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  Structure of the eye
Fig. 1. Structure of the eye
cc.
sc.
ch.
r.
i.
c.
Corpus Ciliare
Sclera
Choroidea
Retina
Iris
Cornea
l.
cv.
vok.
aok.
no.
Lens
Corpus Vitreum
Anterior Eye chamber
Posterior Eye chamber
Optical nerve

Health

Eye diseases

Structure of the eye

The wall of the eye consists of three layers (see Fig. 1). From the outside inwards these layers are:
  • cornea becomes the sclera at the back of the eye
  • uvea, consisting of the iris, corpus ciliare and choroidea
  • epithelium, at the back continuing as retina
The inside of the eye is divided in three parts:
  • anterior eye chamber; between cornea and iris
  • posterior eye chamber; between iris and lens
  • corpus vitreum between lens and retina

The lens

  Structure of the lens
Fig. 2. Structure of the lens
c. 
n. 
k. 
e. 
a. 
p. 
cortex 
nucleus (kern)
capsule
epithelium
anterior (front)
posterior (back)
A double convex lens — the back is a bit more convex that the front — is suspended by fibres of the corpus ciliare. Contraction of the circular muscle in the corpus ciliare causes the lens to become more convex (elasticity).

The lens consists of concentric layers of fibres which are produced by tissue at the front (just below the capsule) of the lens.

Collie Eye Anomaly (CEA)

Is found in the Collie (longhair and smooth coated) and also in the Border Collie, Sheltie and Bearded Collie. Comes in various grades:
TORT
excessive windings of the blood vessels in the retina. Whether this type is part of CEA or not is still subject of discussion.
CRD (ChorioRetinal Dysplasia)
the retina - choroidea is incorrectly developed in certain area's
The types mentioned above pose little to no threat to the vision.
COL (Colobomata or closing defects)
there are holes in the retina; hardly any effect on the vision.
AR (Atresia Retinae)
detachment of the retina. It's obvious that this influences vision.
IOB (IntraOcular Bleeding)
Bleeding occurs inside the eye. Depending on the number and size of the bleedings, vision is deteriorated.
HP (Hypoplastic Papilla or badly developed optic nerve)
It's uncertain whether this is part of CEA.
Normal eye
 
Collie Eye Anomaly
Fig. 3. Normal eye. These pictures are taken through the (enlarged pupil. The light, pink area is the 'blind spot' where the optic nerve enters the eye. The choroidea is visible as a greenish background.
(Photo reproduced from "Erfelijke Oogafwijkingen" (Hereditary eye disorders) with permission of the author1).
Fig. 4. The blind spot shows a coloboma (yellow arrow) at the bottom. The blood vessels on the left are numerous and irregularly shaped. Between these vessels white-yellow spots are visible, where the retina-choroidea is incorrectly developed (CRD).
(Photo reproduced from "Erfelijke Oogafwijkingen" (Hereditary eye disorders) with permission of the author1).

Inheritance and control

Until recently it was only possible to find affected animals by examining the eye. By analysing pedigrees you could find a number of the carriers. Some breeders also had their pups examined at the age of seven weeks to find affected pups before they were sold. This started the discussion about the phenomenon "go normal". This is a dog which was diagnosed with CEA as a pup but which shows no signs of the disease at an adult age.

Some time ago a commercially available test was developed (OptiGen) which makes it possible to find carriers too. The research needed to develop this test showed that CEA is a single recessive gene. The possible test results are 'normal', 'carrier' and 'affected'.

Progressive Retinal Atrofia (PRA)

Is seen in many breeds and crosses. The symptoms vary from breed to breed. The disorder consists of a deterioration of the retina (Fig. 1) - the light-sensitive layer of the eye - which results in a diminished sight. The age of onset varies from breed to breed; the Collie and the Irish Setter show the symptoms at a very early age (from six weeks), while the Labrador is free of symptoms till about four to six years. The disease always ends in blindness. Later on often cataract is found as well.

The two most important types are:

PED (Pigment Epithelium Dystrophy)
pigment accumulations in the retina, followed by degeneration of the cones. At the age of 3 to 5 years eyesight diminishes. At a later age also the rods are affected and blindness follows.
PRA-night-blindness
major types:
  1. At an early age by incorrect development (dysplasia) and later on by deterioration (atrofia) of the rods and sometimes the cones. Blindness follows at the age of 1-2 years. Found in Setters, Collies, Dachshund and Norwegian Elkhound.
  2. This type shows no dysplasia, but instead a degradation (atrofia) of the retina. Slowly increasing until blindness follows at the age of 5-10 years.
The disease is most likely inherited by a simple, autosomal, recessive gene. Two (genetically different) types have been found; research show that the Setter has a different type than the Collie (crossing a Setter and a Collie who are both affected produces pups that are free of PRA). Considering the genetic background it should be possible to develop a genetic test. For the Irish Setter this is already the case. In the Netherlands eye examinations are performed for the Hirschfeld foundation for breeding programmes. The advantage of (genetic) blood tests would be that affected dogs at an early stage and also carriers van be detected.

Glaucoma

The pressure in the anterior eye chamber increases which causes the lens to become clouded. The disease ends in blindness. Often both eyes are affected. Some types of glaucoma are considered to be hereditary. Symptoms include redness of the sclera, blue discoloration of the cornea, enlarged pupil, tears, sensitivity to light or even an enlarged eye. The dog will most likely lose the eye, despite treatment.

Primary glaucoma is often hereditary, with a recessive or polygenous inheritance. About 10-20% of the dogs are genetically affected, but only ½% actually develops glaucoma.

Cataract

Is common in dogs and is often inherited. Since the dogs often get used to a clouded or misty lens, the owner notices hardly anything until a severe stage has been reached.

Primary Cataract

Directly caused by a defect in the eye lens itself.
Congenital cataract
Is present at an early age (6-8 weeks). Causes can be: hereditary disorders, inflammations, poisoning or disease during pregnancy. A white, dense discoloration of the lens is found; often seen in both eyes in equal amounts. Inheritance is unknown and differs from breed to breed.
Juvenile cataract
Originates between 8 weeks and about six years of age. Causes:
Inherited
Both eyes often affected equally. Type of inheritance often unknown.
Radiation
Rare; for example as a side effect from cancer treatment.
Nutrition
With our modern dog food this can only be found in experiments.
Poisoning
For example Naftalene and Dinitrophenole.
Trauma
A wound that perforates the eye or a hit on the head can cause cataract (often in one eye).
Senile cataract
Pretty rare. Is seen at a later age. In parts of the lens the lens fibres are decomposed. Often a case of lens sclerosis (clouding of the lens due to a diminishing amount of water and water solvable proteins in the lens).

Secondary cataract

Cataract caused by another disorder. One can think of diabetes, where substances accumulate in the lens. This accumulation results in a swelling of the lens fibres (attraction of water), which results clouding of the lens. After a while the lens fibres are damaged irreversibly.

Another cause can be PRA. Besides degeneration of the retina, after a while cataract also occurs.

Retinal Dysplasia (RD)

Comes in different types:
  • complete dysplasia
    Rather rare. Pups are born blind. Appears to be a simple recessive gene. Contrary to the next type, no bone disorders are to be expected.
  • Retinal folds
    This is "Retinal and vitreum dysplasia with bone disorders". Three phenotypes exist for the eye disorder:
    1. Normal
    2. Local retinal dysplasia (folds)
    3. Completely detached retina.
    And two phenotypes for the bone disorder:
    1. Normal
    2. Dwarfism
    The gene behaves recessive in case of the bone disorder and incompletely dominant in case of the eye disorder. So:

    *
    - - normal eyes, normal skeleton
    rd - local retinal dysplasia and normal skeleton
    rd rd complete retinal dysplasia and dwarfism
    *

    The retinal folds can disappear at a later age, which can result in false negatives.

Persisting Hyperplastic -Tunica Vasculosa Lentis and -Primary Vitreum (PHTVL/PHPV)

  PHTVL/PHPV
Fig. 5. PHTVL/PHPV
Cross section of the eye. The small, distorted lens is the gray object. Right behind that are the brown-white remains of the blood vessels.
(Photo reproduced from "Erfelijke Oogafwijkingen" (Hereditary eye disorders) with permission of the author1).
Rare disorder, where during the development of the eye remains of the blood vessels, that play a role in the nutrition of the backside of the lens, stay behind. Severeness is expressed in grades:
TW
Transitional case; minute amounts present, often in one eye.
1
light form, often in one eye, small amounts of debris that remain the same
2-6
increasingly severe types, in both eyes, layer of coloured scar tissue situated on the back of the lens, lens can be malformed and can slowly show signs of cataract.

Probably caused by an autosomal, incompletely dominant gene. Heterozygous animals most likely show grade TW or 1.

More severe cases can be operated on, producing positive results in half of the cases.

Membrana Pupillaris Persistens (MPP)

Rare disorder, where during the development of the eye remains of the blood vessels, that play a role in the nutrition of the front side of the lens, stay behind. These remains can often be seen as white threats at the front of the lens or on the iris.
  Eye with MPP Fig. 6. MPP
The remains are visible as white fibres on the iris.
(Photo reproduced from "Erfelijke Oogafwijkingen" (hereditary eye disorders) with permission from the author1).

In severe cases a net of white fibres is found. Sometimes combined with other eye disorders, for example disorder of the retina. Is found to be inherited in a number of breeds.


1) STADES, F.C., M.H. Boevé; Erfelijke Oogafwijkingen; Amsterdam, 1993; W.K. Hirschfeld Stichting.


Copyright © 1998-2013 Jigal van Hemert & Danielle Boshouwers
URL: http://www.bordercollies.nl/eheaeye.shtml
This page last modified: Wednesday, 30-Jul-2008 16:44:47 CEST
 
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