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Ophthalmology > Equine ophthalmology > Flashcards

Equine ophthalmology Flashcards

1
Q

Adaptations of the horse eye

A
  • Large horizontal eye and cornea increase the amount of light able to rech the retina
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2
Q

Visual acuity of the horse in relation to the dog and cat

A
  • Approaches 20/20 and exceeds the dog and cat
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3
Q

Are horses better at peripheral vision or binocular vision?

A

Peripheral vision

Up to 350 degrees

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4
Q

Blind spots for the horse

A
  • Forehead, below the nose, and directly behind the horse like the width of the head
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5
Q

Characteristics of horse fundus

A
  • Large tapetum fibrosum (paurangiotic)
  • No retinal arteries or veins
  • Only capillaries the periphery of the optic nerve head
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6
Q

What color is the horse lens?

A
  • Yellow
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7
Q

Role of the yellow horse lens

A
  • Improves visual acuity
  • Decreases glare
  • More prominent with age
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8
Q

What shape is the horse pupil?

A
  • HOrizontal

- Can dilate and become circular

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9
Q

Function of corpora nigra (iridica)

A
  • Shade from the posterior of the iris epithelium coming forward
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10
Q

Ability of horse to constrict and dilate pupil

A
  • Can dilate 3-6x more than dogs and humans

- Ability of the pupil to constrict to form 2 pupils; thought to improve visual acuity

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11
Q

What’s the problem with corpora nigra cysts?

A
  • Cause visual impairment, especially when the pupil is constricted
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12
Q

Treatment for corpora nigra cysts

A
  • Diode laser to destroy cyst or manual destruction (referral)
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13
Q

What causes pathology to the corpora nigra most commonly?

A
  • Chronic uveitis

- Posterior synechia or atrophy indicates chronic inflammation from ERU

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14
Q

Reflex uveitis in horses

A
  • Often occurs secondary to pain
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15
Q

How does a collapsed iridocorneal angle look in the horse?

A
  • Bright white line
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16
Q

What can cause visual impairment in the horse?

A
  • Iris cysts
  • Cataracts
  • Vitreal opacities
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17
Q

Is asteroid hyalosis in horses normal?

A
  • No
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18
Q

Who gets congenital stationary night blindness?

A
  • Appaloosa horses with leopard gene (LpLp)
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19
Q

Appearance of retina in horses with congenital stationary night blindness?

A
  • Normal

- ERG will be abnormal

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20
Q

What is the primary issue with congenital stationary night blindness?

A
  • ERG abnormal

- Neural transmission defect in retina

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21
Q

Lp gene

A
  • Dominant and associated with coat color (few spot, leopard, etc.)
  • Commonly have striped hooves, white sclera, and mottled skin around mouth, eyelids, anus, and genitalia
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22
Q

Multiple ocular abnormalities - who gets?

A
  • Rocky Mountain Horse
  • Kentucky Saddle Horse
  • Mountain Pleasure Horse
  • Associated with silver dapple gene
  • Chocolate coat with white mane and tail most affected
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23
Q

Congenital ocular disorders in horses

A
  • Microphthalmia

- Cataracts

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24
Q

Naso-lacrimal duct atresia

A
  • Tears go down the face
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25
Q

Scrolled cartilage

A
  • Flipped over TEL cartilage
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26
Q

Diagnosis of naso-lacrimal duct atresia

A
  • N-L flush required to make diagnosis

- If it doesn’t flush, there’s atresia

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27
Q

Entropion in horses - risk factors?

A
  • Foals with neonatal maladjustment syndrome, corneal ulcers, and secondary to microphthalmia
  • Hereditary in TB and QHs
  • Results from cachexia, scarring, pthisis bulbi
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28
Q

Pthisis bulbi

A
  • SO much damage that the eye stops producing aqueous and huts down
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29
Q

Normal foal eyes at birth

A
  • Open and visual
  • Slight ventromedial strabismus
  • Prominent Y-sutures in lens
  • Have round pupils for about 2 weeks
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30
Q

Episcleral or subconjunctival hemorrhage in foals

A
  • Due to trauma in delivery

- Should clear in about a week or a little over

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31
Q

Neonatal septicemia - which organs does bacteremia spread to?

A
  • Joints, lungs, umbilicus, and eye
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32
Q

Mechanism of uveitis with neonatal septicemia

A
  • Intraocular inflammation –> increased vascular permeability –> proteins and cells passing into the aqueous
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33
Q

Appearance of the eye in a foal with neonatal septicemia and subsequent uveitis

A
  • Green hue to the iris from fibrin initially; progresses to miosis, hyperemia, flare, hypotony, hyphema
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34
Q

How to examine a horse for symmetry?

A
  • Stand several feet away from and at the front of the horse
  • Assess facial orbital and eyelid position
  • Pupil size and position
  • Assess direct and consensual PLR (not as strong as dogs and cats)
  • Elicit blink reflex (eyelids should close completely
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35
Q

Facial nerve paralysis appearance

A
  • Muzzle droops towards the unaffected side

- Ear and eye droop

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36
Q

Causes of facial nerve paralysis

A
  • EPM
  • Trauma
  • Encephalitis
  • Aspergillus
  • Temporohyoid osteoarthropathy (THO)
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37
Q

Sequelae of facial nerve paralysis

A
  • Exposure keratitis and corneal ulceration
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38
Q

Treatment for facial nerve paralysis

A
  • Have to place a sub-palpebral lavage system to keep the cornea hydrated
  • Topical abx for corneal ulcers
  • Lubricants
  • Temporary partial tarsorrhaphy
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39
Q

PNS and facial nerve paralysis

A
  • Possible decreased tear production
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40
Q

Prognosis for facial nerve paralysis

A
  • Ultimately the horse should learn to retract the globe and spread tear film with the third eyelid
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41
Q

Which nerve do we block for motor with eye exams?

A
  • Auriculopalpebral, a branch of the facial nerve
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42
Q

Where is the auriculopalpebral nerve located for a block?

A
  • Zygomatic arch
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43
Q

Function of the facial nerve in relation to the eye

A
  • Closes the eye
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44
Q

Which nerve is the sensory supply to the eye?

A
  • Trigeminal nerve

- Frontal nerve is what we technically block to block sensation

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45
Q

Where do we block for sensory?

A
  • Supraorbital foramen to get the frontal nerve out of the trigeminal nerve
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46
Q

What does the frontal nerve block sensory to?

A
  • Upper eyelid

- If you want to do medial or lateral canthus, that nerve block will not cover it

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47
Q

How to block the frontal nerve?

A
  • Place 25 ga needle into supraorbital foramen and inject 1-2 mL lidocaine
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48
Q

How to block auriculopalpebral nerve?

A
  • Palpate nerve over the zygomatic arch, and inject SQ over the nerve
  • May need IV sedation or a twitch first or in addition
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49
Q

What are the more common equine eyelid abnormalities?

A
  • Lacerations**
  • blunt trauma

-

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50
Q

Other causes of equine eyelid abnormalities that are less common

A
  • Entropion (not common)
  • Distichiasis (uncommon but may lead to delayed corneal ulcer healing)
  • Meibomian gland adenitis/eosinophilic granuloma
  • Parasitic disease with habronema, onchocerca, thelazia
  • Neoplasia with actinic dermatitis, SCC, sarcoid, melanoma
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51
Q

How well do eyelid lacerations heal in the horse?

A
  • Quite well due to vascular supply
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52
Q

Treatment of eyelid lacerations in horses

A
  • Minimal debridement to save the lid margin
  • Precise lid margin apposition
  • 2 layer closure, no suture against the cornea (Figure of 8)
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53
Q

How to close an eyelid laceration on a horse?

A
  • 2-layer closure
  • Conjunctiva and skin
  • Close lid margin first
  • Use 6-0 vicryl SQ (DO NOT let sutures contact cornea or penetrate conjunctiva)
  • 6-0 or 5-0 silk for skin
  • Rule out corneal intraocular and orbital lesions
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54
Q

What is the issue if an eyelid laceration is either not repaired or poorly repaired?

A
  • Leaves notch defect and uneven pressure on the cornea
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55
Q

Orbital fracture treatment

A
  • If small and non-displaced, the fractures can be left to heal if they do not impose on the eye
  • Be sure the eye is not ruptured
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56
Q

Treatment for a ruptured eye?

A
  • Emergency enucleation
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57
Q

Eosinophilic granuloma sequela

A
  • Exposure keratitis

- Eyelid does not contact cornea resulting in corneal ulceration/stromal abscess

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58
Q

Treatment of eosinophilic granuloma

A
  • Dermatologic condition (blepharitis) treated with local and systemic steroids, antibiotics, and/or anti-fungals based on cytology/culture/histopath
  • May require aggressive intra-lesional injection with dexamethasone UNLESS there is an ulcer
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59
Q

Eosinophilic granulomas - what are they?

A
  • Meibomian glands can get granulomas (parasitic; Habronema)
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60
Q

Eosinophilic granuloma prognosis

A
  • If soft, they may go down; once hard they’re almost impossible to fix
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61
Q

Treatment of SCC

A
  • Surgical excision, cryotherapy, radiation, photodynamic therapy, intralesional chemo
  • EARLY aggressive treatment for best results
  • Clean margins
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62
Q

Behavior of SCC in horse eyes

A
  • Most will recur
  • Locally invasive
  • Later metastatic
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63
Q

Who gets SCC (horses)?

A
  • Light skinned horses
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64
Q

How do normal horse TELs look?

A
  • Curly

- Should be smooth and healthy conjunctival tissue

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65
Q

What are the two most common sites of SCC in horses>

A
  • Third eyelid

- Lateral limbus

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66
Q

What will give you the best prognosis for conjunctival and TEL SCC?

A
  • Early excision with clean margins for best prognosis

- Other treatment options include cryotherapy and photodynamic therapy

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67
Q

Appearance of conjunctival or TEL SCC

A
  • COuld be petechiation and rough looking
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68
Q

TEL Adenocarcinoma how to diagnose?

A
  • Biopsy (must cut out the third eyelid)

- MRI for margins

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69
Q

Treatment for TEL Adenocarcinoma in horses

A
  • Agressive surgical excision

- Radiation therapy

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70
Q

Where is the bulbar conjunctiva normally pigmented in horses? What can happen if it’s not pigmented?

A
  • Usually pigmented medially and laterally in the horse

- Lack of conjunctival pigment over lateral sclera orTEL predisposes to SCC

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71
Q

How do we identify cause of conjunctivitis?

A
  • Exam and elimination
  • ook for trauma, foreign body, or parasite
  • Look for corneal ulcer or intraocular disorder
  • Then look at systemic disease (fever, LN, anorexia)
  • Cytology
  • Culture
  • Biopsy
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72
Q

Appearance of conjunctivitis in horses

A
  • Hyperemia, chemosis, discharge serous to mucopurulent, blepharospasm
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73
Q

Do clinical signs of conjunctivitis change based on the etiology?

A
  • NO
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74
Q

Causes of conjunctivitis in horses

A
  • Trauma
  • Ulcer
  • Bacterial infection
  • Fungal infection
  • Parasitic infection
  • Eosinophilic inflammation
  • Uveitis
  • Non-ulcerative keratitis
  • Glaucoma
  • Neoplasia
  • Etc.
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75
Q

Distal L-N catheter placement for flushing in horses vs mules

A
  • Infero-medial location in the horse where the pigmented and non-pigmented areas meet
  • In the mule the distal puncta is located superior-lateral nasal fold
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76
Q

Treatment of conjunctivitis in horses

A
  • Treat primary disease (ulcer, foreign body, parasites, neoplasia, etc.)
  • Environmental irritants/allergies often respond to BNP ointment
  • Rule out intraocular and systemic disease
  • May need BNP-HC if no ulcer
  • Careful with dexamethasone
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77
Q

What to do about depigmentation over the temporal or lateral bulbar conjunctiva?

A
  • Biopsy it with excisional biopsy

- Cytology and histopathology

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78
Q

Habronema - how does it occur?

A
  • Larvae deposited on wounds near the eye by flies
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79
Q

Diagnosis of Habronema

A

appearance or biopsy

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80
Q

Appearance of Habronema

A
  • Gritty necrotic debris
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81
Q

Biopsy of Habronema

A
  • Granulomatous reaction with eosinophils and mast cells
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82
Q

Treatment for Habronema

A
  • Ivermectin

- Topical and sytemic-anti-inflammatory drugs

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83
Q

Prevention of Habronema

A
  • Control fly population

- Use fly masks

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84
Q

What can ocular onchocerciasis cause?

A
  • Lateral conjunctival vitiligo (depigmented)
  • Keratitis
  • Keratoconjunctivitis
  • Anterior uveitis
  • Posterior uveitis
  • Peripapillary chorioretinitis
  • Really should always be on the dfdx list
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85
Q

Diagnosis of ocular onchocerciasis

A
  • Diagnose (eyelid, cornea, conjunctiva) with biopsy
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86
Q

Treatment of ocular onchocerciasis

A
  • Systemic ivermectin or moxidectin
  • Systemic NSAID
  • Topical steroids
  • Need to control ocular inflammation with infection and as parasite dies
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87
Q

In general should you use steroids in horses?

A
  • No

- Can cause ulcers

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88
Q

Causes of ulcerative keratitis in horses

A
  • Usually traumatic
  • Sharp or blunt or both
  • May be viral (herpes)
  • EHV2, EHV5
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89
Q

What are ulcer categories in horses?

A
  • Uncomplicated
  • Indolent
  • Infected
  • Melting
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90
Q

Uncomplicated ulcers

A
  • Superficial, not infected
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91
Q

How quickly should uncomplicated ulcers heal?

A
  • 3-5 days
92
Q

Indolent ulcers

A
  • Non-healing ulcer with loose epithelium, older horse
93
Q

Infected ulcers

A
  • Bacterial, fungal
94
Q

Melting ulcers characteristics

A
  • can be infected or sterile
95
Q

Treatment for loose epithelium on an ulcer in horses depending on if they are young or older-

A
  • If younger, look for FB, distichia, infection

- If older, needs debridement

96
Q

Clinical signs of ulcerative keratitis

A
  • Pain due to corneal pain and reflex uveitis
  • Blepharospasm
  • Photophobia
  • Epiphora
  • Miosis
  • Discharge - serous to mucopurulent
  • Fluorescein stain uptake
97
Q

What causes the pain with ulcerative keratitis?

A
  • Corneal pain and reflex uveitis
98
Q

Cause of uncomplicated superficial corneal ulcers

A
  • Mostly traumatic
99
Q

How to treat uncomplicated superficial corneal ulcers?

A
  • Broad spectrum abx (neomycin/polymixin/bacitracin)

- Atropine, Systemic NSAID like flunixin, and pain management (preventing reflex uveitis)

100
Q

How does atropine prevent reflex uveitis?

A
  • Mydriatic and cycloplegic
101
Q

What pain management for horses with superficial corneal ulcers that are uncomplicated?

A
  • Topical morphine
102
Q

What should a circular ulcer make you think in a horse?

A
  • Foreign body
  • Look for underlying cause
  • Especially if it’s deep or infected by non-healing
103
Q

Indolent ulcer appearance

A
  • Loose epithelium
104
Q

Stromal injury in horses healing time

A
  • Longer healing time than superficial ulcers
105
Q

When do blood vessels enter the cornea?

A
  • After 1 week

- Advance 1 mm/day until cornea has healed

106
Q

Treatment for stromal injury

A
  • Continue antibiotics, atropine

- Banamine +/- diclofenac until no stain uptake

107
Q

Equine herpes keratitis signs

A
  • Painful
  • Punctate or dendritic ulcers
  • Can be ulcerative or non-ulcerative
108
Q

Diagnosis of Equine Herpes keratitis

A
  • Careful examination to rule out traumatic injury such as dirt and debris
  • Clinical signs or PCR
109
Q

Which strains of EHV cause keratitis?

A

EHV 2 and 5

110
Q

Treatment for equine herpes keratitis

A
  • Oral lysine and topical trifluridine
111
Q

How might you differentiate ocular disease vs another disease from two horses that look quite similar with funky eyes?

A
  • if the eye is slammed shut, that could indicate pain

- In an abscess, there might be copious ocular discharge but the eye itself might not hurt

112
Q

For a terrible looking eye with copious ocular discharge and severe blepharospasm, what are your differentials?

How might you differentiate?

A
  • Fungal, bacterial, or eosinophilic

- Differentiate with cytology

113
Q

Eosinophilic keratitis treatment (with bacteria and stromal abscesses)

A
  • Keratectomy probably
  • Topical mast cell blockers
  • Cyclosporine
  • Systemic cetirizine
114
Q

What should you do with any complicated ulcers?

A
  • Cytology
  • Culture
  • Sensitivity
115
Q

Bacteria present with secondary infections on equine corneal ulcers?

A
  • Staph
  • Pseudomonas
  • Strep
116
Q

Fungi that can be present as secondary invaders for equine corneal ulcers

A
  • Aspergillus, Fusarium, Penicillium, Alternaria
117
Q

What is the most virulent bacteria with bacterial keratitis?

A
  • Pseudomonas aeruginosa

- Produce endotoxins, exotoxins, proteases

118
Q

Beta-hemolytic strep and bacterial keratitis

A
  • Produces exotoxins, can digest conjunctival and amnionic graft and sutures
  • Strep eat everything
  • Compound IV penicillin, chloramphenicol, ofloxacin
119
Q

Treatment of bacterial keratitis

A
  • C&S (start treatment pending results based on cytology)
  • SPL (Sub-palpebral lavage
  • Chloramphenicol
  • Gentocin
  • Atropine
  • Flunixin
  • Doxycycline orally
  • Topical NSAID
120
Q

When is surgery indicated for treatment of bacterial keratitis?

A
  • if not responsive to medical treatment or if there’s an abscess or melting cornea
  • She will cut the badness out and put a graft over it
121
Q

Appearance of fungal keratitis

A
  • Minor abrasions to deep ulcers or stromal abscesses
  • Fluffy to plaque-like
  • Gray, yellow, brown
  • Punctate rose bengal positive (similar to herpes)
  • Often a history of extensive treatment with antibiotics or steroids
122
Q

Diagnosis of fungal keratitis

A
  • Culture and cytology
  • PCR
  • Histopathology
123
Q

Treatment for fungal keratitis

A
  • Topical antifungals (natamycin, clotrimazole, silver sulfasalazine)
  • Serum
  • EDTA
  • Doxycycline
  • Atropine
  • Antibiotics
  • Oral fluconazole
  • IV or oral flunixin
  • Surgery
124
Q

When to consider fungal keratitis?

A
  • All non-healing or relapsing corneal ulcers in horses, or horses treated with steroids and multiple antibiotics
125
Q

Prognosis of fungal keratitis

A
  • Ulcers can melt rapidly

- Guarded if stromal abscess or rupture

126
Q

What is the only effective treatment in general for melting fungal keratitis?

A
  • Enucleation
127
Q

Treatment for melting ulcers (that maybe aren’t as severe)

A
  • Serum Q2 alternating with EDTA q2hr
  • Topical antibiotic (chloramphenicol, BNP, gentocin)
  • Anti-fungal if indicated
  • Atropine
  • Systemic NSAID
  • N-acetylcysteine 10%

All topical meds should be separated by at least 15 minutes; SPL rinsed between meds

  • Doxycycline (topical and oral)
128
Q

Stromal abscess appearance

A
  • Solid creamy white or yellow stromal opacity

- Painful

129
Q

Possible etiologies of stromal abscess

A
  • Bacterial
  • Fungal
  • Sterile
130
Q

Treatment for stromal abscess

A
  • Need antibiotic (chloro, ofloxacin) or antifungal (voriconazole) that penetrates cornea
  • Best option is surgical excision with graft
131
Q

Endothelial ulcer prognosis?

A
  • guarded prognosis
132
Q

Clinical signs of equine acute uveitis dependent on cause

A
  • They are the SAME regardless of the cause
  • Trauma
  • Corneal ulcer
  • Stromal abscess
  • Etc.
133
Q

Systemic infectious diseases with ocular signs

A
  • Equine infectious anemia
  • Rabies
  • Adenovirus
  • Influenza
  • West Nile Virus
  • Strangles
  • Encephalitis
  • Apsergillus
  • Strep Equi
  • EHV
  • EVA
  • Brucellosis
134
Q

Clinical signs of Acute uveitis (and one of the most important ones first)

A
  • Miosis**
  • Blepharospasm
  • Conjunctival hyperemia
  • Periocular swelling
  • Lacrimation
  • Corneal edema
  • Flare
  • Hypopyon
  • Corneal vascularization
  • Low IOP (hypotony)
135
Q

Definition of Equine Recurrent Uveitis

A
  • Any case that presents with uveitis WITHOUT evidence of underlying disease and the horse has had previous episodes of uveitis
136
Q

Leading cause of blindness in horses

A
  • ERU
137
Q

What is thought to be an inciting cause of ERU in horses?

A
  • Leptospirosis
138
Q

Who gets ERU?

A
  • ANY age, breed, or sex

- Appaloosas, Fresians, Warmbloods

139
Q

What are the three types of ERU?

A
  1. Insidious
  2. Classic
  3. Posterior segment
140
Q

Insidious ERU

A
  • Low grade inflammation (not usually seen clinically) and leads to gradual/cumulative destruction
141
Q

Classic ERU

A
  • Most common
  • Episodes of active inflammation followed by “quiet” periods
  • Squinting, painful, tearing
142
Q

Posterior segment ERU

A
  • Inflammation in vitreous and retina
  • More common in Warmbloods and drafts
  • I guess they see it in Europe more
143
Q

Who is at highest risk of ERU?

A
  • Appaloosas
  • Higher incidence of blindness with ERU
  • Higher % associated with Leptospirosis
  • 88% are bilaterally affected
144
Q

Warmbloods and ERU

A
  • More prone to posterior segment but can get any form of the disease
  • German and Dutch Warmbloods may have a genetic correlation
145
Q

Leptospirosis and ERU

A
  • Leptospira interrogans
  • Lepto antibodies have been found in serum, aqueous humor, and vitreous in affected horses
  • Interaction between Lepto and equine immune system
146
Q

Vaccination for Lepto as prevention

A
  • NOT PROVEN

- Currently not recommended

147
Q

Treatment of Uveitis

A
  • Atropine to effect (monitor for colic; check IOP)
  • NPDex if NO ULCER
  • Topical NSAID to facilitate pupil dilation
  • Flunixin (Banamine is gold standard)
  • +/- Ciprofloxacin
  • +/- Doxycycline
  • Sub-palpebral lavage
  • Treat EARLY AND BE AGGRESSIVE IN TREATMENT
148
Q

Cyclosporine implants

A
  • EARLY referral is critical

- Referral procedure

149
Q

Who should be referred for cyclosporine implants?

A
  • Horses with episodes of uveitis that are responsive to topical anti-inflammatories
150
Q

Where does the cyclosporine implant live?

A
  • Between sclera and uvea/choroid

- Absorbed in the choroid

151
Q

Signs of previous uveitis

A
  • Iris depigmentation and atrophy
  • Pigment on anterior lens capsule
  • Corpora nigra atrophy
152
Q

Chronic ERU signs

A
  • Cataracts (can be small)
  • Glaucoma
  • Blindness
  • Butterfly lesions
  • Stria (signs of glaucoma)
153
Q

Chorioretinal scarring appearance on fundic exam

A
  • Bullet hole lesions (can be incidental)

- Scarring

154
Q

Sequelae of chronic uveitis

A
  • Glaucoma and lens luxation or pthisical eye
155
Q

What form of uveitis do Appaloosas get?

A
  • Insidious or non-painful form of uveitis

- Appaloosas and Fresians often present with end-stage disease

156
Q

How does glaucoma happen?

A
  • Sink analogy
  • Tap: ciliary body, never over-produces fluid
  • Drain: iridocorneal angle and uveoscleral outflow (important in the horse)
  • Chronic inflammation creates cellular debris and PIFMs with fibrin –> clogs the drain –> fluid cannot get out –> increased pressures
157
Q

Appearance of glaucoma in horses

A
  • Corneal edema with glaucoma or eye may appear normal with high IOP until buphthalmic
  • Diffuse severe edema
158
Q

Striae

A

Descemet’s membrane break

159
Q

What are striae pathognomonic for?

A
  • previous IOP elevation
160
Q

Treatment of glaucoma

A
  • Dorzolamide/timolol for life

- Horses do NOT respond to latanoprost

161
Q

If visual, glaucoma treatment?

A
  • Referral for surgery

- Buying them time

162
Q

If blind, glaucoma treatment?

A
  • Enucleation
163
Q

Glaucoma surgery?

A
  • Laser surgery
  • Transccleral cyclophotocoagulation (kills the ciliary body)
  • Micropulse
  • Ahmed valves
164
Q

Heterochromic iridocyclitis/keratitis

A
  • newly described form of uveitis
165
Q

Appearance of heterochromic iridocyclitis/keratitis

A
  • Corneal edema
  • Endothelial pigmentation
  • Mild inflammation
  • Painful
166
Q

How does heterochromic/iridocyclitis/keratitis respond to medication?

A

Poorly

167
Q

Who gets HIK?

A

Warmbloods

168
Q

Cow retrobulbar disease

A
  • Orbital cellulitis
  • Frontal sinusitis
  • LSA
169
Q

Causes of orbital cellulitis

A
  • Trauma
  • Punctures
  • FB
  • Actinobacillus
  • Clostridium
  • Panopthalmitis
170
Q

Frontal sinusitis causes

A
  • Dehorning related in 67% of cases (Actinomyces pyogenes)

- Respiratory tract disease (Pasteurella multocida)

171
Q

Lymphosarcoma cause

A
  • Bovine Leukemia virus
172
Q

BLV transmission

A
  • Horizontal (vaccines, dehorning, castration, ear tags) or vertical (in utero)
173
Q

How long are cattle infected with BLV?

A
  • Permanently

- Permanent carriers

174
Q

What % of cows infected with BLV will seroconvert?

A
  • 30%

- Lymphocytosis months to years after infection

175
Q

Appearance of lymphoma with bovine orbital neoplasia

A
  • Exophthalmos
176
Q

Economic impact of bovine ocular SCC

A
  • Ocular squamous cell carcinoma has serious economic impact
  • 4th leading cause of carcass condemnation post-mortem
177
Q

Signalment of bovine OSCC

A
  • Older cattle (~8 years)
  • Herefords are over-represented as well as Ayrshires (dairy)
  • Black baldies
178
Q

Risk factors for bovine OSCC

A
  • Increased risks at higher altitude
  • Higher UUV light
  • Depigmented eyelids
179
Q

What % of cattle are affected bilaterally?

A
  • 35% of cattle are affected
180
Q

Clinical signs of bovine OSCC

A
  • Lesions on bulbar conjunctiva or cornea that starts as a plaque
  • Carcinoma in situ arises directly from a plaque (grossly like a papilloma) –> progress and invade
181
Q

Metastatic potential of bovine OSCC

A
  • It exists
  • Most commonly to LN or intracranial, can extend hematogenously to multiple organs
  • Animals with invasive OSCC have a higher level of metastasis
182
Q

Diagnosis of bovine OSCC

A
  • Cytology +/- histopath
183
Q

Treatment of bovine OSCC

A
  • need a biopsy
  • Not all precancerous lesions progress
  • About 1/3 cspontaneously regress
  • Salvage procedures (extenteration)
  • Cryotherapy (Success with small lesions)***
  • Immunotherapy
184
Q

Extenteration

A
  • Taking out the eye plus everything around them
185
Q

Bovine orbital neoplasia and transpalpebral exenteration

A
  • Because SCC invades the retrobulbar space
  • 81% of cows were exenterated due to SCC
  • Holsteins over-represented with lymphoma
  • Recurrence is fairly common
186
Q

Infectious bovine keratoconjunctivitis losses

A
  • World-wide distribution
  • Economic losses are HUGE ($150+ million in US)
  • Decreased weight gain and milk production
187
Q

What causes IBK?

A
  • Moraxella bovis
188
Q

What is Moraxella bovis?

A
  • Gram negative bacillus
189
Q

What other pathogens contribute to severity of IBK?

A
  • IBR, Mycoplasma, Thelazia, Listeria
190
Q

***What form of M. bovis causes IBK acute disease?

A
  • Piliated, hemolytic form of M. bovis***
191
Q

What form of M. bovis causes IBK carrier disease?

A
  • Nonpiliated, nonhemolytic forms
192
Q

Risk factors for IBK

A
  • herefords and Murray Grays
  • Age (younger <2 years)
  • UV radiation
  • Comorbidities
  • Face flies
  • Bovine tears lack lysozyme
  • Herds vaccinated for IBR
193
Q

What enzyme do bovine tears lack?

A
  • Lysozyme
194
Q

How does herd vaccination act as a risk factor for IBK?***

A
  • Modified live and shipping can lead to outbreaks of pink-eye***
195
Q

Transmission of IBK

A
  • Us!
  • Sources
  • Direct contact, handles, fomites, and mechanical vectors (flies)
196
Q

Source of IBK

A
  • New animal or carrier in the herd

- Non-pathogenic strain reverts to pathogenic strain over winter and the ninfects calves

197
Q

Clinical signs of IBK

A
  • Day 1 pain –> ulcer that progresses rapidly –> may perforate by day 5-6
  • By weeks 2-3 the eye has perforated and begun to heal
  • By 1-2 months only a faint scar may remain
198
Q

Treatment of IBK difficulties

A
  • Self limiting, so epople don’t want to treat a bunch

- No one treatment is effective always

199
Q

Resistance to IBK treatment

A
  • Tylosin, lincomycin, erythromycin
200
Q

Selection of therapy for IBK: what to consider in dairy vs beef?

A
  • Dairy: milk withdrawal times

- Beef: Infrequent handling +/- respiratory disease

201
Q

Treatment for IBK

A
  • Topical isn’t realistic
  • Bulbar subconjunctival
  • Parenteral antibiotics
  • Surgery?
  • ALWAYS CHECK FDA REGS of antibiotics for food animal
202
Q

Bulbar subconjunctival antibiotics for IBK

A
  • PPG lasts ~40 hours

- Oxytet can have severe reactions - don’t do

203
Q

Parenteral antibiotics for IBK

A
  • SQ PPG lasts about 67 hours

- Oxytet may cause necrosis at injection site

204
Q

Vaccination for IBK

A
  • Controversal - incomplete protection

- True effective vaccine may be available later

205
Q

Current IBK vax recommendations in severely affected herds***

A
  • Culture and swab
  • Vaccinate 6 weeks before onset of disease season and 3 weeks before fly season
  • Calves should be vaccinated at 21-30 days of age and booster 3 weeks later
  • Adults receive 2 initial vaccines then yaearly boosters
  • DO NOT GIVE IBR (MLV) and then stress cattle
206
Q

Malignant catarrhal fever - is it reportable?

A
  • YES
207
Q

Agent of malignant catarrhal fever?

A
  • OHV2
208
Q

Signs of malignant catarrhal fever

A
  • Corneal edema, corneal ulcers, uveitis
  • Non-improvement of corneal edema is associated with poorer prognosis
  • You can’t tell prognosis based on initial appearance
209
Q

Vitamin A deficiency in cows -

A
  • Can cause blindness

- optic nerve atrophy and retinal degeneration

210
Q

Entropion in sheep and goats - how often?

A
  • Quite common
211
Q

Entropion in sheep and goats breeding recs

A
  • Do not keep for breeding
212
Q

Treatment for sheep and goats with entropion

A
  • Treat early before developing multiple issues

- Affected animals should NOT be kept for breeding

213
Q

Infectious keratoconjunctivitis in sheep and goats - most common agents?*** KNOW THIS

A
  • Chlamydophila
  • Mycoplasma
  • Branhamella
  • Moraxella bovis (IBK)***
214
Q

What is the most likely agent in a goat with a cloudy eye?

A
  • Chlamydophila percorum
215
Q

Chlamydophila percorum and effects on goats and sheep

A
  • Primary cause of KCS but also encephalitis, pneumonia, enteritis, polyarthritis, and abortions
216
Q

When do chlamydia outbreaks occur with sheep and goats?

A
  • Lambing

- Confined, high stress

217
Q

Reservoirs for chlamydia in sheep and goats

A
  • Carriers
218
Q

Immunity for chlamydia in sheep and goats

A
  • Short-lived

- Animals are re-infected

219
Q

Can Chlamydia spread between goats and sheep?

A
  • You bet it can
220
Q

Signs of chlamydia in sheep and goats

A
  • Epiphora, chemosis
  • Serous/purulent discharge
  • Lymphoid follicles
  • Severe keratitis and edema
221
Q

Diagnosis of chlamydia in sheep and goats

A
  • PCR (gold standard)

- Conjunctival cytology or culture

222
Q

Treatment for chlamydia in sheep and goats

A
  • Self-limiting
  • Tetracyclines shorten the course of disease
  • Always check FDA for current abx and treatment recommendations
223
Q

Who gets mycoplasma keratoconjunctivitis?

A
  • Older sheep

- More common than chlamydophila in sheep

224
Q

Clinical signs of Mycoplasma KCS in sheep?

A
  • Blepharospasm, conjunctivitis, keratitis (corneal vessels), uveitis
225
Q

Clinical signs of Mycoplasma KCS in goats?

A
  • Corneal abscesses with panopthalmitis can occur +/- permanent damage
  • Goats do NOT OFTEN have uveitis*
226
Q

Diagnosis of Mycoplasma KCS?

A
  • Conjunctival cytology
  • Intracytoplasmic coccobacillary and ring shaped bodies in epithelial cells
  • Culture and serology
227
Q

Treatment for Mycoplasma KCS

A
  • Self-limiting
  • Tetracycline (oxytet topically or IM) in severe cases
  • Some concern that use of tetracyclines promotes carriers in the herd

Ophthalmology (8 decks)

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