Sleeping sickness was a devastating epidemic which had depopulated whole districts of Africa.

The symptoms of the disease begin very insidiously, some slight change in the former mental attitude of the patient being the first thing noticed by the relatives of the patient.
Next, a disinclination to work, with a tendency to sit about and rest more than usual, appears, and at this time headaches and other transient pains may be complained of, especially pains in the upper part of the chest.
The facial aspect now also changes, and a previously happy and intelligent looking negro, becomes, instead, dull, heavy and apathetic.
Once these changes have appeared, the disease may run an acute or more or less chronic course, progressing however to its ultimate fatal termination... The temperature – a very important point – is elevated, rising in the evenings to 101° or 102° F., falling to subnormal in the morning, the range often extending over four degrees or more, and the pulse of very low tension is accelerated, varying from 90 to 130 beats per minute.
These two symptoms are of the greatest diagnostic importance in the early recognition of the disease... Drowsiness, which has gradually been increasing, now passes on to coma, from which the patients can only be roused with difficulty; the temperature falls to subnormal, in rare cases convulsive fits appear, and the patient dies in a complete state of coma.
This is the common course of an ordinary acute case of the disease, the different changes taking about a month or six weeks for completion.

By 1903, researchers had determined that sleeping sickness was caused by a trypanosome, a parasite that lived and multiplied extracellularly in the blood and tissue fluids of its human hosts.
Researchers also knew that trypanosomes were transmitted by a species of tsetse fly.
It had been suggested that preparations of arsenic might be useful in treating the disease, but an effective treatment had not been found.

At the Rockefeller Institute, Simon Flexner organized a group to test arsenical compounds.
Building on the work of Paul Ehrlich in Germany, who had developed an arsenic-derived drug called Salvarsan for the treatment for syphilis, chemist Walter A. Jacobs and immunologist Michael Heidelberger synthesized 243 possible arsenicals, varying methyl groups, amides, and complex side chains.
 Pearce and Brown studied animal models of the disease in rats, mice, and rabbits, to better understand the course of the disease, and tested all the potential treatments to initially assess effectiveness.
In mice and rats the parasites tended to remain in the bloodstream, while in rabbits they invaded the central nervous system, a more comparable model to what happened in humans.
 The most successful of the possibilities was tryparsamide, a derivative of atoxyl, in which a carboxyl group was converted into an amide to reduce toxicity of the drug.
They announced successful results in the Journal of Experimental Medicine in 1919.

The Rockefeller Institute sent Louise Pearce to Léopoldville in the Belgian Congo in 1920 to test tryparsamide, "trusting her vigorous personality to carry out an assignment none too easy for a woman physician and not without its dangers".
 There she worked with a local hospital and laboratory to design and carry out a drug testing protocol for human trials to establish tryparsamide's safety, effectiveness, and optimum dosage.
Almost all early cases of the previously fatal disease were successfully treated, and most patients, even in the later stages of sleeping sickness, could be saved.
 Human trials also revealed that a side effect of other arsenical compounds, damage to the optic nerve and loss of vision, could occur with high or repeated doses of tryparsamide.

Nonetheless, tryparsamide became the drug of choice for chemotherapy of sleeping sickness for several decades.
 The compound was able to enter the central nervous system, making it the first drug that could be used to treat later-stage sleeping sickness.
It was easy to administer, acted quickly, and cured more than 80%
Sleeping sickness was a devastating epidemic which had depopulated whole districts of Africa.
The symptoms of the disease begin very insidiously, some slight change in the former mental attitude of the patient being the first thing noticed by the relatives of the patient. Next, a disinclination to work, with a tendency to sit about and rest more than usual, appears, and at this time headaches and other transient pains may be complained of, especially pains in the upper part of the chest. The facial aspect now also changes, and a previously happy and intelligent looking negro, becomes, instead, dull, heavy and apathetic. Once these changes have appeared, the disease may run an acute or more or less chronic course, progressing however to its ultimate fatal termination... The temperature – a very important point – is elevated, rising in the evenings to 101° or 102° F., falling to subnormal in the morning, the range often extending over four degrees or more, and the pulse of very low tension is accelerated, varying from 90 to 130 beats per minute. These two symptoms are of the greatest diagnostic importance in the early recognition of the disease... Drowsiness, which has gradually been increasing, now passes on to coma, from which the patients can only be roused with difficulty; the temperature falls to subnormal, in rare cases convulsive fits appear, and the patient dies in a complete state of coma. This is the common course of an ordinary acute case of the disease, the different changes taking about a month or six weeks for completion.
By 1903, researchers had determined that sleeping sickness was caused by a trypanosome, a parasite that lived and multiplied extracellularly in the blood and tissue fluids of its human hosts. Researchers also knew that trypanosomes were transmitted by a species of tsetse fly. It had been suggested that preparations of arsenic might be useful in treating the disease, but an effective treatment had not been found.
At the Rockefeller Institute, Simon Flexner organized a group to test arsenical compounds. Building on the work of Paul Ehrlich in Germany, who had developed an arsenic-derived drug called Salvarsan for the treatment for syphilis, chemist Walter A. Jacobs and immunologist Michael Heidelberger synthesized 243 possible arsenicals, varying methyl groups, amides, and complex side chains.  Pearce and Brown studied animal models of the disease in rats, mice, and rabbits, to better understand the course of the disease, and tested all the potential treatments to initially assess effectiveness. In mice and rats the parasites tended to remain in the bloodstream, while in rabbits they invaded the central nervous system, a more comparable model to what happened in humans.  The most successful of the possibilities was tryparsamide, a derivative of atoxyl, in which a carboxyl group was converted into an amide to reduce toxicity of the drug. They announced successful results in the Journal of Experimental Medicine in 1919.
The Rockefeller Institute sent Louise Pearce to Léopoldville in the Belgian Congo in 1920 to test tryparsamide, "trusting her vigorous personality to carry out an assignment none too easy for a woman physician and not without its dangers".  There she worked with a local hospital and laboratory to design and carry out a drug testing protocol for human trials to establish tryparsamide's safety, effectiveness, and optimum dosage. Almost all early cases of the previously fatal disease were successfully treated, and most patients, even in the later stages of sleeping sickness, could be saved.  Human trials also revealed that a side effect of other arsenical compounds, damage to the optic nerve and loss of vision, could occur with high or repeated doses of tryparsamide.
Nonetheless, tryparsamide became the drug of choice for chemotherapy of sleeping sickness for several decades.  The compound was able to enter the central nervous system, making it the first drug that could be used to treat later-stage sleeping sickness. It was easy to administer, acted quickly, and cured more than 80% 
Louise Pearce