Role of metabolism in pathogenesis of bacteremia due to Diplococcus pneumoniae in rabbits.

Abstract

Since the lethal factors in most bacterial infections have not been defined, the role of metabolic alterations was investigated. Bacteremia was produced in rabbits by infection with Diplococcus pneumoniae, and the animals were grouped by severity of the disease as determined by progressive increments in the level of bacteremia, concentration of lactate in whole blood, and change in body temperature. Adenosine triphosphate and adenosine diphosphate in blood, liver, heart, and skeletal muscle were normal. Hepatic glycogen was variably decreased, and 45% of the animals were hypoglycemic despite normal hepatic glucogenesis. Concentrations of lactate in heart and liver increased. In-vitro oxidation of glucose, acetate, and pyruvate decreased in liver only. Glycolysis was normal in liver, heart, and muscle, but it was markedly increased in the lung. Hepatic synthesis of the triglyceride from acetate increased markedly. Hepatic microsomal protein synthesis apparently was normal, but amino acids in plasma, liver and skeletal muscle were increased. Complex multifaceted alterations in metabolism occurred. It is doubtful that anyone of these could be responsible for death, but the role played by these changes as a whole is unknown.