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Edwin A. Deitch, MD; Rodney Berg, PhD; Robert Specian, PhD

Arch Surg. 1987;122(2):185-190.

Abstract
• Experiments were performed in mice to determine whether endotoxin could cause bacteria normally colonizing the gut to spread systemically, a process termed bacterial translocation. Endotoxin given intraperitoneally promoted bacterial translocation in a dose-dependent fashion from the gut to the mesenteric lymph node (MLN). The incidence of bacterial translocation to the MLN was similar whether the endotoxin was administered intramuscularly or intraperitoneally, although the number of bacteria colonizing the MLN was greater with intraperitoneal endotoxin. The incidence and magnitude of endotoxin-induced bacterial translocation were similar between CD-1 and C3H/HeJ (endotoxin-resistant) mice, indicating that bacterial translocation is not prevented by genetic resistance to endotoxin. Thus, it appears that the gut may serve as a reservoir for bacteria causing systemic infections during endotoxemia.

(Arch Surg 1987;122:185-190)

Author Affiliations
From the Departments of Surgery (Dr Deitch), Microbiology (Dr Berg), and Anatomy (Dr Specian), Louisiana State University Medical Center School of Medicine, Shreveport.

Footnotes
Accepted for publication Sept 15, 1986.

Read before the Sixth Annual Meeting of the Surgical Infection Society, Chicago, April 21, 1986.

Reprint requests to LSUMC School of Medicine, PO Box 33932, Shreveport, LA 71130 (Dr Deitch).

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