Table 1. Five current anti-human African trypanosomiasis (HAT) chemotherapies.
Drugs | Mechanism | Advantages | Disadvantages |
Pentamidine (pentamidine Isethionate) | Accumulates in trypanosomes; disrupts mitochondrial processes | Effective against stage I Trypanosoma brucei gambiense | Ineffective against stage II T. b. gambiense and both stages of Trypanosoma brucei rhodesiense |
Suramin* (Bayer 205, Germanin) | Binds to enzymes in the glycosome; disrupts glycolysis | Effective against stage I T. b. rhodesiense | Ineffective against stage II T. b. rhodesiense and stage II T. b. gambiense |
Melarsoprol (Mel B) | Disrupts trypanosomal redox metabolism and glycolysis | Effective against both subspecies at both stages | Toxic; around 5% of patients die as a result of post-treatment reactive encephalopathy (PTRE); trypanosomal resistance reported to be as high as 30% |
Eflornithine (difluoromethylornithine) | Irreversibly inhibits ODC; disruption of proliferation and vulnerability to oxidative attack | Effective against stage II T. b. gambiense | Ineffective against both stages of T. b. rhodesiense; treatment is time-consuming |
NECT (nifurtimox–eflornithine combination treatment) | Eflornithine inhibits ODC; nifurtimox induces oxidative attack upon weakened trypanosomes | High cure rate for both stages of T. b. gambiense; low rate of adverse effects; no death rates | Potential for resistance to the treatment in the field |
*Suramin is also effective against stage I T. b. gambiense, but its use remains confined to infections causes by stage I T. b. rhodesiense