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A single ion is changing how we read the story of canine heart failure. We sit down with cardiologist Dr. Darcy Adin and internist–nephrology researcher Dr. Autumn Harris to unpack why hypochloremia—once dismissed as collateral damage from diuretics—now stands out as a powerful predictor of survival in dogs with stable congestive heart failure. The conversation moves from physiology to practice, showing how chloride levels map to renin–angiotensin activation, diuretic resistance, and risk, and how that knowledge can guide smarter, earlier interventions.

We trace the research arc: early work that spotlighted chloride as more than a bystander, data linking low chloride to advanced disease stages and higher diuretic needs, and the pivotal finding that hypochloremia predicts outcomes even after controlling for other variables. Along the way, we break down renal salt sensing at the macula densa, why chloride depletion ramps up neurohormonal stress, and how this affects real dogs with mitral valve disease and congestive heart failure. If you manage CHF cases, this is practical cardiology and nephrology in lockstep.

Most importantly, we translate the science into steps you can use tomorrow. We talk thresholds and trend-watching, ensuring chloride is on every chemistry panel, covering RAS inhibition, adjusting diuretic strategies to spare chloride, and when to consider chloride supplementation. We also preview active trials targeting chloride to improve diuretic responsiveness, cut hospital time, and lift quality of life. Owners get a clear takeaway too: lab values are not just numbers; they’re signals that help personalize care and extend good days.

If you care for dogs with heart failure—or love one at home—this deep dive reframes a humble electrolyte as a crucial guide. Listen, share with your team, and help push the field forward. Enjoyed the conversation? Subscribe, leave a review, and tell us how you monitor chloride in your CHF workflow.

JAVMA article: https://doi.org/10.2460/javma.25.08.0526

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A spike in feline H5N1 cases has many of us asking the same question: how did bird flu end up in our living rooms? We sit down with author and clinician Dr. Jane Sykes to map the path from migratory birds to household pets, spotlighting the two biggest drivers of risk for cats—predation on infected wildlife and contaminated raw diets. The conversation is candid, practical, and rooted in current data, with clear guidance for veterinarians and pet owners who want to reduce danger without fear or hype.

We break down the clinical pattern that should trigger suspicion: a rapidly worsening illness with fever, lower respiratory signs, neurologic changes like ataxia or seizures, hypersalivation, and even sudden vision loss. Jane shares a step-by-step plan for what to do next: preserve the suspect diet for testing, notify local public health partners, and coordinate diagnostics through NAHLN labs with NVSL confirmation. We also unpack why household cases typically arise from common exposure rather than cat-to-cat spread, and why ending raw feeding across the home is the first and most effective intervention. The oseltamivir question comes up too; Jane weighs the risks, pharmacologic unknowns, and stewardship concerns around antivirals in cats.

Listeners get concise takeaways: cooked diets are safer, indoor life or secure catios cut exposure, and detailed dietary histories matter more than ever because many raw products look like pasteurized foods. We touch on the evolving clade 2.3.4.4b, the possibility of reassortment in cats, and why dogs appear more resistant yet still susceptible to infection. Jane points to the research we still need—serology to find silent infections, better food-chain surveillance, and communication tools that help us talk about diet without blame. Subscribe, share with a colleague or pet-loving friend, and leave a quick review to help more people find evidence-based guidance on companion animal health.

JAVMA article: https://doi.org/10.2460/javma.25.06.0388

Washington Post article: https://wapo.st/49isM8M

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A small structural “bump” on a molecule might be the big breakthrough EPM care has been waiting for. We sit down with researcher and clinician Izabela de Assis Rocha to unpack how bumped kinase inhibitors exploit a tiny difference between parasite and mammalian kinases to hit Sarcocystis neurona where it hurts—motility, invasion, and replication—while sparing the horse. It’s a molecular strategy with practical promise, and the conversation bridges the stall, the lab, and the future of equine neurology.

We break down the science behind CDPK1, the gatekeeper residue that drives selectivity, and why unique parasite structures like the apical complex and apicoplast open new therapeutic lanes. Then we move into what really matters for care: pharmacokinetics and clinical fit. BKI-1708 shows strong systemic distribution that positions it as a prophylactic candidate, while early data on BKI-1553 suggests better CNS penetration and a path toward active EPM treatment. Isabella explains how EPM’s dead-end host biology may lower the risk of widespread resistance, a rare bright spot in the antiparasitic landscape.

Clinical trials are the hard part. With no robust experimental infection model and fewer than 1% of exposed horses developing disease, enrolling enough cases takes patience and teamwork. We talk about building pragmatic, clinician-led studies, harmonizing diagnostics and neurologic scoring, and tracking relapse to find outcomes that matter to horses and owners. The One Health angle also shines through: BKIs show activity against equine piroplasmosis and have potential roles in toxoplasmosis and cryptosporidiosis, linking equine research to human and livestock health.

If you care about evidence-based equine neurology, new antiparasitic strategies, and turning elegant biochemistry into barn-side change, this is your roadmap. Subscribe, share with a colleague who manages EPM cases, and leave a review to help more veterinarians find the show. What question would you ask about bringing BKIs into practice?

AJVR article: https://doi.org/10.2460/ajvr.25.07.0270

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