Show Notes
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
More from The Skin Flint Podcast
CHAPTER 1 – Rosanna’s 2 Pennies Worth This month, Sue, John and Paul welcome Rosanna Marsella to the platform - Diplomate of the American College of Veterinary Dermatology and Professor at the University of Florida. 03:57 – John invites Rosanna to introduce herself. Thirty years as a veterinary dermatologist at the University of Florida, teaching, researching and treating small-animal allergy alongside some large-animal work; Florida's climate means plenty of infections. 04:42 – John asks how she'd categorise pyoderma. Rosanna explains it's classified by depth: surface pyoderma (often the "hot spot"), superficial pyoderma (essentially bacterial folliculitis), and deep pyoderma, where infection breaches the follicle wall into the dermis (furunculosis). 05:35 – Sue asks how dysbiosis differs from surface pyoderma. Allergic dogs already have reduced microbiome diversity, which shifts sharply toward Staphylococcus during a flare; dysbiosis is that pre-pustular shift, while surface pyoderma is the acute inflammatory skin-barrier damage that follows. 07:45 – Sue asks what AMD looks like clinically. Rosanna describes the classic picture: thick-coated dogs developing intensely pruritic, erosive lesions almost overnight on the face, rump or hips, driven by an acute trigger plus moisture trapped against the skin. 09:01 – John asks how important it is to find the trigger rather than just treat the lesion. Miss it, Rosanna says, and the dog either won't fully respond or will relapse. 09:54 – John runs through the usual suspects - fleas, allergic skin disease, ear disease, trapped moisture, pain, boredom. Rosanna splits these into predisposing factors (thick coat, heat, humidity, swimming) and primary triggers, ranking fleas top: an oral flea product still needs the flea to bite before it works, so a flea-allergic dog may also need a repellent. 13:37 – Sue asks whether lesion distribution helps distinguish flea-driven AMD from other allergies. Rosanna's rule of thumb: the back half of the body is fleas until proven otherwise; facial lesions warrant a work-up for pollen allergy or Malassezia otitis, both intensely itchy in their own right. 17:07 – John asks Sue whether "fleas first" holds in the UK climate too. Sue agrees fleas should be ruled out in every case, even with fast-acting isoxazoline parasiticides on board. CHAPTER 2 – More Than Skin Deep
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 interdigi
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.
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