Lethal Factors in Experimental Infections of Trypanosoma equiperdum in Rats. ∗

Abstract

A biochemical and pathological study of experimental Trypanosoma equiperdum infections in laboratory-bred rats has disclosed that the animals died with a significantly reduced blood pH, lowered alkali reserve, and greatly diminished blood oxygen content, i. e., they finally succumbed to a condition of non-volatile, uncompensated acidosis. These findings are in harmony with the previously reported excessive lactic acid content and reduced oxygen content of the blood of trypanosome-infected rats (Kligler and Geiger; 1 Kligler, Geiger and Comaroff 2 ). A progressive hypoglycemia accompanied these terminal manifestations as has been demonstrated by a number of investigators.

Tissue changes found at death were pronounced vasodilatation and congestion throughout the body, extreme enlargement of the spleen, varying degrees of pulmonary edema and occasionally emphysema, distension of the right heart and engorgement of the coronary vessels. The most significant development was the formation of intravascular blood clots which were most prominent in the left side of the heart, but which were also found in the right heart and the vessels of the lungs. These clots were not post-mortem clots nor were they typical laminated thrombi. They were composed of red cells in a mesh of fibrin enclosing an agglomeration of trypanosomes.

It is believed by the authors that the obstruction to the circulation occasioned by these blood clots results in pulmonary edema which leads progressively to the manifestations of dyspnea, suffocation, and finally asphyxia. These changes account for the terminal syndrome, viz., convulsions, almost total lack of oxygen and excessive amounts of lactic acid in the blood, lowered alkali reserve and subsequently reduced pH of the blood. The reduction of blood sugar is tentatively explained as follows: the utilization of glucose by the rapidly multiplying trypanosomes exercises a progressively increasing demand upon the glycogenolytic function of the liver.