You are here


6 April, 2016 - 17:26

T. brucei, the parasite that is responsible for African sleeping sickness, confounds the human immune system by changing its thick layer of surface glycoproteins with each infectious cycle (Figure 13.17). The glycoproteins are identified by the immune system as foreign matter, and a specific antibody defense is mounted against the parasite. However, T. brucei has thousands of possible antigens, and with each subsequent generation, the protist switches to a glycoprotein coating with a different molecular structure. In this way, T. brucei is capable of replicating continuously without the immune system ever succeeding in clearing the parasite. Without treatment, African sleeping sickness leads invariably to death because of damage it does to the nervous system. During epidemic periods, mortality from the disease can be high. Greater surveillance and control measures have led to a reduction in reported cases; some of the lowest numbers reported in 50 years (fewer than 10,000 cases in all of sub-Saharan Africa) have happened since 2009.

In Latin America, another species in the genus, T. cruzi, is responsible for Chagas disease. T. cruziinfections are mainly caused by a blood-sucking bug. The parasite inhabits heart and digestive system tissues in the chronic phase of infection, leading to malnutrition and heart failure caused by abnormal heart rhythms. An estimated 10 million people are infected with Chagas disease, which caused 10,000 deaths in 2008.

Figure 13.17 Trypanosomes are shown in this light micrograph among red blood cells.


This movie ( the pathogenesis of Trypanosoma brucei, the causative agent of African sleeping sickness.