The Skin Flint Podcast

• Episode 33 - Bulldogs, Pugs and Plenty of Folds; A Deep Dive into Brachy Skin

  Chapter 1 – Intertrigo: Prevention, Work-Up, and When (Not) to Use Antibiotics (00:11) John introduces the podcast episode and the hosts. (02:39) John welcomes Dr Laura Buckley (Senior Lecturer, Veterinary Dermatology, University of Liverpool) and asks what “brachycephalic” means and which breeds it covers. Laura explains shortened muzzles and broad, domed heads; the most extreme include French and British Bulldogs, Pugs and Boston Terriers, with Cavaliers, Chihuahuas and Dogue de Bordeaux also affected. (04:00) Sue notes their huge popularity in UK primary care. Laura adds that around 40% of her clinic can be French Bulldogs, with brachycephalics a very large overall share. (04:33) Sue asks which skin problems are most common. Laura explains that atopic dermatitis and otitis (externa/media) lead, with interdigital furunculosis also frequent. Cavaliers often show primary secretory otitis media. Skin-fold dermatitis (intertrigo) and muzzle furunculosis are common, and lesions can form over bony prominences where itchy dogs rub. (06:15) Sue asks what intertrigo is and why brachys get it. Laura explains shortened muzzles leave redundant skin that folds around eyes and muzzle, creating humid, low-airflow pockets that accumulate keratinous/sebaceous debris. Microbial overgrowth follows; bristly coats plus rubbing traumatises follicles and escalates inflammation. (08:06) Sue asks about prevention. Laura suggests daily fold hygiene from the start: clean away debris; consider antiseptic wipes (e.g., chlorhexidine) once or twice daily, and increase during flare-prone periods. (09:15) Sue highlights how early routines improve compliance and handling; Laura agrees it gives a “head start,” especially as atopy often appears within the first three years. (10:08) John asks how early disease presents and how to work it up. Laura explains earliest signs are diffuse erythema in the fold, then partial/complete alopecia, erosion/ulceration, crusting; severe untreated cases may progress to folliculitis and even deep pyoderma. (11:48) Sue asks about cytology. Laura explains it’s pivotal: expect keratinous debris with cocci (staphylococci) or Malassezia in overgrowth; neutrophils with intracellular bacteria indicate infection and guide therapy. (12:57) John asks if systemic antibiotics are ever needed. Laura explains they’re rarely indicated: most cases respond to topical antiseptics/antimicrobials plus strong anti-inflammatory control. Consider systemic antibiotics only for genuine deep, painful, draining pyoderma, immunosuppression, poor feasibility for topicals, or proven topical failure - always post culture & susceptibility. (15:47) John asks how she controls inflammation. Laura uses topical glucocorticoids (often in combination products). For severe inflammation, short anti-inflammatory courses of prednisolone (~0.5–1 mg/kg for a few days before tapering) can calm tissue so topicals can work. (16:48) Sue asks about long-term routines and when to consider surgery. Laura advises daily fold cleaning (once–twice daily) and twice-weekly topical anti-inflammatories (e.g., hydrocortisone aceponate or mometasone) with minimal systemic absorption; discuss surgery if medical care is impractical, or if maintenance fails with frequent relapses or recurrent infections. Chapter 2 – Viral Pigmented Plaques (VPP) (19:33) John moves to VPP and asks which brachy breeds are affected. Laura most often sees Pugs, plus Boston Terriers, Chihuahuas and French Bulldogs. (20:25) Sue asks what they look like. Laura describes numerous, heavily pigmented, slightly raised plaques that may begin flatter and become scaly, verruciform and hyperkeratotic over time. (22:00) Sue asks how to differentiate melanoma. Laura says biopsy/histopathology is the diagnostic choice; FNAs from plaques are often low-cellularity keratinocytes, whereas melanoma cytology differs. (23:43) John asks if plaques regress. Laura explains most persist or increase, likely due to a virus-specific, genetically influenced immunodeficiency in otherwise healthy, often young dogs. For treatment, Laura notes most are cosmetic, but very rarely plaques can transform to SCC, so monitoring matters. Limited numbers can be removed surgically or with laser; for numerous lesions consider systemic/medical options (e.g., azithromycin, interferon, retinoids, vitamin A, topical imiquimod) with variable success. (25:35) Sue summarises a primary-care approach: monitor unless numerous, pruritic, function-limiting or rapidly changing. Laura agrees; schedule regular reviews. Chapter 3 – Seasonal Flank Alopecia (SFA) (26:30) Sue introduces SFA and asks what it is and why it happens. Laura explains it’s a localised cyclic follicular dysplasia linked to photoperiod and melatonin; predisposed breeds include Boxers, Affenpinschers, British Bulldogs, Staffies and Chihuahuas. (29:40) John asks about geography. Laura notes seasonality is more marked away from the equator where day-length swings are greater. Sue recalls light-box data suggesting equal photoperiod may prevent SFA; both agree the pattern fits a light/melatonin mechanism. (30:18) Sue contrasts the clinical picture with endocrine alopecia. Laura explains SFA shows sharply demarcated, bilateral flank patches (± hyperpigmentation). Endocrinopathies tend to be diffuse, affect coat quality and other sites (e.g., tail). (32:27) Sue asks differentials and work-up. Laura highlights hypothyroidism and Cushing’s; use signalment and systemic signs, then haematology/biochemistry ± T4/TSH and targeted endocrine tests as indicated. (33:03) Sue asks about monitoring. Laura expects regrowth in spring within 1–4 months as day length rises, though a minority become permanently alopecic. (35:45) John asks about treatment. Laura reassures it’s cosmetic once endocrinopathies are excluded; many owners opt to observe. For those wanting intervention, oral melatonin and increased light exposure are reasonable. (37:30) John thanks Laura and invites her for episode 2!

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• Episode 32 - Resistance is Futile! Managing MRS in Practice

  Chapter 1: Meet the Microbes (02:41) John opens the episode, introducing Dr Vanessa Schmidt and inviting her to share her background. Vanessa explains her role at the University of Liverpool, her PhD in antimicrobial resistance in staphylococci, and her leadership in infection control and antimicrobial stewardship. (03:38) John asks whether staph infections in pets are usually caught or part of their natural skin flora. Vanessa replies that most infections come from an animal's own commensal microbiota, which coexist harmlessly but can cause disease when the immune system or skin barrier is compromised. (05:07) Sue asks whether humans and animals share the same commensals. Vanessa explains that while many organisms are shared across species, each host also harbours unique flora. Cross-species transfer is possible but not common. (06:16) Sue asks whether different body sites have different staph species. Vanessa says this is well-mapped in humans, while in pets we know carriage is common in the nose, mouth, and perineum, but site-specific species need more study. (07:28) John asks about coagulase-positive vs coagulase-negative staph. Vanessa explains that coagulase-positive staph are generally more virulent, while coagulase-negative species can still be important, especially in immunocompromised hosts or in association with implants. (09:37) Sue asks how to interpret a coagulase-negative result on a lab report. Vanessa advises considering clinical context, immune status, culture growth level, and cytology to judge significance. (12:34) Sue emphasises the value of cytology. Vanessa agrees, explaining it's routine in dermatology and helps identify intracellular bacteria and neutrophilic inflammation.   Chapter 2: Resistance Training (14:30) John transitions to methicillin resistance. Vanessa explains MRSP carries the mecA gene, conferring resistance to beta-lactam antibiotics. It spreads clonally and is more stable than resistance in Gram-negatives. (17:40) Sue asks whether antibiotic use can switch the resistance gene on or off. Vanessa says it's about selection pressure - resistant strains survive when antibiotics are overused. (19:03) Sue shares her “rucksack” analogy. Vanessa agrees, adding that over time resistant strains adapt, carrying resistance genes more efficiently. (20:15) John asks about zoonotic risk. Vanessa confirms bacteria like MRSP can pass between pets and owners, though actual infections are rare.   Chapter 3: Less is More: Treating MRS the Smarter Way (22:33) Sue asks about managing MRSP pyoderma in practice. Vanessa outlines a tiered approach: treat the underlying disease, apply barrier nursing, and use topical therapy like chlorhexidine, aiming to avoid systemic antibiotics. (27:00) Sue raises chlorhexidine use and guideline updates. Vanessa recommends 2% or above concentrations of chlorhexidine and warns that dilution reduces effectiveness and may lead to treatment failure. (30:05) Sue mentions suspected resistance. Vanessa confirms resistance is reported and linked to bacterial efflux pumps. She uses hypochlorous acid or bleach as follow-up options in certain MRSP cases. (33:15) John asks what Vanessa avoids. She avoids systemic antibiotics in superficial MRSP unless absolutely needed, and tailors treatment to the underlying disease. Immunosuppressives are avoided if the infection arose due to immune compromise. (35:00) Sue asks about treating MRSP otitis. Vanessa explains that lower chlorhexidine concentrations are potentiated by TRIS-EDTA, so she still uses them as first-line ear cleaners. (36:40) John asks about long-term carriage. Vanessa explains MRSP can persist for months or even years. Decolonisation before high-risk surgery is common, but long-term clearance is difficult and evidence is limited. (39:42) Sue summarises the discussion: in MRSP, less is more - fewer antibiotics and more topicals. New guidelines offer hope for better resistance control.   ISCAID guidelines https://onlinelibrary.wiley.com/doi/10.1111/vde.13342?af=R&utm_campaign=Nextmune%20-%20Nextmune%20UK%20Updates&utm_source=hs_email&utm_medium=email&_hsenc=p2ANqtz--e1aa7hsXEupaiUzNH8tbxLSDEH8s4jALF4ScLWjefX83QJvKt5H20n5xE--r0sn9CVwFI   Protect Me guidance from BSAVA https://www.bsava.com/Resources/Veterinary-resources/PROTECT-ME/

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• Episode 31 - Son of a Birch! The Pollen Predicament

  Show Notes On this month's episode, Sue, John and Paul invite Darragh O'Hanlon (@thetopicalvet)  onto the pod to discuss pollen allergies. Chapter 1 – How Pollens Affect Animals (02:32) John introduces the topic of pollen allergies and welcomes guest Darragh O’Hanlon. Darragh shares how Sue’s lecture on otitis sparked his dermatology journey, and how John’s CPD also played a role. (04:09) John asks how pollens cause allergic reactions in animals. Darragh explains that pollens are airborne reproductive grains from grasses, trees, and weeds, and describes their microscopic structure and typical transmission routes. He shares the story of Mitzi the fox terrier, one of the first dogs documented with airborne pollen allergy. (06:30) Sue asks whether pollens affect more than just the skin. Darragh explains that: In dogs, pollens mostly trigger atopic dermatitis but can also affect eyes and ears. Cats may show respiratory and skin symptoms, including asthma and eosinophilic conditions. Horses show skin reactions like urticaria and, in some regions, respiratory issues like heaves. (08:45) John asks why grass pollens are so problematic over say garden flowers. Darragh notes a rising trend in grass pollen allergy and explains the volume and dispersal of wind-pollinated plants. Garden flowers are less allergenic due to heavier, insect-borne pollen; wind-pollinated plants like grasses and trees produce vast quantities of light airborne pollen. Sue discusses tree flowers and their pollen production. (11:30) Sue asks which trees cause the worst reactions. Darragh highlights birch as a major allergen in Northern Europe. He explains its cross-reactivity with other tree pollens and regional variations such as cypress (Mediterranean) and cedar (Japan). Conifers and pines, though present in air samples, are less allergenic due to their size and resin content. Chapter 2 – Seasons, Cross-Reactions, and Geography (14:20) Sue asks about pollen season overlap and the role of allergy testing. Darragh agrees and describes how pollen calendars can predict seasonal challenges. He outlines Ireland’s pollen calendar, from alder and hazel in winter through to weeds in autumn. (16:20) John asks if pollens cross-react with each other or be linked to food sensitivities. Darragh explains: Cross-reactivity is common among grasses and within trees and weeds. Birch is highly cross-reactive. Some food cross-reactions exist in humans (e.g. Mugwort-Birch-Celery Syndrome), but evidence in dogs is limited. (19:55) Sue mentions bee foraging and asks about using tape strips to detect pollens on animals. Darragh shares anecdotes and online interest in identifying pollens via tape stripping. (21:36) Sue asks about ragweed in Ireland. Darragh says it’s rare locally but problematic in the US. He discusses its introduction to Europe and control measures. (23:20) John asks how pet owners can reduce pollen exposure. Darragh shares advice: Allergen avoidance is difficult; pollens travel long distances. Regular washing, foot rinsing, and barrier-supporting shampoos help. Avoid walking dogs on freshly cut grass or on high pollen days. (26:10) John asks about environmental factors like altitude or proximity to the sea. Darragh explains: Pollen can travel thousands of kilometres. Grass pollen is more localised than tree pollen. Higher altitudes and coastal winds can reduce exposure. (29:12) Sue mentions a 2023 study on reactions to grass sap, not just pollen. Darragh reflects on cases that may fit contact dermatitis patterns seen with grass sap exposure. Chapter 3 – Testing, Treatment & Takeaways (31:14) Sue asks for practical advice on pollen avoidance and resources. Darragh recommends: Monitoring pollen forecasts (e.g. Met Office, Met Éireann). Using allergy maps from dermatology providers. Avoiding warm, dry, windy days; walking dogs after rain. Understanding how weather affects pollen counts, including the impact of thunderstorms and urban pollution. (35:15) John asks about immunotherapy and vaccine formulation. Darragh explains: Allergen-specific immunotherapy aims to desensitise. Earlier intervention is better. Cross-reactivity helps simplify formulations. (38:36) Sue stresses that vaccine components must reflect relevant, local allergens. Darragh notes the importance of seasonal coverage and discusses challenges with mixing mould and pollen extracts. (41:05) Sue shares an anecdote about a mismatched allergy vaccine and wraps up with thanks to Darragh. Useful Links: Nextmune – Veterinary allergy diagnostics and immunotherapy. https://nextmunelaboratories.co.uk/

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• Episode 30 - Understanding The New ISCAID Pyoderma Guidelines

  This podcast is based upon the new 'Antimicrobial use guidelines for canine pyoderma by the International Society for Companion Animal Infectious Diseases (ISCAID)' available HERE   (00:00) John introduces the podcast with his co-hosts Sue Paterson & Producer Paul.   Chapter 1 – Understanding Pyoderma and the Need for New Guidelines   (02:56) Sue welcomes Dr. Anette Loeffler, who introduces herself and her background in veterinary dermatology. Originally from Germany, she studied in Munich and has worked in the UK for over 30 years. She is currently a dermatologist at the Royal Veterinary College (RVC) and has a special interest in Staphylococcus and bacterial skin infections and this has led her to work over the last 4 years on the new pyoderma treatment guidelines, aimed at improving antibiotic use and promoting topical therapy.   (04:30) Sue asks Anette to explain antimicrobial stewardship and why it is important. Anette describes antimicrobial resistance as a major global threat. Overuse of antibiotics leads to resistance, so it is crucial to avoid unnecessary prescriptions and focus on appropriate diagnostics.   (06:10) Sue asks how common pyoderma is in domestic species, particularly dogs and cats. Anette explains that staphylococcal pyoderma is very common in dogs due to their unique skin structure, making them more prone to bacterial overgrowth. While cats and other species can develop bacterial skin infections, it is far less frequent and usually not recurrent.   Chapter 2 – Diagnosing and Classifying Pyoderma   (08:00) John discusses evolving perspectives on pyoderma classification and asks if the traditional categories of superficial and deep pyoderma are still relevant. Anette confirms that the new guidelines still use these classifications as they help determine treatment:   Surface pyoderma (dysbiosis): Often in skin folds where bacteria and yeast overgrow due to friction and moisture. Superficial pyoderma: Involves hair follicles and is the most common type. Deep pyoderma: A more serious infection requiring systemic antibiotics.   (10:19) Sue notes that past treatment approaches lacked strong clinical evidence. Anette explains that many historical treatment protocols were based on anecdotal evidence rather than research. While deep pyoderma has more robust studies, superficial cases often lacked proper research, leading to overuse of antibiotics.   (13:04) John asks how vets can determine whether a case is surface, superficial, or deep pyoderma. Anette explains that clinical examination alone can often differentiate them:   Surface infections show redness and are in friction areas (e.g., nasal folds, hotspots). Superficial pyoderma presents with papules, pustules, and epidermal collarettes. Deep pyoderma causes swelling, draining tracts, haemorrhagic crusting, and pain.   (16:04) Sue asks how to confirm true bacterial pyoderma and rule out mimicking conditions. Anette stresses the importance of cytology, a simple and cost-effective test that can quickly confirm bacterial involvement. Cytology can also differentiate between bacterial infections, yeast overgrowth, and sterile pustular diseases.     Chapter 3 – Treatment Approaches and Key Takeaways from the New Guidelines   (19:36) John asks about traditional treatment approaches and why they need updating. Anette outlines how older guidelines recommended unnecessarily long courses of antibiotics (e.g., 3-4 weeks for superficial pyoderma, 4-6 weeks for deep pyoderma). While this was logical before antimicrobial resistance became a concern, modern research supports shorter, targeted treatments. (26:13) Anette explains the new recommendations:   Surface pyoderma should be treated topically only – systemic antibiotics are inappropriate. Superficial pyoderma should primarily be treated with topical therapy – which has been shown to be as successful as a course of antibiotics. Deep pyoderma requires systemic antibiotics but can benefit from adjunctive topical treatment.   (32:40) Sue asks about helping vets communicate these new approaches to pet owners. Anette explains that the guidelines include tables, visual aids, and quick-reference guides to support busy practitioners.   (33:28) John asks about when systemic antibiotics are still necessary. Anette explains that systemic therapy is still essential for deep pyoderma or when topical treatment alone is impractical (e.g., large dogs, owner limitations). In such cases, culture and susceptibility testing should guide antibiotic choice.   (38:15) Sue asks which antibiotics should be the first choice if empirical treatment is necessary. Anette recommends clindamycin, lincomycin, cephalexin, or co-amoxiclav as first-line choices, with fluoroquinolones reserved for resistant infections.   (42:32) Sue asks Anette for her top five takeaways from the guidelines:   Read the dog, not just the textbook. Diagnose based on clinical lesions and determine if the infection is surface, superficial, or deep.   Use cytology whenever possible. It’s quick, inexpensive, and helps confirm bacterial involvement.   Always look for the underlying cause. Pyoderma often recurs due to allergies or hormonal conditions.   Prioritise topical therapy. Topical antimicrobials alone are effective for many skin infections, reducing antibiotic use.   Use systemic antibiotics responsibly. Empirical choices should be limited to first-line drugs, and culture should guide second-line therapy.   (45:45) Sue mentions that the full guidelines will be available online via: WSAVA, ISCAID, and WAVD. Sue also mentioned a  WAVD webinar Anetta hosted, which is a must watch. The guidelines are currently available HERE   (47:29) Outro – As always, Sue & John wrap up before John asks his co-hosts a light-hearted question to end on

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• Episode 29 - How Complex is Eosinophilic Granuloma Complex?

  Show Notes This month, the Skin Flint team welcome RCVS & European Specialist Debbie Gow to the platform to explore Eosinophilic granuloma complex (EGC). (00:00) John Sue and Paul introduce the podcast.   Chapter 1 – What on Earth Is Eosinophilic Granuloma Complex?   (02:55) Sue welcomes Debbie Gow to the podcast and invites her to introduce herself. Debbie shares that she is a specialist in veterinary dermatology, working at a busy referral hospital outside Edinburgh. She describes her role in setting up the dermatology service, working with a resident and derm nurse, and her continued involvement in CPD and writing.   (04:05) Sue introduces the topic: eosinophilic granuloma complex (EGC) in cats. She jokes that it’s sometimes referred to as “eosinophilic granuloma confusion” due to its complexity and terminology. She asks Debbie to break it down explaining that EGC is an umbrella term for three lesion types: Linear granulomas: Seen on the backs of legs, chin, or in the mouth. May or may not be itchy. Plaques: Often pruritic, ulcerated, and secondarily infected. Found on the ventrum or medial thighs. Indolent ulcers: Located on the upper lip, may appear crater-like.   (07:28) Sue asks about miliary dermatitis. Debbie considers it a separate reaction pattern, not part of EGC, though also common and allergy-associated. (08:15) John asks about age, breed, or sex predispositions. Debbie explains that while any cat can be affected, young adult cats (6 months to 5 years) are most likely to develop these lesions. Females may be slightly overrepresented, but evidence is limited. (09:27) John inquires about geographical prevalence. Debbie confirms EGC is seen globally wherever cats are present and exposed to allergy triggers.   Chapter 2 – Lookalikes, Lip Lesions & Licking Cats: Sorting the EGC Puzzle (10:21) Sue asks whether EGC lesions are pathognomonic or if there are important differentials. Debbie stresses the importance of not assuming a diagnosis without investigation whilst they can have a classical appearance: Cytology is key to identifying eosinophils. Differentials include squamous cell carcinoma (particularly for lip ulcers), mycobacteria, fungal infections, and viral diseases.   (12:37) Sue asks about a minimum diagnostic approach. Debbie advises: Cytology Wood’s lamp and trichogram to rule out dermatophytosis Consideration of biopsies if in doubt   (14:08) Sue asks how to perform cytology. Debbie describes: Tape prep for dry lesions Cotton bud for moist/crusted areas Direct impression with a slide   (14:59) Sue asks how often infection is present. Debbie says: Infections are uncommon but more likely with plaques due to licking Cytology helps assess if antibiotics are needed Most cases are treated with anti-inflammatories rather than antibiotics   (16:52) John asks about allergic patterns in cats. Debbie describes four main reaction patterns: Miliary dermatitis Head and neck pruritus Ventral overgrooming Eosinophilic lesions She notes cats may display multiple patterns and also non-skin signs like conjunctivitis, otitis, or sneezing. (19:02) John asks if specific allergies present with specific signs. Debbie says it’s inconsistent. While flea allergy is often associated with miliary dermatitis and food allergy with head/neck pruritus, patterns vary and aren’t reliable for diagnosis.   Chapter 3 – Practical Approaches: From Kitchen Floor to Referral Door   (21:23) John asks what owners might notice or try at home. Debbie recommends: Observing behaviour Keeping a diary Ensuring flea control Considering recent diet or environmental changes   (23:30) Sue asks about food trial myths. Debbie emphasises: Over-the-counter “hypoallergenic” foods are not suitable for true food trials Prescription hydrolysed diets or novel proteins (e.g. ostrich, kangaroo, crocodile) are required Food trials should run for ~8 weeks She also recommends: Treat toppers to help encourage eating Short-term feeding is usually nutritionally safe Veterinary nutritionist input for longer-term plans   (28:43) Sue asks how to start a food trial if a cat is self-traumatising. Debbie uses concurrent systemic treatment (usually steroids) to control inflammation during the trial, tapering meds over 4–6 weeks if possible. (30:05) John asks for the first steps as a guide for primary care vets. Debbie recommends her first steps would be to rule out ectoparasites with full household flea control, possibly whilst beginning topical/systemic treatment as needed for comfort (32:10) Sue asks what to do when left with suspected environmental allergy. Debbie describes: Referral approach: Intradermal testing and immunotherapy if cost allows (40–75% success rate) Primary care approach: Use steroids at the lowest effective dose Importance of prioritising flea control and food trial first as they are often curative   (36:50) Sue and Debbie have a healthy debate on the relative benefits of allergy testing when immunotherapy is not being considered as an option.  (41:08) John wraps up the episode, thanking Debbie for simplifying a complex topic and helping listeners better understand eosinophilic granuloma complex in cats. John asks Paul and Sue another probing - if not questionable - question.

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