The adsorption of D-glucosamine (2-amino-2-deoxy-D-gIucose) in the protonated or neutral form on homoionic Cu2+-bentonite was investigated by infrared (IR) and electron spin resonance (ESR) spectroscopy and chemical analyses of solution. The results show that the interaction of the glucosamine hydrochloride with the clay complexed a small fraction of interlayer metal ions with neutral amino sugar molecules. In contrast, the adsorption of free glucosamine was much more favorable and resulted in interlayer copper(II) complexes, mainly those in which the ligand was coordinated through amino and deprotonated hydroxyl groups. Part of the amino sugar molecules, however, were transformed into glucosammonium, replacing copper as the saturating ion.

We are studying early events in the establishment of Trypanosoma brucei in the tsetse midgut using fluorescent trypanosomes to increase visibility. Feeding flies with the lectin-inhibitory sugars D-glucosamine (GlcN) or N-acetyl-glucosamine (GlcNAc) has previously been shown to enhance fly susceptibility to infection with trypanosomes and, as expected, we found that both sugars increased midgut infection rates of Glossina morsitans morsitans with T. brucei. However, GlcNAc did not show the inhibitory effect on salivary gland infection rate reported previously for GlcN. Both sugars significantly slowed the movement of the bloodmeal along the midgut. GlcN also significantly increased the size of the bloodmeal taken and fly mortality. The most surprising finding was that GlcNAc stimulated trypanosome growth not only in the midgut, but also in vitro in the absence of any factor derived from the fly. Thus our direct comparison of the effects of GlcN and GlcNAc on the trypanosome-tsetse interaction has shown that these sugars impact on trypanosome growth and tsetse physiology in different ways and are not interchangeable as suggested in the literature. The sugars cause multiple effects, not restricted solely to the inhibition of midgut lectins. These findings have implications for current models of tsetse susceptibility to trypanosome infection.