Épisodes

  • Ep.42 - The 2p Piece Sized Problem: Acute Moist Dermatitis Explained (feat. Rosanna Marsella)

    Ep.42 - The 2p Piece Sized Problem: Acute Moist Dermatitis Explained (feat. Rosanna Marsella)
    Oct 12 2026
    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 18:30 – John asks what else sits on the differential list. Rosanna adds food allergy, pollen allergy and mite infestations including scabies, noting that food allergy - once considered rare in her caseload - now seems far more common and has moved up her checklist. 23:03 – Sue asks what diagnostics she'd reach for to rule out mimics such as mast cell tumours or diffuse neoplasia. Cytology is quick and informative, and she'll skip a deep skin scrape if the dog's already on a reliable flea/mite product. Older dogs with cutaneous lymphoma (mycosis fungoides) can present with hot spots as just one sign - something she sees fairly often in Florida's chronic atopic dogs. 25:59 – Sue asks how to tell surface from deep pyoderma. Largely a clinical call, Rosanna says: clip and check the edges for papules (superficial) versus draining tracts, nodules and infiltrated tissue (deep) - surface cytology can under-represent a deep infection, since it only samples the tip of the iceberg. 28:19 – John asks what the treatment priorities are once AMD is confirmed. Stop the itch and self-trauma first: clean the lesion, add an antimicrobial, and control inflammation with a steroid or JAK inhibitor while working out the cause - both act at a similar speed. CHAPTER 3 - No Quick Fixes 30:58 – John asks about physical barriers such as buster collars. Rosanna avoids them, preferring gabapentin to settle the dog and keep it off the area, given the known overlap between itch and pain. 31:59 – John asks when she'd reach for systemic antibiotics. Only for confirmed deep infection after an exam and cytology, with the choice guided by the patient's antibiotic history and resistance risk. 33:38 – Sue underlines that antibiotics should never be dispensed without an exam and cytology confirming deep infection, and that a five-day course is inappropriate under current guidance. Rosanna agrees: deep infections need around three weeks with a recheck; anything more superficial needs only a short course. 35:12 – Sue asks about newer adjuncts - fluorescent light energy, ozone, medical lasers. Rosanna's experience with fluorescent light energy is mixed: occasionally useful for antibiotic-resistant deep pyoderma, but rarely justified given the cost, repeat visits and unclear benefit. 37:04 – Sue asks for Rosanna's final thoughts. Client education is the headline: owners need to understand a hot spot usually signals a bigger underlying picture, not a one-off, and that resistant infections are a one-health issue that can pass between pets and owners in the same ...
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    45 min
  • Ep.41 - Down Under the Ear Canal (feat. Peter Hill)

    Ep.41 - Down Under the Ear Canal (feat. Peter Hill)
    Sep 22 2026
    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 ...
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    44 min
  • Ep.40 - The Real Sheep Detective (feat. Stephen D. White)

    Ep.40 - The Real Sheep Detective (feat. Stephen D. White)
    Aug 7 2026
    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...
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    48 min
  • Ep. 39 - I'm All Right, JAK! (feat. Stephen Shaw)

    Ep. 39 - I'm All Right, JAK! (feat. Stephen Shaw)
    Jul 22 2026

    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
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    38 min
  • Episode 38 - Cat.exe Has Stopped Working; FOPS and the Furious Face (Clare Rusbridge)

    Episode 38 - Cat.exe Has Stopped Working; FOPS and the Furious Face (Clare Rusbridge)
    Mar 31 2026
    (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 ...
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    53 min
  • Episode 37 - Bow Ties and Blink Reflexes

    Episode 37 - Bow Ties and Blink Reflexes
    Feb 21 2026
    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 ...
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    44 min
  • Episode 36 - Hives, Lesions and Lumps; Urticaria in Horses

    Episode 36 - Hives, Lesions and Lumps; Urticaria in Horses
    Jan 7 2026
    Episode Overview Join us as we venture into the stables to explore urticaria in horses - those mysterious swellings that appear seemingly out of nowhere and may disappear just as suddenly. Expert guest Dr. Valerie Fadok shares her extensive experience as both a veterinary dermatologist and immunologist to help us understand what causes these puzzling conditions, how to differentiate them from other lumps, and when to investigate further rather than automatically reaching for steroids. Featured Guest Dr. Valerie Fadok - A dual specialist bringing unique expertise as both a veterinary dermatologist and immunologist. With experience across three veterinary schools, private practice, and as a field specialist with Zoetis, Val brings a wealth of practical knowledge from working with veterinarians and horse owners around the world. Episode Breakdown Introduction to Urticaria in Horses Val discusses how horses are the most commonly affected species with urticaria among the animals veterinarians treat, and how this condition can drive both horses and their owners to distraction. The disease presents unique challenges, with sudden onset cases that sometimes resolve on their own, and chronic cases where horses experience repeated outbreaks over time. Clinical Presentation and Diagnosis What Urticaria Looks Like: Val emphasizes the importance of palpation—urticarial lesions tend to be soft compared to nodular diseases like eosinophilic granulomasIndividual lesions wax and wane, even if the horse has hives every dayLesions can take fascinating shapes: round, linear, or ring-like configurations (serpiginous patterns)Not all horses with urticaria are particularly itchy Papular Urticaria: Papular (miliary) lesions are commonly associated with insect bitesVal shares examples of horses moving from northern US states to Florida developing papular urticaria in their first year due to high insect pressure from mosquitoes and CulicoidesThese cases often resolve after the first yearSue confirms similar patterns in the UK with Culicoides Immunological vs Non-Immunological Reactions The Role of Mast Cells: Urticaria involves mast cells in the skinImmunological urticaria occurs when allergens bind to IgE on mast cells, triggering the reactionNon-immunological causes involve "twitchy" mast cells that react to physical triggers Physical Urticaria: Pressure urticaria and dermatographism—where a handprint appears on the horse's flank after touchingCold-induced urticariaHeat-induced urticariaExercise-induced urticariaSome horses have both immunological and physical components, making diagnosis particularly challenging History is Key: Observant owners can provide crucial information (e.g., "hives appeared after training session" or "outline of saddle appeared after removal")Owner observations are often the best way to differentiate between causes Acute vs Chronic Urticaria Acute Urticaria Management: Most acute urticaria in horses is drug-related (antibiotics, pain medications) or from blood transfusionsVal's approach: Don't do an intense workup immediatelyTreat with antihistamines (Val prefers hydroxyzine) for a few months to let mast cells settleIf it recurs after stopping medication, then investigate furtherSue agrees: not chronic unless present for 8+ weeks or recurring annually When to Investigate: Sue and Val agree: 8-12 weeks or recurrent episodes warrant deeper investigationBoth emphasize the value of owners who keep detailed calendars noting when hives appear50% of urticaria in people remains idiopathic—same often true for horsesCompetition horses present particular challenges due to medication restrictions Investigation and Testing Seasonal Cases: For seasonal urticaria, Val recommends intradermal or serum allergy testingHorses with urticaria respond well to allergen immunotherapy compared to other speciesMost horse owners are comfortable giving injections Non-Seasonal Cases: Consider dietary factors and whether feed changes throughout the yearHorse owners are surprisingly open to food trialsVal has only proven a handful of food-related urticaria cases (alfalfa and grains)Diet trials are difficult in horses, though owners are willing Environmental Allergens: House dust mites and storage mites are the most commonly identified allergens across all speciesMolds are important triggers, especially in humid environmentsVal notes regional differences: Florida has unusual pollens and insects, Texas is drier with mainly pollens, Pacific Northwest sees more mold allergiesSue observes autumn cases in UK when horses start wearing rugs, potentially related to house dust mites, temperature, dampness, or molds Allergen-Specific Immunotherapy Val's Approach: Uses traditional step-up procedure for injection immunotherapyConsults pollen charts (from Greer allergy company, pollen.com, Google searches)Selects major allergens relevant to the horse's region and historyDoesn't include everything that tests positive—focuses on major ...
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    38 min
  • Episode 35 - Ferrets, Fur and Fun; Taming The Beastmasters (Madonna Livingstone)

    Episode 35 - Ferrets, Fur and Fun; Taming The Beastmasters (Madonna Livingstone)
    Nov 29 2025

    In this month's episode, Sue John and Paul invite exotics guru Madonna Livingstone onto the podcast to discuss general and skin issues in ferrets.

    Overview of ferrets as pets:

    - Ferrets have been domesticated for over 3,000 years, evolving from the European polecat.

    - They are highly social and prefer to be kept in groups of at least two.

    - Ferrets have high protein and fat dietary requirements, and need a lot of space and environmental enrichment.

    Common Skin Conditions in Ferrets:

    - Ectoparasites:

    - Fleas (usually dog and cat fleas) are the most common ectoparasite, causing pruritus and alopecia.

    - Ear mites are very common in ferrets, often asymptomatic.

    - Sarcoptic mange can affect the feet, causing severe pruritus and scabs.

    - Allergies:

    - Skin allergies are rare in ferrets, but environmental contact dermatitis can occur.

    - Food allergies are very uncommon.

    - Hormonal Imbalances:

    - Hyperadrenocorticism (adrenal gland disease) is less common than hyperestrogenism in female ferrets.

    - Hyperestrogenism can lead to alopecia, bone marrow suppression, and even death if untreated.

    Treatment Approaches:

    - Ectoparasites: Use of selamectin, fipronil, or moxidectin is recommended.

    - Allergies: Antihistamines, steroids, and omega-3/6 fatty acids can be used.

    - Hormonal Imbalances:

    - Hyperestrogenism is often managed with deslorelin implants or HCG injections.

    - Hyperadrenocorticism may require surgical adrenalectomy or deslorelin implants.

    Insights and Takeaways

    - Ferrets are unique and fascinating pets, with specific care and medical needs.

    - Skin conditions in ferrets can present similarly to dogs and cats, but there are some key differences in diagnosis and treatment.

    - Ectoparasites, especially fleas and ear mites, are very common and should be the first consideration when a ferret presents with skin disease.

    - Hormonal imbalances, particularly hyperestrogenism in females, are an important cause of skin problems in ferrets and require prompt recognition and management.

    - Veterinarians should be familiar with ferret-specific care and be prepared to handle ferret skin cases, as they may be uncommon but can be challenging.

    Conclusions and Decisions

    - Ferrets are becoming increasingly popular pets, and veterinarians should be equipped to provide appropriate care for their skin conditions.

    - Developing a good understanding of ferret biology, common skin diseases, and treatment approaches can help build confidence in managing these cases.

    - Consulting resources like the BSAVA Exotic Animal Formulary and seeking advice from experienced exotic animal veterinarians can be invaluable when caring for ferrets with skin problems.

    - Promoting proper husbandry and preventive care, such as regular ectoparasite control and monitoring for hormonal imbalances, can help minimize skin issues in ferrets.
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    49 min