The gut microbiome as the basis of health:
biofilm, dysbiosis and system repair
Why do complaints in dogs and cats keep coming back despite treatment? The role of pathogenic biofilm, low-grade inflammation, intestinal permeability and the intestinal axes: substantiated with literature.
By Stefan Veenstra DVM
The gut microbiome: more than bacteria
The gut microbiome of dogs, cats, and humans includes an estimated10-11 to10-12 microorganisms per gram of gut contents, consisting of bacteria, archaea, fungi, viruses, and their metabolites. [1] This ecosystem performs functions that extend far beyond digestion alone: it produces short-chain fatty acids (butyrate, propionate, acetate) that serve as a source of energy for colonocytes and directly strengthen the intestinal barrier, it synthesizes vitamins (B12, K2, folate), modulates immune maturation via pattern recognition receptors (TLR, NOD) and produces neurotransmitter precursors including 90% of the body’s serotonin. [2]
When this ecosystem is disrupted, it is called dysbiosis: a qualitative and quantitative change in the microbiome composition that undermines the normal physiological functions of the microbiome. Dysbiosis in dogs is associated with inflammatory bowel disease (IBD), atopic dermatitis, behavioral problems, and metabolic syndrome. [3]
NatuurlijkGezondeDieren.nl: An Introduction to Integrative Bowel Therapy in Dogs and Cats
StefanVeenstra.nl: Systems Biology and Chronic Disease in Animals
Pathogenic biofilm: the hidden factor
One of the central mechanisms by which dysbiosis becomes persistent and maintains chronic symptoms is the formation of pathogenic biofilm. Biofilm is a structured community of microorganisms embedded in a self-produced extracellular matrix (ECM) of polysaccharides, proteins and extracellular DNA. [4] In the gut, pathogenic bacteria such as certain Proteobacterial species (including E. coli and Helicobacter pylori) and yeasts such as Candida albicans attach to the intestinal mucosa, forming a protective layer that effectively shields them from the immune system, antibiotics, and antimicrobial supplementation.
Biofilm continuously produces toxins and enzymes that weaken the host and strengthen its own structure. This generates a chronic, low-grade immune activation that rarely has the sharpness of an acute infection but puts a constant strain on the body. Diagnostically, pathogenic biofilm is difficult to see: the encapsulated bacteria evade regular culture tests and sometimes show false negative results. [5]
Low-grade inflammation and intestinal permeability
Pathogenic biofilm and the associated dysbiosis are almost always accompanied by increased production of lipopolysaccharide (LPS), the endotoxin of gram-negative bacteria. LPS activates TLR4 receptors on enterocytes and immune cells, leading to NF-κB activation and production of pro-inflammatory cytokines (TNF-alpha, IL-1β, IL-6). [6] This chronic cytokine production damages the tight junctions between enterocytes, making the gut barrier more permeable to undigested dietary proteins, bacterial fragments, and LPS itself. This mechanism is referred to as increased intestinal permeability or, popularly, “leaky gut”.
The result is a positive feedback mechanism: the leaked endotoxins enhance systemic immune activation, which in turn further suppresses tight junction expression. This explains why chronically ill animals often become progressively more sensitive to food and environmental triggers, develop more symptoms at once and are difficult to stabilise with symptom-oriented treatments.
The intestinal axes: why complaints manifest themselves everywhere
The intestine is connected to the entire body via multiple bidirectional communication routes. These intestinal axes explain why a disturbed intestinal environment can manifest itself in complaints that at first glance seem to have nothing to do with the intestine.
Intestine-skin axis
Dysbiosis increases systemic LPS burden and pro-inflammatory cytokines that damage the skin barrier and increase mast cell activity. Associated with atopic dermatitis, hot spots, and recurrent skin infections. [7]
Gut-brain axis
The vagus nerve, enteric nervous system, and microbiome metabolites such as butyrate and tryptophan modulate behavior, stress response, and serotonin production. Dysbiosis correlates with anxiety, hyperactivity, and cognitive changes in dogs. [8]
Intestine-joint axis
Systemic LPS loading increases inflammatory tone in joints. Increased intestinal permeability facilitates passage of antigens that can trigger cross-reactive immune responses in joint tissue. [9]
Intestinal immune axis
Approximately 70 to 80% of the immune system is located in and around the intestines (GALT: gut-associated lymphoid tissue). Dysbiosis shifts the Th1/Th2 balance, reduces regulatory T cell activity and increases the likelihood of autoimmune reactions. [10]
The NGD Care Gut Protocol: phasing and mechanisms of action
The Gut Protocol is built around a mechanistically coherent sequence: first biofilm degradation and inflammation inhibition, then microbiome building and barrier repair. Build-up in a still inflamed or biofilm-loaded intestine has limited effect because the pathogenic environment hinders the colonization of desirable microorganisms.
Approximately 80% fresh feed (KVV or BARF), approximately 20% vegetables. Ultra-processed dry food increases the glycemic load of the intestine, stimulates the growth of fermentative bacteria on simple sugars and lowers the production of butyrate through fiber fermentation. Dry food always causes dysbiosis and limited variation in the microbiome. Fresh feed provides prebiotic fiber and bioactive phytonutrients that directly support microbiome recovery. Nutrition is not an afterthought but a biological condition for the success of the protocol.
Biofilm Balance contains enzymes, NAC and lactoferrin and breaks down the extracellular biofilm matrix via proteolytic and mucolytic activity. NAC specifically breaks through the disulfide bridges in the ECM. Liposomal Curcumin inhibits NF-κB activation and downregulates pro-inflammatory cytokines through multiple pathways. Liposomal Vitamin C provides high intracellular concentrations of ascorbate as a cofactor for collagen synthesis and antioxidant protection of enterocytes. Green detox contains chlorella, spirulina and alfalfa and supports hepatic and renal clearance of toxins released during biofilm degradation. Prebiotics stimulate bacteria from all families as microbiome preparation for the build-up phase.
Water kefir provides a broad spectrum of live bacterial and yeast strains that actively restore microbiome diversity. L-glutamine is added in this phase as direct fuel for enterocytes: it is the most commonly used amino acid by intestinal epithelium and essential for rapid regeneration of damaged intestinal mucosa and tight junction repair. In chronic intestinal damage, L-glutamine is mechanistically indispensable as a building material for the intestinal wall itself, separate from microbiome structure.
Shilajit is the first choice in phase 2, especially for humans. Shilajit is a concentrated source of fulvic acid, more than 84 minerals in ionic form, and dibenzo-alpha-pyrones that directly support mitochondrial function in enterocytes. Fulvic acid stimulates Akkermansia muciniphila, the key species for tight junction expression and barrier integrity, and enhances mineral absorption via chelation. For animals, fulvic and humic acids are a proven and useful alternative to the shilajit. Liposomal Vitamin B Complex supports the neural repair of the enteric nervous system and energy production in enterocytes. In this phase, the microbiome composition consolidates and the intestinal barrier stabilizes.
Phase 3 is not a standard component but a targeted supplement for chronically weakened animals and humans where intestinal recovery is going well but energy, resilience and immune resilience do not recover sufficiently. Long-term chronic intestinal problems are almost always accompanied by mitochondrial dysfunction in intestinal cells and systemic tissues: the persistent inflammatory load and oxidative stress deplete the mitochondrial respiratory chain. Phase 3 focuses on this level.
Longevity Complex (NAD+, resveratrol, and ergothioneine) restores the NAD+ pole that is essential for mitochondrial energy production and sirtuin activation. Liposomal Coenzyme Q10 as an electron carrier in the mitochondrial respiratory chain. Liposomal Glutathione restores the intracellular antioxidative capacity that is structurally depleted in chronic infection and inflammation. Optionally, Myco Immune Complex can be added for further immune modulation via beta-glucans and additional microbiome support in the consolidation phase.
Scientific substantiation of the phasing
The logic of cleaning before building up is underpinned in microbiome science. Studies show that probiotic colonization in a dysbiotic environment with pathogenic biofilm is significantly less effective than in a remediated environment: the pathogenic flora suppress the colonization of commensal bacteria via production of bacteriocins and competitive exclusion of adhesion sites. [11] NAC as a biofilm disruptor has been documented for multiple pathogenic species, including the most prevalent intestinal pathogens in dogs. [12] Curcumin directly modulates the gut microbiome through selective inhibition of pathogenic species and stimulation of Lactobacillus and Bifidobacterium populations, in addition to its anti-inflammatory action. [13] Akkermansia muciniphila, stimulated by fulvic acid, has been identified in multiple studies as a central species for tight junction expression and barrier integrity. [14]
L-glutamine is the most commonly consumed amino acid by intestinal epithelial cells and supports tight junction protein expression (claudine-1, occludin) via direct enterocyte energetics and inhibition of apoptosis in intestinal wall damage. Clinical studies in people with increased intestinal permeability show recovery of lactulose/mannitol ratio after L-glutamine supplementation, a direct measure of barrier integrity. [15] Fulvic and Humic acids, or Shilajit, whose bioactivity is primarily attributed to fulvic acid and dibenzo-alpha-pyrones, modulates mitochondrial function via complex I-II stimulation and has demonstrated prebiotic activity in recent microbiome studies. [16]
Why do individual supplements or antibiotics not work enough for chronic intestinal problems?
Individual probiotics do not colonize sustainably in a dysbiotic, biofilm-laden environment. Antibiotics eliminate both pathogenic and commensal bacteria, decrease microbiome diversity, and increase the risk of Clostridioides difficile infection as secondary dysbiosis. Symptom-focused interventions (antihistamines, corticosteroids) suppress the immune response without addressing the underlying microbiome dysregulation. The Intestinal Protocol works in the opposite logic: first clean up the environment, then bring back the right residents.
Indications for the Intestinal Protocol
Chronic or recurrent bowel complaints (IBD, changing stools, SIBO, dysbiosis). Skin and allergy problems via the gut-skin axis. Behavioral changes, stress sensitivity, and cognitive decline through the gut-brain axis. Chronic joint inflammation via the gut-joint axis. Decreased resistance and recurrent infections via the gut-immune axis. As a basis for any chronic protocol, can be combined with Skin Protocol, Giardia Protocol and other specific protocols of NGD Care.
Conclusion
The gut microbiome is not a peripheral organ but a central regulatory system that influences the health of the whole body through multiple axes. Pathogenic biofilm, low-grade inflammation and increased intestinal permeability are the three mechanistic pillars on which chronic, multilocalistic complaints in dogs and cats rest. The NGD Care Bowel Protocol addresses these three pillars in a mechanistically coherent order over four months.
Intestinal recovery is not a quick intervention but a biological process that takes time. When the microbiome stabilizes and the gut barrier restores, health improves on multiple levels at once: skin, resistance, behavior, energy, and joints. This is not an accidental by-catch, but the logical consequence of systemic recovery.
View the NGD Care Intestinal Protocol and choose the right package for your animal
Literature
- Suchodolski JS. Intestinal microbiota of dogs and cats: a bigger world than we thought. Fat Clin North Am Small Anim Pract. 2011; 41(2):261–272.
- Yano JM, Yu K, Donaldson GP, et al. Indigenous bacteria from the gut microbiota regulate host serotonin biosynthesis. Cell. 2015; 161(2):264–276.
- Marsilio S, Pilla R, Salavati Schmitz S, et al. Comparison of the fecal microbiome in dogs with or without chronic inflammatory enteropathy. J Vet Intern Med. 2021; 35(2):851–863.
- Flemming HC, Wingender J. The biofilm matrix. Nat Rev Microbiol. 2010; 8(9):623–633.
- Hall-Stoodley L, Costerton JW, Stoodley P. Bacterial biofilms: from the natural environment to infectious diseases. Nat Rev Microbiol. 2004; 2(2):95–108.
- Cani PD, Amar J, Iglesias MA, et al. Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes. 2007; 56(7):1761–1772.
- Salem I, Ramser A, Isham N, Ghannoum MA. The gut microbiome as a major regulator of the gut-skin axis. Front Microbiol. 2018;9:1459.
- Simpson CA, Diaz-Arteche C, Eliby D, et al. The gut microbiota in anxiety and depression: a systematic review. Clin Psychol Rev. 2021;83:101943. [Mechanism Applicable to Veterinary Gut-Brain Axis]
- Tito RY, Cypers H, Joossens M, et al. Brief report: Dialister as a microbial marker of disease activity in spondyloarthritis. Arthritis Rheumatol. 2017; 69(1):114–121.
- Vighi G, Marcucci F, Sensi L, et al. Allergy and the gastrointestinal system. Clin Exp Immunol. 2008; 153 (Suppl 1):3–6.
- Maldonado Galdeano C, Cazorla SI, Lemme Dumit JM, et al. Beneficial effects of probiotic consumption on the immune system. Ann Nutr Metab. 2019; 74(2):115–124.
- Zhao T, Liu Y. N-acetylcysteine inhibits biofilms produced by Pseudomonas aeruginosa. BMC Microbiol. 2010;10:140.
- Shen L, Liu L, Ji HF. Regulatory effects of curcumin spice administration on gut microbiota and its pharmacological implications. Food Nutr Res. 2017; 61(1):1361780.
- Plovier H, Everard A, Druart C, et al. A purified membrane protein from Akkermansia muciniphila or the pasteurized bacterium improves metabolism in obese and diabetic mice. Nat Med. 2017; 23(1):107–113.
- Kim MH, Kim H. The roles of glutamine in the intestine and its implication in intestinal diseases. Int J Mol Sci. 2017; 18(5):1051.
- Winkler J, Ghosh S. Therapeutic potential of fulvic acid in chronic inflammatory diseases and diabetes. J Diabetes Res. 2018;2018:5391014. [Fulvic acid and mitochondrial function; shilajet as a supplier of fulvic acid and dibenzo-alpha-pyrones]
This information is educational in nature and based on available scientific literature. The studies mentioned are not always directly veterinary or specific to the formulation described here. This text does not replace a veterinary consultation and does not contain any therapeutic claims.