No abstract

Some metabolic disorder treatments require patients to follow a specific diet or to consume supplements that, over time, can lead to oral microbiome alterations. Well-known disorders requiring such treatment are phenylketonuria (PKU), an inborn error of amino acid metabolism, and type 1 diabetes (T1D), a metabolic disorder that requires a specific diet regimen. Therefore, the aim of this study was to investigate the oral health and microbiome characteristics that might contribute to caries activity and periodontal disease risk in PKU and T1D patients. In this cross-sectional study, 45 PKU patients, 24 T1D patients, and 61 healthy individuals between the ages of 12 and 53 years were examined. Their anamnestic data and dental status were assessed by one dentist. Microbial communities were detected from saliva-isolated DNA using 16S rRNA gene V3–V4 sequencing on Illumina MiSeq sequencing platform. Results revealed that the PKU patient group displayed the highest number of extracted teeth (on average 1.34), carious teeth (on average 4.95), and carious activity (44.44% of individuals) compared to the T1D and CTRL groups. The lowest numbers of filled teeth (on average 5.33) and extracted teeth (on average 0.63) per individual were observed in T1D patients. Gingivitis appeared more often in the T1D group; however, possible risk of periodontal disease was seen in both the T1D and PKU patient groups. The highest number of differentially abundant genera was detected in the PKU group (n = 20), with enrichment of Actinomyces (padj = 4.17 × 10−22), Capnocytophaga (padj = 8.53 × 10−8), and Porphyromonas (padj = 1.18 × 10−5) compared to the CTRL group. In conclusion, the dental and periodontal health of PKU patients was found to be significantly inferior compared to T1D patients and healthy controls. T1D patients showed early signs of periodontal disease. Several genera that correlate with periodontal disease development were found in both groups, thus suggesting that T1D and PKU patients should seek early and regular dental advice and be educated about proper oral hygiene practices.

The spread of extended-spectrum beta-lactamases (ESBLs) in nosocomial and community-acquired enterobacteria is an important challenge for clinicians due to the limited therapeutic options for infections that are caused by these organisms. The epidemiology of these infections is complex and combines the expansion of mobile genetic elements with clonal spread. Insufficient empirical therapy for serious infections caused by these organisms is independently associated with increased mortality. Here, we developed an ESBL coding gene panel, evaluated the abundance and prevalence of ESBLs encoding genes in patients undergoing H. pylori eradication therapy, and summarized the effect of eradication therapy on gut microbiome functional profiles. To assess the repertoire of known beta lactamase (BL) genes, we divided them in clusters according to their evolutionary relation, designed primers for amplification of cluster marker regions and assessed efficiency of this amplification panel on 120 fecal samples acquired from 60 patients undergoing H. pylori eradication therapy. In addition, fecal samples from additional 30 patients were used to validate the detection efficiency of designed ESBL panel. The presence for majority of targeted clusters was confirmed by NGS of amplification products. Metagenomic sequencing revealed that the abundance of ESBL genes within the pool of microorganisms was very low. The global relative abundances of the ESBL-coding gene clusters did not differ significantly across the treatment states. However, at the level of each cluster, classical ESBL producers, such as Klebsiella sp. for blaOXY (p = 0.0076), Acinetobacter sp. for blaADC (p = 0.02297), and others, differed significantly with a tendency to decrease compared to the pre- and post-eradication states. Only 13 clusters were common among all three datasets, suggesting a patient-specific prevalence profile of ESBL-coding genes. The number of AMR genes detected in the post-eradication state was higher than that in the pre-eradication state, which at least partly might be attributed to the therapy. This study demonstrated that the ESBL screening panel was efficient for targeting ESBL-coding gene clusters from bacterial DNA and that minor differences exist in the abundance and prevalence of ESBL-coding gene levels before and after eradication therapy.

It has been hypothesised that the establishment of stable adult microbiota is programmed in infancy, and therefore early life gut colonisation may lead to a lifelong microbiota pattern with significant effects on health. The aim of the study was to analyse the composition of gut microbiota and influencing factors in infants up to seven months of age in Latvia. A cross-sectional study was performed at primary healthcare centres. The parents of healthy infants filled out a questionnaire and brought the child’s faecal sample. 16 rRNS gene sequencing was performed to identify the bacterial taxonomic units. The composition of gut microbiota was compared between children with different risk factors. The final participant sample group included 55 infants with median age 4.0 months. The infant gut microbiota of the sample group had typical and rather healthy microbiota — the main phyla detected were Firmicutes and Actinobacteria, the main family was Bifidobacteriacea and genus — Bifidobacterium. A significant effect of the type of delivery and feeding type was identified, as well as negative correlation between Lactobacilli and gestational age. Further, it would be important to analyse the changes of microbiota prospectively to identify the association with environmental factors and health status in dynamics.

The spread of extended-spectrum beta-lactamases (ESBLs) in nosocomial and community-acquired enterobacteria is an important challenge for clinicians due to the limited therapeutic options for infections that are caused by these organisms. Here, we developed a panel of ESBL coding genes, evaluated the abundance and prevalence of ESBL encoding genes in patients undergoing H. pylori eradication therapy, and summarized the effects of eradication therapy on functional profiles of the gut microbiome. To assess the repertoire of known beta lactamase (BL) genes, they were divided into clusters according to their evolutionary relation. Primers were designed for amplification of cluster marker regions, and the efficiency of this amplification panel was assessed in 120 fecal samples acquired from 60 patients undergoing H. pylori eradication therapy. In addition, fecal samples from an additional 30 patients were used to validate the detection efficiency of the developed ESBL panel. The presence for majority of targeted clusters was confirmed by NGS of amplification products. Metagenomic sequencing revealed that the abundance of ESBL genes within the pool of microorganisms was very low. The global relative abundances of the ESBL-coding gene clusters did not differ significantly among treatment states. However, at the level of each cluster, classical ESBL producers such as Klebsiella sp. for blaOXY (p = 0.0076), Acinetobacter sp. for blaADC (p = 0.02297) and others, differed significantly with a tendency to decrease compared to the pre- and post-eradication states. Only 13 clusters were common across all three datasets, suggesting a patient-specific distribution profile of ESBL-coding genes. The number of AMR genes detected in the post-eradication state was higher than that in the pre-eradication state, which could be attributed, at least in part, to the therapy. This study demonstrated that the ESBL screening panel was effective in targeting ESBL-coding gene clusters from bacterial DNA and that minor differences exist in the abundance and prevalence of ESBL-coding gene levels before and after eradication therapy.