Bacterial Translocation of Coagulase-Negative Staphylococci in Rats following Intestinal Ischemia-Reperfusion Injury

Abstract

Many patients with sepsis have bacteremia for which no septic focus is identified either clinically or by autopsy. This study was designed to determine the relationship between the ischemia-reperfusion injury (IRI) and bacterial translocation that might be involved in the pathogenesis of necrotizing enterocolitis. In the first experiment, a total of 32 Sprague-Dawley rats weighing 150–200 g were divided into four groups. The mesentery to isolated loop was occluded for 30, 60, and 90 min following 30-min reperfusion in the three groups of experimental animals with a micro-bulldog clamp. A control group involved the same technique and exposure, without occlusion of the mesentery. Two sets of blood culture were taken through a catheter in the portal vein immediately and 15 min after the reperfusion, respectively. In another experiment, bacteria isolated were fed in different doses to control rats and those after 30- or 60-min ischemia and 30-min reperfusion. Two sets of blood culture were taken following the procedure. Invasion and transcytosis of the bacteria through epithelial cells were studied in vitro using a Madin-Derby canine kidney (MDCK) cell monolayer model. PCR for delta toxin gene was performed on all bacteria isolated, using Staphylococcus epidermidis as the control. Coagulase-negative staphylococci (CoNS) were invariably isolated from mice with prolonged ischemia (90 min) and reperfusion. When bacteria were fed into mice with only 30-min ischemia, an inoculum as low as 5 × 10⁵ CFU/ml could induce bacteremia. No bacterial translocation was found in control mice even fed with a higher dose of bacteria (5 × 10⁸ CFU/ml). In vitro experiments showed that CoNS failed to transcytose MDCK monolayer. These isolates were not cytotoxic to MDCK cells and contained no delta toxin gene. Bacterial translocation of CoNS occurred following severe bowel ischemia and reperfusion injury. Intact mucosa integrity readily prevented bacterial translocation; however, bacterial translocation could occur in rats following mild IRI in the presence of a higher number of CoNS in the gut.

Maternal Factors in Extremely Low Birth Weight Infants Who Develop Spontaneous Intestinal Perforation

“…27 In an animal model, bacterial translocation of CONS occurs after intestinal ischemia/reperfusion injury. 28 The role of Candida in the pathogenesis of SIP remains unclear. Two of the histopathologic surgical reports showed evidence of yeast within the intestinal tissue.…”

Update on Colon Ischemia: Recent Insights and Advances

“…It is unlikely that a randomized controlled trial will ever be completed given the disease's benign nature and the number of patients that would be required to power such a study. Our current knowledge regarding the potential benefits of antimicrobial therapy come from murine models that show antimicrobials decrease inflammatory responses and bacterial translocation into the blood in the setting of CI [37,38]. Older studies have shown antimicrobials to reduce the severity and extent of bowel damage in the murine model [39].…”

Low mortality in necrotizing enterocolitis associated with coagulase-negative Staphylococcus infection

“…Mollitt et al [39] reported an incidence of 30% for CoNS blood infection within 72 h of the operative procedure, with an overall mortality of 33%. It has been suggested that organisms isolated in blood during enterocolitis come from the bowel through translocation [40]. Our study, unfortunately, did not allow confirming the nature of the colonization of the bowel by stool cultures.…”

“…A total of 52% were female and 48% were male; seven infants (15.9%) were full-term neonates. Mean birth weight was 1,666 ± 740 g (range 710-3,450) and mean gestational age was 32 ± 4 weeks (range of [25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41]. Twenty-two percent were extremely low birth weight (ELBW, birth weight under 1,000 g).…”