Corneal ulcer in a dog - treatment, symptoms, diagnosis. Corneal dystrophy Lipid protein corneal dystrophy in a dog

A dog with severe thinness and lack of appetite is clearly an unhealthy animal. The first, associative diagnosis for the "shy" is dystrophy. However, dystrophy in dogs is not only a lack of weight and an apathetic state, first of all, it is a violation of metabolic processes, and secondly, a serious threat to life.

The disease is classified depending on the nature of the disruption of processes into protein carbohydrate, mineral and fatty, the latter being the most common. Violation of metabolism and breakdown of substances leads to the accumulation of fat (droplets) in the tissues of the liver (lipidosis of the liver), less often, in the kidneys or myocardium of the heart.

The term "dystrophy" means a violation of metabolic processes in the body, which led to starvation, modification, degradation or death of cells and tissues. As you know, cells feed through membranes (walls), which are formed from lipids and proteins (proteins). In case of violation of the functioning of cell membranes, there is a deposition of fat droplets in the tissues of organs - the heart, kidneys, liver.

Note! Golden Retrievers are prone to muscular dystrophy. The disease can be called pedigree. It occurs due to a lack of dystrophin protein. Puppies and adult dogs get sick, effective methods of treatment do not exist, although research in this area is actively underway.

Causes of fatty degeneration in dogs

The disease is secondary, that is, the consequence of a violation that affects the body for a long time. Identification of the cause of the development of dystrophy is extremely important for subsequent treatment. As practice shows, the most common root cause is feeding poor-quality dry food.

Read also: Ear diseases in dogs: causes and main pathologies

Possible violations include:

• Violation of the heart muscle and respiratory system, hypoxia, anemia.

• Acute infectious diseases or chronic ailments that occur secretly.

• Unbalanced diet, lack / excess of proteins or fats, beriberi.

• Systematic treatment with antibiotics or other drugs that adversely affect the intestinal microflora.

• Eating foods that have expired.

• Poor chewing of food due to malocclusion, diseases of the oral cavity or teeth.

• Food or chemical poisoning that affects the functioning of the central nervous system.

• Hormonal imbalance, including diabetes.

• Diseases of the digestive system.

• Changes that led to degenerative processes in the body, including hunger.

Important! If you find a starving dog with obvious dystrophy and want to help her, in no case do not feed the animal with ordinary food. Live yogurt or kefir, egg yolk (in small amounts, but often) and medicines that restore the intestinal microflora are all that is needed so as not to kill the dog before visiting the veterinarian.

Signs of fatty degeneration in dogs

Most often, the disease proceeds in a sluggish form and becomes acute after stress or injury. In a visually healthy animal, there is rapid weight loss and a complete refusal of food, for no apparent reason. The acute stage proceeds quickly, however, the owners often confuse fatty degeneration with poisoning and lose precious time. In fact, the acute form of dystrophy is manifested by toxication with the following symptoms.

The eyes of animals, just like those of humans, are an indicator of their health. Bright and shiny eyes indicate that the animal is all right. If the owner notices cloudy eyes in the dog, then you should immediately take your pet to the veterinarian, as this may be a sign of a serious illness. In addition to such a natural cause of cloudy eyes as old age, the disease can be caused by serious pathologies that can lead to complete loss of vision.

Features of cloudy eyes in dogs

If the dog's eyes become cloudy, the owner needs to show his pet to a veterinarian who will examine the animal and make the correct diagnosis. Depending on the disease that caused clouding of the eye in a dog, you can see various manifestations of this condition:

• cataract;
• clouding of the cornea.

If you carefully examine the cloudy eyes of a dog in the photo, you can sometimes see signs of a clouded lens. In this case, the cloudy film on the dog's eye is located not far from the pupil. You can determine that the pet’s lens has become cloudy using a table lamp - under bright lighting, the clouded spot decreases in size, but if the dog is in a dimly lit room, then it expands.

If the dog has clouding of the cornea, then the entire surface of the eye becomes cloudy. It loses its luster and takes on a whitish or bluish appearance, which will be clearly visible in the photo.

If the pet has a cloudy eye due to old age, then a bluish or whitish spot appears directly near the pupil, which has become a sign of clouding of the lens.

Cloudy eyes in a dog - causes of corneal clouding

When the cornea of ​​the dog's eye is clouded, its surface becomes bluish or whitish, and may also lose its luster, which is clearly seen in the photo. The main reasons for this phenomenon:

1. Glaucoma

In this case, a cloudy film on the eye of a dog appears as a result of an increase in intraocular pressure. If this situation occurs abruptly, then the cornea loses its transparency. If you do not carry out emergency treatment, then after just a few days the dog may develop atrophy of the optic nerve and complete loss of vision.

2. Keratitis

This is an inflammation of the cornea of ​​​​the eye, which spreads to it in just a few days and leads to a sharp deterioration in vision, as well as to its loss. The main causes of keratitis are conjunctivitis, infectious hepatitis, poisoning of the body and other diseases.

3. Conjunctivitis

With this disease, inflammation of the areas around the eyeball (the edge of the inner surface of the eyelids) occurs. When a pet is in a serious condition, a large amount of pus forms on the surface of the eye, which causes clouding of the cornea.

The cause of conjunctivitis can be a fungal or viral infection, bacteria, dust in the eye, foreign bodies, allergies, and a violation of the release of lacrimal fluid.

4. Corneal dystrophy

This is a hereditary disease of a dystrophic-degenerative nature that does not cause any pain to the animal. Corneal dystrophy can be epithelial, stromal or endothelial. In the first case, the process of formation of the epithelial layer is disrupted; in the stromal form of the eye disease, it acquires a bluish tint. With endothelial dystrophy, cellular "influxes" appear on the cornea of ​​​​the eye in the form of a cloudy film, due to which the dog's vision practically disappears.

5. Erosion or ulcer of the eye

These are corneal defects that are caused by a variety of reasons. The main symptoms of an ulcer or erosion are a cloudy eye in a dog and reddening of its cornea. Treatment of this condition involves strengthening the immunity of the pet.

6. Corneal degeneration

This condition develops when there is a metabolic disorder inside the cornea, which leads to the deposition of cholesterol, amyloid, and calcium crystals in it. With cloudy eyes in a dog, treatment may include both therapeutic and surgical measures (according to indications).

7. Belmo

It can be easily seen in the photo, since the thorn appears at the site of various sores, burns and injuries and is a clouding of the cornea of ​​​​the dog's eye. Timely treatment will completely remove the thorn from the eye.

All these reasons explain why the dog's eyes became cloudy. However, in addition to the cornea of ​​​​the eye, its lens may also suffer, which is also caused by certain reasons.

Clouding of the lens of the eye

In this case, the clouding is located deep in the eye, in the pupil. This process is called cataract and occurs in older dogs. The main causes of cataracts are metabolic disorders, weakened immunity, exposure to toxic substances on the pet. This is one of the most common age-related problems that leads to visual impairment. A predisposition to this disease is noted in poodles and cocker spaniels, in which cataracts can appear even at a young age.

If you shine a bright lamp on the sore eye, you can see how the opacity narrows, while in low light it expands. It is worth knowing that with partial clouding of the lens, the dog's vision decreases, and in the event that a mature cataract (complete clouding of the lens) is observed, then the pet becomes completely blind.

Before you treat a cataract, you need to remember that the therapy used will not completely cure the disease. With the help of drugs that improve the metabolism in the eyes, it will only be possible to slow down the development of the disease. If the last stage of the disease has come, then the clouded lens is replaced with an artificial one.

The dog has cloudy eyes - how to treat the disease

After the reason why the dog's eyes became cloudy has been established, treatment of the pet can begin. Sometimes you can cope with the disease on your own, but most often you have to resort to the services of a veterinarian. In any case, every dog ​​owner should know why his pet has cloudy eyes, what signs various diseases have, and how to treat the pathology. Only in this way will it be possible to provide first aid to your pet if the dog has cloudy eyes.

1. How to treat glaucoma

This is an intractable disease that can affect all layers and parts of the eye. In the event that the condition of a sick dog only worsens, doctors have to remove the affected eye from it.

The main task of the attending physician who helps a pet with glaucoma is to prevent complete loss of vision and reduce the pain that occurs with increased intracranial pressure. If the owner of the dog notices the primary signs of glaucoma in her, he should immediately seek medical help, since the treatment of this disease takes a very long time. At the same time, as a result of taking medications, it will only be possible to stabilize intracranial pressure, but it will not be possible to completely get rid of the disease.

Drugs used in the treatment of glaucoma include beta-blockers, prostaglandin analogs, osmotic diuretics, locally applied miotics, and carbonic anhydrase inhibitors.

2. Treatment of keratitis

With this disease, inflammation of the cornea of ​​​​the eye or the anterior part of the eyeball occurs. The main symptoms of this condition are tearing, corneal clouding, and sensitivity to light. The film that appears on the eye of a dog can be very different - from yellowish gray to milky bluish. In some cases, a film on the cornea may appear for no reason, but it disappears on its own after a certain time.

If a dog develops purulent keratitis, small sores appear on the surface of the eye (in an advanced case, large, shapeless and purulent ulcers are observed). After all the ulcers have been removed as a result of the treatment, scars will remain on the treated areas, preventing the pet from seeing normally.

At the very beginning of the development of the disease, the veterinarian prescribes hydrocortisone to the dog in the form of an ointment or drops. Later, for the treatment and prevention of a sick animal, antibiotics are prescribed (especially effective for infection) - Levomycetin, Tetracycline, Penicillin in the form of an ointment or drops.

When pus appears, the conjunctival sac is washed with solutions of penicillin, furacilin, boric acid, furagin, lactate or ethacridine. To prevent a sick pet from rubbing his eyes with his paws, he needs to wear a special collar on his head. In addition, this measure will speed up the treatment process, since the main active component will remain directly in the diseased organ and have a healing effect on it.

3. Treatment of conjunctivitis

Sometimes in the photo you can see a red or cloudy eye in a dog, the treatment of which is easy and fast. In this case, the pet's eyes are washed with an antiseptic, an ointment is placed under the eyelids, which will contain antibiotics, and antihistamines are prescribed (if there is an allergy).

4. Treatment of corneal dystrophy

Currently, it is impossible to completely cure corneal dystrophy, because even during a surgical operation, scars remain on the animal's eye that do not improve the pet's vision.

In particularly severe cases, a corneal transplant is recommended, but the results after the operation are not very encouraging, since the eye still remains obscured by a bluish film. And the cost of surgery is quite high.

The process can be stopped by taking antioxidants and vitamin complexes. It is worth knowing that dogs with corneal dystrophy should not be bred, as the offspring will be diagnosed with the same disease.

5. Cataract treatment

The main method of treating cataracts is surgical intervention, while diet drugs can only slow down the development of the disease.

It is believed that cataract is a hereditary disease, and approximately 80 breeds are at risk, in which the incidence of this pathology is maximum.

In the case of a surgical operation, the cloudy lens is removed from the eye, and an artificial transparent lens is put in its place.

These and other diseases of dogs should be treated only under the guidance of a doctor, since improperly performed therapy will not only lead to complete loss of vision, but also cause a lot of pain to the pet. If the owner of the dog notices some eye problems in time and turns to the veterinarian, this will avoid many problems in the future and help the animal lead a full life.

Aspects of hereditary eye disease in a purebred dog

R. G. C. Bedford BVetMed, PhD, FRCVS, DVOphthal, DipECV
Royal Veterinary College, UK
L. J. S. Bedford is Head of the Small Animal Medicine and Surgery Department at the Royal Veterinary College, University of London, UK.
http://www.dog-beauty.ru/nasledstvennye_zabolevaniia_glaz.html

Summary
Genetic eye diseases in dogs represent a significant category of diseases in some breeds.
Control programs based on conventional ophthalmoscopic examination are possible.
Vision loss and pain are powerful arguments for mass adoption of such programs.
Introduction
The spectrum of hereditary ocular diseases in the modern pedigreed dog population is relatively complex. These diseases are recorded in many breeds of dogs and, as a rule, with different frequency, but all parts of the eye are affected. Despite the interest shown by ophthalmologists around the world and the few national data collection projects that exist, data on disease incidence and inheritance patterns are unfortunately far from complete. In the UK, information is collected and analyzed through collaborative projects between veterinary ophthalmologists and kennel clubs rather than through existing national data collection projects. In Europe, a notable exception has been the Swedish Kennel Club program, which has now made it possible to provide a consistent analysis of data from some hereditary diseases. This program owes its existence to a number of breeders who have shown an increased interest in establishing control over the spread of hereditary eye diseases in rare breed dogs. Of course, the popularity of certain breeds varies in different countries. Accordingly, the types and frequency of hereditary diseases will differ. At the same time, the presence of an international market for dogs now creates the conditions for hereditary diseases to cross traditional geographic boundaries.

Prevention of genetically determined diseases should be a high priority in the reproduction of healthy dogs. It is difficult to prescribe a panacea that could eradicate inherited diseases, but there is no doubt that a routine eye examination as part of the registration policy of any kennel club could bring about a change for the better. The mere knowledge that a hereditary disease exists should motivate us to make every effort to ensure that future dog populations are protected from constant threat, and the opposite view, based on the observation that most dogs lead a healthy lifestyle, is largely misleading. You can never accept the presence of a hereditary disease within the breed. Rather, it should encourage us to recognize the potential threat and cooperate to control the spread of the disease. At present, it is the routine eye examination that is the most effective way to control the disease, and the voluntary participation of the breeder or kennel club in it will benefit everyone. Legislative action through kennel clubs and breed societies is always possible, but some may view it as compulsory. Future promising DNA-based tests will allow accurate genotype analysis, prognosis of present disease, and identification of heterozygous carriers for recessive diseases. Currently, however, only the genetic defect responsible for rod/cone dysplasia in the Irish Setter can be identified using this method. Although some other eye diseases, including hereditary cataracts and collie eye anomalies, are investigated in a similar way.

In the UK, positions regarding the control of the spread of hereditary eye diseases vary among individual breeders and within the respective breed societies, but control is clearly the shared responsibility of both the breeder and the breed society. Of the 157 breeds currently registered with the Kennel Club, 41 suffer from nine of the most common eye conditions. Unfortunately, exact figures for the incidence of some of these diseases are rarely available due to the inadequate attitude of breeders to both official and club research projects. In 1995, about 12,000 dogs were examined under the auspices of an official British Veterinary Association/Kennel Club/International Shepherd Society project with an overall incidence rate of 4.23%, and there is evidence that the overall range of hereditary diseases appears to be increasing. More recent figures regarding this project are not available, and yet the range of hereditary diseases is clearly on the rise. The incidence of an eye defect, possibly of a hereditary nature, for the other 42 breeds is potentially expected to be greater than a random sample can take into account. The spectrum of disease in the UK may differ from other countries, but international awareness of the problems among British dog owners will only be helpful in the general control of hereditary diseases.

The hereditary disease is manifested at birth or can develop clinically at any age, but the basis of the disorders is formed in the process of organogenesis. It is necessary to distinguish between the terms "congenital" and "hereditary". The former refers to malformations presenting clinically at birth, while the latter refers to any malformation that is genetically determined. Therefore, some hereditary defects may appear already at birth, while others do not become clinically manifest until early adolescence or even later in life. It follows that many congenital malformations are not inherited, but arise simply as a result of impaired differentiation of fetal tissues. In the world of purebred dogs, many eye defects show a clear breed predisposition to them, but the exact mode of inheritance may remain undetermined. Congenital eye defects, reflecting the breed's predisposition to them, in dogs are:

Various types of retinal dysplasia (RD), cataracts, persistence of hyperplastic primary vitreous elements (PHPV), persistence of remaining pupillary membrane (PPM), and various collie ocular anomalies (CEA) lesions. Goniodysgenesis is a congenital defect in which the differentiation of the iridocorneal angle is disturbed, which predisposes to primary glaucoma of the eye. It usually occurs in older dogs or middle aged dogs. An inherited disease that develops clinically after birth can be defined as an evolving disease, although strictly speaking the term "evolving" refers to the process of organogenesis. There are several such developing eye diseases in purebred dogs. These are various anomalies of the eyelid and other appendages of the eye, hereditary cataract, dislocation of the lens, primary glaucoma, progressive retinal atrophy and retinal pigment epithelial dystrophy. There are clear indications that some other ocular anomalies may also be hereditary. This group includes corneal lipidosis, uveodermatological syndrome, chronic superficial keratitis, pigment dispersion syndrome, and keratoconjunctivitis sicca.

Congenital hereditary disease
retinal dysplasia

Retinal dysplasia (RD) includes those hereditary diseases of the retina in which abnormal differentiation results in the formation of a neuroretinal fold and rosette, degeneration, or nonattachment of the retina. The possibilities of ophthalmoscopy are limited in that simple folds cannot be clinically differentiated from those in which there is a structural abnormality. In the future, the situation is complicated by the “disappearance” of some folds, since the eye develops to the end in the early period of life. The question of whether or not all folds should be classified as retinal dysplasia is debatable, and opinions are divided here. It should also be remembered that in the complex of progressive retinal atrophy (PRA) there is dysplasia of both rod and cone photoreceptors in the Irish Setter and Rough Collie, and rod dysplasia is accompanied by cone degeneration in the Norwegian Elkhound.
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Figure 1 Retinal dysplasia (RD) in a 12-month-old Hungarian Puli. Some neuroretinal folds are visible in the covered fundus.

The simplest ophthalmoscopic manifestation of RE) is a fold in the neuroretin when the affected tissue separates from the underlying retinal pigment epithelium (RPE) (Figure 1). Several shapes are possible in which linear, round, and Y-shaped outlines are observed. In adult dogs, the folds are limited to a band-like covering of the bottom, but in puppies, the entire bottom may be affected. As the posterior segment develops, several folds may not be visible when examined with an ophthalmoscope. But in the future, their early presence may be evidenced by increased reflex sensitivity of the coating due to retinal degeneration. Complex folds in which there is a proliferation of photoreceptor elements and RPE are also commonly referred to as “rosettes”. This form of RD is inherited in the Cavalier King Charles Spaniel, Hungarian Puli, and Rottweiler as a recessive trait. In the English Springer Spaniel, neuroretinal folds can be accompanied by varying degrees of retinal degeneration: these lesions take on the appearance of classic post-inflammatory retinopathy caused by increased reflex irritability of the fundus covering and the possible presence of melanin pigmentation (Figure 2). Sometimes this clinical picture is complicated by retinal detachment, and both intraocular bleeding and cataract formation can be observed. The frequency of this lesion is especially high in working carriers of this breed, and again heredity is a simple recessive trait. Complete neuroretinal nonattachment has been described in the Selig Terrier, Bedlington Terrier, Samoyed and Labrador Retriever, but the incidence is currently exceptionally low. In the last two breeds, skeletal dysplasia may accompany congenital neuroretinal nonattachment. The affected dog shows growth retardation of the radius, ulna, and tibia. In addition, there are sometimes observed: separation of the hypoplastic olecranon and coracoid processes, delayed development of the epiphyses and hip dysplasia. Vitreous rudiments may also be seen, and subsequently cataracts cannot be ruled out.
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Figure 2 Retinal dysplasia (RD) in a 20 month old English Springer Spaniel. Neuroretinal folds, retinal degeneration and pigmentation are clearly visible in the covered fundus.

Cataract

A cataract is defined as any clouding of the lens and/or its capsule. Congenital hereditary cataracts affect the central nuclear part of the lens of the embryo and fetus, although those fibers of the lens that make up the nucleus and cortex in the adult usually remain unaffected (Figure 3). Therefore, congenital nuclear cataracts are often described as stationary, affecting the dog's vision depending on the size of the opacity. Patients are treated with long-acting mydriatic drugs. But when the cortical layer is involved, it may be necessary to remove the lens. This disease occurs as a recessive trait in miniature schnauzers and can be diagnosed in bobtail, golden retriever, white scotch terrier - if the breeders of these breeds respond correctly to the data of the first studies. Congenital cataracts may also accompany microphthalmos in breeds such as the English Cocker Spaniel, Cavalier King Charles Spaniel, Rottweiler, Rough Collie, Doberman Pinscher, English Bobtail, Standard Poodle, and White Scotch Terrier as part of a possibly inherited multiple eye defect.

Figure 3 Nuclear cataract in the left eye of a 4 year old Cocker Spaniel. The lens cortex is not affected, and the fundus covering reflex around the cataract is not altered.

Congenital cataracts sometimes involve the lens capsule as a secondary sign of PHPV or PPM. Rudimentary pupillary membrane often presents with anterior capsule opacities at attachment sites, while PHPV may accompany varying degrees of posterior capsule opacification and posterior cortical cataracts.
PHPV/PPM

The role of the primary vitreous during organogenesis is to nourish the developing lens through its vascular component. The posterior and anterior branches of this vessel, together with elements of the annular artery in the anterior rim of the optic vesicle, form a vasculature around the lens, the choroid of the lens. All parts of this network should be resorbed by the 14th day after birth, but elements of both the anterior and posterior components may persist when attached to the lens capsule. Anterior rudiments, together with mesenchymal elements, appear as a persistent pupillary membrane, while a rudiment of the primary vitreous can undergo hyperplasia and involve a significant part of the lens in the process. PPM is described as a simple recessive trait in the Basenji but appears to be an accidental finding in many other breeds, including Bullmastiff, Basset Petit, Griffin, Vendin, Rottweiler, Siberian Husky, Cocker Spaniel, and White Scotch Terrier (Figure 4) . The mechanism of inheritance remains unclear, and rudiments of PPM may also be present in microphthalmos. PHPV (Hyperplastic Primary Vitreous Persistence - this also refers to PHTVL/PHPV, where the first abbreviation stands for persistent lens choroid) has been described as a primary malformation in the Doberman Pinscher and Staffordshire Bull Terrier. Perhaps it is inherited as an incomplete dominant trait. Lesions range from small brown isolated opacities of the posterior polar parts of the capsule to extensive capsular and cortical opacities with occasional intralenticular hemorrhages (Figure 5).

Figure 4 Persistent pupillary membrane (PPM) in the left eye of a 12-month-old Cocker Spaniel. Dark bands of PPM are attached to the anterior lens capsule. There is a cataract.

Figure 5 Persistent hyperplastic primary vitreous (PHPV) in the right eye of a 2-year-old Staffordshire Bull Terrier. Fibrovascular spot is a significant obstruction to vision.
Collie Eye Anomaly (CEA)

CEA is the most common hereditary eye disease in the UK pedigreed dog population. An accurate estimate of the incidence of the disease is not possible, but 40-60% of the disease has now been identified in the Rough Collie, Smooth Collie and Sheltie breeds. CEA is also seen in Border Collies, but the frequency is low: between 1 and 2%. This disease is considered to be inherited as a simple recessive trait and is multiform, involving some structures in the posterior segment region. Ophthalmoscopic features used in the diagnosis: choroid hypoplasia, coloboma of the optic nerve papilla and peripapillary region; both defective attachment, and detachment of the neuroretina and intraocular hemorrhage.

During organogenesis, it is the posterior wall cells that invaginate into the optic vesicle that form the primary retinal pigment epithelium. Deficiency in growth hormone secretion affects the subsequent differentiation of ocular tissues. In CEA, the choroid remains hypoplastic in the area lateral to the optic disc (Figure 6), and failure to close the embryonic fissures leaves a colobomatous defect in the papilla and peripapillary tissue (Figure 7). The degree of choroidal hypoplasia and the size of the coloboma vary greatly among affected individuals and even between the eyes of the same individual. All affected puppies show choroidal hypoplasia, but from 12-16 weeks of age, many of the smaller lesions may be masked by melanin pigmentation. Estimates vary, but it is likely that around 30% of affected puppies in the UK show this masking pattern: somewhat confusing, the process is described as 'going back to normal'. This phenotype then appears ophthalmoscopically as normal, but these dogs are genetically diseased and can only be cured of the disease by control programs. This is a significant aspect of the disease, necessitating screening of all litters at 6-7 weeks of age.

Figure 6 Collie Eye Anomaly (CEA): Choroidal hypoplasia of the right eye of a 4 year old Rough Collie. Scleral protein is visible through a lesion lateral to the optic nerve head.

Figure 7 Collie Eye Anomaly (CEA): A typical papillary coloboma in the right eye of a 2 year old Smooth Collie. A coloboma is a dark area occupying the ventral part of the optic disc. A patch of choroidal hypoplasia is seen lateral to the disc.

About 30% of dogs that show choroidal hypoplasia as adults also have colabomatous defects. Papillary colobomas invade the optic disc and vary considerably in size when the disc is completely affected. Peripapillary colobomas are not so common, but they can also vary in size. It is believed that colobomas are caused by insufficient development of scleral tissues during the closure of the embryonic fissure, but the explanation for the development of an atypical coloboma is not easily attributed to this process. Peripapillary colobomas are surrounded by degenerative neuroretinal tissue, and dogs with an extensive papillary colobomatous process should have poor vision. The role of coloboma in postnatal retinal detachment has not been fully elucidated, but the neuroretina may first flake off from the ends of the defect. Without double choroidal hypoplasia, however, CEA is inherited as a recessive trait, and yet there is evidence suggestive that although coloboma is considered part of the same anomaly, this defect may be inherited as a separate disorder. If so, then the high frequency of choroidal hypoplasia indicates that coloboma is most often a concomitant phenomenon.

In a small percentage of affected dogs, the neuroretin is not attached at birth, although in individuals with a significant colabomatous defect, the neuroretin may detach in the first three years of life. About 1% of affected dogs have intraocular hemorrhage, but the etiology of this complication remains open to speculation. It is believed that preretinal capillaries in the equatorial regions of the eyeball may develop in response to retinal hypoxia and that these unstable vessels may rupture. However, hemorrhage in puppies may be associated with persistence of the vitreous vasculature. The presence of unstable blood vessels within the papillary coloboma offers an alternative explanation for spontaneous hemorrhage in both young and adult dogs. Ophthalmoscopic observation alone is insufficient to determine the cause of the hemorrhage.

To be continued

Continuation of the article

developing hereditary disease
Anomalies of the century

The terms "entropion" (inversion of the eyelid) and "ectropion" (inversion of the eyelid) are familiar to everyone involved in breeding dogs. Both of these conditions have, as a rule, an origin in the breed standard, which dictates the appearance of the “eye”. Both of them are the consequences of euryblepharon, in which the discrepancy between the size of the eyeball and the length of the eyelids leads to deformation of the palpebral fissure. In entropion, the rim of the eyelid is turned inward relative to the surface of the eye, causing irritation, inflammation, and possible ulceration. With ectropion, the lower eyelid hangs outward from the eyeball, exposing the nictitating membrane, the lower palpebral membrane, and the surfaces of the conjunctiva and the eyeball. The nature of inheritance remains unknown, and a focus on deviations from the breed standard is the only real solution to the problem. Corrective surgery is possible to alleviate discomfort and preserve vision, but considerable difficulty arises in correcting the combined entropion/ectropion defect in the St. Bernard and Bloodhound breeds, commonly described as "diamond eye".

Figure 8 Ectropion/entropion combination - diamond eye, right eye lesion in an 8 month old St. Bernard.

In distichiasis, additional eyelashes arise from the edge of the eyelid, creating the possibility of contact with the surface of the cornea. This disease is no doubt hereditary in the Miniature Wirehaired Dachshund and Cocker Spaniel breeds, but it also appears to be in many other breeds. The clinical picture may vary:

The expected irritation may not be due to the protective effect of the precorneal tear film. But if distichiasis is significant, it can cause trigeminal irritation, keratitis, and even corneal ulcers. A variant of distichiasis is an ectopic eyelash that breaks into the conjunctiva of the eyelid from its outgrowth inside the tarsal plate and causes trauma to the corneal epithelium. Intense irritation and keratitis are also characteristic features of trichiasis, in which the eyelashes are abnormally curved in relation to the surfaces of the cornea and conjunctiva.

hereditary cataract

Lens cloudiness is a relatively common occurrence among different types of dogs and can occur for a variety of reasons, from amino acid deficiencies in young dogs to age-related changes associated with aging. Hereditary developing cataract can occur at any age after birth, but mostly affects individuals from young to middle age. It is the nature of the opacification associated with age that confirms the diagnosis of hereditary cataract (HC). There are currently 16 breeds affected by developing NS in the UK, and it is suspected in another 10 breeds, among which control studies are currently underway.

Affected breeds are listed in Table 1 along with age (beyond which HC is unlikely to occur), heredity (where known) and pattern of turbidity observed.
Table 1
Breeds affected by hereditary cataract

Breed Age Inheritance Haze pattern
Boston Terrier - two forms:
Early 3 years Recessive Progresses to full lens involvement
Late 8 years Unknown Usually clouding wedges
Cavalier Books Charles Spaniel 8 years Possibly recessive Progresses to full lens involvement
German Shepherd 3 years Recessive Slight progression in bark
Large Munsterlander 9 years Possibly dominant Opacification of the posterior pole, sometimes involving the entire cortex
Miniature Schnauzer 3 years Recessive Progresses to complete clouding of the lens
Norwegian Buhund 5 years Possibly recessive Blurring in the back of the bark
English Bobtail 3 years Unknown Progresses usually to total lens opacity
Poodle (standard) 18 months Unknown Progresses to full lens involvement
Retriever (Purebred Beagle) 3 years Probably dominant Posterior pole clouding
Retriever (golden) 9 years old Dominant Clouding of the posterior pole, sometimes of the entire cortex
Retriever (Labrador) 9 years old Dominant Clouding of the posterior pole, sometimes of the entire cortex
Siberian Husky 5 years Probably recessive Clouding of the back of the bark
Spaniel (American Cocker) 6 years Recessive Extremely variable in both stable and progressive turbidity
Spaniel (Welsh Springer) 3 years Recessive Progresses to full lens involvement
Staffordshire Bull Terrier 18 months Recessive Progresses to full lens involvement

There is now sufficient evidence to confidently include the Irish Red and White Setters and the Belgian Shepherd in this list of breeds with posterior cataracts.

The lens increases throughout life due to the constant production of new fibers. These new fibers make up the lens cortex, and their abnormal formation is caused by factors that (as yet not well established) are responsible for the development of cataracts. Both dominant and recessive hereditary traits are involved in the development of NS, and there are significant variations in the presented clinical picture and in the associated prognosis. For example, the 5% incidence of posterior cataracts in Labrador Retrievers and Golden Retrievers (Figure 9) may be mitigated by the fact that only 5% of these dogs develop generalized cortical cataract requiring surgery. While a young Boston Terrier or Miniature Schnauzer always develops complete cortical opacity on both sides, the Siberian Husky (Figure 10) and the Norwegian Buhund develop cataracts that rarely involve the anterior cortex. The American Cocker Spaniel can show bilateral blindness, but it can also be unilateral, in which the cataract is limited to a very small portion of the lens cortex.

Figure 9 Hereditary cataract in the right eye in a 16-month-old Labrador Retriever. Opacification of the posterior pole is seen as a whitish, roughly defined triangular spot that stands out sharply in relation to the reflection of the green coating (the pink spot over the cataract is out of focus of the optic disc).

Figure 10 Hereditary cataract of the right eye in a 10-month-old Siberian husky. Diffuse posterior opacification of the cortex is visible.

Cataract surgery is attempted only when the eye becomes functionally blind, or when there is a sure sign that the developing opacification will involve the entire cortex of the lens. Fortunately, surgery will save the animal's vision, but perhaps no less effective measure in the fight against the disease could be the organization of proper selection work at the breed level.

Dislocation of the lens

The lens is held in position by a ligament of zon and is attached to the vitreous by its posterior capsule. The ligament fibers are attached to the equatorial part of the lens capsule and embedded in the epithelium of the ciliary processes. A recessively inherited structural defect in these fibers can cause them to rupture early in life and the lens then shifts, usually towards the pupil or anterior chamber of the eye (Figure 11), blocking the flow of pupillary fluid from the ciliary processes into the anterior chamber. Fluid pressure inside the iris rises and the iriocorneal angle is broken. The result is secondary glaucoma, and only urgent removal of the displaced lens restores intraocular fluid pressure (IOP) to normal and prevents damage to the optic nerve. Primary lens luxation occurs almost classically in middle age in terrier breeds, including the Tibetan Terrier, and has also been noted in the Border Collie.

Figure 11 Dislocation of the lens of the left eye in a three-year-old Selig Terrier. The lens is clearly defined in the depth of the anterior chamber of the eye by the internal reflection of light along its equator.

Glaucoma - a pathological process in which all eye structures are affected, as a result of an increase in JR, which is constantly maintained above normal physiological norms. Undoubtedly, this is one of the most severe eye diseases of a hereditary type in purebred dogs. It is a painful, blinding disease in which treatment is often ineffective or completely ineffective. It requires real urgency, and hours spent trying to diagnose or select an ineffective treatment means irreversible progressive degeneration of the optic nerve and, as a result, blindness.

The lens and cornea are devoid of blood vessels and depend on a constant influx of fluid to meet their metabolic needs. The rate of fluid inflow is balanced by the constancy of its drainage from the anterior chamber of the eye to the vascular network of the sclera through the iridocorneal (drainage) angle. All glaucomas in dogs are caused by a defect in this structure. Secondary glaucomas result from a tear in the iridocorneal angle due to a previous or concomitant eye disease, while primary glaucomas result from a genetically determined hereditary defect. There are two types of primary glaucoma in the dog, and the terms "open angle" and "angle closure" are descriptive and generally acceptable. The nature of inheritance is still uncertain. In open-angle glaucoma, the defect is at the level of the trabecular meshwork or vascular plexus, which is responsible for the increase in IOP. Fortunately, this disease is very rare in the UK, and only Elkhounds and Poodles suffer from it, in which, with some degree of probability, we can talk about inheritance in the breed. In contrast, angle-closure glaucoma is relatively common and includes primarily the Basset Hound, Cocker Spaniel - both English and American, Welsh Springer Spaniel, Great Dane, Siberian Husky, and Smooth-Coated Retriever. This form of glaucoma is caused by the closure of a congenital defective iriocorneal angle, usually in middle-aged and older dogs. The angle develops from the mesodermal tissue and its incomplete splitting is indicated by a narrow entrance to the ciliary gap and a dysplastic pectinate ligament. This defect can be easily identified in 4-6 month old dogs by gonioscopy, and this screening method represents the basis for disease control (Figures 12 and 13).

Figure 12 Narrowed iriocorneal angle in a 7 year old Cocker Spachel. The pectineal ligament is anomalous and barely visible opposite the severely narrowed ciliary inlet.

Figure 13 Narrowed iriocorneal angle in a 7 year old Cocker Spaniel. The pectinate ligament and the entrance to the ciliary fissure cannot be identified.

Progressive retinal atrophy.

Progressive retinal atrophy (PRA) is a term adopted to describe a range of hereditary neuroretinal degenerations. Generalized PRA or simply PRA describes degenerations in which the photoreceptor is the primary focus of the disease. Such degenerations are characterized by night blindness, which progresses to total blindness and contributes to a high incidence of secondary cataract formation. All these diseases are inherited by simple autosomal recessive traits. Central PRA (CPRA) is a retinal degeneration in which photoreceptors are affected, but is secondary to a dystrophic defect in the retinal pigment epithelium (RPE). Subsequently, CPRA was reclassified as retinal pigment epithelial dystrophy (RPED). It begins with fundus occlusion, and peripheral vision is often preserved. The nature of inheritance remains unclear. Both PRA and RPED can be found in the same breed.

Ophthalmoscopically, all generalized PRAs are characterized by increased reflex irritability of the fundus coating due to progressive thinning of the neuroretin during degeneration, as well as weakening and virtual shutdown of the superficial retinal vasculature (Figure 14). Depigmentation of the retinal pigment epithelium in the uncovered fundus can lead to patchy repigmentation. Optic nerve degeneration caused by ganglion cell death is characterized by serrations and pallor of the disc. The etiology of hereditary retinal degeneration is largely unknown, but at least three types of PRA have been described among UK dog breeds. Rod/cone photoreceptor dysplasia was first characterized in the Irish Setter (rod/cone dysplasia type I) and more recently photoreceptor dysplasia has been described in the miniature schnauzer. In the latter breed, these signs of the disease may not be visible during ophthalmoscopy until the 5th year of life. But in the Irish Setter, the disease has an early onset with severe visual impairment beginning at 6-8 months of age and complete blindness at 12 months of age. In this breed, a photoreceptor defect is an enzyme abnormality in the light conversion cascade. Retinal cyclic guanosine monophosphate (cGMP) nucleotide levels are elevated to about 10 times normal due to reduced cGMP phosphodiesterase activity. Recent studies have shown that the genetic defect is an abnormality in the beta subunit of cGMP phosphodiesterase and it is now possible to predict the disease and establish the genotype of dogs with a normal phenotype by a relatively simple DNA test. PRA is not thought to have been seen in the general population of Irish Setters in the UK since 1978, but the possible presence of carriers in the present population is an understandable risk to future breeding programs.

Figure 14 Progressive Retinal Atrophy (PRA) in a 6-year-old Miniature Poodle. Here there is an increased reflex irritability across the entire width of the bottom cover; the superficial retinal arteries are no longer visible and its veins are extremely thinned.

Interestingly, dominantly inherited rod/cone dysplasia, also characterized by elevated levels of cGMP, has also been described in the Abyssinian colony in this country.

A second form of PRA, in which the rod photoreceptor unit is dysplastic and there is subsequent regeneration of normal cone photoreceptors, has been described in the Norwegian Elkhound, but the disease appears to have been eradicated from this breed in the UK. The initial rod defect remains unrecognized as it is the cause of the third form of PRA, a disease seen classically in Miniature and Toy Poodle, English Cocker Spaniel and Labrador Retriever breeds (rod/cone degeneration). Here there is a normal development of both photoreceptor units, but blindness is caused by their premature degeneration in adulthood. Little is known about the etiology, but it is assumed that this is the same genetic anomaly that causes the disease in all three breeds, which has been demonstrated in mating experience. X-linked PRA has recently been described in the Siberian Husky developed in the USA, but this form of PRA has not been found in any breed in the UK.

Retinal pigment epithelial dystrophy (RPED)

This disease was originally thought of as a primary degeneration of the photoreceptor, but in reality it is caused by a defect in the RPE. There is progressive neuroretinal degeneration, mostly limited to the unpigmented part of the fundus, the occlusion zone. Therefore, there is increased reflex irritability of the fundus coating, but the weakening of the circulatory network is less noticeable than with PRA. A characteristic ophthalmoscopic feature is the appearance of a light brown pigment in the covered fundus, first as spots and later as confluent plaques (Figure 15).

Figure 15 Retinal pigment epithelial dystrophy (RPED) in a 5 year old Briard. Plaques of lipopigment are clearly visible. There is a characteristic weakening of the vascular network.

Peripheral vision is usually preserved and there is no secondary cataract formation.

The pigmentation seen with the ophthalmoscope is caused by the accumulation of lipopigment within the RPE cells. One of the many important functions of these cells is to degrade the photoreceptor outer segment (POS) substance, which is used in light conversion. There is a rapid turnover of POS, but dystrophic RPE cells can neither degrade used POS rapidly enough nor participate effectively in POS production. Their cytoplasm accumulates phagocytosed POS material, and these phagosomes contain a lipopigment observed with ophthalmoscopy. As more and more lipopigment accumulates, the function of the RPE in terms of neuroretinal nutrition is impaired. Photoreceptors and in fact all of the neuroretin located on top of dystrophic RPE cells undergo degeneration. Undoubtedly, there is a genetic predisposition to this disease, as evidenced by breed-specific involvement, but many factors influence the course of degeneration. Vitamin E deficiency causes the same retinal degeneration, and RPED-affected dogs may have low concentrations of both vitamin E and taurine. Recent studies have shown that affected dogs may exhibit hypercholesterolemia. Over time, RPED may simply be an ocular manifestation of hereditary antioxidant deficiency or abnormal lipid metabolism.

Other developing anomalies

Corneal lipidosis in breeds like the Cavalier King Charles Spaniel, Rough Collie, and Sheltie is likely caused by a primary defect. This disease is of little clinical importance because it rarely has any noticeable effect on vision. The same cannot be said for uveo-dermatological syndrome, in which severe uveitis can lead to retinal detachment or glaucoma. This disease occurs on an autoimmune basis, and the melanin-containing tissue undergoes inflammatory changes. There is loss of skin pigment (vitiligo) and hair (graying), but panuveitis is a problem in treatment. There is a clear predisposition to certain breeds, with the Japanese Akita predominantly affected in the UK. Similarly, breeds such as the German Shepherd and keratoconjunctivitis sicca are clearly predisposed to autoimmune chronic superficial keratitis (pannus) and the white Scotch terrier to keratoconjunctivitis sicca. More recently, pigment resorption syndrome has been described in the Cairn Terrier, in which pigment that has disappeared from the iris can lead to blockage of aqueous humor outflow tracts, and chronic glaucoma can develop in old age.
Conclusion
The control of a congenital eye disease, known as hereditary, should present little difficulty, since defects can be identified by simple examination methods at the earliest possible age: 5-6 weeks in many breeds. As such, testing pairs and selecting them for future breeding programs is fairly straightforward. Poor subscription to litter screening projects means that these congenital problems continue to exist and knowledge of emerging congenital anomalies remains insufficient. About 50 breeds are currently screened for multiple eye defects, cataracts and retinal dysplasia in the UK, but many breeds are not signed up for the voluntary screening project. Routine screening of all litters as part of the Kennel Club registration procedure would make a significant contribution to the overall control of inherited congenital eye defects.

Age of onset is one of the most difficult factors in implementing projects to control developing eye diseases. The late onset of clinical symptoms means that breeding may occur before the disease genotype is established. Only through the cooperation of all the breeders of the breed can the full picture of the disease be determined and advice given for breeding. The future offers the reality of DNA-based testing, but for the time being, only the mass adoption of routine eye examination programs will reduce the incidence of hereditary eye diseases. This is the responsibility of the breeder and breeding society, working with the help and guidance of kennel clubs and veterinary specialists.

The state of the cornea is of great importance for making a diagnosis, predicting the course of the disease and developing adequate treatment tactics for ophthalmic pathologies in animals. The cornea is the anterior most convex part of the eyeball and the main light-refracting medium. Normally, it is transparent, shiny, spherical, smooth and even. To ensure a normal act of vision, it is necessary to have all of the above characteristics of the cornea of ​​​​the eye.

A decrease in the transparency of the cornea indicates pathological processes in it, and is associated with a certain change in the color of the cornea. Pathological reactions include vascularization (red), edema (blue), scarring (grey-white), lipid or protein deposits (glossy white), pigmentation (black), inflammatory cell infiltration (yellow-white). All of the above pathological reactions occur both separately and together.

If the cornea of ​​a dog or cat turns red

Cause of red color cornea - vascularization (Fig. 1). Vascularization indicates a chronic inflammatory process. The direction, length and depth of the blood vessels provides information about the location and depth of the pathological focus.

Vascularization is accompanied by deep ulcerative keratitis and corneal trauma affecting the stroma and accompanied by the multiplication of pathogenic microorganisms. Vessels grow into the cornea in order to isolate healthy tissues from damaged ones.

Differentiation of deep and superficial vascularization is crucial for the choice of further diagnostic steps and for the separation of intraocular diseases from superficial irritants.

Superficial vessels grow into the cornea from the conjunctiva, crossing the limbus. They are thin, branched and look like branches of a tree (Fig. 2). These vessels indicate a disease of the stratified squamous epithelium and superficial layers of the corneal stroma, arising from insufficient protection or excessive irritation.

Deep vessels grow into the cornea from ciliary or scleral vessels. They are darker, shorter, straighter and do not branch (Figure 3). They are not seen crossing the limbus, they come from the sclera and look like a hedge or panicle. As a rule, deep vessels characterize such diseases as deep keratitis, uveitis or glaucoma.

Blue animal cornea

With corneal (stromal) edema, the cornea acquires blue color(Fig. 4). Corneal edema occurs due to dysfunction of one or both of the cell layers (stratified squamous epithelium and posterior limiting membrane or endothelium) responsible for corneal turgor. Edema associated with impaired function of the anterior limiting membrane is accompanied by corneal ulceration with loss of stratified squamous epithelium. In this edema is weak, focal and the basis of corneal opacity is an infiltrate consisting of inflammatory cells (leukocytes).

Endothelial dysfunction can be either an independent disease (primary endothelial dysfunction) or a consequence of concomitant eye pathologies (secondary endothelial dysfunction). At the same time, attention is paid to soreness, the presence of inflammation in the cornea and intraocular pressure. With endothelial degeneration and endothelial dystrophy, diffuse edema and the absence of the above clinical signs are observed. Primary endothelial dysfunction is more common in dogs than in cats because the endothelium in cats is more resistant to ageing. Primary endothelial dystrophy is common in Boston Terriers and Chihuahuas, and senile endothelial degeneration occurs in older dogs of all breeds. Outbred animals are less susceptible to primary hereditary diseases, so primary endothelial dystrophy is extremely rare in them.

Secondary endothelial edema occurs in dogs and cats with glaucoma and lens luxation. Such edema is accompanied by soreness, limited inflammation, and other specific clinical signs.

The pathology in which corneal edema is the main clinical sign is bullous keratopathy (Fig. 5). With this disease, the function of not only the endothelium, but also the stroma is impaired. Collagen fibers of the stroma lose their density and allow moisture to pass into the cornea. Violation of the function of the corneal endothelium leads to impregnation of the stroma with fluid from the anterior chamber of the eye with the formation of characteristic vesicles. The stroma becomes cloudy and protrudes in the form of a keratoglobus. Then moisture penetrates under the epithelium, exfoliating it in the form of separate bubbles and forming eroded areas on the surface of the cornea. The epithelium exfoliates over a considerable extent, which leads to clouding of the entire cornea and a sharp decrease in trophism.

Ophthalmic examination and diagnostic tests can determine the cause of corneal edema.

The cornea of ​​a cat or dog is gray

Gray "smoky" color in the cornea is observed during the formation of cicatricial opacities (Fig. 6). Scars are formed in the stroma of the cornea as a result of its injury or deep ulceration, which accompanies parenchymal ulcerative keratitis and is the outcome of inflammatory diseases of the cornea with the formation of a defect in its tissue. Normal stromal cells are replaced by connective tissue, upsetting the density of stromal collagen. In this case, the depth of the spread of the ulcerative process is important, since the density of the scar and the visual abilities of the eye depend on the depth of the connective tissue. When normal corneal tissue is replaced, the precorneal tear film is disturbed and the function of the physiological barriers of the eye is reduced.

Scar tissue does not retain fluorescein. Formed scars are the result of deep lesions of the cornea and, depending on the density of questionable tissue and the size of the affected area, are divided into nubecula, macula and leukoma.

If the animal's cornea is white (transparent)

Lipid or protein deposits look like shiny transparent or white limited areas on the cornea (Fig. 7). These deposits often contain cholesterol or amyloid. There are both primary hereditary dystrophies and secondary ones resulting from metabolic disorders, more often protein ones. Lipids or protein are deposited in the central and peripheral parts of the cornea, often in the form of a circle or oval. As a rule, deposits accumulate in the stroma, they are painless and are not accompanied by clinical signs of diseases of the anterior segment of the eye.

In case of metabolic disorders, an excess of certain metabolic end products accumulates in the blood. As a result, lipids (usually cholesterol), proteins (usually amyloid) and minerals (usually calcium) accumulate in the cornea, nourished by osmosis and diffusion from intraocular fluid and limbal vessels.

Hereditary primary dystrophies are more common in young animals. Secondary dystrophies are observed in older animals that have somatic diseases (diseases of the liver, kidneys, pancreas).

The animal has a black cornea

Black color on the cornea, this is corneal pigmentation (Fig. 8).

The pigment melanin passes to the cornea from the limbus with prolonged mechanical irritation. Dog breeds Pekingese, Shih Tzu, pugs, chow-chow are most predisposed to pigmentary keratitis. That is, those animals that have a nasolabial fold.

Melanin in this case is deposited as a factor in protecting the cornea from mechanical damage. In cats, the deposition of melanin in the cornea occurs when the integrity of the stratified squamous epithelium is violated, accompanied by stromal necrosis, detachment of collagen fibers from each other and is called corneal sequestration (Fig. 9). Corneal pigmentation is often accompanied by vascularization, as the pigmented areas are undernourished.

The cornea is yellow-green. What's this?

Infiltration by inflammatory cells of the corneal stroma is accompanied by yellow-green color change cornea.

Color change is observed on the posterior surface of the cornea, directly in the stroma and on the anterior surface of the cornea (Fig. 11). Inflammatory cells (leukocytes) come from the tear, limbus, and sometimes the uveal tract, and the infiltration develops quite rapidly, indicating a strong stimulation of chemotaxis. Stroma infiltration occurs with blunt trauma (contusion or contusion of the cornea).

Yellow-green staining of the posterior surface of the cornea is observed with the accumulation of precipitates on the endothelium (Fig. 10). Precipitates are multiple accumulations of inflammatory cells and fibrin and are a pathognomonic sign of iridocyclitis. With staphyloma, fibrin and leukocytes accumulate on the anterior surface of the cornea, staining it yellow-green.

With staphyloma, the condition of others

corneal tissue is edematous.

The main diagnostic criteria, as well as a comprehensive method for examining the animal, make it possible to make the correct diagnosis and prescribe treatment. A change in the color of the cornea is observed both as an independent disease and as a consequence of concomitant diseases of the eyes and internal organs.

If you notice a change in the color of the cornea in your pet, then contact the veterinary city clinic "VetState", where experienced ophthalmologists conduct the appointment. A veterinary ophthalmologist will conduct all the necessary examinations, provide the necessary assistance and help maintain vision 7 days a week, 365 days a year.

Without holidays and days off, we are glad to see you from 10.00 to 21.00.
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Corneal dystrophy is a hereditary pathology in which substances are deposited in the cornea that impair its transparency. The pathology always appears symmetrically in both eyes in the form of round/oval white-gray opalescent spots in the central part of the cornea. Both eyes can be affected at the same time, or with a slight difference in time: first one, and after a while the second eye. The area, depth and intensity of the lesion are variable in different animals.

In most cases of corneal dystrophy, cholesterol/phospholipids/fatty acids/calcium salts are deposited in the stromal layer, just below the epithelium. This is a painless process, however, as it progresses, the amount of deposits will increase, which can provoke corneal ulceration. The more deposits, the more vision deteriorates.

Corneal dystrophy in a dog, right eye Corneal dystrophy in a dog, left eye

Diagnosis of corneal dystrophy in dogs and cats.

A patient with suspected corneal dystrophy needs an ophthalmological examination. Based on the results of the examination, additional studies may be prescribed for Cushing's syndrome, hyperthyroidism, hyperlipoproteinemia, and diabetes mellitus.

Differential diagnosis.

Corneal lipidosis, corneal degeneration, corneal edema.

Treatment of corneal dystrophy.

Since the process is genetically determined, there is no specific and effective treatment. Sometimes the process progresses more with improper feeding (an excess of fat in the diet). In this case, the patient is recommended to adjust the diet. In the event that the deposits began to provoke ulceration of the cornea, the patient begins to experience pain. Pain syndrome develops (blepharospasm, lacrimation, redness of the eye). This condition is an indication for superficial keratectomy. During this surgical operation, the zone of dystrophy is removed, and the cornea restores its transparency. The treatment is temporary, as corneal dystrophy will develop again in the same place in the future. However, this is a rather lengthy process and can take from several months to a year. In the event that ulceration develops again, a second keratectomy is performed.

An alternative to surgical treatment can be keratotomy with a diamond bur, which has proven itself in the treatment of this disease. Recently, more and more of my patients are treated and cured by this method. Unlike surgery, it is performed without general anesthesia, which at times increases the relevance of the procedure. Since this procedure may have contraindications, a face-to-face consultation with a veterinary ophthalmologist is mandatory before performing a keratotomy with a diamond burr.

Ulceration in corneal dystrophy Positive staining with fluorescein

Predisposed dog breeds.

The disease can manifest itself in any dog, cat, but more often this disease is diagnosed in the following: