Role of anaerobic bacteria in intra-abdominal septic abscesses in mediating septic control of skeletal muscle glucose oxidation and lactic acidemia.
Altered glucose metabolism and lactic acidemia are features of Gram-negative polymicrobial abscesses, but the relationship between carbohydrate metabolism and the aerobic or anaerobic organisms is unclear. Since reductions in the % active pyruvate dehydrogenase complex (PDHa) limits glucose oxidation in sepsis, the effect of a 7-day monoclonal (E. coli or B. fragilis) vs. biclonal (E. coli + B. fragilis) intra-abdominal abscess (IA) on PDHa and lactate concentrations in skeletal muscle (SM) and plasma was studied in rats. A chronic IA was created by the intraperitoneal introduction of a sterile rat fecal-agar pellet (1.5 ml) inoculated with a known bacterial flora [sterile (S); E. coli 10(6) CFU/ml (EC); B. fragilis 10(8) CFU/ml (BF); E. coli 10(3) CFU/ml + B. fragilis 10(4) CFU/ml (ECLBF); E. coli 10(3) CFU/ml + B. fragilis 10(8) CFU/ml (ECHBF)]. Neither SM PDHa nor SM nor plasma lactate were altered from control in animals with either sterile (S) or E. coli (EC) monoclonal IA, but SM PDHa was significantly (p less than 0.001) reduced and SM lactate increased (p less than 0.05) in rats with B. fragilis 10(8)/ml (BF) monoclonal IA. In biclonal IA, the effect of sepsis on SM PDHa depended on the concentration of B. fragilis in the IA fluid (ECLBF = 10(4) CFU/ml vs. ECHBF = 10(8) CFU/ml) since the E. coli were constant (10(3) CFU/ml). At the lower B. fragilis IA concentration (ECLBF), the SM PDHa was not different from control. However, when the IA B. fragilis concentration was increased to 10(8) CFU/ml (ECHBF), the SM PDHa was significantly (p less than 0.001) decreased relative to control. A decreased muscle PDHa was always associated with elevated SM and plasma lactate concentrations. These results suggest that IA which permit a threshold of relatively nonlethal (BF = 0% mortality) anaerobic B. fragilis (greater than or equal to 10(8) CFU/ml) to enter the circulation are more important in altering metabolic control of skeletal muscle glucose oxidation and in producing lactic acidemia than are IA with only aerobic E. coli. However, in biclonal intra-abdominal abscesses, B. fragilis potentiated the early mortality from E. coli (EC = 6% vs. ECHBF = 37% mortality), suggesting that the metabolic effect of the B. fragilis-induced lactic acidemia is synergistic with the direct toxic effects of the E. coli.
Vary
T C
TC
Maryland Institute for Emergency Medical Services Systems, Baltimore 21201.
Siegel
J H
JH
Tall
B
B
Morris
J G
JG
D000005:Abdomen; D000038:Abscess / Q000378:metabolism* / Q000382:microbiology; D000818:Animals; D001442:Bacteroides Infections / Q000150:complications / Q000378:metabolism*; D001441:Bacteroides fragilis; D004927:Escherichia coli Infections / Q000150:complications / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism*; D007773:Lactates / Q000097:blood*; D019344:Lactic Acid; D007964:Leukocytosis / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D009132:Muscles / Q000378:metabolism; D010084:Oxidation-Reduction; D051381:Rats; D011919:Rats, Inbred Strains
D007773:Lactates; D019344:Lactic Acid; D005947:Glucose