Exotics Flashcards
What adaptations does the rabbit eye have?
Lateral position + large ocular surface - prey, wide field of view
(prone to traumatic damage/evaporative loss)
Haderian gland (accessory lacrimal gland) - keep large cornea supplied with tears
Lens = near spherical to focus light from wide cornea (focal distance only 8mm), to compensate for spherical aberration the lens has concentric layers of different refractive index (can make it appear that nuclear sclerosis is occurring even in young rabbits)
Merangiotic retina - horizontal band of blood vessels and myelinated nerve fibres but otherwise no retinal blood vessels.
Describe the retina of the rabbit.
Merangiotic (dogs/cats = holangiotic)
Horizontal blood vessels and myelinated nerve fibres but no retinal blood vessels
Band of retina containing high density of photoreceptors ventral to vascularised strip - allows to see in higher resolution along the horizon as prey species
Retina mostly rod based - night vision (nocturnal/crepuscular animal)
Cone receptors in ventral retina (looking dorsally) most responsive to blue light, dorsal fundus (looking ventrally) most responsive to green light - attuned for detection of predators.
Why is dacryocystitis so common in the rabbit?
Single ventral nasolacrimal punctum
Nasolacrimal duct courses across roots of both molar and incisor teeth
Maxillofacial bone abnormality, molar tooth root abscess or overgrown incisor teeth can lead to nasolacrimal duct pathology and inflammation
How can we diagnose dacryocystitis in the rabbit?
Usually suspect based on clinical signs - copious white discharge from NL punctum, matting of fur/dermatitis around eye, epiphora.
Dacryocystorhinography can be valuable to evaluate degree of nasolacrimal duct dilation or rupture
What type of bacteria are usually isolated from rabbit dacryocystitis cases?
Pastuerella (gram -ve) and Staphylococcus (gram +ve)
Broad spectrum AB cover
Often commensal within rabbit respiratory tract and nasal mucosa
Only when pathology occurs that become pathogenic.
How is dacryocystitis treated in the rabbit?
Topical agents unlikely to treat infection deep in NL duct
Nasolacrimal duct flushing regularly until condition resolved to remove discharge (cannulation with 23G NL cannula) - sterile water/saline
Treat underlying disease - usually associated with dental disease/husbandry.
Another therapeutic regime = systemic enrofloxacin/azithromycin, useful where persistent flushing unsuccessful but does not cure - merely control and relapse common.
What causes are there for conjunctivitis in the rabbit?
Conjunctival inflammation - dusty hay/foreign body
Alongside dacryocystitis
Infectious causes - Pasteurella or other gram -ve organisms, myxomatosis (with fulminant blepharitis)
Which ocular signs are seen in rabbits with myxomatosis?
Conjunctivitis with fulminant blepharitis and copious white discharge
DNA pox virus - hijacks genes from host and mutates them to reduce vital immune functions - allows range of commensals to become pathogenic.
Vaccinated individuals - myxomatous tumour growths (sometimes around eyes/eyelids)
What causes are there of blepharitis in rabbits?
Myxomatosis
Allergic reaction to Staphylococci (lid swelling can then lead to entropion which is rarely seen in the rabbit) - warm compresses can help resolve
Ulcerative blepharitis associated with Treponema canaliculi (rabbit syphilis) - diagnosis skin scrape or histopath
Treatment with 50,000 i.u/kg of depot penicillin by s/c injection for 3-4 weeks
What is conjunctival overgrowth/centripetalisation/epicorneal membrane/pseudopterigium?
Condition only seen in rabbits
Annulus of conjunctiva growing over cornea from the limbus
Not common 1 in 1000
Narrow band of tissue or sizeable ring with only a small aperture centrally.
Resection of tissue only leads to regrowth
Can suture then band of tissue back onto sclera to prevent excessive growth occluding vision.
What is the difference between the orbit of the cat/dog and orbit of the rabbit.
Rabbit orbit = contains large venous sinus - important for performing enucleations.
List the common causes of exophthalmos in the rabbit
Most common = retrobulbar abscess (tooth root) - can be difficult to manage. ?Endoscopic curettage after dental extraction
Neoplasia
Parasitic cysts
Intermittent exophthalmos = thymoma (most often seen when animal handled). Mass wraps itself around jugular veins preventing adequate return of venous flow from head region. Engorges venous sinus in retrobulbar space and causes painless exophthalmos while blood pressure raised.
Cervical mass preventing venous return is difficult to remove in many cases.
What are the orbital glands in the rabbit?
How should prolapse of any of these glands be managed?
Nictitans
Haderian
Accessory
Basal
Treatment of any orbital gland prolapse - replace using Morgan pocket technique
Why is corneal ulceration common in the rabbit? How quickly should a simple erosion heal and how should they be managed?
Large lateral and prominent ocular surface
Prone to traumatic corneal ulceration - hay etc
Superficial corneal ulcers/erosions should heal in under a week
Initial management = lubricant (carbomer based product) + prophylactic AB cover
Describe SCCED/dystophic type ulcers in the rabbit. How are they treated?
Adhesion between basement membrane and epithelial cells can be poor such as in SCCED’s in dogs.
Edge of ulcer = ring of devitalised epithelium around ulcer preventing healthy cells migrating and adhering to ulcer bed
Treated - topical anaesthesia applied, cotton bud debridement
Sometimes will combine with grid keratectomy to breach abnormal basement membrane.
Carbomer based lubricant +/- contact lens
(Third eyelid flaps not really done in rabbits as cannot be readily extended >1/2 way across cornea + retracted by powerful muscular extension of levator palpebrarum superioris muscle - sutures prone to pulling through TEL conjunctiva.
What type of ocular changes can be associated with Encephalitazoan caniculi?
How can it be diagnosed?
Cataracts
E.canaliculi = obligate intracellular microsporidian
Infects rabbits through ingestion of contaminated urine and can also cause renal/neurological symptoms (head tilt)
Involvement with cataract formation = parasite transmitted transplacentally and enter rabbit whilst still in utero.
Migrate to developing lens = lie dormant for many months before moving through lens causing cataract.
Eventually can erupt through anterior lens capsule releasing lens material into anterior chamber - phacoclastic uveitis
Signs of phacoclastic uveitis = miosis, iridial redness and swelling, hypopyon, white/pink mass protruding into anterior chamber.
E.canaliculi titre always helpful in rabbit presenting with signs of uveitis as above.
What is the treatment for E.canaliculi?
Phacoclastic uveitis = topical steroid drop (prednisolone acetate, Pred Forte) or dexamethasone (Maxidex)
+ fenbendazole orally to treat parasite
Other option - consider phacoemulsification of lens and associated parasites with pre-emptive tx of topical steroids
List the common causes of uveitis in the rabbit.
What diagnostic option is there?
What treatment options are there?
E.canaliculi - miosis, hypopyon, pink/white (sometimes some neovascularisation)
Pastuerella/staphylococcal infection - yellow-cream abscess filling large proportion of eye
Diagnosis = could consider aqueocentesis with 25G needle for bacteriology/cytology sample
Treatment = fenbendazole (E.canaliculi), topical antibiosis, atropine, topical steroid drops covers other eventualities.
Which breed of rabbit is genetically predisposed to buphthalmos/glaucoma.
New Zealand White
Increased IOP early on in life leading to buphthalmos
Bu gene also causes prenatal mortality and small litter sizes
Recessive but does appear to affect NZW crosses and giant breeds
List the causes of glaucoma in the rabbit
Genetic - NZW
Secondary to uveitis - hypopyon/purulent material accumulation/phacoclastic uveitis
What is the normal IOP in the rabbit.
How can glaucoma be managed in the rabbit?
Normal IOP 15-20mmHg
Tx - topical carbonic anhydrase inhibitors - dorzolamide TID
Which technique for enucleation should be performed in the rabbit and why?
Transconjunctival approach - allow removal of globe but not exenterate the orbit and its contents.
Conjunctiva incised
EOM transected at their insertions
Optic nerve then transected
TEL often retained and incorporated into closure of orbital fascia prior to skin closure so no risk of penetrating orbital venous sinus.
(Transpalpebral = risk of entering orbital venous sinus and significant haemorrhage)
What type of fundus does the guinea pig have?
Paurangiotic (fundoscopy - fundus appears almost devoid of blood vessels, can be mistaken for retinal atrophy)
What type of vision do guinea pigs have?
Hypermetropic (long sighted) refraction
Albinos - predisposed to myopia (short sightedness)
What congenital conditions of the globe can be present in guinea pigs?
Microphthalmos and anophthalmos
Obvious from birth as precocious and born with eyes open
Often associated with mucopurulent discharge which builds up in orbit
Entropion can occur as globe too small for size of orbit
Association between lens and development of globe means often congenital cataracts associated with microphthalmos
Clinical management (possibly topical antibiotic if discharge within orbit, entropion - Hotz-celsus)
How does entropion present in the guinea pig and how may it be managed?
In turning of eyelid
Blepharospasm, epiphora, corneal ulceration
May occur secondary to microphthalmos or defect with tarsal plate of lid
Can be secondary from irritation of conjunctivitis, KCS, trichiasis
Topical anaesthesia to assess if primary or secondary to another cause
Hotz celsus can be performed (often only around 1mm needs to be removed as thin delicate lid)
What types of guinea pig are prone to trichiasis?
Rex and Texel = thick bristly coats, can get ocular abrasion within 1st hours of life
Secondary corneal ulceration/entropion can ensue and further ocular abrasion
Petroluem jelly at birth to keep hairs away from eyes
Lubrication of eye to relieve discomfort
NSAID - keratolac
How can dermoids be managed in the guinea pig?
Similar to dogs - aberrant development of dermal tissue in abnormal place
Superficial keratectomy = curative
Very little tissue to remove as thin cornea (less than 500um)
Magnification essential
List the causes of conjunctivitis in the guinea pig.
Infectious - Chlamydia + Listeria monocytogenes + Salmonella
Allergic - poor hay quality/dusty hay
Foreign bodies - hay awn
Dietary - Vitamin C deficiency - one of the earliest signs
What stages of work up would you consider in guinea pig with conjunctivitis?
Examine for physical factors/foreign bodies
Diet appropriate
?Infectious - topical AB cover treatment trial, sample for bacteriology/PCR
What type of fluid can guinea pigs normally produce for lubricating eye/cleaning face?
Can normally produce milky white ocular secretion - cell free fluid
Differentiate from dacryocystitis - copious white to purulent discharge
Discuss KCS in the guinea pig
Signs of ocular irritation (partial closure of palpebral aperture)
Lack of clear sharp reflection of light from ocular surface
Potentially mucoid discharge
Normal STT 3-12mm/min reported in literature
Phenol red test (given small size of eye) - 16-21 = average
Unclear if same immune mediated destruction of lacrimal gland as in dogs
Topical ciclosporin effective
Replacement tears - carbomer based gel
What is the most common cause of keratitis in the guinea pig?
How do we manage?
Ocular trauma - hay/grass awn
Acute phase - corneal epithelial erosion and sometimes also stromal damage but often little blepharospasm
Later changes = scar with inflammatory cell infiltrate and fibrosis
Tx = removal of any foreign body, topical AB cover (chloramphenicol)
Chronic phase significant scarring - could consider superficial keratectomy (rarely done unless very significant scarring impacting vision)
What is “fatty eye/flesh eye” in guinea pigs?
Fatty eye = deposition of lipid within bulbar conjunctiva - appears as white/pink lesion
Flesh eye = pink/red-pink mass in medial canthus (similar to cherry eye)
Fatty eye - can be managed by reducing calorific dietary input but reduction in size of lesion will take time
How does corneal lipidosis present in guinea pigs?
Circular to oval white area in central/paracentral cornea
Triglyceride/cholesterol crystals
?Dietary fat plays a role
?Genetic - stromal lipid dystrophy
Often no specific treatment - may affect vision being in central axis but often not enough to have significant impact
How does heterotopic bone formation present in guinea pigs?
White lesion at limbus protruding slightly into cornea
Often no other ocular changes - IOP often unaffected
Ascorbic acid/vitamin C promotes calcium deposition when at high concentrations in tissue
Ciliary body secretes vitamin C into the AH potentially to ensure sufficient enough levels in lens to prevent cataract formation. High levels = can lead to calcium build up at limbus causing the heterotrophic bone formation.
Most cases = no treatment as often does not impede vision/lead to discomfort
?Tonometry and IOP monitoring
How can cataracts appear in guinea pigs?
Small nuclear cataracts/posterior subcapsular cortex to full complete mature cataract.
Up to 40% have some degree of lens opacity in one study
GP require dietary input of ascorbic acid (prevent oxidative changes at heart of many cataracts) - low levels Vitamin C may be associated.
Diabetic cataracts also seen in GP
?Phacoemulsification but ?value/ethics
What is the difficulty with applying mydriatics to rodents?
Mydriatics bind to melanin within pigmented irises - less effective in albinos
Rodent eyes contain atropinase which degrades mydriatics making less effective - fundoscopy challenging.
What size lens is appropriate for viewing the rodent fundus?
90 dioptre with slit lamp
28D lens or 2.2 panretinal lens with indirect headpiece
How does the volume of the ocular tear film affect administration of drops in our rodent population ?
Very small volume of tear film and lacrimal lake
Even 1 drop will overflow eye and lead to nasolacrimal overflow
Potential s/e due to systemic absorption
What test may be useful for assessing the tear film of rodents?
Phenol red
STT test strips too large for rodent eye
What is conjunctivitis often associated with in rodents?
Often related to mycoplasmal respiratory disease
Young animals often more severely affected
OR
Environmental irritants - ventilation currents in rodent cages may cause airborne suspensions of fine bedding matter (leading to severe keratoconjunctivitis)
What is sialodacryoadenitis virus infection in rodents?
Coronavirus associated with ocular irritation with conjunctivitis, periocular swelling followed by sneezing and cervical swelling
Usually self limiting - 1-2 weeks but can take longer to clear secondary effects
Present within 45% of rat laboratory colonies in UK
Which gland produces porphyrin pigmented tears in rats - exhibited as red crusting around eyes in cases of ocular irritation or URT infections?
What is the excess production of tears with red deposit called?
Haderian gland
Called chromodacryorrhea - diseases such as mycoplasmosis, sialodacryoadenitis, nutritional deficiencies and other physiological stresses are factors that may cause.
List ocular problems of the globe that may be seen in rodents.
Microphthalmos
Corneal opacificaition/dystrophies - elliptical paracentral opacifications (basophilic material in sub epithelial stroma)
Exposure keratopathy - post GA/surgery most commonly (especially xylazine/ketamine)
Glaucoma - often associated with persistent pupillary membranes causing pupil-block glaucoma
Persistent hyaloid artery (can be associate with vitreal haemorrhage)
Cataracts - often occur spontaneously or secondary to retinal degeneration due to release of metabolic by products
Which retinal disease can be seen in rodents?
Inherited retinal dystrophies/degenerations
Rd gene = albino mice, retinal degeneration and blindness
What ocular condition is often seen in degus associated with diabetes?
High amounts of aldose reductase - secondary cataracts
How can prolapse of the globe in hamsters associated with rough handling be treated?
Temporary tarsorrhaphy but poor prognosis for full eye function subsequently
What are the key features of the avian eye anatomy?
Eyelids - lower more mobile than upper, meibomian glands absent
Lacrimal gland inferior and lateral to globe + Haderian gland acting as secondary lacrimal gland at base of nictitating membrane
Dorsal and ventral lacrimal punta drain secretions into nasal cavity
Nictitating membrane moves across eye - pyrimidalis muscle, posterior sclera, loops through optic nerve in sling via bursalis muscle (quadratus muscle)
Orbit = open and occupied predominately by globe
EOM not particularly well developed (torsional movements 2-5 degrees only)
Close proximity of globe to infraorbital diverticulum of the infraorbital sinus - sinusitis = periorbital swelling, orbital compression, conjunctivitis, exophthalmos or intraocular inflammation.
Owls - tubular posterior segment allowing considerably magnified image to be projected onto retina
Passerines/Psittaciformes - anterior-posteriorly flattened globe = oblate spheroid with hemispherical posterior segment
Cornea = reduced thickness compared to mammals, anterior stroma acellular
Scleral ossicles behind limbus - bony structures, firm origin for muscles which allow accomodation (make enucleations more challenging)
Shallower anterior chamber than mammals (except owls - can see iridocorneal angle without gonioscopy in owls)
Iris = thin, striated muscle (rather than autonomically innervation constrictors/dilator muscles in mammals) - allows conscious control of pupil dilation/constriction, complicates evaluation of PLR
Can be used for communication/sexual attraction/signal sexual dimorphism. Pharmacological dilation of pupil more complicated non depolarising muscle relaxants required rather than parasympatholytic drugs (e.g tropicamide/atropine)
Decussation at optic chiasm ABSENT in birds - integration of sensory information from each visual field occurs in midbrain. Direct/consensual PLRs redundant in birds.
Lens generally soft with annular pad lying under lens capsule in equatorial region allowing considerable attachment between lens and muscles of accommodation (change in focal length)
Accommodation - change in focal length of lens produced in ciliary muscles divided in 2 portions - Crampton’s muscle (anterior) - originates on sclera beneath scleral ossicles and its contraction flattens cornea at peripheral margin - central bulging increasing refractive power.
Posterior = Brucke’s muscle = pulls ciliary body forward, lessening tension applied to annular pad by the tenacular ligament from ciliary body.
How is the avian fundus adapted?
Can see in 3 colours (red, green, blue) + UV light
Exceptional vision
Fundus = no blood vessels or choriocapillaris instead have pecten
Pecten = protrudes into posterior vitreous and supplies oxygen and nutrients. Continual torsional movements of globe cause pecten to move backwards and forwards within vitreal fluid to diffuse oxygen and nutrients.
No tapetum
Distinct fovea - increased density of photoreceptors for increased visual resolution
Why is the avian eye prone to sinusitis and what clinical signs are there?
Close proximity of globe to intraorbital sinus and diverticulum = prone
Exophthalmos/strabismus of globe - acute phase, space occupying lesion
Enophthalmos - chronic condition where sinus collapses due to fibrotic change
Avian abscesses = solid caseous material - due to heterophils rather than neutrophils
Surgery to resect and remove caseous material - shell out through infraorbital sinus through skin incision below lower eyelid. Needs careful reconstruction.
Irrigation may be possible if softer material
AB cover based on C+S
What type of virus can cause blepharitis in birds?
Pox virus
Range of variation depending on bird - epiphora, lid swelling, proliferative cutaneous growths, ulcerations of eyelids, eyelid oedema, mucopurulent discharge.
Fibrosis/scarring- irregular eyelid margin and chronic corneal damage/blindness
Prevention of self trauma to prevent scarring = key (dilute baby shampoo around lids - softens scales and makes less irritating)
Antiviral medications not effective.
How does hypovitaminosis A present in birds?
Vitamin A deficiency = periocular and conjunctival swelling with ocular discharge
(Other ddx - poxvirus/blepharitis/sinusitis)
Consider contributory factor when above disease seen.
White plaques in and around mouth, open mouth/laboured breathing, nasal discharge, sneezing, crusted nares, dermal dyskeratosis, feather abnormalities = systemic disease.
Vitamin A = key for normal epithelial growth
Seed based diet - especially sunflower seeds - dietary deficiency of fat soluble Vit A
Long term - dietary change and management
Injectable Vit A short term/oral beta carotene
Care of periocular area with lubricant/topical AB cover
List causes of conjunctivitis in avians.
- Foreign bodies
- Infectious disease (usually systemic and associated with septicaemia) - Chlaymdophila, Mycoplasma, Cryptosporidia, M.avium, Poxvirus
- Sinusitis
- Hypovitaminosis A
How would you investigate conjunctivitis in birds?
1.. History - other in contacts? New cagemate etc
2. Ophthalmic exam
3. Full PE - is conjunctiviits purely local or other systemic signs
4. Further testing (STT/phenol red), cytology, bacteriology - PCR
Which antibiotic is a good first line choice for avian conjunctivitis?
Bacterial infection = most common cause avian conjuncitivitis
Tetracycline/fluoroquinolone if high likelihood mycoplasma or chlamydophila
Systemic + topical AB cover
What are the usual signs of corneal ulceration in birds?
How do the majority of corneal ulcerations occur?
Blepharospasm, epiphora, self trauma
Majority = trauma
More chronic non healing ulcers can be seen in older birds - may have basement membrane dystrophy similar to SCCED’s in dogs
Normal healing time within 1 week
Serum can be used for melting corneal ulcers
Temporary tarsorrhaphy can be done with sterile non healing corneal ulcers for additional protection
What stage of cataracts do we often see birds with? How does lens induced uveitis present in these birds?
Often full/mature cataracts by time we see
Dull/dark homogenous hue to the iris face = lens induced uveitis
Also assess for retinal detachment (ocular ultrasound)
What is the most common cause of cataracts in birds?
How can they be treated?
Trauma = most common
Other ddx - inherited (canaries), age related, dietary deficiency of anti-oxidants
Phacoemulsification can be used in larger eyes
Irrigation/aspiration in smaller eyes
Lens induced/post traumatic uveitis - steroid drops up to 5x daily to reduce intraocular inflammation
What is lens luxation often associated with in birds? How does it present?
Majority Trauma but can be secondary to increased tension on zonules from mature cataract (often larger birds e.g owls with already very spherical lens)
Aphakic crescent often visible (subluxation)
Often other ocular abnormalities - mature cataracts, lens induced uveitis
If only mild inflammation best to leave in place
Other option = intracapsular lendectomy/phaco to remove
Describe enucleation in avians - what structure makes this surgery more challenging than in other species?
Scleral ossicles - make accessibility for enucleations more challenging
2 techniques
1. Enlarge palpebral aperture by joining to aural meatus
2. Evisceration - intraocular contents removed and resultant space filled with sphere/gelfoam mesh is possible
Evisceration often preferred in birds as easier approach but does make histopath examination of eye difficult compared to an enucleation approach.
Discuss the adaptations of the reptilian eye.
Lizards - anterior corneal and posterior orbital segments
Cornea = thin stroma but thick Bowman’s later devoid of cells and covered by thin epithelium
Iridocorneal angle poorly developed
Overlapping scleral ossicles (10-14 in lizards) found behind limbus overlying ciliary body and equator of lens (form Ringwulst) bringing lens into contact with ciliary body.
Ciliary muscle - Cramptons muscle and Brucke’s muslce as in birds - radial and circumferential fibres
Snake eyes - covered by spectacle formed from fused transparent eyelids
Haderian gland - seromucous fluid between spectacle and cornea
Do not have scleral ossicles but fibrous sclera with cartilagenous cap posteriorly
Cornea - thin with epithelium of only few layers as spectacle = main defence
Chelonians - large lacrimal and Haderian glands compared to other reptiles - marine species help with salt excretion.
Predominately cone photoreceptors - oil droplets accentuate colour as in birds
What is the parietal eye in reptiles?
Structure homologous with pineal gland in mammals
Histologically similar to conventional eye but an axial mid brain structure is overlain by a dorsal foramen in the skull and translucent skin allowing the parietal eye to play a central role in seasonal physiological and behavioural cycles through light detection in hardwired manner.
How does hypovitaminosis A present in chelonians?
Eyelid oedema to more severe eyelid swelling, chemosis of conjunctiva (can be severe and blind animal if obscures globe)
Globe can be exophthalmic - orbital glands enlarged through epithelial dyskeratosis
Particularly obvious in terrapins as lacrimal/haderian glands take up large space in orbit
Tx - address diet
Topical tear replacement therapy
Topical/systemic antibiosis (cytology showing heterophils/bacteria) - usually fluoroquinolone
Vitamin A injections - IM (oral dosing unsuccessful as affect GI epithelium and poor absorption))
List some causes of periocular lesions in reptiles.
Hypovitaminosis A
Caiman Pox/Herpesvirus - sea turtles (proliferative/ulcerated lesions)
Bacterial blepharitis - Aeromonas infection, pseudomonas, chamydophila
Physical irritation - e.g substrate
What signs of dacryocystitis are there in reptiles?
Discharge and bubble formation at medial canthus
Tear overflow/purulent ocular discharge
Diagnosis similar to in mammals
Systemic antibiosis more effective than topical drop
NL flushing difficult due to small size of eye
How should a retained spectacle in snakes and some lizard species be treated?
Spectacle = derived from fusion of the eyelids, closed space in which tears form, circulate and are drained via NL duct.
Usually shed with rest of skin (shedding = ecdysis) - becomes oedematous and opaque whilst rest of skin becomes dull.
Retention = raised plaque of retained tissue, often opaque in ocular area. Often not noticed until occurred several times when retained eyecaps are multiple.
DDx = bullous spectaculopathy, opacity from trauma/infection or subspectacular abscess, neoplasia - keratocanthoma
Often seen with incomplete skin shedding in other areas.
Underlying problem = husbandry = too low humidity or infestation with snake mite Ophinyssus natricius
DO NOT REMOVE WITH FORCE - often remove whole spectacle and leads to severe keratitis with poor prognosis for eye
TX - increase humidity, may be enough to remove at next shedding, damp cotton paper in vivarium or soaked cotton wool can help remove. If not working - GA, operating microscope to remove but advise referral to specialist.
What is bullous spectaculopathy in snakes?
Obstruction of NL duct system in snakes = build up of tear film under spectacle leading to enlargement (swelling of this space rather than epiphora)
Appearance = protuberant opaque mass or can be transparent where spectacle remains clear
Mechanical swelling of spectacle
NL obstruction:
1. Congenital - development atresia of duct
2. Acquired physical obstruction - infection/abscess, shed epithelium obscuring duct
Can aspirate fluid but will only give temporary relief (done under sedation/GA) - can be useful for bacteriology/C+S, often viscous fluid
Standard tx: done under GA
Excise triangle ventrally within spectacle allowing continual drainage of tears until the next shed
Perform using operating microscope/specialist
Often inflammatory rather than infectious obstruction
What is a subspectacular abscess in snakes?
Abscess forms between spectacle and cornea - yellow mass in ventral subspectacular space or severe cases occupying whole ocular surface.
Optimal tx = same as with bullous spectaculopathy - making window in ventral spectacle to allow drainage + irrigation
What corneal pathology can we see in reptiles?
Corneal ulceration - often trauma related
Opacification - pigmentation, lipid, calcium, proteinaceous deposit
(Corneal lipidoisis in chelonia - dietary hyperlipidaemia)
What is uveitis associated with in reptiles?
Not very common
Usually sign of systemic infection/inflammation
Main signs = flare, hazy appearance of iris, hypopyon
Majority of reptiles = gram -ve bacteria
TX - antibiosis (systemically) - often enrofloxacin
Topical steroids/NSAIDs for ocular inflammation
Atropine ineffective in reptiles - striated muscle
(Glaucoma not really reported in reptiles)
What are the common causes for cataracts in reptiles?
Nutritional deficiencies - particularly antioxidants
UV illumination in enclosures in captive reptiles
Freeze artifact during hibernation (tortoises)
Age related change
What may microphthalmos and anophthalmos in reptiles be associated with?
Congenital abnormality
Can affect feeding as high visually motivated feeders
Concurrent orbital infections due to lack of filled orbit space
May be associated with incubating eggs at too high temperature
Describe the adaptations of the amphibian eye.
Has to be adapted to both aquatic and terrestrial environments.
Eyelids - protect ocular surface
Harderian gland - tears to moisten corneal surface
Globe spherical with cornea and sclera having same radius and curvature
Retractor oculi - pulls eye in and down and forms integral part of roof of buccal cavity when swallowing.
Iris = thin and well vascularised, striated iridial muscle also autonomous activity allows pupil to constrict directly on light stimulation with contraction (does this even in enucleated eye so care with PLR intepretation)
Why must the use of topical antibiotics for corneal ulceration be considered with caution in amphibians?
Risk of toxicity due to systemic absorption through highly permeable skin
Fluoroquinolones/chloramphenicol preferred over aminoglycosides - renal toxicity
How may UV ocular pathology present in the amphibian?
Inflammatory keratitis or degenerative white opacity (sparser more crystalline appearance than lipid)
Intraocular changes - opacification of lens
What is the most common ocular disease seen in captive amphibians? How does it present?
Lipid keratopathy
White opacity of cornea, often protruding from corneal surface
DDX - corneal scarring/UV radiation
Raised surface and intense white colouration pathognomonic
? more common in females ready to spawn but unable to find appropriate place in captive environment and elevated blood lipid levels for long periods
What type of infection often causes periocular dermal ulceration in amphibians?
Fungal infections
Chromomycosis and Phycomycosis = skin ulceration wih/without reddening
Saprolegnia = fluffy white deposit on skin
Treatment = immersion in Malachite Green for periods of 5 minutes/laying gauze swabs soaked in medication over the area but not touching ocular surface.
What is uveitis associated with often in amphibians?
Often secondary uveitis - systemic gram -ve septicaemia
Systemic disease most likely so should be isolated
Blood culture/post mortem of any deceased amphibians vital
Tx - enrofloxacin s/c or IM once daily or oxytetracycline
Rifampicin baths or baths of methylene blue or malachite green
Why are carbonic anhydrase inhibitors not recommended for glaucoma in amphibians?
Glaucoma occurs in amphibians secondary to intraocular inflammation.
Carbonic anhydrase in amphibians = acid-base regulation and muscle contraction.
Drug can be absorbed across skin - severe s/e and risk death so not advised
Why is enucleation not recommended in amphibians?
Enucleation not recommended in amphibians - eye retracted caudally and ventrally when swallows to form dorsal buccal cavity as amphibians do not have a hard palate.
Frogs/toads retropulse eye into buccal cavity to provide intraoral pressure for swallowing.
Enucleation = great difficulty swallowing and poor QOL
?evisceration and implantation of prosthesis but not been reported.
