Uveitis is an inﬂammatory process involving the middle of the three layers in the eye. To understand uveitis, it is important to know the basic anatomy of the eye. The outer layer enclosing the eye is composed of the clear cornea and the white sclera. The innermost layer is the nerve layer or the retina. The middle layer, which is rich in blood vessels, is the uveal tract. It is composed of the iris in the front part of the eye, the ciliary body, which produces the ﬂuid (aqueous humor) inside the eye, and the choroid, which nourishes the retina in the back of the eye. Because of its rich blood supply, the uveal tract is a natural target for diseases originating in other parts of the body. When inﬂammation attacks specific segments of the uveal tract, the disease is further classified as iritis (inﬂammation of the iris), cyclitis (inﬂammation of the ciliary body) or choroiditis (inﬂammation of the choroid), depending on the affected structure. If all the structures are inﬂamed then it is called panuveitis (inﬂammation of all uveal structures of the eye).
Uveitis may produce vague signs that can include excessive blinking, squinting, watery discharge and photophobia (sensitivity to light) without any obvious changes to the eye itself. In more advanced cases, changes to the eye are visible without special instruments. The eye may appear dull, cloudy or red due to changes in the cornea or due to inﬂammatory cells accumulating inside the eye. Uveitis is usually diagnosed following an examination of the ocular structures by your veterinarian or veterinary ophthalmologist utilizing instruments, which magnify and illuminate the uveal tract. Once uveitis is diagnosed, a general physical examination should be performed in case the uveitis is actually an early sign of internal or systemic disease. The evaluation may include blood profiles or specific tests if a certain disease is suspected. Ocular examination consists of a visual inspection of the interior of the eye with a slit lamp and the measurement of ocular pressure. If the internal structures of the eye cannot be clearly visualized, ocular ultrasound may be performed to more clearly visualize the position of the retina and lens and to detect any abnormal masses or growths within the eye.
Ocular pressure is maintained by the aqueous humor (ﬂuid) produced by the ciliary body within the eye. Initially, if the ciliary body is inﬂamed, the ﬂuid production slows down and the ocular pressure drops. The aqueous humor produced in the eye normally drains through the angle between the cornea and the iris. The inﬂammatory debris produced in uveitis can block the drainage angle and result in increased intraocular pressure (glaucoma) over time. Once uveitis resolves, glaucoma can remain if drainage structures were damaged by the inﬂammation. A recheck of the eyes following uveitis is important for this reason.
Additionally, disease processes such as uveitis can lead to corneal ulcers (superficial to deep), ocular infections, corneal scarring, corneal vascularization, corneal mineralization, cataract, lens luxation, retinal detachment and keratoconjunctivitis sicca. Uveitis also can lead to secondary complications similar to those to which treatment for uveitis can give rise as discussed under “Prognosis”.
Uveitis is associated with many different diseases. Examples in the dog include Ehrlichiosis and Coccidioidomycosis, two systemic infectious diseases common to the southwestern United States. In the cat, uveitis can be a consequence of Feline Leukemia Virus, Feline Infectious Peritonitis or many other diseases. In any animal, penetrating injuries such as cactus spines or a cat scratch may produce uveitis. Inﬂammation of the uveal tract can occur when the lens capsule is breached (such as following surgery, trauma, or injury of the lens) or in the presence of cataracts where lens proteins leak out of the lens capsule into the eye. Other possible causes of uveitis are local bacterial infection, immune-mediated, and parasitic diseases. Treatment can be more specific if the actual cause is known. It is important to test for some infectious diseases to make sure there is not an underlying cause for the inﬂammation, but unfortunately, in up to 75% of the cases, the cause is never determined.
Uveitis must be treated aggressively in order to prevent glaucoma, scarring of the uveal structures, and possibly blindness. Different medications may be used to treat the underlying, original cause of the uveitis and to attempt to control the inﬂammation itself. Aspirin (not aspirin substitutes) and corticosteroids minimize the inﬂammatory process. Corticosteroids may be administered by injection under the lid of the eye, by drops in the eye, or as an oral medication, depending on the suspected cause of uveitis. Topical use must be postponed if damage to the corneal surface is present because the corticosteroids prevent healing of the ulcer. If certain systemic diseases are suspected, oral corticosteroids may be postponed until test results become available. Atropine dilates the pupil and helps prevent scarring of the iris. This medication may be contraindicated; however if glaucoma is present as it may further decrease the drainage of aqueous humor from the eye. Oral and topical antibiotics are employed when a bacterial infection is present in the eye.
The treatment of uveitis requires therapy to halt the inﬂammation of the uveal tract along with a search for the original cause of the disease. Many tests may be needed to determine possible causes and the results are important for proper treatment.
Treatment for uveitis can involve life-long topical and/or oral medications. Life-long topical medications seldom give rise to complications, which occur in less than 5% of these cases. Nevertheless, potential complications include, but are not limited to, inﬂammation of the pink tissue (conjunctivitis); corneal ulcerations (superficial to deep); corneal scarring, vascularization, and mineralization; ocular rupture secondary to ulceration; worsened inﬂammation inside the eye, secondary to infection or ulceration; glaucoma, secondary to the uveitis; retinal detachment or degeneration, secondary to uveitis or infection; ocular or orbital pain, secondary to uveitis, glaucoma or infection; eyelid rubbing; bleeding inside the eye (hyphema), secondary to uveitis or infection; tearing (epiphora); and/ or lens luxation, secondary to uveitis, glaucoma or infection. Some of these complications can lead to blindness. Some oral medications used to treat these disease processes may cause changes in behavior, gastrointestinal upset (diarrhea, vomiting, decrease/increase in appetite/thirst), panting, decreased white blood cell counts (such as leukopenia), and various changes in chemistry values (liver, kidney, potassium, to name a few).
Your awareness of your pet’s symptoms and compliance with recommendations for recheck examinations and periodic blood work help control these potential complications.
Corneal dystrophy and corneal degeneration are diseases of the cornea characterized by white, opaque mineral (either cholesterol or calcium) deposits within the cornea (the clear front part of the eye). The size, shape, and density of the areas of mineral deposits vary. Although these affected areas can be highly visible, they rarely cause blindness.
Corneal dystrophy may be an inherited trait in several breeds, including the Shetland Sheepdog, Siberian Husky, Beagle, American Cocker Spaniel, Miniature Schnauzer, and Airedale Terrier. Corneal dystrophy affects both eyes and occurs in dogs of any age. It has been reported to occur in dogs with high levels of cholesterol or calcium in their blood. Routine blood work can be performed to evaluate for these possible changes.
Corneal degeneration can affect one or both eyes, and may occur in areas of the cornea that have suffered a traumatic incident or chronic disease process. It is not an uncommon finding at the center of the cornea in our geriatric patients.
Corneal dystrophy and corneal degeneration can lead to corneal ulcers (superficial to deep), ocular infections, and corneal scarring and vascularization arising from continuous sloughing of the mineral deposits. Severe cases can cause visual impairment.
Our goal in treating corneal dystrophy and corneal degeneration with topical medication is to improve the health of normal cells overlying the corneal minerals. We may also treat these diseases through dietary management (low-fat, high-fiber diets).
Some patients may be candidates for treatment with a topical acid treatment (TCA), which helps to dissolve the mineral. This treatment may be performed once or multiple times and is often effective in improving comfort, reducing the mineral and preventing further ulcers.
In cases of severe progression and discomfort, we can remove the mineral deposits through superficial keratectomy, a surgery in which the outer layer of the cornea and the mineral is removed; however, scar tissue may remain present instead of the mineral deposits. If a deep ulcer is found as a result of the degeneration, a grafting procedure may be necessary to allow the cornea to heal. Although most corneal dystrophy patients do not require surgical intervention, some pets will, and their owners should be aware of potential complications. Any surgical procedure can introduce complications, including potential anesthetic risks. Surgical procedures that involve the cornea seldom give rise to complications, which occur in less than five percent of these cases. Nevertheless, potential complications include, but are not limited to…
Some of these complications can lead to blindness.
The cornea is normally the transparent “windshield” of the eye, serving to protect the internal structures of the eye while allowing light to enter for vision. The endothelium is a single layer of cells that lines the inside of the cornea. Though only a single cell layer thick, this layer is vital in maintaining a clear cornea for functional vision. The cornea normally maintains its clarity through a number of factors, including a very regular arrangement of supportive ﬁbers and a relatively dehydrated state compared to other body tissues. If water is allowed to build up, the corneal ﬁber arrangement will be disrupted and the clarity of the cornea will be reduced.
Endothelial cells in domestic animals are not able to repair themselves. Therefore, if cells are lost, the remaining cells attempt to spread out to take the place of the lost cells. As long as the number of functional endothelial cells remains above a critical threshold number, they will be able to prevent a gap in this lining and successfully keep the cornea clear. If the number of cells falls below this threshold, or if the cells become unhealthy, they will no longer be able to keep the entire cornea dehydrated and clear. The result is a progressive blue cloudiness that develops across the cornea.
This situation can develop due to an inherited condition in certain breeds, such as Dachshunds, Chihuahuas and Boston Terriers. In these breeds, the condition is referred to as endothelial dystrophy. It can occur spontaneously in these dogs without an inciting cause.
Endothelial degeneration also occurs following death or damage to the endothelial cells as a secondary disease to many intraocular disorders. These can include severe inﬂammation (uveitis), elevated intraocular pressure (glaucoma) or mechanical damage due to a luxated lens.
Fluid accumulation within the cornea is not a painful condition by itself; however, this ﬂuid can sometimes cause the formation of small “water blisters” in the cornea called bullae. If these bullae reach the surface of the cornea and rupture, they will leave a painful corneal ulcer. These ulcers can heal quickly with appropriate medications but, if they become a recurrent problem, we may recommend a surgical procedure to help minimize bullae formation and heal the erosion.
This condition cannot be reversed with topical medications. However, treatment often begins with a topical hyperosmotic, non-irritating salt ointment, which may help to draw out the excess ﬂuid in the cornea. The amount of time that this ointment will be used depends on your pet’s individual situation. Other eye medications that may be used include anti-inﬂammatory drops to reduce inﬂammation inside of the eye (uveitis) that may be contributing to the loss of endothelial cells. Topical antibiotic drops should be used if corneal ulcers are found.
If corneal bullae and ulcer formation become a recurrent problem, we may recommend one of two procedures, “Laser Keratoplasty” or “Thermokeratoplasty”. These procedures are designed to use concentrated energy, or heat, to create a layer of scar tissue within the cornea. These procedures typically do not help improve the clarity of the cornea, but rather stimulate healing of corneal erosion. With fewer ulcers, your pet will be more comfortable and will require fewer eye drops.
Any surgical procedure can introduce complications, including potential anesthetic risks. Surgical procedures that involve the cornea seldom give rise to complications, occurring in less than 5% of cases. Nevertheless, potential complications include, but are not limited to:
•Inﬂammation of the conjunctiva (the pink tissue around the eye)
•Infections at the surgical site, which may extend to other internal and/or external areas of the eye (intraocular/extraocular infections)
•Corneal ulcerations (superﬁcial to deep holes in the thin cornea)
•Corneal scarring, vascularization, or mineralization
•Rupture of the eye, secondary to ulceration
•Inﬂammation inside the eye (uveitis)
Ehrlichiosis (also called “tick fever”) is an infectious disease seen across the continental U.S. and occurs with the most frequency in the southern states and desert states. Since systemic signs of this disease are often vague and mild in the early stages, ocular changes may be the first indication to test for Ehrlichiosis. Ocular manifestations include uveitis, retinal disease, and corneal opacities. Early detection, diagnosis, and treatment greatly increase chances for saving vision and even the life of a pet. Rhipicephalus sanguineus, the common brown dog tick, transmits ehrlichiosis to dogs. The disease is spread by a bite from an infected tick; in other words, direct contact between a healthy dog and an infected dog will not spread the disease. Canine ehrlichiosis does not cause disease in humans. Ticks may not always be present when the first signs of disease appear because of the long incubation period of eight to twenty days and the tick’s ability to transmit disease for many months after it becomes infected. Surprisingly, the majority of patients diagnosed do not have a history of tick infestation as it only takes one bite for transmission to occur. Ehrlichiosis may appear at any time during the year, not just tick season, due to the chronic nature of the disease, and because of this tick’s ability to survive indoors throughout the year.
History and clinical signs may be suggestive of ehrlichiosis while general blood tests may increase suspicion. Ehrlichiosis commonly causes changes in blood screening tests. Once suspected, ehrlichiosis can be diagnosed by sending a blood sample to a laboratory for specific testing. Diagnosis is important for treatment and prevention.
Symptoms of ehrlichiosis are often diverse, vague and can vary during the three different phases of the disease. The first phase, called the acute phase, occurs eight to twenty days following exposure. During this phase, mild signs including fever, nasal discharge, anorexia, lymph node enlargement, and breathing difficulty may occur. Unfortunately, these signs are not specific for ehrlichiosis. After one to two weeks, the pet recovers. The next phase, the subclinical phase, shows no signs and lasts up to four months. During this time, the pet may mount a sufficient immune response to rid itself of the disease. If not, the chronic phase begins. Signs during this phase can be severe and may include depression, weight loss, abdominal tenderness, and bleeding tendencies.
Signs of a poor ability to clot the blood include bleeding from the nose or gums, coughing up blood, or the formation of small bruises. This phase generally continues until a diagnosis can be made and treatment begun.
Treatment of ehrlichiosis depends on the severity of the disease at the time of detection. In severe cases, immediate supportive care may include blood transfusions and ﬂuid administration. To treat ocular diseases associated with ehrlichiosis, therapy may include corticosteroids. The ehrlichiosis organism is susceptible to many different antibiotics, but the current antibiotic of choice is doxycycline. This type of antibiotic is works quickly and is effective in most cases. German Shepherds, in particular, are more sensitive to this disease and may require more rigorous and long-term therapy. Once treatment ceases, prevention is important to lower the chances of reinfection. Discuss tick control options with your primary veterinarian.
Unfortunately, no effective vaccine exists to prevent ehrlichiosis. However, due to the life cycle of the brown dog tick, other methods of prevention can be employed. Unlike other ticks, which feed on many different kinds of hosts, the brown dog tick feeds only on dogs and survives mainly in areas where dogs live. This facilitates effective tick control. After treatment of ehrlichiosis, no lasting immunity develops. Tick control is often the best method to prevent reinfection; infected ticks may transmit the disease for five months or longer. Therefore, tick control in the environment and on the dog should be maintained on a regular basis.
Tick fever can be a chronic, debilitating, and even fatal disease if not treated. However, successful treatment of ehrlichiosis is common if the disease is detected early. Ocular disease may provide the first clue in the diagnosis of ehrlichiosis. Most ocular diseases associated with ehrlichiosis require aggressive and prompt therapy to prevent permanent damage. Once treatment is finished, prevention by control of the tick population will help to decrease the chance of reinfection so your pet can continue to lead a normal life.
Horner’s syndrome is a collection of clinical signs that are seen together and often have a limited number of causes. These particular clinical signs seen with Horner’s occur due to damage to the sympathetic nerve supply to the eye:
These symptoms are not painful though they may interfere with vision due to the third eyelid elevation.
The sympathetic nervous system is part of the autonomic nervous system that “automatically” controls a variety of bodily functions, including pupil size, without conscious effort. It also controls the fight or flight response. The sympathetic nerve supply to the eye originates at the base of the brain and has 3 sections. The first section of the nerve then travels down the neck within the spinal cord. The nerve exits the spinal cord in the area near the shoulders and then travels through the chest cavity. The second section of the nerve travels up the neck to the base of the skull. The third section of the nerve then takes an elaborate route through the skull where it is closely associated with the bone of the middle ear before finally reaching the orbit. Inside the orbit, it branches to innervate certain structures of the eye. Damage to this nerve anywhere along its path results in loss of sympathetic innervation leading to the characteristic signs listed above.
Damage can occur anywhere along the nerve pathway:
To try to determine the location of nerve damage, your veterinary ophthalmologist may apply eye drops that stimulate different sections of the nerve and monitor the response. This usually takes about 15 to 30 minutes. Determining the location of the damage is important because it may help to uncover the cause of the damage or other problems in that area. For example, patients with First order Horner’s syndrome may have a history of brain or spinal cord trauma. Studies also have demonstrated a correlation between endocrine diseases, like hypothyroidism or Cushing’s disease, in patients with Horner’s syndrome. Patients with Second order Horner’s syndrome might have thoracic disease, including tumors within the chest cavity or neck trauma. Third order Horner’s syndrome is the most commonly seen form in dogs and is most often associated with inner or middle ear disease. You may be referred back to your veterinarian for evaluation of systemic disease or a close examination of the ear canal. If the Horner’s is suspected to be First or Second order, the help of a veterinary neurologist may be recommended. Many times the location of damage cannot be determined without advanced imaging.
We can temporarily treat the symptoms of Horner’s syndrome with the eye drops used for diagnostic purposes. If your pet is having difficulty with vision due to Horner’s syndrome, your veterinary ophthalmologist may prescribe eye drops called sympathomimetics that mimic the sympathetic system supply. Also, an anti-inﬂammatory may be recommended to symptomatically treat conjunctivitis (inﬂammation of the pink tissue around the eye), if present.
While most patients with Horner’s syndrome do not warrant medical therapy for the eye, determining and treating the underlying cause of this syndrome can be important as some diseases are very serious and potentially life-threatening. Luckily, most patients have few complications from Horner’s syndrome and the signs clear up on their own in a few months.
Collies are prone to several inherited eye defects, including the following:
• Collie Eye Anomaly / Choroidal Hypoplasia (CEA/CH)
• Persistent Pupillary Membranes (PPM)
• Progressive Retinal Atrophy (PRA)
Collie eye anomaly is a disorder caused by incomplete development of the eye. The disorder is found in rough and smooth collies of all colors worldwide, as well as other similar breeds including Border Collies, Shetland Sheepdogs, and Australian Shepherds. This defect can manifest through underdevelopment of the choroid (choroidal hypoplasia), a defect of the optic nerve or adjacent areas (coloboma), an area of thinning in the sclera (staphyloma) and retinal detachment. While the severity of the anomaly ranges from no apparent visual defect to total blindness, most Collies with CEA do not demonstrate vision problems.
CEA is an autosomal recessive defect, which means that an animal must inherit one copy of the abnormal gene from each parent to be affected by this disorder. Affected dogs are termed homozygous dogs. If a normal Collie (no CEA genes) mates with a carrier dog (a heterozygous dog or a dog that has only one copy of the CEA gene) but shows no external signs of the disease the resulting puppies may also be unaffected but may pass the abnormal gene along to their respective litters. Carriers cannot be distinguished from normal dogs based on an ophthalmic examination alone, and should be genetically tested before they are bred.
In the past, an ophthalmic grading system was used to classify affected CEA eyes, with the highest grade (Grade 5) representing the most severe form:
Grade 1: Eye has tortuous retinal vessels with small areas of choroidal hypoplasia
Grade 2: Eye has tortuous retinal vessels and large areas of choroidal hypoplasia
Grade 3: Eye has tortuous retinal vessels and large areas of choroidal hypoplasia with colobomas or areas of ectasia (pits)
Grade 4: Eye has all of the above defects along with a retinal detachment
Grade 5: Eye has all of the above defects along with retinal hemorrhage
While it is possible for one eye to have a different grade than the other eye, both eyes are affected in almost all CEA cases. Originally the hope was that by breeding Collies with eyes that are only mildly affected it would minimize the potential of producing severely affected CEA offspring. Unfortunately, this was not the case. Collies with minor eye defects can and do produce severely affected offspring. In other words, for the purpose of genetic selection, a Collie that shows even the mildest effects of CEA is just as likely as a Collie suffering serious effects to produce offspring with severe CEA defects because even mildly affected dogs carry both copies of the abnormal CEA gene.
Some Collies start with a Grade 1 or Grade 2 as young puppies and then “go normal” as they mature. This means that over time normal pigment grows over the area of choroidal hypoplasia masking the defect so that the eye appears normal in later examinations. These animals are abnormal genetically and can set a breeding program back years. CEA in Collies that have “gone normal” cannot be detected in an eye exam after about 12 weeks of age.
While lesions stemming from CEA can be detected in puppies as early as five- to six-weeks old, we recommend evaluation at six to eight weeks of age. This age facilitates the exam and thus produces more accurate results. There is a genetic test available for CEA and more information is available on testing at www.optigen.com.
Persistent Pupillary Membranes are fine strands of mesodermal tissue (from the middle embryonic layer). In the embryo, the iris is initially formed as a solid sheet of tissue. Later in development, the sheet thins in the center to form a functional hole known as the pupil. Any abnormal remaining strands of this original tissue are described as Persistent Pupillary Membranes (PPMs).
It is not unusual to see such strands in six- to eight-week old puppies and unless the strands are extremely large, they are not typically a cause for concern. If pupillary membranes persist beyond this stage they are considered a defect. Persistent Pupillary Membranes can also form attachments between the cornea and the lens, resulting in permanent opacities and vision defects.
Progressive Retinal Atrophy (PRA) is a collective term used to describe a variety of inherited retinal diseases in dogs. Within this category of diseases is a syndrome called rod-cone dysplasia in the Collie. The rods and cones are the visual cells of the eye within the retina. Dysplasia is used to describe a condition in which tissue does not form correctly.
Collies that are clinically affected by rod-cone dysplasia exhibit night blindness as early as 12 weeks of age. This night blindness progresses to total blindness as early as one year of age. Changes can be seen in the appearance of the retina by six months of age.
Like CEA, rod-cone dysplasia is a recessive defect. Collies will inherit the disease when both of their parents carry the PRA gene. The eyes of carrier dogs appear normal and show no changes in vision and reveal no signs of the disease on ophthalmic examination. To date, no test other than test breeding has been devised to detect carriers in Collies but tests are available for certain other breeds. See information on testing on www.optigen.com.
Test breeding involves breeding a suspected carrier dog with a known affected dog. If the mating produces affected offspring then the suspicion is confirmed that the test dog carries the rod-cone dysplasia gene. Statistically, the more normal puppies produced by the mating the greater the assurance that the suspected dog is a non-carrier.
Keratoconjunctivitis sicca (KCS) results from inadequate aqueous tears. To understand the “dry eye” syndrome, it is necessary to understand the normal health of the cornea as it relates to the tear film. The cornea is the clear, outer windshield of the eye. Like all living tissues, it requires oxygen and nutrients to remain healthy. These are not supplied through blood vessels as in other parts of the body, but through the fluid inside the eye and the three-layered tear film on the surface. The outermost layer is an oily layer supplied by glands in the eyelids. The middle layer is the watery (aqueous) layer produced by the lacrimal glands that are located in the upper eyelid and in the third eyelid. This is the layer affected in KCS. The innermost layer of the tear film that is in direct contact with the cornea is a mucous layer produced by glands located in the conjunctival tissue around the eye. Keratoconjunctivitis sicca is due to dysfunction in the corneal tear film, and it results in patchy, dry areas across the corneal surface. In more advanced cases, widespread and severe corneal drying can occur and lead to permanent damage. The dried cornea, deprived of oxygen and nutrients through the tear film, rapidly undergoes destructive changes. Additionally, the mucous layer tries to make up for the lack of watery tears and an accumulation of mucus can be present on the surface of the cornea. Mucus can provide an excellent home for bacteria, which can lead to ocular infections. Corneal drying can lead to significant patient discomfort, corneal vascularization, corneal pigmentation, corneal scarring, corneal mineralization, corneal ulcers and even corneal rupture.
Diagnosis is based on history, clinical signs and a number of diagnostic procedures. The most important test is the Schirmer Tear Testing (STT), which measures watery tear production. This involves placing a soft strip of paper in your pet’s lower eyelid for 1 minute. Also, fluorescein stain (a bright green stain) is used to define breaks in the corneal surface and to assess the rate of tear film breakup. Sometimes Rose Bengal Stain (a reddish pink stain) may be used to evaluate the health of the outer layer of the cornea called the epithelium. Cytology and/or culture may also be recommended to quantify the health of the conjunctival cells and look for infectious organisms.
A number of causes have been documented to play a role in the development of KCS. These include diabetes, hypothyroidism, infections of the eye and lacrimal glands (e.g.: canine distemper virus), neurologic conditions, birth defects, and immune-mediated disease that negatively impacts the tear secreting glands. Immune-mediated KCS is the most common form in the canine patient. The forms of KCS associated with systemic disease, such as low thyroid hormone, require treatment of the underlying condition, in addition to eye-specific treatments, and may require some routine blood work for diagnosis.
Another cause of keratoconjunctivitis sicca is a toxic effect produced by some sulfa-containing antibiotics and non-steroidal anti-inﬂammatory drugs. Because some of these drugs may be necessary for the treatment of other diseases, it may not be possible to change the patient’s medications. It is very important that you tell your veterinary ophthalmologist about all medications and supplements that your pet currently takes – as well as medications take in the few months before the problem began.
There are several areas to address when treating keratoconjunctivitis sicca. A primary goal is to reduce the overgrowth of bacteria commonly associated with the dry eye syndrome. Topical anti-inﬂammatories are indicated when corneal staining shows no ulceration. This medication helps reduce inﬂammation of the conjunctival and corneal surfaces and reduces the long-term scarring effects. Corticosteroids cannot be used in the face of ulcers because they may decrease healing and increase the spread of infection. Artificial tear preparations are often indicated to supplement the deficient tear film and make your pet more comfortable. In addition to drops or gel preparations, artificial tear ointments are sometimes used to provide prolonged corneal contact overnight and during times when the patient cannot be treated frequently.
The most important medications for immune-mediated KCS are the immunomodulating agents such as cyclosporine (Optimmune) and tacrolimus. These medications reduce inflammation and stimulate a patients’ own lacrimal glands to produce tears. This is important because artificial tears do not contain the nutrients and enzymes that are present in natural tears. The good news is that these medications work in about 80 to 90% of dogs with maximal tear production occurring in 4 to 6 weeks. The bad news is that these medications must be given lifelong to control the dry eye symptoms. We will work to minimize the frequency of medication but many patients require daily treatment. Life- long topical medications seldom give rise to complications, which occur in less than 5% of these cases. Complications of cyclosporine and tacrolimus are typically limited to inﬂammation of the pink tissue (conjunctivitis) as a result of a local allergic reaction to the medication or the preservatives in the formulation. Some newer studies have tried to draw a link between the use of these medications and some cancers. It is unclear, however, whether the medication, the underlying dry eye disease, or some other cause in the cases where neoplastic changes have occurred. Most often the reports are in patients (usually humans) that take the medications by mouth – particularly after organ transplants. Regardless the cause, this is an extremely rare side effect with topical use of these medications. Please do not hesitate to discuss this with the veterinarian, if you have any other concerns.
Your awareness of your pet’s symptoms and compliance with recommendations for medication and recheck examinations will greatly help control the disease and improve your pet’s outcome.
Most patients with keratoconjunctivitis sicca do well if medications are administered on a timely basis. In cases where medicines cannot be given regularly or where medications are not effective, surgical techniques, such as a parotid duct transposition or others may be recommended. Any surgical procedures carry a risk of complication, including potential anesthetic risks, breakdown of the tissue or suture (wound dehiscence), obstruction or deterioration of the salivary gland or duct, salivary stone formation, facial nerve damage, infections at the surgical site, severe periocular wetting, corneal ulcerations, corneal scarring or vascularization, and others. Some of these complications can lead to blindness.
The lens of the eye sits behind the colored iris; its job is to bend light rays to produce a sharply focused image upon the retina. New lens fibers are constantly being formed by cells in the outer portion of the lens called the lens capsule. As new lens fibers are formed, older fibers cannot exit the lens capsule so get pushed toward the lens center. Unfortunately with time and aging, this process turns the crystal-clear lens cloudy due to the compressed fibers. This process is called lenticular or nuclear sclerosis.
Lenticular sclerosis is simply a hardening and thickening of the lens fibers. The lens becomes blue-gray, and the pupil appears cloudy. Occasionally owners will think the cloudiness comes and goes, but this is more likely due to alterations in the size of the pupil based on lighting conditions – rather than any actual change in cloudiness. In other words, the lens stays cloudy but a larger pupil diameter allows you to see more of the hazy lens color. Lenticular sclerosis does not cause blindness though in advanced cases depth perception and near vision may be less accurate.
Animals usually retain enough vision to function well within a familiar environment. No treatment is required unless a true cataract (opacification of the lens) forms, in addition to lenticular sclerosis.
Ocular Melanosis is an eye condition that most commonly affects Cairn Terriers, though it has been reported occasionally in other breeds such as the Boxer. It is also called Pigmentary Glaucoma because this condition often results in glaucoma (which is a high pressure in the eye that can cause discomfort and blindness). Ocular Melanosis is inherited, although the specific genes and mode of inheritance is not completely understood. The condition causes pigmented (i.e. brown) cells to accumulate in the eye and eventually block the drains that are responsible for removing fluid from the eye. These “clogged” drains will cause the pressure inside the eye to increase. The high pressure in the eye will damage the retina (the layer in the back of the eye that senses light) and the optic nerve (the nerve that sends the signal from the retina to the brain). Dark pigment may also be deposited on the sclera (white part of the eye).
Unfortunately, despite ongoing research, there is currently no cure for this condition. Treatment is aimed at controlling inflammation with topical anti-inflammatory medications. Dogs with Ocular Melanosis typically require routine eye exams and intraocular pressure monitoring. If intraocular pressures start to increase, then anti-glaucoma medications can be initiated in an attempt to decrease the pressure. Unfortunately, glaucoma surgeries to preserve vision, such as ECP (endocyclophotocoagulation), have a very low success rate with this condition. In the event that the glaucoma is no longer responsive to anti-glaucoma therapy, alternative surgeries, such as eye removal, may be necessary to ensure long-term comfort.Less Info
Pannus, or chronic superficial keratitis, is a progressive inﬂammatory autoimmune disease of the cornea. Common clinical signs include pigmentation (brown discoloration), vascularization (blood vessel in-growth) and opacification (haziness) of the cornea. These corneal changes may lead to scarring and may progress to severe visual impairment or blindness in severe cases. Active disease may also result in discomfort.
The definitive cause of pannus is not known, but several factors may be involved:
The cardinal sign of pannus is vascular or pigment infiltration into the clear cornea, causing whitish, pink or brown discoloration. This typically starts at the outside edge of the clear cornea nearest to the ear and extends inward. The blood vessel in-growth and pigmentation of the cornea may progress across the entire corneal surface and if left untreated, may result in blindness.
A diagnosis of pannus is usually made on the basis of characteristic clinical signs but sometimes additional diagnostics, including cytology and bloodwork, are recommended.
Despite intensive research efforts, no permanent cure exists. The good news is that the vast majority of cases can be managed with topical medications that halt the disease progress and reverse corneal damage. This condition does, however, require lifelong treatment with the best outcomes seen when therapy is instituted early in the course of the disease. The inﬂammatory cell infiltrations and the vessel invasion usually are reversible with therapy. On occasion, the scarring and pigment depositions are not irreversible but they can often be minimized with regular treatment. Even short periods of interrupted therapy, for example 2 to 4 weeks, may cause severe recurrence with profound effects on your dog’s vision.
There are three categories of therapy:
Your awareness of your pet’s symptoms and compliance with recommendations for medication and recheck examinations help control these potential complications.
Pigmentary uveitis, or Golden Retriever Uveitis (GRU), is a disease primarily seen in the Golden Retriever breed and does not appear to be associated with any systemic disease or infection. While this disease is presumed to be inherited, the cause remains unknown.
Uveitis is inﬂammation of the uveal tract, which is composed of the iris, ciliary body, and choroid (the vascular components inside the eye). The iris is the colored part of the eye, which is brown in most dogs, including Golden Retrievers. The ciliary body is the structure behind the iris that produces ﬂuid in the eye. The choroid is a membrane of blood vessels that line the back of the eye and nourish the retina.
GRU is typically a bilateral progressive disease, however, only one eye can be affected initially. Early in the disease process, inﬂammation in the eye is usually very subtle and may not be evident by casual observation. Symptoms of uveitis include: squinting, increased tearing or discharge, redness, photophobia (light sensitivity), and cloudiness of the eye or eyes.
Pigmentation of the lens capsule in a radial or “spoke wheel” pattern is considered a hallmark of this disease. The iris can also become heavily pigmented and appear dark brown to black in color. Darkly pigmented iris cysts within the eye can be observed as an early sign of GRU. Iris cysts are small ﬂuid- filled structures, which are either attached to the iris, ciliary body, or free ﬂoating inside the eye. These changes in the eye tend to get worse over time and can lead to cataract formation, glaucoma (high eye) and blindness.
Treatment for GRU is aimed at reducing inﬂammation in the eye and preventing or delaying the onset of glaucoma. The treatment protocol will vary for each individual patient, but may include an anti-inﬂammatory eye drop, an oral anti-inﬂammatory, an oral immunosuppressant and/ or medication to delay the onset or treat glaucoma. Routine blood work may be advised if systemic medications are being used in order to monitor for any side effects.
GRU is a chronic concern that will require long-term treatment. In some cases, inﬂammation is mild and easy to control, but many affected dogs eventually develop glaucoma. Glaucoma, which is painful and blinding, has been found to develop in 46 percent of dogs with Golden Retriever Uveitis. Long-term treatment and management are imperative in helping keep a comfortable, visual eye.
To better understand progressive retinal atrophy, one must have a basic understanding of the function of the retina. The retina is a highly specialized tissue that lines the back of the eye. The retina is analogous to film in a camera; it is responsible for integrating light into vision. Without adequate retinal function, vision is not possible. Simplified, the eye can be thought of as a light-collecting organ that focuses light rays on the retina. As light strikes the retina, a sequence of chemical reactions are initiated, propagating an electrical impulse. The impulse passes through the layers of the retina to the optic nerve and finally to the brain (visual cortex) for interpretation. The brain’s interpretation of the light signal is responsible for what we know as vision.
The retinal cells, which transform light energy to chemical energy, are known as rods and cones. Rods are responsible for black and white vision, night vision and vision for movements, whereas cone cells are used for color discrimination, vision in bright light and acute focal vision. Most domestic animals (dogs, cats, etc.) have a dominance of rods. Color vision in dogs is poor compared to people.
As the name progressive retinal atrophy (or PRA) implies, an atrophy or a degeneration of retinal tissue occurs. Progression of this disease occurs slowly and the early signs may be overlooked in many animals. The slow loss of sight is similar to a dimming switch to reduce brightness of light in a room. If light is slowly reduced over a long period of time, our eyes adapt and the change is not noticed until darkness occurs. A similar situation occurs in progressive retinal atrophy in animals; often the condition is not noticed until the condition is significantly progressed. Unfortunately, there is no cure available for progressive retinal atrophy. Identification of affected breeding animals is essential to prevent the spread of the condition within the breed.
The early signs of retinal atrophy include night blindness in most cases, which will frequently progress to day blindness. Night blindness may be manifested in a number of ways, including a pet that is hesitant or afraid to go out in the dark or go into a dark room. Often these pets will get lost in their own home after the lights have been turned off or they may stay near the light in the backyard at night versus wandering the full extent of the yard as they did previously. Pupils may be dilated and/or have a slow response to light. Some pet owners will notice a characteristic eyeshine. This is due to increased reﬂectivity of an iridescent tissue known as the tapetum located underneath the retina. As previously mentioned, retinal abnormalities may not be noticed at home until later in the course of the disease. Other well-developed senses including olfaction (the sense of smell) and hearing help animals adapt to the slow loss of sight. Often sight loss is not noticed until a change of the pets’ normal environment occurs. Examples of environmental changes include furniture rearrangement in the home; an animal that is restricted to a different area of your house or is boarded while you are away on vacation, etc. Because PRA can be difficult to identify, routine ophthalmic examination of all pets is recommended. This is especially important in animals that are being considered for breeding.
When the ophthalmologist views the retina with an instrument called an indirect ophthalmoscope, changes can be seen in the retinal blood vessel pattern, the optic nerve and the tapetum (the reﬂective portion of the eye that is responsible for “eyeshine”). However, some breeds characteristically have little or no early visible changes and may appear normal until the later stages of the disease. Some affected dogs show various rates of progression making generalization difficult.
Cataracts may form secondarily to progressive retinal atrophy in some animals and are generally associated with the later stages of the disease process. Formation of cataracts may interfere with direct visualization of the retina and make other diagnostic modalities essential. Although cataracts are surgically treatable, removal of cataracts in an animal with progressive retinal atrophy is not indicated, as their diseased retina will still result in visual deficits. Cataracts can leak protein within the eye causing inflammation within the eye. Uncontrolled or chronic inflammation can lead to glaucoma (increased intraocular pressure), a painful and blinding disease. Therefore, the retina (and cataracts) should be monitored as they may require topical medications to prevent inﬂammation or glaucoma.
Definitive diagnosis of PRA is supported by electroretinography. An electroretinogram “(ERG)” is similar to an electrocardiogram (ECG) for the heart in that they both measure normal electrical impulses produced by the organ of interest. A special contact lens is placed on the cornea and two tiny needles (electrodes) are placed under the skin around the eye. After a period of dark adaptation, ﬂashing lights are used to stimulate the retina. The electrical response of the retina is recorded by the electrodes, which send a signal to a computer. A healthy retina will produce a characteristic wave pattern on the electroretinograph recording. This instrument is sensitive enough to diagnose affected dogs before they begin to demonstrate clinical signs.
Any diagnostic procedure can introduce complications, including anesthetic risks (in the few patients that require anesthesia for diagnostic procedures). In order to obtain accurate ERG recordings, the veterinary ophthalmologist may recommend sedation or anesthesia. Complications from ERG are very rare, and include, but are not limited to, inﬂammation of the pink tissue (conjunctivitis); ocular infections that may affect internal and/or external areas of the eye (intraocular/ extraocular infections) and corneal ulcerations (superficial to deep). If any abnormalities are noticed in your dog’s eyes following an ERG please notify us immediately so that the condition does not worsen.
Since PRA is an inherited genetic disease, it is possible to identify and test for the defective gene. This test has been developed in some breeds affected by PRA. The test requires a blood sample, which is sent to a diagnostic lab for analysis. The blood test can identify dogs that are affected, as well as normal dogs that may pass the defective gene to offspring. Information on genetic testing can be found at www.optigen.com. A partial list of breeds affected with progressive retinal atrophy follows:
Unfortunately, no treatment has been formulated to prevent, treat or cure progressive retinal atrophy. A number of vitamin therapies have been suggested, however, there is no evidence to suggest that vitamins have any therapeutic effect. As stated previously, affected animals should be identified as early as possible and eliminated from breeding programs.
Progressive retinal atrophy is a painless condition. Animals that lose sight from PRA usually acclimate well to their environment with time, as they utilize their other senses to make up for their vision loss. Maintaining a consistent environment for the affected animals will help the acclimation process. For example, frequent furniture rearrangement during this period should be avoided. When animals are taken from their home environment, the use of leads and harnesses are helpful in addition to reassurance to comfort your pet.
Progressive retinal atrophy refers to a broad category of inherited retinal diseases that result in gradual blindness. Because of the insidious nature of the disease, serial examinations may be required to detect affected individuals. Affected individuals should not be used for breeding purposes.
Sudden Acquired Retinal Degeneration Syndrome (SARDS) is characterized by sudden vision loss in the dog. As the name implies, this disease affects the retina, which is the back part of the eye responsible for sending visual signals to the brain for interpretation. Due to an unknown cause, SARDS patients suddenly lose retinal function and become blind. There is subsequent degeneration or atrophy of the retina that can lead to other complications. In addition to a sudden loss of vision, many owners notice enlarged pupils, as well as, increased appetite and thirst.
In all patients with acute vision loss, an electroretinogram (ERG) is recommended. This test allows for assessment of retinal function, and if the result is negative, it provides a definitive diagnosis of SARDS. An electroretinogram is a non-invasive test that involves placing a specialized contact lens on the surface of eyes that have been numbed with topical anesthetic drops. Some pets require tranquilization or light sedation to reduce movement that can affect the results. After a period of dark adaptation, a standardized series of light flashes are created to stimulate the photoreceptors of the retina. The photoreceptors create an electrical signal that is detected by the contact lens and recorded by a computer. A normal retina produces a waveform, much like an EKG for the heart. In a SARDS patient, the normal electronic responses of the retina are extinguished and no waveform can be detected. In the early stage of the disease, the retina appears normal on ophthalmic examination. After a period of months, signs of degeneration of the retina can be observed on ophthalmic examination.
This syndrome most often occurs in middle-aged female spayed adult dogs No breed is known to inherit the condition, but some breeds appear to be more susceptible than others – including dachshunds and miniature schnauzers. Affected animals are generally in good health, but as described above, some dogs may have a recent history of unexplained weight gain, lethargy, pacing, panting, increased appetite, increased consumption of water and/or increased urination. Blood work is recommended to rule out any systemic problems, such as a condition called Cushing’s that is characterized by high blood cortisol. If affected dogs have systemic problems, an internal medicine consultation may be recommended. The etiology, or underlying cause, of SARDS is currently unknown; however, multiple laboratories are conducting research to find the cause. Possible theories for this syndrome include endocrine disorders, autoimmune disease, toxicity, infection, neoplasia, etc.
Unfortunately, there is currently no proven treatment or prevention for SARDS and the blindness it causes is irreversible. The good news is that SARDS is not a painful condition and that it does not reduce your dog’s life expectancy. Many dogs adjust very well to being blind. It may take a few weeks to months for your dog to fully acclimate, but a recent publication reported that owners of dogs with SARDS find their pets to have a very good quality of life. Animals should also be monitored long-term complications, such as secondary cataract formation or glaucoma that can be painful. If signs of these conditions are seen, prophylactic medical therapy may be required. Safety precautions should be taken for all visually-impaired pets, particularly around swimming pools, stairs, roads, strange dogs, etc. There are many resources for owners with blind pets to help the owners adjust to living with blind dogs, as this condition can sometimes be more difficult for the owners than their dogs.
The Merle gene is responsible for a wide variety of beautiful coat and iris colors in the dog. This dilution gene acts to lighten the coat color. The dappling effect it creates is not evenly spread; rather, it is responsible for spotting of the coat and variations of the iris or colored part of the eye. A combination of colors may be found in one or both eyes. Colors expressed may range from a pale, light blue to greenish to amber. Unfortunately, the same gene that is responsible for the desirable coat and eye appearance is often responsible for many developmental eye defects. Breeds that have been identified as having the Merle gene include the Australian Shepherd, Rough and Smooth Collies, Shetland Sheepdog, Dachshund, Great Dane, Old English Sheepdog, American Foxhound and the Catahoula Leopard dog among others.
With respect to ocular effects, the Merle gene’s most minor manifestation is a blue iris (or irides). The blue appearance may also be as an ‘inclusion’ or as a partial segment of another wise brown eye (heterochromia iridis). A blue iris does not absolutely indicate the presence of the Merle gene; it may also be expressed in dogs carrying the piebald gene, such as the Dalmatian. There is no adverse consequence of the presence of the blue iris alone. Conversely, the other effects of the Merle gene may result in devastating blindness. The abnormalities affect either the front or back part of the eye or a combination of both. When the whole eye is affected, the condition has been referred to as Merle Ocular Dysgenesis.
Since it is understood that multiple congenital ocular abnormalities in the dog may be inherited, a brief review of basic genetics is in order. In any dog, two copies of a gene are present, one from each parent. For the purpose of this discussion, the Merle gene will be termed “m” and the non-merle gene will be called “M”. If both copies are the same for Merle, they are termed homozygous (mm) or a double merle. A double Merle will be a predominantly white dog. If one copy is Merle and one is not, they are called heterozygous (Mm). One Merle gene copy is dominant over the non-Merle gene in that just one copy (Mm) will produce dilution of the coat and potentially different colored eyes, which is considered desirable in many breeds. A dog that is homozygous for non-merle (MM) is a normal, full-colored dog. In the Australian Shepherd dog, multiple ocular abnormalities due to the Merle gene occur secondarily to an autosomal recessive trait. Autosomal implies that this is not a sex-linked condition. Since a recessive trait is expressed only when homozygous, this means that affected dogs must be a double Merle (mm). Double merle animals may also have varying degrees of congenital deafness. The most severe abnormalities occur in homozygous merles with an excessive white hair coat involving the head region.
There are other, more serious ocular problems associated with the Merle gene. Microphthalmia is a congenital defect characterized by a small eye. Severely affected dogs may be blind at birth. Iris changes include thinning of the iris (iris hypoplasia) and possibly an eccentric or off-centered pupil, known as corectopia. An iris coloboma is an abnormality in the development of the iris that usually presents as a notch or cleft of the iris at the edge of the pupil. Another problem that occurs with the iris may be persistent pupillary membranes or PPMs. Pupillary membranes are present in the developing eye in utero but normally regress within the first few weeks of life. When persistent, they represent a congenital defect from blood vessel remnants that fail to regress.
They may appear as strands or sheets of tissue that originate from the iris and attach to another part of the iris, the lens, or the cornea. They range from being of minor significance to causing severe vision impairment. A cataract, or an opacity, of the crystalline lens or its capsule, is yet another possible heritable defect associated with the Merle gene. It may be found independently or in a microphthalmic eye. Cataracts, if focal, may only cause minor impairment of vision, but when cataracts are complete, blindness occurs.
The posterior segment (the back part of the eye) may also be affected. Colobomas, or notch defects, may affect the sclera or the white of the eye. A scleral coloboma indicates the presence of an abnormally thin region of sclera; this condition is known as scleral ectasia. When this occurs the vascular layer bulges out beneath the fibrous coat of the eye. This is known as a staphyloma. These may occur in the front half of the eye, apparent as a bulge underneath the eyelid or they may be in the back of the eye, only visualized using special instrumentation. Choroidal hypoplasia or choriodal colobomas may also be seen. In this condition, the vascular layer at the back of the eye develops incompletely. Posterior segment anomalies may also affect the optic nerve. The optic nerve’s job is transmission of information from the retina to the brain for the interpretation of vision. When a defect at this level of the eye is minor, a patient remains visual; alternatively, a more serious defect of the optic nerve may be the cause of complete blindness.
In addition to the optic nerve, the retina may also be affected negatively. Retinal dysplasia is abnormal development of the sensory retina with focal folds or widespread geographic maldevelopment. This may occur in conjunction with retinal detachment. If the retina becomes completely detached, blindness ensues. In some dogs with a Merle coat, the tapetum or reﬂective layer at the back of the eye is missing. These dogs may have somewhat poorer night vision compared to an eye with a tapetum, but there is no obvious functional abnormality with these dogs.
With an array of problems that may have a common end result of blindness, informed breeders will not breed affected animals because those with ‘mild disease’ may still produce severely affected offspring. It is also understood not to breed merle to merle as this will increase the chances for double merles in the litter. As such, it is advisable to include more ‘solids’ or darkly-colored animals in a breeding program. It is always ideal to have breeding animals evaluated by a veterinary ophthalmologist to rule out structural abnormalities of the eyes. This can be accomplished via an OFA Eye certification exam, formerly known as a CERF exam. The OFA is an organization that tracks heritable diseases in many parts of the body including eyes in dogs with the goal of identifying and eliminating genetic conditions. The certification exam can only be performed by a board-certified veterinary ophthalmologist. A certification exam is valid for one year. Ideally, dogs should be certified every year by a veterinary ophthalmologist to ensure that conditions that may be progressive or develop later in life have not appeared. These exams do not guarantee that the dog is not a carrier of genetic ocular disease; rather, a passing test proves that at that time of exam no genetic ocular disease was diagnosed. If a dog’s status is unknown, it is strongly recommended not to breed. With respect to the Merle gene and ocular dysgenesis, these abnormalities are congenital, which means they are present at birth. They do not show up later in life; therefore, they may be diagnosed in a puppy as young as six weeks old.