FOR ANIMAL USE ONLY — Administer as directed by a veterinarian or as per label instructions. Sustain for Cats is a veterinary nutraceutical synbiotic and postbiotic supplement — not a veterinary medicine; it does not require a prescription but veterinary guidance is recommended for cats with chronic or recurrent GI signs (chronic diarrhoea, vomiting, weight loss, or suspected inflammatory bowel disease). Chronic or recurrent GI signs in cats require veterinary investigation to exclude feline inflammatory bowel disease (IBD), small cell lymphoma (the most important differential for chronic feline GI disease), exocrine pancreatic insufficiency (EPI), hyperthyroidism, and chronic enteropathy before attributing signs to microbiome dysbiosis alone. Sustain for Cats is for daily maintenance gut health and immune support in otherwise healthy cats or cats under veterinary management for GI or immune-related conditions. Keep out of reach of children. Store in a cool, dry place; keep sachets sealed until use.
VetPlus Sustain Synbiotic & Postbiotic Sachets for Cats | Enterococcus faecium SF68 Probiotic, Inulin Prebiotic, Saccharomyces cerevisiae Postbiotic & Beta-Glucan Immune Support | 30 Sachets
VetPlus Sustain for Cats is a veterinary nutraceutical supplement manufactured by VetPlus Ltd (UK), specifically formulated for feline daily long-term gut and immune health maintenance. Sustain for Cats delivers a uniquely comprehensive four-component synbiotic and postbiotic formula in a convenient individual powder sachet: (1) Enterococcus faecium SF68 (NCIMB 10415 — the clinically validated probiotic strain), (2) inulin (the β(2→1)-fructan prebiotic selectively nourishing gut commensals including SF68), (3) a postbiotic derived from Saccharomyces cerevisiae (inactivated baker’s/brewer’s yeast and its cell wall components including mannanoligosaccharides — MOS — and beta-glucans), and (4) beta-glucans (the immunomodulatory β(1→3)(1→6)-linked glucose polymers from S. cerevisiae cell walls). This multi-component formulation extends beyond a simple probiotic or synbiotic: the postbiotic and beta-glucan components provide immune system modulation independent of live bacterial colonisation, making Sustain effective in situations where live probiotic colonisation may be transient or limited. The 30-sachet pack provides a full 30-day supply (one sachet daily), suitable for extended daily microbiome and immune maintenance. The powder format mixes easily into wet or dry food.
Distinguishing Sustain’s Four-Component Formulation: Probiotic + Prebiotic + Postbiotic + Beta-Glucan
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The four functional categories and how they differ: (a) probiotic — live microorganisms that, when administered in adequate amounts, confer a health benefit on the host (FAO/WHO 2001 definition); probiotics act through colonisation, competitive exclusion, bacteriocin production, and direct immune modulation while alive in the intestinal lumen; (b) prebiotic — a selectively fermented substrate that allows specific changes in the composition and/or activity of the gastrointestinal microbiota, conferring benefit to the host (Gibson & Roberfroid 1995; updated ISAPP 2017 definition: a substrate selectively utilised by host microorganisms conferring a health benefit); prebiotics nourish and selectively amplify beneficial commensals; (c) synbiotic — a combination of probiotics and prebiotics designed to work synergistically (the prebiotic is the selective growth substrate for the co-administered probiotic, providing a colonisation advantage in the competitive intestinal environment); SF68 + inulin in Sustain is the synbiotic pair; (d) postbiotic — a preparation of inanimate microorganisms and/or their components that confers a health benefit on the host (ISAPP 2021 definition by Salminen et al., Nature Reviews Microbiology); critically: postbiotics are NOT live organisms — they are inactivated (killed by heat or other means) microbial cells, cell wall fragments, cell wall polymers (MOS, beta-glucans, lipoteichoic acids), intracellular metabolites (SCFAs, enzymes, vitamins), and surface-associated proteins; postbiotics confer immune benefits independently of colonisation: they stimulate pattern recognition receptors (PRRs — Toll-like receptors — TLR2, TLR4, Dectin-1, Dectin-2) on intestinal epithelial cells and dendritic cells via their MAMP (microorganism-associated molecular patterns) content, modulating innate and adaptive immunity without requiring viable microbial survival in the gut; this is a critical advantage: in cats receiving antibiotics, hospitalisation, or with compromised intestinal environments where live probiotic colonisation is difficult, the postbiotic component continues to provide immune benefits regardless of colonisation status
Active Ingredients & Mechanisms of Action
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Enterococcus faecium SF68 (NCIMB 10415) — clinically validated, thermostable probiotic strain: SF68 is the most extensively studied veterinary probiotic strain; mechanisms in cats: (a) adhesion to feline intestinal epithelium via Esp (enterococcal surface protein) MSCRAMM domain binding to sialylated and sulphated feline mucin MUC2 glycoprotein; (b) competitive exclusion of feline enteropathogens (Clostridium perfringens type A, pathogenic Enterococcus spp., Listeria) via bacteriocin production (enterocins) and nutrient competition; (c) secretory IgA (SIgA) stimulation — SF68 activates Peyer’s patch dendritic cells → IL-6/TGF-β co-stimulation of IgA class switch recombination (AID-mediated T-cell-independent switch) in subepithelial dome B cells → polymeric IgA (pIgA) → transcytosis via polymeric immunoglobulin receptor (pIgR) → secretory IgA (SIgA) in the intestinal lumen → immune exclusion of enteropathogens; (d) Treg (CD4+FoxP3+) maintenance via TLR2/TLR9 dendritic cell activation → IL-10/TGF-β → lamina propria Treg differentiation → suppression of Th1/Th17 responses in the feline gut; EFSA QPS (Qualified Presumption of Safety) status for E. faecium NCIMB 10415 in cats; clinical evidence: Bybee et al. (JVIM 2011) — SF68 reduced duration of diarrhoea and improved faecal scores in shelter cats; Torres-Henderson et al. (Front Vet Sci 2017) — SF68 improved Dysbiosis Index in cats; Veir et al. (2007) — SF68 increased faecal IgA in cats
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Inulin (chicory root β(2→1)-fructan prebiotic) — the SF68 synbiotic partner and colonic prebiotic fibre: inulin (β(2→1)-linked fructose oligomers from chicory root Cichorium intybus; DP 10–60, distinguishing it from FOS DP 2–4) is the selective prebiotic substrate for SF68 and colonic Bifidobacterium spp.; mechanisms: (a) SF68 colonisation advantage — SF68 expresses β-fructofuranosidase and a fructose-specific PTS transporter allowing it to ferment inulin intracellularly; inulin selectively amplifies SF68 in the competitive intestinal environment over non-fructan-fermenting bacteria; (b) Bifidobacterium and Lactobacillus selective stimulation (bifidogenic effect) — β(2→1) glycosidic bonds are resistant to mammalian digestive enzymes; inulin reaches the colon intact for selective fermentation by Bifidobacterium (which expresses β-fructofuranosidase and the FOS uptake system) → Bifidobacterium-derived acetate → cross-fed to butyrate-producing Firmicutes (Roseburia intestinalis, Faecalibacterium prausnitzii via the butyryl-CoA:acetate CoA-transferase pathway) → colonocyte butyrate supply, tight junction integrity (claudin-1, occludin, ZO-1 upregulation), and colonic Treg induction; (c) longer-chain inulin (DP 10–60 vs FOS DP 2–4) distributes the prebiotic effect across the full colonic length (proximal to distal) rather than being rapidly fermented in the proximal colon only
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Saccharomyces cerevisiae postbiotic — inactivated yeast cells and cell wall components (mannanoligosaccharides — MOS — and beta-glucans) with gut barrier and immune modulation activity: Saccharomyces cerevisiae (baker’s/brewer’s yeast) postbiotic is produced by controlled heat inactivation of S. cerevisiae fermentation biomass — the inactivation process maintains the structural integrity of cell wall components while eliminating viability; the S. cerevisiae cell wall is a complex layered structure comprising: outer layer: alpha-mannoproteins (glycoproteins with alpha-1,2-, alpha-1,3-, and alpha-1,6-linked mannose chains — mannoproteins; these are the source of mannanoligosaccharides — MOS); inner layer: beta-glucan network (β(1→3)-linked glucose backbone with β(1→6)-linked branches — the dominant structural polysaccharide comprising approximately 60% of the dry cell wall weight); chitin microfibrils (β(1→4)-N-acetylglucosamine polymer — approximately 1–3% of cell wall dry weight — anchoring beta-glucan to the plasma membrane); mechanisms of S. cerevisiae postbiotic action: (a) MOS — pathogen exclusion via mannose receptor competitive binding: type 1 fimbriae-expressing gram-negative enteropathogens (Salmonella spp., Escherichia coli — ETEC/EPEC strains expressing FimH adhesin — the lectin domain of the type 1 fimbrial tip adhesin which binds to mannosylated glycoproteins on intestinal epithelial cells) use FimH to colonise the intestinal epithelium; MOS from S. cerevisiae cell walls provides mannose residues in solution that competitively bind FimH lectins → blocking FimH adhesion to intestinal epithelial cell mannosyl glycoproteins → enteropathogens are unable to colonise the epithelium → they are cleared by intestinal peristalsis; this mannose receptor competitive exclusion mechanism is the basis of MOS use in poultry (reducing Salmonella shedding) and companion animal probiotic/postbiotic products; (b) MOS — beneficial microbiome stimulation: MOS oligosaccharides serve as fermentation substrates for beneficial Lactobacillus and Bifidobacterium species in the colon (mannan-fermenting Lactobacillaceae express alpha-mannosidase and mannanase for MOS hydrolysis) → selective enrichment of commensals; (c) beta-glucan immunomodulation — innate immune activation via Dectin-1 and TLR2/4 (see beta-glucan section below); (d) improvement of intestinal barrier integrity: MOS glycoproteins interact with intestinal mucin producing goblet cells, stimulating mucin MUC2 secretion → increased mucus layer thickness → physical barrier enhancement against pathogen adhesion and luminal antigen translocation; postbiotic heat-killed S. cerevisiae also stabilises tight junction protein expression (claudin-3, claudin-4, occludin) via MyD88-dependent TLR2 signalling → reduces intestinal permeability (‘leaky gut’)
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Beta-glucans (β(1→3)(1→6)-D-glucan from S. cerevisiae cell walls) — the principal innate immunomodulatory component of Sustain: S. cerevisiae beta-glucan (β(1→3)-D-glucan with β(1→6)-linked glucose branches; also termed particulate yeast beta-glucan or whole glucan particles — WGP — when isolated in intact particle form) is the most potent and well-characterised immunomodulatory dietary supplement in companion animals; mechanisms of beta-glucan immune activation: (a) Dectin-1 (CLEC7A — C-type lectin domain family 7 member A) receptor activation: Dectin-1 is the primary pattern recognition receptor (PRR) for β(1→3)-D-glucans on innate immune cells (macrophages, dendritic cells, neutrophils, NK cells, and intestinal epithelial cells); β(1→3)-D-glucan binds Dectin-1’s carbohydrate recognition domain (CRD) → Dectin-1 ITAM (immunoreceptor tyrosine-based activation motif) phosphorylation via Src kinases (Lck, Hck, Fyn) → Syk (spleen tyrosine kinase) recruitment and activation → downstream signalling: (i) CARD9-Bcl10-MALT1 (CBM complex) → NF-κB canonical pathway (p65/p50) → IL-12, IL-6, IL-23, TNF-α pro-inflammatory cytokines in Th1/Th17 context; (ii) CARD9 → IRF5 → IL-12 → Th1 differentiation → antifungal and antibacterial defence; (iii) NLRP3 inflammasome priming (Dectin-1/Syk/CARD9 → NLRP3 upregulation) → IL-1β/IL-18 processing via caspase-1 → inflammatory resolution in the intestinal mucosa; (iv) Dectin-1 synergism with TLR2 (on the same cell surface): Dectin-1 + TLR2 co-stimulation by S. cerevisiae cell walls (which present both beta-glucan for Dectin-1 and mannoprotein/zymosan-associated lipoteichoic acid analogues for TLR2) activates: Myd88 → IRAK4 → TRAF6 → TAK1 → IKKβ → NF-κB; TRIF → IRF3 → type I IFN (α/β interferon); the synergistic Dectin-1/TLR2 co-stimulation on intestinal lamina propria dendritic cells generates a particularly potent IL-12/IL-23-mediated Th1/Th17 response that enhances mucosal anti-pathogen defence without the systemic inflammatory consequences of LPS/TLR4 activation; (b) beta-glucan and NK cell priming (trained immunity): beta-glucans can programme innate immune cells for enhanced responses to subsequent pathogen challenges — a phenomenon termed ‘trained immunity’ (Netea et al., Science 2016); mechanism: beta-glucan exposure → epigenetic reprogramming of monocytes/macrophages via H3K4me3 (trimethylation of histone H3 lysine 4 — an activating epigenetic mark) at the promoters of IL-6, TNF-α, and IL-1β loci (mediated by β-glucan → Dectin-1/Syk/Akt → mTOR → HIF-1α → glycolytic reprogramming from oxidative phosphorylation to aerobic glycolysis [Warburg effect] → fumarate accumulation → TET2 inhibition → DNA demethylation at enhancer regions → H3K4me3 deposition at cytokine promoters); trained innate immune cells maintain enhanced cytokine production capacity for weeks to months after a single beta-glucan priming event — providing sustained mucosal immune enhancement beyond the period of supplementation; this is particularly relevant for the daily 30-sachet course of Sustain − the extended supplementation period allows cumulative epigenetic training of intestinal and circulating innate immune cells; (c) beta-glucan and Treg/Th2 balance: at lower or physiological beta-glucan concentrations (as achieved by dietary supplementation vs pharmacological dosing), Dectin-1 activation tilts the DC phenotype toward tolerogenic DCs expressing IL-10 and TGF-β → Treg (FoxP3+) differentiation → mucosal tolerance → suppression of excessive Th2 responses (relevant for cats with food hypersensitivity or atopic manifestations); (d) feline-specific immunological context: cats are at particular risk of vaccine-preventable infectious diseases (feline panleukopenia — FPV, feline herpesvirus — FHV-1, feline calicivirus — FCV) that are lethal when innate immune defences fail to contain initial viral replication before adaptive immunity generates vaccine memory responses; beta-glucan-mediated trained immunity in cats may provide an adjunctive non-specific innate immune ‘boost’ between vaccination intervals, particularly relevant in multi-cat households, shelters, and cats with known immune compromise
Indications
- Daily long-term maintenance probiotic, prebiotic, postbiotic, and immune support for cats
- Antibiotic-associated gut dysbiosis in cats — concurrent or post-antibiotic supplementation; the postbiotic and beta-glucan components maintain immune benefit even when live probiotic colonisation is suppressed by concurrent antibiotic use
- Immune support during periods of increased infection risk — multi-cat households, boarding, kennelling, new cat introductions, shelter environments
- Stress-associated GI disruption — boarding, rehoming, multi-cat household dynamics, veterinary hospitalisation
- Post-illness microbiome and immune recovery
- Senior cats (≥10 years) with age-associated microbiome changes and immune senescence
- Cats with food hypersensitivity or atopy as adjunctive mucosal tolerance support
- IBD-predisposed breeds (Siamese, Burmese, Ragdoll) as adjunctive microbiome and immune support alongside veterinary IBD management
Directions for Use
- Administer as directed by a veterinarian or per VetPlus label instructions
- Mix the contents of one sachet into wet food, or sprinkle onto dry food daily
- The powder is palatable and designed for easy mixing with food
- 30-sachet pack = 30-day supply at 1 sachet daily; for extended maintenance, use continuously or as directed by a veterinarian
Safety Information
- For animal use only — keep out of reach of children
- E. faecium SF68 is susceptible to all major veterinary antibiotics; the postbiotic and beta-glucan components are not affected by concurrent antibiotic use
- Seek veterinary attention for chronic or recurrent GI signs (lasting more than 7 days)
- Store in a cool, dry place; keep sachets sealed until use