Primary lens luxation (PLL) is thought to be heritable in most breeds in which it is seen,
although clinical signs are generally not seen until the dog is an adult. Secondary lens luxation is not heritable, and occurs secondary to another disease process within the eye. In the terrier breeds (such as the Jack Russell terrier) PLL is associated with an inherited degeneration of the zonules, or the thin ligaments that suspend the lens in place behind the iris (the coloured part of the eye) and in front of the vitreous (a clear, gel-like substance). The genetic mutation has been characterised in a number of breeds, and a genetic test is available.
Lens luxation refers to the lens being in an abnormal position inside the eye. Clinical signs in the fox terrier are usually not seen until the dog is in middle age, and include a sudden onset of pain (squinting, tearing etc), redness, and cloudiness of the cornea.
The lens may partially or fully luxate into the front chamber of the eye, causing acute glaucoma (increased pressure within the eye). Sometimes the lens may fall backwards into the posterior (back) chamber of the eye, which may displace the vitreous forwards. This may then also lead to a blockage of drainage of fluid from the eye and a secondary glaucoma. Glaucoma (increased fluid pressure within the eye) is a common consequence of lens luxation, and can rapidly lead to blindness.
Lens luxation is a veterinary emergency, and if you notice the signs of PLL in your dog’s eye you should see your vet immediately. Diagnosis is by examination of the inside of the eye by a veterinarian, and possibly an ultrasound of the eye. Treatment of PLL is aimed at reducing the fluid pressure within the eye and preserving vision in acute cases, then removing the lens surgically. Blind eyes may be removed to treat pain. Genetic testing is available for the screening of breeding animals, so that two carriers (or any affected animals) are not bred. Although the disease is treated as a recessive one, carrier animals will also occasionally develop lens luxation.
Progressive retinal Atrophy, Rod-cone dysplasia 3 is an inherited eye disease affecting dogs. Progressive retinal atrophy, Rod-cone dysplasia 3 occurs as a result of degeneration of both rod and cone type Photoreceptor Cells of the Retina, which are important for vision in dim and bright light, respectively. Affected dogs have abnormal thinning and degeneration of the retina beginning around 4 weeks of age. Signs of progressive retinal atrophy including changes in reflectivity and appearance of a structure behind the retina called the Tapetum that can be observed on a veterinary eye exam by 6 to 16 weeks of age. Rod photoreceptor cells degenerate first resulting in loss of peripheral vision and night vision. As the disease progresses, cone photoreceptor cells also degenerate resulting in complete blindness. Most affected dogs are completely blind by 1 year of age, but some may retain limited sight until 3 to 4 years of age.
Progressive Retinal Atrophy, Progressive Rod-cone Degeneration (PRA-prcd) is a late onset, inherited eye disease. PRA-prcd occurs as a result of degeneration of both rod and cone type Photoreceptor Cells of the Retina, which are important for vision in dim and bright light, respectively. Evidence of retinal disease in affected dogs can first be seen on an Electroretinogram around 1.5 years of age for most breeds, but most affected dogs will not show signs of vision loss until 3 to 5 years of age or later. The rod type cells are affected first and affected dogs will initially have vision deficits in dim light (night blindness) and loss of peripheral vision. Over time affected dogs continue to lose night vision and begin to show visual deficits in bright light. Other signs of progressive retinal atrophy involve changes in reflectivity and appearance of a structure behind the retina called the Tapetum that can be observed on a veterinary eye exam. Although there is individual and breed variation in the age of onset and the rate of disease progression, the disease eventually progresses to complete blindness in most dogs. Other inherited disorders of the eye can appear similar to PRA-prcd.
Degenerative myelopathy is most commonly seen in the German Shepherd Dog, although other breeds are also predisposed, including the boxer, Cardigan and Pembroke Welsh Corgi, Siberian husky and the Rhodesian ridgeback. This disease is normally seen around middle age, and in general diagnosis can only be confirmed at post mortem examination. Breed surveys of some predisposed breeds indicate a fairly low occurrence rate, but most experts think this rate is actually much higher, due to the lack of post mortem follow up of the majority of suspected cases. Signs are due to the immune-mediated destruction of a part of the nerves in the spinal cord, leading to loss of these nerve fibres. The first sign is knuckling of the hind feet, and hind limb ataxia. Once the spinal cord damage progresses past this initial stage (termed proprioceptive deficits), the effectiveness (if any) of treatment is much diminished. Hence early diagnosis is vital. Following this initial stage, hind limb reflexes are affected, then weakness in the hind limbs develops, progressing to total paralysis. Once a dog shows these signs it will almost always respond poorly to therapy. Eventually destruction progresses from the middle of the spinal cord to the upper cord and brain stem, leading to forelimb weakness and eventually interference with the muscles of breathing, causing death. Most dogs are euthanased for humane reasons before this happens. Treatment is with specific supplements and drugs aimed at interfering with the immune destruction in the spinal cord, to slow further nerve damage. The effectiveness of this treatment is variable, but is only of benefit if started as early as possible. Once nerves are lost, they will not be replaced. Degenerative myelopathy cannot be cured. A DNA test is available for predisposed pure breeds to carry out screening of breeding animals.
Like other toy breeds, the Cresteds can be prone to patellar luxation.
This inheritable condition is caused by shallow knee joints (stifles) and results in kneecaps that pop out of place. Its onset is often at a young age, and can cause temporary to permanent lameness based on the severity. Breeders should have their stock certified free of patellar luxation. The Orthopedic Foundation of Animals (OFA) collects and disseminates the information concerning genetic and orthopedic diseases in dogs to establish a control to lower the incidence of these inherited diseases and works in conjunction with the Canine Eye Registration Foundation (CERF).
Legg-Perthe's Disease is a disabling ailment that causes deterioration and flattening of the hip joint. The disease develops when the animal is between 4 and 8 months old. Lameness can come on suddenly or else develop gradually over 6 to 8 weeks. During this period of time the muscles begin to atrophy, giving the impression that the dog has one limb shorter than the others. There also will be noticeable restricted movement in the animal's joints. When the leg muscles become weakened through atrophy, it slows down the animal's recovery.
Keratoconjunctivitis Sicca (dry eye) is just what it sounds like. It’s a dry eye with inflammation, a condition often mistaken for conjunctivitis, which also has a gooey yellow discharge. Diagnosis is done with a Schirmer Tear Test and treatment consists of drops and ointment.