Your Dog Has Chronic Inflammatory Enteropathy: A Canine Nutritionist’s Guide to Diagnosis, Treatment and Daily Management

· by Glendon Lloyd Dip.Canine.Nutrition Dip.Dog.Nutrigenomics

Canine Chronic Enteropathy_ Diagnosis, Treatments and Outcomes

Summary

Chronic inflammatory enteropathy (CIE) is the umbrella term for a group of persistent gastrointestinal conditions in dogs characterised by recurrent or continuous digestive signs lasting three weeks or longer. It is the most common cause of chronic diarrhoea, vomiting and weight loss in dogs, accounting for a significant proportion of small animal veterinary consultations worldwide. CIE is not a single disease but a spectrum of conditions classified by treatment response into food-responsive (FRE), microbiota-related modulation-responsive (MrMRE), immunosuppressant-responsive (IRE) and non-responsive (NRE) subtypes, with protein-losing enteropathy and granulomatous colitis considered distinct phenotypes within the same spectrum. The 2026 ACVIM consensus statement, the most current evidence-based guidance available, recommends a diet-first stepwise diagnostic approach, discourages empirical antibiotic use, and identifies microbiome-directed intervention as a clinically relevant adjunct following dietary trials. This guide explains what each subtype means for your dog, what the diagnostic process involves, and how to build an evidence-informed daily management strategy.

Introduction

You have come home from your vet with a new piece of information: your dog has chronic inflammatory enteropathy. You may have also seen the abbreviation CIE on a referral letter, or heard your vet use the term inflammatory bowel disease. You may have been told it is a long-term condition that requires management rather than a cure. You may be wondering what exactly that means, what your dog’s gut is doing and why, and what you are supposed to do about it every day.

This guide is written for that moment. It covers the diagnostic process in plain language, explains each CIE subtype and what it means practically, addresses the treatment options in the sequence your vet will likely use, and gives you a framework for daily management that is grounded in the current evidence base, including the 2026 ACVIM consensus statement, the most comprehensive expert guidance on canine CIE published to date.

One important clarification before we begin. The term inflammatory bowel disease is increasingly discouraged in dogs because it was borrowed from human gastroenterology, where it refers to a related but distinct set of conditions. The 2026 ACVIM consensus panel reached formal consensus to use CIE instead, because the canine and human conditions share features but differ in important ways around disease location, cellular infiltrates and treatment response patterns.¹ Throughout this article, CIE is used as the correct, current term.

Key Takeaways

  • CIE is a diagnosis of exclusion: other causes of chronic digestive signs, including infections, parasites, organ disease and neoplasia, must be ruled out before CIE can be confirmed
  • CIE is classified by treatment response into FRE, MrMRE, IRE and NRE; protein-losing enteropathy (PLE) and granulomatous colitis (GC) are considered phenotypes within the CIE spectrum
  • MrMRE is a newly formalised subtype reflecting the shift away from antibiotic use toward microbiome restoration as the appropriate treatment for dysbiosis-associated CIE
  • The 2026 ACVIM consensus recommends diet as the first-line diagnostic and therapeutic intervention; 38-89% of dogs with CIE are food-responsive
  • Empirical antibiotic treatment is formally discouraged in the 2026 ACVIM consensus, as relapse rates are high and long-term microbiome damage is well documented
  • A specific multi-strain probiotic formulation is identified in the 2026 ACVIM consensus as the only probiotic supported by a randomised clinical trial in dogs with CIE
  • Daily microbiome support through prebiotics, probiotics and postbiotics is a rational, evidence-informed complement to dietary management across all CIE subtypes
  • CCECAI score below 8 indicates disease likely to respond to dietary management; above 8 indicates more severe disease requiring consideration of additional treatment

In This Guide

What Is Chronic Inflammatory Enteropathy?

Chronic inflammatory enteropathy describes a group of gastrointestinal disorders in dogs characterised by persistent or recurrent digestive signs and variable intestinal mucosal inflammation, after other causes have been systematically excluded.¹ The defining criteria are duration of three weeks or longer, the exclusion of infectious, parasitic, metabolic and structural causes, and ultimately the classification of the condition by its response to sequential treatment trials.²

CIE is among the most common reasons dogs are referred to internal medicine specialists, and accounts for a significant proportion of all veterinary consultations involving chronic digestive signs. Two studies cited in the 2026 ACVIM consensus suggest that 20-30% of all companion animal visits to vets involve vomiting or diarrhoea as a primary concern.¹ In a large Swedish epidemiological study of 814 dogs presenting at two animal hospitals with chronic enteropathy, the period prevalence was approximately 1.1% of the total hospital population, but this likely underestimates the true burden since many milder cases are managed in primary care without referral.⁵

The clinical signs of CIE vary with the segment of gut involved and the extent of inflammation. Small intestinal disease typically produces soft, voluminous stools, weight loss, and variable appetite. Large intestinal disease produces more frequent, smaller-volume stools, mucus and occasional fresh blood. Many dogs have both simultaneously, and the pattern can shift over time. Vomiting, particularly after meals or in the early morning, is common across all subtypes. Lethargy, coat changes and intermittent nausea, evidenced by drooling, grass eating and lip-licking, are frequently reported by owners but under-recognised as CIE signs.²

What CIE is not is as important as what it is. It is not the same as acute gastroenteritis. It is not caused by a single bacterial or viral pathogen. It is not, in most cases, an allergic condition in the classical immunological sense, though food antigens play a central role in the most common subtype. And it is not, in the majority of dogs, a condition that requires lifelong medication if the correct subtype is identified and managed appropriately.⁸

The CIE Subtypes Explained

CIE is classified by what resolves it, not by a biological test performed at diagnosis. This is a deliberate feature of the diagnostic framework, not a limitation: it reflects the reality that the condition is multifactorial, that a single biopsy or blood test cannot predict treatment response, and that the most clinically meaningful distinction is the one that guides management.¹ There are four primary subtypes, with protein-losing enteropathy and granulomatous colitis now recognised as distinct phenotypes within the spectrum rather than separate diseases.

Food-Responsive Enteropathy (FRE) is the most common CIE subtype, accounting for 38-89% of all cases depending on the study population and diagnostic criteria.¹ It is confirmed when clinical signs resolve or significantly improve within two to four weeks of starting an appropriate elimination dietary trial, conducted strictly and completely. FRE is the first diagnostic and therapeutic target in virtually every dog presenting with chronic digestive signs, and many dogs with FRE maintain long-term remission on dietary management alone without any medication.¹ Affected dogs tend to be younger than those with immunosuppressant-responsive disease and present with lower clinical severity scores.²

Microbiota-Related Modulation-Responsive Enteropathy (MrMRE) is the most recently formalised subtype, proposed in 2024 to replace the earlier category of antibiotic-responsive enteropathy (ARE).³ MrMRE describes cases in which clinical signs resolve or significantly improve in response to interventions targeting gut microbiome composition and function, including prebiotics, probiotics, postbiotics, synbiotics, faecal microbiota transplantation and bile acid sequestrants (commonly cholestyramine), rather than antibiotics per se. The rationale for this reclassification is covered in detail below, but the core point is that the therapeutic objective has shifted from reducing bacteria to restoring a diverse and functional microbial community.³ MrMRE and FRE partially overlap because dietary change itself alters microbiome composition, and some dogs respond to both interventions simultaneously.³

Immunosuppressant-Responsive Enteropathy (IRE) is the subtype most closely aligned with what was historically called inflammatory bowel disease. It applies when clinical signs fail to respond adequately to dietary trials and microbiome-directed interventions, and improvement is achieved with corticosteroids or other immunosuppressive treatment. IRE is diagnosed at endoscopy, with histopathological evidence of significant mucosal inflammation confirming the diagnosis. Affected dogs tend to present with higher clinical severity scores, more advanced weight loss and more pronounced laboratory abnormalities.² IRE carries a more guarded prognosis than FRE, particularly when hypoalbuminaemia is present.⁶

Non-Responsive Enteropathy (NRE) applies when clinical signs fail to respond adequately to dietary management, microbiome-directed intervention and immunosuppressant therapy. NRE accounts for 15-43% of dogs classified at the IRE level, carries the worst prognosis of all CIE subtypes, and is associated with a high rate of euthanasia in referral populations.² Management of NRE may involve additional or alternative immunomodulatory approaches, emerging therapies including faecal microbiota transplantation, or palliative care, depending on the individual dog’s condition.

Protein-Losing Enteropathy (PLE) occurs when intestinal inflammation is severe enough to damage the mucosal barrier and lymphatic vessels, allowing plasma proteins to leak directly into the gut lumen. The hallmark laboratory finding is hypoalbuminaemia, which may progress to panhypoproteinaemia. Clinical complications include abdominal effusion, peripheral oedema and thromboembolism in severe cases. PLE can be food-responsive or immunosuppressant-responsive, and the subtype determines prognosis: food-responsive PLE carries significantly better long-term outcomes than IRE-associated or non-responsive forms.⁷ The 2026 ACVIM consensus treats PLE as a phenotype within the CIE spectrum rather than a separate disease, and this framing is important: it means that the same diagnostic and therapeutic logic applies, with dietary management as the first-line intervention even in dogs with confirmed protein loss.¹

Granulomatous Colitis (GC) is a rare form of CIE characterised by the presence of mucosal adherent and invasive Escherichia coli (AIEC). It is predominantly seen in Boxers and French Bulldogs. Unlike other CIE subtypes, GC requires mucosal culture with antimicrobial sensitivity testing to guide specific antibiotic treatment, because AIEC strains have high antimicrobial resistance rates. The 2026 ACVIM consensus treats GC as a CIE phenotype but makes clear that it is an exception to the general guidance discouraging empirical antibiotic use.¹

MrMRE: The Classification Shift That Changes the Treatment Conversation

The replacement of antibiotic-responsive enteropathy with microbiota-related modulation-responsive enteropathy is not a minor terminological update. It represents a fundamental reframing of what the therapeutic objective is for a significant proportion of dogs with CIE, and it has direct practical implications for every owner managing a dog with chronic digestive disease.

The ARE category existed for decades because dogs whose signs improved on antibiotics, particularly metronidazole or tylosin, clearly represented a recognisable clinical pattern. The problem is that antibiotics do not actually resolve the underlying dysbiosis. They suppress it temporarily while simultaneously damaging the broader microbial community. Studies using validated microbiome analysis tools have shown that metronidazole causes significant alterations in canine gut microbiome composition that persist for extended periods after treatment ends, with reductions in important beneficial taxa that do not fully recover.³ Tylosin produces similar disruptions. More critically, relapse rates after antibiotic discontinuation are high: the same clinical pattern returns because the underlying dysbiotic environment has not been corrected, only temporarily suppressed.¹

MrMRE acknowledges this reality and redirects the treatment logic. If the therapeutic objective in dysbiosis-associated CIE is microbial restoration rather than bacterial reduction, then the appropriate interventions are those that support the growth and diversity of beneficial commensal organisms: prebiotics, probiotics, postbiotics, synbiotics, and where available, faecal microbiota transplantation.³ This is not a fringe proposition. It reflects the direction of the specialist veterinary literature, the 2024 proposed reclassification by Dupouy-Manescau and colleagues, and the endorsement of the principle by the 2026 ACVIM consensus panel, which formally discourages empirical antibiotic use and identifies microbiome-directed intervention as a conditional first-line approach alongside dietary trials.¹

For the dog owner, this means that if your vet has historically prescribed metronidazole for your dog’s recurring digestive signs without diagnostic workup, the current evidence suggests this approach is not addressing the root cause and may be making the underlying dysbiosis harder to resolve over time. It also means that daily microbiome support, through appropriate prebiotic, probiotic and postbiotic supplementation, is not simply a wellness add-on. It is the scientifically grounded primary approach for the subset of CIE dogs whose disease is driven by or maintained by dysbiosis.³

How CIE Is Diagnosed: The Diagnostic Ladder

CIE is a diagnosis of exclusion. No single test confirms it. The process is a structured, sequential elimination of other possible causes, combined with a structured assessment of treatment response. Understanding this process helps owners engage more effectively with their vet and interpret the results of individual tests in context.

The 2026 ACVIM consensus recommends a two-tier diagnostic approach based on clinical severity.¹ Dogs with mild to moderate signs and no alarming features (CIE-I) can begin a dietary trial after basic exclusion tests, without proceeding immediately to endoscopy. Dogs with more severe disease, significant weight loss, hypoalbuminaemia, or failure to respond to dietary trials (CIE-II) require a more comprehensive diagnostic workup including advanced imaging and ultimately endoscopy with biopsy.

Tier 1: Basic exclusion and initial assessment. Before CIE can even be considered, the following must be assessed: full physical examination including body condition score and muscle condition score; complete blood count and serum biochemistry panel including electrolytes; urinalysis with urine protein-to-creatinine ratio if hypoalbuminaemia is present; fecal parasitology including Giardia antigen testing; cobalamin and folate concentrations; pancreatic lipase and TLI to exclude exocrine pancreatic insufficiency; resting serum cortisol to exclude atypical hypoadrenocorticism; and abdominal ultrasonography to exclude focal disease, lymphoma, other organ pathology and to characterise intestinal wall changes.¹

These are not optional steps even for dogs presenting with apparently straightforward digestive signs. Several conditions can produce clinical signs identical to CIE, including atypical hypoadrenocorticism, chronic pancreatitis, hepatobiliary disease and early intestinal lymphoma. Missing any of these before committing to a CIE management approach has potentially serious consequences.¹

Laboratory markers with prognostic relevance. Hypocobalaminaemia (low vitamin B12) is among the most clinically important laboratory findings in a dog with CIE. It affects 19-61% of dogs with the condition and is an established negative prognostic factor, associated with worse outcomes regardless of CIE subtype.¹ Hypocobalaminaemia also contributes to ongoing intestinal dysfunction because cobalamin is required for normal enterocyte metabolism and intestinal repair. Cobalamin supplementation is indicated in hypocobalaminaemic dogs. Low serum albumin, elevated C-reactive protein and elevated fecal calprotectin all provide additional information about disease severity and the likelihood of requiring immunosuppressive treatment.¹

Fecal microbiome analysis. The canine fecal dysbiosis index (DI) is a validated quantitative PCR assay that measures seven bacterial taxa and produces a single composite score. A DI below zero indicates normobiosis; above two indicates dysbiosis. The DI distinguishes healthy dogs from those with CIE with 74% sensitivity and 95% specificity.⁴ While the 2026 ACVIM consensus rates fecal microbiome analysis as a weak recommendation for routine use, it identifies the DI as a clinically useful tool for individual patient management, and for owners managing dogs with CIE day-to-day it provides an objective baseline against which dietary and supplement interventions can be tracked.¹

Abdominal ultrasonography. Ultrasound is recommended in all dogs with moderate or marked clinical signs, weight loss, hypoalbuminaemia or failure to respond to dietary trials. In dogs with PLE, ultrasound findings including hyperechoic mucosal striations carry 75% sensitivity and 96% specificity for intestinal lymphangiectasia.¹ Normal hypoechoic small intestinal mucosa on ultrasound is over 80% sensitive and specific for food-responsive disease, making it a useful early predictor of FRE before a dietary trial is completed.¹

Endoscopy with biopsy. The 2026 ACVIM consensus recommends proceeding to endoscopy only after at least three properly conducted dietary trials have failed to produce clinical remission, not as a first-line investigation in clinically stable dogs.¹ This is a meaningful departure from previous practice in some referral settings and reflects the evidence that dietary management resolves signs in 38-89% of dogs, meaning the majority of CIE dogs never require endoscopy. When endoscopy is performed, both upper (oesophagogastroduodenoscopy) and lower (ileocolonoscopy) should be conducted, with a minimum of 10-15 biopsy samples per site to allow thorough histopathological evaluation.¹ An important caveat: histological findings do not reliably distinguish between dogs that will respond to dietary management and those that will require immunosuppressive treatment, which is one reason the consensus deprioritises early endoscopy.¹

The Dietary Trial: What It Actually Requires

The dietary trial is both the primary diagnostic intervention and the first therapeutic step for almost every dog with CIE. Its proper execution is essential. A poorly conducted dietary trial produces a false negative result, leading to unnecessary escalation to medication. A well-conducted trial either confirms FRE and avoids medication entirely, or rules out food-responsive disease and justifies the next diagnostic step.

The 2026 ACVIM consensus defines an adequate dietary trial as exclusive feeding of a therapeutic diet for a minimum of two weeks, with strict adherence.¹ The diet must be selected based on the individual dog’s dietary history: there is no universal therapeutic diet that works for all dogs. The options are hydrolysed protein diets (proteins broken into peptides too small to trigger an immune response), novel protein or limited-ingredient diets (a single protein source the dog has never previously consumed), elemental diets (protein provided as individual amino acids), high-digestibility diets, fibre-enriched diets, or ultra-low-fat diets (particularly relevant for dogs with suspected fat malabsorption or PLE).¹

The strict adherence requirement is the part most owners underestimate. During a dietary trial, the dog must eat nothing except the therapeutic diet and water. No treats, no flavoured dental chews, no flavoured parasite preventatives, no table scraps, no flavoured medications where alternatives exist. A single contaminating protein source can invalidate the entire trial. If clinical signs improve on the therapeutic diet, that is confirmation of food-responsive disease only if the trial has been conducted completely.

The consensus recommends considering at least three dietary trials with different diets before concluding that a dog is non-food-responsive.¹ Some dogs that do not respond to one hydrolysed diet respond well to a different one, or to a novel protein dog food (e.g. a plant-based dog food without wheat, corn or soy) using a protein source they have genuinely never encountered. The two-to-four week timeframe is a minimum: clinical responses can take longer in some dogs, and owners should monitor weekly rather than expecting immediate resolution.

Once a dog achieves clinical remission on a therapeutic diet, that diet should be fed for at least 12 weeks before attempting to transition back to a maintenance diet.¹ Transitioning too early is a common source of relapse. Dogs with PLE may require the therapeutic diet to be maintained indefinitely, as relapse on dietary non-compliance in this subgroup is well documented.¹

Measuring Severity: CCECAI and CIBDAI Explained

Your vet may use one of two validated scoring systems to measure disease severity: the Canine Inflammatory Bowel Disease Activity Index (CIBDAI) or the Canine Chronic Enteropathy Clinical Activity Index (CCECAI). These are not arbitrary scores. They predict treatment response, guide decisions about escalation to medication, and provide an objective measure of improvement or deterioration over time.⁶

The CIBDAI evaluates six clinical parameters: attitude and activity, appetite, vomiting frequency, stool consistency, stool frequency, and weight loss. Each is scored from 0 (normal) to 3 (severe), giving a maximum score of 18. Scores of 0-3 indicate clinically insignificant disease; 4-5 mild; 6-8 moderate; 9 or above severe.⁶

The CCECAI adds three variables to the CIBDAI: serum albumin concentration, the presence of ascites, and the presence of peripheral oedema or pruritus. This makes it more sensitive to PLE and more predictive of prognosis in dogs with hypoalbuminaemia.⁶ The 2026 ACVIM consensus recommends using either score at every clinical review and interpreting changes over time, with a decrease of 75% or more from baseline indicating complete response or remission, 25-75% decrease indicating partial response, and less than 25% decrease indicating no response.¹

From an owner’s perspective, a CCECAI below 8 is the threshold below which dietary management alone is the appropriate first approach, and above which your vet will begin considering whether additional intervention is warranted. This is not a rigid cutoff, but it is a useful guide for conversations with your vet about whether your dog’s current management is sufficient.¹

The Dysbiosis Connection: Gut Microbiome and CIE

Whether dysbiosis causes CIE or CIE causes dysbiosis remains an open and actively debated question in the research literature. What is not debated is that the two are inseparable in the vast majority of affected dogs.² Dogs with chronic enteropathy consistently show altered gut microbiome composition compared to healthy controls, and these alterations are not peripheral to the disease. They are mechanistically active in maintaining intestinal inflammation and disrupting normal digestive function.

The microbial pattern in canine CIE is characterised by reductions in beneficial, short-chain fatty acid-producing taxa including Faecalibacterium spp., Turicibacter spp., Blautia spp. and Fusobacterium spp., alongside a critical reduction in Clostridium hiranonis, the primary converter of primary to secondary bile acids in the colon.⁴ When C. hiranonis is depleted, primary bile acids accumulate, creating a pro-inflammatory and secretory environment that sustains diarrhoea through a metabolic pathway distinct from immune dysregulation. This bile acid dysmetabolism is now understood as one of the central mechanisms through which dysbiosis perpetuates intestinal inflammation in CIE.⁹

Simultaneously, potentially inflammatory taxa including Escherichia coli and Streptococcus spp. expand in the dysbiotic environment, reinforcing the shift toward an inflammatory microbial community.⁴ The fecal dysbiosis index provides a composite score reflecting this overall shift. In the validation cohort of 95 healthy dogs and 106 dogs with CIE, a DI above zero separated the groups with 74% sensitivity and 95% specificity.⁴

The role of the gut microbiome in CIE extends well beyond bacterial imbalance. Microbial metabolites regulate intestinal immune tolerance, barrier integrity, and the inflammatory threshold of mucosal immune cells. A diverse, functional microbial community produces SCFAs that nourish colonocytes, synthesise vitamin K and certain B vitamins, and maintain the mucus layer that protects the epithelium. When that community is disrupted, these functions are lost, and the intestinal environment deteriorates in a way that perpetuates the very inflammation driving the dysbiosis.⁹

This is why dietary management and microbiome support are not two separate interventions. They are the same intervention seen from different angles: every dietary change that reduces antigenic provocation also changes microbial substrate availability. Every prebiotic intervention changes bacterial community composition. Every probiotic and postbiotic intervention modulates mucosal immune signalling. Managing CIE without attending to microbiome restoration leaves the underlying microbial imbalance intact.

The 2026 ACVIM consensus makes an explicit, strong recommendation: empirical antimicrobial treatment is not recommended in dogs with suspected CIE.¹ This is a significant departure from historical practice in many veterinary settings, where metronidazole was prescribed as a default intervention for any dog presenting with chronic digestive signs. Understanding why this guidance has changed matters for every dog owner who has been through this experience.

The problem with empirical antibiotics in CIE is not that they produce no short-term benefit. Many dogs do improve temporarily on metronidazole or tylosin. The problem is the nature and duration of what they do to the gut microbiome in achieving that improvement. Metronidazole produces rapid, significant reductions in anaerobic bacterial diversity, with measurable effects on key beneficial taxa that persist for weeks to months after treatment ends. Tylosin produces similar disruptions. Both drugs increase antimicrobial resistance in bacterial populations that will then be present in the dog’s gut long-term.³

More fundamentally, antibiotic-induced clinical improvement does not represent resolution of the underlying dysbiosis. It represents a temporary suppression of one part of the dysfunctional microbial community while simultaneously damaging the wider ecosystem. The relapse rates after antibiotic discontinuation in dogs with this clinical pattern are consistently high: the same condition returns because the same dysbiotic environment re-emerges once the antimicrobial pressure is removed.¹ This cycle — antibiotics, improvement, relapse, antibiotics — is precisely what the MrMRE classification is designed to interrupt.

The one clear exception is granulomatous colitis caused by adherent invasive E. coli, where targeted antibiotic treatment based on mucosal culture with susceptibility testing is appropriate and necessary. For all other presentations of CIE, the 2026 ACVIM consensus is clear: dietary management comes first, microbiome-directed intervention is the conditional second step, and antibiotic use without confirmed indication is not justified by the current evidence.¹

Protein-Losing Enteropathy: When CIE Progresses

Protein-losing enteropathy is not a diagnosis separate from CIE. It is a clinical phenotype that develops when intestinal inflammation becomes severe enough to compromise the epithelial barrier and lymphatic system to the point where plasma proteins are lost into the gut lumen faster than they can be replaced.¹ The consequence is hypoalbuminaemia, which may progress to panhypoproteinaemia if both albumin and globulins are lost.

The clinical presentation of PLE ranges from subtle, evidenced only by laboratory findings of low albumin, to dramatically overt, with abdominal effusion, peripheral oedema and in severe cases pleural effusion, thromboembolism and collapse. Dogs with PLE are also at significantly elevated risk of hypercoagulability, affecting 63-100% of PLE dogs, which predisposes to thromboembolic complications that can be life-threatening.¹

The most important clinical point about PLE is the prognostic gradient by subtype. Food-responsive PLE carries the best prognosis. In a retrospective study of 33 dogs with PLE, 23 responded to ultra-low-fat dietary management alone and had significantly longer survival times than those requiring immunosuppressive treatment.⁷ A CCECAI below 8 was the strongest predictor of food-responsiveness.⁷ Non-responsive PLE carries the worst prognosis, with high mortality and limited treatment options.

This prognostic gradient has a direct implication for management timing. Dogs whose PLE is caught at the food-responsive stage, before significant mucosal damage has accumulated and before protein loss has become severe, have substantially better outcomes than dogs who arrive at a veterinary practice with florid hypoalbuminaemia. Regular monitoring of serum albumin in dogs with established CIE is therefore not optional. It is a practical early warning system.

Dogs with confirmed PLE also require vitamin D monitoring, as hypovitaminosis D is detected in up to 35% of PLE dogs and is associated with negative outcomes.¹ Cobalamin supplementation is indicated in hypocobalaminaemic dogs, which is the majority.¹ Thromboembolic prophylaxis should be discussed with your vet for dogs with significant hypoalbuminaemia.

Probiotics and Microbiome Support in CIE

The shift toward microbiome-directed intervention in CIE is supported by both the updated classification framework and the clinical trial evidence. The question for dog owners is what the evidence actually says about which interventions are worth using and how to understand what the research tells us.

The 2026 ACVIM consensus makes a specific, clinically significant observation: a multi-strain probiotic formulation containing eight lactic acid bacterial strains, known as the De Simone Formulation, is the only probiotic supported by a randomised clinical trial in dogs with CIE, and receives a conditional recommendation for consideration after dietary trials.¹ In the original trial by Rossi and colleagues comparing this eight-strain formulation to combination therapy with prednisone and metronidazole in dogs with confirmed IBD, both treatments produced equivalent reductions in clinical and histological scores at 60 days, but the probiotic produced superior immunological outcomes, including significant increases in regulatory T cell markers (FoxP3+) and better normalisation of dysbiosis as measured by Faecalibacterium abundance.¹⁰ The trial was small and open-label, which is why the recommendation is conditional rather than strong, but it is the only probiotic in the veterinary literature for which this quality of evidence exists.

The conditional recommendation for multi-strain probiotic therapy sits alongside dietary management as the core of the MrMRE treatment approach, and the broader category of microbiome-directed intervention includes prebiotics, postbiotics, synbiotics and faecal microbiota transplantation. Prebiotics, particularly inulin-type fructans and beta-glucans, provide the substrate that beneficial bacteria require to re-establish community diversity. In dogs with CIE receiving a hydrolysed diet, prebiotic and glycosaminoglycan co-supplementation showed clinically rational additive effects on intestinal metabolic profiles compared to dietary management alone, even in a small pilot study that did not reach statistical significance on the primary endpoint.¹¹

The practical implication is this: daily microbiome support through a combined prebiotic, probiotic and postbiotic regimen is not simply a precautionary measure. It is the active therapeutic approach for the subtype of CIE now formally recognised as MrMRE, it is endorsed as a conditional adjunct in food-responsive disease by the 2026 ACVIM consensus, and it is the mechanism through which the microbial restoration that underpins long-term remission is achieved.

How Bonza Supports Dogs with CIE

The evidence base for daily management of CIE points consistently toward three priorities: supporting microbiome diversity and function, protecting mucosal barrier integrity, and reducing the systemic inflammatory tone that perpetuates intestinal immune dysregulation. The Bonza product range addresses these three priorities through two products, with a third for dogs whose CIE is producing active digestive signs.

Biotics Bioactive Bites is the daily microbiome foundation for all dogs with CIE, delivering the complete Biotics Triad: prebiotics through chicory root inulin, which selectively feeds beneficial bacteria and supports short-chain fatty acid production that nourishes the colonocyte layer; Calsporin® (Bacillus velezensis DSM 15544), the only live spore-forming probiotic with EFSA authorisation specifically for dogs, selected for its stability across environmental conditions and its documented gut-immune activity; and postbiotics comprising TruPet™, derived through a proprietary fermentation process, and L. helveticus HA-122, a heat-inactivated postbiotic strain. TruPet™ and L. helveticus HA-122 are named individually because they are distinct postbiotics operating through different mechanisms. Combining prebiotics, a spore-forming live probiotic, and two postbiotics in daily supplementation addresses the microbial restoration objective from multiple mechanistic angles simultaneously.

Calsporin® provides a different and complementary mechanism to the lactic acid bacterial strains that form the De Simone Formulation referenced in the 2026 ACVIM consensus. Its spore-forming nature allows it to survive gastric acid and delivery conditions that compromise many conventional probiotic strains, and its EFSA authorisation reflects the regulatory evidence standard for safety and efficacy in companion animals. The broader Biotics Triad is not positioned as a substitute for veterinary diagnosis or treatment: it is a daily foundation that creates and maintains the microbial environment within which all other management interventions operate more effectively.

Belly Bioactive Bites is the targeted recommendation for dogs with active CIE presentations: chronic or intermittent diarrhoea, soft stools, variable stool consistency, excessive flatulence, weight loss or ongoing food-responsive digestive sensitivity. Belly supports gut motility, mucosal barrier function and microbiome stability during active digestive episodes, and is designed to complement Biotics as the daily foundation while addressing the acute-on-chronic presentation that characterises CIE in many dogs.

Biotics remains the appropriate daily foundation across all CIE subtypes and at every stage of management, including during dietary trials. There is no evidence that daily prebiotic and postbiotic supplementation interferes with dietary trial assessment, and there is mechanistic rationale for beginning microbiome support as early as possible in the management pathway.

How To Build a Daily CIE Management Protocol

Building a consistent, evidence-informed daily management protocol for a dog with CIE reduces the likelihood of relapse, provides early warning of deterioration, and gives both owner and vet the information needed to make good clinical decisions.

  1. Start daily microbiome support immediately.

    The microbiome is disrupted in virtually every dog with CIE, and this disruption does not resolve spontaneously. Daily prebiotic, probiotic and postbiotic supplementation provides the microbial substrate and supporting organisms that the gut needs to begin restoration. Begin Biotics as a permanent daily supplement from the point of diagnosis and maintain it through dietary trials, treatment changes and long-term management.

  2. Conduct the dietary trial with genuine rigour.

    Work with your vet to select the appropriate therapeutic diet based on your dog’s dietary history. Commit to full adherence: no exceptions for treats, flavoured supplements or table scraps during the trial period. Monitor stool consistency, frequency, appetite, energy and weight weekly, and record findings in a simple daily log. Provide this log to your vet at every review appointment.

  3. Schedule monitoring appointments proactively.

    CIE is managed rather than cured. A minimum of six-monthly veterinary reviews is appropriate for stable dogs, with more frequent visits for dogs with a history of PLE, severe disease or significant weight fluctuation. Serum albumin and cobalamin should be checked at each review as early markers of deterioration, even when clinical signs appear controlled.

  4. Do not discontinue a therapeutic diet too quickly.

    The 2026 ACVIM consensus recommends maintaining a diet that achieves clinical remission for at least 12 weeks before attempting any transition.¹ Premature transitions are among the most common causes of CIE relapse in dogs who achieved initial remission.

  5. Communicate changes immediately.

    If your dog’s stool consistency deteriorates, if appetite changes significantly, if weight loss resumes or if any new clinical signs appear, contact your vet promptly. Do not wait for the next scheduled appointment. CIE can progress, and early intervention at the first signs of deterioration produces better outcomes than waiting until the situation becomes acute.

Safety, Red Flags and When to Seek Urgent Care

Managing a dog with CIE at home requires knowing which signs represent tolerable day-to-day variability and which require immediate veterinary attention.

Seek emergency veterinary care immediately if your dog shows: profuse or bloody diarrhoea of sudden onset; collapse or extreme lethargy; pale or white mucous membranes; abdominal distension; vomiting that continues for more than six hours; or visible difficulty breathing. These signs may indicate acute haemorrhagic diarrhoea syndrome, thromboembolic complications, severe hypoalbuminaemia, intestinal obstruction or other conditions requiring immediate diagnosis and treatment.

Seek an urgent veterinary appointment, same day if possible, for: weight loss of more than 5% of body weight over two to four weeks; first-time appearance of abdominal fluid or peripheral swelling; sustained refusal to eat beyond 24 hours; stool that is consistently black or tarry; or any sudden and marked change in clinical pattern from a previously stable baseline.

Schedule a non-urgent veterinary review for: gradual increase in stool softness that persists beyond five to seven days; return of intermittent vomiting after a period of remission; gradual weight loss over several weeks; or coat and condition changes that develop slowly over time.

The prebiotic, probiotic and postbiotic support described in this article is appropriate as a daily complement to veterinary management. It is not a substitute for veterinary diagnosis, treatment of established CIE, or emergency care. This article is for informational purposes only and does not constitute veterinary advice. Always consult a qualified veterinarian before making changes to your dog’s diet or supplement regimen.

Frequently Asked Questions

What is the difference between CIE and IBD in dogs?

The 2026 ACVIM consensus reached formal consensus to avoid the term inflammatory bowel disease in dogs because it creates confusion with the human condition, which is related but distinct. CIE is the correct current term for the full spectrum of chronic gut conditions in dogs. When vets use IBD informally, they typically mean the immunosuppressant-responsive subtype (IRE), which is only one part of the CIE spectrum and accounts for a minority of cases. Many dogs described as having IBD are more accurately classified as food-responsive CIE, which responds to dietary management without medication.

How long does a dietary trial need to last?

The 2026 ACVIM consensus recommends exclusive feeding of the therapeutic diet for a minimum of two weeks before assessing response, with weekly monitoring. Some dogs require more time. Three dietary trials with different therapeutic diets should be considered before concluding that a dog is not food-responsive. A diet that achieves remission should be fed for at least 12 weeks before any transition is attempted.

Can CIE be cured?

Food-responsive CIE can be managed to a state of long-term remission in many dogs, and a proportion of dogs with FRE can transition off the therapeutic diet and maintain remission on a maintenance diet without medication. IRE and NRE require ongoing management. PLE outcomes depend on subtype. The goal for most dogs with CIE is sustained clinical remission with good quality of life, rather than cure in the conventional sense.

Should all dogs with CIE have endoscopy?

The 2026 ACVIM consensus recommends endoscopy only after at least three properly conducted dietary trials have failed to produce remission, not as a first-line investigation. The majority of dogs with CIE are food-responsive and never require endoscopy. Endoscopy is reserved for dogs with moderate to severe disease, significant weight loss, hypoalbuminaemia, or no response to dietary management.

Is metronidazole appropriate for my dog’s CIE?

Empirical antibiotic treatment is formally not recommended in the 2026 ACVIM consensus for dogs with suspected CIE, except in granulomatous colitis caused by confirmed AIEC where targeted antimicrobial treatment based on culture and sensitivity is appropriate. For all other CIE presentations, dietary management and microbiome-directed intervention are the first and second steps. Antibiotic relapse cycles do not resolve the underlying dysbiosis.

What is the dysbiosis index and should my dog be tested?

The canine fecal dysbiosis index is a validated quantitative PCR assay that measures seven key bacterial taxa and produces a single number: below zero is normobiosis, above two is dysbiosis. It is available through veterinary referral laboratories. It is useful for establishing a baseline at diagnosis, monitoring response to dietary and supplement changes, and identifying subclinical dysbiosis in dogs whose clinical signs are intermittent or partially controlled.

Can my dog stay on prebiotics and probiotics during a dietary trial?

There is no evidence that prebiotic and postbiotic supplementation interferes with dietary trial assessment, and there is mechanistic rationale for beginning microbiome support early. Daily microbiome support through Biotics can be continued throughout the dietary trial period. Discuss with your vet if you are uncertain about any supplement or treat during a trial.

What does a CCECAI score mean and why does it matter?

CCECAI is a validated clinical scoring tool that assesses disease severity by scoring appetite, stool consistency, stool frequency, vomiting, weight loss, attitude, albumin, and signs of protein loss. A score below 8 indicates disease appropriate for dietary management as first-line intervention. A score above 8 indicates more severe disease that may require consideration of additional treatment beyond diet alone. Tracking CCECAI over time gives both owner and vet an objective measure of whether management is working.

Conclusion

Chronic inflammatory enteropathy is the most common chronic digestive condition in dogs, and it is also one of the most commonly mismanaged, largely because the diagnosis itself has historically been conflated with a single treatment pathway: empirical antibiotics followed by steroids if antibiotics fail. The current evidence, crystallised in the 2026 ACVIM consensus statement, tells a different and more hopeful story.

The majority of dogs with CIE are food-responsive. They do not need antibiotics. They do not need steroids. They need a properly conducted dietary trial, often two or three, the patience to allow the gut time to respond, and daily microbiome support that provides the microbial foundation within which dietary management operates most effectively. The formalisation of MrMRE as a distinct subtype is not a bureaucratic reclassification. It is a formal acknowledgement that microbial restoration is a primary therapeutic objective for a significant and previously under-recognised subset of dogs with CIE, and that the interventions that achieve this, prebiotics, probiotics and postbiotics, belong at the centre of the management conversation rather than at the periphery.

For dogs whose CIE is more severe, that requires endoscopy, histopathology and immunosuppressive treatment, the same foundation applies. Microbiome support does not compete with conventional therapy. It operates alongside it, addressing the dysbiotic environment that conventional therapy cannot reach. The best outcomes in CIE are achieved when dietary management, microbiome support and veterinary clinical oversight work together.

The evidence base for canine CIE continues to mature rapidly. The clinical classification is being refined, the role of bile acid dysmetabolism is being mapped with increasing precision, and the therapeutic potential of faecal microbiota transplantation is being investigated in properly designed trials. For now, the clearest practical guidance is also the simplest: investigate properly, start with diet, support the microbiome daily, monitor closely, and escalate only when indicated.

For further reading on the mechanisms discussed here, see The Gut-Immune Axis in Dogs, Gut Dysbiosis in Dogs: Causes, Symptoms and How to Restore Balance, Best Probiotics for Dogs: Canine Nutritionist’s Guide to Real Gut Impact, and Best Prebiotics for Dogs: Canine Nutritionist’s Complete Guide.

Glossary of Terms – Key Terms Explained

The following terms appear throughout this article, formatted as questions so they can be implemented directly as Yoast FAQ blocks. Each question reflects the language owners commonly search after receiving a CIE diagnosis.

What is chronic inflammatory enteropathy (CIE) in dogs?

CIE is the umbrella term for a group of persistent gastrointestinal conditions in dogs characterised by recurrent or continuous digestive signs lasting three weeks or longer, after infectious, parasitic, metabolic and structural causes have been excluded. CIE is not a single disease. It is a spectrum of conditions classified by treatment response rather than by a single diagnostic test, and is currently the preferred term over inflammatory bowel disease in dogs.

What is food-responsive enteropathy (FRE) in dogs?

FRE is the most common subtype of CIE, accounting for 38-89% of all cases. It is confirmed when clinical signs resolve or significantly improve within two to four weeks of an appropriate elimination dietary trial conducted with strict adherence. Many dogs with FRE maintain long-term remission on dietary management alone, without any medication.

What is microbiota-related modulation-responsive enteropathy (MrMRE) in dogs?

MrMRE is a newly formalised CIE subtype (2024) that replaces the former antibiotic-responsive enteropathy category. It describes cases that respond to interventions targeting gut microbiome composition and function, including prebiotics, probiotics, postbiotics, synbiotics, faecal microbiota transplantation and bile acid sequestrants. The reclassification reflects evidence that microbial restoration, not bacterial suppression, is the appropriate therapeutic objective.

What is immunosuppressant-responsive enteropathy (IRE) in dogs?

IRE is the CIE subtype in which clinical signs fail to respond to dietary trials and microbiome-directed intervention but improve with corticosteroids or other immunosuppressive treatment. IRE is most closely aligned with what is informally called inflammatory bowel disease in dogs. It is confirmed by endoscopy with histopathological evidence of significant mucosal inflammation.

What is non-responsive enteropathy (NRE) in dogs?

NRE is the CIE subtype in which clinical signs fail to respond adequately to dietary management, microbiome-directed intervention and immunosuppressant therapy. NRE accounts for 15-43% of dogs classified at the immunosuppressant-responsive level and carries the worst prognosis of all CIE subtypes.

What is protein-losing enteropathy (PLE) in dogs?

PLE is a clinical phenotype that develops when intestinal inflammation is severe enough to cause plasma proteins to leak from the bloodstream into the gut lumen. It is characterised by hypoalbuminaemia and potentially panhypoproteinaemia. PLE is now classified as a phenotype within the CIE spectrum rather than a separate disease, and can be food-responsive, immunosuppressant-responsive or non-responsive depending on the underlying driver.

What is granulomatous colitis (GC) in dogs?

GC is a rare CIE phenotype caused by mucosal adherent and invasive Escherichia coli (AIEC), predominantly seen in Boxers and French Bulldogs. Unlike other CIE subtypes, GC requires mucosal culture with antimicrobial sensitivity testing to guide targeted antibiotic treatment, and is an explicit exception to the general guidance discouraging empirical antibiotic use in CIE.

What does the CCECAI score measure in dogs with CIE?

The Canine Chronic Enteropathy Clinical Activity Index (CCECAI) is a validated clinical scoring tool used to measure disease severity in dogs with CIE. It scores six clinical parameters (appetite, vomiting, stool consistency, stool frequency, weight loss and attitude) plus albumin concentration, ascites and peripheral oedema. Scores below 8 indicate disease suitable for dietary management as first-line treatment; scores above 8 indicate more severe disease requiring consideration of additional intervention.

What does the CIBDAI score measure in dogs with CIE?

The Canine Inflammatory Bowel Disease Activity Index (CIBDAI) is a validated clinical scoring tool assessing six clinical parameters: attitude and activity, appetite, vomiting frequency, stool consistency, stool frequency and weight loss. Each parameter is scored from 0 to 3. Unlike the CCECAI, the CIBDAI does not include albumin concentration, making it more suitable for dogs without confirmed protein loss.

What is dysbiosis in dogs?

Dysbiosis is an imbalance in the composition, diversity or function of the gut microbial community. In canine CIE, dysbiosis is characterised by reductions in beneficial bacteria including Faecalibacterium spp. and Clostridium hiranonis, and increases in potentially inflammatory organisms such as Escherichia coli and Streptococcus spp. Dysbiosis both contributes to and is perpetuated by intestinal inflammation in CIE.

What is the canine dysbiosis index (DI)?

The dysbiosis index is a validated quantitative PCR-based assay that measures seven bacterial taxa in a fecal sample and produces a single composite score. A DI below zero indicates normobiosis (a normal microbial balance); above two indicates dysbiosis. Available through veterinary referral laboratories, it achieved 74% sensitivity and 95% specificity in separating healthy dogs from those with CIE in the original validation study.

What is hypoalbuminaemia in dogs?

Hypoalbuminaemia is an abnormally low albumin concentration in the blood, most commonly identified on a routine biochemistry panel. In dogs with CIE, hypoalbuminaemia indicates that the intestinal barrier has been compromised to the point where plasma proteins are being lost directly into the gut lumen. It is an important negative prognostic indicator and may signal progression toward protein-losing enteropathy.

What is panhypoproteinaemia in dogs?

Panhypoproteinaemia is the presence of low concentrations of all plasma proteins, including both albumin and globulins, in the blood. It indicates more severe or advanced intestinal protein loss than hypoalbuminaemia alone and is associated with worse clinical outcomes in dogs with protein-losing enteropathy.

What is hypercoagulability and why does it affect dogs with PLE?

Hypercoagulability is an abnormal tendency of the blood to clot. It affects 63-100% of dogs with protein-losing enteropathy, likely because protein loss disrupts the normal balance of clotting and anti-clotting factors in the blood. This predisposes affected dogs to thromboembolic complications, including pulmonary thromboembolism, which can be life-threatening. Monitoring and prophylaxis should be discussed with your vet for dogs with significant hypoalbuminaemia.

What is cobalamin and why does it matter in dogs with CIE?

Cobalamin (vitamin B12) is a vitamin absorbed in the ileum that is essential for normal enterocyte metabolism, intestinal repair and red blood cell production. Hypocobalaminaemia (low cobalamin) is found in 19-61% of dogs with CIE and is an established negative prognostic indicator. Because cobalamin deficiency impairs intestinal repair, supplementation is indicated in hypocobalaminaemic dogs regardless of which CIE subtype is present.

What is bile acid dysmetabolism in dogs with CIE?

Bile acid dysmetabolism is a disruption in the normal conversion of primary bile acids to secondary bile acids in the colon. In canine CIE, depletion of Clostridium hiranonis, one of the key bacteria responsible for this conversion, is the primary cause. The resulting accumulation of primary bile acids promotes secretory diarrhoea and sustains intestinal inflammation through a mechanism that is independent of immune dysregulation.

What is the mucosal barrier and how does CIE affect it?

The mucosal barrier is the protective lining of the intestinal wall, comprising the epithelial cell layer, the overlying mucus layer and the immune cells embedded within the mucosa. A healthy mucosal barrier prevents bacterial products and dietary antigens from entering systemic circulation. In CIE, inflammation and dysbiosis compromise the mucosal barrier, increasing intestinal permeability and allowing bacterial products including lipopolysaccharide to enter the bloodstream, which sustains systemic inflammation.

What is endoscopy and when is it needed for dogs with CIE?

Endoscopy is a minimally invasive procedure in which a flexible camera is passed into the gastrointestinal tract under general anaesthesia to allow direct visualisation of the mucosal lining and collection of biopsy samples. In CIE, the 2026 ACVIM consensus recommends endoscopy only after at least three adequate dietary trials have failed to produce clinical remission. The majority of dogs with CIE are food-responsive and do not require endoscopy.

What is histopathology and what does it show in dogs with CIE?

Histopathology is the microscopic examination of biopsy tissue samples by a pathologist to identify the type, distribution and severity of cellular changes. In CIE, histopathology of intestinal biopsy samples characterises the nature and extent of mucosal inflammation. Importantly, histopathological findings do not reliably predict which treatment a dog will respond to, which is one reason the 2026 ACVIM consensus deprioritises early endoscopy.

What is the De Simone Formulation probiotic?

The De Simone Formulation is an eight-strain lactic acid bacterial probiotic that is, as of the 2026 ACVIM consensus statement, the only probiotic supported by a randomised clinical trial in dogs with CIE. In that trial it achieved equivalent clinical remission to combination therapy with prednisone and metronidazole, while producing superior immunological outcomes including better normalisation of dysbiosis. It received a conditional recommendation from the ACVIM panel for consideration following dietary trials, and is used in the Visbiome Vet product.

References

  1. Heilmann RM, Jergens AE, Kathrani A, Allenspach K, Salavati Schmitz S, Priestnall SL, Dandrieux JRS, O’Connor AM. ACVIM-endorsed statement: consensus statement and systematic review on guidelines for the diagnosis and treatment of chronic inflammatory enteropathy in dogs. J Vet Intern Med. 2026;40(1):aalaf017. doi: 10.1093/jvimsj/aalaf017.
  2. Jergens AE, Heilmann RM. Canine chronic enteropathy: current state-of-the-art and emerging concepts. Front Vet Sci. 2022;9:923013. doi: 10.3389/fvets.2022.923013. PMID: 36213409. PMC: PMC9534534.
  3. Dupouy-Manescau N, Méric T, Sénécat O, Drut A, Valentin S, Leal RO, Hernandez J. Updating the classification of chronic inflammatory enteropathies in dogs. Animals (Basel). 2024;14(5):681. doi: 10.3390/ani14050681. PMID: 38473066. PMC: PMC10931249.
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  8. Dandrieux JRS. Inflammatory bowel disease versus chronic enteropathy in dogs: are they one and the same? J Small Anim Pract. 2016;57(11):589-599. doi: 10.1111/jsap.12588. PMID: 27747868.
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Editorial Information

FieldDetail
Published[Date to be inserted on publication]
Last Updated[To be updated on revision – note update scope in brackets]
Reviewed byGlendon Lloyd, Dip. Canine Nutrition (Distinction), Dip. Canine Nutrigenomics (Distinction)
Next Review12 months from publication
AuthorGlendon Lloyd
DisclaimerThis article is for informational purposes only and does not constitute veterinary advice. Always consult a qualified veterinarian before making changes to your dog’s diet or supplement regimen.

Glendon is the founder of Bonza. He holds Diplomas in Canine Nutrigenomics and Canine Nutrition (both with Distinction) and is committed to advancing evidence-based canine nutrition through continuous study of peer-reviewed research. His expertise spans evidence-based canine nutrition, nutrigenomics, and the connections between diet, the gut microbiome, and long-term health outcomes.
Through the Bonza Health Hub for Dogs, Glendon shares evidence-based articles on preventative canine health, making complex nutritional science accessible to dog owners seeking to make informed decisions about their companions’ wellbeing.

Glendon Lloyd Dip.Canine.Nutrition Dip.Dog.Nutrigenomics

About Glendon Lloyd Dip.Canine.Nutrition Dip.Dog.Nutrigenomics

I have had dogs from the day I was born. Much to my Mum's amusement, my Dad bought home Zetta, a beautiful corgi puppy , as his contribution to our new family!

Fast forward to 2018 and Catherine, my wife, and one of our dogs Poppy, were both diagnosed and treated for cancer within months of each other

Diet and its impact on health, cancer particularly, led me down a rabbit hole of discovery.

I consumed information voraciously - on our diets, our dogs' diets and the impact these have not just on health but also the health of our increasingly fragile planet.

I was humbled by the time and expertise given so freely by doctors and vets, canine nutritionists and scientists, academics and agronomists. The more I learned the more I understood there had to be a better way to improve not just our health but also our dogs and the planet's.

The result of my trip down that rabbit hole is Bonza, a plant-based dog food (and now supplements) that elevate our dogs' diet beyond simple nutrition to a diet that inspires a healthier everyday life for our dogs and the planet.

I am continually researching the nutritional impact our dogs' diets have on their health and wellbeing and the ingredients and nutrients we should include in, and exclude from, their food to deliver longer, healthier lives.

I am delighted that my trip down the rabbit hole has led to me completing a Diploma in Canine Nutrigenomics and a Diploma in Canine Nutrition being awarded a Distinction for both my coursework and theses!

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