CMS- Preventative medicine, dermatology and opthalmology Flashcards

1
Q

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?

A

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

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2
Q

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?

A

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?

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3
Q

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?

A
  1. 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

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4
Q

IBR (Infectious Bovine Rhinotracheitis)

A

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.

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5
Q

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?

A

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

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6
Q

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?

A

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

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7
Q

Puppy vaccine schedule

A

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.

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8
Q

core dog vaccinations

A

Canine Distemper Virus
Canine Adenovirus/ Infectious Canine Hepatitis
Canine Parvovirus

Leptospirosis
Core for the UK, not necessarily in other countries

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9
Q

Adult dog vaccines

A

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).

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10
Q

Leptospirosis vaccination

A

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.

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11
Q

non core dog vaccines

A

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

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12
Q

core feline vaccinations

A

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.

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13
Q

Kitten vaccine schedule

A

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.

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14
Q

Adult cat vaccine schedual

A

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

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15
Q

non core cat vaccines

A

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.

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16
Q

core rabbit vaccines

A

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

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17
Q

Equine influenza vaccination

A

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.

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18
Q

EI vaccination requerments for different regulatory bodies

A

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!

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19
Q

equine tetanus vaccination

A

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.

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20
Q

equine strangeles vaccination

A

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

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21
Q

Equine Herpes Virus vaccine

A

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

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22
Q

Equine Viral Arteritis vaccine

A

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.

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23
Q

Other licensed equine vaccines in the UK

A

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.

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24
Q

cattle vaccines

A

BVD
IBR
Leptospirosis
BRD (Bovine Respiratory Disease)
Calf Scour
Salmonella
Ringworm
Mastitis
Lungworm
Clostridia
Arboviruses (Bluetongue, Schmallenburg)

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25
sheep vaccines
Clostridia Abortion (Toxoplasma, Enzootic) Pasteurella Footrot Orf Ovine Johnes Disease
26
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?
27
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!
28
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!
29
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!
30
grains are
enerrgy based feeds
31
silages are
fibre based feeds
32
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.
33
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
34
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.
35
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.
36
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. 
37
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. 
38
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
39
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)
40
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.
41
RSV balence
a scale used to determine the risk of acidosis from diet
42
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
43
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
44
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
45
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
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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
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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
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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
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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
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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
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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
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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)
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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
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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)
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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
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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
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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!
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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
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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
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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
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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
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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
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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
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occular presentation of BVD
Cataracts
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occular presentation of endotoxaemia
conjected conjunctiva
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occular presentation of septicemia
hypopyon (assosiated with meningitis) pus in anterior chan=mber
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occular presentation of dehydration
sunken eyes
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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.
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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
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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
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adnexa
tissue around the eye – eyelids, extraocular muscles, fascia, orbital bones
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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
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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
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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 
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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
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OPHTHALMIC DYES
Fluorescein stain Jones test Rose bengal stain
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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 `
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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
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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
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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
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categories of topical opthalmic medications
Antibiotics Antifungals Nonsteroidal anti-inflammatories Steroids Lacrimomimetics / Lacrimostimulants Pressure modulators Mydratics
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Solutions
drug is totally dissolved in a given solvent
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Suspension
sterile products containing solid particles of active ingredient dispersed in a liquid. Shake before use
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Ointment
semi-solid substance, gels, creams
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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.
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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TRANSCONJUNCTIVAL ennucliation
Indications: standard, less bleeding, more visualization, less depression of skin over orbit Lateral canthotomy Begin dorsal incision in bulbar conjunctiva approxmately 5mm posterior to limbus Through conjunctiva to level of the sclera Identify extraocular muscles and transect as close to the insertions to the sclera Allows mobilisation of the globe Curved scissors transect optic nerve a few millimeters behind the globe Remove nictitating membrane 3-5mm eyelid margin removed and conjunctival sac Less bleeding more visualization Closure Periorbital deep fascia : continuous pattern Skin : continuous or interrupted Skin: intradermal Small amount of discharge Nasal secretion
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TRANSPALPEBRAL enucliation
Neoplasia, infection, minimise orbit to contamination. Eyelids are sutures together with continuous pattern Elliptical incision is made around the lid margin approximately 5mm behind the lid margins Deep dissection towards the globe to identify the bulbar conjunctiva Then dissection at level of globe at limbus Complete like transconjunctival Slit lamp also 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. Jones test is the timing of the passage of fluorescein through the lacrimal system to the nose to check the nasal lacrimal patency. Rose bengal pink stain is used to assess erosions of the cornea or conjunctiva and not true epithelial loss like in an ulcer.  Closure Periorbital deep fascia : continuous pattern Skin : continuous or interrupted Skin: intradermal Small amount of discharge Nasal secretion
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describe the diagnostic process for an arab gelding with blinking and headshyness. he has just cone back rom an endurance competition on examination there is blepharospasm and piphora in left eye unilateral miosis and anisoscoriaphotophbia swelling of eyelid laceration in eyelid
history- is there anything that makes it worse?- beright light, light transition ect. hat time of year is it, how is he fed. how well did he travel, was the trailer dusty? problem list: physical trauma?- got hit, bedding got in eye is laceration primary or secondary- other issues point to secondary diagnostics- flurosine stain- strips or liquid (strips dont need to be refrigerated). wet strip with saline and place in lower eyelid. ulcers como in horse the flurosine stain shows an ulcer- does not invlove decimaile membrane as stain in uniform and solid
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treatment for corneal ulcer in arab gelding, not involving the decimale
topical broadspectrum antibiotics- ointment mre practical for horses- cloromphenacol, tripple antibiotic- neomicim, polymixin b (something else swab- check for infection- cytology and culture and sensitivity atropine to dilate pupil and open up drainage angle- not dilating pupil can cause fibrin build up and dhesions that cause sight issues lubrication- lacrimopnemetic- prevents dry sticky eyes and discomfort
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after reacheing an eye you have been treating in an arab gelding for an eye ulcer you check back and find corneal opacification deepening of ulcer bed cellular inflitration meiosis what is happening? what will you do next?
may have had infection that was missed treat with antifungal- mycoconazol- irritating to eye
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describe the diagnostic thought process in the case of a 7 year old king xharles spaniel presenting with "wet eye " bluish tinge to cornea in both eyes bilaterally hyperemic conjunctibva thick mucopurulrnyt discharge neo vascularisation
history questions- new or reccurent problem? irritated or ithcing- headshaking, nodding\? problem list- infectious- corneal infection would most lily be secondary uvietis conjunctivitis dry eye bilateral involvment indicates it may just not be an eye issue history of collitis- use of antibiotics can cause keratoconjunctivitis- sulphonamides also breed disposition to kerratoconuntivitis further tests- shchirmerr tear test eye pressure fluroscien
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a 7 year old king xharles spaniel presenting with "wet eye " bluish tinge to cornea in both eyes bilaterally hyperemic conjunctibva thick mucopurulrnyt discharge neo vascularisation it ws previously treated with sulphonomided for collitis a schirmer tear test show a result of 7mm hat is the diagnosis and treatment
keratoconjunctivitis establish if its an infectous cause- cytlogy treat with topical antibiotics, lacrimopneumetics/ lacrimostimulants
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an 11 year old domestic long hair cat presents with strange behaviour and eye problems. desrcibe your diagnostic thought process eating voraciously loosing weight loss of condition bumping into furnature eyes look "funny" stressed tahcycardia very thin bilateral mydriasis with cloudiness in lef eye absent relfexes posterior segment of eye canit be assesed restinal abnomality dectected in right eye
inquire as to hat is meant by strange behaviour eating? drinking? deficating? what changes in the eye problem list- sudden onset blindness can cause strnge behaviour- retinal detechment weight loss not primary eye issue- systemic issue endocrine issues- hyperthyroidism kidney disease resulting in high blood pressure diabetes cardiact isseus- cardiomyopathy issues affecting blood pressure can ead to affect on eye diagnostics- T4- thyroid parameters renal parameters auscultate the heart cbc ultrasound of eyes
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an 11 year old domestic long hair cat presents with strange behaviour and eye problems. desrcibe your diagnostic thought process eating voraciously loosing weight loss of condition bumping into furnature eyes look "funny" stressed tahcycardia very thin bilateral mydriasis with cloudiness in lef eye absent relfexes posterior segment of eye canit be assesed restinal abnomality dectected in right eye the test for hyperthyroidism comes bac positive how do you treat
treat hyperthyrois and prvide supportive are to eyes- blood pressure managment reducting inflaction in eye important- ennucliation an option
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Dermatological examination
Nature and distribution of lesions Extent/ severity of lesions Changes with treatment Presence of pruritis or pain State of the coat perform outside in good light take into acound the seasonal changes in coat can make this difficult- palpation valuble tool with thik coat Primary vs Secondary lesions- Hair loss Pruritis Lumps and bumps Dry scaling and crusting Moist and exudative Pigment changes Skin disease as part of a wider systemic disorder
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Pediculosis
Lice! Common Winter coats- cant reproduce in hotter temps Host-specific obligate parasites Spread by direct contact HIGHLY contagious!! Groups affected Young and geratric Survive in rugs and bedding asymtomatic carriers Clinical signs- Evidence of self-inflicted trauma from pruritis Hair loss where most significant rubbing ‘moth eaten’ appearance Lice visible with magnifying glass in mane and tail
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topical treatment for pediculosis in horses
advised to clip before aplication deosect- 5% cypermenthin- spray dermoline shampoo- 0.08% piperonyl butoxide 0.04%pythrum extract
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deosect-
5% cypermenthin- spray for pediculosis in horses
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dermoline shampoo
0.08% piperonyl butoxide 0.04%pythrum extract for pediculosis in horses
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Hypersensitivities other than sweet itch in horses
Other than Culicides sensitivity, other cutaneous manifestations of hypersensitivities are relatively rare. Pruritus and urticaria are the common clinical presentations of both equine food allergy and equine atopy. To distinguish between the two, horses can be fed a novel exclusion diet to aid the diagnosis of feed allergy. This can be made up of 5 to 10 kg of lucerne nuts per day for four to six weeks. Many horses in the UK have not been exposed to Timothy hay, which is a suitable alternative to lucerne nuts. Should the pruritus resolve, previous feeds can be reintroduced to identify the ofending substance. If pruritis persists despite a food exclusion trial then a diagnosis of atopy can be made
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Insect bite hypersensitivity in horses
sweet itch Most common cause of pruritis in horses Caused by hypersensitivity to the salivary proteins of Culicoides midges, and occasionally other insects Culicoides are more active in warmer temperatures, moisture and habitat components determine the presence and activity of the midges Clinical disease seen more in warmer summer months due to Culicoides activity distrebution of lesions- hairloss and eratosis of skin around tail and neck, doral aspect of bosy, sometimes on stomach may be so itchy it causes abnomal behaviour signalment- Recognised familial component No breed, colour or sex predisposition Age of onset 3-4yrs – clinical signs worsen with age pathophysiology- IgE mediated Type 1 and then Type 5 hypersensitivity with accompanying eosinophil infiltration into the skin. Only horses showing clinical signs will have IgE antibodies, whereas IgG antibodies are found in all horses exposed to midges, not just those that develop the more severe allergic reaction differentials- Miscellaneous Drug reaction Hepatic dysfunction Multisystemic eosinophilic epitheliotropic syndrome Paraneoplastic pruritis diagnosis- managment biopsy of skin to demonstrate eosinophilic folliculitis
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differentials for puritis in horses
Infectious Mites: Chorioptes, Sarcoptes scabiei, Trombicula autumnalis, Dermanyssus gallinae Lice: Haematopinus asini, Damalinia equi Fungal: Dermatophilus congolensis Bacteria: Dermatophytosis, Staphlococcal folliculitis Endoparasite: Oxyuris equi Biting flies and insects Immunological Atopic dermatitis Contact hypersensitivity Food allergy Miscellaneous Drug reaction Hepatic dysfunction Multisystemic eosinophilic epitheliotropic syndrome Paraneoplastic pruritis
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treatment for sweet itch
Control of the pruritic response to prevent self-trauma Resolution of infections and epithelial trauma secondary to self-trauma Prevention of further exposure to Culicoides midges. Management Barrier? Boett rug Stabling at dawn and dusk + netting Washing? Regular shampooing to soother the skin and repair the skin barrier: oatmeal based shampoos- cooling, antipuritic, moisturising, ceanse hair and skin- coatex, episooth, dermallay- bath once-twice weekly skin so soft- jojoba oil- insect repellet, antipuritic, moisturising- apply to affected areas ocne daily topicl therapies- 25% Benzyl benzoate – Pour over the mane and tail and work in 4% w/v Permethrin – Pour over the mane and tail and work in antiinflamitories- corticosteriods- prednisolone, dexmethasone, chlorpheniramine, hydrocortisone, triamcinolone, betamethasone antihystamines- hydroxine hydrochoride- often only effective if administered before exposure and ofter very impractical doses systemic injectoon? one paper suggests trichophyton species vaccine can help- anacdotal and lots of side effects
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Urticaria
hives immunological causes- allegic reactions- atopic dermatitis, food, contact allergy stinging/biting insects snake bite infections and infestations drug reaction plants transfusion reaction vasculitis antisera, bacterins, vaccines non-immunological caused- cold induced cholinergic, exersise induced sunlight, heat stress/phycogenic dermatographism (pressure induced) genetic abnormality idiopathic clinical signs- Multiple, raised, oedematous plaques of varying size over the body surface May be localized – most common over body and trunk Larger plaques can coalesce and pit on pressure Usually non pruritic Recurrent episodes common differentials- Dermatophyte infection eliminate by fungal PCR Insect bites - can identify after clipping showing site of bite Erythema multiforme Contact hypersensitivity Infectious and immune mediated vasculitis Most often diagnosed on clinical recognition… History of sudden onset Clinical appearance is characteristic If its doesn’t respond to treatment or lesions don’t pit on pressure then possible biopsy
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treatment of urticaria
Presents acutely and resolves rapidly Will clear in 24-48hr without intervention Ideally you would identify the cause, most often you don’t It's reasonable to monitor untreated if acute If chronic and recurrent it's important to ID a cause h1 antihastamien receptor blockers- chlopheniramine diphenhydramie hydroxyzine]cetrizine centrallly acting tricyclic drugs- aamitriptyline doxepin trimeprazine
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Pastern dermatitis
(Mud fever) Dermatitis is secondary to damage of the skin barrier allowing bacteria to enter. Triggers: moisture from wet mud, sweat, mites, photosensitisation and disruption to the normal immune system. Often in long standing cases the cause may not be obvious. clinical signs- Any breed-most common in draft breeds due to feathers- holds water Usually affects the caudal aspects of the distal limb, hindlimb more commonly *it can spread to involve the front of the pastern and fetlock* Often seen in non-pigmented skin Oedema Erythema Scaling exudation matting of hair +crusting Pain on palpation +lameness is seen +/ pruritis types- mild- Erythema Alopecia Dry scales and crusts Pruritis Thickened skin exudative- Erythema Erosion alopecia serous -> purulent crusting chronic proliferative- Excess granulation tissue Hyperkeratosis lichenification diagnois- Clinical recognition? Detailed history Often made worse by over-zealous topical ointments Recurrent/unclear cases: Bacterial swabs Hair brushings Skin scrapes Skin biopsy
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treatmemt of mud fever
ID predisposing, perpetuating and primary factors Keep the skin clean and dry out of wet mud! Clip feathers (not popular) If photosensitisation keep white areas covered. If no improvement… Clip the affected area. Bathe with disinfectant/ antiseptic shampoo. Rinse thoroughly. Dry carefully. Remove all crusts and scabs Apply antibacterial or corticosteroid treatment Repeat! medical- Antifungal: lime sulphur dips for localised dermatophytes and mites Topical treatment for bacterial infections: silver sulphadiazine Topical steroids/oral steroids: immune mediated conditions Systemic antibiotics: culture and sensitivity is advised 1st! other considerations- Early diagnosis – swift treatment! Feather mite treatment – Dectomax injection. Photosensitisation – when mud fever is in white haired areas only. Treat cellulitis if present with anti-biotics. Be vigilant!
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Eosinophilic granuloma in horses
Most common nodular skin disease Aetiology unknown; insect bites, skin trauma and environmental allergies?? Clinical signs 3-6mm ->5cm non pruritic intradermal nodules – non painful – often coalesce Over the back and chest walls (pressure from tack) Occasionally lesions open releasing serum or cream coloured granular material – can calcify DDx- Dermoid cysts (midline of the body only due to embryological defect) Insect bites – usually associated oedema Sarcoid? Usually show change in keratin surface Confirmation: Punch biopsy treatment- Intralesional steroid Surgical removal? Does it need treating?
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treatment for chorioptic mange in horses
clip hair and cleam with keryolytic or slenium sulphide shampoo hot lime sulphure spray/ dip repeated every 12 days as needed doramectic- not licnences in horses ivermectin- 200mcg/kg sigle treatment with oral moxidectin- 400mgc/kg NAIDSs- phenylbutazone
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Pruritus
“…the sensation that leads to the desire to scratch... chew, lick, bite or rub at the skin” BSAVA Manual of canine and feline dermatology. Also feather plucking, flashing and leaping behaviour (fish), hair plucking (primates). There are multiple pathways by which pruritus can be mediated – see PCP “structure and function of skin” lecture Pruritus is a very common presenting condition with a long list of potential differentials. Important to manage client expectations at the start of the investigative process. Pruritus is often managed, not cured. Logical approach: History Clinical examination Rule out ectoparasites Rule out infection - Bacterial - Fungal Allergies (excl atopy) - Food - Contact dermatitis Atopy Zebras!
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leason distributions for skin conditions
Sarcoptes scabiei: Axilla, groin and hock Demodex spp.: Face, ears and feet, can be generalised. Exception =Demodex injai (greasy dorsal trunk in terriers). Cheyletiella: usually dorsal, can be more generalised. Fleas: Lumbosacrum, groin, neck, and caudal thighs. Harvest mites: between the digits, Henry's pocket of the pinna. Atopic dermatitis: Affected front feet and ear pinnae, unaffected ear margins and dorso-lumbar area Contact dermatitis: Only dependant surfaces affected e.g. bottom of feet, ventrum etc
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Ectoparasite testing- Coat brushing
Coat brushing Useful for fleas/flea dirt and Cheyletiella. Flea dirt visible with the naked eye – wet towel and they will turn reddish brown. Cheyletiella can be seen with the naked eye (“walking dandruff), otherwise seen under the microscope – most common in rabbits.
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Ectoparasite testing- Hair pluck
Used to examine the structure of the hair and to look for Demodex mites. Not 100% sensitive for Demodex spp. May also be able to see dermatophyte spores, but not always.
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Ectoparasite testing- Tape strip
Used to pick up coat brushings and/or parasites visible with the naked eye for examination under the microscope e.g. cheyletialla, harvest mites etc. Can also be used for cytology (see later).
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Ectoparasite testing- Skin scrapes
Used to look for Demodex or Sarcoptes mites. Low sensitivity, esp for Sarcoptes; take multiple scrapes and prioritise crusted papular lesions. Deep scrapes needed, make sure you get capillary ooze. May require sedation in fractious or excitable patients
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Ectoparasite testing- Sarcoptes IgG
Sensitive and specific test for sarcoptic mange, providing clinical signs have been present for at least three weeks
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Flea allergic dermatitis
Particularly common in cats. Need to treat holistically: Manage pruritus Treat the affected animal Treat in-contacts Treat the environment Ongoing management is also of paramount importance Regular, routine flea control of the affected animal and all in contacts. a single flea bite can cuase this- enviroment needs to be treated
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Demodex spp. presentation and treatment
Most common in dogs and hamsters Localised usually self-limiting, generalised requires treatment. Treatment options- Amitraz (topical ectopraraciticide) Macrocytic lactones (broad-spectrum ectoparasitic)– Ivermectin, milbemycin oxime, moxidectin Isoxazolines (broad-spectrum ectoparasitic) – Lotilaner, fluralaner, sarolaner, afoxolaner
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Sarcoptes scabiei treatment
Treatment options: Macrocytic lactones – selamectin, moxidentin, milbemycin oximime Imidacloprid Isoxazolines – Sarolaner, afoxolaner & fluralaner Amitraz – three dips. seven days apart. Fipronil (not licensed) Ivermectin (not licensed for dogs/cats) Minimum of two treatments 28-30 days apart is required. Other considerations: Contact with foxes = risk factor. 2o pyoderma common – see tx later. Pruritus control – glucocorticoids, off license use of ciclosporin or oclacitinib (dogs). Zoonotic!
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Cheyletiella spp. treatment
Most common in rabbits, occ dogs and cats. Zoonotic Treatment: None licensed but susceptible to most common spot on treatments (except imidacloprid) Avermectins (selamectin, ivermectin) and fipronil (not rabbits) most commonly used. All in contact animals of all species should be treated. Environment should be treated: Remove bedding; routine cleaning. get new enclosure for smal mammels
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Neotrombicula autumnalis treatment
harvest mites Cats and dogs most common Treatment: Fipronil (can apply fipronil spray directly with a cotton bud), permethrins (dogs only)
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Trixicarus caviae treatment
Most common mite of guinea pigs Causes intense pruritus which can  seizure like activity Treatment: Ivermectin, consider analgesia and benzodiazepines to control seizures until treatment takes effect. give benzo before skin scrape so consult doesnt trigger episode
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Ophionyssus natricis treatment
Most common ectoparasite of captive snakes and lizards. May be a vector for viral disease. Treatment: Permethrin, ivermectin, fipronil all reported. Need to also treat the environment – take care to air thoroughly before returning the animal. physically appy it ot enviroment and animal
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Knemidocoptes spp. treatment
Different spp. cause different syndromes (scaly leg, scaly face etc.) Treatment: Ivermectin (non-poultry); physical removal, diatomaceous earth- lacerates bodies of mites
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Dermanyssus gallinae treatment
Red mite in chickens Treatment: Fluralaner, diatomaceous earth
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Infectious skin disease testing- Tape strip cytology
Needs to be stained to assess cytology (cf parasites) Useful for dry skin lesions and folds. Yeasts +++ suggest malassezia overgrowth. Keratinocytes with adherent bacteria +++, but no active response (phagocytosing neutrophils) suggests bacterial overgrowth.
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Infectious skin disease testing- Impression smear
Useful for moist and ulcerative lesions. Glass slide pressed against lesion – not useful for folds! Pyoderma - bacteria with phagocytosing neutrophils. May help guide antibiotic tx (if required) where c+s is not an option.
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Infectious skin disease testing-Culture and sensitivity
Ideally should be used prior to antibiosis in any case of suspected bacterial infection. Strongly advised where large numbers of rods on cytology.
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Infectious skin disease testing- Wood’s lamp exam
Microsporum spp. only. Generally not very useful – false +ve and false –ve possible. Recommended to culture fluorescent hairs to confirm diagnosis.
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Infectious skin disease testing- Dermatophyte culture
Can take a long time, consider performing early on in investigations if any suspicion. Inhouse or external Inhouse tests are cheap and easy to perform and interpret. Identify Microsporum and Trichophyton species
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Infectious skin disease treatment
Factors affecting treatment: Agent involved (bacterial vs fungal) Depth of infection (topical vs systemic) Owner compliance/patient temperament Underlying conditions
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Bacterial skin Disease
Secondary infections involving skin commensals (esp gram positive occi) most common. Any disease which compromises epidermal barrier function can -> 2o infection: Allergic disease (atopy, cutaneous food allergy) Trauma Endocrine disease Ectoparasites Poor husbandry Anatomy (skin folds) Keratinisation disorders Categorised according to extent/depth of infection: Bacterial overgrowth Surface pyoderma Pyotraumatic dermatitis Superficial pyoderma Deep pyoderma
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Bacterial overgrowth in skin
Usually 2o to atopic dermatitis. Erythema but no other lesions present. Managed with topical treatment e.g. shampoo, mousse, wipes etc. Depending on underlying condition, may never fully resolve and require long term management
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Surface pyoderma
Infection confined to the interfollicular epidermal layers  erosions and ulcers. Hot spots usually start as a surface pyoderma (see next). Important to identify and treat any underlying conditions. Need to prevent licking/ scratching take sample before starting antibiotics Treatment generally topical: Clipping Cleaning- Saline only vs shampoo Topical- Spot treatment vs generalised Analgesia/anti-pruritic treatment Prevent further trauma NSAIDs Steroids (contained in some topicals)
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Pyotraumatic dermatitis
AKA hot spot, acute moist dermatitis Surface pyoderma ->ulcer/erosion -> intense pruritus and self-trauma -> progression to superficial or deep pyoderma if left untreated. Treatment depends on tissues affected (see surface, superficial and deep pyoderma tx. Clipping recommended to allow better access for topical management
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Superficial pyoderma
Limited to the epidermis and hair follicles Characterised by pustule formation (rarely seen intact as fragile). Most common form of pyoderma in small animals. Treatment so for surface +/- antibiotics (7-10 days past clinical cure).
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Deep pyoderma
Infection which involves dermal tissue Furunculosis = deep pyoderma with destruction of the hair follicle. Always require antibiotic treatment, ideally based on c+s, alongside topical treatment. Painful condition, analgesia indicated
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Intertrigo (skin fold superficial pyoderma)
Treatment: As superficial pyoderma Management: Chlorhexidine wipes useful once skin has healed puritic bacterial disease
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Bacterial folliculitis
moth eaten appearance Treatment: as for superficial pyoderma. pruritic bacterial diseases
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Impetigo
‘Puppy pyoderma’ Pustules not centred around hair follicles Treatment: as for superficial pyoderma. pruritic bacterial diseases
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Feline acne
Idiopathic keratinization disorder comedones, usually on the chin. Pruritic when 2o infection develops. Treatment: Early stage, wash/shampoo, later stage as for superficial dermatitis.
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Eosinophillic granuloma complex
Hypersensitivity issue in cats Three presentations: indolent ulcer; eosinophilic plaque; collagenolytic granuloma Not painful/pruritic (except eosinophilic plaque) until 2o infection develops. Treatment dependant on underlying cause, often steroid responsive
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Fungal skin Disease
Two main presentations: Yeast overgrowth (dogs primarily) Dermatophytosis (cats and small mammals) Uncommon in non-mammalian species Reptiles suffer from non-pruritic fungal dermatitis: Nannizziopsis in squamates. Ophidiomyces ophiodiicola in snakes. Various spp.  shell infection in chelonia
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Yeast overgrowth
Malassezia pachydermatis most frequently implicated. Generally 2o to an underlying issue Treatment topical e.g. shampoos (chlorhexidine, miconazole), wipes, mousse etc. Ongoing shampooing (chlorhexidine to keep yeast levels down, other components to improve skin barrier) to manage long term. Systemic antifungals rarely indicated
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Dermatophytosis
Microsporum canis most common in dogs and cats, with Trichophyton spp. And M. gypseum less common T. mentagrophytes and M. gypseum most common in small mammals. Zoonotic Treatments: Clipping – pros and cons aids efficacy of topical treatment but risks skin trauma and spreads spores- need to clean room post clipping Topical Shampoo (miconazole, enilconazole, chlorhexidine) Spray/rinse (miconazole, F10, chlorhexidine) Systemic Itraconazole Ketoconazole Terbinafine (not licensed)
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Allergen testing
Not diagnostic of allergic disease! Results used to decide on treatment: Immunotherapy – most common. Allergen avoidance Not diet - unreliable Intradermal testing – Considered the ‘gold standard’ but not generally performed in first opinion practice. Serological testing – Easier to perform and generally more acceptable to owners. more expensive Testing method does not affect treatment outcome for immunotherapy
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Cutaneous food allergy
Dogs, some cats Concurrent GI signs raise suspicion Not common, but identical symptoms to atopic dermatitis and easy to control, so worth ruling out. Investigation indicated in all cases of non-seasonal pruritus. Serology not considered useful for food allergy. Preparation: Need to treat any potential confounding issues (infection, infestation). May be necessary to control pruritus initially (short course steroids). Complete dietary history should be taken. Various types of diet available: Hydrolysed diets Enzymatic hydrolysis disrupts protein structure to reduce the antigenicity of the protein. Varying levels of hydrolysis possible – anallergenic (royal canin) one of the most hydrolysed. For less hydrolysed diets, choosing a novel protein source is also important. Limited antigen diets Novel protein and carbohydrate source (select based dietary history). Less useful than hydrolysed Home-cooked diets Not recommended (labour intensive, unlikely to be nutritionally complete). Food trial should be performed for 6-8 weeks – will identify 90% of food allergic dogs. Owner compliance paramount! If improvement seen, rechallenge with old food one item at a time. Recurrence of symptoms = confirmation of diagnosis Treatment: Ongoing use of exclusionary diet, symptomatic management of flare up.
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Contact dermatitis
Irritant vs allergic contact dermatitis. Irritant = more common form: Usually affecting the sparsely haired skin in areas in contact with the irritant. Chemical cleaners, fertilisers, herbicides, insecticides, cement dust, shampoos, flea tx (rare). Always check mouth esp with cats! Treatment: Remove irritant + supportive care. cats will try to groom irritant off and can cause ulcers on tounge- analgesia needed, may stop eating
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allergic contact dermatitis
Allergic = rarer form: Type IV hypersensitivity reaction – see “POP:​ hypersensitivity and allergy​” lecture Also affecting the sparsely haired skin in areas in contact with the allergen. Plant resins, oils, pollens (less common), cleaning chemicals, flea collars etc. Treatment: Remove allergen + supportive care.
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Atopic Dermatitis
Dogs, less often cats Diagnosis of exclusion – rule out ectoparasites, infections, and food allergy as above. Criteria opposite suggestive of atopy, but full work up still indicated. Pathophysiology: Atopy = a genetically predisposed inflammatory and pruritic skin disease, most commonly directed against environmental allergens. House dust mites and pollens are the most common allergens involved . Lifelong condition – can be managed but not cured. criteria under three years glucocorticoid responsive puritis sleasional puritis at onset affected front feet affected ear poneae unaffected ear margins unnafected dorso-lumbar area No single protocol will work for every animal. Factors which influence treatment protocols include: Pruritic threshold Flare factors Client/patient factors
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Pruritic Threshold
See PCP lecture “structure and function of skin” Basic summary: Some pruritic stimuli can be tolerated without frank pruritus developing. Where multiple stimuli exist simultaneously, the level of itch may exceed the pruritic threshold -> symptoms. Pruritic stimuli (aka flare factors): Infection and infestation Allergen concentration e.g. pollen Environment (dry, humid, hot, cold) Stress (esp cats) An increase in pruritic stimuli in an otherwise controlled animal may -> flare ups. Management plans should aim to limit flare ups by controlling these flare factors. Important to investigate these before increasing anti-pruritic therapy. Flare factors will vary between individuals
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Flare factors - Infection
Bacteria and yeasts can both act as flare factors. Atopic animals also more likely to develop bacterial or yeast overgrowth due to defective epidermal barrier. Active pyoderma or yeast overgrowth/infection should be treated as above. Ears, paws and skin folds common areas of concern. In animals prone to bacterial and yeast overgrowth, routine topical treatment can help control levels. Shampoos: Miconazole/chlorhexidine – effective but can be very drying to the skin. Non-medicated shampoos may contain other ingredients (e.g. emollients) to improve the skin barrier function Mousse May be easier for tricky patients (cats!). Often used between baths to reduce frequency required. Wipes Useful for localised areas e.g. skin folds.
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Flare factors - Ectoparasites
Ectoparasites are a common flare factor, even in animals without flea allergy. Routine treatment of the individual, in contact animals, and the environment recommended.
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Flare factors – Allergen concentration
Allergens may increase at certain times of year e.g. pollens in spring. Avoidance often suggested but may not be possible. May predict times when increased medication or change in routine is required. Antihistamines- Often requested by clients. Poor evidence they are effective for management of atopy. Most useful pre-exposure.
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Flare factors - Environment
Weather e.g. winter when pets are exposed to central heating (drying to the skin) and/or wet conditions ( increased bacterial and yeast levels on the skin) Area e.g. high environmental allergens and or chemicals in fields cf beach.
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Flare factors - Stress
Especially important for cats. Various stress management techniques can be used depending on the source of stress: Remove sources of stress where possible. Inter-pet conflict Pheromones e.g. diffusers, sprays etc. Calming supplements/diet Increase enrichment
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Treatment options for atpic deramatitis
Multifactorial treatment usually most appropriate: Allergen avoidance Anti-pruritic treatment Immunotherapy- Topical treatments Supplements
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Antipruritic treatment
Important for quality of life (owner and animal) and to reduce self-trauma and 2o issues. Glucocorticoids Ciclosporin Oclacitinib Lokivetmab Antihistamines – poor evidence (see above) See dermatology pharmacology lecture for mechanisms of action
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Ciclosporin for puritis pros and cons
Reliably effective, generally few (GI) side effects so useful where the side effects of steroids are unacceptable. Delayed onset of action (up to 8 weeks),expensive, decreased antitumor response, not compatible with live vaccines, can increase risk of life threatening infections e.g. T. gondii
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Oclacitinib for puritis pros and cons
Cheaper than ciclopsorin, fewer side effects than steroids and ciclosporin, rapid onset of action, can be used for short term flare ups. Double dosing needed to start, break through pruritus can be seen on once daily dosing, leukopenia reported so regular blood testing recommended
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Lokivetmab puritis pros and cons
Can be used in dogs from 8 weeks of age, injectable (no oral meds needed), rapid onset of action. Not effective in all dogs,
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Immunotherapy for atopic dermatitis
Tailored to the individual based on allergen testing. Mechanism of action: repeated doses of allergens -> immunological shift from a Th2 response to a Th1 response -> build-up of immunological tolerance. Protocol: s/c injections given at increasing doses and intervals until 1ml per month is being administered. Requires allergen testing to decide which to include in the immunotherapy (see prev). Serology testing most commonly performed allergen testing. No drug withdrawal required for ciclosporin, oclacitinib, lokivetmab or NSAIDs. Glucocorticoids: No withdrawal if short acting and dose <0.5mg/kg q12hr OR <2m treatment Otherwise 4-6 week withdrawal for oral (e.g. pred), 28 day withdrawal for long acting injectable (e.g. depo-medrone), 7 day withdrawal for short acting injectable (e.g. dexadresson). Efficacy variable: ⅓ cures the condition ⅓ will improve symptoms ⅓ will see no effect Must trial for at least 12m before deciding if it is working. Can use antipruritic medication concurrently. Expensive +++ and lifelong treatment required. Possible to teach clients to administer once the initial course has completed
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Topical therapy fpor atopic dermatitis
Multiple functions: Control bacteria and yeast levels on skin Soothe skin and improve epidermal barrier function Antibacterials and antifungals e.g. chlorhexidine, iodine, F10, piroctone olamine, miconazole May be drying to the skin. Minimum contact times required (10 minutes for most) – can be tricky Shampoo, mousse, wipes, spot gel etc. all available Spot treatment for localised infection Antibiotic and antifungal creams Medicated creams/gels e.g. containing topical steroid, sometimes combined with an antibiotic Emoliants (soothe skin/improve epidermal barrier) Colloidal oatmeal, tea tree oil, glycerin Exfoliants (decrease scale) Salicylic acid Client compliance is the biggest issue. Mousse and foam treatments may have better compliance (no need to rinse) Ears – next lecture!
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supplements for atopic dermatitis
Owners commonly ask about supplements for pets with skin disease. Common components: Essential fatty acids –minor evidence these may decrease erythema and pruritus and/or allow lower doses of antipruritic drugs to be used. Bioactive lipids (Palmitoylethanolamide - PEA) – minor evidence of decreased pruritus in treated animals, but dependant on chemical form used. Probiotics –minor evidence of beneficial effect, but dependant on exact strains used. Common components: Vitamin D – minor evidence that patients with higher serum vit D respond better to medical therapy. Vitamin E – minor evidence that atopic dogs have lower serum vit E cf normal dogs, which can be corrected with supplementation. Niacinamide (vitamin B3) – No evidence of effect on veterinary species. Biotin (vitamin B7) – Evidence that deficiency  skin disease, but not that supplementing is useful in the absence of deficiency Zinc – minor evidence that zinc supplementation may decrease pruritus alongside medical therapy.
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Pemphigus foliaceus
Uncommon autoimmune condition -> pustule/vesicles Treatment: Glucocorticoids tapered to lowest effective dose.
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Cutaneous lymphoma
Uncommon( except in hamsters) , diagnosed on biopsy. Chemotherapy protocols have been reported, or palliative care with glucocorticoids. often get secondary infections poor outcome- care often aplliative until euthanasia
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Otitis externa
= most common, up to 20% dogs affected. Pathogenesis = complicated. The PSPP (Primary, Secondary, Predisposing and Perpetuating) model categorizes causes and factors involved with otitis externa. Primary: Diseases that can affect a normal ear canal. Secondary: Infections which occur due to inflammation caused by primary causes. Perpetuating: Chronic changes to the anatomy and physiology of the ear canal, usually as a consequence of disease. Predisposing: Usually breed associated conformational problems of the ear canal anatomy e.g. floppy ears Acute otitis external: Ear pinna – erythema, trauma due to scratching or head shaking. Ear canal – erythema, swelling, vasodilation, increased cerumen, pain. Chronic otitis externa: Ear pinna – erythema, swelling, scaling, crusting, alopecia progressing to hyperpigmentation and lichenification. Ear canal: exudate (brown, purulent, ceruminous etc.), hyperplasia, stenosis. Aural haematoma Potential sequele to otitis externa. Occurs following excessive head shaking  vascular disruption and consequent bleeding into the potential space between the auricular cartilage and skin. Medical and surgical treatments described
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Otitis media
Head tilt Progressing to vestibular syndrome Loss of balance/ataxia; rolling and falling towards affected side Nystagmus and strabismus Vomiting Horner’s syndrome and facial nerve paralysis Concurrent otitis externa Vestibular syndrome Loss of balance/ataxia; rolling and falling towards affected side Nystagmus and strabismus Vomiting Concurrent otitis externa +/- otitis media Unilateral facial nerve paralysis General lethargy and inappetence. Unilateral deafness
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Otoscopic exam
Need to assess for: Foreign bodies Ectoparasites - Otodectes cynotis, Psoroptes cuniculi etc. Discharge Ear canal patency and the degree of stenosis Ear canal lining appearance, and the presence of ulceration Tympanic membrane appearance, perforation etc. The presence of neoplasms or polyps Try to assess before cleaning where possible. If cleaning is needed: Take samples for cytology and c+s before cleaning. Make sure any cleaner used is safe for use on ruptured TM. Examination may be painful, especially where ulceration is present. Consider cone size and tip shape Can use otoscope to remove FB e.g. grass seed during the consult. Often present as very acute onset, very painful ear during a walk. Crocodile forceps needed to reach FBs in the ear canal. Treatment after removal depends on damage.
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Neurological exam for otitis
Assess for: Horner’s syndrome Nystagmus Facial paralysis Presence of these suggests involvement of middle or inner ear. Advanced imaging indicated in these cases
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Cytology for otitis
More important than culture; should be performed in all cases of ear disease. Useful to differentiate bacterial and yeast infections, assess for inflammatory exudates and biofilms.
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imaging for otitis
Indications: Chronic cases where the ear canal is too stenotic to allow direct visualisation. Suspected otitis media/otitis interna. Where polyps or neoplasia are/are suspected to be present Most commonly used to plan surgical interventions. Radiography Poorly sensitive. Ventrodorsal, lateral, right and left lateral oblique and rostrocaudal open mouth views indicated to maximise information gained. CT Modality of choice for otitis media MRI Modality of choice for otitis interna
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otitis treatment
Will depend on the underlying issue Generally topical, symptomatic treatment based on CE and cytology indicated in the first instance: Treatment for specific primary causes e.g. Otodectes, Psoroptes, foreign body. Ear canal cleansing. Treatment of secondary infection (antibacterials, antifungals). Management of inflammation (topical and/or systemic anti-inflammatory drugs). Control predisposing and perpetuating factors. Severe, chronic and recurrent cases merit investigation for underlying disease (allergic skin disease, neoplasia etc.) Medical treatment Ectoparasite treatment Ear cleaners Topical treatments Systemic treatments Ear flushing/ear wicks Aural haematoma Surgical treatment Lateral wall resection Total and partial ear canal ablation Lateral bulla osteotomy Otic and nasopharyngeal polyps ectoparasites- Some topical medications licensed for mites (drowns them!) Systemic antiparaciticides: Ivermectin (tx of choice for Psoroptes cuniculi); injectable (preferred) or spot on. Selamectin – licensed for Otodectes Moxidectin - licensed for Otodectes Fipronil – direct application into the ear canal reported as an off license treatment for Otodectes ear cleaners- Purpose: Removes debris and microbes. Allows medicated topical treatments to reach the tissue. Some help break down biofilms (N -acetylcysteine) Some potentiate the effect of antimicrobials (Tris-EDTA) Usually done at home as part of a treatment protocol Method important, clients often need to be taught how to perform. Initial cleaning may be done under GA in the clinic if fractious or severe, painful disease present.
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ear cleaners
Purpose: Removes debris and microbes. Allows medicated topical treatments to reach the tissue. Some help break down biofilms (N -acetylcysteine) Some potentiate the effect of antimicrobials (Tris-EDTA) Usually done at home as part of a treatment protocol Method important, clients often need to be taught how to perform. Initial cleaning may be done under GA in the clinic if fractious or severe, painful disease present. Types of ear cleaner: Saline – safe with ruptured TM, generally best for flushing under GA. Ceruminolytics - for waxy ears. Antiseptic - for purulent discharges or where bacterial or yeast overgrowth is present on cytology. Some contain a drying agent to prevent further maceration – may be painful where the ear is severely inflamed or ulcerated. Ongoing maintenance cleaning may be indicated with chronic disease: Prevents debris build up Controls bacterial/yeast burden. SOME NOT SAFE WITH RUPTURED TM Most proprietary topical products contain multiple agents  over treatment. May include: Antibiotics Antimicrobial peptides (AMP2041 peptide) Antiseptics (Tris-EDTA) Antifungals Glucocorticoids Most contraindicated with a ruptured TM Other products which may be used off license as topical treatments include: Injectable antibiotics, e.g. marbofloxacin (indicated for severe infection where the TM is ruptured) Silver sulfadiazine cream (let down with water) Injectable steroids (dexadresson) – see later
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Topical treatments for otitis
Topical antibiotics: Chose narrow spectrum drugs where only cocci are seen on cytology. Where rods are seen, aminoglycosides and polymycin B should be used before fluroquinolones (based on c+s). Important to remove discharge/pus – can inactivate antibiotics. Triz-EDTA can enhance antibiotic activity esp aminoglycosides. Topical glucocorticoids: Not with Demodex spp. Gives immediate relief from pruritus +/- pain. Injectable dexadresson sometimes added to ear cleaner for maintenance where antibiotic/antifungals aren’t indicated. Recicort (glucocorticoid + salicylic acid) also useful in these cases.
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systematic treatments- otitis externa
Systemic anti-inflammatory drugs (glucocorticoids, occ NSAIDs) may be indicated if topical treatment is not possible (very stenotic canals, ruptured TM etc. Systemic antibiotics and antifungals poorly effective. Systemic treatment for underlying disease e.g. allergic disease
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Systemic treatments- Otitis media:
Spread from otitis externa – treatment primarily topical unless access limited as prev. Ascending – parenteral antibiosis and NSAID therapy indicated. Investigation and treatment of underlying disease e.g. dental disease in rabbits with ascending otitis media
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Systemic treatments- Otitis interna
Systemic antibiotics +/- anti-inflammatory drugs indicated in all cases. Almost always require surgical drainage of the tympanic bulla.
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Ear flushing and wicks
Where ears are particularly painful or difficult to clean effectively then flushing under GA may be necessary. Warmed sterile saline via a 20ml syringe and a Spreulls needle. Not uncommon for tympanic membrane to rupture during flushing. Ear wicks may be placed post-flushing: Can be used to help topical medications reach the area needed e.g. stenotic canals, otitis media. Injectable antibiotics often used off license for this. Must be placed and removed under GA (painful). Usually removed after 7 days (10 max)
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Aural haematoma
Medical treatment Drain and flush with saline via a small incision or large needle Steroids then given, either directly into the haematoma cavity or systemically. Need to control underlying otitis. Failure rate very high. Surgical treatment S-shaped incision made over the haematoma along the long axis and on the inner surface of the pinna. Haematoma cavity cleaned and flushed with sterile saline. Pinna layers opposed with full thickness mattress sutures placed parallel to the incision. Sterilised lengths of drip line or buttons can be used to minimise ‘cheese-wiring’. Incision left open for drainage. Alternative procedures: Fenestration of the medial pinna over the haematoma to allow drainage without suturing. Passive drainage e.g. with a teat cannula placed through a stab incision at the apex of the haematoma, or a through-and-through Penrose drain Continuous suction drainage with a closed system.
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Lateral wall resection
surgical treatment for chronic otitis Removal of most of the lateral wall of the vertical canal to improve local environment and drainage of the ear canal. Unlikely to be curative, esp where underlying disease exists. Possibly makes topical treatment easier/more effective. Excellent results in animals with congenital ear canal stenosis without hyperplastic changes.
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Total and partial ear canal ablation
treatment for chronic otitis Total (TECA) or partial (PECA) removal of the ear canal. Challenging surgery with a high rate of complications: Often combined with lateral bulla osteotomy (LBO). Results often good with an experience surgeon. Hearing does not appear to be more impaired post op can have facila nerve paralusis, infection, neuro symptems, pinnae avascular necrosis swelling and hyoid aperatus damage leading to repiritory distress
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Lateral and ventral bulla osteotomy
surgical treatment for chronic otitis LBO usually performed alongside TECA or PECA ( decreased complications) Ventral often performed as a standalone procedure where concurrent OE is minimal or not present. Important that all bulla epithelium is removed. Care re:facial nerve.
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PECA + LBO
surgical treatment for chronic otitis Surgical treatment of choice for rabbit middle ear disease. Concurrent dental disease in most cases prevents effective conservative management in most cases. Bulla often left open for flushing (cf dogs/cats) or antibiotic impregnated beads inserted prior to closure.
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Otic and nasopharyngeal polyps
Rare in dogs; result of chronic inflammation  hyperplasia. Common in cats Benign masses arising from the lining of the middle ear. Can extend up into the external ear canal or down into the nasopharynx. Removed via traction in the first instan ce. VBO indicated where there is recurrence or chronic bulla changes.
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anal gland disease
Very similar between all manifestations: Perianal pruritus - scooting, licking, chewing, overgrooming etc. Pungent odour (“fishy”) +/- anal discharge Reluctance to sit or defecate Tenesmus and/or constipation Erythema and swelling Abscessation (usually unilateral) +/- draining fistula Need to differentiate AG disease from other causes of perianal pruritus. AG disease may be 1o or 2o to another cause of skin inflammation History General history and demeanour Any other history or evidence of skin disease? Clinical exam Rectal and general dermatological exam Cytology? Neutrophils, monocytes, yeasts, rods and cocci all commonly seen in non-diseased AG secretions – questionable value. Culture? May guide treatment choice but not as helpful for diagnosis Anal gland impaction Anal sacculitis Anal gland abscess Furunculosis Anal gland neoplasia
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Anal gland impaction
Most common presentation CE: very full AG on rectal palp with no change in secretion or evidence of inflammation or infection. May -> anal saculitis and/or abscessation if not treated. Obese dogs and those with deep set AG may require routine emptying. Treatment: AG emptying External technique – squeeze either side of the anus at 4 and 8 o’clock. Client can be taught this. Internal technique – squeeze each AG separately with one digit in the rectum and the other externally. Both techniques – stand to the side and keep your mouth closed! Management: Teach clients to express externally at home Weight loss – perianal fat pads collapse the duct in obese animals. Increase dietary fibre – increases faecal size  better expression of the glands during defecation Control underlying disease (see pruritus part 1)
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Faecal impaction
Common issue in older, intact male guinea pigs. Thought to be due to testicles/fat deposits in the scrotum  cleft around the anus which can fill with faecal material. 2o infections and pain common tx as superficial pyoderma. Management = routine removal by owners.
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Anal sacculitis
Inflammation and/or infection of the anal sacs, usually 2o to impaction. CE: very full AG + pain, erythema and/or swelling of the perianal tissue. Treatment: AG emptying (conscious or under sedation if painful) Flushing and topical treatment Systemic NSAIDs Antibiotics only indicated for abscessation
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Anal gland abscess
Progression of anal sacculitus – AG rupture -> cellulitis and abscessation. Frequently present with draining fistulas, if not drainage needs to be created. Treatment: Flushing, topical tx as above, NSAIDs, and systemic antibiotics indicated. For chronic, recurrent, and refractory cases anal sacculectomy is indicated.
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Anal sacculectomy
For chronic, recurrent, and refractory cases of anal gland absecss anal sacculectomy is indicated. Open technique: Anal gland incised to allow removal of the secretory lining.- lower complication rate but less effective Closed technique Skin incised and entire gland carefully dissected out. Preferred for neoplastic cases. Higher risk of damage to nerve supply of the external anal sphincter -> faecal incontinence. Overall long term complication rates low in the hands of experienced surgeons.
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Anal gland furunculosis
Ulcers and sinus tracts that spontaneously occur in the skin around the anus. GSDs appear predisposed. Immune-mediated pathogenesis: Local T-cell-mediated inflammation. Affected dogs have ↑ anti-staphylococcal IgG cf normal dogs Presentation: Sinus tracts and ulceration in the perianal area (usually don’t communicate with the rectal lumen). Pain, licking of the perianal area, abnormal tail carriage. GI signs (tenesmus, dyschezia, haematochezia, soft stools, mucus in the faeces and increased frequency of defecation). Diagnosis generally based on CS but rectal exam may also be useful to assess AG. asses for impactin Surgical treatment Resection, cryosurgery, and laser therapy all reported. High risk of complications – referral indicated. Medical treatment - preferred Immunomodulatory therapy Treat 2o infections Analgesia Supportive care
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Anal gland furunculosis treatment
Immunomodulatory therapy: Ciclosporin Treatment of choice. Used BID until remission (8-12 weeks), then tapered to lowest effective dose. Approx 85% remission rate Can be used with ketoconazole to reduce dose needed (care re:liver) Topical tacrolimus -(0.1%) Effective, but application may be tricky in painful patients. Not licensed. Suitable for use alongside oral tx with ciclosporin, or as a sole agent for mild lesions or for maintenance of cases already in remission. Prednisolone and azathioprine – poor evidence + success rates low; avoid. Treat 2o infections Ideally based on c+s TMPS and amoxy/clav good 1st line options Analgesia Multimodal incl NSAIDs (care re:other drugs), and opioids Supportive care Stool softeners
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Anal gland neoplasia
Apocrine gland anal sac adenocarcinoma (ASA) = most common. Locally invasive + high metastatic rate (lymph nodes and lungs). Paraneoplastic hypercalaemia common. Common found incidentaly; CS perianal irritation and pelvic canal obstruction/narrowing. Diagnosis: Biopsy – FNA can be diagnostic, incisional indicated if FNA inconclusive. Radiography – thoracic and abdominal to assess for metastasis. CT – More sensitive for staging; can be useful for surgical planning
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treatment of Anal gland neoplasia
Surgery = treatment of choice. Excision of the primary mass +/- lymph node metastasis. Hypercalcaemia should be stabilised before surgery: Complete ressection difficult due to close proximity of the rectum and anal sphincter – referral indicated. Chemotherapy: Can be used prior to surgery to shrink tumours and allow easier resection, and to control disease post-surgery. Radiotherapy: Can be used to improve survival time post surgery. Prognosis guarded – high rates of local recurrence and metastasis. Disease stage will influence prognosis: Stage I - primary mass <2.5 cm with no metastases = 1200 days Stage II – primary mass >2.5 cm with no metastases = 733 days Stage IIIA – metastases <4.5 cm, only to local LN, + resectable = 492 days Stage IIIB – metastases >4.5 cm = 330 days Stage IV – distant metastases (organs) = 90 days General rule: median survival = 12 months if mets at surgery, 19 months if not.
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Alopecia
Another very common presenting complaint from owners. Pruritic alopecia = work up as per pruritus. Non-pruritic = different set of differentials. Note: Pruritus can occur 2o to infections even where non-pruritic causes of alopecia are present. If alopecia persists after pruritus resolves, move to non-pruritic alopecia work up Non-pruritic alopecia can be focal, multifocal or generalised. Endocrinopathies = most common reason for adult onset generalised or symmetrical alopecia: Hyperadrenocorticism – symmetrical flank alopecia and/or ‘rats tail’. Hypothyroidism – flank alopecia with hyperpigmentation and/or myxoedema History Clinical and dermatological exam Trichogram Haematology and biochemsitry Endocrine testing Skin biospy Breed and genetically related individuals: Hereditary/congenital alopecia Black hair colour dysplasia, colour dilution alopecia. Sex status Sex hormone alopecia in entire animals Waxing and waning? Canine recurrent flank alopecia/ seasonal flank alopecia. Medications Exogenous steroids, sex hormones General health Concurrent evidence of endocrine conditions e.g. PU/PD Other clinical signs e.g. hyperpigmentation, myxoedema, skin thinning, calcinosis cutis, weight gain or loss etc. Evidence of infectious skin disease (pyoderma, dermatophytosis etc.) Examination of the hair shafts Broken hair shafts = self trauma; animal is likely pruritic but the owner hasn’t noticed. Differentiate anagen (growing) vs telogen (resting) hairs - telogen more abundant in animals with an endocrinopathy. Clumped melanin = colour-dilution alopecia or black hair follicular dysplasia. Haematology: Bone marrow suppression (anaemia, thrombocytopenia) – excess of sex hormone (oestrogen) due to e.g. Sertoli’s cell tumour, hyperoestrogenism, drug-induced (oestriol, oestradiol) Biochemistry Changes suggestive of endocrinopathies – see endocrine pathology lectures ACTH stimulation and T4/TSH tests. Should be only performed where there is suspicion of endocrine disease on history, CE, bloods and/or trichogram. Care: low T4 can occur with non-thyroidal illness; common reason for misdiagnosis of hypothyroidism. skin biopsy- Perform when other tests have not provided a diagnosis. Test of choice to diagnose: Follicular dysplasia Sebaceous adenitis Seasonal flank alopecia
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allopecia in ferrets
Non-pruritic alopecia, bilateral alopecia = very common in ferrets Endocrine aetiology: Hyperoestrogensism – entire jills which are not brought out of season; pancytopenia will be present on haematology Hyperadrenocorticism – neutered jills and hobs; reason neutering is not recommended without deslorelin implant.
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Alopecia X
Diagnosis of exclusion Endocrine imitating – often see concurrent hyperpigmentation. Aetiology unknown Cosmetic disease, not a health concern. Treatment: Neutering (if entire) Melatonin Benign neglect mitotane, trilostane etc. report but carry risks.
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types of primary skin lesion
Primary lesions: Macule Papule Nodule Vesicle Bulla Pustule Wheals Alopecia Scale Crust Comedone Follicular Cast
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types of secondary skin lesion
Erosion Ulcer Lichenification Hyperpigmentation Epidermal collarette
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Sheep scab (psoroptic mange)
Psoroptes ovis A Type 1 hypersensitivity reaction occurs – allergic dermatitis in response to mite excretions (faeces) producing host immune response ‘The most important ectoparasitic sheep disease in the UK’ – Sheep Vet Soc. Serious welfare issue for sheep; economic losses substantial Deregulated in England and Wales in 1992 – removed compulsory dipping requirement Lack of enforced control since then, despite legal requirements to treat (E&W)/notify (S&NI)- noted deterioation of disease controle after this point Repeated initiatives, both local and national, to eradicate Annual cost estimated to be between 78 and 202 million pounds in GB (Nixon et al. 2020) Has moved (hopefully) higher up the agenda in recent years – renewed efforts Good diagnostic tests and treatments available, but are they known about/being used in practice? Needs better coordination and renewed determination to eradicate – state v private? serious welfare issue can remain viable off the host for 15-17 days – environmental reservoir pathogenisis- Quiescent phase – reservoir sites in axilla, groin, inner surface of pinna – spring, summer, early autumn – then spreads rapidly in colder months to cover the body (Oct – Feb) – highly contagious Earliest clinical phase – zone of inflammation with small vesicles and serous exudate - hypersensitivity response Lesion spreads – centre dries, yellow crust develops with secondary infection, but edges moisten as mites multiply and move centrifugally Patch of lighter wool, but then sheep responds to intense pruritus and scratches fence posts and gates – larger areas of skin damage, wool becomes stained and ragged, wool loss noticeable Nibbling at flanks also seen clinical signs- Sheep may be suspected as being infected with sheep scab if the sheep are: Rubbing/scratching against fence posts Nibbling and biting at flanks, tossing head Dirty fleece due to rubbing and scratching - especially shoulders – using hind feet to scratch ‘Nibble' response: spontaneous or in response to handling or manipulation of a lesion Staying apart from the flock: may be dull diagnosis- Scab or lice infestation? Skin scrapes: Mites are scraped from the skin surfaces of the most-affected sheep – good approach if clinically affected in early stages of infection - can be difficult to find mites, and there may be lots of sheep in pre-clinical stage and it can be quite time-consuming to collect and examine. Blood ELISA test: Testing for antibodies the sheep produces in response to infestation, with sensitivity of 98% and specificity of 96%. Can be detected as soon as 2 weeks after exposure – early Ab response to infection Sheep scab is still notifiable in Scotland and Northern Ireland Legal requirement in England and Wales to treat infected animals and all others in the flock Enforcement?? differentails- Lice infestation – also pruritus and fleece loss Keds (Melophagus ovinus) – skin damage Blowfly strike (cutaneous myiasis) – larval stages of Dipteran flies Tick infestation – cause some pruritus Scrapie – pruritus and ‘nibble reflex’ – not a flock, individuals Wool slip – no inflammation of skin or pruritus, just wool loss Ringworm – usually Trichophyton verrucosum- from infected cattle contact?- not common in sheep Dermatophilosis – Dermatophilus congolensis infection – serum exudation and scab formation, often around head
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Psoroptes ovis – the sheep scab mite
Entire life cycle of P. ovis occurs on the host – do not burrow into the dermis, feed on skin scales Adult mites (up to 0.75mm long) live on the skin surface - adult females lay eggs (about 90 in 4–6 week lifespan), hatching to release six-legged larvae Larva becomes nymph and then develops to the adult stage Life cycle can be completed in about 10-14 days; can remain viable off the host for 15-17 days – environmental reservoir A Type 1 hypersensitivity reaction occurs – allergic dermatitis in response to mite excretions (faeces) producing host immune response A SERIOUS WELFARE ISSUE
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treatment for sheep scab
Treatment – Plunge OP dipping (not jet spraying!) or injectable Macrocyclic Lactones (ML) parasiticide Establish origin: Where did it come from? Review quarantine protocols if buying in sheep (remeber quesent phase Advise farmer to contact neighbours: Warn them of contiguous spread risk and joint control efforts will help avoid re-infection in local area Review fencing and contiguous contact: Neighbouring sheep with direct contact? Straying sheep through broken fences? Introduced rams? Think biosecurity. There are only two options for treating sheep scab: Plunge organophosphate dip (e.g. diazinon, Bimeda – ‘Gold Fleece Sheep Dip’) – treatment and up to 8 weeks of protection – also kills other ectoparasites Injectables (macrocyclic lactones) – e.g. moxidectin (milbemycin), doramectin, ivermectin (avermectins) – various manufacturers – treatment regimes and withdrawal periods vary according to product Dipper needs ‘Safe use of Sheep Dip’ certificate, Environmental Permit, container to store the chemically treated wastewater, leak-proof dipping tank, crook, timer Sheep should not be dipped on full stomach; thirsty; when they are wet; or with open sores/wounds. Cool, dry day and best in morning. Use full PPE safety equipment for dipper/attendants – hazardous chemical Correct concentration of dip essential. Whole body apart from head and ears must remain immersed for at least 1 minute. Keep sheep moving – head immersed at least twice, but do not hold down – choke/inhalation. Top up dip tank regularly to keep volume/concentration. Empty and refill tank as per instructions - dirty tanks need to be replaced. Holding pen for sheep to drip off before release – environmental considerations. It is illegal to apply OP dip by jets or showers or for SQPs to prescribe dip for these application routes - only licensed to plunge Resistance has developed to macrocyclic lactones (MLs) in the UK Very concerning, given that these products are also used to treat endoparasites
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Ringworm in cattle (Dermatophytosis) in large animals
Zoonosis Very common Mainly calves/youngstock Highly contagious fungal disease Mainly Trichophyton verrucosum Causes grey scaly lesions, especially on the head and neck (hair loss and excessive growth of keratin) Transmission – direct or indirect contact. Bought-in cattle, on-farm spread or contaminated environment - fungus can survive for years off the host Animals recover and develop immunity – a disease of youngstock – but months to resolve Confirmation – microscopic examination of hair samples – spores Treatment – topical antifungal sprays – e.g. enilconazole (Imaverol Cutaneous Emulsion, Audevard) Prevention – live vaccine available, useful where large number of infected animals to reduce the severity of the condition/number of cases – human health protection Current UK supply problems with vaccine (Bovilis Ringvac, MSD Animal Health) VMD has authorized import of a Czech/Netherlands ringworm vaccine A notifiable disease in Norway! Very different attitude to the disease Eliminated using vaccination and herd restrictions
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Bovine papillomatosis (warts/‘angleberries’)
Small, double-stranded viruses (Family Papillomaviridae) with predilection for keratinocytes and some types also for fibroblasts - penetrate minute abrasions Induce benign, hyperplastic, usually regressive lesions – papillomas/warts – on cutaneous and mucosal epithelia in cattle – teats, udder, head, vulva, anus, penis Lesions usually resolve over time, but influenced by environmental carcinogenic co-factors, these lesions may become neoplasias – bladder and upper GIT Complete genomes of BPV-1 up to BPV-27 have been elucidated – lot of genotypes! [BPV-1 and BPV-2 associated with sarcoids in horses – potential cross-species transmission] Mostly young cattle < 2 yrs old – cell-mediated immunity should preclude older animals re-developing lesions Infection by direct contact or contaminated fomites Papillomas and fibropapillomas Usually spontaneously regress and fall off given time – but could be many months Unsightly appearance, but severe infections and widespread lesions can lead to loss of body condition and eventual death Teat lesions can interfere with milking – hard to attach clusters; damaged lesion can lead to infection and mastitis Penile fibropapilloma lesions a problem in breeding bulls BPV-1 and BPV-2 cause fibropapillomas and are prob. the most common genotypes in cattle
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Bovine papillomatosis – Treatment approaches
Conservative, laissez-faire approach – leave and allow to fall off naturally Surgical removal – but can regrow Autogenous vaccines – too expensive? Supportive treatment – antimicrobials responding to secondary infection if required
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Bovine Ischaemic Teat Necrosis (ITN)
Emerging disease of mostly dairy heifers in first lactation – as yet unknown aetiology First report by Blowey (2004): ‘Ischaemic necrosis of the base of the teat in dairy cows’, Vet Rec. 154(7):214. Welfare issue – premature culling and economic loss Initially thought to be linked to digital dermatitis Treponema spp. and Orthopox virus were excluded as major aetiological agents by Crosby-Durrani et al. (2022a) Primarily affects the base of the teat, may extend distally towards the teat end and/or proximally to the adjacent skin of the udder Severe lesions can lead to sloughing of teat – resultant complications Crosby-Durrani et al. (2022b) - Farmers reported 1/5 of cows with ITN were culled, 1/5 recovered, and others had complications such as teat loss and/or mastitis
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Erysipelas infection in pigs
Erysipelothrix rhusiopathiae Gram-positive slender, rod-shaped bacteria Up to 50% of healthy pigs may be carriers – tonsils Excrete in faeces and urine Soil and surface water frequently contaminated – environmental reservoir - survives several weeks outside host The organism causes erysipelas in pigs (and turkeys) worldwide – increasing global prevalence. also post dipping lameness in sheep Zoonotic organism - erysipelas in humans Cutaneous form – ‘Diamond shaped leasions of haemorage" Hyperacute - Pigs found dead – sudden death Generally fattening pigs between 55kg and 80kg Uncommon in adult sows/boars Scarlet flushing of skin – signs of septicaemia Acute- Pyrexia – Can be higher than 42C Reddening and blotching of skin – feels raised initially Pathognomonic purple-red diamond skin lesions appear within 24-48 hrs of onset clinical signs Acute form may kill pigs within 12-48 hrs Older pigs - anorexia and thirst Pigs dull and reluctant to move Abortion may occur in pregnant gilts/sows more chronic forms- Skin lesions (and ear tips/tail) can become necrotic, turn black and slough off Pigs can become chronically-affected with polyarthritis (lame) and/or cardiac insufficiency due to endocarditis (congestive heart failure, death) E. rhusiopathiae is ubiquitous in soil – environmental exposure Note particularly outdoor herds/backyard pigs Responds quickly to penicillin – treat early Prevention: commercial vaccines are available e.g Porcilis Ery (MSD), Eryseng (Hipra) – primary course then boosters Vaccine immunity lasts for 6 months – sows and boars need regular boosters
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Pityriasis rosea in pigs
(‘False ringworm’) Probably a genetic condition – heritable from certain boars Individuals or whole litters, but usually just a few per litter Lesions can appear from about 4 weeks of age (weaning) – hyperaemic patches on flanks, groin, thighs These expand rapidly to form red rings with normal centre Self-limiting with course of few months, then clears Unsightly, but not pruritic - pig grows normally
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bivalent leptospirosis vaccine
Canicola and Icterohaemorrhagiae Icterohaemorrhagiae Most commonly isolated serovar in canine clinical leptospirosis cases in the UK. Canicola Canine adapted; very rare since vaccination introduced.
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Tetravalent leptospirosis vaccine
Canicola, Icterohaemorrhagiae, Australis (Bratislava) and Grippotyphosa. 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.
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describe a treatment plan for a 1 year old english bulldog with cherry eye
Problem List: Eye lesion Mild depression and pawing at eye – likely due to pain/pruritus Differential Diagnoses?- Prolapse of the nictitating membrane (NM) gland Mass Conjunctivitis Treatment Options: Surgical Removal Surgical Repositioning Supportive therapy- Systemic pain medication, Buster collar, Consider prophylactic topical broad pectrum antibiotics Recommended treatment: Surgical Repositioning- Surgical removal is likely to trigger Keratoconjuncitivitis sicca (Dry Eye), especially due to breed predisposition Supportive therapy- Likely to be bilateral eventually- perhaps wait and provide supportive therapy before surgery? Should not breed from this dog
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Simple supportive therapy for uncomplicated, acutely presenting, simple ulcer
Chloramphenicol or triple antibiotic ointment (easier to apply than drops) Atropine to effect to keep pupil dilated Warn owner to cover eye if turned out during the day (e.g. eye patch fabric sewn over eye area of fly mask) Lubrication? Monitor for signs that ulcer is not healing Effects of atropine may linger
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signs an eye ulcer is worsening and what would you do next
Corneal opacification Deepening of the ulcer bed Cellular infiltration Meiosis Likely indolent ulcer and/or infection Swab for cytology, and culture & sensitivity, (consider fungal infection?) Adjust antibiotic based on C&S Debridement Consider sub-palpebral lavage if infected and regular treatments required
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list the problems and differentials and further tests for a 7-year-old male, neutered King Charles Cavalier Spaniel Presenting with “wet eye” Owner has noticed that both eyes have been a bit “gummy” over the last week or two – seems to be getting worse Dog was treated with antibiotics for a bout of colitis recently QAR TPR within normal limits Bilaterally hyperemic conjunctiva Thick, mucopurulent discharge from both eyes Bluish tinge to corneas in both eyes
Problem List: Conjunctivitis Corneal oedema Mucopurulent discharge Differential Diagnoses? Keratoconjunctivitis sicca (KCS) or “Dry Eye”- (Schirmer Tear Test) Infectious conjunctivitis Ophthalmic Exam fluroscien stain Schirmer Tear Test
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treatment plan for Keratoconjunctivitis sicca
Treatment Options: Lacrymomimetics Lacrymostimulants May need to treat secondary infection Consider analgesia Recommended treatment: Lacrymomimetics initially, and lacrymostimulants if no recovery and owner can afford Anything else to consider? May be toxic aetiology due to sulphonamide treatment for colitis If toxic aetiology, there is a chance that the eyes will recover if sulphonamides have been discontinued BUT breed predisposition as well, so may not recover Lifetime treatment required
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describe the problem list, differentails and further tests for a 11-year-old Domestic Longhair Cat Presents with strange behaviour and eye problem Eating voraciously Losing weight Loss of condition Started to bump into furniture and seemed distressed over the weekend Eyes “look funny” BAR, seems stressed Very thin, weighs 2.8kg Tachycardia Unkempt coat, poor condition Bilateral mydriasis, with cloudiness in one eye Bilateral mydriasis, with cloudiness in left eye Pupillary Light, Dazzle and Menace Reflexes absent Posterior segment of globe cannot be assessed in cloudy eye Retinal abnormalities detected in right eye on fundoscopic exam
opthmic exam- Pupillary Light, Dazzle and Menace Reflexes , opthalmoscope Problem List: Weight loss (despite eating) Acute loss of vision Abnormal fundic exam Differential Diagnoses? Systemic disease- Hyperthryoidism Kidney disease Neoplasia Diabetes mellitus (Cardiomyopathy) Secondary ophthalmic disease- Uveitis Retinal degeneration/detachment further tests- Bloodwork CBC Thyroid levels Kidney indicators Urinalysis Blood glucose Ultrasound of eyes- If available, may help to determine prognosis for return of vision
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how would you investigate puritis
Pruritus is a very common presenting condition with a long list of potential differentials. Important to manage client expectations at the start of the investigative process. Pruritus is often managed, not cured. Logical approach: History Clinical examination Rule out ectoparasites Rule out infection - Bacterial - Fungal Allergies (excl atopy) - Food - Contact dermatitis Atopy Zebras! Medical- Any current medications (may affect treatment choice) Previous medical history Any other current signs of illness e.g. GI? In contacts- Any other animals or people affected? (i.e. is it contagious) Environment- House (e.g carpets, laminate flooring) Exercise (e.g. woodland, field, rivers, beaches) Wildlife exposure (e.g. garden visitors) Dietary history- Main diet, treats, supplements Routine management- Parasite control, grooming and bathing etc. When did signs start? Age, time of year etc. Are they continuous, seasonal, intermittent? Has the condition progressed? How? How bad is the pruritus e.g. is the animal non-distractable during episodes of scratching, is it stopping other activities e.g. eating in order to scratch? Any previous treatment? Did it work? clinical exam- leasion?
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disrtibution of leasions for sarcoptes scabiei
Axilla, groin and hock
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disrtibution of leasions for Demodex spp
Face, ears and feet, can be generalised. Exception =Demodex injai (greasy dorsal trunk in terriers).
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disrtibution of leasions for Cheyletiella
usually dorsal, can be more generalised.
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disrtibution of leasions for fleas
Lumbosacrum, groin, neck, and caudal thighs.
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disrtibution of leasions for harvest mites
between the digits, Henry's pocket of the pinna.
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disrtibution of leasions for Atopic dermatitis
Affected front feet and ear pinnae, unaffected ear margins and dorso-lumbar area
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disrtibution of leasions for Contact dermatitis
Only dependant surfaces affected e.g. bottom of feet, ventrum etc.
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Specific tests for ectoparasites
Coat brushings Hair pluck Tape strip Skin scrapes Sarcoptes IgG
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Infectious skin disease tests
Tape strip cytology Impression smear Culture and sensitivity Dermatophyte culture Wood’s lamp exam
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