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Updated: Sep 2, 2025
An In Vitro Batch-culture Model to Estimate the Effects of Interventional Regimens on Human Fecal Microbiota
Published on: July 31, 2019
Inhibition of Cronobacter sakazakii in an infant simulator of the human intestinal microbial ecosystem using a
Alfred Ke1, Valeria R Parreira1, Jeffrey M Farber1
1Canadian Research Institute for Food Safety, Department of Food Science, University of Guelph, Guelph, ON, Canada.
Insights
A synbiotic blend of lactic acid bacteria and Vivinal GOS effectively inhibited Cronobacter sakazakii in infant formula. This synbiotic accelerated pathogen reduction compared to natural gut microbiota alone.
Area of Science:
- Microbiology
- Food Safety
- Gut Microbiome Research
Background:
- Powdered infant formula (PIF) can harbor Cronobacter sakazakii, a pathogen causing severe infant illness.
- Synbiotics, combining probiotics and prebiotics, offer a potential strategy to control C. sakazakii in PIF and the infant gut.
- Limited research exists on synbiotics' efficacy against C. sakazakii inhibition.
Purpose of the Study:
- To evaluate the inhibitory effect of a synbiotic formulation (lactic acid bacteria + Vivinal GOS) on Cronobacter sakazakii growth.
- To investigate the mechanisms by which synbiotics may control C. sakazakii in an infant gut model.
- To compare the efficacy of synbiotics versus lactic acid bacteria alone in reducing C. sakazakii.
Main Methods:
- Utilized a Simulator of the Human Intestinal Microbial Ecosystem (SHIME®) model with infant fecal microbiota.
- Applied a triple SHIME setup with control, lactic acid bacteria (LAB) treatment, and synbiotic (LAB + Vivinal GOS) treatment over two 1-week periods.
- Analyzed Cronobacter sakazakii levels, species diversity, metabolomic profiles, and bacterial abundance (e.g., Bifidobacterium).
Main Results:
- Synbiotic treatment significantly decreased C. sakazakii levels within 1 week (p < 0.05).
- Control groups showed a significant decline in C. sakazakii only after 2 weeks (p < 0.05).
- LAB treatment alone did not significantly reduce C. sakazakii levels (p ≥ 0.05).
- Synbiotic addition slightly increased species diversity and altered metabolomic profiles compared to controls.
- A negative correlation was observed between Bifidobacterium abundance and Cronobacter levels in the absence of treatment (ρ = -0.96; p < 0.05).
Conclusions:
- The potential synbiotic formulation effectively inhibits Cronobacter sakazakii in an infant gut model.
- Inhibition may occur through antimicrobial metabolite production, increased species diversity, or competitive exclusion.
- Native gut microbiota, particularly Bifidobacterium, can inhibit C. sakazakii, a process potentially accelerated by synbiotic intervention.
Abstract:
Powdered infant formula (PIF) can be contaminated with Cronobacter sakazakii, which can cause severe illnesses in infants. Synbiotics, a combination of probiotics and prebiotics, could act as an alternative control measure for C. sakazakii contamination in PIF and within the infant gut, but synbiotics have not been well studied for their ability to inhibit C. sakazakii. Using a Simulator of the Human Intestinal Microbial Ecosystem (SHIME®) inoculated with infant fecal matter, we demonstrated that a potential synbiotic, consisting of six lactic acid bacteria (LAB) strains and Vivinal GOS, can inhibit the growth of C. sakazakii in an infant possibly through either the production of antimicrobial metabolites like acetate, increasing species diversity within the SHIME compartments to compete for nutrients or a combination of mechanisms. Using a triple SHIME set-up, i.e., three identical SHIME compartments, the first SHIME (SHIME 1) was designated as the control SHIME in the absence of a treatment, whereas SHIME 2 and 3 were the treated SHIME over 2, 1-week treatment periods. The addition of the potential synbiotic (LAB + VGOS) resulted in a significant decrease in C. sakazakii levels within 1 week (p < 0.05), but in the absence of a treatment the significant decline took 2 weeks (p < 0.05), and the LAB treatment did not decrease C. sakazakii levels (p ≥ 0.05). The principal component analysis showed a distinction between metabolomic profiles for the control and LAB treatment, but similar profiles for the LAB + VGOS treatment. The addition of the potential synbiotic (LAB + VGOS) in the first treatment period slightly increased species diversity (p ≥ 0.05) compared to the control and LAB, which may have had an effect on the survival of C. sakazakii throughout the treatment period. Our results also revealed that the relative abundance of Bifidobacterium was negatively correlated with Cronobacter when no treatments were added (ρ = -0.96; p < 0.05). These findings suggest that C. sakazakii could be inhibited by the native gut microbiota, and inhibition can be accelerated by the potential synbiotic treatment.
