Show Notes
Intro (00:00) John introduces the team of Sue Paterson and Paul Heasman, ready for another fascinating conversation with the special guest, Ross Walker.
Log this CPD with 1CPD here
Chapter 1 – What is hypochlorous? (02:05) Sue introduces Ross Walker to the podcast. Ross describes himself as Director of Clinical Health Technologies, which manufacture products based on a high purity of hypochlorous solution; this has been in the human market with the Clinisept brand, and is now moving into the animal sector with the Contego brand via Nextmune.
(02:52) Sue asks Ross how he got into working with hypochlorous acid. Ross says having worked in London and then wanting to change, he was approached to work in the field of producing a highly stabilised hypochlorous acid.
(03:35) Sue asks what hypochlorous acid is and Ross describes it as the most effective disinfectant agent known to man, but is also completely skin compatible to any mammals- so it kills things you want to get rid of without doing any harm to humans or animals.
(04:12) Sue asks how this works, and why it isn't a concern that it has the word acid in it. Ross says this is because it is an acid with a skin neutral pH, so it is non-irritant, non-sensitising and non-cytotoxic. He says it originates in our body in order to deal with invading organisms, through the process of phagocytosis - the blood cells in our body produce low concentrations and low quantities of hypochlorous.
(05:37) John ponders what the catch is and why this isn’t already widely used in the human sector and more generally. Ross describes hypochlorous Archilles’ heel - describing the first discovery of hypochlorous occurring during the first world war in 1915, where when soldiers had severe wounds as well as having been exposed to chlorine gas, it was discovered that they healed much quicker than those who had had the severe wounds without the exposure to chlorine gas. This was found to be due to the chlorine forming a solution in the water within the trenches, and this forming a level of cleanliness. The soldiers exposed to the chlorine gas we're also found to have high levels of cleanliness within the wounds. The papers published at the time concluded three things: firstly that hypochlorous was a very effective disinfectant, being bactericidal, fungicidal, viricidal and sporicidal. Secondly that it had a skin neutral pH, so therefore was contributing bacterial resistance without causing skin trauma. And thirdly, that this contributed to the perfect environment for skin healing, maintaining cleanliness without causing tissue trauma.
(08:19) Sue asks the difference between this and hypochlorite (bleach). Ross says that the two are derived from the chlorine chemistry, but that hypochlorite or bleach, is far more skin irritant, as many with no not wanting to have bleach on the skin. But that it is actually also much less effective in killing bacteria then hypochlorous. Ross demonstrates this by saying that an examination of a bottle of bleach would show a very high parts per million concentration, because hypochlorite has to be in very high concentrations in order to be effective; whereas hypochlorous can be in a much lower concentration in order to achieve the same level of efficacy.
Chapter 2: Why isn’t it being used in people? (09:51) John asks again whether this is something that is available on the human market and Ross confirms that over the years the number of companies have bought this product in the market, and much research has been done. However, it never achieves its potential because of the Achilles heel mentioned previously. Hypochlorous has a half life of 48 hours, meaning if you manufacture it you need do something with it quickly before it starts to decay; this is due to its manufacture, which in 1915 was by electrolysis – passing an electric current through a saline solution and generating a quantity of hypochlorous from the anode. This method of manufacture h
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.