Human milk microorganisms contribute not only to the healthy development of the immune system in infants, but also in shaping the gut microbiota. We evaluated the effect of the maternal diet during pregnancy and during the first month of lactation on the human milk microbiota in a cross-sectional study including 94 healthy lactating women. Microbiota composition was determined by 16S rDNA profiling and nutrient intake assessed through food questionnaires. Thirteen genera were present in at least 90% of all samples, with three genera present in all samples: Streptococcus, Staphylococcus, and Corynebacterium. Cluster analysis indicated two distinct compositions: one marked by a high abundance of Streptococcus (cluster 1), and other by a high abundance of Staphylococcus (cluster 2). A global association with milk microbiota diversity was observed for vitamin C intake during pregnancy (p = 0.029), which was higher for cluster 2 individuals (cluster 2 median = 232 mg/d; cluster 1 = 175 mg/d; p = 0.02). Positive correlations were found between Bifidobacterium in the milk and intake of polyunsaturated and linoleic fatty acids during the lactation period (p < 0.01). We show that maternal diet influences the human milk microbiota, especially during pregnancy, which may contribute in shaping the gut microbiota.

We identified different diarrheagenic (DEC) Escherichia coli pathotypes isolated from 1,207 children with and without acute endemic diarrhea in Salvador, Bahia, Brazil collected as part of a case-control study. Since the identification of DEC cannot be based on only biochemical and culture criteria, we used a multiplex polymerase chain reaction developed by combining five specific primer pairs for Enteropathogenic Escherichia coli (EPEC), Shiga toxin-producing E. coli/ Enterohaemorrhagic E. coli (STEC/EHEC), Enterotoxigenic E. coli (ETEC) and Enteroaggregative E. coli (EAEC) to detect these pathotypes simultaneously in a single-step reaction. In order to distinguish typical and atypical EPEC strains, these were tested for the presence of EAF plasmid. The prevalence of diarrheagenic E. coli in this sample of a global case-control study was 25.4% (259 patients) and 18.7% (35 patients) in the diarrhea group (1,020 patients) and the control group (187 patients), respectively. The most frequently isolated pathotype was EAEC (10.7%), followed by atypical EPEC (9.4%), ETEC (3.7%), and STEC (0.6%). Typical EPEC was detected only in one sample. The prevalence of the pathotypes studied in children with diarrhea was not significantly different from that in children without diarrhea.

Gut microbiota composition is influenced by environmental factors and has been shown to impact body metabolism. Objective: To assess the gut microbiota profile before and after Roux-en-Y gastric bypass (RYGB) and the correlation with food intake and postoperative type 2 diabetes remission (T2Dr). Design: Gut microbiota profile from obese diabetic women was evaluated before (n = 25) and 3 (n = 20) and 12 months (n = 14) after RYGB, using MiSeq Illumina-based V4 bacterial 16S rRNA gene profiling. Data on food intake (7-day record) and T2Dr (American Diabetes Association (ADA) criteria) were recorded. Results: Preoperatively, the abundance of five bacteria genera differed between patients with (57%) and without T2Dr (p < 0.050). Preoperative gut bacteria genus signature was able to predict the T2Dr status with 0.94 accuracy ROC curve (receiver operating characteristic curve). Postoperatively (vs. preoperative), the relative abundance of some gut bacteria genera changed, the gut microbial richness increased, and the Firmicutes to Bacteroidetes ratio (rFB) decreased (p < 0.05) regardless of T2Dr. Richness levels was correlated with dietary profile pre and postoperatively, mainly displaying positive and inverse correlations with fiber and lipid intakes, respectively (p < 0.05). Conclusions: Gut microbiota profile was influenced by RYGB and correlated with diet and T2Dr preoperatively, suggesting the possibility to assess its composition to predict postoperative T2Dr.