scott@vtx-cpd.com

Replying to Suzi Bailey 12/05/2025 - 23:27

Hi Suzi,

Thanks so much for your great questions. I really hope you are enjoying the course.

1. Refractory or recurrent Giardia infections

You’re definitely not alone in seeing more of these. My current approach is:

If a dog doesn’t respond to a 5-day course of fenbendazole (50 mg/kg PO SID), I’ll typically repeat the same course first, as I find some dogs need two full rounds before we see clearance—especially in multi-pet households or where environmental contamination is possible.

Only after a second fenbendazole course fails would I consider combining fenbendazole and metronidazole concurrently (the latter at 10–15 mg/kg BID for 5–7 days), although I try to avoid metronidazole unless really necessary due to its potential microbiota impact.

Environmental hygiene is critical—daily bathing, decontaminating surfaces, prompt faeces removal, and sometimes bathing with chlorhexidine-based products if there’s heavy shedding.

I’m increasingly increasing fibre in the diets of these dogs.

I’ve also started incorporating faecal microbiota transplantation (FMT) more routinely for dogs with relapsing diarrhoea or poor recovery post-Giardia—especially those with previous antibiotic exposure or persistent dysbiosis.

2. Acute diarrhoea progressing to chronic enteropathy

Yes, this is something I’m seeing with increasing frequency. Dogs that start out with a single episode of acute diarrhoea (often due to Giardia or dietary indiscretion) seem to lose resilience and go on to develop chronic signs.

Like you, I suspect that:

Early or repeated antibiotic exposure, particularly metronidazole, may contribute to long-term dysbiosis and altered mucosal immune function.

There may be a “tipping point” in genetically susceptible dogs that progresses to immune-mediated enteropathy after an acute GI insult.

This is exactly why I’m cautious now with antibiotics in acute cases. Instead, I often use:

Probiotics (Visbiome, Vivomixx, FortiFlora)

Fibre supplementation (psyllium or canned pumpkin)

Clay binders, and

Close dietary review from the outset.

3. When to use immunosuppressives – before or after biopsy?

You’re absolutely right that this is nuanced. Here’s how I generally approach it:

If there is marked hypoalbuminaemia, GI bleeding, or other red-flag features (weight loss, anaemia, low cobalamin), I prioritise biopsy before steroids.

If the case is moderate and owners are hesitant, I will sometimes trial immunosuppression empirically, but I document the limitations clearly and try to re-approach biopsy if the response is incomplete.

If steroids have already been started and we’re considering biopsies, I usually recommend a washout of 2–4 weeks (depending on severity and taper status) before sampling to avoid histopathological distortion.

4. Metronidazole-responsive or dependent CE cases

Yes—I’ve had similar Golden Retrievers in particular that seem metronidazole-responsive even after extensive trials.

In these truly refractory cases:

I still trial antibiotics—but very much as a last resort, and with awareness of the long-term impacts.

If long-term antibiotics are required, I’m now more inclined to use tylosin over metronidazole, supported by evidence such as the randomized controlled trial by Kilpinen et al. (Acta Vet Scand. 2011):

Tylosin (25 mg/kg SID) was significantly more effective than placebo in dogs with presumed tylosin-responsive diarrhoea, with 85% achieving normal stool consistency during relapse episodes.
PMID: 21489311

I find tylosin to be better tolerated, with less dysbiosis and neurotoxicity risk than metronidazole.

I’ll also continue probiotics alongside to help mitigate any microbiota impact, and will sometimes reintroduce FMT or increase fibre support if relapse occurs on withdrawal.

Thanks again, really appreciated your insight here. Please do keep the questions coming, and I’d love to hear how your Golden cases evolve.

Let me know how you are getting on with the course.

Best wishes,

Scott 🙂

Replying to Anna J. 13/05/2025 - 19:19

Anna!

Welcome. Thank you for joining us!

I really hope that you enjoy the course. 3 children would be enough for me without adding in the dog and the chickens! 🙂

Scott 🙂

Replying to Jon H. 12/05/2025 - 20:48

Hey Jon.

Thank you so much for joining us and for your brilliant contribution.

My list of historical nightmares is too long to share sadly.

Scott 🙂

Replying to Jane Sedgewick 14/05/2025 - 12:07

Hi Jane,

Thank you so much for the great questions. You are definitely not a pest. It’s fantastic that you’re getting so much out of the course.

You’re absolutely right that when you have a collapsed dog with marked hyperkalaemia and hyponatraemia, Addison’s becomes the top differential, especially in the presence of classic clinical signs like lethargy, vomiting, bradycardia, and hypovolaemia. Very few diseases give you that combination in a sick dog. Once sodium is low and potassium is genuinely high (not an artefact), Addison’s should be considered the most likely diagnosis unless something else clearly explains it, like urinary obstruction or acute kidney injury.

That said, regarding your question about differentials for a low basal cortisol, there are a few scenarios where this might occur without true Addison’s:

Critical illness-related corticosteroid insufficiency (CIRCI) is increasingly recognised in dogs with sepsis or SIRS. These dogs may have a flat or blunted ACTH stim but are not Addisonian. A 2021 study by Marchetti et al. found that CIRCI occurred in nearly 50% of dogs with SIRS and was associated with increased CRP and band neutrophils, but not necessarily with hypotension or mortality. Importantly, these dogs may have low delta cortisol on ACTH testing, so we need to interpret results carefully in the ICU setting.

Reference: Marchetti M, Pierini A, Favilla G, Marchetti V. Critical illness-related corticosteroid insufficiency in dogs with systemic inflammatory response syndrome: A pilot study in 21 dogs. Vet J. 2021;273:105677. doi:10.1016/j.tvjl.2021.105677

Iatrogenic suppression from prior steroid treatment, even topical creams or ear medications.

Sampling variation. Basal cortisol is highly dynamic and a low result can sometimes occur transiently in otherwise healthy or mildly stressed animals.

Hepatic dysfunction or severe systemic illness, which can affect cortisol metabolism or binding proteins.

That’s why, even in the face of compatible electrolytes and clinical signs, a low basal cortisol doesn’t confirm Addison’s. It just tells us we can’t rule it out. That’s where the ACTH stim is still essential. On the flip side, a basal cortisol above 55 nmol/L (around 2 µg/dL) is very helpful to exclude Addison’s.

The combination of all three in a collapsed dog dose make Addison’s the most likely thing! It’s questions like this that make the course better, so please do keep them coming.

Happy Sunday!

Scott 🙂