Health of Lapponian herder

Conditions of breeding may vary from country to country, so I write breed conditions of lapinporokoira in the Czech Republic.

HD - HIP DYSPLASIA - prescribed for breeding

Hip dysplasia means abnormal development of the hip joint. It inevitably leads to the development of arthritis (osteoarthritis). Either the hip dysplasia or the secondary arthritis may cause hip pain. Hip dysplasia is a genetic disorder caused by the combination of genes from the parents (dam and sire). During the first few months of life, as the hips are developing, they become unstable. As a result the ball (femoral head) and socket (acetabulum) move apart during weight bearing. This causes abnormal forces on the soft bones which leads to the ball becoming flattened and the socket becoming shallow. The process is self-perpetuating and causes damage to the covering of the bones (the articular cartilage). Cartilage damage is a key feature of the secondary osteoarthritis.
The development of dysplasia depends not only on the genetic equipment of the individual, but also to various extents on other environmental factors. The disease is hereditary to 90%. Although some parents may not show symptoms of the disease themselves, they may still transmit it to their offspring. Even from healthy parents can develop 18-30% of sick puppies. However, in sick parents the probability of disease of puppies is 63-93%.

Dolgi - HD A/A
Pinkie - HD A/A

ED - ELBOW DYSPLASIA - prescribed for breeding

Elbow dysplasia means abnormal development of the elbow joint. This causes damage to the cartilage surface of the joint - a process called osteochondrosis or OCD. Elbow dysplasia and osteochondrosis collectively lead to the development of arthritis (osteoarthritis). Any of these three conditions may cause elbow pain. Elbow dysplasia is a genetic disorder caused by the combination of genes from the parents. The exact detail of how the elbow develops abnormally is poorly understood. An uneven fit (or incongruency) is suspected and this results in abnormal distribution of weight within the joint. Points of increased pressure cause damage to the cartilage covering the bones, and fragmentation of cartilage and the underlying bone may develop (osteochondrosis).

Dolgi - ED 0/0
Pinkie - ED 0/0

PRA-PRCD - Progressive Retinal Atrophy - prescribed for breeding

Progressive Rod-Cone Degeneration, or PRA-prcd, is a form of Progressive Retinal Atrophy (PRA) in which the cells in the dog's retina degenerate and die. PRA for dogs is similar to retinitis pigmentosa in humans. Most affected dogs will not show signs of vision loss until 3-5 years of age. Complete blindness can occur in older dogs. Progressive Rod-Cone Degeneration is a form of PRA known to affect over 40 different breeds. PRA-prcd is inherited as an autosomal recessive disorder. A dog must have two copies of the mutated gene to be affected by PRA. A dog can have one copy of the mutation and not experience any symptoms of the disease. Dogs with one copy of the mutation are known as carriers, meaning that they can pass on the mutation to their offspring. If they breed with another carrier, there is a 25% chance that the offspring can inherit one copy of the mutated gene from each parent, and be affected by the disease.

Dolgi - prcd PRA A
Pinkie - prcd PRA B (carrier)

CMR3 - CANINE MULTIFOCAL RETINOPATHY (Lapphund Type) - recommended for breeding

Multifocal retinopathy 3 is an inherited disorder of the Retina affecting dogs. Affected dogs typically present between 9 months and 2 years of age with multiple discrete circular areas of retinal detachment with underlying fluid accumulation that are visible on an eye exam performed by a veterinarian. These blister-like lesions are typically found in both eyes and can appear gray, tan, orange or pink and vary in number, size and location. Some affected dogs also present with obvious retinal folding. Progression of retinal changes is usually slow. Occasionally as affected dogs age, lesions appear to heal and are no longer visible on an eye exam. Generally the dog’s vision is not affected although vision loss has been described in some cases of multifocal retinopathy 3. CMR is an autosomal recessive hereditary disease. Thus, the disease manifests in individuals who receive the mutated gene from both their parents. These individuals are referred to as P / P (positive / positive). The mutant gene carriers, termed N / P (negative / positive), have the mutated gene from only one parent and are free of clinical symptoms. However, they transmit the disease to their offspring. Thus, when two heterozygotes (N / P) are covered, theoretically 25% of the offspring will be healthy, 50% of the offspring will be carriers and 25% will inherit both genes mutated from their parents and will therefore be affected by CMR.

Dolgi - CMR3 N/N
Pinkie - CMR3 N/N

MH - MALIGNANT HYPERTHERMIA - recommended for all dogs!!!

This syndrome is characterized by abnormally high body temperature and muscle contraction that can potentially lead to death. It can be followed by muscle rigidity, a very rapid and irregular heartbeat, increased breathing rate, bluish tinge to skin and mucous membranes, unstable blood pressure, fluid buildup in the lungs, impaired blood coagulation, kidney failure, and death. Giving certain anesthetics or specific drugs that affect the neurologic and muscular systems also consistently triggers malignant hyperthermia in susceptible animals. Diagnosis is based on development of clinical signs in an animal that has been given an anesthetic agent or is participating in a stressful event. Signs can develop slowly or rapidly. Animals that are not under anesthesia may show open-mouthed breathing and an increased breathing rate, followed by a temporary break in breathing. Blanching and redness of the skin followed by blotchy blue tinges can be seen in light-colored animals. Body temperature increases rapidly and can reach 113°F (45°C). Laboratory tests have been developed to help identify animals susceptible to malignant hyperthermia, but they are not useful for diagnosis of malignant hyperthermia in a sudden crisis.
Inheritance of MH is autosomal dominant. Only a single copy of the mutated gene is sufficient to produce clinical symptoms. The mutation is not linked to specific breeds. Because affected individuals are completely free of clinical signs without the inducing of the inducing agents, some individuals may live a lifetime without a diagnosis of MH during their lifetime. In the case of an affected individual, the risk of transmission of disability to the offspring is 50%.

Dolgi - later
Pinkie - later

DM - DEGENERATIVE MYELOPATHY - recommended for all dogs!!!

Degenerative myelopathy is a condition that slowly progresses over many months, where nerves within the spinal cord gradually lose their ability to transmit impulses. The cause of the nerve degeneration is poorly understood, but it appears to be related to an alteration in the genes of the affected dog. The nerves in the middle of the back (the thoracolumbar spine) tend to be affected initially and from here the degeneration spreads up and down the spine. The first signs of degenerative myelopathy generally develop at around eight years of age, although the onset may be later in life in some dogs. Weakness and loss of co-ordination in one or both of the hind limbs (back legs) is often the initial sign, followed by dragging and scuffing of the digits (toes). Affected dogs have a drunken appearance and will often stumble and fall when turning, especially on slippery surfaces. As the condition gradually progresses over many months, hind limb weakness and loss of co-ordination increase. In some severe cases the fore limbs (front legs) also become affected and affected dogs can become unable to walk and may develop incontinence. Degenerative myelopathy is not a painful condition and, as a result, affected dogs are generally well and keen to exercise, despite their disability.

Dolgi - later
Pinkie - later

GSD type 2 - GLYCOGEN STORAGE DISEASE II. - POMPE DISEASE - recommended for breeding

Canine Glycogen Storage Disease II (GSDII), also known as the Pompe disease, is an inherited disorder caused by deficiency of a specific enzyme active in lysosomes. It is a part of a wider group of disorders known as glycogen storage diseases (GSDs) or glycogenosis, all characterized by defects in glycogen processing or breakdown within muscles, liver or other cells types. GSDs can be divided in two types based on their cause, which can be genetic or acquired through intoxication. Acquired GSD has been identified only in cattle. Another classification of GSDs into different forms is based on type of enzyme that is defected and in which body part the specific enzyme is usually active. Like this, there are about eleven GSD types, classified by a number, the name of the defective enzyme, or by the name of the doctor who first described the condition. Glycogen Storage Disease II (GSDII), or the Pompe disease, has been reported in humans and different animal species, such as Japanese quails, cats, sheep and dogs. Canine glycogen storage disease is known to affect Lapponian dog breeds, such as the Finnish and Swedish Lapphunds and the Lapponian Herder. It was for first tie described in a Swedish Lapland dog in 1970, but the genetic cause of the Pompe disease in dogs was not known until 40 years later.
Canine Pompe disease is inherited as an autosomal recessive disorder. Dog carrying one copy of the mutated gene is heterozygous and will not show the GSDII symptoms. When mating two carriers (heterozygotes) at conception each cub has a 25% chance of being affected, a 50% chance of being an asymptomatic carrier, and a 25% chance of being unaffected and not a carrier.

Dolgi - later
Pinkie - later