117 | The microbiome and its role in gastrointestinal disease: everything vet nurses need to know about it in 2026

The microbiome is probably THE most talked about area of GI disease this year.

And with good reason - because it’s fascinating, and we’re only learning more and more about it as time goes on.

The microbiome is linked to so much more than ‘just’ dysbiosis - from gastrointestinal disease to cancer, emotional health and much more, this unseen but mighty ‘virtual organ’ is hugely important in our patients.

And as our understanding of it grows, so too does our role in supporting patients as veterinary nurses and technicians.

In episode 117 of the Medical Nursing Podcast, we’re discussing exactly what the microbiome is, what we know about it so far, what affects it, and what happens when we see dysbiosis - a disruption in the normal microbial balance.

And, of course, we’ll look at how we can use more of our skills to support patients with dysbiosis - from support during diagnostics, to faecal microbiota transplantation and much more.

Let’s get started.

What is the microbiome, and why is it so important in small animal gastrointestinal disease?

Before we start, I want to quickly explain a couple of terms, because you’ll hear the microbiome called different things.

The microbiota is the community of living organisms - the actual bugs - while the microbiome, to be technically correct, is the collective genome. By this, I mean it’s all the genes that these organisms carry. To be honest, most of the time we use the term ‘microbiome’ as a catch-all term, or some people will use these terms interchangeably. I’ll be using ‘microbiome’ today - but before we get into the episode, I want to point out the technical difference between the two.

With that said, put simply, the microbiome is a collection of microorganisms - bacteria, yeasts, protozoa, viruses, fungi, etc. We have several distinct microbiomes - as well as in our GI tract, we have a microbiome on our skin, in our respiratory system, in our urogenital system, etc.

When looking at the role of the microbiome, we need to remember the different ways that microorganisms exist on or in a host. 

They can either be:

  • Commensal: Where the microorganism (or microorganisms) benefits while the host is neither helped nor significantly harmed. Basically, the commensal organism ‘eats at the same table’ without causing any trouble.

  • Symbiotic: Where there is a mutually beneficial relationship between the microorganism and host. For example, some GI bacteria receive nourishment from things like complex sugars in our food, and we’re better able to digest those nutrients as the bacteria have helped to break them down.

  • Pathogenic: Where the microorganism benefits but also in the process harms the host, causing disease, damage or infection.

In the microbiome, these microorganisms should be commensal or symbiotic - either not harming, or directly benefiting, the host.

Dysbiosis is a disruption in the balance of these microorganisms. This may mean reduced numbers of certain microorganisms, or a shift in the balance between symbiotic and pathogenic species, for example.

In dogs and cats, bacteria make up around 98% of the GI microbiome, and there are a LOT of them - around 100 trillion microbial cells in the intestine.

That’s up to ten times more actual cells in the whole body - so technically, our patients (and us) are more bacteria than we are human, cat, or dog!

And when you count genes, the microbial genes outnumber the host's own genes by something like ten to one. So actually, we could argue that we should think of any animal as a kind of multi-species hybrid, with host cells and microbial cells working together.

Each microbiome is a distinct community, shaped by its own little environment. Current research suggests that we begin as ‘sterile’ beings - ie, with no microbiome at all. During parturition, when that puppy or kitten is born, they pick up many of their first organisms from the dam or queen's vaginal, oral and skin communities. So those maternal microbiomes are literally where life begins for the gut.

Looking at that gut microbiome in more detail, the number and diversity of those microorganisms increase as we move from the stomach down to the colon. The stomach holds relatively few bacteria, mostly Helicobacter species and some lactic-acid producers, because it's an acidic, hostile place - it’s supposed to be; its job is to break down food. 

The small intestine carries a mix of aerobes and facultative anaerobes like Lactobacillus and Streptococcus. And then the colon is the busy end, packed with obligate anaerobes such as Bacteroides, Clostridium and Fusobacteria.

The main bacterial groups across dogs and cats are fairly consistent and include Firmicutes, Bacteroidetes, Proteobacteria, Fusobacteria and Actinobacteria. While we see varying proportions of each of these between individuals, these big bacterial families are seen consistently.

So that’s what the gastrointestinal microbiome is - what affects its composition in cats and dogs?

Well, the biggest factors in cats and dogs are thought to be diet, environment, age and developmental stage, genetics, medications and health status. 

The role of diet in the canine and feline microbiome

In multiple studies, diet has been identified as the primary influence on the structure and function of the gut microbiome, both in the short term and over the long term. 

Diets higher in protein and fat tend to increase levels of things like E. coli, Clostridium perfringens and Fusobacteria. Diets higher in fibre feed the fibre-fermenting bacteria within the gut, like Faecalibacterium, Megamonas, and Prevotella. These bacterial species produce beneficial metabolites - known as ‘post-biotics’ which help the gut. 

The digestibility of the diet also matters - poorly-digestible protein and fat sources have been linked to disruption of the microbiome.

I also want to mention that cats and dogs are not the same here - we know that there are different nutrient needs across species, and their microbiomes respond differently to this. In fact, some studies have shown that the feline microbiome responds more quickly to dietary changes than dogs; however, the most important message here is that they respond differently, rather than the timing itself. We can’t assume that cats and dogs have the same response 

The role of genetics in the canine and feline microbiome

The microbiome, like our patients, is continually evolving. It begins at birth through the maternal skin and vaginal flora, and is shaped by things like maternal grooming, lactation, and then the individual puppy or kitten’s environment.

It varies early on and takes time to stabilise into a mature community of beneficial microorganisms.

Many of the milestones our neonatal patients move through as they grow - weaning, for example, will have significant effects on the microbiome. In the very early stages, before weaning, environment is the biggest factor impacting the microbiome - until diet takes over as the patient begins eating ‘proper’ food.

The role of medications in the GI microbiome

Lastly, we need to talk about medications, because these can significantly impact the microbiome.

Antibiotics are the obvious category to mention, because they can have significant and long-lasting effects on the microbiome. They reduce bacterial diversity and balance within the GI tract, and this change can persist for some time.

In fact, in one study, tylosin caused a persistent drop in bacterial diversity in around 40% of dogs. 

Other medications, like antacids such as omeprazole, can alter the microbiome - though these changes tend to be shorter-lasting and resolve when the medication is stopped.

In fact, this explains why we have really moved away from routine antacid use in recent years, and why we can often see things like diarrhoea with omeprazole use.

How do we assess the gastrointestinal microbiome - and when do we need to?

I don’t want to make this a super deep and scientific episode, I want to make sure it is practical for all of us as veterinary nurses and technicians - but it’s important to mention how we assess the microbiome and how we’ve learned so much about it in recent years.

Until recently, culture was the only way we could assess bacteria, so taking a sample. Incubating it on an agar plate and seeing what grows. The problem with this is that most GI bacteria are anaerobic (i.e., they do not use oxygen for cellular respiration) and will not grow in standard lab conditions.

Culture definitely still has its place in GI disease, though. We use it heavily to detect things like Salmonella and Campylobacter, for example - it’s just not suitable for looking at the entire GI flora.

Now, thanks to things like bacterial DNA sequencing, we have a much better idea of what’s going on in that gut. We also have tests like FISH (fluorescence in-situ hybridisation), which allows us to detect different bacteria within GI tissue, and in fact, this is a test we run relatively commonly on endoscopic biopsies if we suspect invasive bacteria are causing disease.

Lastly, I want to mention something you’ll probably have heard of - the dysbiosis index. This is a panel of PCR tests that looks at key bacteria in the microbiome and then turns that into a single result you can interpret - so we’ll often use this to quantify changes to the microbiome in a patient with GI disease.

All of these different testing methods have taught us a few things about the microbiome.

First, every individual is different.

Each patient carries a unique community of microorganisms, with its own proportions of the major groups. 

Despite this, the genes these microorganisms carry are similar, which is why patients can have changes in the particular makeup of their microbiome, but those different organisms can carry out the same functions.

These highly individualised changes also explain why patients don’t respond to many GI interventions in the same way - different diets, different probiotics, etc, will not reliably have the same effect across individual patients.

Second, measuring the microbiome is challenging and is not without limitations.

If we think about what impacts the microbiome, it’s a lot. In humans, the microbiome is known to be affected by things like diet, sleep, environment, when a person eats, medications, hydration, exercise and much more.

So if the microbiome is ever changing, measuring it will only really give us a ‘snapshot’ of a much bigger picture.

Additionally, there's no standardisation between laboratories, so the same sample can give different answers depending on how the DNA was extracted and analysed. 

Lastly, we need to look at more than ‘just’ the microbiome.

The GI tract will often tell us there’s a problem through systemic signs or wider bloodwork changes - for example, dysbiosis often affects things like B12 and folate results. Because pathogenic bacteria within the gut can ‘eat’ the B12 and excrete folate, a low B12 in the face of a high folate level is highly suggestive of dysbiosis. 

So we need to ask ourselves - is there always a need to perform dysbiosis assessment, if we’re already highly suspicious of this? These are all things our clinicians need to consider when working up a patient with GI disease.

The link between the microbiome and disease in cats and dogs

This is a really important area to discuss because the microbiome plays a bigger role in disease (in general) in our patients than I think we’ve all appreciated.

The microbiome is responsible for, or contributes to, so many important physiological processes, including:

  • Supporting metabolism and energy

  • Creation of vitamins such as B-vitamins and vitamin K

  • Competing for space and nutrients with pathogenic bacteria, controlling levels of them and maintaining balance

  • Regulating the immune system

And much more. So we can see the role of the microbiome extends way past the GI tract - and dysbiosis has a bigger impact on our patient than ‘just’ within the gut.

In fact, alterations to the microbiome have been linked with chronic enteropathy, chronic kidney disease, obesity, diabetes mellitus, atopic dermatitis and immune-mediated disease. And in humans, neurodevelopmental and mental health conditions such as Alzheimer's disease and depression are also highly associated with the microbiome.

The link between the microbiome and disease in veterinary patients

Studies have shown that obese patients have an altered microbiome, with lower populations of energy-harvesting microorganisms than lean cats.

Again, in cats, there is a link between intestinal lymphoma and dysbiosis. Studies suggest that chronic dysbiosis causes inflammation, which in turn changes the environment and can increase the risk of neoplasia.

And another area that we’re learning more and more about is the link between the gut and the brain - and how dysbiosis impacts the emotional health of our patients.

The gut-brain axis and the role of stress in small animal GI disease

There are both neurochemical and anatomical links between the gut and brain. The two communicate via the bloodstream and the nervous system (the vagus nerve), but also via neurotransmitters.

This means the gut and brain are more heavily linked than we’ve previously thought, and this is an essential consideration for us as veterinary nurses and technicians.

Studies looking at germ-free mice raised with no microbiome showed they were generally more anxious, less social, and had exaggerated stress responses - but when the microbiome was recolonised early, these changes resolved. If it was left too late, some of these changes became permanent - so the microbiome seems to be help with brain development.

In fact, around 90% of the body’s serotonin is made and stored in the gut, from bacteria that convert tryptophan in the diet into serotonin. Other bacteria within the microbiome produce GABA, and others are involved in the production of things like dopamine - so we know the role between gut and emotional health is really important.

We also know that stress impacts the gut.

Stress causes the release of things like cortisol and other stress hormones, which can weaken the GI barrier and negatively impact the microbiome, predisposing our patients to dysbiosis.

So this means a stressed patient can develop GI disease, and because we’ve got that bidirectional communication between the gut and brain, GI disease can manifest as emotional or behavioural signs, rather than obvious GI signs.

In fact, one study showed that cats with inflammatory gastrointestinal disease showed increased levels of anxiety and care-soliciting or attention-seeking behaviour than healthy cats, and it’s the same for cats with inflammatory skin disease.

For us, as veterinary nurses, this is really important. We need to be looking beyond the obvious or ‘traditional’ signs of GI disease, and asking our clients about things like the home environment, subtle signs of stress, or other changes that could impact the gut-brain axis.

We need to be on the lookout for signs such as pica, toileting or appetite changes, repetitive licking or overgrooming - and it’s the same in dogs. Many dogs who compulsively lick surfaces or even lick the air have underlying GI disease, and often treating their underlying disease resolves these behaviours.

So that’s the importance of the microbiome and its role in disease - let’s chat a bit more about dysbiosis.

We’ve touched on what dysbiosis is, but in reality, it’s way bigger than just a change in the microbiome.

Dysbiosis means a change in the makeup or the diversity of the gut microbiota that affects how it functions. 

As well as being a change in those microorganisms, it’s also a change in the beneficial effects of them. It’s a change in the metabolites they produce, their genetic makeup, and a weakening of the intestinal barrier - either in one area of the GI tract, or throughout all of it.

There are usually three types of dysbiosis: a loss of beneficial bacteria, a drop in overall bacterial diversity, or overgrowth of pathogenic bacteria. These three types will often overlap in the same patient. 

Other factors suggested to impact dysbiosis include:

  • Abnormal substrates within the gut, like undigested food, which drive metabolites that cause diarrhoea

  • An increase in total bacterial numbers, especially in the small intestine, producing more toxic metabolites

  • An increase in the more invasive, mucosa-adherent bacteria, which cause inflammatory changes in the intestinal wall

And of course, we need to look at how underlying GI disease is linked to dysbiosis as well. In chronic inflammatory enteropathy, we end up in a vicious cycle where the intestinal mucosa is remodelled due to chronic inflammation. This then impacts absorption, meaning undigested substrate sits in the intestinal lumen. This food feeds bacterial overgrowth, which drives more dysbiosis, and the cycle continues.

What signs do we see in a patient with dysbiosis, and how is it managed?

The clinical signs are really variable because it depends on the location and severity of the dysbiosis, and whether there’s an underlying gastrointestinal disease.

Patients may be asymptomatic, or we may see things like vomiting, diarrhoea, inappetence, weight loss, and these signs may be acute or chronic.

Usually, patients with acute diarrhoea have milder microbiome changes compared to patients with chronic enteropathy. Acute patients also tend to have self-limiting changes to their microbiome, and that’s exactly why current evidence recommends NOT using antibiotics in acute diarrhoea - because we’ll worsen the dysbiosis, rather than improve the diarrhoea significantly.

Treating dysbiosis is multimodal, including diet, probiotics, and potentially other treatments - like FMT.

Let’s start by looking at the importance of diet.

Highly digestible diets reduce the amount of undigested nutrients within the gut, and therefore the availability of food for bacteria, meaning it’s harder for them to overgrow.

Just like any other GI patient, if a food sensitivity is suspected, an appropriate hydrolysed or novel-protein diet should be selected - just like we discussed last week in episode 116.

Fermentable fibres are also fantastic in patients with dysbiosis, because they are converted into short-chain fatty acids by colonic bacteria. These fatty acids feed the epithelium in the gut and lower the pH within the intestinal lumen, and this makes it harder for pathogens to thrive.

Then we’ve got pre- and probiotics.

Prebiotics are non-digestible fibres like psyllium and fructooligosaccharides. These act as food for the beneficial bacteria in the gut, boosting production of those short-chain fatty acids.

Probiotics are the actual live beneficial organisms - and they’re really strain-specific. Make sure you know the strain numbers in the probiotics you’re using, and if you’re using them for management of a specific condition, there’s evidence showing that the particular strain of bacteria in your probiotic will help.

And then we’ve got faecal microbiota transplantation, or FMT.

FMT is a growing procedure in small animal GI disease, and one which we’re ideally placed to run as veterinary nurses and technicians.

The concept is exactly what it sounds like - you take faeces from a healthy donor and transfer it into the GI tract of a diseased recipient, to restore a healthy microbiome.

So, how is FMT performed?

Fresh faeces is collected from an appropriate donor, blended with saline, and strained to make a liquid solution.

This is then administered either rectally as a retention enema or endoscopically instilled directly into the GI tract.

Oral capsules are also available, depending on your location. I personally have no experience with the capsules, though I have heard their large size can make at-home administration challenging for clients.

What makes an appropriate faecal donor?

Selecting the right donor is really important - probably more important than we’ve previously considered, given what we now know about the role of the microbiome in behaviour and obesity.

And it’s also one of the biggest areas we’re involved in as veterinary nurses.

We need our donors to be:

  • Clinically healthy

  • Of a normal body condition score

  • Emotionally healthy

  • Without any history of chronic GI signs

  • Dysbiosis index normal

  • Tested negative for infectious agents

  • Antibiotic-free for at least 6 months

  • Not on a raw diet

  • Rescreened regularly (at least every 6 months)

FMT is a safe, well-tolerated and minimally invasive procedure, and this can be performed by veterinary nurses and technicians under direction - so it’s a great use of our skills.

Speaking of, how can we use more of our skills to support dysbiosis patients as veterinary nurses?

Well, if we think about where our role fits in working up GI disease, it’s huge.

History taking is really, really important here, and it's so often nurse-led. We need to look at things like diet, recent medications, any GI signs, and now, after everything we've said today, behaviour too.

Every single visit, we should be asking about toileting patterns and faecal scoring using a standardised chart, such as the Purina faecal score system - and we’re ideally placed to do this as vet nurses.

Where further GI interventions are needed - such as endoscopy, which we’ll discuss in detail in a separate episode - the nursing role is huge. We discussed it in episode 116 so I won’t repeat too much here, but things like anaesthesia support and management, endoscopy assistance and sample handling are really important.

Speaking of sampling, there’s also sample collection and handling for Dysbiosis Index testing, client education around diet, prebiotics and probiotics, and monitoring response over time, including reinforcing that the microbiome takes months to recover even when the patient looks well. We mentioned last week that expectation management and support are essential in GI disease to help with client compliance, and that’s true for dysbiosis patients too.

Antimicrobial stewardship is another big one. We've seen today that antibiotics often aren't the answer in acute diarrhoea, and that they come with significant consequences to the microbiome. And while we’re not prescribing as vet nurses, we are often the ones having those conversations with clients, explaining why diet and supportive care are preferred and why antibiotics are not always the answer.

And then there’s FMT itself. We can - and should - be the ones preparing the product, running and coordinating a donor screening programme, administering the FMT, and looking after both our donors and recipients. As FMT becomes more widely performed - and it is - this is a real area we can champion as veterinary nurses and technicians.

So let’s sum up everything we’ve discussed in today’s episode because it’s been a big one - one of the biggest deep dives we’ve done in a while, actually - and there’s been a lot of science.

The microbiome is a vast, individual, dynamic ecosystem that does a lot more than ‘just’ digest food. 

It trains the immune system, makes metabolites that help maintain the GI barrier, and it's in constant bidirectional communication with the brain.

Dysbiosis is a disruption in the balance within this ecosystem, and it occurs for many reasons - such as dietary changes, environmental changes, underlying disease, and even emotional changes.

We manage it through things like diet, prebiotics and probiotics, and faecal transplant where needed - and avoid antibiotics as routine, instead using them only where specifically indicated because of their long-lasting effects on the microbiome.

And of course, we’re ideally placed to help with all of this as veterinary nurses and technicians - from initial diagnostics, to FMT, to emotional health and stress management and much more.

Did you enjoy this episode? If so, I’d love to hear what you think. Take a screenshot and tag me on Instagram (@vetinternalmedicinenursing) so I can give you a shout-out and share it with a colleague who’d find it helpful!

Thanks for learning with me this week, and I’ll see you next time!

References and Further Reading

  • Albright JD, Haug LI. Bidirectional Communication: The Gut-Brain Axis in Companion Animal Health. Vet Clin North Am Small Anim Pract. 2026;56(3):649-663. doi:10.1016/j.cvsm.2026.01.008

  • P.C. Barko, M.A. McMichael, K.S. Swanson, D.A. Williams, The Gastrointestinal Microbiome: A Review, Journal of Veterinary Internal Medicine, Volume 32, Issue 1, January-February 2018, Pages 9–25, https://doi.org/10.1111/jvim.14875

  • Breczko WJ, Bubak J, Miszczak M. The Importance of Intestinal Microbiota and Dysbiosis in the Context of the Development of Intestinal Lymphoma in Dogs and Cats. Cancers. 2024; 16(12):2255. https://doi.org/10.3390/cancers16122255

  • Bugrov N, Rudenko P, Lutsay V, et al. Fecal Microbiota Analysis in Cats with Intestinal Dysbiosis of Varying Severity. Pathogens. 2022;11(2):234. Published 2022 Feb 10. doi:10.3390/pathogens11020234

  • Gilbert EJ, Powell L, Siracusa C. Cats with inflammatory gastrointestinal or dermatological disorders exhibit increased care-soliciting and anxious behaviors. Am J Vet Res. 2025;86(3):ajvr.24.10.0312. Published 2025 Jan 14. doi:10.2460/ajvr.24.10.0312

  • Huang Z, Pan Z, Yang R, Bi Y, Xiong X. The canine gastrointestinal microbiota: early studies and research frontiers. Gut Microbes. 2020;11(4):635-654. doi:10.1080/19490976.2019.1704142

  • Pellowe, S.D., Zhang, A., Bignell, D.R.D. et al. Gut microbiota composition is related to anxiety and aggression scores in companion dogs. Sci Rep 15, 24336 (2025). https://doi.org/10.1038/s41598-025-06178-4

  • Pilla R and Suchodolski JS (2020) The Role of the Canine Gut Microbiome and Metabolome in Health and Gastrointestinal Disease. Front. Vet. Sci. 6:498. doi: 10.3389/fvets.2019.00498

  • Purina Institute. Intestinal dysbiosis in dogs and cats. 2026, https://www.purinainstitute.com/centresquare/therapeutic-nutrition/intestinal-dysbiosis-in-dogs-and-cats

  • Smith B. The heroes within: utilizing the gut microbiome, microbiome therapeutics, and fecal microbiota transplant in managing companion animal health and disease. J Am Vet Med Assoc. 2025;263(S2):S45-S52. Published 2025 Aug 14. doi:10.2460/javma.25.03.0218

  • Suchodolski JS, Toresson L. Microbiome Modulation in Veterinary Medicine: From Diet to Fecal Microbiota Transplantation. Vet Clin North Am Small Anim Pract. 2026;56(3):619-632. doi:10.1016/j.cvsm.2026.01.009

  • Suchodolski J. Intestinal microbes and digestive system disease in dogs. Today’s Veterinary Practice 2017, https://todaysveterinarypractice.com/gastroenterology/intestinal-microbes-digestive-system-disease-dogs/

  • Wernimont SM, Radosevich J, Jackson MI, et al. The Effects of Nutrition on the Gastrointestinal Microbiome of Cats and Dogs: Impact on Health and Disease. Front Microbiol. 2020;11:1266. Published 2020 Jun 25. doi:10.3389/fmicb.2020.01266

  • Winston J, Suchodolski J, Gaschen F et al. Clinical Guidelines for Fecal Microbiota Transplantation in Companion Animals. Advances in Small Animal Care, 2024; 5, 79-107

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116 | Have we got IBD wrong for years? Here’s what you ACTUALLY need to know about chronic inflammatory enteropathy as a veterinary nurse