Fish & Invertebrate Ophthalmology Flashcards
1
Q
Describe the ocular anatomy of fish.
What species have rudimentary eyes?
What species have large eyes? Why does this matter clinically?
Describe fish eyelids.
Describe fish corneas. What is unique about green moray eels? Do any species have corneal pigmentation? What species have flat corneas?
What is the shape of the iris? Do any fish lack an iris? Can the iris be controlled in any species?
What is the shape of the lens?
What is the function of the choroidal gland? How does it play a role in clincial eye disease?
A
Ocular Anatomy
- Eyes vary greatly by spp.
- Rudimentary eye/eyespot 🡪 hagfish; Eyeless fish 🡪 cavefish
- Large eyes 🡪 squirrelfish, rockfish; seem more prone to issues like gas bubble disease, inflammation
- Do not have opposable eyelids - many have membrane (aka epidermal conjunctiva) covering cornea or tissue around eye
- Some have static eyelids to protect eyes (salmonids, jacks)
- FW fish corneas are thicker than SQ and some have 2-layered corneas
- Green moray eel cornea - dermal layer + scleral layer; common abnormal lipid deposition in dermal layer
- Microanatomical features - epidermal conjunctiva, basement membrane (Bowman’s membrane), and endothelial layer (Descemet’s membrane)
- Some spp. - normal corneal iridescence or pigmentation (pufferfish)
- Most have fixed pupil 🡪 no PLR (some exceptions 🡪 true eels, turbot, flounder, African lungfish)
- Iris - can be round, pear-shaped, elliptical, slit-like
- Deep sea fish lack an iris
- Amphibious fish (mudskippers) - flattened cornea, two pupils in each eye
- Suckermouth catfish 🡪 modified iris called “omega iris” - loop at top can expand and contract
- Lenses - dense, spherical (compensate for lack of refraction underwater), protrude slightly from iris
- No mechanical separation of vitreous and aqueous humor
- Ciliary bodies absent or rudimentary; ciliary processes absent; vitreal fluid production not understood
- Sclera is cartilaginous, orbit is bony - some fish have tenacular ligament anchoring globe to orbit
- Some spp. have scleral ossicles (sturgeon)
- Retina variable; rods and cone present - more cones in diurnal spp.; fovea and tapetum lucidum present
- European eel - only teleost w/ intraretinal vascular circulation
- Other teleosts - organ w/ vascular rete (choroidal gland) that wraps around optic nerve & communicates w/ pseudobranch
- Important in O2 secretion, implicated in intraocular gas bubble formation and potential source of hemorrhage during enucleation
2
Q
Describe the causes and management of exophthalmos and buphthalmos in fish.
What is the difference between exopthalmos adn buphthalmos?
What fish are particularly susceptible?
What are some of the cuases of gas accumulation in the eye?
What about soft tissue or fluid?
How should these cases be managed?
A
-
Exophthalmos or Buphthalmos
- Exophthalmos = protrusion of the globe
- Buphthalmos = enlargement of the globe
- Both are referred to as “popeye”
- Important to differentiate the cause of the distension (gas, soft tissue, or fluid) and the location (intraocular, retrobulbar)
- Signalment
- Any bony fish can be affected
- Some are more susceptible – Groupers, Dhufish, Rockfish, Squirrelfish, soldierfish
- Rare in elasmobranchs
- Clinical Findings
- One or both eyes may be affected
- One or more fish may be affected
- Etiologies
- Gas
- The most common is gas supersaturation and low hydrostatic pressure; inflammation is often secondary
- Metabolic
- Pseudobranch pathology
- Renal disease
- Acidosis
- Trauma
- Cohort, décor, or catch trauma
- Startling stimuli
- Barotrauma
- Life Support System/Environmental
- Gas supersaturation
- Shallow systems for deep water fish
- High or increasing water temperature
- Soft Tissue or Fluid
- If only one eye is affected, trauma and neoplasia are the most common differentials. If both eyes are affected, nutritional or infectious causes are more likely.
- Neoplasia
- Retrobulbar
- Intraocular
- Nutritional
- Excess fat behind eye
- Deficiency of micronutrients (Vit A, C, E, folate, pyridoxine)
- Infectious/Inflammatory
- Viruses, particularly rhabdoviruses, herpesviruses, infectious pancreatic necrosis virus, infectious salmon anemia, cardiomyopathy syndrome.
- Bacteria, particularly vibriosis, Aeromonas, Citrobacter, Pseudomonas, Edwardsiella, Flavobacterium, Yersinia, Streptococcus, Mycobacterium, Francisella spp.
- Fungi or fungal-like organisms, particularly Fusarium spp., Mesomycetozoea.
- Protozoa, particularly scuticociliates.
- Metazoa, particularly philometrid nematodes.
- Myxozoa, particularly Tetracapsuloides bryosalmonae.
- Toxic
- Ammonia
- Trauma
- Cohort, décor, or catch trauma
- Startling stimuli
- Life Support system/environmental
- Stray voltage and poor electrical grounding
- Gas
- Diagnostic Approach
- Review the history- recent additions? Quarantine protocols, habitat dimensions, recent life support system changes, recent catch/transport/handling, external events like light changes, chronicity and progression of clinical signs
- Check water quality – dissolved oxygen and total gas pressures
- Visually assess the animals
- Handling of the fish
- Examine eyes, oral cavity, gills
- Measure intraocular pressure – 10-20mmHg for teleosts. Comparison to a conspecific is helpful.
- Collect fine needle aspirate from the affected space for gas or fluid removal and cytology, fluid analysis, or cultures as indicated
- Examine gill and fin biopsies to check for gas emboli
- Consider ultrasound, radiographs, or CT to identify pathology within and around the eyes
- Management Approach
- Prevent further ocular trauma by removing complex décor, reducing the lighting, and partially covering any windows to reduce startle responses.
- Treat any infection with systemic, topical, conjunctival, or intraocular medications.
- Consider analgesia and anti-inflammatory medications.
- If gas supersaturation is suspected, identify and remove the source. Agitate the water gently to help with offgassing.
- For intraocular or retrobulbar gas, consider recompression treatment. For intransient intraocular gas, consider pseudobranch ablation.
- Prognosis for retrobulbar gas is usually good. In some cases, clinical signs may remain or recur but systemic signs and mortality are rare.
- Prognosis for intraocular gas is worse due to lens and retina damage. Return to normal function is possible, although uncommon with chronic cases.
- The eye may progress to phthisis bulbi.
- Enucleation may improve overall prognosis.
- Enucleation may improve overall prognosis if the disease is not systemic.
3
Q
Describe the causes and management of ocular opacities in fish.
How do differentials change if just one or both eyes are affected?
What are some of the potential etiologies? Nutritional issues? Infectious issues? Traumatic or life support issues?
How should these cases be worked up and managed?
A
-
Ocular Opacity
- Overview
- Can be due to changes in the conjunctiva, cornea, anterior chamber, or lens
- Diffuse ocular opacities are common and often due to keratitis and uveitis. Lesions are frequently traumatic or infectious in origin. Bilateral lesions can suggest a systemic infection
- Cataracts are common
- Clinical Findings
- Affected eyes may also be buphthalmic or exophthalmic
- Reduced appetite, inappetence, weight loss, lethargy, or skin changes are more likely associated with systemic disease
- Etiologies
- If only one eye is affected, trauma is more likely. If both eyes are affected, infectious or environmental causes are more likely
- Nutritional
- Abnormal lipid deposition
- Deficiency of micronutrients
- Infectious/inflammatory
- Bacteria, particularly vibriosis, Aeromonas, Citrobacter, Pseudomonas, Edwardsiella, Flavobacterium, Yersinia, Streptococcus, Francisella spp.
- Fungi or fungal-like organisms, particularly atypical oomycetes.
- Protozoa, particularly Cryptocaryon, scuticociliates (SW); Ichthyophthirius, scuticociliates (FW).
- Metazoa, particularly capsalids (e.g. Neobenedenia spp.), digenes (e.g. Diplostomum spp.), turbellarians, copepods.
- Toxic
- Ammonia, nitrites
- Polycyclic aromatic hydrocarbons
- Trauma
- Cohort, décor, or catch trauma
- Startling stimuli
- Barotrauma
- Lens luxation
- Life support system/environmental
- Rapid change in pH or salinity
- High, low or fluctuating water temperature
- High carbon dioxide
- Insufficient or excessive UV
- Sudden light changes
- Residual oxidants
- Diagnostic Approach
- Review the history- animal additions, quarantine, environmental conditions, recent catch/handling/transport, chronicity and progression of clinical signs
- Check water quality- pH, CO2, oxidants
- Visually assess animals
- Handle fish
- Examine eyes, oral cavity, gills
- Consider corneal cultures particularly if lesions are not healing
- Examine an impression smear of the corneal surface
- Measure intraocular pressure
- Use fluorescein stain
- Consider ultrasonography to evaluate the posterior chamber and retrobulbar space
- Consider aspiration if exophthalmos or buphthalmos is present
- Histology of the eye and retrobulbar tissues following enucleation
- Management Approach
- Prevent further ocular trauma by removing complex décor, reducing the lighting, and partially covering any windows to reduce startle responses
- Treat any infection with systemic, topical, conjunctival, or intraocular medications.
- Consider analgesia and anti-inflammatory medications.
- For lens luxations or cataracts, consider surgical management.
- For ulcerative keratitis, consider a grid keratotomy with a 25 ga needle or cotton-tipped applicator.
- Overview
4
Q
Describe the management of cataracts in fish.
What are some of the proposed etiologies?
What other clinical findings may be present?
How are these cases diagnosed?
What are typical IOPs for fish?
How are they treated?
A
- Cataracts
- Common in fish, can be resolved via lensectomy or phaco
- etiology :
- Genetic, age
- Nutritional - vitamin A, C, B2 (riboflavin), amino acids (tryptophan, methionine, histidine), manganese, zinc; vegetable oil substitutes for fish oil, phytate-phosphorus in diets
- Inflammatory - uveitis
- Infectious - bacterial (vibriosis, Yersinia, Edwardsiella, Strep), fungal, parasitic (i.e. encysted digenes - Diplostomum)
- Toxic - polycyclic aromatic hydrocarbons
- Trauma
- Envtal - rapid salinity change, excess UV exposure, excess ozone, fluctuating water temp, gas supersaturation, high CO2 in water
- Findings
- Opacities of the lens/lens capsule
- Can resolve over time rarely, usually if assoc with osmotic imbalances
- May be no other c/s, may see lethargy, decreased feeding response, other ocular pathology, other evidence of trauma
- Dx
- Slit lamp exam, can use flourescein to r/o ulcers, IOP to ID incr IOP (glaucoma) vs low IOP (uveitis), teleosts reported 10-20 mmHg
- Husbandry
- Resolve any WQ or life support system concerns
- Medical tx
- Consider sx - lens removal (phakectomy) or emulsification (phaco), consider electroretinogram (ERG) prior to determine if retina is visual
- Generally good prognosis with sx if no other pathology
5
Q
Discuss lipid keratopathy in fish.
What species are more suceptible?
What are the findings on the cornea?
What husbandry and medical treatments are available?
How can this be prevented?
A
- Lipid Keratopathy
- Seen in human care, esp moray eels
- Assoc with systemic lipid abnormalities
- Dietary management or surgical resection of lesions can improve signs
- Etiology
- Diet high in fat
- Signalment
- Carnivorous teleosts under human care most susceptible, esp moray eels
- Findings
- Irregular, grey to white dermal opacities in the cornea or dermal layer (spectacle), silver sparkling or shiny crystalline structures visible under magnification
- Ddx
- Mineral deposition, corneal edema, fibrosis, keratitis
- Dx
- May see elevated TP, TG, Cholesterol, AST
- Definitive via histopath
- Husbandry
- Reduce fat/cholesterol in diet, diet analysis with lipid profiles recommended
- Introduce fasting periods, reduce scavenging on high fat foods
- Medical tx
- Surgical resection of lesions → may improve ocular clarity, feeding behavior
- Prevention
- Avoid high fat diets, review nutrition, base diets on natural hx of the species
