Blastomycosis is a fungal infection caused by the fungus Blastomyces dermatitidis. This fungus is commonly found in the river valleys of Tennessee, St. Lawrence, Ohio, Mississippi, and Missouri, as well as, the southern Mid-Atlantic States.
Exposure to this organism usually occurs within areas close to water ways and in areas where the ground has recently been disturbed. This fungus lives in the soil and soil disruption causes aerosolization of the fungal spores that are then inhaled. Inhalation is the primary route of infection. This disease cannot be transmitted directly from your pet to you; however, you live in the same environment as your pet, so you can also be exposed to the organism. . You should seek out the advice of a physician if any symptoms develop.
Once inhaled, the spores of the fungus can spread to other parts of the body. Where the spores end up will determine the clinical signs. Some signs you may notice in your pet include the following:
Eyes: Redness, discharge, swelling, squinting, elevation of the third eyelid, and blindness. Blasto can cause inflammation inside of the eye as well, leading to retinal detachment and glaucoma (see glaucoma handout). Oftentimes, ocular disease is the only sign of infection with Blastomyces. Fifty percent of infected dogs with ocular lesions will have evidence of disease in both eyes.
Skin: Draining or crusting skin lesions that are slow to heal.
Respiratory System: Coughing or increased breathing effort or rapid breathing.
Other: Decreased appetite, weight loss, fever, lameness, enlargement of lymph nodes and changes in mentation (neurologic abnormalities), which are more often observed in cats.
Notice many of these are fairly nonspecific signs and may result from many different disease processes, so an evaluation by your veterinarian is important.
Dogs are at high risk of infection: about 10 times more susceptible than humans and 100 times more susceptible than cats. The typical Blastomycosis patient is a large breed, male dog that spends a lot of time outdoors.
On average, it can take 5-12 weeks from the time of infection to the development of clinical signs (incubation time).
Depending on the clinical signs your pet is showing, your doctor may recommend certain tests. Blood, urine and skin lesion samples are commonly obtained. Sometimes a sample may be directly taken from the eye.
Your doctor may recommend chest radiographs (x-rays) because lung lesions can be present without any other clinical signs. If lung lesions are present, their resolution can be used to determine how long treatment will be necessary.
The treatment of choice is the oral antifungal Itraconazole. Depending on the severity of clinical signs, your doctor may recommend treatment for up to 9 months. While Itraconazole is a very safe drug, side effects may include liver disease and gastrointestinal upset. For these reasons, we recommend regular blood work to monitor for any side effects that may require changes to medication. Appropriate treatment for the eyes often includes anti-inflammatory eye drops, as well as, anti-glaucoma medications. Other oral medications and injections may also be recommended. Depending on the severity of clinical signs and inflammation within the eye, medical therapy may not be successful in keeping your pet visual and/or comfortable. At that point, surgical therapy may be required; if this is the case, your doctor will explain the options available for your pet. General supportive care may be necessary. Your doctor will work together with your referring veterinarian to make sure your pet is getting complete appropriate treatment.
Although some dogs lose their vision due to this infection, most recover from Blastomycosis and live healthy and happy lives following treatment. Most dogs do not have a recurrence of the disease, but re-infection is possible, which is why it is very important to monitor for return of any of the above clinical signs. If you see any, see your veterinarian as soon as possible. Although very rare, some dogs do not survive infection with Blastomyces.
While it is impossible to prevent Blastomycosis, being aware of your environment and knowing what clinical signs to look for are important. Be mindful of when and where you hike with your dog, especially near waterways and areas of significant ground disturbance, as is common with construction sites. Even superficial digging of the ground by your dog can release infectious spores into the air. Become familiar with the clinical signs mentioned above and talk to your doctor. If you are ever in doubt, do not hesitate to ask.
Blepharitis is an inflammation of the eyelids and may also include inflammation of the tiny glands of the eyelid margin called the meibomian glands. There are many causes but, one of the most common we see is immune-mediated and may require long-term management especially if underlying allergies are involved. We also see blepharitis occur spontaneously and your pet may just have one incidence although treatment may take weeks to months. Other cases may require a biopsy in order to determine the cause.
Tiny eyelid glands produce olive oil-like fat needed to delay evaporation of the water in tears. When this fat is gone due to clogging of the glands or the fat changes to a toothpaste-like consistency, evaporation of the watery tears occurs too quickly. The tear film protecting the cornea breaks apart into dry, unprotected spots; the cornea feels dry, so excessive tearing and scar tissue may form.
Blepharitis may be very itchy and, just like a child scratching at a mosquito bite; this can make the inflammation worse. We need to try to stop your pet from doing this. An Elizabethan collar may be needed in the first few days of therapy.
Treating blepharitis may be approached in different ways:
1.Warm compresses may help in the first week to loosen up the clogged glands and clean away debris. Warm tap water on a face cloth can be applied to each eye for 5 minutes twice a day. Keeping the eyelids clean is essential in decreasing mucous buildup and associated bacteria.
2. Topical antibiotics may be used to decrease the bacteria on the eyelid margin. Ointment formulations may be prescribed in that they help to stabilize the water in the tear film by decreasing evaporation.
3. Antibiotics by mouth may also be prescribed. These should be taken with food. At times, these may be given for several weeks and in some cases several months. Doxycycline or Cephalexin are commonly used antibiotics but, others may be employed. Please let us know if your pet is vomiting or shows any signs of gagging while taking these medications.
4. In very inflamed cases, a steroidal anti-inflammatory may be used to decrease severe swelling.
5. No blowing air. Keep your pet away from heating or air conditioning vents and DO NOT let them stick their head out the car window. Grooming should be performed without the aid of blow dryers
6. Keep your pet’s hair around the eyes trimmed short.
Hang in there! Even in people with blepharitis, treatment may take a while.
A variety of cacti thrive in Arizona. The most common are the prickly pear, cholla, saguaro, hedgehog cactus, barrel cactus and button cactus. In addition to the large obvious spines, many of these species have tiny translucent spines called ‘glochids’ that easily embed into tissue. These spines covering local cacti, especially the prickly pear and cholla, are a frequent source of injury to the eyes of dogs and cats.
At Eye Care for Animals, we treat many patients who present with spines impaled in or around the eye. These spines can even penetrate the eye and damage intraocular tissue, such as the iris or lens. Whether the injury is on the surface or deep within the eye, cactus injuries require treatment. Without proper treatment, complications can be vision-threatening or even eye-threatening.
Our goal in treating cactus-related eye injuries is to ensure the health of our patients’ eyes and promote ocular comfort.
Cactus spines embedded in conjunctival and corneal surfaces cause severe irritation and damage to surrounding ocular tissue; thus, these spines must be removed. Some spines can be removed with topical anesthesia, but more often general anesthesia and an operating microscope are required. If the spine leaves a large defect in the cornea, reconstructive surgery or direct suturing of the corneal tissue may be necessary to close the wound. This is often the case with spines that pierce through the entire cornea. Spines that damage the lens can cause cataract and inflammation, which may require more extensive intraocular surgery.
Whether surgery is required or not can only be determined with an ophthalmic examination. Additionally, all cactus-related eye injuries are at risk of infection – either bacterial, fungal or both. Topical and oral medications may be required to control infection, inflammation, and pain involved in this type of injury. And yes – your pet will likely have to wear a cone for at least a short amount of time, but the good news is that these type of eye injuries often heal with minimal complications.
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.
A cataract is an opacity of the lens that prevents light from reaching the retina, which means cataracts lead to vision impairment. Cataracts can develop in one or both eyes and have a variety of causes.
A cataract can take on a variety of appearances. Most owners note a cloudy or white to blue appearance to the eye. The cataract might start as small dots or white lines that progress to include larger areas of the lens or the eye may appear to turn cloudy overnight. The rate of progression is difficult to predict and can vary by underlying cause.
Cataracts can be inherited or acquired. Many dog breeds are known to have cataracts that are inherited – meaning it is in their genes. This is an important consideration for breeding dogs. Acquired cataracts can result from causes such as injury, inflammation, and internal metabolic diseases that affect the eye (such as diabetes mellitus). Dogs also get age-related cataract like humans do. No matter what the cause of cataract, the only definitive treatment is removal.
To date, no known eye drop or medical treatment has been proven to slow progression, prevent formation or reverse the changes caused by a cataract. Surgical removal of a cataract is the only currently available and effective treatment that can restore vision in animals and humans.
If you suspect that a cataract is forming in one or both of your pet’s eyes, call Eye Care for Animals.
Animals and arrange to have your pet examined by one of our veterinary ophthalmologists.
A complete ocular exam involving all structures of the eye is required to fully evaluate the cataract and determine the prognosis for surgery. If a cataract is not completely filling the lens, we can examine the retina and other parts of the eye with relative ease. If a cataract is complete, we are not able to examine the back of the eye – specifically the retina. A few additional tests are recommended before determining whether your pet is a good candidate for cataract surgery. The earlier we examine a cataract case the sooner we can treat vision threatening inflammation in the eye that often occurs with cataract formation. Thus, the earlier we see your pet the better.
We evaluate each eye for the extent and density of cataract formation, rapidity of change, presence and severity of ocular inflammation and extent of vision loss. We may recommend additional testing from your primary veterinarian to determine that your pet is in good physical health and if he/she is a good candidate for general anesthesia. Based on these findings, we will make recommendations on whether or not to pursue surgery.
We recommend cataract surgery for those patients whose vision is significantly impaired by cataract progression. It is a common misconception that a cataract must “ripen” or mature before cataract surgery can be performed. This is not the case. In fact, surgery to remove immature cataracts generally carries a post-operative prognosis and decreased chance of post-operative complications. It is important also to remember that cataract removal surgery is an elective procedure. While removing cataracts generally improves the quality of life in pets, many pets have very satisfactory lives with vision impairment. Your pet’s health, your goals, your finances, your availability, and many other factors should be considered before making a decision.
If we recommend surgery in both eyes, we also discuss with you how we will proceed. In general, we recommend cataract surgery on both eyes simultaneously to reduce anesthetic risk to your pet and improve post-operative outcomes. It also tends to be more cost efficient. There are occasions when we might opt to stage the surgeries, operating first on the most impaired eye. Surgical recommendations are made on a pet by pet basis. The final factor in determining whether your pet is a candidate for cataract removal surgery involves retinal testing. The retina is the structure at the back of the eye that transmits images to the brain. If the retina is not in good condition, removing cataracts will not improve your pet’s vision. The retina is tested in two ways: functionally and structurally. To test the retina’s function, we perform a non-invasive procedure called an electroretinogram (ERG). If the ERG is normal, we perform an ocular ultrasound to make sure there are no holes, tears, or detachments of the retina. These tests generally required your pet to be with us for about half a day. These procedures are not painful, but mild sedation may be used if your pet is nervous. We recommend having these tests performed within 2 to 3 weeks before surgery.
Cataract surgery is performed on an outpatient basis after an initial preoperative period (three to five days) when a few medications are administered at home to prepare the eyes. Your pet will be admitted to the hospital on the morning of the surgery to allow time for IV catheter placement and administration of more eye drops at frequent intervals. Your pet should not be fed breakfast on the morning of surgery – UNLESS he/she is a diabetic. Diabetic pets should get ½ the normal breakfast and ½ the normal insulin – unless otherwise specified by one of our doctors.
For cataract (and any other) surgery, we use the most advanced anesthetic agents and monitoring equipment available. During the surgery, our technicians carefully monitor your pet’s respiration, heart rate, and blood pressure. The actual surgical procedure takes approximately 30 to 40 minutes and the general anesthesia typically lasts 45 to 60 minutes. The procedure involves first making a very small incision at the top corner of your pet’s eye. Small surgical instruments are used to remove a small circular portion of the clear lens capsule that surrounds the cataract. Next, we use a state of the art “ultrasonic vacuum” to remove all of the cataractous lens fibers. Once the lens fibers are removed, an artificial lens, designed specifically for dog or cat eyes, is placed into the lens capsule. There are occasions when the artificial lens cannot be placed because the lens capsule is torn or unstable. Even if an artificial lens is not able to be placed, your pet will still have vision after surgery. He or she will be mildly far-sighted but able to see much better than with a cataract. The final step involves closing the surgical incision. The size of the incision in the eye needed for this procedure is generally less than half of a centimeter.
During post-operative and anesthetic recovery, we continue to closely monitor your pet. Usually, patients are ready to be discharged from the hospital approximately two to three hours after surgery. We will call you after your pet has recovered from anesthesia to set up a specific discharge time. To protect your pet’s eyes after surgery, your pet’s eyelids might be partially sutured to serve as a temporary bandage. If so, we remove these eyelid sutures ten to 14 days after surgery. He or she will also need to wear a cone or e-collar.
Postoperatively, we will want to recheck your pet 4 to 6 times in the first couple of months. You will continue to administer topical and/or oral medications, which we gradually taper to a low-level maintenance regimen. The use of these medications is critical to the success of surgery by helping to prevent infection and to control postoperative inflammation.
With the advent of new therapeutic drugs and microsurgical techniques, the success rate of cataract surgery has improved dramatically in recent years. On occasion, despite our best efforts to prevent them, complications can arise in approximately 5 -10% of patients. These potential complications include the following:
Some of these complications can lead to discomfort and blindness, but many of them can be successfully treated and managed with early intervention. Adherence to the post-operative medication and recheck schedule is critical to minimizing risk of complications.
The surgical removal of a vision-impairing cataract can result in a dramatic improvement of functional vision. Some dogs need more time to adjust than others, but most notice their pets are seeing well within 2 weeks after surgery. The implantation of an intraocular lens will bring your pet’s vision back to as close to normal as possible. As previously stated, pets that do not receive intraocular lenses will still have vision, but their near-vision, depth perception, and visual acuity will be reduced but still much better than with cataract. Some owners may not notice this difference unless their dog performed work or tricks requiring high visual acuity prior to cataract formation.
No. Because we remove all of the lens fibers during surgery, the cataract cannot come back. In some cases, progressive scarring of the capsule that surrounded the lens may result in some cloudiness and a recurrence of visual disturbances many years from the time of cataract surgery. This is uncommon, but if it does occur in your pet, we can attempt to remove this scar tissue with a non-invasive laser procedure, that may be available at some locations.
Coccidiomycosis (a.k.a. Coccidioidomycosis or “Valley Fever”) is an infection caused by the fungus Coccidioides immitis, or a closely related species Coccidiodes posadassii. This fungus is commonly found in the southwestern United States, Mexico and areas of Central and South America. It is found in sandy, dry soils. The organism reproduces during periods of high rainfall and produces spores that become airborne during dry, windy conditions. Coccidiomycosis can infect a wide variety of animals, including dogs, cats, and horses. Humans can also be infected. Immunocompromised humans and animals are at greatest risk for severe infections. It is important to seek an examination by a veterinarian if your pet develops any signs of the disease described below.
Infection occurs by inhalation of fungal spores. Once inhaled, spores from this fungus can infect the lungs and then spread to other parts of the body. It can take 1 to 3 weeks from exposure to the first development of respiratory signs; however, most animals and people that are exposed never show signs of clinical disease. Signs of disease in the eyes and other parts of the body may not occur until 4 months or more after exposure.
Fortunately, infected animals and humans are not directly contagious. This means that a human cannot contract the disease from an infected pet from typical interactions. If multiple pets or people in a household are infected, it is most likely from a common environmental exposure, not from transmission from pets to people, from pets to pets, or from people to pets. Caution should be taken, however, to practice good hygiene and avoid direct contact with bodily fluids or open skin wounds, especially for immunocompromised persons. It is extremely rare but possible for a less severe, localized infection to be transmitted from an infected animal to a person via a bite wound. Any animal bite wound to a person, especially by an animal known to be infected, should be examined by a physician.
Coccidiomycosis can cause a wide variety of clinical signs in different body systems, which may include the following:
Eyes: Redness, cloudiness, discharge, swelling, squinting, elevation of the third eyelid, protrusion or enlargement of the eye, and blindness may occur. These are very non-specific signs and may be indicative of a variety of diseases. Valley Fever can cause inflammation inside of the eye leading to retinal detachment and glaucoma (elevated pressure inside the eye that causes discomfort and vision loss). It can also affect the eyelids and cause swelling or redness. Eyelid involvement is seen more commonly in infected cats than dogs. Occasionally, eye disease will be the only clinical sign of infection with this fungus. In up to 43% of patients, ocular disease is the only sign of infection. One or both eyes may be affected with 80% of dogs with ocular coccidiomycosis only affected in one eye.
Respiratory System: Coughing, increased effort to breathe or lethargy may be noticed. Since the infection starts with inhalation of the spores, the fungus first causes disease in the lungs. In many cases, however, respiratory signs may be mild and non-specific. Also, they may resolve prior to an onset of signs elsewhere in the body.
Skin: Slow-healing draining and/or crusted lesions can develop. These tend to be more common in cats with this infection.
Other: Decreased appetite, weight loss, lethargy, depression, fever, limping, back or neck pain, enlargement of lymph nodes and behavioral/neurologic changes, such as altered gait or seizures.
Your veterinarian will recommend diagnostic testing based on the specific clinical signs your pet is showing. Samples from blood, urine and/or enlarged lymph nodes (if present) are commonly obtained. Tests on these samples are performed both to determine if coccidiomycosis is likely the cause of signs and to evaluate major organ function before starting treatment. Both false positive and false negative test results are possible for coccidiomycosis in endemic areas – such as Arizona. Your veterinarian will consider test results along with history and clinical signs when making a diagnosis and developing a treatment plan.
Radiographs (X-rays) and/or ultrasound are also often needed to search for signs of systemic infection. If neurologic abnormalities are present, an MRI would be recommended. Occasionally, the best method of diagnosis is from testing samples obtained directly from the eye. Some of the diagnostic tests may need to be repeated during the course of treatment to monitor response to therapy.
Coccidiomycosis is treated with a long course antifungal medication. The two most commonly prescribed antifungal medications for dogs and cats with coccidiomycosis are itraconazole and fluconazole. Other antifungal medications may be recommended in some cases. Your veterinarian will make a specific recommendation based on your pet’s signs and overall systemic health. Duration of treatment can vary; however, treatment is generally continued for at least 3 to 6 months past the resolution of all signs of disease and normalization of blood antibody titers. Shorter courses of treatment have been shown to have a high incidence of relapse. Itraconazole and fluconazole are generally safe drugs; however, side effects may include liver damage and gastrointestinal upset (ie: decreased appetite, vomiting, diarrhea). For this reason, your veterinarian may recommend regular blood work to monitor for any potential side effects.
If the eyes are infected, additional treatments such as anti-inflammatory eye drops and/or anti-glaucoma medications may be indicated. Oral anti-inflammatory medications may also be prescribed. Depending on the severity of clinical signs and inflammation within the eye, medical therapy may or may not be successful in keeping your pet visual and comfortable. If medical treatment is not controlling the disease in the eye, surgical therapy may be required. Your doctor will discuss the surgical treatment options available for your pet, if necessary.
General supportive care is sometimes necessary. If so, your pet’s ophthalmologist will work closely with your primary veterinarian to make sure your pet is getting complete and appropriate treatment.
When coccidiomycosis affects the eye, it can be very serious and has the potential to cause permanent blindness. Prognosis for recovery depends on the severity of signs at the time of diagnosis. With the appropriate treatment, approximately 60% of patients (including those that lose vision) are able to fight off the systemic fungus and have healthy and happy lives. Prognosis is better for patients with an early diagnosis and mild signs of disease. After recovery, patients have an approximately 20% chance of relapse and reinfection is possible if your pet remains in the same environment. It is, therefore, very important to monitor your pet for any of the above clinical signs and to call your veterinarian as soon as possible if you notice any of them.
Unfortunately, there are no vaccinations available for coccidiomycosis. Becoming familiar with the clinical signs mentioned above is the best way to help your pet. It is important to contact your veterinarian if signs occur. Being proactive will provide the best chance for recovery. Avoiding outdoor activity during dry, windy conditions and discouraging digging may reduce risk of exposure.
The conjunctiva is the pink tissue that lines the inner surface of the eyelids and covers the white portion of the eyeball (sclera). It is a protective layer that contains special glands that secrete a component of the tear film that helps maintain normal eye health. Conjunctivitis is a condition where the conjunctiva becomes reddened, congested, and painful. It may occur in one or both eyes and has a variety of causes. These include foreign matter, chemicals, pollen, dust, bacteria, viruses, and environmental irritants like smoke.
Other causes may be due to systemic diseases or allergic reactions. The conjunctiva of a sensitive animal can massively swell after an insect sting/bite on any part of the body. Allergies to food and the environment can also cause swelling and redness. Conjunctivitis may lead to, or be a sign of, corneal ulcers (abrasions of the cornea), eye infections, corneal scarring, corneal vascularization, corneal mineralization, corneal sequestrum (primarily in cats), conjunctival adhesions, nasolacrimal blockage (blockage of normal tear flow), and keratoconjunctivitis sicca (dry eye).
Your awareness of your pet’s symptoms and compliance with recommendations for medication and recheck examinations will help control these potential complications. Notify the doctor if any of the following occur:
The cornea is the clear front part of the eye. A thin layer of tissue called epithelium is the cornea’s protective outer layer. The inner surface is called the endothelium and the portion in between is called the stroma. A corneal abscess occurs when bacteria or fungus along with the animal’s own white blood cells enter the cornea through an injury. The injury may heal too quickly and essentially “seal” the bacteria or fungus inside the cornea creating a pocket of infection or abscess. Abscesses may also be sterile, with only white blood cells present.
A horse with a corneal stromal abscess will have a dense white or yellow spot in the cornea representing an accumulation of organisms (bacteria or fungi) and/or white cells. The eye may be cloudy and red with varying levels of ocular discomfort, which may manifest as tearing and squinting of the affected eye. A corneal stromal abscess may weaken the cornea to the point of perforation of the eye, with the possibility of subsequent blindness. It is also possible that the abscess may spread to the inside of the eye causing severe intraocular inflammation and infection, which also may be vision-threatening.
Corneal stromal abscesses are treated intensively with medications prescribed by the veterinary ophthalmologist. The ophthalmologist may remove the corneal epithelium covering the abscess to increase penetration of medication into the lesion to hasten the healing process. Medications may need to be continued for several weeks to several months. Surgical intervention is occasionally necessary to remove the organisms (bacteria or fungi) and prevent rupture of the eye. These surgeries can vary depending on the depth of the abscess and occasionally utilize a corneal or conjunctival graft to cover the surgical site. These grafts incorporate into the cornea at the site of the abscess forming a dense scar in a few weeks. The goal is to preserve the vision and globe by provide structural support to the cornea and bring in blood supply to facilitate healing to the weakened and diseased tissue. Healing of a corneal stromal abscess with or without surgery will result in a scar on the cornea. The size and location of the scar will dictate the degree of vision impairment (if at all). The performance of your horse may or may not be affected by the corneal scar.
While treating for a corneal stromal abscess, the horse should be kept in a darkened stall with limited exercise. Hay should be removed from overhead racks and fed on the ground. An Eye Saver Mask can be used to protect the eye self-trauma and from fly strike. In many cases, frequent medication application can be performed with ease by the placement of a subpalpebral lavage system. Please speak to your veterinarian or veterinary ophthalmologist if you are interested in having a subpalpebral lavage system placed.
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)
•Ocular pain
•Eyelid rubbing
•Excessive tearing
Corneal sequestrum is a disease affecting the cornea (the clear curved transparent part of the front the eye). The sequestrum is usually an area of degenerated or non-living corneal tissue. This develops after an area of chronic corneal irritation or non-healing ulceration. The area of corneal degeneration often turns light brown to dark brown or black in color. The sequestrum may affect only the outer layers of the corneal stroma (tissue), but in some cases the sequestrum extends deeper into the cornea and may lead to deep ulceration, pain and possibly, corneal rupture.
While corneal sequestra have been documented in horses, the disease is most common in cats. Corneal sequestra occur in cats of all breeds, however, the Persian, Himalayan, and Burmese are particularly susceptible.
If your cat develops a corneal sequestrum, you might notice increased tearing, discharge from the eye and squinting. You might also see the brown (or black) area on the cornea.
A corneal sequestrum can lead to corneal ulcers (superficial to deep), ocular infections, corneal scarring, corneal vascularization and corneal mineralization.
Corneal sequestra can occur as the result of chronic eye irritation. A large prominent globe, low tear production, decreased blink response and decreased sensation of the cornea, as seen in brachycephalic (or short-nosed, flat-faced) breeds might create a predisposition to a corneal sequestrum. Another possible cause of this disease is Feline Herpesvirus. Sequestra can recur in the same eye or in the other eye in predisposed patients.
Treatment for a corneal sequestrum usually involves a surgical procedure called a keratectomy. This involves surgical removal of the diseased layers of cornea. Our veterinary ophthalmologists perform this surgery using an operating microscope and specialized microsurgical instruments. Surgery relieves the discomfort associated with the corneal sequestrum, prevents the lesion from deepening and greatly shortens the healing time of the ulcer.
If the sequestrum affects the deeper layers of the cornea we may elect to apply a tissue graft or similar material to strengthen the cornea in that area and hasten healing. This may involve the use of a graft consisting of the patient’s own conjunctiva (the pink, mobile layer covering the white of the eye), adjacent cornea, donor cornea, synthetic biological or collagen discs placed over the surgical defect.
Not all corneal sequestra require surgical intervention. Your veterinary ophthalmologist may recommend medical treatment and monitoring. When surgical intervention is recommended, your doctor will discuss the surgical procedure along with benefits and risks specific to your pet. 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 5% of these cases. Nevertheless, potential complications include, but are not limited to:
•Inflammation of the pink tissue (conjunctivitis)
•Break down or rejection of the tissue or suture (wound dehiscence/graft retraction/rejection)
•Infections at the surgical site, which may extend to other internal and/or external areas of the eye
•Corneal ulcerations
•Corneal scarring, vascularization, or mineralization
•Inflammation inside the eye (uveitis)
Some of these complications, if severe could lead to blindness; however most can be managed with prompt treatment
The cornea is the transparent, domed front part of the eye that acts to protect and maintain ocular integrity while allowing light to enter the eye for vision. The normal cornea is composed of three layers. An outer layer of epithelial cells lines the surface and protects the rest of the cornea. The thicker middle layer is called the stroma and contains multiple supportive cells, collagen fibers, and nerve fibers. The inner lining is called the endothelial layer and it functions to help maintain corneal clarity. A corneal ulcer is a break in the outer epithelial layer of the cornea. Although initially painful, uncomplicated ulcers should heal with appropriate therapy in three to four days. Ulcers that persist beyond this period of time or worsen or progress are considered be complicated ulcers.
Primary tissue healing defects are conditions in which the epithelium fails to remain adherent to the underlying stroma after attempts to heal the superficial ulcer. This condition is common in middle-aged and older dogs as well as certain breeds, such as the Boxer. It is also found in dogs that have underlying hormonal or metabolic conditions that may delay healing such as hypothyroidism, diabetes mellitus or Cushing’s syndrome. This type of ulcer is sometimes called a “Boxer” ulcer or an “indolent” ulcer. The basic defect affects the ability of the outer epithelial cells to anchor themselves and remain adherent to the underlying corneal stroma. Although they continually attempt to grow over and cover the ulcer, they are periodically stripped away either by the eyelids with normal blinking or due to active rubbing of the eye by the animal.
Among the most important instruments required to evaluate a corneal ulcer is the slit lamp, a biomicroscope. The slit lamp permits our veterinary ophthalmologists to carefully evaluate the patient’s cornea with a high degree of magnification and resolution equivalent to that of a microscope. Sometimes, a cause for the ulcer, such as an aberrant eyelash or foreign material stuck in the eye can be identified. The ulcer will generally heal uneventfully after removal of the inciting cause. Often the characteristic loose tissue edges of these ulcers will provide the ophthalmologist with enough information to diagnose the disease.
To further evaluate a complicated corneal ulcer, we might obtain samples for bacterial culture, virus isolation, and cytological evaluation.
Arguably the most frustrating ulcer is the indolent ulcer. Although these ulcers do not typically threaten a patient’s sight, they run a protracted course. Medical therapy for indolent ulcers consists of preventative antibiotics and often hyperosmotic agents and offers only a 15% success rate.
The recommended treatment for indolent ulcers is a surgical procedure called a keratotomy, either a linear grid or punctuate pattern can be used. The purpose of this procedure is to first remove all of the loose epithelial cells that are not able to remain attached to the stroma. A very fine needle is then used to make a series of microgrooves or grids into the superficial corneal stroma. This will help to disrupt the abnormal portion of the cornea and allow new epithelial cells to anchor down to healthy cornea below this unhealthy zone. This can be performed either awake under topical anesthesia or under general anesthesia, depending on the patient and the size of the ulcer. Most indolent ulcers will heal after this procedure; however, refractory ulcers might require a repeat of the procedure or a more invasive surgical procedure called a superficial keratectomy. Here the outer layers of the cornea are surgically removed with a specialized corneal blade that peels the unhealthy layer of the corneal stroma away.
Not all indolent ulcer patients require surgical intervention, but it is important to be aware of potential complications if surgery does occur. Including potential anesthetic risks, procedures that involve the cornea seldom give rise to complications, which occur in less than 5% of these cases. Potential complications include, but are not limited to:
Some of these complications can lead to blindness.
Dermoids are overgrowths of non-cancerous, normal skin in the wrong location that arise because of abnormal development of the embryo in utero. The skin may be pigmented, contain sebaceous and sweat glands, fat, and/or grow hair. These growths have been described in multiple species, and while affected animals are born with the condition, it may go unnoticed until the hair grows sufficiently long to become prominent or cause irritation. Any dog breed can be affected, but they occur more frequently in Australian Shepherds, German Shepherds, Cocker Spaniels, Collies, Dachshunds, Dalmatians, English Springer Spaniels, Golden Retrievers, Poodles, Pugs, Pulis, Siberian Huskies, and St. Bernards. Cat breeds more commonly affected include the domestic shorthair and Burmese.
Around the eye, they can occur as abnormal skin growing on the normal skin of the eyelids or face, on the conjunctiva, or on the cornea. They can affect the normal ability to blink, which is required for a healthy cornea, and they can be vision obstructing. In addition to affecting cosmetic appearance, the haired dermoids can be irritating. Clinical signs may include redness, tearing, discharge, and corneal ulceration. Diagnosis can be made with an ophthalmic exam.
Dermoids are typically treated in order to improve cosmesis or when the associated hair causes irritation and clinical signs. Surgical removal is the treatment of choice and is curative. Outcomes are generally good following surgical excision. Perioperative medications may include anti-inflammatories and antibiotics, depending on the location and size of the dermoid.
Distichiasis is an abnormal condition in which extra eyelashes appear along the eyelid margin(s), where they normally should not grow. This condition is genetically inherited and is common in many breeds. Although some patients with distichiasis will exhibit discomfort, many show no clinical signs and some require no treatment.
Trichiasis involves hairs located in normal sites around the eye but are misdirected toward the eyeball or the cornea. Breeds with long facial hair (i.e. Shih Tzus) commonly have trichiasis. Trichiasis is a common cause of excess tearing and tear staining down the face, as the hairs act as a wick to pull the tears out of the eye. Offending hairs can be permanently removed by freezing the hair follicles if they are causing a problem, such as pain, itchiness, chronic wetness of the skin and associated infections. Although we use lasers for many procedures, they may be too destructive to the eyelid margin if multiple abnormal hairs are present.
Ectopic cilia is an eyelash that emerges from the underside (conjunctiva) of the upper or lower eyelid. This causes the short, stiff eyelash to rub against the eye whenever your pet blinks or sleeps. Ectopic cilia generally cause a great deal of discomfort and can create ulcerations on the surface of the eye. Ectopic cilia generally require surgical excision in order to alleviate clinical signs.
All three conditions may cause excessive tearing, discomfort and ocular scarring. Serious injury to the eye, particularly the cornea, may also occur. Early eye damage is not readily apparent and may be detected only
with the aid of special ophthalmic instruments.
1.Numerous procedures can be used to correct these disorders. The choice of treatment will be based on your pet’s individual needs.
2.Due to the complex, ongoing nature of distichiasis and trichiasis, new eyelashes may appear after the initial corrective procedure. This occurs in approximately 20% of patients and may necessitate a second procedure.
Treatment may not be needed if the condition causes no harm or discomfort.
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.
Episcleritis is an inflammation of the episclera. The sclera is the white outer fibrous covering of the eyeball. The thin outer layer of tissue overlying the sclera is called the episclera. Both the sclera and episclera lie underneath the conjunctiva, the mobile pink outer membrane. The combined conjunctiva, episclera, and sclera make up the “white of the eye” surrounding the clear cornea.
Episcleritis usually appears as an immovable pink lump or nodule on the white part of the eye. It may also be more generalized and appear as redness and apparent swelling of the eyeball. With severe reactions, small blood vessels may grow into the cornea and cause it to become cloudy. The cause of episcleritis is believed to be an autoimmune type reaction. Treatment involves the use of anti-inflammatory and immune- modulating drugs. Without treatment, episcleritis may result in severe and prolonged inflammation, which can affect the structures inside the eye. Lesions affecting the cornea may result in permanent scarring or mineral deposits.
1. A thorough eye examination is essential before treatment. A biopsy (tissue sample) of the tissue may be required to ensure that cancerous tissue is not present, as episcleritis may clinically resemble a tumor.
2. Episcleritis generally responds to treatment, but long-term therapy may be required. Relapses may occur if treatment is discontinued and therapy may need to be re-instituted.
3. In cases that are non-responsive to medical treatment, cryotherapy (freezing) of the episclera and sclera may be recommended.
Please notify the doctor if any of the following occur:
a. No improvement is noted or the condition worsens.
b. The eye appears painful or the medication appears to be irritating your pet.
By definition, a cataract is an opacity of the lens that obstructs passage of light and impedes vision. A cataract may appear as cloudiness or haze in your horse’s eye. Cataracts can develop for a variety of reasons and some types will cause more severe vision impairment than others. Cataracts can also lead to secondary complications, such as glaucoma – a painful eye condition. A horse may be born with cataracts (congenital cataracts), develop them at a young age (juvenile cataracts), or develop them as an adult. In general, this is an uncommon condition in the horse.
Congenital and juvenile cataracts are believed to be due to either hereditary condition or an abnormality during development inside the mare. This type of cataract is fortunately quite rare in horses. The possible hereditary nature of this type of cataract should be taken into consideration when breeding these horses and their close relatives.
The majority of cataracts in horses occur in adult animals. They most commonly develop secondary to diseases that cause intraocular inflammation, such as Equine Recurrent Uveitis (ERU, moon blindness). The second most common cause of equine cataract is trauma – both blunt and sharp trauma. All eye injuries should be evaluated by a veterinarian at the time of injury, as well as, at future rechecks to monitor for development of cataract.
The management of equine cataracts depends on the type and size of cataract present, as well as, the intended use of the horse. Cataracts that remain small enough that vision is not significantly impaired may not require treatment or require topical medical treatment only. A complete or mature cataract may be a surgical candidate. No medication will dissolve cataracts and cataracts are only resolved by surgical removal. Some equine cataracts can be removed by phacoemulsification and replaced by an intraocular lens, but this surgery is not an option for all horses. An in-depth discussion with a veterinary ophthalmologist can help to determine if your horse is a possible candidate. Foals with congenital or juvenile cataracts may benefit from early cataract removal surgery and have improved surgical outcomes. This higher rate of success is due to the smaller size of the foal eye and the decreased association between inflammation and cataract in foals.
The success rate for congenital/juvenile equine cataracts is approximately 85% in terms of vision while that for adult horses with acquired cataracts may be much less. Success rates for adult horses vary depending on the cause of cataract, chronicity, and any underlying disease. For instance, the surgical outcome for traumatically-induced cataracts in adults is highly favorable, while outcome for cataracts from chronic ERU is guarded (50% or even less chance of maintaining vision long-term).
Potential complications of lens removal in the horse may include: persistent or recurring intraocular inflammation, corneal ulcers, corneal cloudiness or edema, loss of vision, glaucoma, and retinal detachment. Leaving the cataract in the eye, unfortunately, has many of the same possible complications. While cataracts are not painful, many of these complications can cause discomfort and/or blindness.
Pre- and post-operative treatment should be discussed as well. If surgical removal is being considered, pre-surgical diagnostic testing is recommended prior to cataract surgery, including an ocular ultrasound and electroretinogram to evaluate retinal function and integrity.
Post-operative treatment should also be a consideration. Medical treatment with topical and oral medications for a month or longer may be required following the procedure to maximize chances of success. Immediately after surgery, medications will be given multiple times per day via a subpalpebral lavage system. Your horse should also wear a protective mask (Eye-Saver) for days to a week after surgery. During the post-operative treatment period, your horse may need to be kept out of bright light and will have marked exercise restrictions.
It is important to realize that a horse with an intraocular lens and a successful surgery is not considered to have normal vision. Fortunately, most horses seem to adapt quite well and are capable of returning to pre-surgical work. If a lens is not placed, your horse will be “far-sighted,” meaning the “close up” vision is poor. It is important that your horse be considered visually impaired and you, as the owner, are responsible for the safety of any other riders you allow on your horse. That said, many owners of visually impaired horses find them to be wonderful companions and athletic partners.
The cornea is the clear dome-shaped structure that forms the front surface of the eye. It allows light to enter the eye and helps to focus it on the retina for functional vision. It also protects the structures inside the eye and maintains ocular shape and integrity. A corneal ulcer is simply a break on the surface of the cornea and leads to loss of the outer layer or epithelial surface of the eye. Ulcers have many possible causes: trauma, lacerations, abrasions, drying due to abnormal tear production, eyelid abnormalities, foreign material, parasites, viral infections, insect stings, chemical sprays or inflammation, intraocular disease, etc. Often the initial cause cannot be determined but treatment is similar for most corneal ulcers, as they are essentially open wounds on the eye. Signs of ulceration include squinting, tearing, discomfort, watery or mucoid discharge, redness and sensitivity to light. Cloudiness of the cornea or discoloration may also be noted.
A superficial, uncomplicated ulcer usually heals uneventfully in about 1 week with minimal scarring after appropriate medical treatment. A corneal ulcer can become secondarily infected with bacteria, fungi, or a mixture of the two. Infected, deep, or complicated ulcers require more intensive medical treatment and sometimes surgery. Corneal ulcers should be evaluated by a veterinarian. In addition to the exam, the veterinarian may take samples of the ulcer for cytology, bacterial and/or fungal culture. These tests will help determine the most appropriate therapy.
In complicated cases, the ulcer may rapidly deepen or the cornea may start a breakdown process called “melting”. A “melting” cornea can even progress to rupture of the eye. Melting and deep ulcers are considered eye emergencies. Secondary inflammation, or uveitis inside the eye, is painful and can contribute to vision-threatening complications. The ulcer may require intensive, frequent treatments for several days to weeks to control infection, reduce melting and control inflammation in order to achieve healing and save the globe. Deep and complicated corneal ulcers generally result in more noticeable scarring after healing. Large or dense white scars can cause visual impairment and the horse’s athletic performance or intended use may be affected.
Deep or melting ulcers that worsen despite therapy may require surgery in addition to medical therapy to save the eye. These surgeries usually involve grafting of additional supportive tissue or biosynthetic material, such as a flap of conjunctiva (tissue from the “pink” part of the eye), into the ulcer. This helps to fill in the tissue defect, bring in a blood supply, and hasten healing. These grafts usually incorporate into the corneal tissue in a few weeks to months but also may result in a permanent scar.
Uveitis means inflammation of the iris and deeper structures inside the eye. Equine recurrent uveitis (ERU) is the most common cause of defective vision or blindness in the horse. ERU is also known as “periodic ophthalmia” and “moon blindness”. It is characterized by multiple episodes of “active” uveitis alternating with periods when the eye is “quiet”, or not inflamed. One or both eyes may be involved in the disease. Chronic ERU may result in partial or complete loss of vision. Signs of “active” ERU include tearing, squinting, sensitivity to light, and a cloudy or red eye. The active episodes of ERU cause permanent changes in the eye, including scarring of parts of the eye and possibly cataracts or retinal detachments. These permanent changes can be seen by a veterinary ophthalmologist even during the “quiet” stages of the disease. During the “quiet” stages, the eye is not painful and inflammation is minimal. ERU is caused by an overly active immune response of the eye to many different sources. The source may be bacterial (such as Leptospira, Brucella, Salmonella, or Streptococcus), viral, parasitic (such as Onchocerca, Strongylus, or Toxoplasma), or fungal. Trauma to the eye or certain diseases of the body can also be sources of ERU. It is important to remember that the source only initiates ERU. The original source may be treated or may go away, but the horse’s own immune system may perpetuate the inflammation and disease in the eye. Relapses of inflammation may continue to occur although the original source of inflammation is no longer there. Identifying the original source of inflammation may prove to be very difficult, and in many cases, the causative agent or original source of inflammation is never identified. A genetic predisposition to ERU as some breeds, such as Appaloosas, which have a higher incidence of the disease, may exist.
Treatment of ERU alleviates the pain associated with the “active” stages of the disease and decreases inflammation in the eye while also attempting to preserve vision. Medications should be prescribed by your veterinarian as soon as signs of ERU are noted. For each “active” stage of the disease, it may be necessary to continue treatment of the eye for several weeks to several months, depending on the severity of inflammation. Although most treatment involves a combination of topical eye drops/ointment and oral or injectable medications, some patients may be candidates for a surgical implant device that slowly releases cyclosporine, an immunomodulatory medication.
Relapses of inflammation of the eye require reinstatement of topical and systemic treatment by your veterinarian. It is important to contact your veterinarian or veterinary ophthalmologist if you feel your horse is having a recurrence of ERU. Signs of ERU can be similar to other conditions such as glaucoma or corneal ulceration and some of the medications used to treat ERU may be contraindicated for these conditions. Thus, it is important that you consult your veterinarian or veterinary ophthalmologist prior to restarting medications for ERU. It is also important that you contact your veterinary ophthalmologist prior to stopping or decreasing the frequency of any prescribed medications. It is helpful to keep the horse in a darkened stall with limited exercise during treatment periods. If treatment fails and the eye becomes blind and painful, the eye may need to be removed to eliminate discomfort.
The prognosis for vision in horses affected with ERU can be poor. Prompt treatment may slow or prevent the occurrence of blindness.
General Information
Eyelid agenesis is a congenital condition (birth defect) in cats where a portion of the eyelid margin is underdeveloped at birth. This disease of the feline eyelid is also referred to as an “eyelid coloboma”, as a coloboma implies an area of missing tissue. This condition generally affects both eyes and most commonly occurs along the upper and outer aspects of the eyelids. The cause of eyelid agenesis is not fully understood; however, hereditary patterns or in utero viral transmission have been proposed. All cats with eyelid agenesis should receive a thorough ophthalmic examination as additional intraocular abnormalities may be present, which could lead to discomfort or vision impairment.
Treatment Strategies
Eyelid agenesis is generally accompanied by varying degrees of corneal irritation (keratitis) due to hairs rubbing on the cornea or improper tear film distribution leading to corneal drying. These side effects can occasionally lead to corneal ulceration varying from superficial to deep wounds.
If a procedure is indicated for your pet, common postoperative care may include the use of short-term systemic antibiotics, anti-inflammatories, and pain medication as well as topical therapy which may include eye drops or eye ointment. An Elizabethan collar should be placed following eyelid surgery to prevent self-trauma. Complications of surgery are uncommon but include wound infection, suture dehiscence, or persistent ocular irritation.
If you have any further questions or concerns regarding eyelid agenesis, please do not hesitate to call us at Eye Care for Animals.
Less InfoEntropion is a condition of the eyelids in which the eyelid margin rolls inward towards the eye. It is most common in puppies and usually results from disproportionate eyelid growth. Many puppies will outgrow the condition by the time they reach one year of age. If the eyelid is causing corneal irritation or damage (signs might include tearing, squinting, redness and/or discharge) then a procedure known as “tacking” or temporary eyelid eversion may be helpful. In adult dogs, permanent eyelid surgery can be performed to correct the abnormality by removing a section of tissue near the eyelid margin and/or shortening the eyelid. Over-correction of entropion can lead to complications and is difficult to fix. For this reason, doctors will generally be conservative rather than risk removing too much tissue, thus, entropion correction may require a second surgery if adequate correction is not achieved initially. Dogs with complicated eyelid abnormalities, severe entropion, or scar tissue from previous injuries or surgeries are more likely to need multiple surgical procedures.
Ectropion is a condition of the eyelids in which the eyelid margin rolls out, away from the eye. This condition can lead to chronic irritation and discharge and can also be surgically corrected.
Entropion and ectropion can lead to corneal irritation corneal ulcers, conjunctivitis, eye infections, corneal scarring, corneal vascularization and corneal mineralization. These complications can be painful and cause vision loss.
If your doctor recommends surgical correction of entropion or ectropion for your pet, he or she will discuss the specific procedure recommended as well as benefits and risks associated with the procedure. Any surgical procedure can introduce complications, including potential anesthetic risks. Surgical procedures that involve the eyelid or skin surrounding the eye rarely give rise to complications, which occur in less than two percent of these cases and are usually minor. Potential complications include, but are not limited to, inflammation of the eyelid (blepharitis); inflammation of the pink tissue surrounding the eye (conjunctivitis); break down of the tissue or suture at the surgical site (wound dehiscence); infections at the surgical site, which may extend to other internal and/or external areas of the eye; corneal ulcerations; corneal scarring, vascularization, or mineralization; or tearing (epiphora). Close post- operative monitoring and adherence to medication and recheck schedules can minimize complications. Any concerning signs should be reported to your doctor immediately to allow any complications to be identified and treated promptly, reducing the risk of progression vision-threatening complications.
Eyelid masses are most often benign in the dog. Cats have a higher incidence of malignant eyelid masses. Depending on the size, location and appearance of the mass your doctor may recommend taking a sample of the mass (biopsy or fine needle aspirate) to determine the mass type prior to definitive surgery. If the eyelid mass involves less than about one-third of the eyelid margin, removal can be performed in a routine fashion. Small masses with minimal involvement of the eyelid margin can often be removed by CO2 laser photoablation under local anesthetic to avoid the need for surgical removal under general anesthesia. If the mass involves more than one-third of the eyelid margin, surgical reconstruction of the eyelid is usually necessary. This may require more complicated procedures, and sometimes more than one surgery will be needed to fully reconstruct the eyelid.
Even benign eyelid masses can lead to corneal irritation and ulcers, eye and eyelid infections, corneal scarring, corneal vascularization, and corneal mineralization. Some of these complications can be painful and cause vision loss.
Any surgical procedure can introduce complications, including potential anesthetic risks. Surgical procedures that involve the eyelid or skin surrounding the eye rarely give rise to complications, which occur in less than two percent of these cases and are usually minor. Potential complications include, but are not limited to, inflammation of the eyelid (blepharitis); inflammation of the pink tissue surrounding the eye (conjunctivitis); break down of the tissue or suture at the surgical site (wound dehiscence); infections at the surgical site, which may extend to other areas of the eye; corneal ulcerations; corneal scarring, vascularization, or mineralization; and tearing (epiphora). Close postoperative monitoring and adherence to medication and recheck schedules can minimize complications. Any disconcerting signs should be reported to your doctor immediately to allow any complications to be identified and treated promptly, reducing risk of progression vision-threatening complications.
Eyeshine refers to the reflection of light off the mirror-like membrane, called the tapetum, in the back of the eye. Many animals, including dogs and cats, have a tapetum, while humans do not. The tapetum improves the low light vision of these animals.
There are multiple veterinary conditions where the presence of increased eyeshine may be a symptom:
Retinal reattachment surgery is offered at our Pasadena, California (626-564-0202) and St. Charles, Illinois (630-444-0393) hospitals, where patients are received from around the country for surgical care.
The retina is a thin membrane that lies against the back wall of the eye. Similar to the way a camera works, images from the outside of the eye are focused by the cornea and lens onto the retina, which can be compared to the film in a camera. If the retina is not properly positioned or becomes damaged, vision is diminished or lost. The retina is only fused to the wall of the eye at its peripheral edges and at the optic nerve. Much of the retina relies on vitreous, a firm molded gel (like Jello), to tamponade it against the back of the eye.
Although there are many types of retinal detachment, there are two main scenarios that require retinal surgery. The first is called vitreal degeneration/dysplasia, where the vitreous humor, instead of forming a semi-firm gel, liquefies. It transforms from a Jello-like consistency to a chicken noodle soup-like consistency and can no longer effectively hold the retina in place. As the eyes move, the swirling liquefied vitreous tugs on the retina, causing tears and fluid flow under the retina, separating it from the wall of the eye. The tears often progress, until the entire retina has peeled off the back of the eye. This type of retinal detachment (rhegmatogenous retinal detachment) is inherited or genetic in many breeds including the Shih Tzu, Italian Greyhound, Boston Terrier, Poodle and Terrier Breeds. Tears may be precipitated or exacerbated by vigorous head shaking during play.
The second main type of retinal detachment occurs secondary to cataracts, cataract surgery or other intraocular surgeries. Inflammation in the eye lead to areas of adhesion between the retina and the vitreous, putting traction on the retina, pulling it off the back of the eye. Retinal detachment can occur due to other causes such as trauma.
Because most dogs continue to behave normally as long as one eye has vision, retinal detachment in the first eye is often missed. Patients often present to a veterinary ophthalmologist for vision loss when the retina in the second eye detaches. Signs of retinal detachment include vision loss, a dilated pupil, increased eyeshine, and sometimes blood within the eye. With cataracts, retinal detachments are often detected during pre-operative screening ultrasounds. They may also be identified following cataract surgery during recheck examinations.
Surgical correction is accomplished by entering the back of the eye via small ports. The diseased vitreous is first removed. The detached retina is then repositioned back against the back of the eye using a heavy oil called PFO. The PFO is replaced by silicon oil, which acts as an artificial vitreous. A laser is also used to strengthen the retina’s attachment to the back of the eye.
The two biggest factors that influence the success of surgery are: the length of time the retina has been detached prior to surgery and the cause of retinal detachment. Predisposed breeds, such as the Shih Tzu, tend to have the highest success rates (often >90%) if retinal detachments are caught early. Retinal detachments following blunt trauma or bite wounds often have the lowest success rate (<50%). The veterinary ophthalmologist performing retinal reattachment surgery will be able to further discuss the estimated success rate for your pet, the details and care involved with retinal reattachment surgery, as well as work with your local veterinary ophthalmologist to provide long-term care for your pet’s eyes.
The success of retinal reattachment surgery has improved over the past decade with state of the art equipment and shorter surgery times. However, complications can arise and include retinal re-detachment and degeneration, glaucoma, chronic inflammation, bleeding inside the eye, corneal ulceration, cataract formation, changes in focusing, or silicon oil migration into the front of the eye.
While most retinal detachments are not initially associated with discomfort, long term, many dogs with an untreated retinal detachment will develop glaucoma, or an elevated pressure in the eye. As this can become an uncomfortable condition, your pet should continue to receive ocular exams over time. Should glaucoma develop, further treatment will be necessary to maintain comfort.
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:
Collie: rod-cone dysplasia under a year
•Irish Setter: rod-cone dysplasia under a year
•Cairn Terrier: rod-cone dysplasia under a year
•Miniature Long-Haired Dachshund: rod-cone dysplasia under a year
Norwegian Elkhound: rod dysplasia, cone 2 to 3 years
•Samoyed: rod-cone degeneration 3 years
•Cocker Spaniel: rod-cone degeneration 2 to 7 years
•Miniature Poodle: rod-cone degeneration 3 to 6 years
•Miniature Schnauzer: rod-cone degeneration 3 to 6 years
•Akita: rod-cone degeneration 3 to 6 years
•Schnauzer: rod-cone degeneration > 3 years
•Golden Retriever: rod-cone degeneration
•Labrador Retriever: rod-cone degeneration
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.
Conjunctivitis and keratitis are common eye problems in all ages of cats. Conjunctivitis refers to the inflammation of the pink membranes surrounding the eye, whereas keratitis refers to the inflammation of the cornea. Cats may either develop signs of conjunctivitis alone, or symptoms coupled with keratitis, which is then termed keratoconjunctivitis. A number of infectious agents, namely viruses and bacteria, have been identified as potential underlying causes of these two conditions. These infections may be contracted as a kitten from the queen shortly after birth or from other cats, and are usually contagious from cat to cat.
The most common clinical signs of feline conjunctivitis and keratitis include red and swollen conjunctiva with excessive tearing, ocular discharge, and/or squinting. The discharge ranges from clear mucous to green- yellow in color. Some cats also rub at the eyes, which indicates discomfort. Sneezing and nasal discharge may also accompany the ocular signs, especially in younger cats. Recurrent bouts of conjunctivitis and keratitis are common, especially in viral cases such as feline herpes virus. Severe infections can cause complications such as permanent scarring of the cornea and conjunctiva. Some cases may have poor tear drainage resulting in chronic tearing onto the face. In young kittens, the inflammatory response may cause adherence of the conjunctiva to the cornea, and the eyelids may scar and fuse partially closed. The most severe cases can lead to rupture of the globe and vision loss, especially if untreated.
Severe keratitis can lead to abnormal blood vessel growth into the cornea. When severe infections occur, such as simultaneous viral and bacterial infections, corneal ulceration (a scratch or abrasion) may lead to perforation of the eye. With long-standing ulcers that are slow to heal, a dark brown to black discolored area of the cornea (corneal sequestrum) can form. When corneal ulceration and/or sequestrum occur, they are usually associated with varying degrees of ocular discomfort or pain.
In addition to history and clinical signs, several diagnostic tests may be required to confirm the cause and magnitude of conjunctivitis and keratitis. When a cause is identified, specific treatment directed at the underlying cause produces a faster healing response. Some or all of the following tests may be necessary.
Conjunctival Cytology
Microscopic evaluation of the cells collected from the ocular surface can help determine the health of the cornea and conjunctiva. Furthermore, it will help identify whether primary or secondary infections are involved. For suspected viral infections, samples can be sent for virus isolation, fluorescent antibody (FA), and/or polymerase chain reaction (PCR) testing by a diagnostic laboratory. Although these tests are highly specific, they are not 100 percent sensitive; therefore, repeated samples may need to be submitted to the lab to achieve a positive result for a definitive diagnosis.
Cultures
Bacterial culture is often warranted to confirm suspected infections. In order to determine if the right antibiotic is used for a bacterial infection, the diagnostic laboratory can perform an antibiotic sensitivity test for the offending bacteria.
Blood Tests
Ocular disease can be the result of internal or systemic conditions; if the patient’s immune system is suppressed or not fully functional, infections are more likely to occur. Specific tests to check the health status of the patient may include a complete blood count, serum chemistry profile, tests for feline leukemia virus (FeLV), and feline immunodeficiency virus (FIV). Blood testing is also available for feline herpes virus.
Common causes of conjunctivitis include feline herpesvirus (FHV-1), chlamydial, and other bacterial infections; a less common cause is allergies. Depending on the cause, certain antibiotic and antiviral agents may be used for treatment. Bacterial and chlamydial infections usually respond well to topical and oral medications. On the other hand, patients infected with viral agents may not respond as well to these treatments. Antiviral therapy requires frequent applications, sometimes as often as every 2-3 hours, in order to achieve the maximal effect. Antibiotic therapy is usually given at the same time as antiviral therapy in order to treat any secondary bacterial infection that may be present. Similar to human cold sores, viral infections are associated with stress; therefore, maintaining a low-stress environment may help reduce recurrences.
Superficial corneal ulcers can usually be treated similar conjunctival abnormalities; however, a large or deep corneal ulcer and corneal sequestrum may require surgical intervention. One specific treatment is surgical removal of infected or devitalized tissue (keratectomy). The cornea may require additional support, such as conjunctival grafting, following the keratectomy. Grafting also enhances the long-term health of a devitalized cornea by introducing blood vessels into a normally avascular area. With chronically infected eyes that contain excessive scarring, scar tissue may be surgically reduced to improve vision or tear drainage.
In general, response to therapy is good with bacterial and chlamydial conjunctival infections. Unfortunately, viral infections may be slow to heal and often recurrent. Because complications can have devastating consequences, such as pain and blindness, it is important that the treatment schedule is followed closely. Re-examinations to monitor progress and to adjust therapy will be advised when necessary.
The iris is the most common origin of primary intraocular tumors in all species of domestic animals. The iris is the most common site of origin for ocular melanocytic (brown pigmented) tumors in canine and feline species. Feline diffuse iris melanoma is the most common type of ophthalmic melanoma (cancer) in cat species, with an average onset age of 11 years. FDIM begins as concentrated or multiple areas of iridal pigmentation that gradually increase in size.
The progression rate of FDIM is highly variable and the disease can have long dormant periods. FDIM can be metastatic (spreading of the tumor to the rest of the body) in felines and may spread to the lung, spleen, liver and other parts of the abdomen. This unpredictability makes it challenging for Veterinary Ophthalmologists to offer advice on when best to remove the affected eye, which may still provide vision.
Photographing the affected eye over time intervals is a very helpful way to document growth of the lesion, iridal pigmentation change, and changes in anterior chamber depth. Other diagnostic options include a full body X-ray to rule out the metastasis and a full blood panel to establish a baseline.
Laser therapy is not recommended for iris melanoma in cats owing to their higher metastatic potential.
Less InfoFeline herpesvirus (FHV-1) is a common cause of eye and upper respiratory infection in the cat. This virus is very common in the cat population, but it is not contagious to people and other species of animals such as dogs. Herpesvirus is easily passed from one cat to another through sneezing, coughing, grooming, and/or simply living in the same household with an infected cat. While it is quite contagious, most cats contract this infection from their mothers before they are even weaned. This virus is in the same family as the chicken pox virus. As you may know, some people will develop ‘shingles’ in their adult lives, which is a re-emergence of the chicken pox virus that has been lying dormant in the body since childhood. The same is true for cats with FHV-1. Clinical signs associated with infection can vary greatly between cats. Some cats will never have signs after the initial infection while other cats will have episodes throughout life.
Some cats affected with FHV-1 may only have mild conjunctivitis (redness and inflammation of the white part of the eye) of one or both eyes. Other cats have more severe disease and may show ocular and nasal discharge, conjunctivitis, coughing and sneezing. Cats may also develop ulcers of the cornea (the clear “window” in the front part of the eye). Corneal ulcers can be very painful and serious enough to cause noticeable scarring or even perforation of the normally clear cornea.
After initial recovery from the herpesvirus infection, an estimated 80% of the cats become a carrier of the disease. In other words, the disease goes into temporary remission but the cat may still be infectious. In these cats, stress and illness can reactivate the virus, causing repeated infections or recurrences of the clinical signs throughout life. Stressors may include moving to a new house, having new pets or houseguests in the household, construction/remodeling, a traveling owner, etc.) Repeated or chronic infections have been associated with diseases such as dry eye, symblepharon (adhesion of the conjunctiva to itself or to the cornea), corneal sequestrum (an abnormal brown plaque formation on the cornea), and possibly eosinophilic keratitis (an immune-mediated condition of the cornea).
The definitive diagnosis of feline herpesvirus infection is accomplished by laboratory testing. Many tests are available through a professional diagnostic laboratory. They include virus isolation, fluorescent antibody (FA) testing, serology such as ELISA or serum neutralizing titers, and polymerase chain reaction (PCR) testing. It is important to realize that these tests may have false negative results. On the other hand, certain cats in the carrier state but without apparent clinical signs can also test positive for some of these diagnostic modalities. Since the disease is extremely common, it is not always necessary to perform diagnostic testing, but your veterinary ophthalmologist will discuss this with you at the examination.
Treatment for herpesvirus is aimed at controlling clinical signs and reducing secondary complications. It is important to note that there is no cure for herpesvirus, and once infected, your cat has the virus for life. Some animals will never have clinical disease after the initial infection while others may have frequent recurrences. Cats that have recurrent outbreaks often have a stressful trigger, which if identified can be avoided or minimized. This can reduce the number of outbreaks. Typically, therapy includes topical antiviral drops or ointment for the eye and occasionally an oral antiviral medication. Sometimes starting medications prophylactically (before a known stressor) the severity of the recurrent infection can be reduced. Some anecdotal reports state that L-lysine, an amino acid dietary supplement, can inhibit viral replication. This has been shown in a laboratory setting but not in cats with natural infection. There are no studies proving that Giving L-lysine as a supplement may benefit cats with herpesvirus as many owners feel it reduces outbreaks. In any event, there are no known side effects of L-lysine documented in the cat.
Vaccination against herpesvirus infection is included in the typical feline vaccination schedule provided by your primary care veterinarian. The vaccine minimizes the clinical signs of the herpesvirus infection but does not prevent future outbreaks. Additionally, the vaccination does not cure cats already infected with the herpesvirus.
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 is the uveal tract, which is rich in blood vessels. 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).
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 ciliary body 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 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 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 diseases 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; high pressure within the eye (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.
Less InfoThe conjunctiva refers to the pink tissue surrounding the eye, third eyelid, and lining the upper and lower lids. This tissue contains numerous structures, called follicles, which are important for the local immune system. In some dogs, the conjunctiva can mount an exuberant reaction to environmental allergens, such as dust and grass, leading to follicular conjunctivitis. This condition is most commonly seen in juvenile dogs up to 18 months of age, as their immune system is still developing.
The most obvious clinical symptoms include eye discharge and an increase in redness of the conjunctival tissue. On closer examination, small semi-transparent, raised follicles are seen, most commonly underneath the third eyelid. They can also be present in the surrounding conjunctiva. These follicles are normally not readily visible to the naked eye. However, in this condition, they become enlarged due to chronic stimulation of the local immune system. This chronic stimulation is often associated with environmental irritants, such as plant matter, and is therefore more common in large breeds with more exposure of their conjunctiva. If large enough, these follicles can also be irritating to the surrounding tissue. Diagnosis of this condition is most commonly made by clinical appearance, although it can be confirmed by sampling the follicles and examining the cells under the microscope.
Treatment usually involves flushing the area with eye wash to remove antigens and debris. In addition, application of a topical steroid solution will help decrease local inflammation. In cases non-responsive to topical therapy, mechanical debridement of the follicles may help to stimulate resolution. Follicular conjunctivitis is typically self-limiting and usually improves once dogs grow older and their immune system matures.
Glaucoma describes a neurodegenerative condition of the optic nerve, which eventually leads to blindness. In humans, elevated intraocular pressure is one of the major risk factors for developing glaucoma; however, in veterinary medicine, glaucoma is always associated with elevated intraocular pressure. In order to understand the mechanisms of glaucoma, it is necessary to understand the normal flow of fluid that maintains the intraocular pressure. The intraocular fluid, also known as aqueous humor, is produced behind the iris in the ciliary body. This fluid flows through the pupil and drains from the eye at the iridocorneal angle, a sieve-like network located between the iris and cornea. Aqueous humor is produced and drained from the eye at approximately the same rate, resulting in a stable pressure within a range of 15 to 25 mmHg (millimeters of mercury). When fluid flow out of the eye is compromised, intraocular pressure rises above normal. High pressures lead to death of the cells, which make up the optic nerve and retina and blindness ensues.
In general, there are two broad categories of glaucoma: primary and secondary. Primary glaucoma occurs without any previous ocular disease. It is known to occur in certain purebred breeds of dogs and thought to have an inherited basis. Primary glaucoma can be further divided into open-angle and narrow or closed angle. Open-angle glaucoma is common in human patients but is very rare in veterinary patients. Narrow or closed-angle glaucoma occurs as a result of a defect in the development of the normal intraocular drainage system, termed goniodysgensis. Secondary glaucoma is a consequence of another primary ocular disease that interferes with the natural flow of ocular fluid. Diseases that commonly cause secondary glaucoma include ocular inflammation, lens dislocation, and ocular trauma.
Glaucoma results in blindness by blocking the nerve impulse through the optic nerve. Once the optic nerve has been permanently damaged, vision cannot be restored. With early, aggressive, and appropriate medical and surgical therapy, vision may be restored. Unfortunately with extreme elevations of pressure, the eye becomes permanently blind and painful. Even if the ocular pressure is restored to normal, enough changes may have occurred already for the eye to remain blind. The aim of therapy at this point is to maintain a pain-free eye and a comfortable patient.
The diagnosis of glaucoma is based on history, clinical signs, tonometry, and gonioscopy. Redness of the conjunctiva (white part of the eye), clouding of the cornea, dilation of the pupil, and pain are common clinical signs of glaucoma. In the later stages, the eye may become enlarged. Tonometry is the measurement of intraocular pressure. A variety of techniques can be used to estimate intraocular pressure, including Schiotz tonometry, applanation tonometry, and rebound tonometry. Gonioscopy is a technique used to evaluate the iridocorneal angle. It involves placing a dome-shaped contact lens (goniolens) on the corneal surface. This lens permits the direct visualization of the drainage angle. Gonioscopy occasionally requires sedation, but in calm and cooperative patients, it can be performed with topical anesthetics alone. This technique is essential in determining the nature of the glaucoma and will provide insight as to whether the unaffected eye is at risk for developing glaucoma.
After the initial diagnosis of glaucoma is made, the patient is generally treated with aggressive medical therapy. This may require a brief period of hospitalization. During periods of hospitalization, osmotic diuretics may be given orally or intravenously to reduce the intraocular pressure quickly. Once the pressure has been controlled, maintenance levels of medications are prescribed for long-term therapy. Medications that are commonly used include those that are aimed at improving the outflow of aqueous humor or suppressing its production. Drugs that can improve aqueous outflow include pilocarpine, demacarium bromide, and latanoprost. Other medications designed to reduce the aqueous production include carbonic anhydrase inhibitors and beta-blockers. Unfortunately, medical management of glaucoma is often unsuccessful in veterinary patients, and the initial response to medication may be short-lived. In many instances, it is impossible to control the pressure with medications alone and a variety of surgical techniques have been developed to aid in the control of pressure.
Surgeries for glaucoma can be divided into vision-saving procedures and surgeries of comfort. Vision-saving procedures are an option for patients with acute glaucoma that still have vision. Once an animal has lost vision due to glaucoma, these surgeries are of no benefit.
Cyclophotocoagulation – In this procedure a laser is used to kill a portion of the cells in the ciliary body that produce aqueous humor, thereby reducing the rate of fluid production. Unfortunately, the laser energy can create significant inflammation inside the eye, which may exacerbate the glaucoma in the days following the procedure. Intraocular hemorrhage and cataract formation (if performed by a transscleral approach) are uncommon but are potential complications. Over time, the fluid-producing cells may regenerate leading to the recurrence of high pressure, necessitating a repeat procedure.
Gonio implants – In order to facilitate outflow of fluid from the eye, a drainage device can be surgically implanted. A tube is placed inside the eye, which drains through a pressure-regulating valve placed beneath the mucous membrane surrounding the eyeball. This procedure can be very effective; however, the body will create scar tissue surrounding the implant causing it to fail over time. Published reports give an average of six months before the implant stops working, although success time periods of over a year are not uncommon. Cyclophotocoagulation is usually performed in combination with this surgery. Complications of this surgery include intraocular hemorrhage, inflammation, infection, and migration of the implant. If too much inflammation occurs within the eye, obstruction of the draining tube can occur. Surgeries of comfort are discussed in more detail in another handout.
Unfortunately, glaucoma remains a leading cause of blindness in animals. Because of the insidious nature of the disease, many animals are presented at a time when it is not possible to restore vision to the initially affected eye. The goal of the veterinary ophthalmologist in treating the patient with glaucoma is to restore vision where possible and to maintain a cosmetic, pain-free eye. Glaucoma is seldom diagnosed early enough to restore vision in the first eye affected. Therefore, during the initial examination, time will be spent to evaluate the “good” eye. Prognosis is dependent upon early diagnosis, appropriate medical therapy, and regular and consistent re-evaluation.
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.
Systemic hypertension (high blood pressure) is a common problem in companion animals, particularly in cats. Frequently, there are no obvious systemic signs indicating your pet has high blood pressure. The first sign observed may be the sudden onset of blindness. The retina lines the back of the eye and functions similarly to film inside a camera. Long-standing elevations in blood pressure lead to damage of the blood vessels throughout the body and this occurs in the retina of the eye as well. These damaged blood vessels leak fluid, which accumulates under the retina and causes it to detach, resulting in blindness. Some owners will notice that their pet’s pupil is very large, that one pupil is a different size than in the other eye, or that the green “eye shine” is more obvious. Other signs may be bleeding within the eye or neurologic changes.
Normal blood pressure in cats and dogs is similar to humans and should be around 120 mmHg. However, due to the effects of stress on our patients in the hospital, even normal animals can have blood pressure readings significantly higher than the normal range. Your doctor will take into consideration many factors in determining a treatment plan for your pet. It is important that your pet has their blood pressure monitored in a quiet setting and in a consistent manner with as little distress as possible for accurate measurements. If your pet is placed on medications it is imperative that these medications be consistently administered as directed by your veterinarian and never be stopped abruptly. If medications are stopped, signs will likely return.
Most cats and dogs affected with high blood pressure have developed this condition as a result of another underlying health problem such as kidney disease, heart disease or an endocrine disease (Hyperthyroidism, Cushing’s disease, Diabetes Mellitus, or others). To manage high blood pressure appropriately, it is important to identify and treat any underlying diseases. Thus, a full health history, current blood work, and urine analysis are extremely helpful when dealing with this syndrome. Early diagnosis and treatment will improve overall health and decrease the risk of ongoing retinal damage and systemic side effects. Systemic hypertension is not only blinding, if severe damage to the other organs occurs, it can be a life-threatening disease as well.
Depending on the degree of retinal detachment, the amount of bleeding and the duration of retinal disease, your pet may regain vision with treatment. Regular eye examinations and blood pressure monitoring will be required long-term. Your veterinary ophthalmologist and your primary veterinarian will work together to determine the best treatment and monitoring plan for your pet.
Hyphema simply means blood inside the eye. It can occur for many reasons and it can be a sign of a serious disease process, such as rat poison ingestion, certain infections, cancer, high blood pressure, trauma, and retinal detachment. As you can see, many of these problems are not just ‘eye diseases.’ The exact cause may be difficult to determine since the blood can mask the location of the injury or disease. Because some of these conditions are quite serious, if the bleeding develops suddenly it is important that your veterinarian or an emergency veterinarian rule out the most serious causes, such as a blood clotting abnormality or a toxicity that is affecting the whole body. Once it is clear that your pet is not in a life-threatening situation, it is important to see the veterinary ophthalmologist.
As seen in the diagram above, sometimes the entire eye is not filled with blood and only a small amount is present. Your awareness of your pet’s symptoms and compliance with recommendations for recheck examinations can reduce the risk of complications. If any complications arise, it is important that they are promptly identified and treated.
Notify the Doctor if Any of the Following Occur:
Immune mediated keratitis (IMMK) occurs when the immune system has been stimulated to attack corneal tissue leading to inflammatory changes within those tissues. Like many other immune-mediated diseases that can affect other tissues in the body, the underlying mechanism of IMMK is not well understood. Changes to the cornea can include color changes due to pigmentation, blood vessel formation, and the formation of opacities. The appearance of each case will vary and may also be dependent on the type of IMMK with which your pet has been diagnosed. Other signs of IMMK may also include reddening of the sclera (white tissue around the cornea), excessive discharge, or squinting; however, these signs can be nonspecific and are seen with a variety of other ophthalmic conditions as well.
Chronic superficial keratitis (or Pannus) and superficial punctate keratitis are two examples of IMMK in the dog. Pannus can be seen in many breeds but has been strongly associated with the German Shepherd and the Greyhound. It manifests as pigmentation and vascularization of the cornea in a characteristic pattern that starts at the corner of the cornea and moves across it. Superficial punctate keratitis has been described in the Shetland Sheepdog and the long-haired Dachshund, but, like Pannus, can be seen in any breed. Superficial punctate keratitis often looks like grey, opaque dots on the cornea, prompting owners to bring their pet into the ophthalmologist. In both forms of IMMK, the patient may or may not be uncomfortable due to irritation and possible corneal ulceration.
The mainstay of therapy for any IMMK is topical medications to stop inflammation and suppress the local immune system. Usually one or two types of medications are used depending on the type of IMMK and the severity of the symptoms. One group is immunomodulatory medications and include cyclosporine and tacrolimus. The other group is steroid medications and include prednisone or dexamethasone. Most dogs with IMMK do very well with medical management; however, medications are often needed very long term or, in some cases, permanently. The veterinary ophthalmologist will recommend a treatment plan for your pet’s specific needs. They will also recommend recheck exams to monitor your pet’s condition. The goal of therapy for IMMK is to allow your pet to be on the lowest amount of medications needed to keep their IMMK controlled. These recheck examinations will be very important as medications will often be adjusted during these visits.
Please call our office if you notice any change in the appearance of your pet’s eyes, such as redness, or your pet seems uncomfortable (squinting or holding the eyes closed).
Less InfoCollies 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.
Iris Atrophy is an age-related thinning of the iris that commonly occurs in cats and dogs. The iris is the colored tissue inside the eye that surrounds the pupil (which is a circular structure in the dog and a slit-like structure in the cat). The iris has a muscle that allows the pupil to become smaller (like a camera aperture) when exposed to light to protect the retina in the back of the eye. However, iris atrophy will occasionally result in thinning of this muscle, which can eventually prevent the pupil from constricting. In these cases, the pupil may remain dilated, or large. In addition, iris atrophy can occasionally result in a “moth eaten” appearance to the iris.
Iris Atrophy is typically not a problem and rarely results in changes to a pet’s functional vision. It is non-painful. Some animals will exhibit sensitivity to and squinting with bright light when the iris atrophy is significant. Since this condition may be mistaken for a potentially serious problem, such as glaucoma or a neurologic condition, an examination with your pet’s veterinary ophthalmologist may be necessary.
Less InfoKeratoconjunctivitis 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 is the focusing structure of the eye, known as accommodation. It is suspended in place by small fibers or ligaments and is located immediately behind the iris and the pupil. If these ligaments that suspend the lens break down, the lens may become partially unstable and may partially dislocate (sub- luxated) or fully dislocate (luxated) from its normal position. Movement of the lens forward through the pupil into the front half of the eye is called Anterior Lens Luxation. Movement of the lens backward into the back half of the eye is called Posterior Lens Luxation.
In general, there are two broad categories of Lens Luxation: primary and secondary. Primary Lens Luxation is caused by an inherent weakness and degeneration of the ligaments that suspend the lens. Primary lens luxation can be inherited in many breeds, including several terrier breeds, Border Collies, Brittany Spaniels, Australian Cattle Dogs, and Shar Pei’s. In these breeds, spontaneous luxation of the lens occurs in early adulthood (most commonly 3-6 years of age) and often affects both eyes, although not necessarily at the same time.
Lens Luxation can also occur secondary to other primary problems of the eye, including inflammation, cataracts, glaucoma, cancer and trauma. Lens Luxation can lead to inflammation and glaucoma (increased intraocular pressure), which can result in painful, teary, red eyes that may look hazy or cloudy. Irreversible vision loss may occur if this condition is not addressed immediately.
If detected early, surgical removal of the lens can be beneficial. Unfortunately, there is a high risk of complication with lens removal; all animals will experience inflammation and will require lifelong topical medication. Glaucoma is not uncommon following lens removal and can lead to blindness. Retinal detachments and bleeding are also potential complications of surgery. Other surgical procedures can be performed at the time of lens removal to reduce the chance of these complications. When a lens is removed, your pet will be able to see, but will be hyperopic (far-sighted). Posterior lens luxations may be treated with medications to constrict the pupil, which traps the lens in the back portion of the eye, where it is less likely to cause a problem. Even with this medical treatment, it is still possible for a posterior lens luxation to become an anterior lens luxation. If the eye is already suffering from severe inflammation or glaucoma, eye removal, or a procedure to place a prosthetic eye, may be recommended.
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.
A limbal or epibulbar melanoma is a deeply pigmented mass that arises from a pigmented shelf at the limbus, which is where the cornea (outer clear portion) and the sclera (white portion) meet. These tumors are typically benign but can be locally invasive. Most of these masses are single tumors that originate from the location in which they are visualized and do not spread from other areas of the body. They are usually smooth and have a dark brown to black pigment and are most often raised above the contour of the eye.
They are more commonly seen in German Shepherds, Golden Retrievers, and Labrador Retrievers but may be seen in any breed of dog and occasionally, in cats.
If the mass is small and not causing any structural changes within the eye, your ophthalmologist may recommend serial monitoring of the size of the mass. If your dog has a mass that is enlarging, then your ophthalmologist may recommend surgery. These masses may become large enough that intervention is not possible. Close monitoring with or without medication and/or surgical intervention may be recommended.
Surgical options may include:
Typically, the prognosis is good for these tumors, as they are most often benign and locally invasive. The best option for your pet will be determined by discussion with your ophthalmologist.
If you have any questions or concerns regarding Limbal Melanomas, please call Eye Care for Animals.
Less InfoLipid Aqueous results in a clouded appearance of the eye and is caused by a high concentration of lipids (the fatty substance in the cells) collecting in the aqueous humor (the thick watery substance located inside of the eye between the lens and cornea). This can occur in a pet of any age, gender, or breed.
Clinical signs of lipid aqueous include:
A thorough physical and ocular examination will be performed on your pet, considering the background history of symptoms and possible incidents that might have led to this condition.
Lipid Aqueous often results from a condition of hyperlipidemia (fat in the blood), and simultaneous breakdown of the blood-aqueous barrier due to uveitis (inflammation in the eye). Hyperlipidemia may also destabilize the blood-aqueous barrier directly. The breakdown of this barrier allows lipids to leak out of the bloodstream and into the eye. High levels of lipids in the circulating blood following a meal may occasionally result in the appearance of lipid aqueous, if uveitis is present.
Lipid Aqueous requires treatment for the associated uveitis, which is usually mild, and for any underlying metabolic disorders. If your pet is diagnosed with hyperlipidemia, you will need to change the pet’s diet to one that is lower in fat and calories, to decrease the amount of fat in the bloodstream. Your pet will also need anti-inflammatory medications to be given at home.
Your veterinary ophthalmologist will continue to monitor your pet closely after the initial treatment. Intraocular (within the eyes) pressure should be monitored to detect possible secondary glaucoma. The frequency of subsequent rechecks will be dictated by the severity of the disease and your dog’s individual response to treatment.
The prognosis is typically good for these patients, but it does depend heavily on the underlying condition that may have contributed to the Lipid Aqueous. The condition generally responds quickly (within 24–72 hours) to moderate anti-inflammatory therapy. Keep in mind that recurrence, and the need for further treatment, is possible.
Less InfoThe Meibomian glands are a special kind of secreting gland at the edge of the eyelids in both dogs and cats. These glands are responsible for the production of meibum, an olive oil-like fat that prevents evaporation of the eye’s tear production. In dogs and cats, there are approximately 20-40 openings of the Meibomian glands on the eyelid margin.
Meibum is the outer layer of the tear film, consisting of a very thin, oily layer of various fats, including fatty acids. Meibum prevents tear spillage, known as epiphora, onto the skin around the eyes by trapping tears between the oiled edge and the eyeball.
Dysfunction of the Meibomian glands often cause a sensation of dry eye, as your pet’s natural tear production will evaporate more rapidly than normal. Your pet may actually look as though he/she is tearing more, and this “drying effect” may cause scar tissue to develop on the eye. Meibomitis, or inflammation of the Meibomian glands, causes these glands to be obstructed by thick, waxy secretions. Commonly, this inflammation is due to another underlying condition, such as allergies. Clinically, this is seen as “pointing” or more swollen Meibomian gland openings that can typically only be observed with microscopic examination of the eyelid margin. This condition can be itchy, and if your pet does rub or paw around the eye, this can make inflammation worse. An Elizabethan collar may be recommended during treatment to prevent any rubbing.
Less Info
The nasolacrimal system is a thin walled tube that drains tears from the surface of the eye into the nasal passages and oral cavity. The nasolacrimal duct begins at two small openings in the conjunctiva at the eyelid margins on the side of the eye nearest the nose. About half of the tears are lost from the cornea and conjunctiva by evaporation and the remaining half drain from these ducts. Most tear drainage into and through the nasolacrimal duct is moved passively by external forces like gravity. Some drainage is due to capillary action and the force of eyelid closure. Blockage of the nasolacrimal duct may occur in dogs, cats, rabbits, and horses. Symptoms include but are not limited to:
A bright green dye called fluorescein is applied to the eye to identify normal passage of fluid through the nasolacrimal system. In addition, the openings into the duct are examined at high magnification using a slit lamp biomicroscope. The slit lamp enables the ophthalmologist to carefully evaluate the patient’s cornea, conjunctiva, and nasolacrimal ducts. If a nasolacrimal duct blockage is diagnosed or suspected, a small blunt cannula may be inserted into the duct openings in the eyelid. Once in the opening, irrigation of the duct with saline is performed. This is done using a local anesthetic applied to the eye in most cases, but occasionally injectable sedation is needed. Flushing the duct with saline may eliminate blockage or it may provide evidence of ductal scarring that can cause permanent occlusion of the duct. Other diagnostics tests that may be recommended include:
Nasolacrimal blockage can occur due to anatomical defects present at birth, breed related eyelid conformational abnormalities, inflammation of or foreign bodies lodged in the ducts, and occasionally tumors pressing on the ducts. Most blocks in dogs occur due to the shape of the eye, nose and face as well as mild inflammation of the pink tissues in the eye. In cats, prior infection with the feline herpesvirus can lead to narrowing or scarring down of the ducts.
Many nasolacrimal blockages can be treated medically with anti-inflammatory and antimicrobial therapy. Some blockages improve but may not completely resolve. Treatment may be used for comfort if resolution is not achievable. For some cases, surgical intervention may be necessary, particularly for conjunctival or scar tissue obstructing the duct openings, foreign bodies in the ducts, or for tumors) Surgery may involve exploration, resection of tissue or reconstruction of normal tissues.
Complications are rare and including anesthetic risks, only account for less than 5% of cases. Complications that may occur include:
Ocular injuries resulting from accidental contact with cactus spines or other plant foreign bodies are the most commonly seen ocular foreign bodies in dogs or cats in desert regions. Other foreign bodies include plastic, glass, pellets or bb’s, grass awns, bristles, thorns, small stones and even popcorn kernels can adhere to the cornea, leading to corneal ulceration, infection, or rupture. Minor injuries may heal without treatment by formation of scar tissue which can lead to decreased vision. More serious injuries may require surgery.
Long cactus spines embedded within the cornea may extend into the deeper tissues of the eye including the iris and lens. These embedded spines are difficult to remove safely without surgery under an operating microscope. During surgery, a precise corneal incision is often required to free the spine from the cornea. If this is required the incision may then be surgically repaired to prevent leakage of the fluid from the eye and seal the wound. In some cases a foreign body may be found completely inside the eye, requiring a more complicated procedure involving a larger incision to facilitate removal. Spines that contact and penetrate the lens can lead to cataracts, as well as, initiate serious inflammation inside the eye. This inflammation can lead to discomfort and even glaucoma.
More commonly we find patients with ocular discomfort associated with multiple small cactus spines called glochids embedded in the pink tissue around the eye (conjunctiva) – in addition to the cornea and eyelids. These spines cause discomfort and can abrade the corneal surface. These tiny bristles require magnification for visualization, and removal is generally performed under anesthesia with the aid of an operating microscope. These bristles can migrate beneath the conjunctival surface and may not be visible, even with the aid of magnification. If they break through the conjunctival surface at a later time, a process which may occur days to weeks following initial exposure, a second procedure is sometimes required to remove additional spines. As with all surgeries, anesthetic and post-operative complications can occur. This is seen rarely with ocular surgery, but serious complications can lead to loss of vision or loss of the globe.
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 InfoPannus, 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.
Prolapsed gland of the third eyelid or “cherry eye” is the most common disorder of the third eyelid. It is most common in puppies and usually results from weakness in the connective tissue attachments that hold the gland in place. This weakness allows the gland, which is normally located behind the third eyelid to flip up and become visible. The prolapsed gland will appear as a smooth, pink to red mass protruding at the lower inner corner of the eye. This condition can be present in one or both eyes.
The gland of the third eyelid significantly contributes to tear production. Therefore, if this condition is left uncorrected chronic conjunctivitis (inflammation of pink tissue around the eye), discharge, and low tear production can occur. Low tear production can lead to corneal scarring, ulcerations, vascularization (blood vessels in the cornea), or ocular rupture. Some of these conditions can lead to blindness.
Surgical repositioning of the gland is recommended as the treatment of choice. Removal of the gland is almost never advised as a treatment. Many surgical techniques are used to anchor the gland back in the normal position. Surgical repositioning has a success rate of 90-95% in patients. If your pet has only one gland prolapsed, your doctor may recommend a prophylactic tacking of the other gland.
At the time of discharge, your pet may have the eyelid(s) partially sutured closed to protect the surgery site. If present, they will be removed in 10-14 days after surgery. An Elizabethan or “cone” collar is also placed after surgery and recommended until your pet’s follow-up examination. Limited activity is also recommended postoperatively to decrease the likelihood of gland re-prolapse.
As with any surgical procedure, complications are possible including anesthetic risks. The most common complication following surgical repositioning of the third eyelid gland is re-prolapse of the gland. This is not limited to but most common in the English Bulldog. Additional complications are rare and include conjunctivitis, inflammation of the third eyelid, break down of the tissue or suture (wound dehiscence), infections at the surgical site, corneal ulcerations (superficial to deep), or corneal scarring.
Eosinophilic keratitis is an inflammatory condition that affects the cornea and/or conjunctiva. The characteristic appearance is white, tan or pink roughened plaques on the corneal surface. These plaques are composed of inflammatory cells known as eosinophils. The cause of eosinophilic keratitis is believed to be related to an underlying feline herpesvirus infection. This disease is progressive and can grow to involve the entire surface of the eye causing blindness and discomfort. Often it is initially detected in one eye; however, the disease often progresses to involve both eyes.
Superficial corneal scraping is usually adequate to obtain a diagnosis, which is confirmed by the presence of eosinophils under light microscopy. Occasionally, microscopic examination is not sufficient for diagnosis and further diagnostics may be recommended.
Due to its suspected association with feline herpes virus (FHV-1), diagnostic testing and/or empirical treatment for herpes virus may also be indicated. Treatment for eosinophilic keratoconjunctivitis consists of topical anti-inflammatory medications and/or systemic hormonal modification. Ovaban (megestrol acetate) is a synthetic progesterone (hormone) used to treat this disease. It is very effective but does have possible side effects, which may include transient diabetes mellitus, enlargement or (rarely) cancer of the mammary gland, and liver toxicity. The length of treatment is variable and some cats may have disease recurrence when medications are discontinued. The majority of patients can remain comfortable and visual when there is client compliance with respect to the medication schedule.
Ocular proptosis is the traumatic forward displacement of the globe out of the orbit, most often resulting in the globe being displaced in front of the eyelids. This is a serious ocular emergency that requires immediate attention to help minimize patient discomfort, damage to the eye, and damage to vision.
Proptosis can occur secondary to acute trauma. The type and degree of trauma to induce a proptosis can vary depending on the pet and breed. Sometimes excessive physical restraint or increased pressure around the neck from leash pulling can cause proptosis in brachycephalic (flat-faced) breeds, where little other than the eyelids maintain the globe within the orbit/”socket”. More trauma is usually required to cause proptosis in non-brachycephalic dogs and cats. In cases of dog-on-dog fight or blunt force injury (hit by car, there may be additional injuries (puncture wounds, fractures) that also require treatment.
Proptosis frequently leads to damage of the globe and associated important structures needed for normal vision. Many factors are considered when determining the patient’s visual prognosis, which may be improved in cases managed promptly after the inciting trauma. Prognosis for maintaining a comfortable eye, regardless of visual outcome, depends on several factors.
Negative prognostic indicators include:
Treatment includes timely globe replacement and temporary sutures in the eyelids to protect the exposed globe until the orbital swelling resolves. Eyelid sutures are left in place for a minimum of two to three weeks while the damaged tissues heal. Postoperative care with oral and topical broad-spectrum antibiotics, a systemic anti-inflammatory, pain medication, and an Elizabethan collar are commonly required.
Long-term complications of proptosis are common, as the traumatic displacement of the globe can damage the optic nerve, extraocular muscles, and the vascular and nervous supply to the eye. Lateral deviation of the globe (strabismus) is often seen due to avulsion of the muscle in the inner corner of the eye (called the medial rectus muscle). This deviation can change the appearance of the eye long term and it may be associated with recurrent corneal ulcers due to changes globe position, tear film quality, and sometimes due to poor or reduced blinking ability. Long term management with medication may be necessary after the injury has healed.
Another treatment option for proptosed globe(s) includes surgical enucleation (removal) of the injured globe, which may be the appropriate option if the patient presents with one or several of the previously listed negative prognostic indicators.
If you have any questions regarding proptosis, please call your Veterinary Ophthalmologist at Eye Care for Animals.
Less InfoRetinal reattachment surgery is offered at our Pasadena, California (626-564-0202) hospital, where patients are received from around the country for surgical care.
The retina is a thin membrane that lies against the back wall of the eye. Similar to the way a camera works, images from the outside of the eye are focused by the cornea and lens onto the retina, which can be compared to the film in a camera. If the retina is not properly positioned or becomes damaged, vision is diminished or lost. The retina is only fused to the wall of the eye at its peripheral edges and at the optic nerve. Much of the retina relies on vitreous, a firm molded gel (like Jello), to tamponade it against the back of the eye.
Although there are many types of retinal detachment, there are two main scenarios that require retinal surgery. The first is called vitreal degeneration/dysplasia, where the vitreous humor, instead of forming a semi-firm gel, liquefies. It transforms from a Jello-like consistency to a chicken noodle soup-like consistency and can no longer effectively hold the retina in place. As the eyes move, the swirling liquefied vitreous tugs on the retina, causing tears and fluid flow under the retina, separating it from the wall of the eye. The tears often progress, until the entire retina has peeled off the back of the eye. This type of retinal detachment (rhegmatogenous retinal detachment) is inherited or genetic in many breeds including the Shih Tzu, Italian Greyhound, Boston Terrier, Poodle and Terrier Breeds. Tears may be precipitated or exacerbated by vigorous head shaking during play.
The second main type of retinal detachment occurs secondary to cataracts, cataract surgery or other intraocular surgeries. Inflammation in the eye lead to areas of adhesion between the retina and the vitreous, putting traction on the retina, pulling it off the back of the eye. Retinal detachment can occur due to other causes such as trauma.
Because most dogs continue to behave normally as long as one eye has vision, retinal detachment in the first eye is often missed. Patients often present to a veterinary ophthalmologist for vision loss when the retina in the second eye detaches. Signs of retinal detachment include vision loss, a dilated pupil, increased eyeshine, and sometimes blood within the eye. With cataracts, retinal detachments are often detected during pre-operative screening ultrasounds. They may also be identified following cataract surgery during recheck examinations.
Surgical correction is accomplished by entering the back of the eye via small ports. The diseased vitreous is first removed. The detached retina is then repositioned back against the back of the eye using a heavy oil called PFO. The PFO is replaced by silicon oil, which acts as an artificial vitreous. A laser is also used to strengthen the retina’s attachment to the back of the eye.
The two biggest factors that influence the success of surgery are: the length of time the retina has been detached prior to surgery and the cause of retinal detachment. Predisposed breeds, such as the Shih Tzu, tend to have the highest success rates (often >90%) if retinal detachments are caught early. Retinal detachments following blunt trauma or bite wounds often have the lowest success rate (<50%). The veterinary ophthalmologist performing retinal reattachment surgery will be able to further discuss the estimated success rate for your pet, the details and care involved with retinal reattachment surgery, as well as work with your local veterinary ophthalmologist to provide long-term care for your pet’s eyes.
The success of retinal reattachment surgery has improved over the past decade with state of the art equipment and shorter surgery times. However, complications can arise and include retinal re-detachment and degeneration, glaucoma, chronic inflammation, bleeding inside the eye, corneal ulceration, cataract formation, changes in focusing, or silicon oil migration into the front of the eye.
While most retinal detachments are not initially associated with discomfort, long term, many dogs with an untreated retinal detachment will develop glaucoma, or an elevated pressure in the eye. As this can become an uncomfortable condition, your pet should continue to receive ocular exams over time. Should glaucoma develop, further treatment will be necessary to maintain comfort.
Less InfoSquamous cell carcinoma is one of the most common periocular tumors in horses, specifically horses located in areas of intense sunlight or high altitude. Non-pigmented regions of the skin are susceptible to the development of this tumor. The tumor may involve the eyelids, third eyelid, cornea or the tissues surrounding the eye itself. Appaloosas, color-dilute breeds, Belgians and other draft horses are particularly susceptible to development of this tumor.
A horse with an early squamous cell carcinoma lesion can be seen with a reddening, roughening or ulcerated area, along with increased tearing of the eye. The tumor soon develops into a small pink or red mass, which if left untreated, can enlarge and spread around and behind the eye, to the skull, sinuses of the skull, brain and to other parts of the body. Squamous cell carcinoma can be diagnosed in its earliest stages by a biopsy of the lesion, which can be performed by your veterinarian or veterinary ophthalmologist. Treatment and prognosis of squamous cell carcinoma vary with the location, size, and the extent of the tumor. Treatments may involve surgical removal, freezing or heating, radiation, laser ablation, immunotherapy, chemotherapy or a combination of the above. In some of these cases, the tumor becomes inoperable and the outcome can be devastating. There is potential for recurrence of the tumor despite the type of treatment used, and additional treatments may be necessary. The prognosis for horses with squamous cell carcinoma is usually good if the tumor is small and can be completely excised. If the tumor is large and extensive or involves the eyelids or space behind the eye, the prognosis may be poor.
The following are recommendations to minimize your horse’s risk of squamous cell carcinoma: avoid peak sun exposure between 10 a.m. and 3 p.m.; provide protection of the eyes from insects, dust, and wind by using an ultraviolet protective mask, sunscreen and fly repellent.
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.
Less Info
The term cyst refers to a fluid-filled structure lined by epithelial cells, similar to a water balloon. When these occur in the eye, they most often originate from the vascular tissues of the eye, called the uveal tract. The uveal tract includes the iris, the ciliary body, and the choroid. The iris is the easiest uveal structure to see, as it is the colored (brown, blue, golden, green, etc.) muscular tissue in the front of the eye that creates the black pupil. A cyst from the iris often appears dark or sometimes transparent, depending on species and how the light catches the cyst. They can be attached or free-floating within the fluid of the eye.
We do not exactly know what causes the cysts to form. There is likely a genetic component since they occur more frequently in certain dog breeds such as Boston Terriers, Golden Retrievers and Labrador Retrievers. While some cysts may result from abnormal contact between layers of the uveal epithelium, others are believed to be caused by inflammation inside the eye.
Cysts often do not cause a problem for veterinary patients, but if they do become a problem, your doctor may discuss options for cyst removal, such as surgical aspiration or laser treatment. Our primary concern with cysts, in most dogs, is that they can interfere with vision. In some dogs and in horses, the cysts can cause behavior changes that are believed to be due to the changes to vision.
We worry more about cysts in specific dog breeds, including Golden Retrievers, American Bulldogs, and Great Danes, because there has been a strong link between the presence of cysts and the development of glaucoma, which is a vision-threatening, painful condition. If you have one of these breeds, medical treatment and/or surgical treatment may be recommended.
It is very important to distinguish uveal cysts from melanoma, which is the most common intraocular cancer in veterinary patients. In general, we can distinguish between the two because cysts will allow light to pass through them (called transillumination) and melanomas will not. Sometimes, particularly in cats and horses, cysts do not transilluminate and may require an ocular ultrasound to determine whether they are fluid-filled (cysts) or solid (possible cancer).
Less InfoUveitis 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.
Uveodermatologic Syndrome is an autoimmune condition affecting the pigmented cells of the body, especially in highly pigmented organs like the eyes and skin. It is generally believed to be due to immune destruction of melanocytes, the pigment cells in the body. This condition is similar to a human condition known as Vogt-Koyanagi-Harada (VKH) syndrome and is often called VKH-like syndrome in dogs. The syndrome occurs most commonly in the Nordic breeds such as the Akita, Samoyed, Siberian Husky and Shetland Sheepdog, but can occur in any breed.
Clinical signs associated with this condition are due to progressive inflammation inside of the eye (known as uveitis). Ocular signs typically precede dermatological disease. Specific manifestations depend on the degree of inflammation, portion of the eye affected, and duration of the disease. Squinting, light sensitivity, and inflammation of the pink tissues surrounding the eye may be the first signs of the disease. Severe inflammation will ensue inside the eye and retinal detachments resulting in sudden vision loss are not uncommon. Progressive loss of pigmentation in the skin and hair (especially around the eyelids, nose, mouth, footpads, and perianal regions) can be noted. Over time, patients can develop skin infections and severe uveitis. Uveitis can lead to cataracts (lens opacity), scarring inside the eye, glaucoma (increased pressure inside the eye) and retinal detachments. These complications are devastating to the eye and result in blindness.
Treatment of the primary disease requires various drugs to suppress the overactive immune system. Symptomatic treatment is also initiated to treat the eyes and skin until the primary disease can be controlled. Initial treatment will likely be aggressive and frequent medications will be required. Medications will be tapered over time as the disease is controlled. Patients remain on long-term immunosuppressive therapy to control this autoimmune disease. Periodic blood testing is recommended to monitor these patients’ overall health and regular ocular examinations are also recommended to ensure good ocular health and control of this potentially blinding disease.