Fecal Microbiota Transplantation in Dogs and Cats. What the veterinary literature actually supports

By Steve Mehler, DVM, DACVS

Bottom line: FMT is a biologically plausible, generally well-tolerated microbiome intervention with the strongest canine signal in parvoviral enteritis and selected chronic enteropathy cases. It is not yet a standardized treatment, a substitute for diagnosis, or a reliably effective therapy across all dysbiosis-associated disease. In cats, evidence remains early and safety deserves particular caution.

Why FMT is more than “transferring good bacteria”

Fecal microbiota transplantation (FMT) transfers a complex biological community from a screened donor into a recipient. That material contains bacteria, archaea, fungi, bacteriophages, metabolites, bile-acid-transforming organisms, microbial proteins and other bioactive components. The therapeutic goal is not simply to add diversity. It is to restore functions that may have been lost during disease or antibiotic exposure: colonization resistance, short-chain fatty-acid production, secondary bile-acid conversion, epithelial support and immune signaling.[1–4]

That distinction matters because sequencing can show that a recipient became more similar to a donor without proving that the patient improved. Conversely, several canine studies reported clinical improvement without consistent donor engraftment or major shifts in standard microbiome indices. FMT is therefore best understood as an ecosystem-level intervention whose clinical effect may depend on the disease, recipient baseline microbiome, donor, product, dose, route and concurrent therapy.

The evidence at a glance

Clinical setting	Best current interpretation	Confidence
Canine parvoviral enteritis	Adjunctive FMT can shorten diarrhea and hospitalization. A mortality advantage has not been proven.	Moderate
Canine acute uncomplicated/AHDS diarrhea	May normalize microbiome recovery better than metronidazole, but controlled studies have not shown a consistent faster clinical recovery than supportive care.	Low–moderate
Canine chronic enteropathy	Some refractory dogs improve, especially with repeated treatment, but a controlled diet-comparator trial found no added benefit from a single enema. Response is heterogeneous.	Low–moderate
Feline chronic enteropathy	A single controlled enema study found no advantage over controls; uncontrolled oral-capsule data show microbiome shifts.	Low
Canine atopic dermatitis	A 2026 blinded trial found reduced lesion scores and medication use, but not superior pruritus scores. Promising adjunct, not replacement therapy.	Moderate, one trial
Diabetes, epilepsy behavior, cognitive dysfunction	Pilot signals only; efficacy is unproven.	Very low
Cats: safety	Adverse events can be clinically important; a nine-cat series reported lethargy, vomiting, diarrhea, anorexia, dehydration and weight loss.	Important signal; incidence unknown

Canine acute gastrointestinal disease

Parvoviral enteritis: the clearest clinical signal

The landmark 2018 randomized trial enrolled 66 puppies with naturally occurring canine parvovirus infection. All received standard care; half also received a single rectal transplant consisting of 10 g of healthy-dog feces diluted in 10 mL saline, administered 6–12 hours after admission. Among survivors, diarrhea resolved faster and median hospitalization fell from six days to three days. Mortality was numerically lower with FMT (21.2% versus 36.4%) but the difference was not statistically significant.[5]

A 2026 prospective double-blinded placebo-controlled study evaluated a broader regimen: one FMT enema followed by 14 days of oral lyophilized capsules. Twenty-seven dogs were enrolled. The placebo arm was stopped after excessive withdrawals for worsening clinical status; FMT-treated dogs had shorter hospitalization and required fewer medications. FMT did not reduce viral shedding or produce a measurable systemic immune response, suggesting that any benefit was more likely related to intestinal ecosystem recovery than antiviral activity.[6]

Clinical interpretation: FMT is a reasonable investigational adjunct to—not a replacement for—fluid therapy, antiemetics, nutritional support, isolation, antimicrobial stewardship and other spectrum-of-care measures. Evidence supports faster recovery more strongly than improved survival.

Acute diarrhea and acute hemorrhagic diarrhea syndrome

The non-parvoviral acute-diarrhea literature is less convincing. In a small 2020 study, 11 dogs given an FMT enema were compared with seven dogs treated with seven days of metronidazole. Both groups improved clinically. By day 28, stool consistency and multiple microbial and metabolic measures were closer to healthy controls after FMT, whereas metronidazole produced more persistent dysbiosis and altered bile-acid profiles.[7] This study supports avoiding unnecessary metronidazole; it does not prove that FMT is required for most self-limiting diarrhea.

A 2021 AHDS pilot found no clinical advantage from FMT, although recipients showed a faster rise in microbial diversity and short-chain-fatty-acid-producing taxa.[8] A larger 2024 double-anonymized trial comparing symptomatic care, FMT and antibiotics likewise found no overall difference in clinical recovery. Dysbiosis persisted longest in antibiotic-treated dogs, and NetF-positive Clostridium perfringens changes were transient regardless of therapy.[9]

Taken together, routine FMT for uncomplicated acute diarrhea or AHDS is not supported. Supportive care is usually sufficient, and antibiotics can delay microbiome recovery when they are not otherwise indicated.

Canine chronic enteropathy

Chronic enteropathy (CE) accounts for most of the canine FMT literature, but the studies vary markedly in diagnosis, disease severity, diet trials, immunosuppressive treatment, donor selection, route, product and number of administrations. Early case reports and uncontrolled cohorts consistently generated encouraging signals, but the controlled evidence is more restrained.

Study	Population / intervention	Main result	Key limitation
Niina et al., 2021	9 dogs with IBD; FMT	Clinical scores fell in all dogs; Fusobacterium increased.	Uncontrolled, small cohort
Toresson et al., 2023	41 poorly responsive CE dogs; median 3 rectal FMTs	31/41 classified as responders; median CIBDAI fell 6 to 2.	Retrospective; concurrent treatment
Gal et al., 2025	7 CE dogs; mostly one enema	Median CCECAI fell from 8 to 3 at week 1 and 1 at day 30; no consistent microbiome change.	No control; donor variability
Bottero et al., 2025	20 diet-refractory CE dogs	17 improved to 3 months; 10 remained stable to 1 year; bile acids and DI improved.	Uncontrolled; mild baseline disease
Toresson et al., 2026	39 refractory CE dogs; 2–3 rectal FMTs	28 responded; 13 tapered corticosteroids. Lower baseline dysbiosis predicted durable response.	Prospective observational, no comparator
JSAP RCT, 2026	42 CE dogs; diet change ± one retention enema	At day 90, owner improvement 76% vs 73%; no significant group differences.	Small; high food responsiveness
TRE trial, 2024/26	13 analyzed dogs; 4 weeks oral FMT vs placebo	Relapse 29% vs 50%, but no clear treatment effect; underpowered.	Very small sample

The strongest practical lesson is that FMT response is not uniform. Repeated-treatment observational work found that dogs with severe baseline dysbiosis and impaired secondary bile-acid production were less likely to sustain a response—counter to the intuitive belief that the “most dysbiotic” patient should benefit most.[10] A plausible explanation is that severe mucosal disease or loss of ecological niches prevents incoming organisms from establishing. In those dogs, FMT alone may be too little, too late, or may require a different donor, route, schedule or concurrent control of inflammation.

A single enema should not be expected to outperform an effective diet trial. The 2026 controlled study in 42 dogs found almost identical owner-reported improvement after diet plus FMT and diet alone.[11] This is a crucial corrective to uncontrolled studies: regression to the mean, concurrent therapy, natural fluctuation and food responsiveness can all be mistaken for an FMT effect.

Current place in therapy: consider FMT only after an adequate diagnostic evaluation and diet trial, most reasonably as an adjunct in refractory CE under specialist oversight. Repeated administration has a stronger observational signal than a single treatment, but an optimal schedule has not been established.

Specific canine enteropathies and antibiotic-associated dysbiosis

Individual case reports describe apparent benefit in a dog with Clostridioides difficile-associated diarrhea, a Toy Poodle with intractable inflammatory enteropathy, a Shiba Inu with nonresponsive enteropathy receiving chlorambucil, a dog with relapsing chronic diarrhea and a French Bulldog with granulomatous colitis.[12–16] These reports are hypothesis-generating only. Concurrent drugs, spontaneous fluctuation and diagnostic uncertainty prevent attribution of response to FMT.

In healthy dogs given tylosin, a randomized study found that fecal microbial and bile-acid abnormalities recovered rapidly after the antibiotic was stopped; neither an enema nor oral FMT accelerated the measured recovery.[17] This argues against automatically using FMT after every antibiotic course. The first intervention should be antimicrobial stewardship.

Evidence outside the canine gastrointestinal tract

Canine atopic dermatitis

An open-label 2023 pilot in 12 dogs found reductions in CADESI-04 and owner pruritus scores after a single oral FMT.[18] More persuasive evidence arrived in 2026: 40 dogs completed a randomized placebo-controlled double-blinded trial of daily lyophilized oral capsules for 90 days plus rectal FMT monthly. CADESI-04 lesion scores and medication scores were lower with FMT at months two and three, and sustained lesion responders were more common (35% versus 5%). Pruritus scores improved in both groups without a significant between-group difference.[19]

This makes atopic dermatitis one of the more interesting extraintestinal indications, but replication is needed. FMT should be framed as an adjunct to allergen control, barrier care, infection management and evidence-based antipruritic therapy—not as a replacement.

Diabetes mellitus

A 2025 double-blinded pilot randomized nine diabetic dogs to oral lyophilized FMT or placebo. FMT was associated with a faster early decline in interstitial glucose, but mean glucose did not differ at study completion. Water intake and Faecalibacterium abundance changed, but the sample was far too small to establish a glycemic benefit.[20] Insulin therapy and standard diabetic monitoring remain indispensable.

Epilepsy-related behavior and cognitive dysfunction

Nine dogs with drug-resistant epilepsy and behavioral comorbidities improved on several owner and behavioral measures after three FMTs in an uncontrolled 2024 pilot; seizure control itself was not established as an FMT outcome.[21] A 2026 open-label study treated 11 aging dogs with oral capsules for 90 days. Only six had complete final cognitive scores: four improved and two worsened.[22] Both studies are intriguing gut–brain-axis signals, but placebo effects, owner expectation, small samples and incomplete outcome data make clinical efficacy unknown.

Performance and stress

A study in Kunming police dogs reported microbiome and performance-related changes after FMT during transportation stress.[23] Its specialized population and endpoints limit generalization to companion animals.

What the feline literature shows

Feline evidence is substantially thinner than canine evidence. A 2023 cohort evaluated 46 cats with chronic digestive problems given 50 oral lyophilized capsules. Donor organisms were detected in recipients and microbial communities shifted, particularly in cats with diarrhea, but the study did not include a placebo control and was designed primarily around microbiome outcomes.[24]

A 2025 prospective study enrolled 28 cats with chronic inflammatory enteropathy or small-cell gastrointestinal lymphoma. Eleven received a single FMT enema and 17 served as controls. Clinical scores improved within the FMT group, but by day 30 neither clinical scores nor the feline Dysbiosis Index differed significantly from controls. The study therefore did not show a specific treatment benefit from one enema.[25]

A 2026 experimental study showed that microbiota from lean or obese donors could shift recipient cats toward the donor microbial profile, but did not change body weight or routine biochemical variables during the study period.[26] This demonstrates transferability, not obesity treatment.

The major feline warning comes from a 2025 nine-cat adverse-event case series. Cats receiving repeated FMT for chronic or treatment-resistant diarrhea developed lethargy, vomiting, diarrhea, inappetence, dehydration and weight loss; some had abdominal pain or ultrasonographic gastroenterocolitis. Most improved with supportive or antimicrobial treatment, and eight ultimately had at least a partial response to the original complaint.[27] Because the series included only cats with adverse events, it cannot estimate incidence—but it proves that clinically meaningful reactions occur and should not be dismissed as benign transient stool changes.

Safety: what can go wrong?

In dogs, published short-term adverse effects are usually mild and self-limiting. A prospective study of 10 healthy recipients given one 5 g/kg enema found transient vomiting, diarrhea, decreased activity or inappetence without meaningful changes in CBC, chemistry, CRP, circulating cytokines or leukocyte subsets.[28] Diseased populations have also reported mild gastrointestinal signs. However, small studies are poorly equipped to detect rare serious events or long-latency consequences.

·       Transmission of recognized pathogens, including parasites, viruses, enteropathogenic bacteria and toxin-producing organisms.

·       Transmission of antimicrobial-resistance genes or multidrug-resistant organisms even when the donor appears clinically healthy.

·       Transfer of an undesirable metabolic, immune or behavioral phenotype; this remains theoretical in routine practice but is biologically plausible.

·       Exacerbation of vomiting, diarrhea, anorexia, abdominal discomfort or dehydration—especially relevant in cats.

·       Aspiration risk with upper-GI or improperly administered oral products, and procedural risks from sedation, colonoscopy or enemas.

·       Failure of engraftment or clinical worsening caused by delay of disease-specific diagnosis and treatment.

FMT material should be treated as a biologic product, not as a probiotic supplement and certainly not as a harmless home remedy. Do-it-yourself transplantation is medically and hygienically inappropriate.

Donor selection and screening

Veterinary donor-screening standards remain incompletely harmonized. Published protocols and expert reviews converge on selecting a consistently healthy, normal-weight donor with normal stool, no chronic gastrointestinal, dermatologic, immune-mediated, metabolic or behavioral disease, no recent travel or high-risk exposure, and no recent antibiotic or immunosuppressive use. Diet and household exposure matter because the donor transfers an ecosystem, not a single strain.[1,29,30]

Domain	Reasonable minimum considerations
History and examination	Normal physical examination, body condition and stool; stable diet; no chronic GI disease, food-responsive disease, recurrent infections, atopy, immune-mediated disease or unexplained systemic illness.
Medication exposure	Exclude recent antimicrobial exposure; document probiotics, immunosuppressants, acid suppressants, raw food and other agents that can alter or contaminate the microbiome.
Routine laboratory testing	CBC, chemistry and urinalysis as appropriate; consider additional testing based on age, region and recipient risk.
Fecal testing	Centrifugal flotation or antigen/PCR testing for parasites; Giardia and Cryptosporidium assessment; pathogen panel tailored to species, geography and recipient.
Canine infectious risks	Consider Campylobacter, Salmonella, pathogenic E. coli, Clostridioides difficile/toxins, Clostridium perfringens toxin genes, canine parvovirus and other locally relevant agents.
Feline infectious risks	Consider FeLV/FIV status, Tritrichomonas foetus, Giardia, Cryptosporidium, Salmonella, Campylobacter, enteric coronavirus context and other locally relevant agents.
Antimicrobial resistance	Culture or molecular screening for multidrug-resistant Enterobacterales and clinically important resistance genes when available, especially for immunocompromised recipients.
Re-screening	Maintain a defined requalification interval and re-screen after illness, medication exposure, travel, diet change or new household animals. Quarantine stored lots until donor health is confirmed when feasible.

No test panel can reduce risk to zero. A negative multiplex PCR panel is not equivalent to a comprehensively safe donor; it only excludes the organisms included in that assay at the time sampled.

Preparation, storage, dose and route

There is no universally validated canine or feline protocol. Published studies have used fresh filtered slurry, frozen glycerol-preserved material, lyophilized products, oral capsules, retention enemas and endoscopic delivery. Doses range widely; several clinical reports used approximately 5–7 g/kg rectally, while the parvovirus trial used a fixed 10 g dose.[5,10,11] This heterogeneity prevents declaring one regimen superior.

Laboratory studies provide several practical clues. Canine stool stored with glycerol at −80°C retained overall community structure better than warmer storage, and donor-to-donor variation exceeded many storage effects.[31] Viability work showed that prolonged storage and lyophilization can reduce viable core organisms, including Peptacetobacter hiranonis; glycerol-preserved frozen preparations performed best in that study.[32] A 2025 companion-animal preparation study found that cryo- or lyoprotectants improved viability up to six months and published a detailed processing framework, but clinical equivalence among products remains unproven.[29]

Route should match the product and patient. Rectal enema is inexpensive and avoids upper-GI delivery, but retention varies and proximal distribution is uncertain. Colonoscopy allows targeted proximal colonic delivery but adds bowel preparation, anesthesia, cost and procedural risk. Oral capsules are convenient for repeated dosing, but capsule integrity, release site, oxygen exposure, dose and palatability matter. A healthy-dog capsule study showed that gelatin and delayed-release products do not necessarily release at identical intestinal sites.[33]

Why studies conflict

·       Different diseases are grouped under the same label. Acute self-limiting diarrhea, parvoviral mucosal injury, food-responsive enteropathy and steroid-refractory protein-losing disease are not one biological problem.

·       Concurrent diet, corticosteroids, antimicrobials and supportive care can drive improvement independently of FMT.

·       The donor is a major source of biological variation. “Healthy” does not guarantee a therapeutically useful community.

·       Single-dose and repeated-dose protocols may not be comparable.

·       16S sequencing describes relative bacterial composition, not absolute load, viability, strain function, viruses, fungi or metabolite activity.

·       Clinical indices and owner-reported outcomes are vulnerable to expectation effects unless studies are blinded and placebo controlled.

·       Most studies are small and underpowered, making both false-positive and false-negative conclusions possible.

·       Follow-up is often too short to measure relapse, delayed adverse effects or stable engraftment.

A practical evidence-based position for clinicians

FMT should currently be discussed as an emerging adjunctive therapy. It has enough evidence to justify controlled, documented clinical use in selected dogs, but not enough standardization to justify casual or indiscriminate use.

Question	Practical answer
When is the rationale strongest?	Parvoviral enteritis as an adjunct; selected refractory canine CE after appropriate diagnostic and dietary workup; possibly canine atopic dermatitis as an add-on.
When is routine use unsupported?	Most uncomplicated acute diarrhea, automatic “repair” after antibiotics, feline CE after one enema, obesity, diabetes, epilepsy, or cognitive dysfunction.
What should be documented?	Indication, donor identity and screening, product preparation and lot, route, dose, concurrent therapies, informed consent, clinical score, stool score, adverse events and follow-up.
What should owners be told?	Benefits are indication-dependent and uncertain; repeat treatment may be needed; pathogens and resistance can be transferred; worsening GI signs require prompt reassessment.
What outcome matters most?	Durable clinical improvement and reduced medication burden—not donor similarity on sequencing alone.

The conclusion

The veterinary FMT literature has moved beyond anecdotes, but it has not yet reached the point of a standardized, broadly validated therapy. In dogs, randomized evidence supports faster recovery from parvoviral enteritis, while acute non-parvoviral diarrhea studies show microbiome preservation more consistently than superior clinical recovery. Chronic-enteropathy cohorts often report benefit, particularly with repeated administration, but controlled data show that a single FMT may add nothing to an effective diet change. A new controlled atopic-dermatitis trial is genuinely promising. Other extraintestinal indications remain exploratory.

For cats, the evidence is earlier and more cautionary: microbial transfer can occur, but clinical efficacy has not been demonstrated in a controlled chronic-enteropathy study, and significant adverse reactions have been reported. Across both species, donor screening, product handling, antimicrobial-resistance risk and careful outcome tracking are central—not optional.

FMT may ultimately become a family of precision microbiome therapies rather than one procedure. The future is likely to involve defined donor phenotypes, disease-specific microbial consortia, functional metabolite profiling and recipient selection based on ecological capacity to engraft. For now, the science supports measured optimism, not microbiome mythology.

References

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