VetPlus Promax 9ml Oral Paste Syringe for Small Breed Dogs & Cats

FOR ANIMAL USE ONLY — Administer as directed by a veterinarian or as per label instructions. Promax is a veterinary nutraceutical oral paste supplement — not a veterinary medicine; it does not require a prescription but veterinary guidance is recommended, particularly for persistent diarrhoea (lasting more than 48–72 hours), diarrhoea with blood (haematochezia or melaena), diarrhoea accompanied by vomiting, lethargy, anorexia, or signs of systemic illness, or diarrhoea in puppies, kittens, or immunocompromised animals. These presentations require veterinary examination to exclude parvoviral enteritis, haemorrhagic gastroenteritis (HGE/AHDS), intestinal obstruction, intussusception, parasitism, and other serious diagnoses. Promax is indicated for supportive management of self-limiting acute diarrhoea and post-antibiotic dysbiosis — it is not a treatment for primary infectious, parasitic, or obstructive GI disease. Keep out of reach of children. Store in a cool, dry place below 25°C; do not refrigerate (cold paste is harder to administer).

VetPlus Promax 9ml Oral Paste Syringe for Small Breed Dogs & Cats | Enterococcus faecium SF68, FOS Prebiotic & Kaolin | Probiotic Gut Support for Diarrhoea, Dysbiosis & GI Recovery

VetPlus Promax 9ml is a veterinary nutraceutical oral paste supplement manufactured by VetPlus Ltd (UK), delivered in a pre-filled 9ml syringe for precise and convenient oral administration to small breed dogs and cats. Promax combines three complementary actives — Enterococcus faecium SF68 (a clinically validated, thermostable probiotic strain), fructooligosaccharides (FOS — a prebiotic fibre that selectively stimulates beneficial commensal bacteria), and kaolin (an inert hydrated aluminium silicate adsorbent clay) — to provide rapid multi-mechanism GI tract support during acute diarrhoea, antibiotic-associated gut dysbiosis, dietary indiscretion, and GI transit stress (kennelling, travel, weaning, rehoming). The 9ml small breed syringe format allows precise dose delivery directly into the mouth or onto food without the need for capsule administration. Promax is designed for short-term acute GI support — not for long-term daily supplementation (for long-term maintenance probiotic support, a daily supplement such as Protexin or Synbiotic DC is more appropriate).

Intestinal Microbiome & Gut Dysbiosis Pathophysiology

• The healthy canine and feline intestinal microbiome: the healthy adult dog intestinal microbiome (primarily the ileum, caecum, and colon) is dominated by the phyla Firmicutes (∼50–60% — including Lachnospiraceae, Ruminococcaceae, Turicibacteraceae, and Erysipelotrichaceae families; Clostridia class genera including Clostridium cluster XIV and cluster IV — short-chain fatty acid SCFA-producing obligate anaerobes) and Bacteroidetes (∼20–40% — Bacteroides, Prevotella, Porphyromonas); minor phyla: Fusobacteria (particularly Fusobacterium spp. — more prominent in dogs than humans), Proteobacteria (Escherichia, Klebsiella — normally a small fraction; expansion of Proteobacteria is a dysbiosis signature), and Actinobacteria (Bifidobacterium spp.); the feline intestinal microbiome differs from the dog’s: cats are obligate carnivores with a shorter GI transit time (∼12–24h vs 24–72h in dogs), lower pH colonic environment, and a microbiome proportionally enriched in Firmicutes (Clostridiales, Lactobacillales) and Fusobacteria, with less carbohydrate fermentation capacity and reduced Bacteroidetes compared to dogs; the intestinal microbiome performs critical functions: (a) colonisation resistance — competitive exclusion of enteropathogens (Salmonella, Campylobacter jejuni, Clostridium perfringens, Clostridium difficile, Giardia) through: resource competition (limiting luminal glucose, iron, and attachment sites), bacteriocin production (anti-microbial peptides produced by Enterococcus, Lactobacillus, and Bacteroides spp. — including class I bacteriocins/lantibiotics and class II bacteriocins/pediocins that disrupt pathogen membrane integrity), bile salt deconjugation (secondary bile acids produced by commensal bacteria — particularly deoxycholic acid DCA and lithocholic acid LCA — are directly toxic to Clostridioides difficile vegetative cells, and the FXR receptor-mediated induction of host antimicrobial peptides REG3γ and β-defensins by bile acids provides direct epithelial protection); (b) short-chain fatty acid (SCFA) production — colonic fermentation of dietary fibre and resistant starch by Firmicutes anaerobes produces acetate, propionate, and butyrate; butyrate (the principal colonic enterocyte energy substrate — colonocytes derive ∼70% of their energy from butyrate oxidation via mitochondrial β-oxidation; unlike glucose which enters via SGLT1 in the small intestine, colonocytes are structurally adapted for butyrate uptake via the SLC5A8 sodium-coupled monocarboxylate transporter and MCT1/SLC16A1 proton-coupled transporter) stimulates colonocyte proliferation, tight junction protein expression (claudin-1, occludin, ZO-1 — reinforcing the paracellular epithelial barrier), and regulatory T cell (Treg/FoxP3+) induction in the colonic lamina propria (via HDAC inhibition of the FOXP3 gene locus — butyrate inhibits histone deacetylases, maintaining the FOXP3 locus in an active, demethylated epigenetic state → Treg differentiation and immunological tolerance in the gut); (c) mucosal immune maturation — commensal microbiota stimulate Peyer’s patch M cell antigen sampling, IgA class switching in subepithelial B cells, and intestinal intraepithelial lymphocyte (IEL) education; germ-free animals have severely underdeveloped gut-associated lymphoid tissue (GALT) — demonstrating the microbiome’s role in mucosal immune development
• Gut dysbiosis mechanisms in dogs and cats: dysbiosis — an imbalance of the intestinal microbiome characterised by reduced diversity, loss of beneficial obligate anaerobes, and expansion of potentially pathogenic bacteria — arises from multiple causes: (a) antibiotic administration — the most common cause of iatrogenic dysbiosis; broad-spectrum antibiotics (amoxicillin-clavulanate, metronidazole, tylosin, enrofloxacin) reduce total bacterial abundance and specifically deplete obligate anaerobes (Lachnospiraceae, Ruminococcaceae, Erysipelotrichaceae — the SCFA-producing core commensals) while often expanding antibiotic-resistant Proteobacteria; metronidazole — despite being commonly prescribed for GI signs in dogs — is associated with particularly marked and prolonged microbiome disruption in dogs (reduced Faecalibacterium, Blautia, and Turicibacter — genera associated with gut health — and increased Escherichia); (b) dietary change — abrupt diet transitions alter fermentable substrate availability → shifts in relative abundances of fermenters vs non-fermenters; (c) enteric pathogens — Parvovirus enteritis, Campylobacter, Giardia, and Clostridium perfringens cause direct mucosal injury and dysbiosis; (d) stress — the gut-brain axis: psychological and physiological stressors (kennelling, rehoming, weaning, surgery, transport) activate the HPA axis → cortisol → mucosal mast cell activation → increased intestinal permeability (‘leaky gut’ — tight junction claudin-2 upregulation by cortisol → paracellular permeability increase); simultaneously, sympathetic innervation of the gut (noradrenaline acting on β-adrenergic receptors on enterocytes and α-adrenergic receptors on smooth muscle) alters motility and secretion → accelerated transit → diarrhoea; stress also directly alters microbiome composition (Lactobacillus spp. abundance correlates inversely with salivary cortisol in dogs); dysbiosis consequence: reduced colonisation resistance → pathogen expansion; reduced butyrate production → colonocyte energy deficit → tight junction weakening → bacterial translocation → systemic immune activation; reduced Treg induction → increased inflammatory tone in the gut lamina propria

Active Ingredients & Mechanisms of Action

• Enterococcus faecium SF68 (NCIMB 10415) — clinically validated thermostable probiotic strain: Enterococcus faecium is a gram-positive, facultative anaerobic lactic acid bacterium (LAB) of the Firmicutes phylum; the SF68 strain (also designated NCIMB 10415 in the National Collection of Industrial, Food and Marine Bacteria; patented by Cerbios-Pharma SA, Switzerland) is one of the most extensively studied veterinary probiotic strains with a documented clinical evidence base in dogs, cats, horses, and calves; the SF68 strain is specifically characterised by: (a) thermostability — SF68 survives ambient temperature storage conditions (critical for an oral paste product) and gastric acid transit (acid tolerance pH 2.5 for 2h — demonstrated in in vitro survival studies; SF68’s acid tolerance is attributed to proton-pumping F0F1-ATPase activity that pumps H+ out of the cell, maintaining intracellular pH above the lethal threshold); (b) bile salt resistance — SF68 tolerates 0.3–0.5% oxgall concentration (a standard in vitro bile resistance assay); bile resistance is mediated by bile salt hydrolase (BSH) enzymes that deconjugate conjugated bile salts (glycocholate, taurocholate) reducing their detergent toxicity to the bacterial membrane, and by altered membrane fatty acid composition (increased cyclopropane fatty acid content providing membrane rigidity against bile salt-mediated phospholipid dissolution); (c) adhesion to intestinal epithelium — SF68 adheres to canine and feline intestinal epithelial cells via surface-expressed adhesins (Esp — enterococcal surface protein, and EF-Tu — the elongation factor Tu moonlighting as a surface adhesin — that bind fibronectin and mucin on the intestinal epithelial surface); intestinal adhesion allows SF68 to: (i) competitively exclude enteropathogens from epithelial attachment sites (competitive exclusion); (ii) persist in the intestinal lumen for the duration of supplementation; (d) colonisation resistance mechanisms: SF68 produces enterocins (class IIa bacteriocins — heat-stable, cationic, amphiphilic peptides of 37–44 amino acids that form pores in the cytoplasmic membrane of gram-positive pathogens by binding to the mannose phosphotransferase system — Man-PTS — as a receptor; Man-PTS-mediated entry → membrane pore → K+ efflux → membrane depolarisation → cell death); SF68-produced enterocins are active against Listeria monocytogenes, Clostridium perfringens, Clostridium difficile, and Enterococcus pathogenic strains; (e) immunomodulation — SF68 activates intestinal dendritic cells (DCs) and macrophages in the Peyer’s patches via TLR2 (recognising lipoteichoic acid — LTA — of the gram-positive cell wall) and TLR9 (recognising unmethylated CpG DNA motifs in E. faecium chromosomal DNA) → MyD88 → NF-κB → IL-10 and TGF-β production by regulatory DCs → intestinal Treg expansion → reduced inflammatory tone in the lamina propria; IL-10 specifically suppresses Th1 and Th17 pro-inflammatory cytokine production (IFN-γ, IL-17A), reducing mucosal inflammation during GI recovery; (f) clinical evidence: multiple randomised controlled trials demonstrate SF68 reduces diarrhoea duration in dogs with acute diarrhoea (Bybee et al. — 14-day trial in shelter dogs: SF68 significantly reduced faecal score vs placebo; Kelley et al. — SF68 normalised faecal microbiome Dysbiosis Index in dogs with acute enteropathy); a key safety advantage of E. faecium SF68: safety surveillance data spanning >25 years of use across millions of doses in companion animals with no documented cases of SF68-mediated endocarditis or antibiotic resistance transfer (unlike some pathogenic E. faecium strains; SF68 is susceptible to all key antibiotics used in companion animal medicine — amoxicillin, ampicillin, vancomycin sensitivity confirmed); note: the EFSA (European Food Safety Authority) and FEDESA granted SF68 qualified presumption of safety (QPS) status
• Fructooligosaccharides (FOS) — prebiotic fibre selectively stimulating beneficial Bifidobacterium and Lactobacillus fermentation: FOS (also termed oligofructose or inulin-type fructans) are β(2→1)-linked fructose oligomers with a terminal glucose (GF2 – kestose, GF3 – nystose, GF4 – fructosylnystose) produced commercially by partial enzymatic hydrolysis of inulin (from chicory root — Cichorium intybus — by inulinase) or by transfructosylation of sucrose (by β-fructosidase/levansucrase from Aspergillus niger or A. oryzae); FOS are classified as non-digestible oligosaccharides (NDOs): they are resistant to hydrolysis by mammalian digestive enzymes (salivary amylase, pancreatic amylase, sucrase-isomaltase, lactase) due to the β(2→1) glycosidic linkage (mammalian digestive enzymes are α-specific — they cleave α(1→4) and α(1→6) glycosidic bonds; the β(2→1) bond in FOS is not hydrolysed) → FOS reach the large intestine intact; in the colon, FOS are selectively fermented by β-fructosidase-producing commensal bacteria (primarily Bifidobacterium spp. and Lactobacillus spp. which express inulinase and β-fructofuranosidase enzymes) via the fructose-specific PTS (phosphotransferase system) — FOS uptake → intracellular hydrolysis → fructose-6-phosphate → glycolysis → acetate, lactate, and formate production (homofermentative pathway in Bifidobacterium — the bifid shunt — via fructose-6-phosphate phosphoketolase generating acetyl-phosphate); FOS selectivity for Bifidobacterium and Lactobacillus is the definition of prebiotic activity (Gibson & Roberfroid’s original prebiotic concept, FEMS Microbiol Rev 1995): FOS consumption increases Bifidobacterium counts (β-diversity increases) while not supporting growth of most Bacteroidetes, Proteobacteria, or Clostridium pathogenic species; Bifidobacterium and Lactobacillus expansion: (a) further contributes to colonisation resistance against Salmonella and Campylobacter; (b) produces lactic acid → lowers luminal pH → inhibitory to acid-sensitive pathogens; (c) produces acetate → protects intestinal epithelial cells from pathogen invasion (E. coli O157:H7 invasion of epithelial cells is inhibited by Bifidobacterium-derived acetate via GPR43 — free fatty acid receptor 2 — activation on epithelial cells → Akt → tight junction stabilisation); FOS also acts as a synbiotic partner to SF68 in Promax: FOS provides the selective fermentable substrate that supports SF68 colonisation and persistence in the intestinal lumen (SF68 expresses β-fructofuranosidase for FOS fermentation); the SF68 + FOS combination is a classical synbiotic formulation (a probiotic paired with its preferred prebiotic substrate)
• Kaolin (hydrated aluminium silicate — Al2Si2O5(OH)4) — inert intestinal adsorbent clay for toxin, water, and pathogen sequestration: kaolin is a phyllosilicate clay mineral (from the kaolinite group — 1:1 tetrahedral Si-O / octahedral Al-O layer structure); as an oral adsorbent in GI preparations: (a) toxin adsorption — kaolin’s high surface area (∼10–20 m2/g for pharmaceutical-grade kaolin) and negatively charged silanol (Si-OH) and aluminol (Al-OH) surface groups adsorb positively charged and amphiphilic toxins from the intestinal lumen; bacterial enterotoxins adsorbed by kaolin include: Clostridium perfringens type A enterotoxin (CPE — a β-pore-forming toxin that binds claudin-3 and claudin-4 tight junction proteins; CPE binding to claudin creates a large protein complex that inserts into the membrane → membrane permeability increase → Ca2+ influx → calpain activation → tight junction disruption → paracellular permeability increase → the mechanism of C. perfringens-associated diarrhoea; kaolin adsorbs CPE before it can bind claudin); E. coli heat-stable enterotoxin (STa — an 18-amino acid disulfide-bonded peptide that activates guanylyl cyclase C/GC-C receptor on enterocytes → cGMP → PKG II phosphorylation of CFTR Cl− channel → Cl− and HCO3− secretion → osmotic diarrhoea; kaolin adsorbs STa reducing its GC-C receptor availability); (b) water adsorption — kaolin adsorbs free water in the intestinal lumen, increasing faecal consistency and reducing stool water content (the mechanical antidiarrhoeal effect independent of toxin binding); (c) pathogen adsorption — kaolin adsorbs Campylobacter jejuni, Giardia lamblia trophozoites, and Cryptosporidium oocysts to its surface (reducing luminal concentration available for epithelial invasion); (d) mucosal coating — kaolin particles form a protective layer over the inflamed intestinal mucosa, reducing direct contact between luminal irritants and the damaged epithelial surface; kaolin in Promax is pharmaceutical-grade (activated/acid-washed kaolin with controlled particle size and purity — not industrial clay); it is physiologically inert — not absorbed from the GI tract, not metabolised, and excreted unchanged in faeces; the combination of kaolin’s rapid mechanical antidiarrhoeal action (effective within hours of administration) with SF68’s probiotic microbiome restoration (effective over 3–5 days of colonisation) and FOS’s prebiotic microbiome enrichment provides a three-phase temporal gut recovery strategy: immediate (kaolin) → early (SF68 colonisation) → sustained (FOS-driven commensal enrichment)

Indications

• Acute self-limiting diarrhoea in small breed dogs and cats — dietary indiscretion, dietary change, mild infectious enteritis, stress diarrhoea
• Antibiotic-associated gut dysbiosis — concurrent or immediately post-antibiotic use to protect and restore the intestinal microbiome
• GI stress events — kennelling, rehoming, weaning, transport, veterinary hospitalisation
• Post-gastroenteritis GI recovery — after resolution of acute gastroenteritis to restore microbiome balance
• Preventive perioperative GI support — around surgical procedures requiring anaesthesia and perioperative antibiosis

Directions for Use

• Administer orally as directed by a veterinarian or per VetPlus label instructions
• The 9ml syringe can be administered directly into the mouth (over the tongue) or squeezed onto food
• Typical course: 3–5 days for acute diarrhoea; up to 5–7 days for antibiotic-associated dysbiosis — confirm with veterinarian
• Refrigeration not required — store at room temperature below 25°C; cold paste is harder to administer

Safety Information

• For animal use only — keep out of reach of children
• Seek veterinary attention for diarrhoea lasting more than 48–72 hours, diarrhoea with blood, or diarrhoea with systemic signs (vomiting, lethargy, anorexia, fever)
• Not indicated for long-term daily supplementation — for maintenance microbiome support, use a dedicated daily probiotic supplement
• E. faecium SF68 is susceptible to all major veterinary antibiotics; Promax can be used concurrently with antibiotic treatment
• Store below 25°C; do not freeze