Observations on the Defense Mechanism in Trypanosoma Equiperdum and Trypano Some Lewisi Infections in Guinea Pigs and Rats

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  • Department of Bacteriology, College of Physicians and Surgeons, Columbia University, New York
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Summary and Conclusion

Artificial hyperglycemia shortens the prepatent period and increases the rate of reproduction of the trypanosomes in guinea pigs infected with T. equiperdum. Death supervenes in such animals from two to three weeks sooner than in control animals with a lower blood sugar. These observations suggest that the trypanosomes in the blood stream require carbohydrates for food and utilize them in a way analogous to the utilization of sugar by bacteria in the test tube.

The intraperitoneal injection of pilocarpine shortens the prepatent period in guinea pigs infected with T. equiperdum. It also causes a significant increase in the number of trypanosomes in the peripheral circulation when injected during the logarithmic phase of development. The increase is only temporary and does not represent a stimulation in the rate of reproduction of the trypanosomes. This increase apparently is due to a contraction of some of the abdominal organs, primarily the spleen which serves as a reservoir for the trypanosomes during the early part of the infection.

The trypanosomes or their products cause an early stimulation of the hematopoietic organs as shown by the temporary increase in the number of red blood corpuscles and in the number of nucleated red blood cells in the peripheral circulation.

The the spleen is the most important and most active individual organ of the reticulo-endothelial system, in the defense against trypanosome infections, is further shown by the correlation of the gross and microscopic changes with the response of the animal to a drug which contracts the spleen.

T. equiperdum infection in pregnant guinea pigs appears to run a milder course in the mother but has a deleterious effect on the offspring.

There is a terminal decrease in the number of trypanosomes in rats infected with T. equiperdum. This occurs within the last few hours of the disease and is associated with a terminal destruction of the red blood corpuscles. We believe that death is in a large part due to the anoxyemia resulting from this hemolysis which is further aided by the presence of a non-volatile acidosis in the blood.

There is no significant change in the resistance of the red blood corpsucles of rats infected with T. lewisi, while in T. equiperdum infection a significant decrease in the resistance of the red cells occurs.

The change in the size of the spleen in rats infected with T. lewisi almost parallels the change in the size of the spleen of guinea pigs infected with T. equiperdum during the first five weeks of the infection.

There is a significant change in the large monocytes and the platelets during the early part of the infection of rats with T. lewisi, with a tendency to return to normal as the infection clears up.

The average duration of life of rats infected with T. equiperdum was lengthened approximately 40 hours in animals previously infected with T. lewisi.

Author Notes

Formerly, Fellow, Howard University Medical School, under a grant from the General Education Board. The first two years of the work reported in this paper were performed in the Department of Bacteriology, College of Physicians and Surgeons of Columbia University, New York City. The remainder of the work was done at Howard University Medical School, Washington, D. C.

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