CMS- Preventative medicine, dermatology and opthalmology Flashcards
Dairy farmer Richard calls you up one morning in a panic because he has had 2 cows die that morning and he wants to know how he could have prevented this loss. When you finally get him to calm down after promising your help he tells you that he thought they looked ‘a bit off’ last night and had runny noses and runny eyes.
1-What are your differentials for this presenting problem?
2-What are you going to do next?
3-How could you confirm your suspicions?
1- IBR, TB, PNEUMONIA
2- history, new animals?, herd health plans, vaccine history, other farms in area, milk drop?, other animals ill? abortion? infertility?, diet change?
3- post mortem dead cattle, take samples
Dairy farmer Richard calls you up one morning in a panic because he has had 2 cows die that morning and he wants to know how he could have prevented this loss. When you finally get him to calm down after promising your help he tells you that he thought they looked ‘a bit off’ last night and had runny noses and runny eyes.
you decide to head on out to the farm that morning and take some samples if appropriate
1-What samples will you take?
2-What animals will you sample?
3-If you could only pick one, which would you choose and why?
4-What questions might you ask?
1- look for gross leasions, bacterial culture and viral pcr, blood samples form herd, bulk milk sampes from herd (antibodies) for BVD(PCR) ,IBR (ELISA), somatic cell count to indicate infection (non specific),
2- animals with resp signs, animals with higher temp, obvious discharge (sample the discharge- viral and nasal swabs),
3- bulk milk cheaper but not as much info, aloow history to inform decision- what are they vaccinated against, what have you had before, are their aniy new animals. nasal swabbing several animals more expensive
4- check housing and husbandry- ventilation? bedding? stocking density? airlow? have walk aorund farm. can you smell amonia?- has effect on breathing and cells involved in resp. any abortions?
IBR has been confirmed on farmer richards farm after the death of two cattle
you call up farmer Richard to share the news. He didn’t answer but you left a concise voicemail including your findings and to call you back if he had any questions.
An hour later you see that Richard is calling you back, clearly he wants to know more! ‘What can I do about it then? I’ve never had this problem before!’
1.What tools are in your arsenal to help him?
2.Will he be able to get rid of this disease from his farm?
- vaccination, information sheets/ leaflets, antibiotics for any secondary bacterial infections.biosecurity
2.There is no specific treatment for IBR, secondary bacterial infections can be managed with antibiotics and animals with a high fever treated with non steroidal anti-inflammatories. Preventative vaccination of the remaining herd members may aid in minimising disease spread.
they may get over the clinical disease but become stressed and shed again
he may choose to cull the infected animals to have his herd free of disease- can do this with bulk testing groups then narrowing it down to individuals
in the future ony animals from confirmed free herds could be bought
IBR (Infectious Bovine Rhinotracheitis)
IBR is a highly contagious and infectious viral disease that affects cattle of all ages. Infection occurs by inhalation and requires contact between animals spreading quickly through the group. The disease is characterised by inflammation of the upper respiratory tract. The virus that causes IBR, Bovine herpes virus 1 (BHV 1) also causes infectious pustular vulvovaginitis in the female, and infectious balanoposthitis in the male and can cause abortions and foetal deformities. IBR is endemic in the UK with around 40% of cattle having been exposed to the virus in the past. Infected cattle develop a latent infection once recovered from the initial infection and despite appearing clinically normal may suffer recrudescence of disease when under stress
Diagnosis of IBR infection is via serology (blood samples) for latent infections or direct detection of the virus (PCR or fluorescent antibody tests on ocular or nasal secretions) for active infection
There is no specific treatment for IBR, secondary bacterial infections can be managed with antibiotics and animals with a high fever treated with non steroidal anti-inflammatories. Preventative vaccination of the remaining herd members may aid in minimising disease spread.
in a case of IBR on a farm you choose to manage the disease by vaccinating
1-Why is it appropriate?
2-When would you do it?
3-What route would you choose in this case?
4-What product would you use?
5-Design a vaccine schedule for future use in this herd. There are multiple correct answers
6-Why are there different options available?
7-What cost:benefit would there be for farmer Richard?
8-What expectations might you have to manage?
9-What animals would you vaccinate?
10-How would you monitor effectiveness?
11- Are there any side effects you should consider?
1- perevents further spread and alloes as few as possible catte to be infecred/ die/ be culled. helps lessen clinical signs so is good or animal welfare
2- if using the nasal vaccine it can be done during pregnancy so the farmer is able to vaccinate whenever is convinient
3- the nasal vaccine works localy and may be most appropriate in a reactive strategy like this where timing cannot be completly handpicked
5- vaccinate every 6 months or in face of outbreak. can follow it up with IM option. calves needs to be revacinated at 3-4 months then every 6-12 months. dont give live vaccines to niave calves- decrease as case decreases
6- live intranasal vaccine treates quickly and locally without timing constraints. some options are . vaccination choice depends on speed of inset, what animals you are vaccinating ect
7- may cost far less to vaccinate than it would to loose more cattle ot the disease
8- this is a longterm problem, the disease will not be enterilry gone
9- those with obvious disease (cows), and then young stock
10- sample bulk milk tank
11- live vaccine temp rise, mild virus symptoms, hypersensitivity reaction, some vaccines can cause abrotions- vaccinate at early stages of second trimester and no later
Mrs Russell calls the practice the next day, from your previous dealings with her you know that she is a very well to do lady, extremely nice but has not a clue about looking after flock of 30 pedigree Suffolk ewes, which live a life of luxury ‘keeping her grass down’ around the manor house.
She has decided that she would quite like to show her sheep next year but is worried about her ‘little darlings’ catching disease from the other sheep, especially when they are in lamb. From speaking to other owners in her breed society she thinks that vaccination might be a good idea but she would like to know answers to the following:
1)How does vaccination work?
2)Is it always 100% effective?
3) Which vaccines should she choose to ensure the complete protection for her flock?
4)When should she give these vaccines to maximise their efficiency?
What other information might you need to ask to complete this part?
Can she give them all at once?
Which vaccine would you advise against giving to her flock?
1- triggers the body to make antibodies to disease so that in futire cases of infection the reaction is quick and clinical disease may be prevented
2- different vaccines have different levels of effectivness. depends heavily on state and age of animal. more extreme leavels of exposure means less effectivness. stress plays a factor
3) toxoplasmosis, clostridium, pasturella, enzoonotic abortion, orf and foot rot is also available but not indcated in his case
4) clostridial diseases and pasturelosis- two vaccinations are given four to six weeks apart followed by annual vaccination four to six weeks before the expected lambing date to ensure adequate accumulation of protective immunoglobulins in colostrum. Lambs are vaccinated from three to four month-old with the programme complete before weaning unless sold for slaughter before waning of maternal antibody at around four to five month-old. not given two weeks before mating and not to pregnant animasls
tox and enzo- 4 months to 4 weeks before tupping, not for use during pregnancy as is ive
orf is alive vaccine so is an unessesary risk
Puppy vaccine schedule
WSAVA VCG recommendation:
1st vaccine at 6-8 weeks old, then every 2-4 weeks until 16
weeks of age (3 or 4 primary vaccinations).
Due to the potential of MDA to last until >12 weeks of age- dobermans and rotweilers nown to last longer so titer tesing may be recomended
Most vaccines are licensed for two doses to finish at 10 weeks old to facilitate early socialisation.
1st Booster
WSAVA VCG recommendation:
DHP+Lepto at 6 months old, therefore up to 5 vaccines
within the first 6 months of life.
Most vaccines are licensed for first booster 12 months after the initial puppy course.
core dog vaccinations
Canine Distemper Virus
Canine Adenovirus/ Infectious Canine Hepatitis
Canine Parvovirus
Leptospirosis
Core for the UK, not necessarily in other countries
Adult dog vaccines
WSAVA VCG recommendation:
After 1st booster at 6 or 12 months old, vaccinate q36m (minimum interval) for DHP, q12m for lepto.
Aligns with most vaccine licenses.
Owners may request serology instead (DHP only).
Leptospirosis vaccination
Bivalent vs tetravalent vaccines:
Bivalent: Canicola and Icterohaemorrhagiae.
Tetravalent: Canicola, Icterohaemorrhagiae, Australis (Bratislava) and Grippotyphosa.
Risk based decision as to which one to use
public perception problem with lep 4
Icterohaemorrhagiae
Most commonly isolated serovar in canine clinical leptospirosis cases in the UK.
Canicola
Canine adapted; very rare since vaccination introduced.
Bratislava
Emerging serovar
Grippotyphosa
Mainland Europe only.
non core dog vaccines
Bordetella bronchiseptica +/- Canine parainfluenza virus (“Kennel Cough” vaccine)- given to dogs that mix with groups of dogs
+/- Canine parainfluenza virus
At risk animals only
Intranasal administration
Live vaccine
Rabies-
Legal requirement for travel to the EU or Northern Ireland.
Must be microchipped and at least 12 weeks of age.
Must be an inactivated vaccine or recombinant vaccine that’s approved in the country of use.
Must wait 21 days after initial vaccination to travel (day 1 is the day after the vaccination).
Boosters should be given according to the vaccine data sheet.
Vaccines must be recorded on an AHC or a pet passport (only in countries which can issue them)
Canine Herpes Virus- Only used in breeding bitches to provide passive immunity to puppies.
Leishmaniasis- Only used in dogs frequently travelling to areas where leishmaniasis is endemic.
Borrelia burgdorferi (Lyme disease
)- Can be considered for high risk individuals e.g. sports/hunting dogs
core feline vaccinations
Feline enteritis (feline parvovirus)
Cat flu (feline calicivirus and herpes virus)
Feline leukaemia (FeLV)
Only for cats that go outdoors or are in contact with cats which go outdoors.
Kitten vaccine schedule
WSAVA VCG recommendation:
1st vaccine at 6-8 weeks old, then every 2-4 weeks until 16
weeks of age (3 or 4 primary vaccinations).
Due to the potential of MDA to last until >12 weeks of age
Most vaccines are licensed for two doses starting from 8-9 weeks of age and with a 3-4 week interval, ending at a minimum of 12 weeks of age.
Where high levels of MDA are present, delaying vaccination start until 12 weeks old is recommended.
1st booster:
WSAVA VCG recommendation:
RCP (+ FeLV) at 6 months old, therefore up to 5 vaccines within the
first 6 months of life.
Most vaccines are licensed for first booster 12 months after the initial kitten course.
Adult cat vaccine schedual
WSAVA VCG recommendation:
After 1st booster at 6 or 12 months old, vaccinate q36m (minimum
interval) for panleukopenia, q12m for calicivirus and herpesvirus.
FeLV = no recommended interval.
TAKE CARE WITH INDIVIDUAL BRANDS!
Owners may request serology instead (RCP only).
Feline injections site sarcomas (FISS) have been recognised since the 1990’s.
Most often associated with rabies and FeLV vaccines.
Risk increases with multiple vaccinations given into the same site.
Requires aggressive treatment – radical excision + radiotherapy.
Very high recurrence rate.
Consider alternative vaccine sites – distal limb (alternated yearly) or tail rather than scruff
non core cat vaccines
Chlamydophila felis
Generally only for breeding colonies with a history of respiratory outbreaks.
Included in some multivalent vaccines
Rabies-
Legal requirement for travel to the EU or Northern Ireland, as per dogs.
Bordetella bronchiseptica-
Generally not used as B. bronchiseptica can be easily treated with antibiotics.
May be requested for cats going into a cattery and/or attending shows.
core rabbit vaccines
Myxomatosis
Viral Haemorrhagic Disease (RHDV1+ RHDV2)
Only one licensed vaccine now available - Myxo-RHD Plus.
Myxo-RHD Plus recommended for previously unvaccinated animals.
1st vaccine from 5 weeks old, single dose only.
Where high levels of MDA are suspected (vaccinated dam) then vaccination is recommended from 7 weeks old.
Booster q12m
Animals which have previously been vaccinated with Myxo-RHD (RHDV1 only) may not develop immunity to the RHDV2 component in Myxo-RHD Plus, even where vaccination has lapsed.
These animals should have an inactivated RHDV2 vaccine, then myxo-RHD plus two weeks later.
FILAVAC- ess side efects- VHD2 vaccine
Equine influenza vaccination
Equine influenza virus (EIV) is constantly changing so vaccine strains need updating.
EIV isolated from all over the world areanalysedto ensure strains in current vaccines are adequate.
Epidemiological data isused.
Horserace Betting Levy Board (HBLB) sponsors surveillance of equine influenza in Great Britain.
An independent panel of worldwide experts, including UK scientists, meet as part of the World HealthOrganisation’s(OIE) Expert Surveillance Panel (ESP) every year.
current recomendations 03/10/2023-
Clade 1 and Clade 2 viruses of the Florida sublineage.
These recommendations have not changed since 2010
Two vaccines available in the UK contain a recommended Clade 1 strain, only one product contains a recommended Clade 2 strain.
No vaccines against EI, nor any other infections, are 100% effective but can leson clinical signs
To ensure maximum protection, vaccines need to be given according to the manufacturer’s instructions on the product label.
Previously FEI and BHA regulations allowed vaccination within a widerrange of dates than the data sheets. Since 2022 BHA have aligned.
e.g ProteqFlu Clade 1 and 2 (Intramuscular injection)
When vaccinating against EI only
Primary course (ProteqFlu):
First injection 5-6months old
Second 4-6weeks later
Third 5months after the second followed by annual boosters
2. When vaccinating against influenza and tetanus
Primary course (ProteqFlu-Te):
First injection 5-6months old
Second 4-6weeks later
Third 5months after second with ProteqFlu-Te
Followed by: ProteqFlu or ProteqFlu-Te ensuring tetanus is covered at a maximum interval of 2years.
Pregnant mares should be vaccinated against EI and tetanus 4-6weeks prior to their predicted foaling dates using the combined vaccine.
Foals receiving adequatematernal antibody should not commenceuntil at least 6 months of age.
EI vaccination requerments for different regulatory bodies
British Horseracing Authority: horses must have been vaccinated against EI within the past 6months, and not been vaccinated less than 7days before racing.
FEI: a booster vaccination must have been givenno more than6months and 21daysprior to competing, and not been given within 7days of competition.
British Dressage and British Eventing: a booster must have been given within6months and 21daysof a competition, and notwithin 7days of a competition.
British Showjumping: booster within365days.
BritishRiding Clubs: booster within 365 days.
THIS IS THE OWNERS RESPONSIBILITY…BUT CHECK CURRENT GUIDELINES!
equine tetanus vaccination
Commonly combined vaccination with EI
Schedule:
Primary (one dose IM)
From 6months old
Second 4weeks later
Revaccination
No later than 17months after the primary vaccination course, thereafter a maximum interval of two years.
in an emergency-
Vaccine can be used together with Tetanus Antitoxin for treatment of injured horses that have not been vaccinated.
In these cases 1st dose Tevaccine+ Te antitoxin at separate injection sites.
2nd Te vaccine dose 4weeks later.
3rd Te repeated at least 4weeks later.
equine strangeles vaccination
Why?
Reduce clinical signs and occurrence of lymph node abscesses
Which horses?-
When horses are at risk of S.equi, due to contact with horses from areas where this pathogen is known to be present
Note: modified-live vaccine may trigger positive results in diagnostic tests for strangles.
strang vac- reduces clinical signs
not used routnely at risk horses
Equine Herpes Virus vaccine
Why?
Specific vaccination of all horses in a herd will raise level of protection within the population against EHV.
Reduces the risk of abortion storms
Which horses?
All horses resident on a stud farm fully vaccinated with a primary course followed by regular 6-monthly boosters.
Pregnant mares additionalboosters at5, 7, 9months of gestation.
Note: vaccine efficacy claims are made for the protection of horses against EHV 1 or 4 related to respiratory disease and abortion NOTneurological disease
can reduce respiritory signs
Equine Viral Arteritis vaccine
Why?
Notifiable disease
Stallions can by asymptomatic and spread to mares who can become clinically affected.
Which horses?
Stallions and teasers
NOT mares- causes false positives on testing
Note: horses seropositive from vaccination cannot be differentiated from those seropositive from infection. Therefore, horses should be blood tested before vaccination and a record kept of the seronegative status, certified by a veterinary surgeon, in the horse’s passport. The vaccine should NOT be administered until the blood result is available.
Other licensed equine vaccines in the UK
West Nile Virus-
Routine vaccination not recommended
Horses travelling to endemic areas should be vaccinated.
Rotavirus-
Mares vaccinated in late pregnancy to establish good colostral and milk levels for passive transfer for foals.
for stud farms with history
Rabies-
Licensed vaccine for multiple species, may be indicated for travelling animals.
cattle vaccines
BVD
IBR
Leptospirosis
BRD (Bovine Respiratory Disease)
Calf Scour
Salmonella
Ringworm
Mastitis
Lungworm
Clostridia
Arboviruses (Bluetongue, Schmallenburg)
sheep vaccines
Clostridia
Abortion (Toxoplasma, Enzootic)
Pasteurella
Footrot
Orf
Ovine Johnes Disease
factors that influence farm vaccination scheduals
What management practices are in place?
What could be altered to reduce infection pressure? E.g. better biosecurity, housing improvements, sourcing policy
Which pathogens are present or present risk to the herd?
E.g. BVD naiive herd that buys in cattle of unknown status and is not monitoring vs high health herd that never buys in cattle and performs regular and consistent monitoring
Are there any
zoonotic concerns for H+S of staff?
E.g. leptospirosis
What is the cost:benefit to vaccinating?
E.g. Vaccinating a herd against salmonella could cost thousands of ££, if herd has never had a confirmed case then it is of little benefit
When is the best time to vaccinate?
Must take in to account risk factors, stage of production, farmer compliance
E.g. All heifers should receive effective protection from BVD prior to first service
What are the practicalities for the farmer for carrying out the vaccine?
Timing, dosage, route, etc (READ THE DATA SHEET!)
Do they have the time/staff/facilities/kit/motivation?
aims of cow BVD vaccination
Aim of vaccination: prevent creation of new PI animals
2 main products available
Bovilis – requires primary course then yearly booster (inactivated)
Bovela – single dose vaccine on annual basis (modified live)
To be effective: animal must have responded to vaccine before service (typically 2w lag time from vaccination)
12m protection after primary course
Block calving systems vs AYR herds
Youngstock can slip through the gaps!
managment of calf scour through vaccines
Who are we vaccinating?
Immunising the COW to ‘vaccinate’ the calf
Dam responds to vaccine by producing antibodies- Enriches dam’s colostrum to deliver immunity to the calf
Requires correct timing of vaccination
Requires excellent colostrum management
Timing of collection AND delivery to the calf
Volume
Frequency
Hygiene
Protective against Rotavirus, Coronavirus and E. coli
Calf scour diagnostics essential!
management of calf pneumonia through vaccines
Intranasal Vaccines-
Provides localised, rapid, short duration (typically 12w) immunity
Avoids maternal antibody interference
Primes upper respiratory mucosa
Protective from 3-4d post vaccination
Give from young age (mostly 7d+)
Parenteral Vaccine -
Protection is systemic, longer in duration (6m) but slower onset of protection
Requires primary course and therefore repeat handling
Protective from 2-3w post vaccine
Give from 2 weeks of age
May be influenced by MDA
Around 8 weeks from first injection to develop immunity!
2 doses 3 weeks apart from 2 weeks of age with a 3 week onset of immunity!
grains are
enerrgy based feeds
silages are
fibre based feeds
ketosis
generation of acetate in the liver for the utilisation of fats requiers proprionate from the rumen (made by fermenting high enerfy firrage such as grains)
if there is not enough propionate th eliver will continue the process but go into ketosis instead and produce ketone bodies
Ketone bodies consist of β-hydroxybutyric acid (βHBA), acetoacetic acid (ACAC), and acetone (AC)- smell sweet on breath
Clinical signs
Earliest signs - reduction in milk yield and a smell of ketones on the cow’s breath (sweet smell).
As severity progresses - appetite falls, followed by decreased liveweight, and faeces which are hard and dry. The cow may also walk in circles.
prevention and treatment of ketosis
managemnt of energy and transition managment
Steroids/ glucocorticoids - both of which are immunosuppressive (need to rule out infection)
Products to boost blood sugar. For example, glucose can be given by intravenous injection
Management of cow body condition score and manipulation of dry cow diets to maximise intake potential - maximise propionate
cows that are overconditioned eat less and are more likley to enter ketosis
milk fever
high milk yeild issue
older cows more suseptable
demand for calcium exeds the rate the parathyroid gland can manage it
Clinical signs
Initially low concentrations of blood Ca lead to hyperexcitability of the conducting membranes - tetany.
In latter stages of the condition - muscle paralysis takes over from the hyperexcitability.
Characteristic S-bend of the neck.
treatment and prevenntion of milk fever
Calcium administered by intravenous injection usually in the form of calcium borogluconate (cow should receive at least 12 g in one dose) - 400 ml of a 40% solution.
Low calcium diets during the dry period - almost impossible with grass silage. maize and straw good combo
Adequate magnesium and phosphorus intakes.
Optimise intakes - same as ketosis.
Optimise dietary cation-anion balance (DCAB) to acidify the gut.
Calcium bolus.
Hypomagnesaemia (grass staggers)
magnesium levels rely on sufficient intake of magnesium at all times. body does not adiqutly store it
lush grass growth in spring / late flushes in autumn doeas not contain sufficient magnesium so animals grazed on this are at risk
Clinical signs-
Magnesium acts as an electrical suppressant of muscle and nerve activity.
Deficiency therefore results in signs which are opposite to this - excitability.
Hypomagnesaemia (grass staggers) Treatment + prevention
If suspected - try to avoid exciting the animal. Magnesium therapy should be given as soon as possible.
Magnesium is not stored, and so prevention is achieved by a regular dietary supply of magnesium.
Animals are at high risk when grazing lush pasture in the spring and autumn months- magnesium supplementation of drinking water or buffer feed during these months with dry forage.
Free access high-magnesium minerals or magnesium bullets.
Improve the magnesium content of grass swards - stitch in clover/regular liming/avoid high-potassium fertilizer.
Ruminal acidosis
Causes
Cattle fed forage have a rumen pH of 6.0-6.5.
pH scale (0-14), pH 7 is neutral, <7 is acidic, >7 is basic
High concentrate diet = lactic acid production by lactic acid producing bacteria causing a drop in rumen pH.
Rumen pH below 5.0 = rumen stops contracting
pH below 4.5 = fluid is drawn from the blood into the rumen to try and dilute the acid, lactic acid leaks back into the blood stream, animal enters shock
highly fermentable feeds creat vfa and drop rumen ph- wheat very dangerous
Clinical signs -
Rumen pH below 5.0 = loss of appetite and decreased weight gain
Rumen pH below 4.5:
foul smelling yellow scour (diarrhoea) containing undigested grain
Late stages = dull, lethargic, panting, sunken eyes, start to stagger, and difficulty standing up
Laminitis??
Simply inflammation of the laminae (site of horn production)
Enteric disease - ruminal acidosis
smeel it before you see it
ruminal acidosis treatment
Treatment
A little too late (Prevention before cure)
Consult herd nutritionist:
Increase forage (fiber) content of the diet = grass silage/straw - stimulates rumination where the saliva produced (bicarbonate and phosphate) is swallowed and increases rumen pH
To feed artificial neutralising agents = Acid buff (rumen buffer)
ruminal acidosis prevention
Always offer long fiber (e.g. straw) to encourage rumination. Intake likely to be ~1.5 kg/day
Gradual adaptation to concentrate diets, over 2 weeks or longer
Do not feed finely ground cereals = powdery texture gives a greater risk of acidosis - formulate diets according to their rumen stability
If not feeding concentrate ad-libitum (all you can eat), avoid meal sizes greater than 2.5 kg/head
When feeding ad-libitum, never let feed hoppers run out as animals can gorge themselves when they are refilled. If you do, you may have to restart adaptation.
RSV balence
a scale used to determine the risk of acidosis from diet
Allergic skin disease
Common cause of pruritus
Particularly in companion animals
Can be triggered by
Ectoparasites
Environmental antigens : Atopic dermatitis- Domestic mite proteins, pollens, moulds, microbial
Foods (hypersensitivity cf intolerance)
Contact allergens
Drugs
allergerns trave across a potentially defective skin barrier and activate t lymphocytes
activated t cells release cytokineswhich act as messengers
certian cytokines activate an intch respone by binding to receptors
others stimulate inflamation
t heper cels stimulate class awithcing in b cells which produce allergen specific IGE
this means it is ow sensitised to the allergen
mast cels bind the ige and also become sensitised and sit in wait of the allergen
Atopic Dermatitis
Affects 10-15% dogs in the population….. Common!
Classic definition = ‘Inherited predisposition to develop a Type I hypersensitivity reaction to environmental allergens’
SENSITISATION: Epidermal barrier defect
Type 1 Hypersensitivity
Type (immediate) hypersensitivity
Occurs with ~30 mins
IgE mediated
Serum IgE bound to high affinity receptors on mast cells and basophils
Degranulation via antigen contact releaseing histamine, heprin, orotyitic enzymes
Leukocyte stimulation occurs
Direct neuronal stimulation on re-exposure
Presents allergen to primed Th2 cells
Proinflammatory cytokines released (e.g. IL-31)
Activation of JAK enzymes
Stimulation of nerves
this is a pathway that bypasses IGE whcih can expain why when testing the IGE is somtimes not a sensitive method
drugs to treat allegric skin disease
Consider-
Owner compliance
Efficacy
Cost- its a lifelong problem!
Side-effects of medication
Manage owner expectations!
Communication is key!
1.Glucocorticoids
2. Ciclosporin (cyclosporine)
3. Oclacitanib (Apoquel)
4. Lokivetmab (Cytopoint)
5. Antihistamines
can be used in combo with other theraputics such as Essential Fatty Acids
Allergen-specific Immunotherapy
Medicated Shampoos
Use 1-2x weekly – allow adequate contact time before rinsing!!- allows itch scratch cycle to be broken and managing secondary infections
Physical Prevention of self-trauma
Glucocorticoid tablets – effective in nearly 100% cases
Ciclosporin – effective in approx 80% cases
Oclacitanib – effective in approx 70% cases
Lokivetmab – effective in approx. 75% cases
Immunotherapy – effective in approx 65% cases
Antihistamines – ?effective in approx 20% cases
EFAs – effective in approx 20% cases (but benefit barrier function)
Medicated shampoos – helpful to treat/prevent infection, soothe skin
Antibiotics – effective when infection present
side effects reduce as eficacy reduces
Glucocorticoids
Mode of action:
pass through cell memberanes and bind to high affinity receptors in cytoplasm of all cells. then migrates to nuclues
- act on both cell mediated and humoral immunity
- induce transcription of anti-inflammatory genes
- decrease production of inflammatory cytokines, enzymes and receptors
Low dose:
Anti-inflammatory
High dose:
suppress antibody production
lymphotoxic
Different Glucocorticoids have different potencies and absorption rates:
Oral GC are rapidly absorbed
Parental GC can be:
Soluble – rapidly absorbed, last days
Insoluble – slowly absorbed, last weeks
Efficacy and Side effects -
Highly effective treatment and acts rapidly and cheapest.
* But most side-effects…
→ And dose-dependent so use the lowest dose possible!
Short-term
Polydipsia, polyuria, polyphagia
Panting
Long-term use
Liver problems
Bladder infections
Diabetes mellitus
Muscle wasting
Gastric ulcers
Pancreatitis, hair loss
Skin changes e.g. thinning, calcinosis cutis in dogs
Pyoderma…
+ suppression of HPA axis, esp if daily dosing
Use systemic glucocorticoids only when necessary – eg
Short-term treatment of severe pruritic flare-up
During early stages of immunotherapy to give immediate relief whilst waiting for therapy to work.
Seasonal pruritus requiring only 3-4months’ treatment per year
When other treatments inadequate
When financial constraints preclude other treatments
oral glucocorticoids
Prednisolone (most common) or methylprednisolone (more expensive) most appropriate
Anti-inflammatory vs immunosuppressive doses
Start daily (eg 0.5-1mg/kg prednisolone sid) then reduce to lowest effective alternate day treatment (aim for <0.5mg/kg prednisolone eod)
Taper gradually – never stop suddenly! - (Risk of iatrogenic Addisonian crisis)- mimic natural glucocorticoids and can stimulate feedback loop
injectable glucocorticoids
Long-acting injectable glucocorticoids
higher risk of HPA axis suppression
poorer dose control with the injectable forms (cf oral forms)
* methylprednisolone acetate (Depomedrone V)
→ 6-8 weeks of action
Topical glucocorticoids
Used for pyotraumatic dermatitis (surface pyoderma)
Also for short-term flare up affecting small areas.
Wear gloves!
Some contain antibiotics (e.g. fusidic acid)
Consider potency of glucocorticoid…
Higher potency products (containing betamethasone/dexamethasone) can be used initially, but 1% hydrocortisone preferable for long-term use.
Hydrocortisone aceponate-
spray - converted to more potent steroid in skin (with similar potency to betamethasone)
But
less systemic absorption/HPA suppression
less skin-thinning
Licensed in dogs for 7 days’ use
Allows us to deliver a topic steroid without an antibiotic
Hydrocortisone aceponate
Topical glucocorticoid
spray - converted to more potent steroid in skin (with similar potency to betamethasone)
But
less systemic absorption/HPA suppression
less skin-thinning
Licensed in dogs for 7 days’ use
Allows us to deliver a topic steroid without an antibiotic
Ciclosporin (cyclosporine)
Anti inflammatory/Immunosuppressive
Licensed for atopic dermatitis in dogs and cat
when t cells are activated it causes intracellular calcium to be released. this causes calcineurin to be released. this activates transciption factors which cause proinflamitory cytokines to be released and stimulate b cell production of ige
Action: Calcineurin inhibitor
Blocks release of inflammatory mediator molecules
eg cytokines, interleukins
Inhibits cells of allergic reaction
eg T lymphocytes, eosinophils, mast cells
Reduces pruritus & inflammation
Atopica - capsule for dog, liquid for cat
Care - potential interactions with drugs involving:
Cytochrome P450 – metabolises ciclosporin –> inactive/weakly active metabolites
Drugs also metabolised by cytochrome P450 potentially result in increased bioavailability
Erythromycin: 2-3x increase in CsA levels
Enzyme inducers reduce bioavailability – phenobarbitone
P-glycoprotein – drugs inhibiting efflux pump → increase bioavailability → increase brain penetration –> potential toxicity
Ketoconazole: 2-3x increase in CsA levels
THOROUGH HISTORY
For dogs:
Efficacy
Effective in approx 80% cases
Slower to effect than glucocorticoids – upto 4-8 weeks for full effect
Side-effects
Generally well-tolerated
Often initial vomiting/diarrhoea but usually settles
In dogs, occasional reversible anorexia, hirsuitism, gingival hyperplasia, papillomatosis
BETTER TOLERANCE WHEN GIVEN WITH FOOD
Some risk of immunosuppression -
Bacterial infection, demodicosis, dermatophytosis
Avoid use 2 weeks either side of live vaccination
Not for use in
dogs <6 months old or <2kg in weight (no data)
breeding, pregnant or lactating animals (no data)
animals with history of malignant disorders - as we are suppressing the T cells which are suppressing the neoplasia.
Diabetics - may affect circulating insulin
Renal insufficiency
Alongside drugs metabolised by cytochrome P450
For Cats:
Liquid oral ciclosporin for cats (Atopica Cat®)
Need to test for FeLV, FIV and toxoplasmosis prior to commencement of treatment
Mild GI signs and weight loss are most common adverse effects
Tacrolismus-
0.1% tacrolimus (Protopic)
Topical calcineurin inhibitor (unlicensed in animals)
Can be helpful for small hairless areas – apply twice daily, wearing gloves
Apparently minimal side effects; possibly mild stinging on application
Costly and oflicence
Oclacitanib (Apoquel)
Licensed only for pruritus associated with allergic skin disease, particularly clinical manifestations of atopic dermatitis. Dogs only.
Effective 60-70% cases
Rapid onset (as fast as prednisolone in most cases) - see a response within 24 hours - 1 week.
dont need to taper
Useful for short-term and ?long-term use (need to monitor with periodic haematology/serum biochemistry)
Mode of Action
JAK inhibitor (JAK1 and JAK3)- binds to it and blocks the transduction pathway to prevent stimulation. breaks itching cycle
Prevents direct stimulation of nerves causing pruritus (inhibits action of IL31)
Reduces inflammation
Side effects less than prednisolone (vomiting/diarrhoea most common)
Does not interfere with intradermal testing/IgE serology
Can vaccinate during treatment (unlike cyclosporine)
Not for dogs <1yo or <3kg
May increase susceptibility to infection
Not if immunosuppressed/ with progressive neoplasia (untested)
Not in pregnancy/lactation/breeding males (untested)
Lokivetmab (Cytopoint)
Caninised IL-31 monoclonal antibody
Highly specific
Only licensed for dogs
Reduced side effects
Long half-life Monthly (q.28 days) SC injections
Fast acting within 8 hours (full efficacy 1-3 days)
Can be used with concomitant disease, alongside vaccinations, all age groups
Not to be used in dogs <3kg
Mode of Action
IL-31 Monoclonal Antibody
Binds IL-31 extracellularly to prevent binding to it’s receptor
Antihistamines
Block H1 histamine receptors of C neurones (+/- some central sedative effect)
Several different types – individual response varies so try several, each for 14-21 days, before excluding
Not very effective, but may allow reduction of dose of other drugs
Unlicensed in animals
May help with mild pruritis.
Side effects
Rare except drowsiness – care especially with cats!
Reported: anorexia, vomiting, cardiac arrhythmias, excitability
All off-license as they are human drugs.
when trying antihistamines try severla types and give enough time to work (few weeks)
Essential Fatty Acids for allergic skin disease
Improves the skin epidermal barrier function
Most important oils:
Gamma-linoleic (GLA)
Linoleic
Alpha-linoleic
Eicosapentanoic acid (EPA)
2-3 months for them to get to efficacy
~20% response rate
Use in combination with other therapies
fly eye/ ibk
new foreest diseas/ pink eye
gram neg bacteria moraxella bovis- can be cultured from normal eyes too
clinical signs-
lacrymation
blepharospasm
kaeratitis to varying degrees (test with fluorecein)
can progress to ulceration, corneal pannus vascularisation
spred by flys
cmost often seen in summer but also in winter in housed cattle
initially just serious tear production, then conjunctivitis, reddening of eye, sensitivity to light
risk factors- flys
woodland
sust/chaff
uv light
viral pneumonia- reduced immune system + occular discharge?
prevention-
fly control- pour on/ ear tag/permethrins/ parasitic waspa/ slurry managment
graze away for wodland (prime fly habitat)
correct ventilation
vaccine available
treatment for fly eye
long acting eye ointment- cloxacillin
systematic/ subconjunctival injection-
amoxyxillin/oxytetracycline
systematic solutions use more antibiotic
best placed in bulbar conjunctiva
can suture 3rd eyelid + eyelid closed- nerve blocks
pain relief!
silage eye
linked to big bale silage feeding- seen in winter
secondary to trauma?
listeria monocytogenes infect conjunctiva
clinical sigs-
pupil consticted
blepharospasm
corneal opacity
fluacoma
fibrin acumulatons in anterior chanmebr
can progress to corneal vascularisation
when compared to IBK
sings on inside of cornear
negative result with flwurosine, no corneal ulceration
silage eye treatment
acute-
good response to oxytetracycline (2-3ml) mixed with 0.5-1ml of dexmethasone injected into conjunctiva
topical atropine if miosis present
chronic case-
treatment of little effect
can reslove without treatment
prevention-
remove ring feeder!
atterntion to detail on bailing and wrapping silage to prevent listeria monocytogones growth- dont leabve bales too long
cancer eye
squamus cell carcinoma
common in older beef cattle (>5y) breed dispositions in heriford and simmental cattle
uv exposure
can occur anywhere in subconjunctival sac
usuallin 3rd eylid/ conjunctival membrane
clinincal presentaion -
unilateral blepharospasm + ocular discharge
swelling and tumour grows
local invasion of occular tissue
managemnt-
third eyelid envolvment- surgical exision under loca
more serious- enucliation
can re-occur- pretty high, most procedures are to get the cow to some short term goal (abbitoiur ext)
enucliation-
standing surgery- zylazine sedation and retrobulbar block
suture eyelid toghther
blunt dissection of conjunctival tissues to scces retrobulbr space
ligate optic vessels if possibel control haemorage with orbitabl packing)
remove eye by cuting optical nerve and vessles
suture eyelid margines together (simple interupeted)
packing removed 3-5 days later
malignat cattarhal fever
seen sporadically
affects single animal
caused by ovine herpes virus 2-
contact with sheep and goats, no cow to cow transmission
clinicla signs-
head and eye form most common
suddent onset depression anorexia and pyrexia (40.5-42)
eyes- congested, blateral kerititis and corneal opacity
mucopurulant discharge
leads to blindness
nasal dishcharge and crusting/ sloughing of muzzle in some case
stomatitis on oral exam
generalised peripheral lympadenopathy
enteritis > diarrhoa
mild chronic form reported- poorly grown youngster, suspicous of bvd but antogen negative, ab post for mcf
ciagnosis- clinical signs + MCF ab+ve on serum / post mortem findings
prevention- avoid sheep cotact
Secondary IBR
herpes virus- BHV1-
latency of disease
recurdesense - stress
vaccine available
clinical signs-
pyrexia _ t= 40 +
conjunctivitis + discherge
coneal odema
nasal lesions + discharge
respiritiory pathology inclusing trachitis
acute milk drom
secondary listeriosis
listeria monocytogones
infection via trigeminal or facial nerve
clinical signs-
encepahlitis- circling disease
unilaterak facial paraycis (droopy eye, ear lip)
depressiqon
pyrexia
abortions
blindness (-ve menace test)
sry eye keratitis
occular presentation of BVD
Cataracts
occular presentation of endotoxaemia
conjected conjunctiva
occular presentation of septicemia
hypopyon (assosiated with meningitis)
pus in anterior chan=mber
occular presentation of dehydration
sunken eyes
eye exam from a distance
Observe movement
Shape of the face and eyelids
Position of the eyes
Position of eyelids
Blepharospasm
Epiphora
Discharge
Shine a light from distant
Conformation of orbit and periocular region (brachy dogs and cats) and there blinking
Looking at symmetry of the face.
Eyelid length, fissure length
Position of the eyes, is one more swollen or is there exophthalmus – anterior protusion of the eye.
Exophthalmia – protusion of globe, enophthalmia sinking in of globe, buphthalmia – enlargement of globe size
Blepharospasm – spasm or closing of the eyelids which is generally due to ocular pain. Upper eyelash angle – horses with longer eyelashes
Tearing also known as epiphora
Discharge, mucoid, crusty discharge (KCS), mucopurulent discharge - infection
Shine a light from a distant to assess the way the light travels through to the back eye. We are looking for a tapetal reflection, the tapetum is like a mirror in the back of the eye which reflects light back at us. This sits within the choriud deep to the retina and is not present in all species. In domestic animals it is usually gives a greeny reflection but sometimes can be red or blue. We are also assessing if we can see anything blocking our line of view with the light for example a cataract.
SCHIRMER TEAR TEST
First test performed, sometimes even before neurophthalmic examination
Measurement of the aqueous component of tears
Normal range in a dog 15-25mm/min
Dry eye (Keratoconjunctivitis Sicca) is <15mm/min
Perform early due to the light stimulating tear production
Tears are made up of three components, aqueous or water component, lipid component and mucus component. The aqueous component makes up 90%
Dogs – KCS most common
Common misconception is that discharge means not dry but can over produce mucus but be devoid of aquoeus component which is the majority of your tear film
The test strip is bent at the notch and the short portion is placed inside the lower eyelid (ventral conjunctival sac).
Place between the eyelid and the cornea, without poking the cornea and the dye on the strip is going to tell us the numerical value
Fear, sedation and general anaesthesia all reduce the values, ulcers and entropion (rolling in of eyelids), find out when the owner last gave topical medication as this could falsely elevate the resultcan result in a falsely elevated reading. lateral to middle third of the lower lid. The strip is in contact with the cornea as reflex tear production
NEURO-OPHTHALMIC EXAMINATION
Neurophthalmic reflexes: Disturbances to any cranial nerve pathways peripherally or centrally:
Loss of vision
Loss of pupil movement or different-sized pupils (anisocoria)
Loss of the ability to blink
Loss of sensation to face, eyelids, cornea.
Abnormal globe position – strabismus, nystagmus
Neurophthalmic reflexes: Disturbances to any cranial nerve pathways peripherally or centrally:
Loss of vision
Loss of pupil movement or different-sized pupils (anisocoria)
Loss of the ability to blink
Loss of sensation to face, eyelids, cornea.
Abnormal globe position – strabismus, nystagmus
Will have been covered in other parts
Eye has CN 2,3,4,5,6,7,8
Vision, Eyelid muscle innervation, Extraocular muscle movement, corneal sensation, blinking, vestibulocular reflex
Crude assessments but helpful
Neurophthalmic just means a merging of the nervous system and the ocular system. Neurophthalmic reflexes are the way we test these nerve systems are working. With these reflexes. If there is any disturbance in this communication between the brain and the eye it can interfere with the neurophthalmic reflexes.
Menace response
Following or placing reflexes
Maze test or obstacle course, tracking reflex
LACK OF MENACE DOESN’T MEAN IRREVERSIBLE BLINDNESS!
Menace from 12 weeks in puppies and kittens
Menace from 14-16 days in foals – slower in foals with postnatal problems
Be careful not to move to quickly to make noise / with a watch etc. produce air movement and not to elicit a tactile response by touching whiskers. We can also assess vision by following tests with a treat or cotton ball. Also dropping the cotton ball and see if they follow it.
A placing reflex is when you cover one eye and move the small dog or cat towards the edge of the table and they should on seeing the edge of the table lift a leg onto the table so as to not hit it with their leg.
Maze tests with obstacles on the floor, so you can place them on side of the room call them and see how they navigate to you. Can be done in normal and dim light.
Dazzle reflex
Direct pupillary light reflex
Consensual pupillary light reflex
Palpebral reflexes
Dazzle present from birth
Dazzle reflex is a bright light response so when a bright light is shown into the eye the eye blinks.
Pupillary light reflexes are when you shine a bright light into the eye and you get pupil constriction which is a called a direct pupillary light reflex. You have probably seen this diagram before but this explains that when the light is shone into the eye is travels done a nerve pathway to the brain and back to the pupil to cause constriction.
The consensual pupillary light reflex is when you shine a light in one eye you get constriction of the pupil in the other eye.
DON’T interpret lack of menace response to be blindness if you haven’t checked palpebral reflexes
adnexa
tissue around the eye – eyelids, extraocular muscles, fascia, orbital bones
OPHTHALMIC EXAMINATION of the cornea
Ulcer
Abscess
Pigment
Oedema
Mineral
Inflammatory infiltrate
Vessels
Limbus junction of bulbar conjunctiva and cornea grey / pigmented line
Iridocorneal drainage angle (pectinate ligments on `Descemets membrane’ not seen in dogs (because of presense of scleral shelf), some cats but generally driect gonioscopy lens or indirect gonioprism required but can be seen in horses
Main problem we see if ulcers.
So the cornea is lots of layers like an onion the layer to the outside is the epithelium and any break in this layer is termed an ulcer. The the depth of the ulcer can be at any point through these layers until we get to the deepest layer before an eye ruptures that type of ulcer at the last layer is a descemetocele and is at significant risk of rupture. So a few pictures of ulcers.
We also see mineral deposits in corneas, FBs corneas, inflammation or keratitis.
Vessels time
Ciliary flush vs arborising vessels - keratitis
OPHTHALMIC EXAMINATION of the by adnexa
Eyelids – hairs (distichia,ectopic cilia, trichasis), masses, entropion, ectropion
Conjunctiva – bulbar and palpebral
Nictitating membrane or third eyelid
What we mean by adnexa: tissue around the eye – eyelids, extraocular muscles, fascia, orbital bones
Size of eyelids – already assessed in distant examination but again when examining eyelids
Eyelid: upper more mobile in mammals, lower in birds, Hairs: distichia, trichasis (periorbital hairs - contacting the cornea), medial entropion, ectopic cilia, masses, meibomion glands – sebaceous secretions as part of tear film
Bulbar conjunctiva is the conjunctiva that over the eye and palpebral in on the inside of the eyelids – conjunctivitis cats (infectious cats, allergic in dogs - unless been abroad)
NM: any thickening, masses, FB, cherry eye (prolapsed nicitatans gland)
NL puncta hard to seen with ophathlmoscope usually need magnification but about 2-5mm from medial canthus dog and 8-9mm in horse and usually at pigmented / non pigmented junction. Or surrounding pigment
Lacrimal caruncle just inside medial canthus – can be haired and normal
Complete fusion of upper and lower eyelid creates spectacle in snakes and geckos
TONOMETRY
Tonovet
Tonopen
Ideally prior to dilating the pupils
Measurement of IOP
Tonovet most practices
Rebounds a probe and measures the returning velocity - does not require local anaesethsia but tonopen which is applied directly onto the cornea requires local anaesthesia as it measures the pressure that is required to flatten the cornea. contacting surface of cornea
Variastion between machines know your practices normal – if you have more than one machine try to record which machine or use the same one
Avoid restrain
Pressure on eye of jugular
Sedated horse, head in normal position – above heart
All falsely elevate pressure
Tonopen can read a little higher but if consistent with technique then you can get consistent comparisons
Make sure not putting pressure on the globe
Tonometry can be either performed with a pen with contacts the eye so topical anaesthesia is required for this method or a rebound probe which
FUNDOSCOPY
Fundoscopy – term for examination of posterior segment so vitreous, retina, optic nerve
Direct – close and looking through ophthalmoscope.
Indirect -
Vitreous should be clear
Discolouration in uveitis is horses – leading cause of blindess in horses, especially appaloosas and spotty horses, especially ERU which can have posterior component with inflammatory deposition in the vitrous
Vitreal degeneration in older dogs, dots suspended – asteroid hyalosis (crystalline formation), snow globe effect (synchysis scintillans) can be seen on ultrasound
DIRECT
Using refractive power of patients cornea and lens
Magnified real view
Systematic approach
Describe things in relation to ONH and clock face
INDIRECT
Image inverted and reversed
Aerial view
Less magnification, wider field of view
Different diopters of lens: different field of view and magnification
OPHTHALMIC DYES
Fluorescein stain
Jones test
Rose bengal stain
FLUORESCEIN STAINING
Most commonly used for detection of ulcers but can detect conjunctival ulceration or erosions too.
Used to assess tear film and the rate at which the tear film dries / disipates on the cornea – tear film break up time
Slit lamp or ophthalmoscopy have a blue light on it to highlight the fluorescein dye even further so we have a picture of fluorescein stain on a ulcer in the light and then with the blue light.
Fluroescein lipophobic so runs off the lipid containing cell membranes of epithelium but fluorescein is hydrophilic so adheres or absorbed by any stroma
Fluorescein does not stain Descemet membrane so if you have a deep ulcer where the edges highlight with fluorescein with exposed stroma on the wall of the ulcer
`
JONES TEST
Assessment of nasolacrimal drainage fluorescein dye applied to eye and evaluate from nose
Jones test is the timing of the passage of fluorescein through the lacrimal system to the nose to check the nasal lacrimal patency.
Remember in some brachycephalic breeds it can drain into the mouth
ROSE BENGAL
Not a vital stain
Hear it talked about for assessment of tear film and tear film abnormalities
Superfical erosions of cornea or conjunctiva– cats with conjunctivitis but often fluorescein will show these lesions anyway
Horses – superficial corneal abnormalities so can help in early detection of SCC
Dyes can come as strips or pipettes
Only use a small amount
Wet the strip, put on conjunctiva not the cornea
when to use CYTOLOGY, CULTURE AND SENSITIVITY for opthamology
Any fluorescein positive lesion especially with opacity
Any ulcer which has a dimpled type appearance
Any corneal ulcer where corneal not holding normal shape
Cytology results can be done in house quickly or give results quicker than culture results
Take two slides
CT, MRI, SD-OCT, pachymetry, fluorescein angiography or green
Can immediately influence course of treatment
Fungal hyphae
Bacteria – cocci / rods
Neutrophils infection
Eosinophils
Epithelial cells
Diff Quik or Gram stain in house
One in house
Send one away
Ultrasound globe size pressure applied varies
Corneal oedema cant see through
Uevitis closed pupil cant see through
Lens in correct position
Swirling in vitreous
Strands in vitreous
categories of topical opthalmic medications
Antibiotics
Antifungals
Nonsteroidal anti-inflammatories
Steroids
Lacrimomimetics / Lacrimostimulants
Pressure modulators
Mydratics
Solutions
drug is totally dissolved in a given solvent
Suspension
sterile products containing solid particles of active ingredient dispersed in a liquid. Shake before use
Ointment
semi-solid substance, gels, creams
considerations in formulations of eye medication
Solution: drug is totally dissolved in a given solvent
Suspension: sterile products containing solid particles of active ingredient dispersed in a liquid. Shake before use
Ointment: semi-solid substance, gels, creams,
Preservative vs Unpreserved
Topical medications
absorbed cornea, conjunctiva, sclera- typically poor penetration into anterior chamber
Lost through blood or nasolacrimal system
Solutions and suspensions have as near to physiology tear pH as possible humans 7.0-7.7
Osmolarity similar to that of humans – a range of osmolarities recored in tears of dogs, cats, horses but the eye seems to tolerate a range of osmolarities
May contain buffers or organic or inorganic carriers
Drug Particles in a suspension less than 10um and uniform in size
More possibility of irritation with suspension – disperse particles throughtout
Enhanced contact time so can decrease the freq of use
Disburance of tear film so can blur vision more administration
Unpreserved refridgerated 2-8 C
Disposed after 7 days
Opened bottles disposed of after 28 days
Fluroscein- can support significant bacterial contamination once opened
Formulations are important with how they penetrate into the eye
Drugs can be converted from prodrugs which are inactive into active parent drug once reached a certain area of the eye
The way different formulations repel or attract lipid or water affect how they penetrate can penetrate
Topical medications as a general rule are affective at reaching the cornea, conj, sclera and some have concetrations in anterior chamber poor pepnratrtion into the posterior segment.
topical antibiotics for eyes
Classes: Penicillins, Aminoglycosides, Tetracyclines, Chloramphenicol, Fusidic acid, Fluoroquinolones
Different mode of actions and spectrum of activity
Indications: ulcers, infectious conjunctivitis, ideally based on culture and sensitivity results
Species differences
Penicillin – orbinin
Aminoglycosides – gent not as common to need gram negative spectrum as gram positive and can be irritant
Tetracyclines – conjunctivitis in cats – chlamydophilia or mycoplasma conjunvitis or morexlla bovis in cattle
Tetracyclines can inhibit marrix mellanoproteinases and other inflammatory mediators which dugest corneal proteins leading the keratomalacia or corneal melting - systemic use showing concerntrations in tears
Anticollagenase serum, edta
Chloramphenicol – good spectrum of activity and well tolerated
Fusidic acid – more resistance but licenced in dogs cats rabbits so uncomplicated ulcers we should consider this as first line
Frequency of use – most eye preparations are epithelial toxic and could slow healing so select your medication and frequency accurately
Most ophthalmic drugs are used off licence
Select by organism and following the cascade
Not many species difference to report – cats can have ocular side effects to systemic use of high doses of fluroquinolones but this is not reported with topical use
They have done multiple studies looking at common
antifungals for opthamology
Classes: Azoles, Polyenes, Echinocandins
Indications: fungal organisms on cytology or culture and sensitivity
Country differences
We don’t see as much fungal as other countries but in the change in climate we are starting to see more
Azoles – miconazole voriconazole, itraconazole, clotrimazole
Cytology helpful as fungal culture takes 5-7 days minimum. may be too late once results come back
Different organisms seen in different counties and different part of the countries
Aspergillis candida fusarium
Different ways of destroying the organism such as inhibiting viral replication
No fungal eye preprations use iv or topical creams
can be very irritating as ph hasnt been talored
topical NONSTEROIDAL ANTI-INFLAMMATORIES for eyes
Ketorolac, Bromfenac, Voltarol
Indications: uveitis, post operative inflammation, analgesia
Uncommon to have side effects
Adjunctive or instead of steroids
Can help reduce frequency
When don’t need potency of topical steroids
Relatively uncommon to have side effects
topical steriods for the eye
Dexamethasone, Prednisolone
Indications: uveitis, immune mediated / non ulcerative corneal disease, blepharitis, episcleritis,
Side effects: not used in the ulcer or infection, slow wound healing, corneal mineralisation or thinning.
Risk of overwhelming infection
Slow ulcer healing
Chronic useage can result in corneal mineralization which can be painful and in term cause ulceration or corneal thinning
LACRIMOSTIMULANTS / LACRIMOMIMETICS
Classes:
Lacrimostimulants / immunomodulators – ciclosporin, tacrolimus
Lacrimomimetics – sodium hyaluronic acid, carbomer based gels
Frequency
Indications: KCS, lubrication, improving corneal health, post ocular surgery
Species differences
Tear stimultants vs tear substitutes
Stimulants: immunomodulators, modulating the immune response in immune mediated KCS allow lacrimal gland to produce more tears
Substritutes:
Preserveative free single use bottles
Preservative and preservative free
PRESSURE MODIFIERS
Classes: Carbonic anhydrase inhibitors, beta – blockers, prostaglandin analogs
Indications: Glaucoma
Side effects: local intolerance, photophobia, blepharoconjunctivitis, hypokalemia in cats, marked miosis, uveitis, conjunctival hyperemia and iris darkening
Species differences
Decrease aqueous humor formation – CAI, BB,
Increase outflow PA
Local intolerance BB CAI
Hypokalemia with CAI cats
Miosis cats and horses p analogs
Uveitis p analogs
Conjunctival hyperemia, iris darkening, eyelash changes PA
MYDRIATICS
Classes: Cholinergic antagonists
Tropicamide, Atropine, Cyclopentalate
Pupillary dilation +/- relieve ciliary spasm
Tropicamide only for examination purposes
Should be avoid in glaucoma- closes drainage angle, profuse salivation from the bitter taste and occasional vomiting.
Species differences: Birds – striated muscle in their iris sphincter muscles
Visualisation in surgery
Tropicamide most species onset in 0.5-1 hour can be longer in horses and in animals with more pigmented irises can last up to 12 hours – warn owner
Atropine – longer acting analgesia from relief of ciliary spasm 1-2 hours again can be longer in horses duration 3-5 days in dogs and cats can be up to 2 weeks in horses
Cyclopentalate – newer medication provides ciliary spasm relief as well as dilation, longer duration then tropicamide but shorter than atropine 1 hour duration 3-5 days
Neuromuscular blocker such as vecuronium and rocuronium birds
TRIAGE ACUTELY PAINFUL EYE
History / Signalment
Sedation
Appropriate restraint
Topical anaesthesia – tetracaine, proxymetacaine
Nerve blocks – large animals
Analgesia
Full assessment – don’t be drown to one thing
Blepharoedema or chemosis – ultrasound
Small animals this may be combined together with the use of opiods with sedative agents such as alpha 2 agonists
Horses / cattle separate
Appropiate restraint with stablisation of the head, support under chin or gently hold of muzzle
Topical anaesthesia such as tetracaine ( )or proxymetacaine (15-20mins) different durations of action between drugs and species, onset 1-5 mins
Nerve blocks such as AP blocks and supraorbital or frontal blocks will be covered in practical lectures
Proxmetacaine maximal effect last 15 mins
Tetracaine can cause mild irritation and slightly shorter acting than prox
Proxy kept in fridge - difficult in LA
Tetracaine tolerated well in horses
differentials from ACUTELY PAINFUL EYE
Ulcers
Abscesses
Lacerations / trauma
Foreign bodies
Uveitis
Glaucoma
Lens luxation
Evaluating the visible step from the corneal surface into the ulcer helps to give an idea of depth.
If the ulcer involves the stroma then anti-collagenase treatment (acetylcysteine, EDTA - ethylenediamine tetraacetic acid, serum – doing cytology
Corneal abscesses can have a white or yellow, consolidated appearance and usually cause significant discomfort (f
primary suture closure is ideal, however the cornea rapidly becomes oedematous and the edges contract, often making closure impossible
Corneal foreign bodies must be differentiated from iris prolapse, which occurs when the cornea is perforated and a portion of iris moves anteriorly to plug the corneal defect and seal the anterior chamber. Prompt removal of a corneal foreign body (fig.9) is important and referral should be considered
Corneal repairs of deep, infected, descemetoceles or acute perforations
Surgical procedures for eyelid conformational issues, abnormal hairs
Phacoemulsifcantion so lens removal – cataract
ADVANCED OPHTHALMIC treatment OPTIONS
Advanced eyelid and conformational surgeries
Lacerations repairs and foreign body removal
Corneal ulcer repair of deep ulcers or Descemetoceles or acutely ruptured eyes
Phacoemulisification
Uveitis surgery – ciclosporin implants, vitrectomy
Glaucoma surgery
Retinal re-attachment surgery.
Early stages of corneal and endothelial transplants
ENUCLEATION
Always check both eyes
Just because it looks bad doesn’t mean it isn’t fixable
Be sure - Always offer referral
Indications; painful, uncontrollable disease, blind financial
Histology
Transconjunctival approach
Transpalpebral approach
Removing globe, nictitating membrane, conjunctiva sac and lid margins
Leaving as much soft tissue as possible
Minimise bleeding
Analgesia
Minimise swelling – cold compress, pressure bandage
DIFFERENT SPECIES-
Dog – oculocardiac reflex- Oculocardaiac reflex from traction on extraocular muscles or pressure on the globe
Cat – don’t pull on optic nerve- Damage contralateral optioc nerve fibres at optic chiasm and cause contralateral blindness
Horses – standing, nerve blocks
Cattle – nerve blocks
Rabbits – orbital venous plexus- use of ligasure - quatery
