No abstract

The purpose of this study was to evaluate the composition and richness of bacterial communities associated with low-birthweight (LBW) infants in relation to host body site, individual, and age. Bacterial 16S rRNA genes from saliva samples, skin swabs, and stool samples collected on postnatal days 8, 10, 12, 15, 18, and 21 from six LBW (five premature) infants were amplified, pyrosequenced, and analyzed within a comparative framework that included analogous data from normal-birthweight (NBW) infants and healthy adults. We found that body site was the primary determinant of bacterial community composition in the LBW infants. However, site specificity depended on postnatal age: saliva and stool compositions diverged over time but were not significantly different until the babies were 15 days old. This divergence was primarily driven by progressive temporal turnover in the distal gut, which proceeded at a rate similar to that of age-matched NBW infants. Neonatal skin was the most adult-like in microbiota composition, while saliva and stool remained the least so. Compositional variation among infants was marked and depended on body site and age. Only the smallest, most premature infant received antibiotics during the study period; this heralded a coexpansion of Pseudomonas aeruginosa and a novel Mycoplasma sp. in the oral cavity of this vaginally delivered, intubated patient. We conclude that concurrent molecular surveillance of multiple body sites in LBW neonates reveals a delayed compositional differentiation of the oral cavity and distal gut microbiota and, in the case of one infant, an abundant, uncultivated oral Mycoplasma sp., recently detected in human vaginal samples.

In this review, we examine the major known risk factors and technical considerations that have been implicated as factors in leakage. Although surgical technique has evolved over the past several decades with the advent of newer surgical staplers, laparoscopy, and robotics, we have not witnessed a decrease in the incidence of colorectal anastomotic leaks suggesting that the fundamental pathogenesis of anastomotic leak remains unknown. Among the factors contributing to anastomotic healing, intestinal bacteria remains largely overlooked even though compelling evidence exist that intraluminal microbes could play a major role in pathogenesis of anastomotic leak. Further investigation focusing on intestinal microbes could be one such avenue for uncovering the elusive cause of colorectal anastomotic leak.

SYNOPSIS Important advances in the study of bacteria associated with the human gastrointestinal tract have significant implications for clinicians striving to meet the metabolic and nutritional needs of critically ill patients. A transition from culture-based to culture-independent studies of the intestinal microbiota has ushered in a new era of laboratory and clinical studies in this field. These studies are helping to clarify the important role of bacteria in carbohydrate metabolism, and are providing new evidence that highlights the role of bacteria in protein and lipid homeostasis. We know that during periods of caloric excess or deprivation, microbial populations in the GI tract are clearly altered; however the molecular etiology for such changes remains elusive. Similarly, little is known about how microbial ecology changes before, during, and after critical illness. Nevertheless, several approaches, e.g. probiotic administration, have been employed to manipulate gut microbial communities in the ICU. In this review we offer a broad overview of the importance of the host-microbe relationship, discuss what is currently known about the role of gut microbes in nutrition and metabolism in the healthy human host, review how gut microbes are impacted by critical illness, and discuss interventions that have already been utilized to manipulate the gut microbiome in ICU patients.

To date, no single change in the gut microbiota has definitively been identified as a risk factor or cause of NEC. The findings at present suggest that NEC does not result from growth of a single causative pathogen, but rather that the disease results from a generalized disturbance of normal colonization patterns in the developing gut.