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Surgical removal of the intestine, lifesaving in catastrophic gastrointestinal disorders of infancy, can result in a form of intestinal failure known as short bowel syndrome (SBS). Bloodstream infections (BSIs) are a major challenge in pediatric SBS management. BSIs require frequent antibiotic therapy, with ill-defined consequences for the gut microbiome and childhood health. Here, we combine serial stool collection, shotgun metagenomic sequencing, multivariate statistics and genome-resolved strain-tracking in a cohort of 19 patients with surgically-induced SBS to show that antibiotic-driven intestinal dysbiosis in SBS enriches for persistent intestinal colonization with BSI causative pathogens in SBS. Comparing the gut microbiome composition of SBS patients over the first 4 years of life to 19 age-matched term and 18 preterm controls, we find that SBS gut microbiota diversity and composition was persistently altered compared to controls. Commensals including Ruminococcus, Bifidobacterium, Eubacterium , and Clostridium species were depleted in SBS, while pathobionts ( Enterococcus ) were enriched. Integrating clinical covariates with gut microbiome composition in pediatric SBS, we identified dietary and antibiotic exposures as the main drivers of these alterations. Moreover, antibiotic resistance genes, specifically broad-spectrum efflux pumps, were at a higher abundance in SBS, while putatively beneficial microbiota functions, including amino acid and vitamin biosynthesis, were depleted. Moreover, using strain-tracking we found that the SBS gut microbiome harbors BSI causing pathogens, which can persist intestinally throughout the first years of life. The association between antibiotic-driven gut dysbiosis and enrichment of intestinal pathobionts isolated from BSI suggests that antibiotic treatment may predispose SBS patients to infection. Persistence of pathobionts and depletion of beneficial microbiota and functionalities in SBS highlights the need for microbiota-targeted interventions to prevent infection and facilitate intestinal adaptation.

Background: Indices for prediction of surgical site infection (SSI) are well documented in the adult population; however, these factors have not been validated in children., Study Design: A retrospective case-control study was performed by examining the medical records of children (0 to 18 years) who developed an SSI within 30 days of selected class I and class II procedures at our institution from 1996 to 2008. Two controls were selected from among patients undergoing identical procedures within 12 months of each case. Statistical analysis was performed using Wilcoxon test for continuous and chi-square test for categorical variable. Factors thought a priori to be associated with risk of SSI and statistically significant variables from a univariate analysis were used to create a logistic regression model., Results: Of 16,031 patients, 159 children (0.99%) developed an SSI. Univariate analysis showed race, postoperative location, skin preparation, urinary catheter, procedure duration, and implantable device as risk factors for development of an SSI. Independent predictors of SSI in multiple conditional logistic regression were age (adjusted odds ratio [aOR] 4.97 neonate vs adolescent; 95% CI 1.38 to 17.90), race (aOR 2.36 for African American vs white; 95% CI 1.32 to 4.18), postoperative location (aOR 6.55 ICU vs home; 95% CI 1.58 to 27.21), urinary catheter placement (aOR 3.56; 95% CI 1.50 to 8.48), and implantable device (aOR 3.05; 95% CI 1.14 to 8.21). Wound classification and antibiotic administration were not independent predictors of SSI., Conclusions: Postoperative location, urinary catheter insertion, and use of an implantable device are potentially modifiable risk factors for an SSI in children. The higher risk of SSI in younger patients and non-white race suggest a possible developmental, socioeconomic, or genetic marker for impaired host defense., (Copyright © 2011 American College of Surgeons. Published by Elsevier Inc. All rights reserved.)