Minisatellite marker analysis of Trypanosoma brucei: Reconciliation of clonal, panmictic, and epidemic population genetic structures

The African trypanosome, Trypanosoma brucei, has been shown to undergo genetic exchange in the laboratory, but controversy exists as to the role of genetic exchange in natural populations. Much of the analysis to date has been derived from isoenzyme or randomly amplified polymorphic DNA data with parasite material from a range of hosts and geographical locations. These markers fail to distinguish between the human infective (T. b. rhodesiense) and nonhuman infective (T. b. brucei) “subspecies” so that parasites derived from hosts other than humans potentially contain both subspecies. To overcome some of the inherent problems with the use of such markers and diverse populations, we have analyzed a well-defined population from a discrete geographical location (Busoga, Uganda) using three recently described minisatellite markers. The parasites were primarily isolated from humans and cattle with the latter isolates further characterized by their ability to resist lysis by human serum (equivalent to human infectivity). The minisatellite markers show high levels of polymorphism, and from the data obtained we conclude that T. b. rhodesiense is genetically isolated from T. b. brucei and can be unambiguously identified by its multilocus genotype. Analysis of the genotype frequencies in the separated T. b. brucei and T. b. rhodesiense populations shows the former has an epidemic population structure whereas the latter is clonal. This finding suggests that the strong linkage disequilibrium observed in previous analyses, where human and nonhuman infective trypanosomes were not distinguished, results from the treatment of two genetically isolated populations as a single population.

Loss of speciation rate will impoverish future diversity

Human activities have greatly reduced the amount of the earth's area available to wild species. As the area they have left declines, so will their rates of speciation. This loss of speciation will occur for two reasons: species with larger geographical ranges speciate faster; and loss of area drives up extinction rates, thus reducing the number of species available for speciation. Theory predicts steady states in species diversity, and fossils suggest that these have typified life for most of the past 500 million years. Modern and fossil evidence indicates that, at the scale of the whole earth and its major biogeographical provinces, those steady states respond linearly, or nearly so, to available area. Hence, a loss of x% of area will produce a loss of about x% of species. Local samples of habitats merely echo the diversity available in the whole province of which they are a part. So, conservation tactics that rely on remnant patches to preserve diversity cannot succeed for long. Instead, diversity will decay to a depauperate steady state in two phases. The first will involve deterministic extinctions, reflecting the loss of all areas in which a species can ordinarily sustain its demographics. The second will be stochastic, reflecting accidents brought on by global warming, new diseases, and commingling the species of the separate bio-provinces. A new kind of conservation effort, reconciliation ecology, can avoid this decay. Reconciliation ecology discovers how to modify and diversify anthropogenic habitats so that they harbor a wide variety of species. It develops management techniques that allow humans to share their geographical range with wild species.