Equine Flashcards
When does puberty occur in a filly? When are mares in oestrous? When is the natural breeding season for horses in the southern hemisphere?
* 2nd spring of a filly’s life
* Mares are seasonally polyoestrous- 21 days- anoestrous period every year
* October to March is the natural season in the Southern Hemisphere
How long is the average oestrous cycle for a mare? How long is the mean duration of dioestrus?
21 days
Duration of dioestrus: 15 days
When do you do a clitoral swab, what are you mostly testing for?
Pseudomonas aeruginosa, Klebsiella pneumoniae, Taylorella equigentitalis (all causing contagious equine metritis (CEM)
When should you take endometrial samples in horses? Why?
Dioestrous
* because the uterus should be free of pathogens in dioestrous
* Exudates are easier to detect
* oedema should not be present (problem in oestrous: inflammatory or oestral oedema)
* Biopsy evaluation will be more meaningful with no oestral oedema or inflammatory cells
BUT DAY 5 or after… because the CL is responsive to PG2alpha so that you can clear out the uterus
Beware: uterus is very susceptible to infection in dioestrous
What does an endometrial sample tell us?
* Only comment on breeding soundness, not on fertility
* Helps describe mares chance of falling pregnant
* Determine if tubular or endocrine disorder present and if it can be treated
How might you induce oestrus earlier in season in a mare? How long is required until well into transition? How many hours per day?
* Artificial/ supplemental light
* Requires minimum of 60 days of stimulation (16 hours per day) until well into transition- may need 90 days to result in ovulation– maintain under lights until diagnosed safely in foal
( same effect shown with 1 hour of light exactly 9.5 hours after sunset)
How do you suppress oestrous in a mare?
* Progesterone e.g. oral Regumate, long acting injectable
* GnRH vaccines (Equity); follicular activity may not return
* Marble in uterus (only 50% successful)
* Infusion of plant oils in uterus in dioestrous (delays luteolysis in 92% when administered at day 10)
How can you synch oestrous?
* Planned matings
* AI and embryo transfer
* Silent oestrous
* Persistent CL–> allows advanced planning
* If mare is in luteal phase, PGF2alpha- luteolysis after single dose– standing oestrus after 3 to 6 days– may take longer to come into heat if small/ atretic follicles, (Granulosa (theca) cell tumour), if they are in dioestrous but less than 5 days ago won’t work, if they aren’t in luteal phase (anoestrous, silent oestrous, transitional oestrus, >35 days pregnant)
* Combined oestrogen-progesterone treatment
How does combined oestrogen- progesterone treatment?
IM injection of 150 mg progesterone and 10 mg of oestradiol in oil for 10 days, PGF2alpha on day 10, progesterone stimulates dioestrous- small amount of oestradiol suppress growth of small follicles… at time of withdrawal all mares start with new follicular wave…. At start of treatment– mares in heat: ovulate in first few days of treatment, mares in early mid-dioestrous will have responsive CL, mares in late dioestrous: will have undergone spontaneous luteolysis
Pros and Cons of PGF2alph, P& E, Regumate for synchronization of oestrous in mares?
Why would you induce ovulation in a mare?
* Accurately time OV in mares scheduled for breeding, AI
* Part of synchronization program
* Means of interrupting transitional oestrous
* Treatment of anovulation (extremely rare condition)
* Induced OV assumed to be as fertile as spontaneous one
How do you induce ovulation in a mare?
* Human chorionic gonadotropin (hCG): LH like function, IV injection of 1500 IU, results in antibody production (probably no interference with action), if given with a 35 mm follicle and some oedema 85% of mares ovulate between 36 and 42 hours— Might not work in transition when lack of LH receptors
* GnRH analogues- deslorelin (ovuplant or injectable)- ovulation between 42 and 48 hours if given as soon as largest follicle is 30 mm, implant should be removed to prevent downregulation
How should you time your ovulation induction?
* Trade off between sperm longevity vs. uterine clearance of bacteria, debris introduced by AI
* Ideally to be done at a time of insemination/breeding (except frozen semen!)
* If semen stored more than 30 hours, induce OV 24 hours before AI
When should you re-examine the mare after OV induction?
* 48 hours later, if induced early enough
* 80% of mares follow the book
* Rest might not ovulate at all that cycle
* in that case discuss if more semen is to be invested (wasted)
What are tests that determine time for breeding a mare?
* Teasing, rectal exam: palpation and ultrasound, (vaginal exam)
How do you conduct teasing with a mare?
* Most important management tool for breeders (especially TB studs)
* Preferably done by same person every day
* Keep records
* Mares must be teased regularly (ideally daily) from 3 days post-partum until 60 days pregnant
When is the mare ready to be bred?
* Ovulatory follicle: usually +/- 5 mm of same size each cycle (individual differences are large)
* Increasing oedema
* Cervix relaxes in oestrus, open in ovulation, then it closes
Problems with natural breeding
* Stallions can only breed limited number of mares, mare and stallion same location, risk of disease, injuries, difficult to assess semen quality (dismount sample)
Advantages of AI over natural service
* more mares can be bred to a single stallion
* mare and stallion do not have to be in the same location
* limiting transmission of venereal disease
* in case of incompatibility (size, temperament, physical disability) breeding still possible
*minimum contamination breeding technique possible
* semen quality can be monitored
What is the avg AI dose in equine? How do you count? How do you assess motility?
500 million progessively motile sperm, haemocytometre, motility assessment (heated phase contrast microscope) done at 37C
Advantages and Disadvantages of raw semen?
Advantages:
* Minimize injuries
* Assess semen quality
* Breed multiple mares from same ejaculate
Disadvantages:
* dirtiest of all AI methods
* Risk of iatrogenic infection especially when done in early or late oestrous
* AI does not dilate cervix as stallion’s penis would do (clearing contaminants)
How do you AI with raw semen?
* Collect, remove gel fraction, assess motility, deposit desired dose into uterus within 30 minutes
Fresh extended semen
* minimizes contamination for mares suscpetible to endometritis
* 1 part semen: 4 parts extender
* extend sample to a concentration of 25-50 million/ ml
* should be used within 3 hours at room temp
Cool extended semen
* Cooled extended semen: 75% first service conception
* not all stallions can have semen successfully shipped
* Stallion collection schedule: MWF or TTS
* Cooled to 5C
* Cooling rate critical 1C/ 3 minutes (commercially available shipping containser to cool at ideal rate)
Set time AI with ovulation induction schedule example
Frozen semen
* Advantages: semen available without regard to stallion’s racing/show schedule, can be shipped worldwide, even decreased stallion’s semen can be used for breeding
* Disadvantages: 12 hours prior to 6 hours after ovulation; advanced planning, ability of stallion’s sperm to survive freezing process, management more expensive* Management more expensive* Management more expensive
* Liquid nitrogen or vapor
* avg 30-35% success/ cycle– increase success if mare is of ideal breeding health– try on 3 successive cycles, if not by 3rd cycle switch to fresh or chilled
With AI, what should you do if the mare does not ovulate when expected?
* Owner makes the decision if that cycle has to be skipped or mare must be scanned every 6 hours to be inseminated again once ovulation is detected
* Mare should not be AI’d again until at least 18 hours after 1st AI (inflammatory uterine reaction)
Considerations with breeding a maiden mare
* Transrectal palpation, ultrasound
* If normal: vaginal check for hymen
* Uterine cylture: “true” maiden has a sterile uterus at start of season and can’t infect the stallion unless/ until bred to infected horse and/or bred ith poor technique–> good candidate for all methods
Considerations with breeding a barren mare?
Bred in prior season(s); not currently pregnant
* Age > 13-14 years??
* Vulvar conformation?
Quick review on events after sperm deposited (where?) in equine
* Sperm deposited into uterus
* fertilization in ampulla of oviduct
* transport of conceptus into uterus (5 to 6 days after OV)
* Unfertilized ova remain in oviduct
Maternal recognition:
* conceptus signals its presence by traversing whole uterus
* prostaglandin inhibitory factor produced (PIF)
* mobility phase until D 16
* then conceptus “get stuck” at the base of uterine horn
When does fixation occur in a mare? Implantation? Where does the embryo get its nutrition at this stage?
* Fixation occurs at D16/17
* Implantation D35
* nutrition through histiotroph (“uterine milk”) and yolk sac
When does early embryonic death (EED) normally occur? Causes?
* Most often before D11 (before detection) (5-25%)
* D14- 40 (6-10%)
* Causes: endometritis, endometrosis, P4 deficiency (progesterone), nutrition; stress, heat, embryonic factors (chromosomal abnormalities)
Where does eCG come from?
* Secreted by endometrial cups (EC)– EC formed from trophoblast cells invading the uterus
What are 5 alpha pregnanes?
* Progestagens of feto-placental unit
* Start rising around D 40
* sole source of progestagens from D 150
*Cross-react with antibodies used in RIA
At what day are ECs retained even if pregnancy is lost?
* after D35
What is responsible for maintenance of pregnancy until D 50? When is the secondary CL functional? When is peak progesterone? When do CLs regress?
* Primary CL resp. for maint. of preg. until D 50
* secondary CL functional after D 40
* Peak progesterone around D 80
*CL slowly regresses until D 150
When is there no value to measure progesterone?
After D 150
What is the profile of oestrogen in horse pregnancy?
* Ovarian oestrogens begin to rise at D 38-40
* D 70-80 a second rise of oestrogens from the foetal-placental unit occurs (peak D 210)
When might you give exogenous progestones?
* NOT in a mare with a history of pregnancy loss
* Anything that might cause luteolysis: endotoxaemia, high plasma cortisol levels, failure of conceptus to signal maternal recognition of pregnancy
* Suspect lack of maternal recognition: start exogenous progesterone at D 5, if pregnant on D 14 : check for CL (+/- serum P4 levels), if not pregnant: withdraw P4
How do you give exogenous progesterone before D 100 to a mare?
* Before D 100:
* first use short-acting P4 (e.g. regumate or injectable)
* if fetus still alive after insult disappears–> can switch to longacting injectable (LA)
* Check fetal viability weekly
* Withdraw over 5 days (reduce dose by 20% daily)
How do you give exogenous progesterone after D 100 to a mare?
* High doses have to be given if premature udder development occurs and fetus is still alive
* 500 mg BID
* Adjust dose according to udder
*Viability of fetus has to be checked weekly
* Withdraw immediately if fetus is dead
Pregnancy Diagnosis in a mare
* Ultrasounds from as early as D 10 (D14 routine)
* Rectal palpation - from D 18 (too late for twins)
* Oestrone sulphate- from D 44 (peak 80)
* eCG- D 40 to 120 (false positive if fetal loss)
Routine pregnancy exam in mare
* D 14 post ovulation (before D 16)
* D 25- 28 post ovulation (viability)
* D 40 often time when stud fee is due
* D 60-70 fetal sexing if they want
What are > 90% of twins in mares a result of ? What percent result in unilateral fixation? When do you crush one of the twins?
Double ovulation… 70% unilateral fixation- 83% chance that one of the unilateral twins will disappear “deprivation hypothesis”
** Crush one of the twins before fixation, in the mobility phase– after fixation– 83% should reduce to singleton pregnancy– reexamine D 33-34
If you do not catch twins before fixation what are you options?
* PGF2alpha (esp early in season)
* Transvaginal, us-guided needle aspiration (50% success that one goes to term)
* Manual crushing (not very successful)
When does placenta take over progesterone production?
D 100
A single shot of PGF2alpha on day 33 will lead to a drop in progesterone and loss of pregancy
True
What should you do if you have twin fixation bilaterally?
* Spontaneous reduction extremely unlikely, crush immediately, might still lose both, keep teasing mare
Signs a mare is close to parturition
What should you do about twins after D40?
* Season is lost
* Owner’s decision- inform about risks (dystocia, premature foals, non-viable/athletic foals)
* If he wants to take on risk: decapitation can be done later, wait and see–mare may abort due to sudden drop in progestagens when one fetus dies; both aborted– when mare develops udder prematurely (because of falling progestagens)–> assess viability of fetus & give large dose of exogenous progestagens (500 mg BID– BID = two times per day)
Speak through normal parturition in a mare– stages, time, and what happens each stage
Stage I: 1-4 hours (up to 12 hours); uterine contractions, positioning of fetus, restlessness, frequent urination, defecation, sweating, laying down/rolling
Stage II: 5-20 minutes, fetal expulsion- starts with rupture of chorioallantois (breaking water), abdominal contractions, mare becomes recumbent, rapid delivery (if > 60 minutes foal likely to die)
* Stage III: expulsion of membranes, usually delivered 30 to 90 minutes after end of stage II… RFM if not released 4-6 hours postpartum
What should you always do to ensure you don’t miss twins in a mare?
Check both ovaries
Signs and cause of placentitis? Consequence? Diagnosis? Treatment?
* Signs: premature udder development and/or udder development
* Usually ascending (e.g. Sc. equi sp zooepidemicus, E. coli, Klebsiella pneumoniae)
* Impending abortion threat believed to be due to decrease in placental progestagens
Diagnosis: transrectal ultrasound (transabdominal if haematogenous), measured CTUP (combined thickness of uterus and placenta)
* Treatment: ABs (e.g. Penicillin/gentamycin, trimethroprim sulfamethoxazole) exogenous progesterone, flunixin meglumine, pentoxifylline ** check fetal viability regularly at least weekly
Red bag- failure of cervical star to rupture
* Don’t wait to get there, tell someone to cut the chorioallantois and deliver foal ASAP
Normal gestation length in a horse? What plays a role in length?
340 days (wide range 320-365 is normal)
* Season plays a role, fetal sex of the foal
Causes a “red hood” over the foals head if cervical star doesn’t rupture but the other part ruptures
* Membranes came out with the foal
* Chorion looks oedematous
When do mares foal?
Between sunset and midnight
Indications for induction of parturition in a mare? How do you induce?
* Very few indications– e.g. prepubic tendon rupture
* Induction protocol:
- Give 10 IU of oxytocin IV
- If water does not break within 40 minutes: vaginal exam
- if straining for 10 minutes without water breaking: incise chorioallantois
- if straining for 10 minutes after water has broken: check for malpressentation/position
How common is dystocia in mares? Why does it occur?
Rare 1.5- 2.5 % of parturitions
* Mares birth canal easily traumatized
* Foals tend to get stuck with their shoulder (hip lock rare)
* Abnormal presentation, position, posture of legs or neck (‘wry neck’)
(foals are likely to die if not delivered within 60 minutes of chorioallantoic rupture)
Treament for dystocia in a mare?
* Get mare up and walking
* Epidural should be given if manipulation is not quick
* Clenbuterol injection can help relax uterus
What is the foal heat? Is it a good time to breed her?
* Ends with first ovulation post-partum
* Onset usually 6 to 9 days post foaling (5-12 normal)
* Interval shorter later in season
* Higher EED rate if bred in foal heat esp if OV before D10
** trade off between getting mare in foal as early as possible and ensuring successful outcome of pregnancy
Why is an epidural given?
Stops contractions because mare no longer has sensation of the cervix
* analgesia
Anaesthesia during equine castration
Eg for 450 kg yearling colt poorly handled: Sedate with 10-20 mg ACP usu im or iv, give about 550-600mg xylazine iv, either diazepam 10-20 mg or butorphanol 10mg or both, then ketamine about 1500mg iv bolus. This would usually give me enough time for the procedure, but if not would mostly top up with about 3-4 ml ketamine. Second top up would include some xylazine too.
Thio gives quicker response but may be better to use catheter. Triple drip if encounter problems, again use catheter.
Can use 10-20 mg ACP with 5 ml (10 mg/ml) methadone im if needle shy
RFM in a mare treatment? Consequences?
* Can try 10 IU oxytocin 45 minutes
* If no progress within 2 hours, start treatment
* Treatment:
- Broad spectrum AB (e.g. Penicillin/ Gentamycin)
- Flunixin meglumine (anti-toxic dose 0.25 mg/kg if concerns for renal function)
3 Oxytocin 10 IU
- IV fluids
- septic metritis happens very fast
- life threatening consequences e.g. laminitis, septicaemia, toxic shock and death
Diagnosis and locating cryptorchid horse
What is the most common approach for cryptorchid castration?
* Inguinal approach
First PD in a mare? Fixation occurs? When is it too late?
Day 14 PD, Fixation occurs D18 (too late)
What is this? Most common cause?
kicked when mating mares
Priapism- persistent and painful erection of the penis
What are the venereal pathogens we worry about in horses? What samples would you take?
* Equine Viral Arteritis
* EHV 3 (coital exanthema)- genital herpesvirus of equines
* Contagious Equine Metritis (CEM) caused by Taylorella equigenitalis
* Pseudomas aeruginosa and Klebsiella pneumoniae can cause uterine infections
Examination parts to Establish Fertility in a Stallion
Shire mare Bella, 12 yo, pieces of membrane hanging from vulva, foul smell, due date May 23rd (presented May 15th), udder full of colostrum, smelled terrible… Clinical exam showed: WNL (within normal limits) dead fetus in ventral neck flexion and bilateral carpal flexion. What would you recommend?
Fetotomy with IV fluids, broad spectrum antibiotics (penicillin, Gentamicin, Polymixin B), Flunixin- meglumine, Sedation (detomidine/ butorphanol), epidural (lignocaine/ xylazine)
What are the three symptom classifications of mare infertility and reasons why they might be in that category?
Why might a mare be anoestrus?
What are the types of abnormal cycle length? Examples of causes?
Causes of AHF? Diagnosis? Treatment?
Causes, diagnosis and treatment of persistent CL?
Causes of regular cyclicity but infertility?
Causes, symptoms, diagnosis, and treatment of ovarian haematoma?
Causes of cervical lesions, symptoms, diagnosis and treament of cervical lesions?
Causes, symptoms, diagnosis of endometrial fibrosis?
Causes, symptoms, diagnosis, treatment, effects of uterine cysts?
What is the most common cause of infertility in the mare? Specific species associated?
Why does Persistent mating induced Endometritis (PMIE) occur?
What are reasons a mare might be more susceptible to PMIE?
Causes of PMIE?
Symptoms and Diagnosis of PMIE?
D) Persistent CL does not have all the septa in between
** look at the other ovary to compare
** you have to look several times
* Treat with PGF2alpha, should go away– GTCT would not get smaller– the other two would
* If she is cycling normally, not a GTCT
DDX?
Twins or a cyst and an embryo
C
Common place for lesions? Common age? Where in Australia? Treatment?
* Age of onset 2-4 years (young adult horses)
* Northern Australia- warm, tropical climates
* Treatment– PREVENTION IS THE KEY– can’t have them on corticosteroids all the time (but can manage them with corticosteroids when intense)– horses indoors at dawn and dusk, spray with insect repellent, fans or drafts
Problem? Transmission? Geographically? Treatment? Signs and symptoms? Who? Diagnosis?
* Onchocerca cervicalis- common filarial dermatitis
* Adults live in nuchal ligament– microfilaria migrate through superficial dermis
* Infection transmitted between horses by Culicoids spp. (IH– larvae develop to L3)
* Worldwide
* Treatment- ivermectin (also used for routein deworming)
* Can sometimes cause a hypersensitivity to dying microfilariae (treatment can temporarily exacerbate)
* Ocular and cutaneous lesions– uveitis, conjunctivitis, keratitis, depigmentation, diffuse/patchy alopecia, erythema, scaling
* Older horses, non-seasonal
* Diagnosis: biopsy but many normal horses have microfilariae– so clinical findings, hisotry, exclusion other DDX, response to treatment
* Treatment: ivermectin (moxidectin), no effective adulticide
What? When? Diagnosis? Treatment?
* Lice- biting and sucking
* autumn, winter (carrier animals remain infested during spring, summer and serve as source of re-infestation)
* Diagnosis: lice visualized, mane, tail (sucking), body (biting), anemia with severe sucking lice infestations
* Treatment: 2-3 treatments 2 weeks apart– ivermectin (moxidectin) - sucking lice only OR topical insecticides
What are the mites that cause mange in horses?
Specific cause? When? Diagnosis?
* Chorioptic mange
* mainly on distal limbs and perineum
* Entire life cycle spent on the host
* More common in winter
* Skin scrapings
Infestations beginning on head and ears of horses and spreading to the rest of the body? Signs and symptoms? Diagnosis?
Causes? Diagnosis? Treatment? Prevention?
* Several causes:
- allergic- environmental allergens, drug eruptions, contact allergies, food allergies (rare) (Type I HS reaction– allergen causes degranulation of inflammatory cells– vasodilation usually 24-48 hours after exposure)
- common drugs causing HS reactions- penicillin, sulfa drugs, NSAIDs, phenothiazines
- physical non-immunogenic pathogenesis (rare)
* Diagnosis: systemic approach to eliminate causese (parasites, insects, drugs, vaccines, plants, feed)
* Treatment: urticaria usually resolves in 24-48 hours, corticosteroids often useful, antihistamines +/- useful, hyposensitisation- approx. 65-70% success, prolonged injection course
* Prevention: avoid cause
* Usually benign (grey horses)– malignancy more common in other coloured horses but incidence rare
* Diagnosis is usually clinical
* May interfere with normal function of the surrounding structures when large
- anus
- genitalia
- upper airway
What is it? Different types? Cause? Diagnosis? Treatment?
* Most common tumour of equids, may appear slow growing
* Fibroblastic, non-regressing, locally invasive
* Dermis and subcutis (as lesion progresses start to involve subcutis, fascia, muscle (locally invasive and aggressive))– can infiltrate through and along fascial planes and present distant to palpable mass
* Epidermal and dermal involvement–> variable, evolving appearance
* Different types: occult, verrucous, fibroblastic/nodular, mixed (transition)
* Cause: associated with BPV 1 and 2
* Diagnosis: biopsy, excise completely at same time if possible– clinical diagnosis wrong about 30% of the time
Treatment: often best left alone and monitor, early recognition and treatment improves prognosis… no universally accepted best treatment….but aim to destroy all tumour cells, minimise damage to healthy tissue, excise early with complete margins– if incomplete topical treatments a must
Diagnosis? Treatment? Prevention?
* Surgical excision, wide margins (but often difficult due to locations and general lack of excess skin in horses)
* Cryotherapy
* Topical 5-FU
* Intralesional cisplatin
*(Radiation therapy)
* (Piroxicam)
* Prevention- minimize UV exposure
Non-tumour, nodular skin disease
- Aetiology unknown, insects?
- Diagnosis
–biopsy
–Granulomatous inflammation
–eosinophils,histiocytes, some lymphocytes
•Treatment
–Surgical excision (care areas in contact with tack)
–Sublesional triamcinolone
–Systemic corticosteroids (multiple, diffuse lesions)
Possible causes?
* Habronemiasis, Pythiosis, Nodular sarcoids, SCC, exuberant granulation tissue
* Often on distal limbs
* Diagnosis: biopsy, culture, cytology
Dermatophilosis
Dermatophilosis treatment plan
* Circular lesions “ringworm”
* usually start around girth/axillary region
* spread over trunk, rump, dorsum, neck, head
* Lesions may be superficial or deep, may form crusts
* Diagnosis: microscopic examination of hair shafts, skin scrapings, fungal culture, wood’s lamp generally not useful
* Treatment: usually self limiting and lesions resolve without treatment (can take months to regrow hair)
– severe cases: medicated shampoos e.g. Malaseb, topical antifungal treatment/ washes (enilconazole), occasionally systemic antifungals may be needed (rare)– Griseofulvin (NOT in pregnant mares)
* common- causes: dermatophilosis, folliculitis/furunculosis, etc.
* Circular lesions “ringworm”
* usually start around girth/axillary region
* spread over trunk, rump, dorsum, neck, head
* Lesions may be superficial or deep, may form crusts
* Diagnosis: microscopic examination of hair shafts, skin scrapings, fungal culture, wood’s lamp generally not useful
* Treatment: usually self limiting and lesions resolve without treatment (can take months to regrow hair)
– severe cases: medicated shampoos e.g. Malaseb, topical antifungal treatment/ washes (enilconazole), occasionally systemic antifungals may be needed (rare)– Griseofulvin (NOT in pregnant mares)
* common- causes: dermatophilosis, folliculitis/furunculosis, etc.
Questions to ask regarding the equine eye
- DO NOT trim lid margin
- May need to delay surgery
- Cover eye/wound with pad covered in antibiotic cream
- Careful debridement if necessary, then suture
- Eyelid margins have a very important role - specialised tissue
- DO NOT REMOVE EYELID MARGIN
- Use appropriate suture material - 4/0-6/0 Nylon
* Purulent discharge
* Check under third eyelid
* May need ocular ultrasound
* Surgery common
Treatment: may need ocular ultrasound, surgery common- GA, exploration of any sinus tracts, antibiotics, anti-inflammatories
What will you see in corneal disease in horses? (most common ocular disease)
* oedema, vascularisation, scarring, pigmentation, cellular infiltration, other abnormal infiltrates
Tests? What can occur with this?
* Tests: corneal cytology, MC&S, fluorescein stain, wash stain from conjunctival sac, do not confuse stain uptake in corneal granulation
* Corneal ulceration–> melting cornea chemotaxis for neutrophils, neutrophils important in melting corneas, not all ulcers are infected… caused by Pseudomonas, Staphs, Strep, Fungi (more common in horses, rare in dogs)…
- you would see: usually stromal loss, toxins and enzymes released by bacteria
Treatment: topical antibiotics/antifungals, consider compounded oral antifungal medication, serum topically…surgery- keratectomy/ conjunctival graft, consider transpalpebral lavage tube, pain control important- Bute twice daily
- Use dedicated topical ophthalmic antibiotics eg. Ofloxacin - Gram negatives
- Can use fortified drops eg. fortified cefazolin (50mg/ml - add 750 mg cefazolin to 12 ml artificial tears) - Gram positives
- Fungal infections in cornea most common in horses
- Use in horses with unresponsive chronic keratitis
- Topical - Voriconazole 1% drops or itraconazole 1% ointment (compounded), fluconazole (Diflucan), silver sulfadiazine (Silvazine), miconazole
- Oral - fluconazole (compounded)
What will you see with corneal infection?
From a corneal ulcer in a horse, what is the likely bacterial spp?
Pseudomonas
From corneal ulcer in a horse
Fungal hyphae
Used after keratectomy/ conjunctival graft
Describe what you see
Describe? Treatment?
- Most corneal lacerations need surgery - suture cornea
- Need suitable instruments, suture material
- Replace iris prolapse as suturing
- Fencing wire, tree branch laceration
- If a corneal laceration is suspected, examine very carefully to prevent expulsion of intraocular contents
- Prognosis poor if laceration extends into the sclera
Tests? DDX? Diagnosis? Treatment?
Tests: Fluorescein stain, cytology, MC&S
DDX: trauma- whip/lead injuries, corneal infection, corneal ulceration
Diagnosis: Bullous keratopathy (horses cornea sucks in a lot of fluid)
- trauma- usually whip/lead injuries; corneal infection
DDX: Trauma, corneal oedema/infection, hypopyon
Tests: Fluorescein stain, tonometry
Diagnosis: acute uveitis (uncommon)… primary or secondary?
Treatment: treat primary cause, timely anti-inflammatory therapy- corticosteroids, NSAIDs, other immune modulating agents; atropine, poor treatment- loss of vision
* Adhesions- synechia; Darkened iris; cloudy pupil- cataract
Diagnosis? What are the signs and symptoms?
Chronic Uveitis (phthisis bulbi, cataract formation, posterior synechia, retinal detachment (ocular ultrasound), hyperpigmented iris, vitreous opacity, lens luxation, glaucoma)
