount of exercise, etc. Subtle changes in gait may be characterized by excessive inward deviation of the paw which raises the outside of the paw so that it receives less weight and distributes more mechanical weight on the outside (lateral) aspect of the elbow joint away from the lesions located on the inside of the joint. Range of motion in the elbow is also decreased.

 

Exzamining ED

 

 Hip  Displasia

 

         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.

 

The material above have been reprinted from http://www.offa.org/

 

 

Genetics of inherited eye disease

 

- The retina atrophy - is characterized by sudden

deterioration of sight or approach of a total blindness.

Pupils are expanded, response to light the slow. In case

of a full atrophy of a retina treatment is useless.

  - Entropy - the wrong provision of a century in case of which its edge is wrapped inside, to an eyeball. Thus skin and eyelashes of an eyelid injure a conjunctiva, causing its inflammation.

  -Ektropiya - when part of an eyelid or all eyelid it is turned out outside and droops, and the conjunctiva is naked. It is often watched congenital выворот.

 Problems of eyelids are eliminated with an operational way, operation often doesn't leave any visible traces.

But it is necessary to remember that dogs with such problems shall be excluded from breedings.

 

Idiopathic Hypothyroidism

 

Autoimmune thyroiditis is the most common cause of primary hypothyroidism in dogs. The disease has variable onset, but tends to clinically manifest itself at 2 to 5 years of age. Dogs may be clinically normal for years, only to become hypothyroid at a later date. The marker for autoimmune thyroiditis, thyroglobulin autoantibody formation, usually occurs prior to the occurrence of clinical signs. Therefore, periodic retesting is recommended. The majority of dogs that develop autoantibodies have them by 3 to 4 years of age. Development of autoantibodies to any time in the dog’s life is an indication that the dog, most likely, has the genetic form of the disease. Using today's technology only a small fraction of false positive tests occur. As a result of the variable onset of the presence of autoantibodies, periodic testing will be necessary. Dogs that are negative at 1 year of age may become positive at 6 years of age. Dogs should be tested every year or two in order to be certain they have not developed the condition. Since the majority of affected dogs will have autoantibodies by 4 years of age, annual testing for the first 4 years is recommended. After that, testing every other year should suffice. Unfortunately, a negative at any one time will not guarantee that the dog will not develop thyroiditis. The registry data can be used by breeders in determining which dogs are best for their breeding program. Knowing the status of the dog and the status of the dogs lineage, breeders and genetic counselors can decide which matings are most appropriate for reducing the incidence of autoimmune thyroiditis in the offspring.

 

The material above have been reprinted from http://www.offa.org/