Tag Archives: Clostridium

Identifying what makes some gut bacteria strains life-threatening in pre-term babies

Researchers from the Quadram Institute and University of East Anglia have identified what makes some strains of gut bacteria life-threatening in pre-term babies.

The findings will help identify and track dangerous strains and protect vulnerable neonatal babies.

A major threat to neonatal babies with extremely low birth weight is necrotizing enterocolitis (NEC).

Rare in full-term babies, this microbial infection exploits vulnerabilities destroying gut tissue leading to severe complications. Two out of five cases are fatal.

One bacterial species that causes especially sudden and severe disease is Clostridium perfringens. These are common in the environment and non-disease-causing strains live in healthy human guts.

So what makes certain strains so dangerous in preterm babies?

Prof Lindsay Hall and Dr Raymond Kiu from the Quadram Institute and UEA led the first major study on C. perfringens genomes from preterm babies, including some babies with necrotizing enterocolitis.

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The research team analyzed C. perfringens genomes from the faecal samples of 70 babies admitted to five UK Neonatal Intensive Care Units (NICUs).

Based on genomic similarities, they found one set had a lower capacity to cause disease. This allowed a comparison with the more virulent strains.

The less virulent group lacked genes responsible for production of a toxin called PFO and other factors needed for colonization and survival.

This study has begun to construct genomic signatures for C. perfringens associated with healthy preterm babies and those with necrotizing enterocolitis.

Exploring genomic signatures from hundreds of Clostridium perfringens genomes has allowed us potentially to discriminate between ‘good’ bacterial strains that live harmlessly in the preterm gut, and ‘bad’ ones associated with the devastating and deadly disease necrotizing enterocolitis.

We hope the findings will help with ‘tracking’ deadly C. perfringens strains in a very vulnerable group of patients – preterm babies.”

Prof Lindsay Hall, UEA’s Norwich Medical School and the Quadram Institute

Larger studies, across more sites and with more samples may be needed but this research could help identify better ways to control necrotizing enterocolitis.

The team previously worked alongside Prof Paul Clarke and clinical colleagues at the Norfolk and Norwich University Hospital NICU. And they demonstrated the benefits of providing neonatal babies with probiotic supplements.

The enterocolitis gut microbiome of neonatal infants is significantly disrupted, making it susceptible to C. perfringens overgrowth.

Prof Hall said: “Our genomic study gives us more data that we can use in the fight against bacteria that cause disease in babies – where we are harnessing the benefits of another microbial resident, Bifidobacterium, to provide at-risk babies with the best possible start in life.”

Dr Raymond Kiu, from the Quadram Institute, said: “Importantly, this study highlights Whole Genome Sequencing as a powerful tool for identifying new bacterial lineages and determining bacterial virulence factors at strain level which enables us to better understand disease.”

This research was supported by the Biotechnology and Biological Sciences Research Council, part of UKRI, and the Wellcome Trust.

The study was led by researchers at Quadram Institute and the University of East Anglia, in collaboration with colleagues at Imperial College, London, the University of Glasgow, the University of Cambridge, Newcastle University and Northumbria University.

‘Particular genomic and virulence traits associated with preterm infant-derived toxigenic Clostridium perfringens strains’ is published in Nature Microbiology.

Journal reference:

Kiu, R., et al. (2023). Particular genomic and virulence traits associated with preterm infant-derived toxigenic Clostridium perfringens strains. Nature Microbiology. doi.org/10.1038/s41564-023-01385-z.

Breast milk microbes shape infant gut health

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A new paper published in the Frontiers in Microbiology explores the contribution of human breast milk to the establishment of the infant gut microbiome.

Study: Human milk-associated bacterial communities associate with the infant gut microbiome over the first year of life. Image Credit: Pavel Ilyukhin / Shutterstock.com Study: Human milk-associated bacterial communities associate with the infant gut microbiome over the first year of life. Image Credit: Pavel Ilyukhin / Shutterstock.com


Breastfeeding is encouraged as the first and exclusive food of infants for at least the first six months of life. In addition to its nutritional content, breast milk contributes significantly to the formation of the infant gut microbiome. This is because of its high content of immune cells, oligosaccharides carrying glycosyl residues, fatty acids, and some microbes.

Both breast milk bacteria and skin microbes from the maternal nipple reach and establish themselves in the infant’s gut. Bacteria may be shielded by secretory immunoglobulin A (sIgA) covering the immune system, thus allowing them to enter the gut intact.   

The infant gut microbiome (IGMB) is important for both infant development and immunity, as well as modulating conditions like atopy and body mass composition. However, earlier research on potential associations between the IGMB and breast milk microbiota has been limited to analyzing samples from corresponding time points.

The current study included almost 190 dyads from New Hampshire. Breast milk and infant stool samples were collected at around six weeks, four months, six months, nine months, and one year from birth, which allowed the scientists to identify correlations that developed over time.

What did the study show?

In the study population, with a mean age of 32 years, most were White and had a normal body mass index (BMI) during pregnancy. About 25% of deliveries occurred through Cesarean section (C-section), and antibiotic exposure prior to lactation occurred in over half of mothers.

Most babies were almost full term at birth, with only 3% being exposed to antibiotics by four months of life. By one year, about 30% of infants had been exposed to antibiotics.

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About 75% and 40% of infants did not receive any formula up to six weeks and four months, respectively. Most infants began eating solid food by six months.

Three breast milk microbiome types (BMTs) were identified in the six-week breast milk samples. These could be differentiated by the relative proportions of four bacterial genera, including Streptococcus, Staphylococcus, Pseudomonas, and Acinetobacter, as well as by the microbial diversity.

At six weeks, the gut microbiome in infants exhibited four six-week infant gut microbiome types (6wIGMTs). These had different abundances of Bifidobacterium, Bacteroides, Clostridium, Streptococcus, and Escherichia/Shigella.

The 6wIGMT correlated with the 6wBMT in male infants and those born by C-section. Notably, the same microbe was likely to be the most abundant within the dyads at this point.

By age one, the predominant difference in microbiome composition was due to Bacteroides. There was no association between the 6wBMT and 12mIGMT, which is likely due to the intake of solid foods by infants at this age. The transition to a primarily solid diet causes the infant microbiome to be dominated by other microbes, such as Bifidobacterium and Bacteroidetes, both of which are more abundant in the adult gut.

At six weeks, the BMT was associated with 6wIGMT in all infants but more strongly in male infants born by C-section. Male infants also had a higher proportion of microbes from breast milk present in their stool.

While infants delivered by C-section have a reduced colonization by maternal stool microbiota, their colonization by breast milk microbiota is higher than vaginally delivered infants.”

This could be due to the reduced microbial diversity and Bacteroides depletion in the IGMB of C-section-delivered infants, which makes it easier for breast milk microbes to colonize the gut.

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Male infants appeared to show a greater effect of the breast milk microbes on their gut microbiome. This may be because they exhibit less microbial diversity, with fewer Clostridiales and more Enterobacteriales abundance than is observed in female infants. The male infant’s gut microbiota is also more susceptible to stress and environmental exposures.

Overall, the breast milk microbial communities correlated most strongly with those found in infant stool samples that were collected at a later time point. For example, Pantoea in breast milk at four and six months was correlated with infant stool collected at nine and twelve months, respectively. These findings require further validation in future research.

What are the implications?

The identification of microbial clusters in human milk and infant feces that were shared within the mother-infant pair at six weeks is a striking finding in this study. The delay in cluster sharing and the association with C-section were associated with stronger correlations.

The findings of this study agree with earlier reports on the associations of various microbes in breast milk and the infant gut. Notably, the current study adds to previous data by identifying correlations between different taxa in these two sites.

The scientists postulate that microbes within communities may show direct interactions, such as the transmission of a microbe present in the infant oral cavity to the breast in this case, as well as the intake of breast milk by the infant. In addition, they may show indirect interactions through nutrients like fatty acids and milk sugars or other bacterial metabolites that influence both communities.

With the observed shift in breast milk microbial diversity over time, long-term studies may be needed to understand the breadth of microbial exposures during infancy. The change in IGMTs over time should also be better characterized and their relevance assessed.

These results suggest that milk microbial communities have a long-term effect on the infant gut microbiome both through sharing of microbes and other molecular mechanisms.”

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Journal reference:
  • Lundgren, S. N., Madan, J. C., Karagas, M. R., et al. (2023). Human milk-associated bacterial communities associate with the infant gut microbiome over the first year of life. Frontiers in Microbiology. doi:10.3389/fmicb.2023.1164553.

Discontinuing oral antibiotics after breast reconstruction does not lead to an increase in infections

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For breast cancer patients undergoing breast reconstruction after mastectomy, avoiding postoperative oral antibiotics does not reduce the risk of infections, reports a study in the May issue of Plastic and Reconstructive Surgery®, the official medical journal of the American Society of Plastic Surgeons (ASPS). The journal is published in the Lippincott portfolio by Wolters Kluwer.

Our experience suggests that discontinuing routine oral antibiotic treatment after implant-based breast reconstruction does not lead to an increase in surgical site infections, and will eliminate a small but significant risk of allergy and other antibiotic-related complications.”

Mark Sisco, MD, ASPS Member Surgeon, NorthShore University HealthSystem, Evanston, Ill

No increase in infections after policy change on preventive antibiotics

A growing number of breast cancer patients are undergoing breast reconstruction after mastectomy, particularly immediate reconstruction using implants. Surgical site infections (SSIs) occur in 10% to 25% of patients undergoing this procedure, leading to increased rates of hospital readmission, repeat surgery, and reconstructive failure.

Historically, plastic surgeons have given extended antibiotic prophylaxis (EAP) to reduce the risk of SSI. The use of postoperative oral antibiotics has continued despite a lack of evidence for its effectiveness, and amid rising concerns about antibiotic resistance. In 2016, the authors’ health system joined the growing trend toward ending routine EAP for post-mastectomy breast reconstruction.

To evaluate the impact of this practice change, Dr. Sisco and colleagues compared outcomes in two groups of patients: 654 women (1,004 breasts) receiving EAP and 423 women (683 breasts) not receiving postoperative oral antibiotics. Both groups received a single dose of intravenous antibiotic before surgery.

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After surgery, the overall infection rate was similar between groups: 7.9% with EAP and 9.1% without EAP. After adjustment for differences in patient characteristics, the risk of SSIs was not significantly different between groups. This was even though patients in the non-EAP were more likely to receive some newer techniques – including nipple-sparing mastectomy and pre-pectoral (“above the muscle”) implant placement – thought to carry an increased risk of complications.

‘Thousands of women nationwide’ may have adverse reactions to EAP

Meanwhile, patients receiving EAP had some “infrequent but not insignificant” adverse events, including a two percent rate of moderate to severe allergic reactions. At least four women in the EAP group developed infection with antibiotic-resistant Clostridium difficile (“C-diff”) bacteria. Neither of these complications occurred in patients who did not receive extended antibiotics.

There was also evidence that EAP affected the types of bacteria isolated from patients who developed infections, including a higher rate of gram-negative bacteria. Extended antibiotic use was associated with a “broader range of pathogens” and more frequent need for second-line intravenous antibiotics.

“Although the use of EAP does not appear to worsen clinical outcomes, marked differences in the microbiology of associated infections may make them more difficult to treat,” Dr. Sisco and coauthors write. Especially at a time when breast reconstruction rates are rapidly increasing, “Our findings suggest that thousands of women are having adverse reactions to EAP nationwide, and some of these are likely to be serious,” the researchers add.

While acknowledging some important limitations of their study, the authors note that a definitive randomized trial of ending routine EAP is unlikely to be performed. Dr. Sisco and colleagues conclude, “We hope that our experience will give surgeons additional evidence and courage to change their practice.”

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Journal reference:

Sisco, M., et al. (2022). Oral antibiotics do not prevent infection or implant loss after immediate prosthetic breast reconstruction: Evidence from 683 consecutive reconstructions without prophylaxis. Plastic & Reconstructive Surgery. doi.org/10.1097/prs.0000000000010073

Can a disrupted gut microbiota contribute to anorexia nervosa pathogenesis?

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In a recent study published in the journal Nature Microbiology, researchers investigated whether intestinal microbial alterations contribute to anorexia nervosa (AN) pathogenesis.

AN, a disorder associated with altered eating, has caused considerable mortality, especially among women. However, therapies based on scientific evidence are scarce. AN pathogenesis likely involves several environmental and genetic factors. Studies have reported intestinal microbial dysbiosis among AN-affected individuals. However, data were obtained from small sample sizes, and genus-level microbial alterations were analyzed by amplicon sequencing.

Study: The gut microbiota contributes to the pathogenesis of anorexia nervosa in humans and mice. Image Credit: Tatiana Shepeleva / ShutterstockStudy: The gut microbiota contributes to the pathogenesis of anorexia nervosa in humans and mice. Image Credit: Tatiana Shepeleva / Shutterstock

About the study

In the present study, researchers assessed the association between the intestinal microbiome and AN.

The team performed metabolomics and shotgun metagenomic analyses on serum and fecal samples, respectively, that were obtained from women with AN (n=77) and age- and sex-matched healthy controls (n=70). Further, the fecal microbiome was transplanted from anorexia nervosa cases to murine animals fed calories-limited diets over three weeks to simulate AN eating behavior for in vivo analysis. In addition, the team explored causal associations in silico by bidirectional mediation analysis. The intestinal microbiome was analyzed at functional, taxonomic, and genetic levels.

The team used the eating disorder inventory-3 (EDI-3) questionnaire to assess eating behaviors and insulin resistance was assessed using the homoeostatic model assessment for insulin resistance (HOMA-IR) tool. The team examined covariations between bacterial abundance at species and genus levels and clinical variables for AN cases and controls. Linear regression modeling was performed, adjusting for confounders such as age, smoking status, medications, and body mass index (BMI).

Further, the team evaluated the growth dynamics of gut bacteria by calculating peak-to-trough ratios (PTR) using the metagenomic dataset. The functional modules of gut bacteria were identified using gut-brain modules (GBMs) and gut metabolic modules (GMMs). Differences in bacterial genomics were explored based on the Canberra distance of bacterial structural variant profiles.

​​​​​​​Graphical abstract of the study workflow and findings.

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Several bacterial organisms (including Clostridium) were altered among individuals with anorexia nervosa and were associated with mental well-being and eating behavior estimates. Bacterial functional-type modules related to neurotransmitter degradation were enriched among those with anorexia nervosa. Further, several structural variants (SVs) in bacterial organisms were associated with the metabolic characteristics of anorexia nervosa.

The findings indicated a probable role of the intestinal microbiome in AN-associated changes concerning satiety and the metabolism of secondary bile acids. The metabolomic analysis indicated an elevation in metabolites linked to lowered food consumption (including taurine-hyodeoxycholic acid, taurine-α-muricholic acid, and indole-3-propionic acid molecules). Causal inference analysis indicated that serological bacterial metabolites probably mediate the effect of gut microbial alterations on anorexia nervosa. At the phylum level, AN microbiome samples showed lowered Actinobacteriota and Bacteroidota counts. Among families of bacteria, Christensenellaceae species, particularly CAG-138, showed the most significant enrichment in AN.

At the genus level, elevated Lactobacillus counts were observed in the AN microbiota. The Ruminococcacea-enterotype was more prevalent in cases of AN. Species-level analysis indicated greater β-diversity among AN-affected women. In AN, Roseburia inulinivorans and Roseburia intestinalis were depleted, whereas those of Erysipelatoclostridium ramosum, Blautia species CAG, and Enterocloster bolteae innocuum (Clostridium) were increased. Clostridium counts correlated positively with eating disorder scores. The abundance of Bifidobacterium and Parasutterella, in absolute terms, showed positive correlations with perfectionism and body dissatisfaction, respectively.

Absolute Brachyspira count showed a positive association with ‘drive for thinness’ markers in anorexia nervosa. Median values for PTR markedly differed between individuals with AN and controls. Women with AN were leaner, had lower fasting serological insulin, glucose, and C-reactive protein (CRP) levels, and were more sensitive to insulin than controls. Bacterial organisms with significant growth retardation, among AN case individuals included Alistipes finegoldii, Akkermansia muciniphila, Eubacterium siraeum, Coprococcus catus, SS3/4, and Odoribacter splanchnicus.

In addition, the intestinal virome was altered among AN-affected individuals, including lowered bacterial-viral interactions, due to attenuated interactions of viruses with short-chain fatty acid (SCFA)-producing bacteria, including Roseburia inulinivorans, Roseburia hominis, and Faecalibacterium prausnitzii. The team observed greater viral richness and Shannon diversity in the fecal samples of AN cases compared to controls. Notably, 25/30 viruses increased in AN were Lactococcus bacteriophages. The abundance of GBMs for serotonin synthesis and degradation of tryptophan, glutamate, and dopamine, were enriched in AN.

The team detected 2,423 and 5,056 variable SVs and deletion SVs, respectively, across 56 species of bacteria, including Bacteroides uniformis, Faecalibacterium prausnitzii, Parabacteroides distasonis, Methanobrevibacter smithii. Individuals with AN lacking the genomic region of B. uniformis had greater scores for self-denial and bulimia. The genetic deletion in B. uniformis could result in the deficiency of thiamine, a vitamin associated with intestinal and mental health. The serotonin synthesis module causally affected BMI through glycoursodeoxycholic acid, which is upregulated by serotonin.

Serum leucine mediated the influence of B. vulgatus counts on glucose homeostasis. Mice receiving AN individuals’ fecal transplants initially lost more weight with a slower gain of weight with time than those receiving fecal transplants of control individuals. The finding was related to greater levels of hypothalamic appetite-suppressing genes and thermogenesis-associated genes in the adipose tissues of mice receiving fecal transplants from individuals with AN.

Based on the study findings, gut microbial disruptions may contribute to the pathogenesis of AN.

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Journal reference:

Some bacteria cells get hangry too, study finds

Have you ever been so hungry that you become angry, otherwise known as “hangry?” New research by Adam Rosenthal, PhD, assistant professor in the Department of Microbiology and Immunology, has found that some bacteria cells get hangry too, releasing harmful toxins into our bodies and making us sick.

Rosenthal and his colleagues from Harvard, Princeton and Danisco Animal Nutrition discovered, using a recently developed technology, that genetically identical cells within a bacterial community have different functions, with some members behaving more docile and others producing the very toxins that make us feel ill.

Bacteria behave much more different than we traditionally thought. Even when we study a community of bacteria that are all genetically identical, they don’t all act the same way. We wanted to find out why.”

Adam Rosenthal, PhD, Assistant Professor, Department of Microbiology and Immunology

The findings, published in Nature Microbiology, are particularly important in understanding how and why bacterial communities defer duties to certain cells – and could lead to new ways to tackle antibiotic tolerance further down the line.

Rosenthal decided to take a closer look into why some cells act as “well-behaved citizens” and others as “bad actors” that are tasked with releasing toxins into the environment. He selected Clostridium perfringens – a rod-shaped bacterium that can be found in the intestinal tract of humans and other vertebrates, insects, and soil – as his microbe of study.

With the help of a device called a microfluidic droplet generator, they were able to separate, or partition, single bacterial cells into droplets to decode every single cell.

They found that the C. perfringens cells that were not producing toxins were well-fed with nutrients. On the other hand, toxin-producing C. perfringens cells appear to be lacking those crucial nutrients.

“If we give more of these nutrients,” postulated Rosenthal, “maybe we can get the toxin-producing cells to behave a little bit better.”

Researchers then exposed the bad actor cells to a substance called acetate. Their hypothesis rang true. Not only did toxin levels drop across the community, but the number of bad actors reduced as well. But in the aftermath of such astounding results, even more questions are popping up.

Now that they know that nutrients play a significant role in toxicity, Rosenthal wonders if there are particular factors found in the environment that may be ‘turning on’ toxin production in other types of infections, or if this new finding is only true for C. perfringens.

Perhaps most importantly, Rosenthal theorizes that introducing nutrients to bacteria could provide a new alternative treatment for animals and humans, alike.

For example, the model organism Clostridium perfringens is a powerful foe in the hen house. As the food industry is shifting away from the use of antibiotics, poultry are left defenseless from the rapidly spreading, fatal disease. The recent findings from Rosenthal et al. may give farmers a new tool to reduce pathogenic bacteria without the use of antibiotics.

As for us humans, there is more work to be done. Rosenthal is in the process of partnering with colleagues across UNC to apply his recent findings to tackle antibiotic tolerance. Antibiotic tolerance occurs when some bacteria are able to dodge the drug target even when the community has not evolved mutations to make all cells resistant to an antibiotic. Such tolerance can result in a less-effective treatment, but the mechanisms controlling tolerance are not well understood.

In the meantime, Rosenthal will continue to research these increasingly complex bacterial communities to better understand why they do what they do.

Journal reference:

McNulty, R., Sritharan, D., Pahng, S. H., Meisch, J. P., Liu, S., Brennan, M. A., Saxer, G., Hormoz, S., & Rosenthal, A. Z. (2023). Probe-based bacterial single-cell RNA sequencing predicts toxin regulation. Nature Microbiology. doi.org/10.1038/s41564-023-01348-4.

Differences in gut microbiome diversity attributed to dietary patterns in children with obesity

In a recent study published in Microbiology Spectrum, researchers found that differences in the dietary patterns of children with normal weight and those who were overweight or obese contributed to variations in the gut microbiome diversity, virulence factors of gut bacteria, and metabolic function.

Study: Virulence factors of the gut microbiome are associated with BMI and metabolic blood parameters in children with obesity. Image Credit: Africa Studio / Shutterstock.com

Study: Virulence factors of the gut microbiome are associated with BMI and metabolic blood parameters in children with obesity. Image Credit: Africa Studio / Shutterstock.com


A growing body of evidence indicates that gut microbiota has a significant role in various aspects of host metabolism, including digestion, harvesting of energy, and induction of low-grade inflammation. In addition, the genetic factors of the host, as well as other characteristics such as age, diet, immunity, and gender, influence the gut microbiome composition.

Research shows that bacterial diversity in the gut and the individual’s functional capacity vary between those with normal weight and obese individuals. Gut microbiome profile variations have also been linked to metabolic disorders, lipid accumulation, and inflammation.

Lipogenesis in the liver and the regulation of appetite through hormones are also associated with gut microbiome genes.

Aside from its role in adipogenesis, superoxide reduction, and the metabolism of vitamins, gut microbiota also regulates innate immunity and the systemic, low-grade inflammatory state that can contribute to fat deposition and obesity. Therefore, Dysbiosis, which is the imbalance of gut microbiota, combined with diet, likely has a significant role in the development of obesity.

About the study

In the present study, researchers conducted a cross-sectional analysis of data from 45 children between the ages of six and 12 to determine the association between gut microbiota and obesity.

Questionnaires were used to obtain information on dietary frequencies, gender, age, and body mass index (BMI). Based on the World Health Organization (WHO) z-scores, in which BMI is adjusted for gender and age, the children were classified into two categories of overweight and obese (OWOB) and normal weight (NW).

Data from food frequency questionnaires were used to classify the dietary habits of children into two nutritional patterns. To this end, Pattern 1 was characterized by complex carbohydrates and proteins, whereas Pattern 2 comprised simple carbohydrates and saturated fats.

Shotgun metagenomics was used to assess the taxonomic diversity of the gut microbiota and metabolic capacity from genomic deoxyribonucleic acid (DNA) extracted from fecal samples. Clade-specific markers were used for the taxonomic and functional assessment of the gut bacteria. Additionally, reverse Simpson and Shannon diversity indices were calculated.

The virulence factor database was used to screen for virulence factor genes, whereas multivariate linear modeling was used to determine the association between the taxa, virulence factors, and function of gut microbes and covariates of diet, serology, and anthropometric measurements.

Study findings

Significant differences between the alpha and beta diversity of the gut microbiota were observed between the children in the NW and OWOB groups, thus suggesting that specific phyla of bacteria contribute to higher levels of energy harvest.

Furthermore, species such as Ruminococcus species, Victivallis vadensis, Mitsuokella multacida, Alistipes species, Clostridium species, and Acinetobacter johnsonii were linked to healthier metabolic parameters.

In contrast, an increase in the abundance of bacteria such as Veillonellaceae, Lactococcus, Fusicatenibacter saccharivorans, Fusicatenibacter prausnitzii, Eubacterium, Roseburia, Dialister, Coprococcus catus, Bifidobacterium, and Bilophila was identified in children with pro-inflammatory conditions and obesity.

Bacteria such as Citrobacter europaeus, Citrobacter youngae, Klebsiella variicola, Enterococcus mundtii, Gemella morbillorum, and Citrobacter portucalensis were associated with higher lipid and sugar intake, as well as higher blood biochemistry values and anthropometric measurements.

Diets high in fats and simple carbohydrates have been associated with the abundance of Citrobacter and Klebsiella species in the gut. Moreover, previous studies have indicated that these bacterial species are potential markers of inflammation, obesity, and an increase in fasting glucose.

The metabolism of menaquinones and gamma-glutamyl was negatively associated with BMI. Furthermore, the microbiomes of children in the NW group preserved a more consistent alpha diversity of virulence factors, while OWOB microbiomes exhibited a dominance of virulence factors.

Differences in the metabolic capacities pertaining to biosynthesis pathways of vitamins, carriers, amino acids, nucleotides, nucleosides, amines, and polyamines, as well as the degradation of nucleotides, nucleosides, and carbohydrate-sugars, were also found between the NW and OWOB groups.


Dietary profiles and the diversity of gut microbiota were found to be interconnected and associated with changes in metabolic parameters, the dominance of virulence factors, and obesity. Changes in gut microbiome diversity and relative abundance have been linked to obesity, inflammatory responses, and metabolic disorders.

Taken together, the study findings suggested that the prevalence of virulence factors, as well as the metabolic and genetic roles of gut microbiota in increasing inflammation, can help identify individuals at an increased risk of childhood obesity.

Journal reference:
  • Murga-Garrido, S. M., Ulloa-Pérez, E. J., Díaz-Benítez, C. E., et al. (2023). Virulence factors of the gut microbiome are associated with BMI and metabolic blood parameters in children with obesity. Microbiology Spectrum. doi:10.1128/spectrum.03382-22