SA skin Flashcards
Definition of Canine Atopic Dermatitis (cAD)? Aetiology?
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)
Define Atopic like dermatitis?
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
Pathogenesis of cAD?
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
Which types of hypersensitivity are involved in cAD?
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
What causes the subacute/chronic reaction of cAD? And what does it result in?
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
Why is there a defective barrier function in cAD?
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
What microbial colonisation is seen with cAD? Why? What problems does this cause?
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)
Common causes of atopic flares?
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
Treatment aims for cAD?
Improve skin barrier
Allergen avoidance and ASIT
Control inflammation and pruritus
Control flare factors
Diagnosis basis of cAD?
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)
Differential diagnoses for pruritus?
Ectoparasites - Sarcoptic mange, Cheyletiellosis, flea infestation and hypersensitivity, Trombiculiasis, pediculosis, Otodectic mange, Demodex canis/injai/gatoi
Allergic skin disease - cAD, contact dermatitis
Microbial infection - bacterial pyoderma, Malassezia dermatitis
Pemphigus foliaceus
Epitheliotropic lymphoma
Compatible history for cAD?
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
cAD: Signs of pruritus? Primary lesions? Secondary lesions? Distribution of lesions?
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
Favrot’s criteria (2010) for diagnosis of cAD?
- Onset of signs <3yo
- Dog mostly lives indoors
- Glucocorticoid-responsive pruritus
- Pruritus sine materia at onset
- Affected front feet and/or ear pinnae
- Non affected ear margins
- Non affected torso-lumbar area
5/7 signs = 85% se, 79% sp
How to exclude differential diagnoses for cAD?
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
Food hypersensitivity - Aetiology? History? Signs?
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
Comparison between cAD and FIAD?
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
Food trials for FIAD/CAFR? How long for? Common allergens? Options?
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
Environmental allergen testing for cAD?
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
Reasons for negative allergy testing with cAD?
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
Aims to improve skin barrier function for cAD?
Reduce transepidermal water loss
Reduce exposure to environmental allergens and irritants
Reduce microbial colonisation
Reduce cutaneous inflammation
Treatments for improving the skin barrier function of cAD?
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
Anti-inflammatory and anti-pruritic therapies for cAD?
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
Systemic glucocorticoids for cAD - Advs? Adverse signs? When to avoid? How best used?
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
Topical glucocorticoids for cAD - How works? Side effects? How to use?
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
Oral clacineurin inhibitors for cAD? - How does it work? Adverse effects?
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
Topical calcineurin inhibitors for cAD - what is available?
Tacrolimus ointment Suggested efficacy Expensive Not licensed Valuable in dogs with skin atrophy 'Burning sensation' reported in people
Janus Kinase Inhibitor for cAD - How does it work? Adverse reactions? Contraindications?
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
What is Lokivetmab for cAD? How does it work? Contraindications?
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
Antihistamines for cAD?
Poor efficacy, good safety
Chlorpheniramine and hydroxyzine may have medium efficacy combined - best used as preventative before flare occurs (continuous daily basis)
Allergen avoidance for cAD?
House dust mires most important source of allergens - environmental flea sprays can reduce levels
Sleep in cages etc
What is allergen specific immunotherapy for cAD (ASIT)? How is it made? How quick does it work?
= 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
Controlling flare factors for cAD?
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
Monitoring of cAD therapy?
Assess every 2-6 weeks until stable
Continue to assess every 6-12mo if good control, more frequently if poor control
Tailor to individual
What is the middle ear lined by?
Modified respiratory epithelium
Some ciliated and secretory cells (mucus)
Ear margin seborrhoea - Breeds? Signs? Treatment?
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
Ear physiology?
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
Normal ear canal flora?
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
Otitis externa pathophysiology?
Most important factor is humidity - this changes the epithelial defences and microbiological proliferation
Predisposing factors for otitis externa?
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
Primary causes of otitis externa?
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
Otodected cynotis (ear mites) - Signs? Treatment?
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
Grass seeds causing otitis - Signs?
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
Grass seeds causing otitis - Signs?
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
Which bacteria tend to cause secondary acute and chronic otitis externa?
Acute: gram positive: - Staph - Strep - Corynebacterium Chronic: gram positive: - Enterococcus Chronic: gram negative: - Pseudomona - Proteus - E.coli
What pathological changes can happen to the external ear canal as a result of otitis externa? Acute and chronic changes?
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
Changes to the tympanum as a result of otitis externa?
Dilation, rupture, diverticulum
Clinical signs of otitis externa?
Aural pruritus or head shaking Mild to marked exudate Malodour Head tilt Deafness Erythema, swelling, scaling, discharge Pain Secondary pineal lesions, pyotraumatic dermatitis, haematoma
How does otitis externa progress from primary to secondary disease?
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)
Consequences of Otitis media?
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])
Horner’s syndrome - Signs?
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)
Primary secretory otitis media (PSOM)? Which breeds? Signs? Treatment?
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
Clinical signs of otitis media?
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
How to investigate otitis media?
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
When is myringotomy used?
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)
How is myringotomy done?
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)
BAER for otitis media? What is it?
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
Otitis interna: Aetiology? Clinical signs? Treatment?
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
Options for otoscope if ear very painful?
Don’t look
Admit for chemical restraint
Treat for short period and then reassess
Examination of the ear canal with an otoscope - What to look for?
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)
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)
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
What must always be done for an otitis??
Cytology!
+/- bacteriology and susceptibility - affected by previous antibiotic ear creams and cleaners - flawed when considering topical treatment!!!
Indications to flush an ear?
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)
What should be used to flush ears?
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
What are the 3 principles for treating otitis? What do medications contain?
- Remove/reduce microbes
2/ Reduce swelling, discomfort or pain - Normalise canal lumen and function
Polypharmacy - antibiotic, antifungal, anti-inflammatory agent
How to decide with otitis ear cream/ointment to use?
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
Which drugs are ototoxic?
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
What ear cleaners are available?
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
What to do before using ear cleaner and ointment for severe, very swollen or great deal of discharge acute otitis?
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
Indications for bacteriology in otitis?
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
What to do with chronic allergic otitis? What organisms are involved?
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)
Pseudomonas otitis - what type of bacteria is it? Problems? When seen? Signs? Associations?
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
Risks of flushing/treating/disease process of otitis?
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
Process of treating otitis?
Assess skin and ears Cytology Bacteriology Flush to clean and observe Use disinfectant cleaner Apply suitable antibiotic Provide anti-inflammatory and analgesia
Example of treating otitis case?
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
What is ear canal stenosis a consequence of?
Chronic low grade trauma
Severe acute disease - untreated
Trauma
Mucinosis +/- conformation in Shar pei
What to do about stenosis with otitis?
Potent topical steroids for extended course - beware systemic side effects
Oral steroids -Pred
Tacrolimus ointment
Intralesional steroids
When does an ear reach the end stage?
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
What are the most common bacteria and fungus commensal and also cutaneous infections of the skin?
S.pseudintermedius
Malassezia
Which organism is not a skin commensal so is a primary skin pathogen, but can be carried asymptomatically in some cats?
Dermatophytes
Poxvirus (cowpox) in cats: Signs? Transmission?
Initial lesion: crusted nodule on head or forelimbs Later develop multiple macules, vesicles, erosions, crusts Not pruritic Usually self limiting From rodent bites Diagnosis: - history and signs - biopsy - virus isolation - EM - serology Don't give steroids! Antivirals Generally self limiting Zoonotic
What underlying diseases could there be to bacterial pyoderma?
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!
Which bacteria can cause bacterial pyoderma?
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)
Define intrinsic and acquired antibiotic resistance? Define multi drug resistance (MDR)?
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
Risk factors for AMR and MDR bacteria?
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
Diagnosis of Meticillin resistant S.pseudintermedius (MRSP)? What are they resistant and susceptible to?
- Oxacillin resistance - resistance breakpoint >0.5ug/mL or <17mm
- mecA gene positive (PCR or PBP2a latex agglutination)
Presume resistant to all beta-lactams and fluroquinolones
What MDR bacteria are we concerned about?
MR-Coagulase positive Staph (CoPS): - MRSP - MRSA MR-coagulase negative Staph (CoNS) MDR Gram negative bacteria: - E.coli - Pseudomonas - Proteus
Classification of bacterial pyoderma?
- Surface = superficial epidermis, overgrowth not infection as not pyogenic
- Superficial folliculitis = epidermis and hair follicles
- Deep = epidermis, hair follicles, dermis +/- subcutaneous fat
Surface overgrowth (1st level bacterial pyoderma) - clinical presentations?
- ‘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 - 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 - 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
Malassezia overgrowths - which species? which breeds over represented? causes?
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
What sample technique should you use for Malassezia?
Dry, erythematous, scaly alopecia patch on ventral neck -> acetate tape
Greasy brown wax between digits -> indirect smear using cotton bud
Superficial folliculitis (2nd level bacterial pyoderma) - What are the primary lesions? Clinical signs?Which bacteria usually?
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.pseudintermedius
Define pyogenic?
= Degenerative neutrophils and phagocytosis of bacteria
Deep pyoderma (3rd level bacterial pyoderma) - Features? Signs?
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)
What causes acral lick lesions?
Obsessive licking
Could be due to allergy, orthopaedic pain etc
Diagnosis of pyoderma?
Cytology!! Direct impression smear Cotton tip/swab smear Adhesive tape strip FNA
Degenerative neutrophils and intracellular bacteria is the key finding - mostly Staph pseudintermedius
What is nuclear or DNA streaming?
Neutrophils casting out ‘nets’ to catch bacteria
Good sign of degenerate neutrophils on pyoderma cytology
What does it mean if Simonsiella app found by skin cytology (train tracks)?
Indicates self trauma - been licking self as bacteria from mouth
When to perform c+s for bacterial pyoderma?
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
What samples to get for culture of bacterial pyoderma?
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
Treatment for confirmed pyoderma?
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)
Treatment of Malassexia dermatitis?
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
What is the most common species of dermatophyte affecting dogs and cats? Others?
Most common in dogs and cats: Microsporum canis
Others:
- Microsporum gypseum from soil
- Trichophyton mentagrophytes from rodents (more inflammatory)
Presentation of dermatophytes? Diagnosis? Treatment?
Signs:
- Multifocal patches of alopecia
- Scaling +/- hyperpigmentation
- Follicular casts
Mostly non pruritic
Diagnosis:
- wood’s lamp of hair (only 50% of M canis will fluoresce)
- trichography: arthrospores around hair shaft, hyphae within hair
- in house dermatophyte test medium (false positives and negatives)
- external lab fungal culture (gold standard/test of choice)
Treatment:
- can spontaneously resolve in 12 weeks but should be treated
- consider clipping long coated breeds
- treat until 2 negative cultures 2-4 weeks apart
- need systemic treatment to achieve mycological cure
- systemic itraconazole licensed in cats (also effective in dogs), 7 days on, 7 days off
- systemic ketoconazole licensed in dogs
- environmental decontamination (M canis viable for 18m) - sodium hypochlorite 1:10
Which demodex mites are follicular (long bodied) and surface mites (short bodied)?
Follicular mites (long bodied): - Demodex canis - Demodex injai - Demodex cati Surface mites (short bodied): - Demodex cornei - Demodex gatoi
Presentation of canine demodicosis?
Juvenile onset:
- immature immune system
- localised (<6 patches alopecia)
- generalised (includes body, feet, head)
- alopecia
- scaling
- blue-grey hyperpigmentation
- comedones
- follicular casts
- mostly resolves by self
Adult onset:
- immunosuppressive disease (e.g. HAC, hypothyroidism, neoplasia, DM, FIV, FeLV) or idiopathic
- often generalised
- often secondary bacterial infection: papules, pustules, enlarged lymph nodes
- needs aggressive treatment (lifelong treatment if idiopathic)
How does demodex present in cats?
Demodex cati: - non pruritic alopecia - minimal skin changes - often immunosuppressive disease/drugs - idiopathic Demodex gatoi: - pruritic (often self induced) alopecia, scaling - infectious (cats)
Treatment for demodicosis?
Clip long haired animals and bathe to remove debris
Treat any secondary pyoderma
Amitraz licensed in dogs
Imidacloprid/moxidectin (Advocate®): licensed, questionable efficacy
Milbemycin oxime (Milbemax®): unlicensed for demodicosis
Fluralaner (Bravecto®): unlicensed for demodicosis
Ivermectin (Panomec®): unlicensed in dogs and cats
Treat until 2-3 consecutive negative skin scrapes taken every 4 weeks
Alopecia areata
Immune mediated
Presentation of alopecia due to endocrine disease?
Symmetrical to generalised Dull and dry coat Scaling Comedones Hyperpigmentation Atrophic skin Poor wound healing Post-clipping alopecia (failure to regrow)
HAC:
- truncal alopecia
- comedones
- skin atrophy and striae (wrinkles)
- prominent blood vessels
- calcinosis cutis
- fragile skin in cats
Hypothyroidism:
- Truncal and extremity alopecia
- Myxoedema ‘tragic’ facial expression
- Weight gain
- Lethargy
- Heat seeking
Sertoli cell tumour alopecia: presentation?
More common in cryptorchid testes Testicular discrepancy Pendulous prepuce Linear preputial erythema Feminisation syndrome (attractive to male dogs, gynectomastia) Metastasis rare Local lymph nodes Rare myelosuppression Neutering curative
Telogen defluxion (effluvium): Presentation? When happens?
Sudden loss of hair - hairs synchronised into telogen
Shed as new hairs develop
Occurs 1-3 months post-stressful incident (pregnancy, lactation, severe illness, shock, surgery)
Biopsy non specific - need good history
Feline paraneoplastic alopecia: presentation?
Pancreatic and bile duct carcinomas Alopecia ventrum and legs Skin shiny and translucent Surgical excision curative Has to be early stage disease Poor prognosis - Advanced disease at presentation - Hepatic metastasis
Alopecia X: Which breeds? Cause? What happens? Diagnosis?
Plush coated breeds (pomeranians, chow chows)
Unknown aetiology – local hormone aberrance?
Primary hairs lost first (puppy coat), later complete alopecia and hyperpigmentation
Spares extremities
Diagnosis of exclusion:
- Rule out endocrinopathies
- Biopsy: follicular dysplasia
- Sex hormone alopecia profile (pre & post ACTH 17-OH-progesterone)
Treatment:
- none consistently effective, recurrence common
- neutering (males)
- melatonin
- trilostane
- may be spontaneous regrowth
Cyclical flank alopecia: presentation? Cause? Diagnosis? Treatment?
Seasonal alopecia restricted to flanks Often skin hyperpigmentation Linked to changes in day length - Reduction in day length, follicular atrophy and dysplasia - Alopecia seen as day length increases Regrowth variable Can be progressive Diagnosis: Skin biopsy Treatment: Melatonin
Post clipping alopecia: Cause? Treatment?
Unknown pathogenesis – some form of follicular arrest Rule out Endocrinopathies, severe illness Plush coated breeds Good prognosis Regrowth 6 months
Injection alopecia: Cause? Signs?
Unknown pathogenesis
- Glucocorticoids, vaccines (esp. rabies), depot antibiotics
Follicular atrophy with no inflammation (but may be immune mediated – panniculitis)
Focal alopecia +/- hyperpigmentation & atrophy
Usually local but may be remote from injection
Usually spontaneously regresses
May be permanent scarring
Congenital alopecia: Which breeds? What does it affect? Aetiology?
Defect in hair follicles Also: - Adnexae - Skin - Teeth - Claws Dominant, recessive, X-linked Hairless breeds e.g. Mexican hairless, Chinese crested, Sphinx Dysplastic hair follicle can be prone to SBI
Pattern alopecia?
Various syndromes Later onset alopecias Miniaturisation of hair Yorkshire terriers: - Pinnae, dorsal muzzle - Occasionally extremities - Alopecia and hyperpigmentation Dachshund pinnal alopecia - hyperpigmentation Greyhound: - Caudal thigh Dachshund, Boston terrier, Chihuahua, Manchester terrier, Italian greyhound - Pre and post auricular, ventral neck, ventrum, caudal thighs
Follicular dysplasia: Which breeds? What happens?
Familial disorder: - Irish water spaniel - Portugese water dog - curly coat retriever - airedale - others Dysplastic hair follicles Hairs fail to develop Shaft fractures Progressive hair loss Breed specific & wear points Regrowth of abnormal hairs
Black hair follicle dysplasia?
Familial disorder
One or more genetic defects in melanisation
Defect in pigmentation and hair formation
Progressive changes:
- Born normal, coat changes by 4 weeks
- Black hairs become dull
- Hair fracture and loss
Colour dilution alopecia?
Dilute colour coats: - Blue or fawn One or more genetic defects in melanisation Macromelanosomes (melanin clumping): - Hair fragility Progressive changes: - Hair fracture and loss - Scaling - +/- bacterial folliculitis
Treatment for weird follicular alopecia?
Avoid damage to coat
High quality nutrition (including essential fatty acid supplementation)
Gentle anti-scaling shampoos
Prevent/treat secondary bacterial infection
Protect from sun
Melatonin?
Anagen deflexion (effluvium): What happens? Cause? Signs?
Sudden hair loss: - chemotherapy - severe illness Damage to growing hair/follicle Patchy to incomplete loss - fractured/distorted hairs Loss of whiskers
Sebaceous adenitis: Breeds? Aetiology? Clinical signs? Diagnosis? Treatment?
Standard poodles, akitas
Lymphocytic immune attack on sebaceous glands
Needed for production of normal hair
Clinical signs:
- Alopecia and dull, dry coat
- Large adherent scales and follicular casts
- Bacterial folliculitis
Diagnosis:
- Trichography: non-specific follicular casts
- Skin biopsy diagnostic
Treatment:
- Skin care, replenish natural skin moisturisers: Manage SBI, shampooing, EFAs, intensive moisturisation (propylene glycol, coconut oil)
- Variable response to ciclosporin
- steroids
Causes of hyperpigmentation?
Parasites - demodicosis Hypersenstivity Trauma Infections Endocrinopathies Cyclical flank alopecia
Causes of hypopigmentation?
Immune mediated disease
Scars
Neoplasia - lymphoma
Vitiligo - immune mediated disease of melanocytes, multifocal depigmentation
What is Chediak-Higashi syndrome?
Partial albinism and neutrophil abnormalities
Blue smoke persian
What may cause secondary bacterial infection of the claws?
Hypothyroidism
What can cause fungal infection of the claws (onchomycosis)?
Dermatophytosis - often claws brittle and broken
Malassezia - often paronychia (inflammation or infection of claw folds), brown exudate under claw fold
Most common neoplasia of the claw/distal phalanx?
Squamous cell carcinoma
Symmetric lupoid onychodystrophy: Breed? Signs? Cause? Treatment?
GSD Sloughing of claws, abnormal soft, brittle claws regrow Diagnosis: - history - clinical signs - cytology - biopsy and histopath (remove third phalanx and claw bed): lichenoid interface dermatitis Treatment: - responds to corticosteroids - regular claw clipping - EFAs Aetiology unknown - classed as immune mediated
How do feline herpesvirus and calicivirus affect the skin?
Facial and nasal erosions and crusting Early lesions are pruritic Resp signs usually too (FeLV and FIV similar) No specific treatment - can try antivirals, interferon etc
Cutaneous lupus erythematosus: Clinical signs? Diagnosis?
Depigmentation, erosions, ulcers, crusting
Immune mediated
Biopsy diagnostic
Bullous phemphigoid and pemphigus vulgaris: What are they?
Similar rare conditions with disruption above (PV) or below (BP) basement membrane
Initially form fluid filled bulla or vesicle
Rapidly ulcerates
Ulceration and crusting of mucocutaenous junctions, nose, ventral body, footpads
Painful and depressed
Erythema multiforme and TEN: What are they? Cause? Signs?
• Rare diseases with necrosis of keratinocytes • Drugs, infections, neoplasia, idiopathic
• Erythema multiforme:
- Erythema, scaling, circular to arcing plaques, erosions and crusts
• TEN:
- Widespread full thickness necrosis
- Treat as severe burns
- Poor prognosis
Vesicular cutaneous lupus: What is it? Breeds? Diagnosis?
- Shetland sheep dogs and collies
- Erosions and ulcers
- Mainly face and ventral body surfaces
- May wax and wane
- Biopsy
Notoedres cati mange in cats: type of mite? Signs? Diagnosis?
Cat form of scabies - burrowing mite
Affects face - extensive crusting and pruritus around pineal margins and eyes
Diagnosis - skin scrapings
Idiopathic facial dermatitis in cats - breeds? signs?
Persians and their crosses
Inflamed, itchy, dirty faces
Commonly complicated by secondary bacterial or Malassezia infection
Difficult to manage, would probably refer
Proliferative necrotising otitis externa in young cats and kittens: Signs? Diagnosis? Treatment?
Tissue coming out of ear canal
Young cats and kittens
Biopsy diagnosis
Immunomodulatory treatment eg ciclosporin
What are the 4 feline cutaneous reaction patterns (most commonly seen with allergic skin disease)?
- Symmetrical self induced alopecia
- Head and neck excoriation/pruritus
- Miliary dermatitis
- Eosinophilic granuloma complex (eosinophilic plaque, granuloma, ulcer)
Causes of self induced symmetrical alopecia in cats?
Mostly allergic - flea bite hypersensitivity most common Pruritic: - cheyetiella - lice - otodectes - demodex gatoi - neotrombicula - bacterial folliculitis Non pruritic: - anxiety - pain (UTI, orthopaedic)
Non pruritic causes of alopecia in cats?
May or may not be symmetrical
Parasitic: Demodex cati (may be pruritic if 2ndary infection)
Infectious: Dermatophytosis (rare cases pruritic)
Internal disease:
- Hyperadrenocorticism
- Thymoma (exfoliative dermatitis)
- Paraneoplastic alopecia (shiny skin)
Causes of head and neck pruritus in cats?
Parasitic: - Otodectes - Neotrombicula - (Notoedres) - (Sarcoptes) Infectious: - Bacteria - Malassezia - (Dermatophytosis)
Causes of military dermatitis?
Most common lesion seen with flea bite hypersensitivity Parasites: - Cheyletiella - Lice - Otodectes - Neotrombicula - Endoparasites Microorganisms: - Bacterial pyoderma - Dermatophytosis Miscellaneous - Hypereosinophilic syndrome - Drug reaction - Fatty acid or other dietary deficiencies - Pemphigus foliaceus
Eosinophilic granuloma in cats: presentation?
Alopecic, raised plaque/nodule
Intact skin or eroded-ulcerated - Ulcerated lesions central white accumulations
Non-pruritic (unless secondary infection)
Caudal thighs - spontaneous regression, ?genetic
Hard/soft palate +/- necrosis
Swelling of chin (asymptomatic)
Often cats up to 1 year old
Eosinophilic ulcer in cats: presentation?
Upper lip
Well circumscribed, red/brown ulcer with raised border
Non-pruritic
Non-painful
How to rule out flea bite hypersensitivity and food induced hypersensitivity in cats = non flea non food hypersensitivity?
Ectoparasite treatment trial 8 weeks
Elimination diet 8 weeks
Treatment for non flea non food hypersensitivity in cats?
Skin barrier care - EFAs, moisturising shampoos
Anti-inflammatories/immune modulators - steroids, ciclosporin, oclacitinib (off license), antihistamines
Allergen avoidance and ASIT if allergy testing positive
Control flare factors
Which bacteria are likely in a cat, dog and rabbit’s abscess?
Cat - Pasteurella, Streptococcus, Fusiformis
Dog - Staph
Rabbit - Pasteurella
Nocardia infection: Signs? Cause? Treatment?
Rare Cats and dogs Nodular skin disease/chronic draining sinus tract Respiratory disease Entry through wound Treatment: - TMPS - enrofloxacin - amoxiclav - C+S - surgery
Juvenile cellulitis (juvenile sterile pyogranuloma): Presentation? Diagnosis? Treatment?
Puppies - big head disease, puppy strangles Facial swelling: - serous to mucopurulent discharge - otitis externa - lymphadenopathy, pyrexia, joint pain Diagnosis: clinical signs, biopsy Treatment: glucocorticoids, antibiotics
Panniculitis: what is it? Signs?
Inflammation of subcutaneous fat
Nodules with fatty, haemorrhagic discharge
Ulceration
Non healing wounds
Can be infection, immune mediated, pancreatitis
Diagnosis - cytology, biospy
Immunosuppression
Sterile granulomas and pyogranulomas: Cause? Clinical signs? Breeds?
Cause: - immune response? - persistent antigenic stimulus e.g. Leishmania, bartonella, Borrelia, Rickettsia - tick bites? Breeds: - Great dane - boxer - labrador - golden retriever - weimeraner - collies Signs: - multiple papules, plaques, nodules - muzzle, nose, periocular skin, ears, head, feet - firm, non painful, non pruritic, erythematous - may become alopecia, ulcerated, crusted and infected - systemic signs rare Diagnosis: - cytology: mature neutrophils and macrophages - biopsy: granulomas - serology - Aspergillus, crypto coccus - PCR - leishmania, Borrelia, Bartonella, Ehrlichia Treatment: - may resolve, relapse or wax and wane - surgical excision - prednisolone - niacinamide and tetracycline - azathioprine (dog) - chlorambucil (cat) - ciclosporin
Sterile granulomas and pyogranulomas: Cause? Clinical signs? Breeds?
Cause: - immune response? - persistent antigenic stimulus e.g. Leishmania, bartonella, Borrelia, Rickettsia - tick bites? Breeds: - Great dane - boxer - labrador - golden retriever - weimeraner - collies Signs: - multiple papules, plaques, nodules - muzzle, nose, periocular skin, ears, head, feet - firm, non painful, non pruritic, erythematous - may become alopecia, ulcerated, crusted and infected - systemic signs rare Diagnosis: - cytology: mature neutrophils and macrophages - biopsy: granulomas - serology - Aspergillus, crypto coccus - PCR - leishmania, Borrelia, Bartonella, Ehrlichia Treatment: - may resolve, relapse or wax and wane - surgical excision - prednisolone - niacinamide and tetracycline - azathioprine (dog) - chlorambucil (cat) - ciclosporin
Systemic histiocytosis: Presentation?
Most common in Bernese Mountain Dogs (Also Golden Retrievers, Labradors, Boxers and Rottweilers) • Age range 4-7years • No sex predisposition • Skin lesions • Single to multiple nodules or plaques • Head, neck, perineum and perigenital skin, and extremities • Haired or alopecic and erythematous • Non-painful and non-pruritic • Older lesions may have central necrosis and scarring Systemic lesions and clinical signs: • Conjunctiva, sclera, retro-bulbar tissues • Nasal cavity • Lymph nodes • Internal organs • Liver • Spleen • Lungs • Bone marrow
Systemic histiocytosis: Presentation?
Most common in Bernese Mountain Dogs (Also Golden Retrievers, Labradors, Boxers and Rottweilers) • Age range 4-7years • No sex predisposition • Skin lesions • Single to multiple nodules or plaques • Head, neck, perineum and perigenital skin, and extremities • Haired or alopecic and erythematous • Non-painful and non-pruritic • Older lesions may have central necrosis and scarring Systemic lesions and clinical signs: • Conjunctiva, sclera, retro-bulbar tissues • Nasal cavity • Lymph nodes • Internal organs • Liver • Spleen • Lungs • Bone marrow Treatment: - similar to cutaneous - not surgery - ciclosporin? Guarded prognosis
Presentation of sarcoptes scabiei mange?
Pruritus, crusts, papules, scale, alopecia
Ears, ventral chest, elbows, hocks
Superficial necrolytic dermatitis: Cause? Treatment?
Cause: - end stage liver disease - glucagonomas - diabetes mellitus Treatment: - hepatic support diet, zinc, EFAs, high quality protein, parenteral amino acid solutions - surgical removal of tumour
Zinc responsive dermatosis: Syndromes? Presentation? Treatment?
2 syndromes: - diets high in soya, cereals, calcium - zinc malabsorption Causes bilaterally symmetrical scaling and alopecia of the face, pinnae, elbows, hocks, paws, genitalia and footpads Treatment: - zinc sulphate - zinc methionine
Pemphigus foliaceus: What is it? Cause? Presentation? Diagnosis?
Most common autoimmune skin disease
Primary (idiopathic) in most cases
Diagnosis: histopathology (neutrophils and acanthocytes)
Signs:
- severe crusting, scale, erythema, pustules
- distribution: ears, periocular, dorsal nose, lips, becoming generalised
- pad hyperkeratosis
- may be pruritic
Idiopathic keratinisation disorders (primary seborrhoea): What is it? Breeds? Clinical signs? Diagnosis? Treatment?
Hereditary defect with increased epidermal turnover Breeds: - Cocker and English Springer Spaniels - Irish Setters - Dobermans - Persian cats
Spaniels: - Thick, adherent scales, erythema, seborrhoea - Lips, periocular, ventral neck and body, tail and feet - Otitis externa
Other breeds:
- Diffuse dry scaling
Diagnosis:
- difficult
- history and clinical signs
- compatible biopsy findings
- rule out other causes
Treatment:
- control secondary infections
- topical therapy
- EFAs
- retinoids (isotretinoin or acitretin)
Vitamin A responsive dermatosis: Breeds? Signs? Diagnosis? Treatment?
Cocker spaniels Signs: - marked scaling, plugging of hair follicles and frond like extrusions Biopsy strongly suggestive Treatment: vitamin A
Schnauzer comedo syndrome: breed? Signs? treatment?
Miniature schnauzers Papules, comedones, scaling and crusting along back Treatment: - keratinolytic shampoos - retinoids
Icthyosis: What is it? Signs? Prognosis?
Rare hereditary and congenital defect of keratinisation
Several types
Moderate to severe
scaling with tightly adherent scales, alopecia and secondary infection
Poor prognosis
Lethal acrodermatitis: Breed? Signs? Prognosis?
Rare hereditary condition of Bull Terriers Signs: - Stunted from birth - Scaling, crusting, erosions of extremities, footpads - Onychodystrophy - Concave hard palate - Immuodeficiency syndrome - Malassezia and Candida dermatitis - Respiratory and GI infections Prognosis very poor
Feline acne: Signs? Treatment?
Dark, waxy, scales, comedones, inflammation, Malassezia, pyoderma, furunculosis
Treatment:
- topical antimicrobials and cleansers
- retinoids
What is tail gland hyperplasia in cats? Treatment?
'Stud tail' Scale and adherent greasy material the becomes reddish brown down the dorsal tail Treatment: - neuter - topical antimicrobials and cleansers - retinoids
Diagnose: A 5-year-old, male, cocker spaniel with moderate to severe generalised scaling and patchy alopecia. The dog is overweight (BCS 7/9) but is otherwise bright and well. The scales are large, greasy, and tightly adherent. The patches of alopecia are predominantly on the trunk and are associated with papules, pustules and epidermal collarettes
Sebaceous adenitis
