SA skin

Question 1

Definition of Canine Atopic Dermatitis (cAD)? Aetiology?

Answer 1

Genetically predisposed inflammatory and pruritic allergic skin disease with characteristic clinical features, associated with IgE Abs most commonly to environmental allergens
But 10-30% cases have no detectable allergen-specific IgE
Allergens e.g. house dust mites, pollens, mould spores, food allergens
High heritability (>0.5)

Question 2

Define Atopic like dermatitis?

Answer 2

An inflammatory and pruritic skin disease with clinical features identical to those seen in CAD, in which an IgE response to environmental or otherallergens cannot be demonstrated

Question 3

Pathogenesis of cAD?

Answer 3

Cutaneous inflammation and pruritus:
- allergen sensitisation and Type I and IV hypersensitivity
- the role of the T-cell
- acute virus chronic inflammation
Defective skin barrier function
Microbial colonisation
Other flare factors

Question 4

Which types of hypersensitivity are involved in cAD?

Answer 4

Type 1 hypersensitivity:
- IgE bound to mast cells
- Allergen bound by IgE causes mast cell degranulation
- Products of mast cell degranulation cause tissue inflammation and pruritus
Type IV hypersensitivity (TH2 bias)
- Allergen peptides presented to T-cells by Langerhans cells
- Induce clonal expansion
- T-cells produce pro-inflammatory cytokines which cause tissue inflammation and pruritus (IL-4, IL-5, IL-13 and IL-31) - IL-31 most important
- T-cells produce cytokines which direct B-cells to produce IgE

Question 5

What causes the subacute/chronic reaction of cAD? And what does it result in?

Answer 5

Influenced by secondary infection
TH2 bias reduced (e.g. IL-31, IL-4, IL-13)
Chronically TH1 cytokines also involved (e.g. IL-2, γ-IFN)
Tissue inflammation results in:
- Skin thickening through hyperplasia
- Increased numbers of Langerhans cells
- Reduced cutaneous barrier function
- Increased bacterial numbers on/in the skin

Question 6

Why is there a defective barrier function in cAD?

Answer 6

Increased transepidermal water loss (TEWL)
Wide intercellular spaces between corneocytes
Disorganised & fragmented lipid matrix
Decreased levels of certain proteins and lipids in some breeds
n.b. can be primary or secondary

Question 7

What microbial colonisation is seen with cAD? Why? What problems does this cause?

Answer 7

Increased carriage of Staphylococci
- Increased binding sites (due to inflammation)
- Reduced lipids and proteins (barrier function)
- Damage to skin surface (due to self trauma)
- Dysbiosis
- Reduced diversity
- Reduced balance between commensals and immune system
Very common to see secondary staphylococcal pyoderma and otitis and malassezial dermatitis in cAD = atopic flares
Induce further inflammation and pruritus - often not alleviated by specific anti-pruritics (e.g. Lokivetmab or oclacitinib)

Question 8

Common causes of atopic flares?

Answer 8

Bacteria and yeast secondary infection
Increases in allergens seasonally/changes to environment
Fleas, scabies etc
Reduction of therapy by owner/vet:
- attempts to minimise treatment
- cost
- running out of meds
- reducing meds through fears of adverse drug reactions

Question 9

Treatment aims for cAD?

Answer 9

Improve skin barrier
Allergen avoidance and ASIT
Control inflammation and pruritus
Control flare factors

Question 10

Diagnosis basis of cAD?

Answer 10

Compatible history
Clinical signs
Exclusion of differential diagnoses
Once done these, can make diagnosis (don't need allergy testing esp as 20% may be negative)
(Ie there are no pathognomonic signs)

Question 11

Differential diagnoses for pruritus?

Answer 11

Ectoparasites - Sarcoptic mange, Cheyletiellosis, flea infestation and hypersensitivity, Trombiculiasis, pediculosis, Otodectic mange, Demodex injai
Allergic skin disease - cAD, contact dermatitis
Microbial infection - bacterial pyoderma, Malassezia dermatitis
Pemphigus foliaceus
Epitheliotropic lymphoma

Question 12

Compatible history for cAD?

Answer 12

Pruritus seasonal or perennial or both
- pruritus precedes skin lesions
- 75% of dogs develop signs <3yo (up to 6yo)
- NB FIAD more commonly starts <1yo
Certain breeds predisposed (e.g. WHWT) but can be any breed
Certain breeds may have certain distribution
May have affected relatives

Question 13

cAD: Signs of pruritus? Primary lesions? Secondary lesions? Distribution of lesions?

Answer 13

Main sign is PRURITUS and precedes other lesions
Signs of pruritus = scratching, rubbing, chewing, excessive grooming or licking, scooting, and/or head shaking
Primary lesions may also include erythema +/- papules
Secondary lesions due to pruritus:
- alopecia
- excoriations
- salivary staining
- lichenification
- pustules, epidermal collarettes and crusts
- hyperpigmentation
- otitis
Distribution:
- face and chin
- periorbital areas
- ear pinna (not pineal margins)
- elbow creases
- feet (dorsal interdigital spaces and plantar/palmar)
- ventral abdomen and axillae
- perianal area
Usually bilateral symmetrical

Question 14

Favrot’s criteria (2010) for diagnosis of cAD?

Answer 14

1. Onset of signs <3yo
2. Dog mostly lives indoors
3. Glucocorticoid-responsive pruritus
4. Pruritus sine materia at onset
5. Affected front feet and/or ear pinnae
6. Non affected ear margins
7. Non affected torso-lumbar area
   5/7 signs = 85% se, 79% sp

Question 15

How to exclude differential diagnoses for cAD?

Answer 15

Exclude ectoparasites:
- flea combing
- scale exam
- acetate tape strops
- hair plucks
- skin scrapes
- treatment trials needed for parasites that are in the environment or hard to find (scabies, fleas) and treat house
Identify and treat S.pseudointermedius and Malassezia pachydermatitis (commensals of skin, overgrow due to underlying allergic skin disease):
- cytology from impression smear and/or acetate tape impression
- fungal culture no value for Malassezia

Question 16

Food hypersensitivity - Aetiology? History? Signs?

Answer 16

May be immune mediated, toxic, or non immunological
Most are food allergy and ‘atopy like’ or food-induced atopic dermatitis (FIAD)
15-60% have concurrent GI disease
Non seasonal, pruritic skin disorder associated with a new substance in the diet
Many cases are young dogs (<1yo) but not always
Pruritus is only consistent finding
May be associated with wheals, papules, erythema etc
Pruritus may be poorly responsive to steroids
Breeds predisposed: WHWT, boxer, Rhodesian ridgeback, pugs, GSD

Question 17

Comparison between cAD and FIAD?

Answer 17

Clinical signs identical except

• Poss increased Malassezia overgrowth in FIAD
• No seasonality in FIAD
• Young age of onset for FIAD
• GI signs more common in FIAD

Question 18

Food trials for FIAD/CAFR? How long for? Common allergens? Options?

Answer 18

Minimum 6 weeks (8 weeks better)
Common allergens: beef, lamb, milk (avoid these!)
Home cooked
- gold standard
- problems with identifying appropriate ingredients, unsuitable for long term use/growing animals, labour intensive, palatability, GIT upsets, cost
Commercial novel protein diets:
- nutritionally balanced
- improved owner compliance
- problems: availability of novel ingredients?, hidden allergens/additives? ‘Hypoallergenic’ means nothing on dog food so look for diets with research backing
Hydrolysed protein diets:
- assumes type I hypersensitivity so benefit for dogs with non-IgE mediated hypersensitivity unknown
- lowest allergenicity with more hydrolysation but gets expensive

Question 19

Environmental allergen testing for cAD?

Answer 19

Not a diagnostic test (false positives and negatives)
Used to identify enviro allergen-specific IgE for use in management where cAD has been confirmed
Raised serum IgE in >75% of patients
IDT or IgE serology using FcER1 technology/dog specific monoclonal Ab
- serology measures circulating allergen-specific IgE
- IDT indirectly measures cutaneous mast cell reactivity due to the presence of IgE
- poor correlation between tests
- success of ASIT not significantly different using either test
- not useful for diagnosis of food allergy

Question 20

Reasons for negative allergy testing with cAD?

Answer 20

Age of patient (<12mo often negative)
Improper technique/allergen concentration
Drug interference
Intrinsic host factors (breed differences in IgE production)
Incorrect selection of allergens
IDT performed too long after (>60d) or during peak allergy season
Atopic-like dermatitis

Question 21

Aims to improve skin barrier function for cAD?

Answer 21

Reduce transepidermal water loss
Reduce exposure to environmental allergens and irritants
Reduce microbial colonisation
Reduce cutaneous inflammation

Question 22

Treatments for improving the skin barrier function of cAD?

Answer 22

Non irritating shampoos
- emollient shampoos likely to be most soothing
- anti-seborrheic for skin greasiness or scaling
- antiseptics for infections
- add topical moisturisers to prevent excessive drying
- intensity and frequency of bathing may be most important factor
- consider impact on topical flea products (use tablets if poss)
Oral EFAs supplements/enriched diet:
- omega 3 and 6 oils
- safe
- take 8-12 weeks
- glucocorticoid and small cyclosporin sparing effect
Topical EFA-containing formulations:
- help to normalise existing stratum corner defects
- likely no benefit compared to oral supplement

Question 23

Anti-inflammatory and anti-pruritic therapies for cAD?

Answer 23

Glucoroticoids:
- systemic (pred, methyl pred, dex)
- topical (betamethasone, hydrocortisone aceponate)
Calcineurin inhibitors
- systemic (ciclosporin)
- topical (tacrolimus ointment)
Novel Janus Kinase inhibitor - Oclacitinib
Biologics - Lokivetmab
Antihistamines

Question 24

Systemic glucocorticoids for cAD - Advs? Adverse signs? When to avoid? How best used?

Answer 24

Advs - consistent efficacy with minor and predictable adverse effects
Adberse effects - polypagia, PUPD, panting, behaviour changes, iatrogenic HAC, increased UTI risk
Avoid as sole therapy in young dogs and perennial clinical signs
Good used as ‘crisis busters’:
- maintain on non-GC baseline therapy
- treat acute exacerbations with systemic GCs for 3-5 days
- if flares too frequent then need more aggressive baseline therapy

Question 25

Topical glucocorticoids for cAD - How works? Side effects? How to use?

Answer 25

Hydrocortisone aceponate Topical diester glucocorticoid Potent anti-inflammatory effect Metabolised within the dermis - very little active drug reaches circulation so minimal systemic effects Effective Major safety risk is skin thinning with prolonged use - prevented by intermittent application E.g. use twice weekly - delays recurrence of flares

Question 26

Oral clacineurin inhibitors for cAD? - How does it work? Adverse effects?

Answer 26

Ciclosporin Inhibits T lymphocyte function via blocking calcineurin Adverse effects: - GI signs - gingival hyperplasia - viral papillomas - hirsutism Effective and adverse effects usually minor Comparable efficacy to oral GCs but slower onset of action (4-8 weeks for full response) so often start with steroids then taper off

Question 27

Topical calcineurin inhibitors for cAD - what is available?

Answer 27

``` Tacrolimus ointment Suggested efficacy Expensive Not licensed Valuable in dogs with skin atrophy 'Burning sensation' reported in people ```

Question 28

Janus Kinase Inhibitor for cAD - How does it work? Adverse reactions? Contraindications?

Answer 28

Oclacitinib JAK1-enzymes involved in signal transduction of pro-inflammatory, pro-allergic and pruritogenic cytokines (IL-2, IL-4, IL-6, IL-13, IL-31) JAK2 - dependent signally associated with changes in the haematopoetic system Preferential inhibitor of JAK1 Effective and safe Rare adverse effects - mainly mild GI signs Haematological/biochem changes - significance? Haematology/biochemistry/urinalysis recommended regularly on data sheet (usually before, 6-8 weeks after and then 6 monthly) May increase susceptibility to infection and exacerbate neoplastic conditions Contraindications: <12mo or <3kg BW, breeding dogs, dogs with serious infections, underlying neoplasia, immune suppression Quick onset of action

Question 29

What is Lokivetmab for cAD? How does it work? Contraindications?

Answer 29

Anti-canine IL-31 monoclonal antibody Caninised monoclonal antibody that specifically targets and neutralises canine IL-31 (pruritogenic cytokine) Highly targeted -> minimal impact on normal immune functions Eliminated via normal protein degradation pathways (minimal involvement of liver or kidneys) Contraindicated <3kg BW

Question 30

Antihistamines for cAD?

Answer 30

Poor efficacy, good safety Chlorpheniramine and hydroxyzine may have medium efficacy combined - best used as preventative before flare occurs (continuous daily basis)

Question 31

Allergen avoidance for cAD?

Answer 31

House dust mires most important source of allergens - environmental flea sprays can reduce levels Sleep in cages etc

Question 32

What is allergen specific immunotherapy for cAD (ASIT)? How is it made? How quick does it work?

Answer 32

= administering gradually increasing quantities of an allergen extract to ameliorate symptoms associated with subsequent exposure to the causative agent. Use allergen specific intradermal testing or IgE serology to identify specific hypersensitivities Must be based on these results and history Slow onset: 4-6 months (trial for 12 months) Uncommon adverse effects but serious if occurs

Question 33

Controlling flare factors for cAD?

Answer 33

Control parasites - topical monthly treatment, treat house q4-6 months Antimicrobials (topical if poss) if signs of infection or colonisation are present Avoid known flare factors Treat secondary infections Chlorhexidine shampoos to avoid infection Stress - work related pressure, behavioural therapy, adaptil Environment - irritants, temperature, humidity Food allergens

Question 34

Monitoring of cAD therapy?

Answer 34

Assess every 2-6 weeks until stable Continue to assess every 6-12mo if good control, more frequently if poor control Tailor to individual

Question 35

What is the middle ear lined by?

Answer 35

Modified respiratory epithelium | Some ciliated and secretory cells (mucus)

Question 36

Ear margin seborrhoea - Breeds? Signs? Treatment?

Answer 36

Relatively uncommon Marked breed predilection in Dachshunds Can be a feature of hypothyroidism Adherent keratin on both medial and lateral sides of the pinna Follicular casts and plugs may trap hair Rubbing produces erosions and ulceration Pruritus is variable Fissuring and secondary infection can be problematic Treatment: emollient rinses, vaseline, propylene glycol, surgery

Question 37

Ear physiology?

Answer 37

Temp 38-2-38.4C Humidity 88.5C pH 6.2 Sebaceous glands Ceruminous glands (modified sweat glands) Lipids and sloughed keratinocytes form cerumen - traps small FB, anti-bacterial/yeast, epithelial migration moves wax from TM to external space

Question 38

Normal ear canal flora?

Answer 38

Gram +ve cocci predominate (but no growth in some dog’s ears) Similar species to those found on the skin Micrococcus spp. Coagulase negative staphylococci, Staphylococcus schleiferi and Staphylococcus pseudintermedius Streptococcus species Malassezia

Question 39

Otitis externa pathophysiology?

Answer 39

Most important factor is humidity - this changes the epithelial defences and microbiological proliferation

Question 40

Predisposing factors for otitis externa?

Answer 40

``` Conformation: - Excessive hair growth in canals (e.g. poodle) - Hairy concave pinna (e.g. cocker spaniel) - Pendulous pinna (e.g. basset hound) - Stenotic canals (e.g. shar pei) Excessive moisture: - Environment (heat & high humidity) - Water (swimmer’s ear, grooming, cleaners) Obstructive ear disease: - Feline apocrine cystadenomatosis - Neoplasia - Polyps Primary otitis media - PSOM in CKCS, tumour or sepsis Treatment effects - Altered normal microflora (e.g. inappropriate cleaner) - Trauma from cleaning or plucking ```

Question 41

Primary causes of otitis externa?

Answer 41

``` Parasites: - Otodectes cynotis - Demodex spp. - Scabies Foreign bodies: - Grass awns Hypersensitivity: - Atopic dermatitis - Food hypersensitivity - Medications Keratinisation disorders: - Primary idiopathic seborrhoea - Hypothyroidism Glandular disorders: - Cocker spaniels, English springer spaniels & Labrador retrievers have increased ceruminous glands Miscellaneous: - e.g. feline proliferative & necrotising otitis externa ```

Question 42

Otodected cynotis (ear mites) - Signs? Treatment?

Answer 42

Common cause of otitis Dark wax, small white mites (photophobic) Hypersensitivity disease Most ear creams are effective with localised disease Selamectin or moxidectin spot-on Evidence that the isoxazoline group are effective May need a cleaner ± steroids for secondary disease

Question 43

Grass seeds causing otitis - Signs?

Answer 43

Late spring to end of summer Often stimulate violent response in the affected individual - sudden onset Check the other ear! Can be hidden in discharge and migrate into middle ear

Question 44

Grass seeds causing otitis - Signs?

Answer 44

Late spring to end of summer Often stimulate violent response in the affected individual - sudden onset Check the other ear! Can be hidden in discharge and migrate into middle ear Painful - chemical restraint essential in most to remove

Question 45

Which bacteria tend to cause secondary acute and chronic otitis externa?

Answer 45

``` Acute: gram positive: - Staph - Strep - Corynebacterium Chronic: gram positive: - Enterococcus Chronic: gram negative: - Pseudomona - Proteus - E.coli ```

Question 46

What pathological changes can happen to the external ear canal as a result of otitis externa? Acute and chronic changes?

Answer 46

Inflammation causing failure of epithelial migration Acute change: oedema, hyperplasia Chronic change: proliferative change, canal stenosis, calcification of pericartilaginous fibrous tissue Hyperplasia of ceruminous and sebaceous glands Hidradenitis

Question 47

Changes to the tympanum as a result of otitis externa?

Answer 47

Dilation, rupture, diverticulum

Question 48

Clinical signs of otitis externa?

Answer 48

``` Aural pruritus or head shaking Mild to marked exudate Malodour Head tilt Deafness Erythema, swelling, scaling, discharge Pain Secondary pineal lesions, pyotraumatic dermatitis, haematoma ```

Question 49

How does otitis externa progress from primary to secondary disease?

Answer 49

Often Malassezia -> Staph -> Gram negative rods If treated inadequately, potential for antimicrobial resistance In many cases, Pseudomonas aeruginosa is end point Progressive pathoglocial changes: - Epidermal hyperkeratosis and hyperplasia - Dermal oedema - Fibrosis - Ceruminal gland hyperplasia and dilation - Abnormal epithelial cell migration - Tympanic membrane alterations - Otitis media (16% of acute OE, 50–80 % of chronic OE)

Question 50

Consequences of Otitis media?

Answer 50

Conductive deafness: - Loss of drum - High pressure fluid/mucous in the middle ear - Chronic OE or OM ± cholesteatoma Horner’s syndrome/facial paralysis: - Ear and lip droop, asymmetrical lips, dribbling - Keratoconjunctivitis sicca, neurogenic dry nose - Anisocoria with ipsilateral miosis, ptosis of the upper eyelid etc. Vestibular syndrome (otitis interna [OI])

Question 51

Horner's syndrome - Signs?

Answer 51

Drooping of eyelid on affected side (ptosis) Pupil of affected eye will be constricted (miosis), or smaller than usual Affected eye often appears sunken (enophthalmos) Third eyelid of affected eye may appear red and raised or protruded (conjunctival hyperemia)

Question 52

Primary secretory otitis media (PSOM)? Which breeds? Signs? Treatment?

Answer 52

CKCS and brachycephalic breeds Presented for deafness or neck pain! Marked mucoid build-up in the middle ear Bulging middle ear noted on otoscopy Repeated flushing and myringotomy (3-5 times) Sputolysin (mucolytic) has been used by some Steroids are used to reduce mucous production

Question 53

Clinical signs of otitis media?

Answer 53

Pain - often localised to head/neck, with spontaneous episodes of vocalisation and a guarded and horizontal neck Neurological signs: ataxia, facial paralysis, nystagmus, head tilt or seizures Pruritus around ears without external otitis Otitis externa Deafness Fatigue Signs of OI if progression

Question 54

How to investigate otitis media?

Answer 54

``` Appearance of the drum on video otoscopy Sampling of the middle ear for Bacteriology Fungal culture Cytology via myringotomy or ruptured TM Palpation of granulation tissue in the middle ear BAER (hearing testing) Imaging ```

Question 55

When is myringotomy used?

Answer 55

Bulging TM with pain or neurological signs (Horner's, vestibular signs, facial paresis) Radiographic/MRI bulla changes and intact TM Evidence of tissue or fluid behind the TM Medically unresponsive vestibular disease with an intact TM Chronic otitis cases longer than 6 months that have not responded to treatment for otitis externa (requires judgement)

Question 56

How is myringotomy done?

Answer 56

Clean and dry the external ear canal Incision made Passed through either hand held or video otoscope Position: - caudoventral aspect of the pars tensa to avoid damaging the tympanic germinal epithelium and the structures of the middle ear Sampling: - Pass swab(s) for cytology and bacteriology - instilling and then withdrawing a small amount of sterile saline solution Flush with saline (± other agents depending on the cytology results)

Question 57

BAER for otitis media? What is it?

Answer 57

Brainstem auditory evoked response Click applied to tested ear (white noise to other) Peaks of response respond to transition through differing structures (e.g. peak I = vestibulocochlear nerve) Normal dog – threshold <10dB

Question 58

Otitis interna: Aetiology? Clinical signs? Treatment?

Answer 58

``` May develop from OM extension (majority) or haematogenous and ascending infection via auditory tube Clinical signs: - head tilt to affected side - spontaneous or rotatory nystagmus - assymetric limb ataxia with preservation of strength - falling - V+ and/or anorexia Long term systemic antibiotics ```

Question 59

Options for otoscope if ear very painful?

Answer 59

Don't look Admit for chemical restraint Treat for short period and then reassess

Question 60

Examination of the ear canal with an otoscope - What to look for?

Answer 60

Is the surface of the epithelium smooth? Is the surface of the canal red? Is the lumen open and consistently so? Nature of discharge? Epithelial migration? Check for swelling, ulceration, hyperplasia, hair, masses Check for wax, pus, ear mites, foreign bodies and occlusion in lumen Drum present or absent, changes in colour, bulging? No wax in unusual, heaped or spread along canal? (Crude measure of epithelial migration)

Question 61

What does the nature of the ear canal exudate in otitis suggest for possible pathogens: - dry coffee granules? - moist brown? - purulent yellow/green (malodorous) - ceruminous discharge (often little smell)

Answer 61

Dry coffee granules - Otodectes cynotis Moist brown - Staph, Malassezia Purulent yellow/green (malodorous) - Gram -ves (esp. Pseudomonas) Ceruminous discharge (often little smell) - allergy, endocrine (esp hypothyroidism), keratinisation defects, bacteroides

Question 62

What must always be done for an otitis??

Answer 62

Cytology! +/- bacteriology and susceptibility - affected by previous antibiotic ear creams and cleaners - flawed when considering topical treatment!!!

Question 63

Indications to flush an ear?

Answer 63

Diagnostic: - To see epithelium of ear canal (hyperplasia, ulceration, masses etc) - Check integrity of drum Therapeutic: - Dilutes and removes, bacteria, yeasts and inflammatory mediators - Antimicrobial effects of some cleaners - Removes pus which may inactivate antibiotics - Removes old treatments Anaesthesia needed for adequate flushing of severe/chronic otitis (Et tube protects aspiration, hearing often present with sedation)

Question 64

What should be used to flush ears?

Answer 64

Normal saline (most often used) - safe, sterile, widely available Dilute povidine iodine - some recommend, some think ototoxicity Chlorhexidine - problematic at higher concentrations, 0.15% safe in dogs (not cat) Others for use after drum known to be intact: - cerumolytics emulsify ear wax for easy removal e.g. squalene, alcohols - aqueous solutions aid in removing pus, mucus and serum - drying agents decrease moisture and desiccate surface keratinocytes e.g. boric acid

Question 65

What are the 3 principles for treating otitis? What do medications contain?

Answer 65

1. Remove/reduce microbes 2/ Reduce swelling, discomfort or pain 3. Normalise canal lumen and function Polypharmacy - antibiotic, antifungal, anti-inflammatory agent

Question 66

How to decide with otitis ear cream/ointment to use?

Answer 66

Potency of steroid: - highly inflamed ear -> need greater potency (dexamethasone) - diabetic -> low systemic absorption (hydrocortisone aceponate) Antibiotic: - correct for cytological organisms sean - potential for ototoxicity (e.g. not gentamycin) - antibiotic stewardship (e.g. fucidic acid) Antifungal - less need for choice Ease of use - e.g. Osurnia

Question 67

Which drugs are ototoxic?

Answer 67

``` Gentamicin Polymixin B Ticarcillin and imipenem Propylene glycol Chlorhexidine at moderate concentrations If have to use, avoid concurrent use of drugs which may increase ototoxicity: - frusemide and other loop diuretics - cis-platin - erythromycin - NSAIDs ```

Question 68

What ear cleaners are available?

Answer 68

TRIZchlor - watery, disinfectant (needed for pus), doesn't sting Cleanaural - more cleaning/ceruminolytic Malacetic otic - intermediate cleaning and drying Always warm these before use! Infections - TRIZ EDTA and chlorhexidine based cleaners best Waxy - oily or alcohol based cleaners best

Question 69

What to do before using ear cleaner and ointment for severe, very swollen or great deal of discharge acute otitis?

Answer 69

Severe - consider putting charcoal swab in fridge, send off if rods always! Very swollen - steroids for 1-2 days before further otoscopic exam Great deal of discharge - admit for flush etc, treat as chronic case

Question 70

Indications for bacteriology in otitis?

Answer 70

Rods seen - most suitable antibiotic can only be chosen if organisms are known Marked purulent discharge without organisms being notes, organisms found may be relevant pathogens or irrelevant clinically Pyogranulomatous inflammation - organisms difficult to see with cytology so culture is essential In treatment failures Suspicion of MRS

Question 71

What to do with chronic allergic otitis? What organisms are involved?

Answer 71

Long term Malassezia and S.pseudintermedius overgrowth, secondary to inflammation Avoid use of antibiotics Control microflora through cleaning and overall control of cAD Use local topical steroids to control inflammation (no licensed products)

Question 72

Pseudomonas otitis - what type of bacteria is it? Problems? When seen? Signs? Associations?

Answer 72

``` Gram negative rod Highly drug resistant capsule and bacterial wall - resistant to many antibiotics and rapid development of resistance Often follow a poorly managed or untreated Malassezia or Staph otitis Swelling, pain, malodour common Green to brown-black discharge May be associated with: - immunosuppression - swimming - prior use of antibiotics ```

Question 73

Risks of flushing/treating/disease process of otitis?

Answer 73

``` Horner's syndrome/facial paralysis Hearing loss Cost - expensive if severe to treat medically Possibility of need for TECA Non licensed products Increased risk in cat ```

Question 74

Process of treating otitis?

Answer 74

``` Assess skin and ears Cytology Bacteriology Flush to clean and observe Use disinfectant cleaner Apply suitable antibiotic Provide anti-inflammatory and analgesia ```

Question 75

Example of treating otitis case?

Answer 75

Clean with saline Disinfect with TRIZChlor - 10 min soak Antibiotics e.g. Marbofloxacin/dexamethasone cream Analgesia - intraoperative opioid (e.g. morphine) and home on opioid and paracetamol Anti-inflammatory - dexamethasone IV at end of procedure Home on: - Marbofloxacin/Dexamethasone cream for 7 days - TRIZChlor starting on day 2 - Prednisolone - Reassess at 7 days, increase dose of steroids if doing well and reduce frequency of drops and cleaner

Question 76

What is ear canal stenosis a consequence of?

Answer 76

Chronic low grade trauma Severe acute disease - untreated Trauma Mucinosis +/- conformation in Shar pei

Question 77

What to do about stenosis with otitis?

Answer 77

Potent topical steroids for extended course - beware systemic side effects Oral steroids -Pred Tacrolimus ointment Intralesional steroids

Question 78

When does an ear reach the end stage?

Answer 78

When welfare of pet and family unacceptable When ear disease is intractable or very quickly recurrent due to: - stenosis - marked granulation in the middle ear - ceruminous and sebaceous gland hyperplasia Cost of repeated medical interventions is unacceptable Inability to treat ear by owner

Question 79

What are the most common bacteria and fungus commensal and also cutaneous infections of the skin?

Answer 79

S.pseudintermedius | Malassezia

Question 80

Which organism is not a skin commensal so is a primary skin pathogen, but can be carried asymptomatically in some cats?

Answer 80

Dermatophytes

Question 81

Transmission of poxvirus in cats?

Answer 81

From voles? bites -> skin lesions Don't give steroids!

Question 82

What underlying diseases could there be to bacterial pyoderma?

Answer 82

Allergy (cAD) - top! often causes recurrent pyoderma Ectoparasites - e.g. demodicosis Self trauma - pain Other infections - dermatophytosis, leishmaniasis Immune deficiency - endocrinopathy, chemotherapy, drug induced Keratinisation defects Folicular dysplasia Environment/hygiene issues Neoplasia Etc!

Question 83

Which bacteria can cause bacterial pyoderma?

Answer 83

Usually commensal bacteria from mucosal or GIT: - Staph psuedintermedius most common - S.aureus, S.schleiferi, S.hyicus less common - Gram negative or atypical bacterial uncommon-rare, usually deep infections (e.g. E.coli, Protes, Pseudomonas)

Question 84

Define intrinsic and acquired antibiotic resistance? Define multi drug resistance (MDR)?

Answer 84

``` Intrinsic resistance = expected inherent resistance to at least one drug class due to lack of target or inability to access eat cell e.g. Pseudomonas and tetracycline Acquired resistance = resistance to antibiotics that were originally effective Multidrug resistance (MDR) = acquired resistance to at least one agent in 3 or more antibiotic classes ```

Question 85

Risk factors for AMR and MDR bacteria?

Answer 85

Recent health care contact/hospitalisatiob Recent antimicrobials - particularly multiple courses or broad spectrum Coprophagia or eating raw meat diets are risk factors for faecal carriage of MDR E.coli

Question 86

Diagnosis of Meticillin resistant S.pseudintermedius (MRSP)? What are they resistant and susceptible to?

Answer 86

1. Oxacillin resistance - resistance breakpoint >0.5ug/mL or <17mm 2. mecA gene positive (PCR or PBP2a latex agglutination) Presume resistant to all beta-lactams and fluroquinolones

Question 87

What MDR bacteria are we concerned about?

Answer 87

``` MR-Coagulase positive Staph (CoPS): - MRSP - MRSA MR-coagulase negative Staph (CoNS) MDR Gram negative bacteria: - E.coli - Pseudomonas - Proteus ```

Question 88

Classification of bacterial pyoderma?

Answer 88

1. Surface = superficial epidermis, overgrowth not infection as not pyogenic 2. Superficial folliculitis = epidermis and hair follicles 3. Deep = epidermis, hair follicles, dermis +/- subcutaneous fat

Question 89

Surface overgrowth (1st level bacterial pyoderma) - clinical presentations?

Answer 89

1. 'Hotspots' = pyotraumatic dermatitis (PTD) - lesions develop within hours due to self trauma - underlying allergy (FAD) or pruritic/painful trigger - rottweiler, golden retriever, GSD predisposed - lesions usually on cheek, neck or rump - well demarcated flat eroded moist lesion with erythematous halo - treatment: clip, clean, topical antiseptic/antimicrobial, systemic/topical anti-inflammatory 2. Skin fold pyoderma = intertrigo - compromised barrier (loss of ventilation, accumulation of fluids, altered micro-climate, friction) - microbes proliferate, produce toxins and create inflammation - may have concurrent skin disorder e.g. cAD - treatment: topical antiseptics/antimicrobials and anti-inflammatories - erythema and moist exudate 3. Bacterial overgrowth - common in dogs with underlying allergic skin disease - ventral trunk and interdigital spaces - can be very pruritic - erythema, hyper pigmentation, lichenification, excoriation, alopecia - ddx Malassezia - treat with topical antiseptics/anti-inflammatories and treat underlying disease

Question 90

Malassezia overgrowths - which species? which breeds over represented? causes?

Answer 90

Usually M.pachydermatis (commensal) Basset hounds, WHWT, cocker spaniels Overgrowths secondary to underlying disease: - trigger/exacerbate pruritus and clinical lesions of cAD - some dogs are also hypersensitive Less common in cats - Devon Rex cats may be predisposed, may be flare factor for feline hypersensitivity dermatitis

Question 91

What sample technique should you use for Malassezia?

Answer 91

Dry, erythematous, scaly alopecia patch on ventral neck -> acetate tape Greasy brown wax between digits -> indirect smear using cotton bud

Question 92

Superficial folliculitis (2nd level bacterial pyoderma) - What are the primary lesions? Clinical signs?Which bacteria usually?

Answer 92

Primary lesions = follicular papule and pustules -> erythema, crusts, epidermal collarettes (rims of scale), erosions, hyper pigmented macules 'Moth eaten' in short coated breeds = annular macule of alopecia Can be pruritic or non pruritic Usually Staph.intermedius

Question 93

Define pyogenic?

Answer 93

= Degenerative neutrophils and phagocytosis of bacteria

Question 94

Deep pyoderma (3rd level bacterial pyoderma) - Features? Signs?

Answer 94

Folliculitis and furunculosis May be local, multifocal or generalised Heat, swelling, erythema, furuncles, nodules, bullae, plaques, sinus tracts, ulcers, exudation and crusts Lesions are usually haemorrhagic Pain, systemically ill, fever, lymphadenopathy Neutrophils, macrophages +/- eosinophils (chronic disease with pyogranulomatous inflammation)

Question 95

What causes acral lick lesions?

Answer 95

Obsessive licking | Could be due to allergy, orthopaedic pain etc

Question 96

Diagnosis of pyoderma?

Answer 96

``` Cytology!! Direct impression smear Cotton tip/swab smear Adhesive tape strip FNA ``` Degenerative neutrophils and intracellular bacteria is the key finding - mostly Staph pseudintermedius

Question 97

What is nuclear or DNA streaming?

Answer 97

Neutrophils casting out 'nets' to catch bacteria | Good sign of degenerate neutrophils on pyoderma cytology

Question 98

What does it mean if Simonsiella app found by skin cytology (train tracks)?

Answer 98

Indicates self trauma - been licking self as bacteria from mouth

Question 99

When to perform c+s for bacterial pyoderma?

Answer 99

Recurrent or chronic infection Poor response to adequate empirical therapy Rod shaped or unusual organisms on cytology Degenerate neutrophils bu absence of bacteria on cytology Deep infections Non healing wounds Post-op infections Life threatening infections

Question 100

What samples to get for culture of bacterial pyoderma?

Answer 100

Superficial infections: - rupture and sample intact lesion if present - sample erosion under a crust or at the edge of a collarette Deep infections: - fresh tissue sample (biopsy) - rupture intact lesion if possible - deep in sinus tract

Question 101

Treatment for confirmed pyoderma?

Answer 101

Identify and treat underlying primary disease Use topical treatment in every case where possible Topical only for surface infections, otitis externa and many cases of superficial pyoderma Systemic antibiotics if severe/widespread or deep pyoderma: - empirical if first time pyoderma, groups of cocci on cytology and no risk for AMR - S.pseudintermedius usually susceptible to B lactams (beware MRSP) Skin antiseptics: - chlorhexidine shampoo/conditioner/sprays etc Treat superficial for 2-3 weeks Treat deep for 4-12 weeks Treat past clinical and cytological cure (and palpable for deep)

Question 102

Treatment of Malassexia dermatitis?

Answer 102

Shampoo first line treatment: - chlorhexidine 2% + miconazole 2% or chlorhexidine 3% Other topical preparations - clotrimazole, miconazole etc Systemic antifungals - only if severe or chronic and underlying disease addressed Allergy vaccine if patient hypersensitive