Hereditary eye disease in dogs

The British Veterinary Association and the Kennel Club

— working together for excellence in canine health

Revised by Sheila Crispin, August 2018

With acknowledgements to past and present members of the

Eye Panel and Eye Panel Working Party and with grateful thanks

to Dr Cathryn Mellersh and the Animal Health Trust

Hereditary

eye disease

in dogs

2 Hereditary eye disease in dogs

Hereditary eye

disease in dogs

Over the years, since its inception in the 1960s, the Eye Scheme

has been expanded to include assessment not just of the eye,

but also of adjacent (adnexal) structures such as the eyelids. The

result of this expansion is that certiﬁcation under the Eye Scheme

has important subsidiary beneﬁts; notably, recording anomalies

(ﬁndings of no clinical signiﬁcance) and abnormalities (ﬁndings

of potential or actual clinical signiﬁcance) whatever their origin.

Examples are provided at the end of this section (Part I).

It is clearly sensible for all dogs (pure bred and cross bred)

which are to be used for breeding to be examined under the

Eye Scheme prior to being bred from, as this is the simplest way

of identifying breed-related and potentially inherited problems.

Advice on the frequency of re-testing is provided each time

the dog is examined under the Eye Scheme. Examination and

certiﬁcation of older dogs, usually those no longer used for

breeding, should be regarded as essential, because longitudinal

information collected over time is a crucial means of providing

owners and breeders with the information that they need in

order to make informed breeding decisions and, in addition, a

reduced fee provides a ﬁnancial incentive for certiﬁcation of

dogs aged eight years and older. In summary, examination of

the older dog is recommended for a number of reasons:

● Enabling longitudinal information to be collected. A

longitudinal study is an observational research method in

which data is gathered for the same subjects repeatedly

over a period of time;

● Ensuring that the dog remains free of the inherited eye

diseases listed for the breed being examined under

Schedule A of the Eye Scheme. A number of inherited eye

problems may only be detected later in life (for example,

various types of hereditary cataract and some forms of

progressive retinal atrophy);

● Indicating whether late onset, potentially inherited, conditions

are emerging in older animals;

● Identifying age-related ocular and generalised diseases with

ocular manifestations, some of which may need treatment.

Further information is provided in Why should we check the eyes

of older dogs? (available from www.bva.co.uk/chs).

PART I

Clinical Examination for inherited eye disease

By Sheila Crispin

The main purpose of the British Veterinary Association/Kennel Club/International Sheep Dog Society (BVA/KC/ISDS)

Eye Scheme is to ensure that there is no clinical evidence of hereditary eye disease in dogs that are to be used for

breeding. A secondary purpose is to identify breed-related problems which may be inherited, especially if they have

welfare implications for the dog. Following examination of the eye an Eye Examination Certiﬁcate is issued which records

the inherited eye disease status (Schedule A) relevant to the breed being examined as either ‘clinically unaected’ or

‘clinically aected’ together with any additional comments about other clinical ﬁndings. In breeds in which primary

glaucoma is recognised clinical examination is supplemented by examination of the drainage angle — gonioscopy

(primary closed angle glaucoma) or measurement of intraocular pressure — tonometry (primary open angle glaucoma).

In addition, clinical examination of puppies when they are still part of a litter (litter screening) can be used to identify

signs of congenital/early onset inherited eye disease in aected puppies. When new potentially inherited conditions

are considered for listing under Schedule A, their inclusion is based on the scientiﬁc evidence including a clinical

prevalence of at least 1% over a minimum three-year period and/or the peer-reviewed scientiﬁc literature.

Healthy eyes enhance dogs’ quality of life

The normal eye

Hereditary eye disease in dogs 3

1: Normal adult eye of

a Border Collie with a

pigmented iris. 2: Ocular

fundus of that eye, showing

the tapetal fundus (yellow)

dorsally and heavily

pigmented non-tapetal fundus

ventrally.

7: Normal ocular fundus of

the eye of the Border Collie

puppy pictured on the left.

8: The eyes of newborn

puppies are not fully

developed at birth and the

tapetum has not yet formed

in this five-week-old puppy.

3: Normal adult eye of

a Crossbred dog with

variations of pigmentation

(heterochromia) in different

sectors of the iris. 4: Ocular

fundus of that eye. Note

that there is less pigment

ventrally, corresponding

with the area of reduced

pigmentation in the iris.

5: Subalbinotic eye of a

normal adult Border Collie.

6: Ocular fundus of that eye.

Both retinal and choroidal

vessels are visible and there

is no tapetum.

Picture, Sue Jones

4 Hereditary eye disease in dogs

The inherited eye conditions currently certiﬁed under the Eye

Scheme are reviewed in Part I of this article, together with

examples of some other conditions of the eye and adnexa

which may be inherited, as well as other examples of non-

inherited conditions. The potentially inherited and non-inherited

conditions are currently recorded in the middle section of the

certiﬁcate.

Inherited eye disease status (Schedule A) is recorded in the

bottom section of the certiﬁcate, as congenital (present from

birth) and non-congenital (acquired later in life) in type. This

simple classiﬁcation is not entirely satisfactory as the eyes of

puppies cannot be examined until the puppy is at least 4 weeks

of age, so there is a presumption that abnormalities viewed at

this stage are of congenital origin, whereas it is possible that

some of the conditions identiﬁed may actually be neonatal

rather than congenital. In addition, because the eye is immature

at birth, it is possible that some developmental conditions may

not be apparent at litter screening (puppies of up to 12 weeks

of age) and others may become less obvious (for example,

Collie eye anomaly) because of postnatal maturation. It is more

rational to describe inherited congenital conditions as those

identiﬁable during the neonatal stage (congenital/neonatal).

In summary, clinical examination for certiﬁcation (Schedule A

conditions) under the BVA/KC/IDS Eye Scheme includes:

1. Litters of puppies in breeds with congenital/neonatal

inherited ocular disease (Litter Screening Eye Examination

Certiﬁcate);

2. All dogs, whether purebred or cross bred, before they

are used for breeding and when they are subsequently

bred from (Eye Examination Certiﬁcate). For dogs that are

bred from year on year (for example, popular sires), annual

re-examination (Eye Examination Certiﬁcate) is required

throughout the dog’s breeding life;

3. Breeds in which primary glaucoma is recognised require

additional assessment as part of certiﬁcation (Eye Examination

Certiﬁcate) under the Eye Scheme. Clinical examination should

be supplemented by gonioscopy to assess the drainage angle

in breeds susceptible to primary closed angle/angle closure

glaucoma and tonometry to measure the intraocular pressure

in breeds susceptible to primary open angle glaucoma. Both

these procedures may need to be repeated in later life;

4. Dogs of eight years of age or older should be examined, at

a reduced fee, in order to check ocular and general health,

to provide valuable longitudinal data and to ensure that

later onset inherited conditions are recorded accurately

(Eye Examination Certiﬁcate).

Inherited eye diseases certiﬁed under

the Eye Scheme Schedule A

Glaucoma

Glaucoma is the term used to describe the eects of a

sustained pathological elevation of intraocular pressure. In

normal eyes the rate of aqueous humour formation and

the rate of aqueous outﬂow are in balanced equilibrium

and the normal canine intraocular pressure (IOP) measured

with an applanation or rebound electronic tonometer is

approximately 10–25mmHg. The clinical features shown are

those which are the result of structural ocular damage and

the consequent visual impairment or blindness. In particular,

it is the damage to the retinal ganglion cells and axons of the

optic nerve, particularly the prelaminar portion, which is the

most signiﬁcant feature in sight loss. Once the process of

retinal ganglion cell and optic nerve degeneration has begun,

the most that appropriate therapy can achieve is slowing

down the loss of sight.

Glaucoma is not a single disease entity, but rather a

degenerative process with a number of possible causes and

a ﬁnal common pathway. Two broad categories of glaucoma

are recognised — primary and secondary. In primary glaucoma

there is no antecedent intraocular disease and, although the

aetiology is complex, all the canine primary glaucomas are

due to impairment or cessation of aqueous outﬂow from

the anterior chamber of the eye. Aqueous outﬂow is through

the iridocorneal (drainage) angle and in the dog the angle is

extended posteriorly into the ciliary body as the ciliary cleft. It

is within the ciliary cleft that the trabecular meshwork is found

and the canine equivalent of the primate canal of Schlemm, the

aqueous plexus, is situated in the scleral tissues which form the

outer wall of the cleft. In cases of primary glaucoma, a defect

of the iridocorneal angle and the structures associated with the

ciliary cleft is responsible for inadequate drainage, leading to an

increase of intraocular pressure. The secondary glaucomas are

associated with antecedent eye disease such as uveitis, primary

lens luxation, trauma and neoplasia.

Classiﬁcation

Currently, two types of primary glaucoma may be distinguished,

primary closed angle glaucoma (or primary angle closure

glaucoma) and primary open-angle glaucoma (see Primary

Glaucoma — available from www.bva.co.uk/chs). The

nomenclature has been ‘borrowed’ from human medicine

and, although acceptable, does not describe the situation

completely. When these terms are used to describe primary

glaucoma in the dog they denote the appearance of the

entrance to the ciliary cleft. Thus, in closed angle glaucoma the

cleft is closed and in open-angle glaucoma the cleft is open.

Hereditary eye disease in dogs 5

● Primary closed angle glaucoma (PCAG)/primary angle

closure glaucoma (PACG):

In the normal dog, the ciliary cleft entrance is between 1.5

and 2 mm in width and spanned by a number of iris root

processes or ﬁbres, collectively referred to as the pectinate

ligament. Dogs which develop primary closed angle glaucoma

demonstrate a congenital predisposition, in that the entrance

to the ciliary cleft is abnormal and both eyes are aected.

The pectinate ligament is dysplastic, or abnormal, and may be

seen as sheets of undierentiated mesenchymal tissue rather

than the normal ﬁbrocellular processes. Pectinate ligament

abnormality with, or without narrowing of the iridocorneal

angle, is referred to as goniodysgenesis. To assist owners and

breeders and as part of data collection for goniodysgenesis

a simple grading system is being piloted to help in the initial

assessment of the drainage angle and any changes to the

drainage angle over time. A grading scheme will almost

certainly replace the ‘Clinically Unaected’ or Clinically

Aected’ classiﬁcation that was used previously to record the

results of examination (see Primary Glaucoma — available

from www.bva.co.uk/chs).

The age at which glaucoma develops tends to vary with

breed but, in most, the disease is one of middle age

and the presentation can be acute. In addition to raised

intraocular pressure the common clinical signs of acute

closed angle glaucoma include pain, episcleral congestion,

corneal oedema and a dilated non-responsive pupil. The

canine drainage angle cannot be viewed directly and a

goniolens is needed to assess the pectinate ligament

and drainage angle width. The Barkan and Koeppe direct

goniolenses are used most commonly for assessment of

the iridocorneal angle under the Eye Scheme. Gonioscopy

9: Anterior segment – gross globe – the iris root processes that comprise the pectinate ligament span the entrance to the ciliary cleft. The iris, from which the

processes arise, is on the left and the posterior cornea, where the processes insert, is on the right. 10: Acute closed angle glaucoma. 11: Welsh Springer Spaniel –

chronic closed angle glaucoma with globe enlargement (left eye). 12: Gonioscopy, Barkan goniolens in situ, a column of saline within the silicone tubing creates a

negative pressure to keep the lens in place. 13: Gonioscopy – Koeppe goniolens in situ, coupling gel keeps the lens in place. 14: Normal drainage angle of a Siberian

Husky. The drainage angle is of normal width and is spanned by the pectinate ligament. In this poorly pigmented eye, the white band of the scleral shelf is clearly

distinguished. There is great variation in the number, width, pigmentation and distribution of the fibres that comprise the pectinate ligament in different breeds, but

the width of the normal drainage angle is not subject to such variation. 15: Normal drainage angle of a Flat Coated Retriever. The width of the drainage angle is normal

and the fibres of the pectinate ligament are clearly defined. This eye is more heavily pigmented than the one pictured on the left and the scleral shelf is obscured by

pigment. 16: Goniodysgenesis in a Flat Coated Retriever. There is extensive pectinate ligament dysplasia and sheets of mesenchymal tissue occlude the majority of the

drainage angle. Aqueous drainage is via a limited number of ‘flow holes’. The drainage angle is slightly narrowed and normal pigment obscures the scleral shelf. The eye

was normotensive at the time of examination (intraocular pressure of 18 mmHg measured with a Mackay-Marg tonometer), despite the compromised drainage angle.

17: Welsh Springer Spaniel – goniodysgenesis.

Primary closed angle/angle

closure glaucoma breeds

under Schedule A

Basset Hound

Dandie Dinmont Terrier

Japanese Shiba Inu

Leonberger

Retriever (Flat Coated)

Siberian Husky

Spaniel (American Cocker)

Spaniel (Cocker)

Spaniel (English Springer)

Spaniel (Welsh Springer)

Spanish Water Dog

can be used as a method

of screening to determine

those animals that are

predisposed before

the disease makes its

appearance and aected

animals should not be

bred from. Routine

gonioscopy can be

performed at ﬁve to six

months of age in most

breeds and should be

repeated, as progression

of pectinate ligament

abnormality over time has been reported in a number of

breeds, including the Flat Coated Retriever, Basset Hound,

Dandie Dinmont Terrier and Welsh Springer Spaniel. The

Eye Panel Working Party has suggested that gonioscopy

is performed at approximately 1, 4 and 7–8 years of age in

breeds at risk.

The precise modes of inheritance have not been

determined for aected breeds, but clear breed and line

predisposition indicate a genetically determined cause,

albeit with a likely complex mode of inheritance.

● Primary open angle glaucoma (POAG):

Primary open angle glaucoma presents both dog breeder

and clinician alike with real problems in its early diagnosis,

for the usual clinical features of glaucoma are not present.

It is silent in onset, with either vision impairment or globe

enlargement usually being the ﬁrst abnormalities reported

by the owner. Goniodysgenesis is not a feature of this

109 1211

14 15 16 17

6 Hereditary eye disease in dogs

type of glaucoma and there are no other predisposing

features that can be used to forecast the advent of the

disease. It is inherited as a simple recessive trait and has

been described extensively in the Beagle. In this breed the

causal mutation has been identiﬁed in the ADAMSTS 10

gene and a DNA based test has been developed. POAG

has been reported in other breeds, notably the Norwegian

Elkhound and, most recently in the UK, the Petit Basset

Grion Vendeen (PBGV), Basset Hound and Basset Fauve

de Bretagne and DNA tests are available.

In the PBGV the earliest clinical presentation is either lens

instability (phacodonesis), lens subluxation in a normotensive

eye, or actual globe enlargement with possible lens

subluxation/luxation and vision impairment. The disease

aects most dogs from 3 to 6 years of age, but a later onset

is possible. When the intraocular pressure (IOP) increases,

variable degrees of episcleral congestion and mild corneal

oedema may be seen. The pupil may be partially dilated, but

with the passage of time the pupillary light reﬂex (PLR) is

eventually impaired or lost. Signs of ocular pain are subtle and

aected dogs are usually lethargic and sleep more; systemic

non-steroidal anti-inﬂammatory drugs beneﬁt such patients.

With progression globe enlargement occurs, but it is only in

advanced disease that cupping of the optic disc and retinal

degeneration characterised by increased tapetal reﬂectivity

and blood vessel attenuation are seen. Lens subluxation may

occur even before there is a rise in IOP, but total lens luxation

would appear to be unusual unless there is gross globe

enlargement. The elevation of IOP is moderate, with pressures

between 30 and 40 mmHg being routinely recorded.

In terms of the BVA/KC/ISDS

Eye Scheme as applied to POAG,

gonioscopy is not necessary,

for closure of the iridocorneal

angle occurs only in late disease

where there is marked globe

enlargement, but tonometry can prove helpful where early

disease is present. Annual examination in dogs of 3 to 9 years of

age is advisable. Lens subluxation is common before and after

the rise in IOP, but POAG should not be confused with primary

lens luxation (see below).

18: Tonopen in use. 19: Tonovet in use.

20: Primary open angle glaucoma

— the globe is enlarged and

secondary lens luxation has occurred.

Persistent hyperplastic primary vitreous

The embryonic lens is supplied with nutrients by the hyaloid

artery (which grows forward from the optic stalk to reach

the posterior lens surface at about day 25 of gestation) and

the tunica vasculosa lentis (which is formed by day 30 of

gestation). Regression of the vascular supply starts at about

day 45 of gestation and is complete some two to four weeks

after birth. Persistence of these vessels and proliferation of

associated mesodermal elements of the tunica vasculosa

lentis posterioris produce the main lesion of ﬁbrovascular

plaque formation on the posterior lens capsule. This plaque

appears as a dense yellow/white opacity with multiple

pigment foci attached to the posterior lens capsule. Blood

vessels may be visible within the plaque and at its periphery.

Other features of persistent hyperplastic primary vitreous

include persistent capsulopupillary vessels (iridohyaloid

vessels), coloboma of the lens, posterior lenticonus,

intralenticular and retrolental haemorrhage, secondary

cataract, persistence of the hyaloid artery and Bergmeister’s

papilla (remnant of the glial sheath around hyaloid vessels on

the optic disc), and retinal dysplasia.

Currently, the Dobermann and Staordshire Bull Terrier are

certiﬁed for persistent hyperplastic primary vitreous under

the Eye Scheme. The mode of inheritance is complex and to

date no mutations have been identiﬁed that play a role in

the development of this disease, although the genetic data

available suggest an autosomal dominant gene with variable

or incomplete penetrance.

Signiﬁcance

Severe lesions cause marked visual loss or blindness. Yellow/

brown focal dots on the posterior lens capsule, the mildest

form of PHPV, have no discernible eect on vision. Small

areas of retrolental plaque formation may spare the lens

periphery and allow adequate vision. More extensive plaques

and cataract, or other lens abnormalities, usually cause severe

visual impairment or blindness. The Staordshire Bull Terrier

suers less from the posterior lens capsule deformities, but

has more widespread retinal folds and rosettes than the

Dobermann. The condition is not common in either breed in

the UK, but represents a serious congenital inherited problem

in some aected dogs. Surgical treatment of those cases with

visual problems is fraught

with diculty and there is

a high risk of postoperative

complications.

Primary open angle glaucoma

breeds under Schedule A

Basset Hound

Petit Basset Grion Vendeen

Shar Pei

Persistent hyperplastic primary

vitreous breeds under Schedule A

Dobermann

Staordshire Bull Terrier

2018 19

Hereditary eye disease in dogs 7

Retinal dysplasia

The term retinal dysplasia embraces a number of congenital/

neonatal conditions resulting from disorderly proliferation

and atypical dierentiation of the retina during embryonic

life. In addition to genetically determined hereditary retinal

dysplasia, a wide variety of extraneous insults (for example,

infectious agents such as canine herpes virus and irradiation)

to the developing retina may cause acquired, non-inherited,

retinal dysplasia. Defective retinal development results in

extremely varied clinical and microscopic appearances so that,

for example, folds, ridges, rosettes, geographic abnormalities

and localised detachments are all possible manifestations of

multifocal retinal dysplasia, whereas total retinal dysplasia is

most commonly associated with non-attachment or complete

detachment of the retina.

Classiﬁcation

● Multifocal retinal dysplasia:

Linear folding of the sensory retina and the formation of

rosettes composed of variable numbers of neuronal retinal

cells are the histological characteristics of multifocal retinal

dysplasia. Typically, the lesions range from vermiform grey

streaks, dots and circles to multiple focal sites of tapetal

hyperreﬂectivity, which may or may not be associated with

hypertrophy of the retinal pigment epithelium. Irregularly

shaped (geographic) areas of retinal dysplasia may also be

encountered. In most cases, the lesions are most obvious

in the tapetal fundus dorsal to the optic disc. In the English

Springer Spaniel, dysplastic changes occur in the developing

sensory retina at 45 to 50 days of gestation. The other

breeds at present certiﬁed under the Eye Scheme for

multifocal retinal dysplasia are the Cavalier King Charles

Spaniel, Hungarian Puli, Rottweiler, Golden Retriever and

American Cocker Spaniel.

Litter screening is useful, although subtle changes are not

always clearly deﬁned. In older animals remodelling of some or

all multifocal lesions may result in them becoming less obvious,

even disappearing, over time. This does not appear to be the

case with the geographic form.

● Total retinal dysplasia:

Somewhat more complex, this form of retinal dysplasia is

associated with non-attachment or complete detachment of

the retina. Non-attachment may result from apparent failure

of contact of the inner (retinal) and outer (retinal pigment

epithelial) layers of the optic cup during embryogenesis; other

ocular abnormalities, such as microphthalmos and nystagmus,

are often present in these cases. The Bedlington Terrier,

Labrador Retriever and Sealyham Terrier are certiﬁed for

total retinal dysplasia under the Eye Scheme, although total

retinal dysplasia has been recorded in other breeds, including

the Yorkshire Terrier and Samoyed. In the Bedlington Terrier

most aected dogs have an infundibular retinal detachment.

Puppies are blind from birth and may present with leukocoria,

a white pupil, because the retina is immediately behind

the posterior lens capsule. Retinal neovascularisation may

result in intraocular haemorrhage. In the Sealyham Terrier

a total detachment of the retina is similarly present and

microphthalmos and nystagmus are common. Two forms

of total retinal dysplasia are recognised as inherited in the

Labrador Retriever. In one form associated with complete

21: Persistent hyperplastic primary vitreous in a Dobermann. The white opacity visible through the pupil involves the vitreous and posterior lens capsule. 22:

Persistent hyperplastic primary vitreous with intralenticular haemorrhage ventrolaterally. The intralenticular haemorrhage progressed to involve the whole

lens. 23: Persistent hyperplastic primary vitreous. In this dog, the hyaloid vessel has remained patent and there is haemorrhage into the lens. Note the numerous

vacuoles within the lens cortex, which are indicative of progressive cataract formation. 24: The same eye as that pictured in 23 some months later after cataract

formation.

25: Golden Retriever — multifocal retinal dysplasia. 26: Multifocal retinal dysplasia in an English Springer Spaniel. Some of the larger focal lesions with pigmented

centres to the right of the dorsal primary retinal vessels resemble inactive chorioretinopathy, but there are also classical rosettes and vermiform lesions to the

left of the vessels. 27: Cavalier King Charles Spaniel puppy — geographic retinal dysplasia. 28: Cavalier King Charles Spaniel — geographic retinal dysplasia. 29:

Golden Retriever — geographic retinal dysplasia and haemorrhage.

22 2421 23

282625 27 29

8 Hereditary eye disease in dogs

detachment, the defect

seems to result from an

inability of the developing

retina to match the rapid

growth of the choroid

and sclera. The resulting

detachment leads to

degeneration of the

neurosensory retina

because of ischaemic

anoxia and such animals are

blind.

Other ocular defects,

such as microphthalmos,

nystagmus and cataract,

may be present. The

second form of total

retinal dysplasia, which

has not been reported in the UK, is ocular-skeletal dysplasia

associated with severe ocular defects and short-limbed

dwarﬁsm. In addition to the Labrador Retriever (dwarﬁsm

with retinal dysplasia type 1 — DRD1) it has also been

reported in the Samoyed (dwarﬁsm with retinal dysplasia

type 2 — DRD2). This phenotype is inherited as an autosomal

recessive in both breeds and mutations have been identiﬁed;

a 1-base insertional mutation in exon 1 of COL9A3 in the

Labrador Retriever and a 1,267-bp deletion mutation in the 5’

end of COL9A2 in the Samoyed.

Signiﬁcance

A simple autosomal recessive gene is responsible for

retinal dysplasia in most of the breeds studied. Diagnosis

is complicated by the fact that retinal dysplasia may be

the result of both genetic and non-genetic inﬂuences, the

ophthalmoscopic changes may be more dicult to detect in

the developing eye (ie, in puppies of less than six months of

age) and there is not always a clear distinction between the

various ocular manifestations of the multifocal and total types.

To add yet further complexity, remodelling of dysplastic lesions

may occur over time.

While many dogs with multifocal retinal dysplasia will have

no obvious visual defect, some are severely visually impaired,

as are all dogs aected with total retinal dysplasia. There is,

therefore, no question of not examining ‘at risk’ breeds under

the Eye Scheme.

Collie eye anomaly (CEA)

The prevalence of Collie eye anomaly in the UK is high, in

excess of 60% in the Rough Collie, Smooth Collie and Shetland

Sheepdog, with the Lancashire Heeler and Border Collie much

less aected. The condition has a worldwide distribution and

ocular lesions of identical ophthalmoscopic appearance have

been described in a number of other collie and non-collie

breeds, such as the Bearded Collie and Australian Shepherd.

CEA is a complex disorder aecting retinal, choroidal and scleral

development. The classical lesion is of choroidal hypoplasia in

the lateral or dorsolateral region of the fundus near the optic

disc. In some animals the hypoplasia may be more extensive

and it is not uncommon for the two eyes to be dissimilar. The

lesion is apparent as a ‘pale patch’ and is due to a localised lack

of some, or all, retinal and choroidal pigment and tapetum.

The choroidal vessels in the aected region are also abnormal,

usually in size, number and disposition. In merle dogs, with

little pigmentation in the fundus and no tapetum, choroidal

hypoplasia will be less obvious and the appearance of the

choroidal vessels then becomes the important diagnostic

feature. In addition to choroidal hypoplasia, colobomas and

staphylomas of the optic nerve head and/or adjacent tissues

may be part of the extended phenotype and can sometimes be

the only visible abnormality. It has been suggested that adult

dogs in this category may be examples of so-called ‘go normals’.

The term ‘go normal’ has been applied to cases where post

natal development (pigmentation and tapetal development)

obscures the choroidal hypoplasia which is the key diagnostic

feature, so that adult dogs have a fundus of ‘normal’

appearance; however, this description might be regarded as

inappropriate because such dogs are genotypically aected.

The phenomenon is common enough to call into question the

relevance of examining dogs as adults rather than as puppies.

Data on Collie eye anomaly in the Rough Collie in Norway, for

example, has indicated that the diagnosis of the condition in a

group of dogs of more than three months of age was almost

half that for a group of puppies of seven weeks to three

months of age. Furthermore, when puppies which had been

diagnosed as having Collie eye

anomaly with mild choroidal

hypoplasia at between seven

weeks and three months of age

were re-examined at about one

year of age, 68 per cent had a

fundus of normal appearance.

30: Total retinal dysplasia in a Labrador Retriever puppy. 31: Close-up of the eye of this puppy. The retina can be visualised

behind the lens. 32: Gross globe — total retinal dysplasia with infundibular retinal detachment.

Collie eye anomaly breeds

under Schedule A

Border Collie

Collie (Rough)

Collie (Smooth)

Lancashire Heeler

Shetland Sheepdog

Multifocal retinal dysplasia/ Total

retinal dysplasia breeds under

Schedule A

Certiﬁed – Schedule A (TRD)

Bedlington Terrier

Sealyham Terrier

Certiﬁed – Schedule A (MRD)

Cavalier King Charles Spaniel

Hungarian Puli

Retriever (Golden)

Rottweiler

Spaniel (American Cocker)

Spaniel (English Springer)

Certiﬁed – Schedule A

(TRD and MRD)

Retriever (Labrador)

TRD Total retinal dysplasia, MRD

Multifocal retinal dysplasia

3130 32

Hereditary eye disease in dogs 9

Complications such as retinal detachment and intraocular

haemorrhage are fortunately rare; thus, the majority of dogs

with Collie eye anomaly show no apparent visual defect.

Tortuosity of the retinal vessels and retinal folds, the latter

usually in the form of vermiform streaks, are not now regarded as

part of the syndrome, but may relate to the smallness of the eye.

Signiﬁcance

A variety of fundamental issues combine to make this

a dicult clinical diagnosis on occasions, however, it is

worth emphasising that Collie eye anomaly is a congenital

condition which can be diagnosed as soon as eye

examination is possible (ie at ﬁve to six weeks of age), and

that it is diagnosed clinically with greatest accuracy in

such young dogs. In aiming to eliminate CEA from a breed,

litter screening, combined with DNA testing is the best

approach. Advances in canine genetics have shown that the

primary CEA mutation has arisen as a single disease allele in

a common ancestor of herding breeds and that all aected

dogs share a homozygous deletion of 7.8 kb in the NHEJ1

gene. The availability of a DNA test has proved of great value

in devising comprehensive breeding strategies.

Hereditary cataract (HC)

The canine lens is an asymmetrical, transparent, biconvex sphere,

with the more convex aspect posteriorly. The adult lens consists

of a central nucleus surrounded by cortical lens ﬁbres and the

nucleus itself is divisible into various regions according to age:

the oldest, central, portion of the lens is the embryonic nucleus;

surrounding that is the foetal nucleus; and the outermost portion

is the adult nucleus. The whole lens is contained within an

acellular capsule (the anterior capsule is thicker than the posterior

capsule). A single layer of epithelial cells lies immediately beneath

the anterior capsule and it is these cells which form the germinal

cell layer that produces new

lens ﬁbres throughout life.

The epithelial cells migrate

peripherally and elongate at

the equator (circumference)

of the lens. Each ﬁbre extends

anteriorly and posteriorly to

meet ﬁbres to the front and rear

to form the suture lines. The

suture lines form an upright ‘Y’

anteriorly and an inverted ‘Y’

posteriorly.

Cataract is deﬁned as

any opacity of the lens

or its capsule. There are

many reasons for cataract

formation — cataracts may

be congenital, due to in utero

insult; traumatic, as a result

of blunt or penetrating injury

to the eye; metabolic, as a

consequence of, for example,

diabetes mellitus; toxic, caused

by some drugs; nutritional,

produced by inappropriate diets; or a complication of

other primary ocular diseases such as uveitis and neoplasia.

Cataracts may also form in dogs with generalised progressive

retinal atrophy.

Additionally, primary inherited cataracts have been reported in

a number of breeds and it is these with which the Eye Scheme

is concerned. Fortunately, the age of onset, appearance and

evolution of the cataracts which are certiﬁed under Schedule A

of the Eye Scheme are usually quite speciﬁc within the aected

breeds, enabling inherited cataracts to be distinguished from

Hereditary cataract breeds

under Schedule A

Alaskan Malamute

Australian Shepherd

Belgian Shepherd Dog

Bichon Frise

Boston Terrier*

Cavalier King Charles Spaniel

German Shepherd Dog

Giant Schnauzer

Irish Red and White Setter

Large Munsterlander

Leonberger

Miniature Schnauzer*

Norwegian Buhund

Old English Sheepdog

Poodle (Standard)

Retriever (Chesapeake Bay)

Retriever (Golden)

Retriever (Labrador)

Siberian Husky

Spaniel (American Cocker)

Spaniel (Welsh Springer)

Staordshire Bull Terrier*

*More than one type of

hereditary cataract can occur

within an individual breed

33: Collie eye anomaly in a five-week-old Border Collie puppy. A region of chorioretinal hypoplasia (pale patch) is obvious lateral and slightly dorsal to the optic

nerve head. 34: Border Collie — Collie eye anomaly right eye. 35: Border Collie — Collie eye anomaly left eye. 36: Collie eye anomaly in an adult Rough Collie. The most

striking feature is the peripapillary coloboma ventral to the optic nerve head. 37: Collie eye anomaly in an adult Border Collie. This image is dominated by a large

colobomatous defect to the right of the picture and there is also extensive chorioretinal hypoplasia lateral to the coloboma. 38: Rough Collie — Collie eye anomaly

with retinal detachment. 39: Shetland Sheepdog — Collie eye anomaly with intraocular haemorrhage.

3533

10 Hereditary eye disease in dogs

other non-inherited types of cataract. At present, congenital

cataract in the Miniature Schnauzer is the only congenital

inherited cataract included in the Eye Scheme; the remainder

are all non-congenital types and, as some of them have a

variable age of onset, it is important to examine dogs of over

eight years of age to ensure that animals that have been used

for breeding remain free of inherited cataract.

Signiﬁcance

Quite apart from the undesirable perpetuation of abnormality

within breeding lines, a proportion of inherited cataracts progress

to produce visual impairment and blindness. The only treatment

for cataract is surgical and, although modern techniques give

good results, the procedure is expensive.

Primary lens luxation (PLL)

Primary lens luxation is a condition in which an inherent defect

in the zonule (the suspensory ligament of the lens) leads to

partial or complete dislocation of the lens at approximately

four to ﬁve years of age; clinical signs are not usually observed

before three years of age or later than seven years of age. It

is a common cause of secondary glaucoma and, as such, an

important disease to recognise because of the potential for pain

and visual loss. Primary lens luxation is recognised as a familial

problem in certain of the terrier breeds (Miniature Bull Terrier,

Smooth Fox Terrier, Wire Fox Terrier, Parson Jack Russell Terrier

and Sealyham Terrier), the Tibetan Terrier (which is not a true

terrier breed), the Lancashire Heeler and the Border Collie. A

single nucleotide substitution in the ADAMTS17 gene has been

shown to be the cause of PLL in 17 breeds (the Australian Cattle

Dog, the Chinese Crested Dog, the Jagdterrier (also known as

the German Hunt Terrier), the Lancashire Heeler, the Miniature

Bull Terrier, the Jack Russell Terrier, the Parson Russell Terrier,

the Patterdale Terrier, the Rat Terrier, the Sealyham Terrier,

the Tenterﬁeld Terrier, the

Tibetan Terrier, the Toy Fox

Terrier, the Volpino Italiano, the

Welsh Terrier, the Wire-haired

Fox Terrier and the Yorkshire

Terrier). This mutation has been

excluded from involvement in

the Border Collie and the Shar

Pei, indicating other mutations

are the cause in these breeds.

The condition is essentially bilateral, but almost invariably

presents as a uniocular condition, as one eye may be aected

weeks or months in advance of the other. Observant owners

may notice a change in the appearance of the aected eye

which correlates with the lens moving out of its normal position.

When the lens moves anteriorly, secondary glaucoma develops

rapidly and pain, blepharospasm, photophobia and lacrimation,

an increase in intraocular pressure, together with a widely

dilated non-responsive pupil, visual loss and episcleral and

conjunctival congestion, are the most obvious clinical features.

With posterior lens luxation, secondary glaucoma is less likely,

although most lenses will move forward at some stage. Careful

observation will reveal the displaced lens (usually the lens

equator is highlighted by the penlight used for examination), in

addition vitreal prolapse and instability of the lens may also be

apparent (phacodenesis). In addition, the iris trembles slightly

with head and eye movement (iridodonesis) because it has lost

the support of the lens.

Primary lens luxation breeds

under Schedule A

Border Collie

Bull Terrier (Miniature)

Fox Terrier (Smooth)

Fox Terrier (Wire)

Lancashire Heeler

Parson Russell Terrier

Sealyham Terrier

Tibetan Terrier

44: Primary lens luxation in a Miniature Bull Terrier. The changes were acute, and the eye painful and red (episcleral congestion), indicative of glaucoma (the

intraocular pressure measured with a Mackay-Marg tonometer was 60 mmHg). The other eye was normotensive (intraocular pressure 22 mmHg). The lens has luxated

anteriorly and an area of corneal oedema is apparent as a result of endothelial damage from contact with the lens. The lens equator is highlighted by illumination

from a penlight. 45: Tibetan Terrier – primary lens luxation (anterior). 46: Tibetan Terrier – primary lens luxation, the anteriorly dislocated lens has developed

cataract.

40: Congenital hereditary cataract in a Miniature Schnauzer. The nuclear portion of the lens is affected and there is a pyramid-shaped extension medially. Picture:

Dr Keith Barnett. 41: Hereditary cataract in a Norwegian Buhund. There is an obvious opacity, located posteriorly, involving the posterior pole and posterior suture

lines. In this breed pulverulent nuclear cataracts have also been reported as inherited (see Figure 85). 42: Hereditary cataract in a Golden Retriever. The characteristic

Y-shaped cataract is located in a posterior polar subcapsular position. 43: Total hereditary cataract in a Labrador Retriever.

4544 46

4140 42 43

Hereditary eye disease in dogs 11

Signiﬁcance

Primary lens luxation is an inherited problem which can

cause persistent pain and blindness without prompt surgical

intervention. Aected dogs should not be bred from and the ‘at

risk’ breeds that are to be used for breeding should be examined

under the Eye Scheme.

Progressive retinal atrophy (PRA)

Progressive retinal atrophy (PRA), is a generic term for a range

of genetically heterogeneous inherited retinal diseases aecting

many breeds of dog. PRA involves the retinal photoreceptors

and two major types are recognised — developmental

(dystrophies) and degenerative. The developmental disorders

are of early onset and involve the rod or cone photoreceptors,

or both, the loss of photoreceptors and rate of progression is

usually rapid as the aected photoreceptors fail to dierentiate

normally. The degenerative disorders by contrast usually

involve photoreceptors that have dierentiated normally and

the age of onset is later and progression slower. For example,

in a breed such as the Irish Setter, with rod/cone dysplasia,

the photoreceptors are abnormally formed and begin to

degenerate before they are mature. The disease, therefore,

aects these dogs at a relatively young age. The age of onset

is later in, for example, the rod/cone degeneration of the

Miniature and Toy Poodle, as the photoreceptors degenerate

after reaching maturity.

The clinical ﬁndings in PRA are strikingly similar whatever

the underlying pathogenesis. Owners usually notice a loss

of night vision, especially when the dog is in unfamiliar

surroundings. The condition progresses to produce a loss

of vision under all lighting conditions and there is a poor

pupillary light reﬂex with dilated pupils. In time, secondary

cataract formation is common. Ophthalmoscopic examination

indicates a generalised, bilaterally symmetrical increase in

tapetal reﬂectivity (a consequence of retinal atrophy). There

is attenuation (narrowing) of the retinal vessels, especially

the small peripapillary arterioles, which may become barely

visible (‘ghost vessels’) or invisible on ophthalmoscopy. In dogs

with a poorly developed tapetum or an atapetal fundus, the

attenuation of the retinal vessels may be the only obvious

ophthalmoscopic sign of early progressive retinal atrophy,

necessitating careful observation. Later in the course of the

disease the optic disc becomes paler due to atrophy of its

capillaries and nerve ﬁbres. The non-tapetal fundus also shows

extensive areas of depigmentation as the condition progresses.

Cataracts, which form late

on in the condition, may

manifest as opacities in the

posterior cortex, or as radial

opacities, before progressing

to total cataract.

In those disorders in which

the cones or rods are

preferentially aected (for

example, cone degeneration

in the Alaskan Malamute,

or rod dysplasia in the

Norwegian Elkhound) the

visual defect will reﬂect

the type of photoreceptor

involved — tending to

day blindness when cone

photoreceptors are abnormal

and night blindness when

rod photoreceptors are

abnormal.

Signiﬁcance

Most types of PRA are autosomal recessive traits but, less

commonly, autosomal dominant and X-linked types of PRA have

also been reported.

There is currently no eective treatment for these conditions, so

it is DNA testing that underpins eorts to eliminate PRA in many

breeds, including a form of PRA, breed speciﬁc retinopathy, in the

Swedish Vallhund.

Retinal pigment epithelial dystrophy (RPED) /

central progressive retinal atrophy (CPRA)

Retinal pigment epithelial dystrophy, for many years referred

to as Central Progressive Retinal Atrophy (CPRA), is a disease

of the retinal pigment epithelium cells. The breeds at present

certiﬁed under the Eye Scheme are the Border Collie, Briard,

Rough Collie, Smooth Collie, Golden Retriever, Labrador

Retriever, Shetland Sheepdog, Cocker Spaniel, English Springer

Spaniel and Cardigan Welsh Corgi. Ophthalmoscopic signs

may be detected on occasion in dogs of just over 12 months

of age, but it is more usual to make the diagnosis from about

18 months of age onwards. Electroretinography is not of value

in early diagnosis.

Progressive retinal atrophy breeds

under Schedule A

Australian Cattle Dog

Collie (Rough)

Dachshund (Miniature Long-Haired)

Finnish Lapphund

Glen of Imaal Terrier

Gordon Setter

Irish Setter

Irish Wolfhound

Lhasa Apso

Miniature Schnauzer

Norwegian Elkhound

Poodle (Miniature)

Poodle (Toy)

Retriever (Chesapeake Bay)

Retriever (Golden)

Retriever (Labrador)

Retriever (Nova Scotia Duck Tolling)

Spaniel (American Cocker)

Spaniel (Cocker)

Spaniel (English Springer)

Swedish Vallhund

Tibetan Terrier

Welsh Corgi (Cardigan)

47: Progressive retinal atrophy in a Cocker Spaniel. Attenuation of the retinal vessels and pallor of the optic nerve head are the most obvious features as tapetal islets (a

normal variant) do not produce the striking hyperreflectivity seen with a more extensive tapetum. Vision was seriously compromised in this dog. 48: Progressive retinal

atrophy in a Miniature Poodle. Tapetal hyperreflectivity is obvious, the optic nerve head is pale and the retinal vessels scarcely visible. The animal was almost totally

blind. 49: Progressive retinal atrophy in a Cocker Spaniel. An abnormal zone is apparent slightly dorsal to the optic nerve head. The zone appears dull or hyperreflective

depending on the direction of the light source. The retinal vessels are marginally narrower than usual and the animal’s vision was apparently unaffected.

4847 49

12 Hereditary eye disease in dogs

The disease is caused by the inability of the retinal pigment

epithelial cells to degrade spent photoreceptor metabolites,

with the resultant accumulation of lipopigment within the

retinal pigment epithelium. There are focal concentrations of

lipopigment-laden cells which migrate into the true retinal layers.

Degeneration of the photoreceptors (rods and cones) and retinal

atrophy are secondary to the lipopigment accumulation and

retinal pigment epithelial cell malfunction.

In dogs of working breeds, the owner may notice an inability to

work in bright light, while vision in dim light may be adequate until

the disease is advanced. In pet dogs, suspect vision may not be

noticed as early. Aected dogs may exhibit a central visual defect,

but the pupillary light response is often reasonable and complete

blindness is unusual.

Ophthalmoscopic examination of early cases indicates light

brown foci in the tapetal fundus. These become more numerous

and eventually coalesce into

larger areas of lipopigment

with hyperreﬂective areas

between. In advanced cases the

pigment becomes less obvious

as hyperreﬂectivity increases.

The retinal blood vessels may

become attenuated late in the

disease, but the appearance

of the non-tapetal fundus and

optic disc alters little. Both eyes

are aected.

The Briard is of interest in that a defect in retinal polyunsaturated

fatty acid metabolism may underlie a form of congenital night

blindness in which the appearance of the ocular fundus is initially

normal, but by two to three years of age subtle hyper-reﬂectivity

of the tapetal fundus is apparent, together with sparse greyish

spots, which increase in number as the disease progresses,

accompanied by moderate attenuation of the retinal vessels.

Signiﬁcance

Unlike generalised progressive retinal atrophy, retinal pigment

epithelial dystrophy rarely causes blindness and secondary

cataract formation is also unusual. However, when the

disease develops in a working dog, the eects are predictably

serious. The inheritance of the disease appears complex and

environmental factors (for example, poor quality diet) may

inﬂuence the phenotypic expression. It is prudent to advise

against breeding from aected dogs and their relatives,

although the mode of inheritance has not been conﬁrmed.

Examples of

conditions recorded

in comments section

Written descriptive comments can be made on both the Eye

Examination Certiﬁcate and Litter Screening Eye Examination

Certiﬁcate providing further information on any Schedule A

inherited eye diseases identiﬁed and as a means of recording

other conditions identiﬁed in the course of the clinical

examination. Examples include:

● Breed-related eye diseases which may be inherited, currently

designated as ‘Under Investigation’ (Schedule B);

● Other breed-related anomalies and abnormalities of the eye

and adnexa which may be inherited;

● Acquired ocular abnormalities (for example, post-traumatic

damage, neoplasia, active/inactive inﬂammation);

● Ocular changes indicative of systemic disease.

Such observations are important if the abnormalities identiﬁed

have welfare implications, particularly so if they might be passed

on to subsequent generations. Examples of relevant breed-

related abnormalities with a genetic component include ocular

problems associated with excessive amounts of loose skin,

imperfect eyelid anatomy (for example, entropion, ectropion

and combinations of entropion and ectropion) and ocular-

related disease associated with brachycephaly (for example,

lagophthalmos and corneal damage).

50: Retinal pigment epithelial dystrophy in a Cocker Spaniel. At this relatively early stage, multiple focal accumulations of

lipopigment are the most obvious feature, together with some vascular attenuation and a slightly pale optic nerve head.

51: Cocker Spaniel – retinal pigment epithelial dystrophy, other eye of the same dog (as 50) photographed in blue light. 52:

Retinal pigment epithelial dystrophy in another Cocker Spaniel at a later stage of disease. The lipopigment has migrated to

produce a more cobweb-like appearance.

Retinal pigment epithelial

dystrophy (RPED/CPRA) breeds

under Schedule A

Border Collie

Briard

Collie (Rough)

Collie (Smooth)

Retriever (Golden)

Retriever (Labrador)

Shetland Sheepdog

Spaniel (Cocker)

Spaniel (English Springer)

Welsh Corgi (Cardigan)

5150 52

Hereditary eye disease in dogs 13

Breed-related ocular conditions that may be inherited, currently listed under Schedule B

Other breed-related ocular conditions of known and potential inheritance

53: Multiocular defects in a Cocker Spaniel. The eye is microphthalmic and a congenital cataract is present. Retinal

dysplasia was an additional finding. 54: Multiocular defects in an Old English Sheepdog. The eye is microphthalmic and

both a congenital cataract and persistent papillary membrane remnants are present. 55: Persistent pupillary membrane.

Most of the remnants arise from the iris collarette and extend anteriorly to the cornea where a discrete opacity is present

at the point of contact. 56: Persistent pupillary membrane. Most of the remnants arise from the iris collarette and extend

posteriorly to the lens. Note the associated pigment deposition on the anterior lens capsule. 57: Congenital hereditary

cataract and uveitis in a Golden Retriever. Note the darkly pigmented iris cyst in the pupillary aperture medially. 58:

Ocular melanosis (abnormal pigment deposition) in a Labrador Retriever. 59: Ocular melanosis (abnormal pigment

deposition) in a Cairn Terrier – secondary glaucoma has resulted in an enlarged globe. 60: Optic nerve hypoplasia in a

Miniature Poodle. 61: Papillary coloboma.

53 55

6968

64 65

66 67

58 59 60

62: Pug – brachycephaly is associated with respiratory and ocular problems. The

common anatomical-related problems that render the eye more susceptible to

mechanical insult can be summarised as a prominent eye, macropalpebral fissure

and lagophthalmos. Chronic pigmentary keratitis is also present in this dog.

63: Shar Pei – multiple skin problems (including poor eyelid conformation and

entropion) associated with hereditary cutaneous hyaluronosis. 64: Neapolitan

mastiff puppy – excessive skin folds and poor eyelid conformation. 65: Bulldog –

prolapsed nictitans gland, sparse distichia, subtle medial lower lid entropion.

66: Golden Retriever – lower eyelid entropion. 67: Boerbel puppy – severe

bilateral entropion (right). 68: Boerbel puppy – severe bilateral entropion (left).

69: Great Dane – lower eyelid ectropion. 70: St Bernard – ‘diamond eye’ –

combined entropion and ectropion (right). 71: St Bernard – ‘diamond eye’ –

combined entropion and ectropion (left).

14 Hereditary eye disease in dogs

76 77

8180

85 86 87

72 73 74

72: Basset Hound – combined entropion and ectropion and trichiasis.

73: American Cocker Spaniel – distichiasis and cataract. 74: Shetland Sheepdog

– ectopic cilia and corneal ulcer. 75: Cocker Spaniel – epiphora (right) associated

with lower lacrimal punctal aplasia (imperforate punctum). 76: West Highland

White Terrier – keratoconjunctivitis sicca. 77: Boxer – epithelial basement

membrane dystrophy. 78: Cavalier King Charles Spaniel – crystalline corneal

dystrophy (Schnyder-like corneal dystrophy). 79: Labrador Retriever – macular

corneal dystrophy. Picture: Animal Health Trust. 80: English Springer Spaniel –

endothelial dystrophy. 81: German Shepherd Dog – corneal arcus (arcus lipoides

corneae) secondary to hypothyroidism (right eye). 82: German Shepherd Dog –

corneal arcus (arcus lipoides corneae) secondary to hypothyroidism (left eye). 83:

Golden Retriever – lipid keratopathy. 84: Labrador Retriever – iris melanoma. 85:

Multiple iris cysts and early, non-inherited, cataract in an aged Labrador Retriever.

86: Senile nuclear sclerosis in an aged Border Collie. 87: Alaskan Malamute –

pulverulent nuclear cataract. Opacities involving the lens or its capsule are

frequently observed as incidental findings under the Eye Scheme

and there are many causes, of which possible inheritance is just one.

88: Akita – uveodermatological syndrome. 89: Cocker Spaniel – immune-mediated

thrombocytopenia.

Hereditary eye disease in dogs 15

BVA/ KC/ ISDS Eye Scheme Schedule A 2018

Alphabetical list of breeds and eye conditions for certiﬁcation under the Inherited Eye Disease Status section of the Certiﬁcate of Examination (ie those speciﬁed in

Schedule A of the current Procedure Notes and for which “Clinically Unaected” or “ Clinically Aected” boxes should be ticked):

Examples of other conditions observed as part of examination under the Eye Scheme

● Alaskan Malamute – HC

● Australian Cattle Dog – PRA

● Australian Shepherd – HC

● Basset Hound – G, POAG

● Bedlington Terrier – TRD

● Belgian Shepherd Dog (all varieties) – HC

● Bichon Frise – HC

● Border Collie – CEA, RPED, PLL

● Boston Terrier – HC (two forms)

● Briard – RPED

● Bull Terrier (Miniature) – PLL

● Cavalier King Charles Spaniel – MRD, HC

● Collie (Rough) – CEA, PRA, RPED

● Collie (Smooth) – CEA, RPED

● Dachshund (Miniature Long–Haired) – PRA

● Dandie Dinmont Terrier – G

● Dobermann – PHPV

● Finnish Lapphund – PRA

● Fox Terrier (Smooth) – PLL

● Fox Terrier (Wire) – PLL

● German Shepherd Dog – HC

● Giant Schnauzer – HC

● Glen of Imaal Terrier – PRA

● Gordon Setter – PRA

● Hungarian Puli – MRD

● Irish Red and White Setter – HC

● Irish Setter – PRA

● Irish Wolfhound – PRA

● Japanese Shiba Inu – G

● Lancashire Heeler – CEA, PLL

● Large Munsterlander – HC

● Leonberger – G, HC

● Lhasa Apso – PRA

● Miniature Schnauzer – CHC, PRA, HC

● Norwegian Buhund – HC

● Norwegian Elkhound – PRA

● Old English Sheepdog – HC

● Parson Russell Terrier – PLL

● Petit Basset Grion Vendeen – POAG

● Poodle (Miniature) – PRA

● Poodle (Standard) – HC

● Poodle (Toy) – PRA

● Retriever (Chesapeake Bay) – PRA, HC

● Retriever (Flat Coated) – G

● Retriever (Golden) – MRD, PRA, RPED, HC

● Retriever (Labrador) – MRD, TRD, PRA, RPED, HC

● Retriever (Nova Scotia Duck Tolling) – PRA

● Rottweiler – MRD

● Sealyham Terrier – TRD, PLL

● Shar Pei – POAG

● Shetland Sheepdog – CEA, RPED

● Siberian Husky – G, HC

● Spaniel (American Cocker) – MRD, G, PRA, HC,

● Spaniel (Cocker) – G, PRA, RPED

● Spaniel (English Springer) – MRD, G, PRA, RPED,

● Spaniel (Welsh Springer) – G, HC

● Spanish water Dog – G

● Staordshire Bull Terrier – PHPV, HC

● Swedish Vallhund – PRA

● Tibetan Spaniel – PRA

● Tibetan Terrier – PRA, PLL

● Welsh Corgi (Cardigan) – PRA, RPED

Inherited eye disease status (NB: For a

number of breeds a DNA test is available

for certain eye conditions – please refer to

current list)

CEA = Collie Eye Anomaly

CHC = Congenital Hereditary Cataract

G = Goniodysgenesis/Primary

Glaucoma

HC = Hereditary Cataract

MRD = Multifocal Retinal Dysplasia

PLL = Primary Lens Luxation

PHPV = Persistent Hyperplastic Primary

Vitreous

POAG = Primary Open Angle Glaucoma

PRA = Progressive Retinal Atrophy

RPED = Retinal Pigment Epithelial

Dystrophy (formerly Central

Progressive Retinal Atrophy

= CPRA)

TRD = Total Retinal Dysplasia

92 93

90: Corneal foreign body (thorn). 91: Briard – nevus identified at examination

under the Eye Scheme and then followed over several years. 92: Briard –

nevus some two years later. 93: Focal granuloma (ocular larva migrans).

94:Border Collie – inactive focal chorioretinopathy lesions (probably ocular

larva migrans originally). 95: Systemic hypertensive disease associated with

hyperadrenocorticism.

16 Hereditary eye disease in dogs

Summary

● The BVA/KC/ISDS Eye Scheme oers a means of identifying the

presence or absence of inherited eye disease in a variety of

breeds of dog. There is little doubt that conscientious breeders

of all types of dog, both purebred and crossbred, wish to use

sound stock with known freedom from inherited eye disease

and breed-related ocular disorders as part of their breeding

programme. However, in the context of a comprehensive

breeding programme, it is important to recognise that

inherited problems without any impact on the dog’s quality

of life may well rank below maintaining genetic diversity and

ensuring that breeding pairs are of good temperament and ﬁt

for function, an aspect of particular importance in working

dogs. Understanding the welfare implications of inherited

disease and breed-related ocular disorders is crucial and those

conditions that may be a cause of pain or blindness, require

surgical correction, or lifelong medical therapy should be

regarded as priorities for elimination, as they have substantial

eects on the individual’s quality of life. All veterinary surgeons

involved in clinical practice can help to achieve this ideal by:

● Checking puppies’ eyes when they are seen for the ﬁrst time;

● Informing all pet owners, not just breeders, about the Eye

Scheme; and

● Ensuring that owners recognise the need for eye

examination in any dog which is to be used for breeding and

are aware of the importance of annual examination for dogs

used regularly for breeding.

● In addition, older dogs (those over eight years of age)

should be examined, in order to ascertain the dog’s status in

relation to possible later onset inherited ocular conditions,

any changes that may have occurred with pre-existing

inherited ocular conditions and as a way of assessing ocular

and general health.

Up to date information on the Eye Scheme, which includes

the conditions certiﬁed in individual breeds and those under

investigation (see tables) can be obtained from the BVA website.

Litter screening checklist BVA/KC/ISDS Eye Scheme synopsis sheet 2018

Alphabetical list of breeds and congenital inherited ocular diseases (those ophthalmoscopically identiﬁable during the neonatal stage) for those speciﬁed in Schedule A

of the current Procedure Notes:

● Bedlington Terrier – TRD

● Border Collie – CEA

● Cavalier King Charles Spaniel – MRD

● Collie (Rough) – CEA

● Collie (Smooth) – CEA

● Dobermann – PHPV

● Hungarian Puli – MRD

● Lancashire Heeler – CEA

● Miniature Schnauzer – CHC

● Retriever (Golden) – MRD

● Retriever (Labrador) – TRD, MRD

● Rottweiler – MRD

● Sealyham Terrier – TRD

● Shetland Sheepdog – CEA

● Spaniel (American Cocker) – MRD

● Spaniel (English Springer) – MRD

● Staordshire Bull Terrier – PHPV

Congenital inherited ocular diseases

CEA = Collie Eye Anomaly

CHC = Congenital Hereditary Cataract

PHPV = Persistent Hyperplastic Primary

Vitreous

TRD = Total Retinal Dysplasia

MRD = Multifocal Retinal Dysplasia

● Akita – PRA

● Australian Shepherd – C

● Beagle – MRD

● Bloodhound – MOD

● Border Collie – HC (early developing), G

● Border Terrier – HC (late onset)

● Bullmasti – PPM

● Cairn Terrier – APD

● Cavalier King Charles Spaniel – MOD

● Collie (Rough) – MOD, MRD

● Dachshund (Miniature Long–Haired) – ONH

● Dachshund (Miniature Smooth–Haired) – PRA

● Dachshund (Miniature Wire–Haired) – PPM

● Dandie Dinmont Terrier – G

● Dobermann – MOD

● Finnish Lapphund – MRD, PHPV, HC, PPM

● French Bulldog – HC (early developing)

● German Shepherd Dog – MRD

● German Spitz – MRD

● Giant Schnauzer – MRD

● Great Dane – G

● Greenland Dog – HC (early developing)

● Grion Bruxellois – HC (early developing)

● Hungarian Vizsla – G

● Irish Setter – PRA (late onset)

● Lancashire Heeler – HC (early developing), PPM

● Norwegian Elkhound – MRD

● Old English Sheepdog – MOD, CHC

● Papillon – PRA

● Petit Basset Grion Vendeen – PPM

● Polish Lowland Sheepdog – RPED

● Poodle (Miniature) – ONH

● Poodle (Standard) – MOD

● Poodle (Toy) – ONH

● Retriever (Flat Coated) – PRA

● Retriever (Golden) – MOD, CHC, G

● Retriever (Labrador) – APD

● Rottweiler – MOD, PPM

● Siberian Husky – PPM

● Spaniel (Cocker) – MOD, PPM

● Spaniel (Field) – HC (early developing), MRD

● Spaniel (Sussex) – MRD

● Staordshire Bull Terrier – HC

(variable age of onset)

● Tibetan Terrier – HC (early developing)

● Welsh Terrier – G

● West Highland White Terrier – MOD, CHC, PPM

● Yorkshire Terrier – HC (late onset), PRA

APD = Abnormal Pigment Deposition

C = Coloboma

CEA = Collie Eye Anomaly

CHC = Congenital Hereditary Cataract

G = Goniodysgenesis/Primary

Glaucoma

HC = Hereditary Cataract

MOD = Multi-ocular defects

MRD = Multifocal Retinal Dysplasia

ONH = Optic Nerve Hypoplasia

PHPV = Persistent Hyperplastic Primary

Vitreous

PLL = Primary Lens Luxation

PPM = Persistent Pupillary Membrane

PRA = Progressive Retinal Atrophy

RPED = Retinal Pigment Epithelial

Dystrophy (formerly Central

Progressive Retinal Atrophy

(CPRA)

BVA/KC/ISDS Eye Scheme Schedule B 2018

Conditions under investigation (i.e those that are not yet included in Schedule A of the Procedure notes, but for which information is being actively sought by

examination of the breeds for the conditions speciﬁed). These conditions should be commented upon only in the middle section of the eye certiﬁcate.

Hereditary eye disease in dogs 17

PART II

DNA testing for inherited eye diseases

By Cathryn Mellersh

Most of the inherited eye diseases for which DNA tests are

currently available are ‘simple’ or single gene diseases. This means

that the disease is a result of a single mutation; no other genes or

environmental factors are involved. For these diseases the results

of DNA tests are easy to interpret and an individual dog’s risk of

developing the disease can be estimated with virtual certainty

from the DNA test results. Most simple inherited eye diseases

have a recessive mode of inheritance. Every dog has two copies

of each gene, one inherited from the dam and one from the sire,

so any individual dog has one of three possible genotypes with

regard to each single gene disorder:

● normal or clear, with two normal copies of the relevant gene;

● carrier, with one normal copy of the relevant gene

and

one recessive, mutant copy;

● genetically aected, with two copies of the recessive

mutation.

Recessive mutations cause a loss of function of a gene. Carriers

that have inherited a single copy of the normal gene from one

parent and a single copy of a mutant gene from the other parent

usually have sucient normal protein encoded by the normal

gene to have healthy functioning eyes. It is only when a dog

inherits a faulty gene from both parents that it becomes clinically

aected. Consequently, if a mutation is recessive then dogs with

zero (normal/clear) or one copy of the mutation (carriers) will

remain clinically free of the disease, although carriers will pass

the mutation onto around half of their ospring. Dogs with two

copies of the mutation (genetically aected) will almost certainly

develop the disease during their lifetime. The age at which

dogs typically develop clinical signs depends on the disease so

although a dog with two copies of a particular disease mutation

is genetically aected from birth it may not be become clinically

aected until later in life. It follows, therefore, that a genetically

aected dog may be clinically unaected at the time it has an

eye examination, especially if it is very young at the time. Some

carriers can be identiﬁed by pedigree analysis, once an aected

dog has been diagnosed; for example, the clinically normal parents

of an aected puppy are both carriers, as are all the clinically

normal ospring of clinically aected animals.

The past 10 years have seen remarkable progress in the ﬁeld

of canine molecular genetics. Since the publication of the

canine genome sequence in 2004 the genetic tools available to

researchers have become increasingly sophisticated and the ease

with which mutations responsible for inherited eye diseases in

dogs can be identiﬁed has increased accordingly. Table 1 contains

details of the genes that have been associated with inherited

eye diseases in dogs to date. Once a particular mutation has

been identiﬁed, it is usually a relatively simple task to develop

a DNA test that can be used to determine an individual dog’s

genotype with respect to the disease. Worldwide there are now

many facilities oering canine DNA tests. The process of DNA

testing involves the submission of a sample of a dog’s DNA to an

appropriate testing laboratory. The DNA can usually be submitted

as a simple cheek swab that an owner can take themselves,

although some tests/laboratories may require a blood sample. The

testing laboratory analyses the DNA for the presence or absence

of the relevant mutation and will report back, usually within a few

weeks, with the result (the dog’s ‘genotype’).

DNA testing and eye examinations should be regarded as

complementary; one does not replace the need for the other.

During an eye examination the ophthalmologist examines the

eye and adnexa, so will detect any ocular abnormality a dog may

have. DNA tests, on the other hand, usually only detect a single,

speciﬁc mutation, and cannot be used to detect all abnormalities

a dog may be suering from, or detect newly emerging

conditions within a breed. For example, Golden Retrievers can

suer from three dierent forms of progressive retinal atrophy

(PRA), known as i) progressive rod cone dystrophy (prcd), ii)

Golden Retriever PRA 1 (GR_PRA1) and iii) Golden Retriever

PRA2 (GR_PRA2). These diseases are caused by mutations in

three dierent genes so a DNA test for prcd, for example, does

not provide any information about a dog’s risk of developing

GR_PRA1 or GR_PRA2. Routine eye examination could detect

the clinical signs of PRA, providing the dog was old enough to be

showing clinical signs, but would not determine which form a dog

was suering from. DNA tests are able to detect carriers, which

an eye examination cannot do and a DNA test can be used from

birth to determine whether a dog is genetically aected, before

it may have developed clinical signs of disease.

Table 1

Genes associated with inherited eye disease in dogs

Disease Locus or

Abbreviation

Gene Breed

(A) denotes that the breed is examined under Schedule A

Cone-rod dystrophy CRD3

ADAM9

Glen of Imaal Terrier (A)

Primary open angle glaucoma POAG

ADAMTS17

Basset Hound (A), Beagle, Petit Basset Grion Vendeen (A), Shar Pei (A)

Primary lens luxation PLL

ADAMTS17

Australian Cattle Dog, Chinese Crested Dog, Jagdterrier, Lancashire Heeler

(A), the Miniature Bull Terrier (A), Jack Russell Terrier, Parson Russell Terrier

(A), Patterdale Terrier, Rat Terrier, Sealyham Terrier (A), Tenterﬁeld Tterrier,

Tibetan Terrier (A), Fox Terrier (A), Volpino Italiano, Welsh Terrier, Wire-

haired Fox Terrier (A), Yorkshire Terrier

18 Hereditary eye disease in dogs

Disease Locus or

Abbreviation

Gene Breed

(A) denotes that the breed is examined under Schedule A

Rod cone degeneration RCD4

C2orf71

Gordon Setter (A), Irish Setter (A), Tibetan Terrier (A)

Generalised progressive retinal atrophy gPRA

CCDC66

Schappendoes

Macular corneal dystrophy MCD

CHST6

Labrador Retriever

Progressive retinal atrophy PRA

CNGB1

Papillon

Cone degeneration CD

CNGB3

Alaskan Malamute

Cone degeneration CD

CNGB3

German Shorthaired Pointer

Dwarﬁsm with retinal dysplasia

(oculoskeletal dysplasia)

DRD2 (OSD2)

COL9A2

Samoyed

Dwarﬁsm with retinal dysplasia

(oculoskeletal dysplasia)

DRD1 (OSD1)

COL9A3

Labrador Retriever

Hereditary cataract HC, EHC

HSF4

Staordshire Bull Terrier (A), Boston Terrier (A), French Bulldog

Hereditary cataract HC

HSF4

Australian Shepherd (A)

Collie eye anomaly CEA

NHEJ1

Rough Collie (A), Smooth Collie (A), Border Collie (A), Shetland Sheepdog (A),

Lancashire Heeler (A)

Cone-rod dystrophy

NPHP4

Standard Wire-Haired Dachshund

Photoreceptor dysplasia PD PDC Miniature Schnauzer (A)

Rod cone dysplasia RCD1

PDE6B

Irish Setter (A)

Rod cone dysplasia RCD1

PDE6B

Sloughi

Rod cone dysplasia RCD3

PDE6A

Cardigan Welsh Corgi (A)

Progressive rod-cone degeneration PRCD PRCD Multiple breeds, including Australian Cattle Dog (A), American Cocker

Spaniel (A), Cocker Spaniel (A), English Springer Spaniel (A), Rough Collie (A),

Chesapeake Bay Retriever (A), Miniature Poodle (A), Toy Poodle (A), Golden

Retriever (A), Labrador Retriever (A)

Rod cone dysplasia RCD2

RD3

Rough Collie (A), Smooth Collie (A)

Autosomal dominant progressive

retinal atrophy

ADPRA

RHO

Bull Masti, English Masti

Congenital stationary night blindness CSNB

RPE65

Briard (A)

X-linked progressive retinal atrophy XLPRA2

RPGR

Mixed breed dogs

X-linked progressive retinal atrophy XLPRA1

RPGR

Siberian Husky, Samoyed

Cone-rod dystrophy CORD1 (CRD4)

RPGRIP

Miniature longhaired Dachshund (A)

Progressive retinal atrophy GR_PRA1 SLC4A3 Golden Retriever (A)

Early retinal degeneration ERD

STK38L

Norwegian Elkhound (A)

Progressive retinal atrophy GR_PRA2

TTC8

Golden Retriever (A)

Canine multifocal retinopathy CMR1

VMD2/BEST1

Great Pyrenees, English Masti, and Bullmasti dogs

Canine multifocal retinopathy CMR2

VMD2/BEST1

Coton de Tulear

Canine multifocal retinopathy CMR3

VMD2/BEST1

Lapponian Herder

Progressive retinal atrophy PRA

MERTK

Swedish Vallhund

Dogs that are to be used for breeding should have all DNA tests

that are relevant to their breed (unless they are hereditarily

clear, see Recording Results). They should also be examined

and certiﬁed under the Eye Scheme, prior to breeding and

subsequently, as outlined in the introduction to this pamphlet,

including a ﬁnal examination when the dog is over eight years

of age. In those breeds in which inherited congenital/neonatal

eye diseases are known or suspected it may also be sensible

to carry out litter screening of puppies as outlined earlier.

Dogs that are carriers of disease mutations can be bred

from safely. Provided all carriers are paired with DNA-tested,

clear mates only clear and carrier puppies will be born; no

clinically aected dogs will be produced and breeders can

select a clear dog to breed on from the resulting litters.

Table 2 details the outcomes of mating dogs with dierent

genotypes (with respect to a recessive mutation) and

whether they can result in clinically aected ospring.

Hereditary eye disease in dogs 19

Eye examination results for all Schedule A conditions are

recorded in the Kennel Club’s Registration Database, with

the information being added to the relevant ﬁeld of the

dog’s record. A similar process is in place to deal with the

results of DNA testing for inherited eye disease. Breed clubs

that have one or more DNA test are encouraged to establish

an Ocial DNA Testing Scheme for the condition(s),

whereby the DNA test results for individual dogs are sent

directly to the Kennel Club and are added to the dog’s

registration data. For those puppies resulting from two DNA

“clear” tested dogs, an automatic status of “hereditarily

clear” is assigned and published as described below.

For breeds examined under the Scheme that are not

included in Schedule A, where the dog is registered with the

Kennel Club, a note will be added to the dog’s record on the

Kennel Club’s database conﬁrming that an examination has

taken place and the date of the examination.

The addition of health screening results to the Kennel Club

Registration Database triggers dissemination via a number of

dierent routes. The result(s) will appear:

● On any new registration certiﬁcate issued for the dog;

● On the registration certiﬁcates of any of the dog’s

future progeny;

● In the Kennel Club Breed Records Supplement (BRS), a

quarterly publication.

The Kennel Club also maintains lists of DNA test results for

all Ocial DNA Testing Schemes on the health pages of its

website (www.thekennelclub.org.uk).

Table 2

Recessive inheritance — expected outcomes of breeding combinations

Combination of Dogs Outcome Possibility of clinically

aected ospring?

Clear X Clear All puppies will be clear No

Clear X Carrier Approx. 50% of puppies will be clear

Approx. 50% of puppies will be carriers

Clear x Aected All puppies will be carriers No

Carrier x Carrier Approx. 25% of puppies will be clear

Approx. 25% of puppies will be aected

Approx. 50% of puppies will be carriers

Yes

Carrier x Aected Approx. 50% of puppies will be aected

Approx. 50% of puppies will be carriers

Yes

Aected x Aected All puppies will be aected Yes

Recording results

Eye Examination Certificate

Any appeal against the results of an eye

examination must be lodged in writing

with the British Veterinary Association

(BVA) within 30 days of the examination.

BVA’s address is shown overleaf.

The owner may then take the dog,

together with the certificate issued by

the first panellist, for examination by

the Chief Panellist, a panellist from the

Eye Panel Working Party, or another

panellist. The second panellist will

charge the normal fee. If the second

panellist agrees with the first panellist

the appeal will be deemed to have failed

and the second panellist will inform BVA

accordingly. In such an event no further

appeal is possible.

The decision of the Chief Panellist at

second examination is final, as also is

the decision of a panellist from the

Eye Panel Working Party acting in

consultation with the Chief Panellist

and provided that the Chief Panellist

agrees with the findings reported. In

all other circumstances, if the second

panellist disagrees with the first panellist

the dog shall be referred to the Chief

Panellist for further examination

without additional fee to the owner. The

decision of the Chief Panellist will be

final and the Chief Panellist will advise

BVA of the result accordingly. Owners

may choose to see the Chief Panellist as

the second panellist once an appeal has

been lodged with BVA. If so, the normal

fee will be charged.

The final result of any appeal must be

received by BVA within 90 days of

examination, otherwise the first result

may be sent to the Kennel Club and/or

the International Sheep Dog Society for

publication.

Litter Screening Eye Examination

Certificate

Any appeal against the results of litter

screening must be notified to BVA and/

or Chief Panellist as soon as possible so

that suitable arrangements may be made

for the whole litter to be re-examined

before the puppies reach 12 weeks of age.

No appeal will be granted unless all the

puppies are re-examined on the same

occasion and the puppies are less than

12 weeks of age.

Appeals procedure

BVA

ISDS CHS Eye Scheme

England

Professor P G C Bedford BVetMed PhD

DVOphthal DipECVO FHEA FRCVS

Village Vets Cayton

601 Hatfield Road, Smallford

Hertfordshire AL4 0HL

Telephone 01727 852667

B T Blacklock BVSc(Hons) DipECVO MRCVS

Dick White Referrals

Station Farm, London Road, Six Mile Bottom

Cambridgeshire CB8 0UH

Telephone 01638 572012

N J Burden BVSc CertVOphthal MRCVS

The Hale Veterinary Group

19 Langley Road, Chippenham

Wiltshire SN15 1BS

Telephone 01249 653561

J Carter BVetMed DVOphthal DipECVO MRCVS

South Devon Referrals

The Old Cider Works, Abbotskerswell

Newton Abbot

Devon TQ12 5GH

Telephone 01626 367972

Mrs B Cottrell MA VetMB CertVOphthal MRCVS

109 North End

Meldreth, Royston

Hertfordshire SG8 6NX

Telephone 01763 261674

Professor S M Crispin MA VetMB BSc PhD

DVA DVOphthal DipECVO FRCVS

Cold Harbour Farm

Underbarrow, Kendal

Cumbria LA8 8HD

Telephone 020 7908 6380

Telephone (home) 01539 568637

S R Ellis BVSc CertVOphthal MRCVS

Riverbank Veterinary Centre

16/22 Watery Lane, Preston

Lancashire PR2 2NN

Telephone 01772 726745

Miss H J Featherstone BVetMed

DVOphthal DipECVO MRCVS

The Ralph Veterinary Referral Centre

Fourth Avenue, Globe Business Park

Marlow SL7 1YG

Telephone 0800 689 4298

K J Fraser BVM&S CertVOphthal MRCVS

The Anima Veterinary Clinic

Church Road, Iver Heath

Buckinghamshire SL0 0RA

Telephone 01753 911300

G V Fricker BVSc CertVOpthal Dip ECVO MRCVS

Davies Veterinary Specialists

Manor Farm Business Park

Higham Gobion

Hertfordshire SG5 3HR

Telephone 01582 883950

J V Goodyear BVMS CertVOphthal MRCVS

29 Park Road

Barton-under-Needwood

Staffordshire DE13 8DW

Telephone 01283 713359

Dr D J Gould BVM&S BSc (Hons) PhD

DVOphthal DipECVO FRCVS

Davies Veterinary Specialists

Manor Farm Business Park, Higham Gobion

Hertfordshire SG5 3HR

Telephone 01582 883950

R Grundon BSc VetMB CertVR CertVOphthal

MANZCVS (Surgery) FANZCVS (Ophthal) FRCVS

Eye Veterinary Clinic

Marlbrook, Leominster

Herefordshire HR6 0PH

Telephone 01568 616616

D Habin BVMS DVOphthal MRCVS

Paragon Veterinary Referrals

1 Red Hall Crescent

Paragon Business Village, Wakefield

West Yorkshire, WF1 2DF

Telephone 01924 908333

C Hartley BVSc CertVOphthal DipECVO MRCVS

Small Animal Hospital

Langford Vets, Langford

Bristol BS40 5DU

Telephone 0117 394 0513

Miss C L Heinrich DVOphthal DipECVO MRCVS

Eye Veterinary Clinic

Marlbrook, Leominster

Herefordshire HR6 0PH

Telephone 01568 616616

C Kafarnik Dr MedVet DipECVO MRCVS

The Animal Health Trust

Lanwades Park, Kentford, Newmarket

Suffolk CB8 7UU

Telephone 01638 552700

M P C Lawton BVetMed CertVOphthal

CertLAS CBiol MIBiol DZooMed FRCVS

12 Fitzilian Avenue

Harold Wood, Romford

Essex RM3 0QS

Telephone 01708 384444

R Linn-Pearl BVsc DipECVO MRCVS

Eye Veterinary Clinic

Marlbrook, Leominster, Herefordshire, HR6 0PH

Telephone 01568 616616

R C Lowe BVSc DVOphthal MRCVS

Optivet Referrals Ltd

3 Downley Road, Havant

Hampshire PO9 2NJ

Telephone 01243 888091

Miss S P Manning BVSc CertVOphthal

DVOphthal MRCVS

Pride Veterinary Centre

Riverside Road, Pride Park

Derby DE24 8HX

Telephone 01332 678333

P McPherson BVMS CertVOphthal MRCVS

Minster Veterinary Centre

Orchard Lodge, Newark Road, Southwell

Nottinghamshire NG25 0ES

Telephone 01636 812133

I K Mason MA VetMB CertVOphthal MRCVS

Seadown Veterinary Hospital

Frost Lane, Hythe

Hampshire SO45 3NG

Telephone 023 8084 2237/01590 679921

J R B Mould BA BVSc DVOphthal MRCVS

Eye Veterinary Clinic, Marlbrook, Leominster

Herefordshire HR6 0PH

Telephone 01568 616616

Mrs L J Newman BVM&S CertVOphthal MRCVS

West Midlands Referrals

Errisbeg House, Barton Turn

Barton Under Needwood, Burton-on-Trent

Staffordshire DE13 8EB

Telephone 01543 414248

J Oliver BVSc CertVOphthal DipECVO MRCVS

Dick White Referrals

Station Farm, London Road, Six Mile Bottom

Cambridgeshire CB8 OUH

Telephone 01638 572012

R Pontefract BVMS CertVOphthal MRCVS

43 Empingham Road, Stamford

Lincolnshire PE9 2RJ

Telephone 01780 764333

M Rhodes BVM&S CertVOphthal DipECVO MRCVS

Website: www.focusreferrals.co.uk

Email: info@focusreferrals.co.uk

Ms K Smith BVetMed CertVOphthal

DipECVO MRCVS

Davies Veterinary Specialists

Manor Farm Business Park, Higham Gobion

Hertfordshire SG5 3HR

Telephone 01582 883950

Ms S Turner MA VetMB DVOphthal MRCVS

The Mandeville Veterinary Hospital

15 Mandeville Road

Northolt UB5 5HD

Telephone 020 8845 5677

C G B WARREN BA VetMB CertVOphthal MRCVS

Westmoor Veterinary Centre

Brook Lane, Tavistock, Devon PL19 9BA

Telephone 01822 612561

J Yellowley BVSc CertVOphthal MRCVS

St. Clair Veterinary Care

87 Bridge Street, Blyth

Northumberland NE24 3AE

Telephone 01670 457271

Panel of Examiners as at July 2019

Chief Panellist: Professor Peter Bedford

Canine Health Schemes

7 Mansﬁeld Street, London W1G 9NQ

Tel: 020 7908 6380 Fax: 020 7908 6389

Email: chs

bva.co.uk

www.bva.co.uk/chs

International Sheep Dog Society

Clifton House, 4a Goldington Road

Bedford MK40 3NF

Tel: 01234 352672 Fax: 01234 348214

Email: oce@isds.org.uk

The Kennel Club

10 Clarges Street, London W1J 8AB

Telephone 0844 4633 980

hbs@thekennelclub.org.uk

www.thekennelclub.org.uk/doghealth

Scotland

M G Davidson BVM&S CertVOphthal MRCVS

19 Hillhouse Road

Edinburgh EH4 3QP

Telephone 0131 332 0458

A T Mckenzie BVMS CertVOphthal MRCVS

MBM Veterinary Group

21 Hill Street, Kilmarnock

Ayrshire KA3 1HF

Telephone 01563 522701

A E Wall BVM&S CertVOphthal MSc MRCVS

Scottish Vet Referrals

14a Inverness Campus

Inverness IV2 5NA

Telephone 01463 21882

Wales

H Cormie BVMS CertVOphthal MRCVS

Cormie Referrals

Ty Pen-y-Coed, Glangrwyney, Crickhowell

Powys NP8 1EW

Telephone 07813 197222

Mrs G E Hubbard BVetMed CertVOphthal MRCVS

Cibyn Veterinary Clinic

Llanberis Road, Caernarfon

Gwynedd LL55 2BD

Telephone 01286 673026

Northern Ireland

I Millar BVMS CertVOphthal MRCVS

Earlswood Veterinary Hospital

193 Belmont Road

Belfast BT4 2AE

Telephone 028 9047 1361

Ireland

Dr T D Grimes BVetMed PhD DVR

DVOphthal DipECVO MRCVS

Department of S A Clinical Studies

Faculty of Veterinary Medicine

University College Dublin

Belfield

Dublin 4, Ireland

Telephone: + 353 1 716 6022

N Mitchell MVB DVOphthal MRCVS

Eye Vet, Crescent Veterinary Clinic

Dooradoyle Road

Limerick

Ireland

Telephone: + 353 61 301 841