 |
 |

Effect of Starvation, Malnutrition, and Trauma on the Gastrointestinal Tract Flora and Bacterial Translocation
Edwin A. Deitch, MD;
John Winterton;
Rodney Berg, PhD
Arch Surg. 1987;122(9):1019-1024.
Abstract
 |  |
We have previously shown, In an animal model, that viable indigenous bacteria will cross the intact gastrointestinal (GI) mucosa and spread systemically, a process termed bacterial translocation, if the normal bacterial ecology of the gut was sufficiently disrupted to allow bacterial overgrowth or if the animals were severely immunosuppressed. Starvation or protein malnutrition disrupts the normal indigenous GI tract microflora and impairs host antibacterial defenses. Consequently, we tested the effect of the combination of starvation or protein malnutrition plus burn trauma In promoting bacterial translocation from the GI tract. Bacterial translocation was measured by quantitatively culturing the mesenteric lymph nodes, spleens, livers, blood, and peritoneal cavities of normal or burned (30% of total body surface area) CD1 mice deprived of food for three days or fed a low-protein (0.03%) diet. The effect of starvation or protein mainutrition on the gut microflora was determined by quantitatively measuring the levels of bacteria present In the ceca. Both starvation and protein malnutrition increased the cecal levels of gram-negative enteric bacilli and decreased the levels of lactobacllli and strict anaerobes. Surprisingly, neither starvation nor protein malnutrition promoted bacterial translocation, even though these animals lost over 20% of their body weight and the ecology of the gut microflora was disrupted. In fact, the protein-malnourished animals exhibited lower Incidences of bacterial translocation than normally nourished animals when both groups were monoassociated with Escherlchia coli C-25 or monoassociated and burned. Thus, It appears that protein malnutrition does not promote bacterial translocation, even when combined with burn trauma.
(Arch Surg 1987;122:1019-1024)
Author Affiliations
From the Departments of Surgery (Dr Deitch and Mr Winterton) and Microbiology (Dr Berg), Louisiana State University Medical Center, Shreveport.
Footnotes
Accepted for publication April 29, 1986.
Reprint requests to the Department of Surgery, Louisiana State University Medical Center, PO Box 33932, Shreveport, LA 71130 (Dr Deitch).
CiteULike Connotea Del.icio.us Digg Reddit Technorati
What's this?
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
 |
Hepatobiliary Complications in Healthy, Intra-abdominally Infected, and High-Output Fistula Rats Receiving Total Parenteral Nutrition
Mok
JPEN J Parenter Enteral Nutr 1993;17:449-453.
ABSTRACT
Intestinal, Pancreatic, and Hepatic Effects of Gastrointestinal Hormones in a Total Parenteral Nutrition Rat Model
Mok and Meng
JPEN J Parenter Enteral Nutr 1993;17:364-369.
ABSTRACT
Dietary Manipulation of Methotrexate-Induced Enterocolitis
Jian Shou et al.
JPEN J Parenter Enteral Nutr 1991;15:307-312.
ABSTRACT
Enteric Bacteria and Ingested Inert Particles Translocate to Intraperitoneal Prosthetic Materials
Mora et al.
Arch Surg 1991;126:157-163.
ABSTRACT
Bulk Prevents Bacterial Translocation Induced by the Oral Administration of Total Parenteral Nutrition Solution
Spaeth et al.
JPEN J Parenter Enteral Nutr 1990;14:442-447.
ABSTRACT
Effects of Protein Malnutrition and Endotoxin on the Intestinal Mucosal Barrier to the Translocation of Indigenous Flora in Mice
Ma Li et al.
JPEN J Parenter Enteral Nutr 1989;13:572-578.
ABSTRACT
Induction of Hypermetabolism in Guinea Pigs by Endotoxin Infused Through the Portal Vein
Arita et al.
Arch Surg 1988;123:1420-1424.
ABSTRACT
|