The prehistory of African trypanosomiasis indicates that the disease may have been an important selective factor in the evolution of hominids. Ancient history and medieval history reveal that African trypanosomiasis affected the lives of people living in sub-Saharan African at all times. Modern history of African trypanosomiasis revolves around the identification of the causative agents and the mode of transmission of the infection, and the development of drugs for treatment and methods for control of the disease. From the recent history of sleeping sickness we can learn that the disease can be controlled but probably not be eradicated. Current history of human African trypanosomiasis has shown that the production of anti-sleeping sickness drugs is not always guaranteed, and therefore, new, better and cheaper drugs are urgently required.

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In this review article the history of leishmaniasis is discussed regarding the origin of the genus Leishmania in the Mesozoic era and its subsequent geographical distribution, initial evidence of the disease in ancient times, first accounts of the infection in the Middle Ages, and the discovery of Leishmania parasites as causative agents of leishmaniasis in modern times. With respect to the origin and dispersal of Leishmania parasites, the three currently debated hypotheses (Palaearctic, Neotropical and supercontinental origin, respectively) are presented. Ancient documents and paleoparasitological data indicate that leishmaniasis was already widespread in antiquity. Identification of Leishmania parasites as etiological agents and sand flies as the transmission vectors of leishmaniasis started at the beginning of the 20th century and the discovery of new Leishmania and sand fly species continued well into the 21st century. Lately, the Syrian civil war and refugee crises have shown that leishmaniasis epidemics can happen any time in conflict areas and neighbouring regions where the disease was previously endemic.

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Abstract. In Trypanosoma brucei, the products of two genes, ESAG 6 and ESAG 7, located upstream of the variant surface glycoprotein gene in a polycistronic expression site form a glycosylphosphatidylinositolanchored transferrin-binding protein (TFBP) complex. It is shown by gel filtration and membrane-binding experiments that the TFBP complex is heterodimeric and binds one molecule of transferrin with high affinity (2,300 binding sites per cell; K D = 2.1 nM for the dominant expression site from T. brucei strain 427 and KD = 131 nM for ES1.3A of the EATRO 1125 stock). The ternary transferrin-TFBP complexes with iron-loaded or iron-flee ligand are stable between pH 5 and 8. Cellular transferrin uptake can be inhibited by 90% with Fab fragments from anti-TFBP antibodies. After uptake, the TFBP complex and its ligand are routed to lysosomes where transferrin is proteolytically degraded. While the degradation products are released from the cells, iron remains cell associated and the TFBP complex is probably recycled to the membrane of the flagellar pocket, the only site for exo-and endocytosis in this organism. It is concluded that the TFBP complex serves as the receptor for the uptake of transferrin in T. brucei by a mechanism distinct from that in mammalian cells.T RANSFERRIN (TF) 1 is the major serum glycoprotein that transports iron to most tissues in mammals. Diferric-TF (holo-TF) binds to a specific cell-surface receptor, the ligand-receptor complex is endocytosed and delivered to endosomes (for reviews see Crichton and Charloteaux-Wauters, 1987;Huebers and Finch, 1987). The low pH of endosomes triggers the release of iron from holo-TF but the resulting iron-free TF (apo-TF) remains bound to the receptor and is recycled back to the cell surface where, at neutral pH, apo-TF dissociates from the receptor. The human TF receptor is a transmembrane glycoprotein composed of two identical disulphide-linked subunits of 90 kD; each monomer can bind one molecule of TF. The intracellular domain of the receptor subunits contains specific signals for uptake in clathrin-coated vesicles (Trowbridge et al., 1993).African trypanosomes, the causative agents of sleeping sickness in humans and Nagana in cattle, are unicellular, flagellated protozoa that live extracellularly in the blood Address all correspondence to P. Overath,