August 2022

In this VETgirl online veterinary continuing education blog sponsored by Purina ProPlan Veterinary Diets, Dr. Jan S. Suchodolski reviews dysbiosis and the microbiome of the dog and cat.

Please note the opinions in this blog are the expressed opinion of the author and not directly endorsed by VETgirl.

Dysbiosis and the Microbiome: Dispelling Myths about Managing GI Patients

By Dr. Jan S. Suchodolski, MedVet, DrVetMed, PhD, AGAF, DACVM, Associate Professor of Small Animal Internal Medicine, Associate Director for Research, GI Lab, Texas A&M University, Veterinary Medicine and Biomedical Sciences

The gut microbiome is much more than a collection of bacteria and other organisms living in an animal’s gastrointestinal (GI) tract. The microbiome works like a metabolic organ, producing compounds and metabolites that connect and activate all of the organ systems in the body through the digestive tract.

Growing knowledge about the role of the gut microbiome in host health is shifting long-accepted beliefs about the management of veterinary patients with GI disease—and relegating some of these beliefs to the status of myths.

Myth #1: Dysbiosis alone always causes disease. Think about the body as a garden and the microbiome as the soil where the garden grows. An abundance of diverse beneficial bacteria produces rich, fertile “soil,” while a lack of diversity and beneficial species produces poor “soil,” that is prone to overgrowth of undesirable microorganisms.

It is true that disruptions to the homeostasis of the microbiome can contribute to disease, but dysbiosis does not by itself always cause it. One or more additional factors must be present. The GI tract has a mucus layer that forms a barrier in the gut, protecting it from harmful bacteria. If an animal has antibiotic-induced dysbiosis but the rest of its GI tract is functioning normally, the individual typically can withstand those changes. However, if the animal has a chronic GI disease that causes inflammatory changes in the epithelium, the mucus layer in the intestine will be compromised. And if there’s a dysbiosis on top of this, the dog may develop a complex, long-term condition that requires multiple therapeutic interventions.

Purina dog gastrointestinal image

Myth #2: Most cases of diarrhea are caused by bacterial infection. Many of us were taught in veterinary school to treat acute and chronic diarrhea with antibiotics because of the accepted wisdom that the diarrhea was likely caused by an enteral pathogen. The reality is that very few diarrhea cases in dogs have an infectious cause. For example, a two-year, multilaboratory survey evaluating the presence of Salmonella prevalence in dogs determined that only 2.5% of dogs were infected—and only 55% of the infected dogs were diarrheic.1 Antibiotic therapy may temporarily improve clinical signs in patients with diarrhea due to the overall decrease in bacteria which, in turn, can alleviate the burden on the immune system. However, the moment we stop treatment, the diarrhea is likely to recur. Meanwhile, the antibiotic has now induced a dysbiosis state in the patient.

This is not to say antibiotics do not have a role in treating infections—they obviously do. But we don’t want to overuse them. Studies conducted in human medicine with thousands have patients have demonstrated that administration of broad-spectrum antibiotics—especially in childhood when the microbiome is still developing—can be a significant factor in the development of problems such as allergies and GI disease later in life. It’s a good assumption that the same is true of young animals.

Changing this approach requires educating clients who come to us seeking treatment for dogs with acute diarrhea. We need to help them understand that it is not in their dogs’ best interest to go home with antibiotics. And contrary to what we as veterinarians have been conditioned to believe, we don’t need to stop the diarrhea right now. Instead, we can assure the owner that their dog’s acute diarrhea is often caused by stress or dietary indiscretion and that we can expect it to resolve on its own in five to seven days. Should the owner ask about antibiotics, we can explain that a course of antibiotics would likely make little difference in the duration of clinical signs2—and potentially do more harm than good. Rather than sending these patients home with a broad-spectrum antibiotic, we should send them home with a highly digestible therapeutic diet. If a clients report a lack of improvement over a week or two, we can consider adding an additional component such as dietary fiber (e.g., psyllium).

Myth #3: If the microbiome is out of balance, it can easily be fixed. While acute diarrhea typically causes only minor, transient shifts in the microbiome, chronic GI disease is a very different story. The affected dog’s protective intestinal villi are shortened, which leads to malabsorption and a shift in balance of beneficial and potentially harmful bacteria in the lumen. Unfortunately, once dysbiosis occurs it can be hard to reverse it because we damaged intestinal villi cannot regrow.

Correcting an abnormal microbiome requires a multimodal approach that may involve two or more of the following elements.

• Diet should be considered the lead strategy when managing patients with dysbiosis. An estimated 50 to 70 percent of dogs with chronic GI disease respond positively to dietary changes. I recommend starting with a highly digestible diet, that allows nutrients to be readily absorbed, then re-evaluating the dog’s clinical signs 10 to 14 days later to see if there has been improvement. If not, I recommend trying a second and even a third diet (e.g., a hydrolyzed, novel protein or amino acid-based diet) before moving on to an immunosuppressive medication or an antibiotic.

• Dietary fiber can serve multiple functions, depending on the fiber used in the diet. Fibers with high solubility and viscosity can bind water and form gelts to prolong gastric emptying and slow intestinal transit time. Meanwhile, prebiotic fibers, such as psyllium or inulin, are fermented by gut bacteria and produce beneficial short-chain fatty acids that provide energy for the cells lining the colon (colonocytes) and stimulate the growth and activity of beneficial bacteria in the gut. Fiber can be added via a supplement or a fiber-enriched GI diet.

• Probiotics, which are typically live beneficial bacteria, may also help maintain gut barrier function. However, probiotics should be viewed as an adjunct versus a primary therapy for dysbiosis. We cannot necessarily change the microbiome itself with a probiotic, but there can be true therapeutic benefits to probiotic administration. For example, administering a probiotic to patients alongside an antibiotic can provide immune stimulation and may help ameliorate some of the diarrhea and vomiting associated with antibiotic administration.

• Fecal microbiota transplantation (FMT) is another adjunct treatment that is becoming much more commonplace. In my experience, it works in roughly one-third to one-half of dysbiosis cases. But while FMT alone would seem to be the perfect treatment for dysbiosis because of its potential to change the recipient’s gut microbial composition, it is important to consider why the animal has dysbiosis in the first place and design the intervention strategy accordingly.

The ideal patient for FMT alone is a young animal that requires an antibiotic for an infection of some type, with a significant disruption in the microbiome being a consequence. Because the dog’s GI tract is probably still physiologically normal, one or two FMTs will probably be sufficient to restore the microbiota. However, a dog with chronic GI disease is unlikely to be completely cured with FMT alone. While a three- to six-month improvement period may be noted following an initial FMT administration, clinical signs are likely to return. Reversing the underlying dysbiosis in these patients typically requires a year or two of treatment with a multimodal therapeutic approach that includes diet, FMT, immunosuppressants and other agents.

It has taken me more than 20 years of study of the microbiome to get to this juncture and the insights garnered by other researchers and me are changing the way practitioners address GI disease. Our long-term goal should be to identify chronic GI disease in its early stages before extensive changes in the microbiome have taken place. We can then deploy management strategies with greater success.

References:
1. Reimschuessel R, Grabenstein M, Guag J et al. Multilaboratory Survey To Evaluate Salmonella Prevalence in Diarrheic and Nondiarrheic Dogs and Cats in the United States between 2012 and 2014. J Clin Microbiol. 2017 May;55(5):1350-1368. doi: 10.1128/JCM.02137-16. Epub 2017 Feb 15. PMID: 28202802; PMCID: PMC5405253.
2. Shmalberg J, Montalbano C, Morelli G, Buckley GJ. A Randomized Double Blinded Placebo-Controlled Clinical Trial of a Probiotic or Metronidazole for Acute Canine Diarrhea. Front Vet Sci. 2019 Jun 4;6:163. doi: 10.3389/fvets.2019.00163. PMID: 31275948; PMCID: PMC6593266.

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