The Skin Flint Podcast

Show Notes
 

This month Peter Hill (Adelaide) joins Sue and John to talk chronic otitis externa — how it develops, when it's still reversible, and how far medical management can take a case before surgery is the only option left.

Chapter 1 – Thickening the Plot

(03:04) John asks Peter to introduce himself. Peter describes training in the UK, a US dermatology residency, a mast cell PhD in Scotland, academic posts at Edinburgh, Bristol and Adelaide, and now full-time clinical work at a specialist hospital in Adelaide.

(04:42) Sue and John ask when acute ear disease becomes “chronic.” Peter says there's no fixed cut-off — chronic change means pathological remodelling of the canal lining that narrows it, making infection more likely and harder to clear.

(05:43) Peter explains the mechanism: chronic inflammation drives hyperplasia of the epidermis, dermis and glandular tissue. With nowhere else to go, this excess tissue folds into the lumen, producing corrugated, pitted linings that shelter organisms from treatment.

(08:23) Sue asks about the accompanying microbial shift. Peter frames this as dysbiosis rather than true infection — resident organisms overgrowing once the ear's natural defences are compromised, with no contagious element.

(10:05) Sue cites allergy as a trigger in up to 75% of otitis cases. Peter questions that figure as referral-population bias — in his own caseload, large numbers of poodle-cross (“oodle”) breeds get recurrent Malassezia overgrowth with no signs of allergy at all.

(12:15) Sue asks whether this matches published reports of a distinct, biofilm-associated, hard-to-resolve form of Malassezia otitis. Peter says no — his oodle cases are simply standard otitis with huge organism numbers on cytology but no inflammatory response (see References).

(13:41) Sue asks how Peter decides between medical and surgical management. He says the threshold for surgery has moved: 15–20 years ago it was pulled too early, whereas now he attempts medical reversal even in severe chronic change.

Chapter 2 – A Primary Care Problem?

(15:36) Sue asks how a primary care vet without CT or video-otoscopy should assess reversibility. Peter says history and otoscopic exam alone can't reliably predict it — safer to assume potential reversibility — while advanced imaging adds detail on lining thickness, cartilage mineralisation and otitis media.

(18:06) Sue asks whether primary care vets should refer or manage these cases themselves. Peter backs GPs to have a go, provided they think mechanistically about each treatment's purpose — he draws a parallel with allergic skin disease, where severe chronic change won't respond to a standard product any more than a standard course of ear drops will.

(21:08) John moves to treatment. Peter says the toolkit is really only antimicrobials plus corticosteroids, used in a acute phase (frequent, potent treatment) transitioning to maintenance. Systemic steroids suit acute-on-chronic inflammation and oedema; topical steroids are the better long-term option for controlling proliferative change.

(24:09) John asks which steroids Peter reaches for. Systemically, prednisolone at 2 mg/kg for a short (roughly two-week) course to settle severe acute-on-chronic inflammation, then tapering onto topical treatment — not a sustainable long-term dose.

(25:35) Sue queries 2 mg/kg against the usual 1 mg/kg anti-inflammatory dose. Peter admits it's dogma from his training rather than evidence-based, but a short, sharp high dose reliably opens an ear fast — reserved strictly for acute-on-chronic flares, never for prolonged hyperplastic change, which he treats with long-term topical steroid instead.

(27:17) Sue suggests a two-week prednisolone trial as an informal test of whether an ear will respond medically. Peter agrees only for the right case selection — used generally, on any unresponsive chronic ear, it's too simplistic a test.

Chapter 3 – Beyond the Drops

(29:29) John asks about ciclosporin and the oral JAK inhibitors. Peter first runs through topical steroid potency — a high-potency mometasone gel at the canal entrance for proliferative folds, tapering to a liquid formulation deeper in the canal. Ciclosporin is too slow for acute management but valuable long-term once the canal is functional again; oclacitinib has less dramatic impact on chronic change, but the newer JAK inhibitor (only ~6 months on the Australian market) is reportedly more effective, per colleagues elsewhere.

(34:11) John asks about tacrolimus. Not a go-to for Peter — the skin-thinning side effect that limits topical steroid use elsewhere is actually the desired effect in a thickened, hyperplastic ear canal.

(35:36) John asks how to prevent recurrence once an ear is reversed. Peter says it depends on the primary cause — allergic cases are maintained with the same anti-inflammatory drugs used for the allergy (ciclosporin, JAK inhibitors) plus routine cleaning to limit microbial overgrowth.

(37:05) John asks about surgical options. For the chronic proliferative cases discussed today, Peter's choice is total ear canal ablation — pathology is centred on the horizontal canal, which lateral wall resection or vertical canal ablation won't resolve. He reserves those procedures for congenital canal stenosis, such as in Shar Peis.

(38:12) (Outro) Sue closes by flagging designer/oodle breeds as a growing, under-explored cause of otitis worth its own future episode, and notes that despite newer anti-allergy drugs, topical and systemic steroids remain the workhorse treatment for otitis externa.

References mentioned

Nunes Rodrigues, T.C. & Vandenabeele, S.I. (2021) ‘Pilot study of dogs with suppurative and non-suppurative Malassezia otitis: A case series’, BMC Veterinary Research, 17, 1–7. PubMed

Nolitt et al. (2025) ‘Suppurative Malassezia Otitis Externa: Clinical Features, Treatment, and Preliminary Isolate Identification’, Veterinary Dermatology. PubMed

In this month's episode, Sue, John and Paul welcome Professor & Chief of Service (Dermatology) at UC Davis, Stephen D White to the podcast.

Chapter 1: Sheep Skin Detectives
(03:09) Sue sets the scope: primary-care perspective rather than rare autoimmune disease. Stephen confirms autoimmune skin disease is vanishingly rare in sheep (pemphigus foliaceus essentially unreported, bar one Barbary sheep case in a zoo).

(06:10) Sue asks whether clinical distribution helps localise the cause in a pruritic sheep the way it does in a dog or cat. Stephen explains it's less reliable — thick wool can mask hair loss even with significant pruritus, though rubbing behaviour is usually evident. Lice are visible with a hand lens; mites are not.

(08:07) Question on empirical response to treatment. Stephen notes lice usually respond well to licensed ectoparasiticides (mainly avermectins); isoxazolines are unlicensed in ruminants and unreported in sheep specifically (though used in camelids, and anecdotally a bighorn sheep). Repeat treatment at 2–4 weeks is usually needed to catch hatching eggs.

Chapter 2: Suspect Number 1 - Ectoparasites
(11:30) John asks for top differentials in a pruritic sheep, Stephen answers: “ectoparasites, ectoparasites, and ectoparasites” — mites, lice and sheep keds (which are insects, not mites). He stresses checking in-contact sheep, since one animal may be subclinical while another is severely affected.

(13:49) Sue asks why would a referral centre see an ectoparasite case at all? Stephen: usually a failed or incomplete owner-applied treatment, or a backyard sheep simply not monitored closely enough for early signs.

(15:29) On technique: always scrape if pruritic, using a medical-grade spatula rather than a blade (sheep are skittish; a slip with a blade causes injury). An otoscope with the cone removed doubles as a magnifier and light source. Dermatophytosis should also be considered — often presenting as facial alopecia rather than fleece loss — and can coexist with ectoparasitism.

(15:09) John ask about photosensitisation. Stephen distinguishes hepatogenous causes (impaired phylloerythrin metabolism from hepatotoxic plants, or a genetic defect in Corriedale lambs) from primary photodynamic plant ingestion (e.g. St John's Wort). Lesions favour the head and distal limbs. Flock-wide cases point to an environmental cause (send hay/pasture samples to the local extension lab); idiosyncratic reactions (as seen with clover in horses) may occur but are poorly documented in ruminants.

Chapter 3: Dermatological Movie Stars
(26:48) John introduces orf, referencing its cameo in Sheep Detectives. Stephen describes it as a parapoxvirus infection, usually self-limiting, but causing anorexia through oral pain — a problem in production settings. A non-resolving “super orf” form causes severe weight loss. Stephen shares data from the retrospective study: of ten orf-affected sheep, five were euthanised, due to generalised cutaneous lesions or concurrent Corynebacterium pseudotuberculosis abscesses — evidence that orf can significantly compromise immune function. One case of orf-associated facial alopecia resolved fully once the virus cleared.

(31:07) On zoonotic risk and management: gloves are essential when handling any crusting lesion in sheep or goats. Management includes moistening hay to ease painful feeding, antibiotics for secondary bacterial infection, and parenteral treatment or stomach tubing in severe anorexia.

(33:17) Sue asks about bacterial skin disease. Stephen identifies C. pseudotuberculosis and staphylococcal abscesses as the main presentations — often large, anywhere on the body, commonly peri udder in females. Internal abscessation (lungs, liver) is a key concern; aspirated purulent masses warrant involving a large-animal colleague, with caution against environmental contamination during drainage. Dermatophilosis is discussed as globally widespread and rain-associated, presenting dorsally, or interdigitally as “strawberry footrot.” Stephen references a 2008 paper (Norris) linking resistance to greasy, high-wax, low-pH, fine-fibre wool with higher suint content — traits that reduce moisture retention.

(41:10) Wrap-up: Stephen credits the study's primary author, a veterinary student, and flags Aidan Foster's JAVMA review of skin disease in alpacas, goats, pigs and sheep as further reading (both for show notes).

(42:00) Sue closes with a reflection that sheep dermatology follows the same diagnostic logic as small animal practice — FNA, impression smears, skin scrapes, hair plucks — and should feel less daunting to primary-care vets than expected.

Silly question to end: what's the most ridiculous thing you've done purely because everyone else was doing it?

 

References mentioned (from Sue’s closing remarks)

Lauth et al. (2025) – Skin disease in sheep (Ovis aries): a retrospective report of 299 cases at a university veterinary medical teaching hospital (1986–2020). Veterinary Dermatology. This is the retrospective study Stephen co-authored, discussed throughout the episode.

Wiley Online Library: https://onlinelibrary.wiley.com/doi/abs/10.1111/vde.13338 

PubMed: https://pubmed.ncbi.nlm.nih.gov/40091266/ 

Foster AP (2023) – Challenges in the diagnosis and management of skin diseases in alpacas, goats, pigs, and sheep. Journal of the American Veterinary Medical Association, 261(S1). The review article flagged in the wrap-up as further reading.

AVMA Journals: https://avmajournals.avma.org/view/journals/javma/261/S1/javma.22.12.0572.xml 

PubMed: https://pubmed.ncbi.nlm.nih.gov/36917614/

In this episode of Skinflints, we are joined by veterinary dermatologist Dr Stephen Shaw to discuss the role of JAK inhibitors in managing canine atopic dermatitis. Stephen explains the underlying disease process, highlighting the key cytokines involved in itch and inflammation, and how JAK inhibitors provide rapid, broad-spectrum control by blocking these signalling pathways.

The discussion explores how treatment should be tailored to each individual dog, considering disease severity, secondary infections and long-term management goals. Stephen also explains the benefits of using JAK inhibitors during food trials, their role alongside other therapies, and practical considerations such as monitoring, vaccination and managing concurrent disease.

The episode concludes by emphasising the importance of evidence-based treatment, informed owner discussions and regular clinical assessment, reinforcing that successful management relies on selecting the right therapy for each patient rather than adopting a one-size-fits-all approach.

This episode is kindly sponsored by MSD Animal Health

(00:00:00) John introduces a new episode on Feline Orofacial Pain Syndrome (FOPS) — a baffling condition where cats can flip from calm to frantic self-injury around the mouth and face in seconds.

 

Chapter 1: Not Toothache — Neuropathic Pain With Teeth

 

(00:03:21) Clare Rusbridge introduces herself as a veterinary neurologist focused on neuropathic pain. She first recognised FOPS working alongside dentist Norman Johnston, then developed a rare multi-disciplinary collaboration with internist Danièle Gunn‑Moore and behaviourist Sarah Heath — a clue to how complex FOPS can be.

 

(00:05:05) What it looks like: the defining feature is mutilation — cats injuring themselves trying to get at the tongue/oral mucosa (and sometimes face). Clare’s headline: don’t call simple dental pain “FOPS”. Dental disease hurts, but in “normal” pain, self-trauma should stop once it becomes painful. In FOPS, the cat may keep going, causing extreme damage.

 

(00:07:51) Clare uses a neuropathic itch analogy: ordinary itch tends to stop once it hurts; neuropathic syndromes can drive continued self-trauma despite escalating injury.

 

(00:09:03) What it isn’t: Clare cautions against over-attributing dramatic grooming/rubbing to neurology — many cats shared online as “neurological” actually have facial pruritus/dermatitis. FOPS often looks unilateral (one-sided facial targeting), though that’s harder to see if the cat is focused on its tongue.

 

(00:10:07) Classic signalment: a Burmese (or related) kitten around five months, often during teething (commonly canine eruption). Owners may find a “bloodbath” with frantic tongue trauma. Some Burmese breeders bandage paws during teething to reduce injury.

 

(00:11:29) The life-course pattern: kitten episodes may resolve once teething ends, then recur later with periodontal disease. Adult episodes are often triggered rather than continuous.

 

(00:14:57) Why it behaves like this: Clare points to trigeminal nerve pain as the leading candidate (teeth/buccal mucosa), with glossopharyngeal also plausible given tongue focus. Adult signs may be triggered within minutes after eating, drinking or grooming, echoing trigeminal neuralgia in humans where mouth movement can trigger paroxysms of pain.

 

Chapter 2: Diagnosis With a Fine Tooth Comb

 

(00:17:39) Breed/genetics: a five-month Burmese kitten is highly suspicious; Clare says she hasn’t seen the teething presentation outside Burmese/very closely related breeds (for example Siamese crosses). Genetic work suggested a likely inherited component and a strong candidate region/gene involved in neural processing, but no funded clinical test exists.

 

(00:20:10) In older cats it’s harder: Clare insists on two anchors — there must be mutilation, and it should be disproportionate to the visible dental disease (often “just a bit of gingivitis” by everyday feline standards). Dental disease remains the most common trigger.

Dentistry is central: proper evaluation usually needs sedation/GA and ideally dental radiographs to identify lesions that are easily missed on casual inspection (Clare describes cats sent to neurology as “no dental lesions” who later prove to have pathology).

 

(00:22:40) A caution for clinicians: FOPS can be worsened by suboptimal dentistry or iatrogenic irritation near trigeminal nerve roots. Clare often advises referral to a colleague with strong dentistry skills/equipment, both for patient welfare and to reduce the risk of treatment-triggered deterioration.

 

(00:24:30) When dentistry is required, she recommends appropriate nerve blocks and careful peri-dental analgesia to reduce pain wind-up.

 

(00:25:15) Neurological exam (keep it simple): focus on trigeminal sensation and compare left vs right. Clare suggests gently stimulating inside each nostril, tickling whiskers to see facial twitch, and checking medial/lateral canthal reflexes. Remember the blink/whisker/ear movement includes a motor component via the facial nerve, which is worth assessing too.

 

(00:26:40) Don’t miss other head pain: Clare highlights ocular/retrobulbar disease as an important differential and recalls a rare, very painful post-lens-trauma tumour that once presented like FOPS (she can’t remember its name).

 

Chapter 3: Stop the Mutilation, Then Treat the Triggers

 

(00:28:40) Clare splits management into three parts: acute control, chronic management, and behaviour/environment.

 

(00:29:52) Acute priorities: prevent further injury (often a buster collar) — but “collar for life” is framed as unacceptable welfare. Then move quickly to neuropathic pain control; NSAIDs/opioids may help a little but are rarely enough alone.

 

(00:31:04) Common options in practice: pregabalin (noting availability of a licensed cat product for anxiety) and gabapentin. Clare notes trigeminal pain can respond differently, and some cases need alternatives.

 

(00:32:10) Anti-epileptic drugs in FOPS: Clare describes historical acute response to a benzodiazepine during a “seizure vs pain” debate, and subsequent benefit from phenobarbital. She frames this as pain modulation rather than “treating seizures”, notes modern caution around diazepam in cats, and points out injectable phenobarbital (where available) can be very effective.

 

(00:36:00) Duration/weaning: in teething kittens, medicate through the teething window (around four weeks) then wean, especially with phenobarbital (not stopped abruptly). Warn owners about later recurrence with periodontal disease.

 

(00:37:11) Dental-triggered episodes: treat dental disease properly and continue analgesia longer than “routine”. Clare notes dental pain in normal cats can persist about a week post-procedure; FOPS-prone cats may need longer coverage plus neuropathic pain medication.

 

(00:39:32) Behaviour and environment: around 1 in 5 cases had a stress-related trigger. Common themes include multi-cat households, new cats, catteries/cat shows, builders, and environmental disruption. Clare highlights the “five pillars” approach and even unusual triggers such as strong smells (perfume/air fresheners).

 

(00:43:52) Prognosis: generally good if triggers are identified and owners accept dental investigation/management. Poorer prognosis includes refusal/inability to investigate dental triggers under sedation, or inability to medicate.

 

(00:46:05) Hard-to-treat cases: Clare mentions off-licence use of Solensia (frunevetmab) in a difficult-to-medicate cat, stressing careful risk–benefit discussion and informed consent.

 

(00:50:23) John thanks Clare for clear, primary-care-friendly guidance and points listeners to the follow-up resources she’s provided for the show notes.

 the show notes.

 

Links:

 

https://neurovet.co.uk/neuropathic-pain-syndrome/

 

https://journals.sagepub.com/doi/10.1177/1098612X241246518 Case 3

 

https://www.youtube.com/playlist?list=PLsBrqYVMr5vOBgQSAVDNKJaKfvP7gxnPd

Bow Ties and Blink Reflexes: Periocular Perils on SkinFlint

 

In this month's episode, Sue & John invite a well known vet with his eye on pet eyes - David Williams.

(00:00) John opens SkinFlint. Today’s focus is the periocular region — small real estate, big consequences — from itchy eyelids and rogue hairs to lumps and lesions that can threaten vision.

 

Chapter 1: The Eyelid Is the Windshield Wiper

 

(03:54) David Williams joins: associate lecturer in veterinary ophthalmology at Cambridge, teaching students and travelling between practices to manage eye cases. He’s been operating that morning on a severe corneal ulcer — a reminder that “eyelid problems” often matter because of what they do to the cornea.

 

(06:10) Mucocutaneous junction basics. David frames the eyelids as protective, moving structures that maintain the ocular surface. The lid margin is more than skin: it includes meibomian gland openings that support tear film stability.

 

(07:21) Tear film (briefly, promise). David describes modern tear film understanding as a mixed mucin and aqueous layer with a lipid surface. The eyelid spreads it over the cornea; tears behave as a non Newtonian fluid, becoming “runnier” as the lid moves, which helps smooth distribution during blinking.

 

(09:08) Rubbing: skin itch vs eye pain. Sue highlights the GP dilemma: is the dog rubbing because periocular skin is pruritic (allergy) or because the eye is painful? David describes the vicious cycle (irritation → rubbing → more inflammation) and stresses looking at both eyelids and the globe. Stopping self trauma (sometimes a collar) can be part of breaking the loop.

 

(11:01) Red eye triage and eyelid eversion. David’s practical tip: clinicians don’t evert eyelids enough. If both palpebral conjunctiva (inside the lid) and bulbar conjunctiva (on the globe) are inflamed, conjunctivitis is more likely. If the globe looks red but the inner lid does not, widen your differential (including uveitis and glaucoma). Don’t guess from the outside.

 

(11:45) The lash trio explained.

 

Trichiasis: normal hairs rub the cornea due to lid conformation.

Distichiasis: extra lashes from the meibomian gland orifices at the lid margin.

Ectopic cilia: a lash emerges through conjunctiva and points at the cornea — often very irritating.

 

David suggests checking for allergy clues elsewhere (paws, general pattern) if you suspect pruritus is the driver.

 

(13:33) Distichiasis: common, not always guilty. Many dogs have distichiae in both eyes without ulcers. Lashes may delay healing rather than cause the initial lesion. Plucking, freezing or electrolysis can lead to regrowth (sometimes shorter and more abrasive). If treatment is truly needed, David prefers approaches that remove the lash follicle within the eyelid to reduce recurrence.

 

(16:45) Older Cockers and “saggy lash syndrome”. David describes age related lid changes in Cocker Spaniels where long lashes start rubbing persistently. He flags the importance of a Schirmer tear test, as dry eye commonly co exists and must be addressed alongside lid conformation.

 

(18:15) Two quick diagnostics. A topical local anaesthetic drop can be used diagnostically (briefly) to see if discomfort reduces, but repeated use is unsafe for the corneal epithelium. David also reminds listeners to check the third eyelid: lymphoid follicles on its inner surface can keep an eye irritated and are only found by everting it.

 

Chapter 2: Lumps, Bumps and the Cat Exception Clause

 

(22:56) Eyelid masses: chalazion or tumour? David frames the common dilemma as meibomian gland inflammation versus neoplasia, though many cases end up managed surgically either way. In dogs, most eyelid tumours are benign (often meibomian adenomas/epitheliomas) and are usually suitable for wedge resection. His bias: remove earlier rather than later (smaller surgery, lower anaesthetic risk than waiting).

 

(24:38) When heat helps. If you suspect a meibomian gland abscess or granulomatous lesion, David suggests warm compresses applied regularly (as hot as comfortably tolerated) to encourage drainage and reduce the lump.

 

(26:20) Cats: higher suspicion. David contrasts this with cats, where eyelid tumours are more likely malignant (including squamous cell carcinoma) and may look ulcerated or invasive. He mentions photodynamic therapy as a tissue sparing option in delicate areas like eyelids.

 

(27:40) A feline oddity to remember. A dark, round medial canthus mass in a Persian cat may be an apocrine hidrocystoma (benign), and similar lesions can appear at other mucocutaneous sites.

 

(29:03) Melanomas. Behaviour varies by species and site. David is generally more concerned in cats than dogs and flags mucocutaneous junction melanomas as potentially more aggressive — excise when feasible.

 

Chapter 3: VKH — The One You Don’t Sit On

 

(30:45) Sue brings up VKH (Vogt Koyanagi Harada) syndrome, a true derm ophthalm crossover where delay can cost vision. David describes it as autoimmune disease against melanocyte associated antigens, classically seen in Akitas (but not exclusively).

 

(31:49) Clues and consequences. Skin signs may include periocular poliosis and vitiligo (white hairs/depigmentation) around the eyes and lips. The urgent issue is ocular: chorioretinal inflammation that can progress to retinal detachment and blindness.

 

(33:38) Treat early, treat hard. David cautions against slow escalation. Steroids alone for weeks may waste time, especially because azathioprine takes time to reach effect. If the posterior segment looks inflamed, he favours starting azathioprine early alongside steroids.

 

(35:06) Sue agrees: start decisively, get ophthalmology input, and monitor closely with baseline and follow up bloods due to bone marrow suppression risk (especially noted in Akitas).

 

(35:51) They land on the headline: periocular cases reward teamwork — dermatology and ophthalmology together can prevent wrong turns and speed up patient comfort.

 

(38:33) Closing banter: David’s bow tie collection and his case sharing on social media get a final mention.   Insagram @bow_teye