HEREDITARY DISEASES IN DOGS

It is also known as CH because its main manifestation is choroidal hypoplasia (defective development of the dark and vascular layer of the eye located behind the retina and whose function is to nourish it and the lens).

It is a disease for which there is no treatment. In its most benign manifestation, the dog retains vision throughout its life, however, these specimens can produce seriously affected offspring. In its most severe manifestation, hemorrhages can occur inside the eye, leading to a serious loss of vision. It usually manifests at two years of age and can affect one or both eyes.

The disease is easily recognizable in an ophthalmologic examination of the fundus at 5-8 weeks of life, as the choroid appears pale and thin, almost transparent, and the blood vessels are easily visible. Once the retina changes to its adult color (around 3 months of age), the pigment masks the deficiencies in the choroid.

It is an inherited neurological disorder characterized by a set of inherited neuronal disorders, characterized by the accumulation of autofluorescent lipopigments (ceroid and lipofuscin) in neurons and in other types of soft tissue cells. This leads to progressive degeneration of brain and eye cells, severe neurological impairment and early death.

Affected dogs begin to exhibit symptoms at one year of age (loss of motor coordination, cognitive degeneration, visual loss and abnormal behavior). Due to the severity of the disease, affected animals rarely survive more than 26-28 months.

The disease has no treatment.

It is a disease in which the bone marrow produces neutrophils (white blood cells) but cannot effectively release them into the bloodstream. This leads to an impaired immune system that makes the affected animal unable to effectively fight common infections.

The disease has not been diagnosed until recent dates because, being an immunodeficiency disease, the symptoms are very diverse depending on the infection that each individual suffers.

Most affected specimens die before reaching six months of age.

Also called «multi-drug resistance gene» is responsible for producing a transporter protein (P-glycoprotein) that represents a functional protective barrier for the brain against drugs and other toxins.

When the gene suffers mutation and is not functional, certain medicinal substances accumulate in the brain and other organs such as the liver and kidneys, become toxic and cause neurological, hepatic, renal damage and even coma and death of the animal.

Various commonly used drugs can cross the blood-brain barrier in case of MDR-1 gene deficiency. The best known are ivermectin (antiparasitic) and loperamide (antidiarrheal loperamide – antidiarrheal marketed in Spain as Fortasec and Salvacolina).

Through a test it can be determined whether a specimen has the functional gene, in which case these medications can be administered normally, or mutated, then it will be necessary to find an alternative treatment.

Also known as cobalamin malabsorption, it is a disorder that causes the inability for the dog to absorb adequate levels of vitamin B12. Cobalamin or vitamin B12 is normally taken up through the small intestine, but affected dogs cannot absorb the vitamin and quickly begin to show symptoms of deficiency.

Symptoms usually appear within the first 6 to 12 weeks after birth as the puppy is born with a certain amount of vitamin B12, but when this stored vitamin is depleted, the puppy begins to show signs of deficiency. Symptoms include anemia, lethargy, lack of growth, and lack of appetite.

IGS cannot be cured but the disorder can be alleviated with regular cobalamin supplementation.

It is a progressive disease of the spinal cord. Generally, the disease manifests between 8 and 14 years of age. It begins with a loss of coordination (ataxia) in the hind limbs. The affected dog staggers when walking, leans on its knuckles or drags its feet. At first it may occur in one hind limb and then affect the other. As the disease progresses, the limbs become weak and the dog begins to have difficulty standing. The weakness progressively worsens until the dog cannot walk.

The clinical course can vary from 6 months to 1 year before the dog becomes paraplegic. If the symptoms continue for a longer period of time, loss of urinary and fecal continence can occur and, finally, it also develops in the front limbs. A key characteristic of DM is that it is not a painful disease.

There is no treatment that has proven clear efficiency in stopping or slowing its progress.

It is an inherited alteration of skeletal muscle characterized by cardiac dysrhythmias, generalized contraction of skeletal muscle, rhabdomyolysis, hypercarbia and renal failure, which appear after exposure to succinylcholine or volatile anesthetic agents.

In the reversal of the symptoms of this canine syndrome, specific actions can be performed, including the use of the calcium release channel antagonist dantrolene.

Developmental disorder of the teeth characterized by high wear of the teeth, with development of a light brown color and soft enamel and gum inflammation.

Symptoms are caused by severe hypomineralization of the teeth. Symptoms develop at an early age.

It is characterized by axonal degeneration and loss of nerve fibers that involve mainly sensory nerves. Mixed sensory and motor nerves deteriorate to a lesser extent. As a consequence, progressive ataxia, intermittent knuckling of the paws and self-mutilation occur.

Symptoms appear at 5-7 months of age: loss of coordination, joint laxity, loss of proprioception, and inability to perceive pain and in all cases progresses to the point where euthanasia is necessary.