Ep.41 - Down Under the Ear Canal (feat. Peter Hill)

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