Theories of speciation, in the past often couched in verbal terms, should explain how ecological divergence and genetically determined reproductive isolation evolve between lineages that originate from single, genetically homogeneous ancestral populations. As Will Provine highlights in Chapter 2, the predominant perspective for a long time was that reproductive isolation emerges as a by-product of other evolutionary processes, through the incidental accumulation of genotypic incompatibility between related species. It is easiest to imagine that such incompatibilities arise when subpopulations become geographically isolated and henceforth evolve independently: genetic distance between them is then expected to increase with time. Thus, “given enough time, speciation is an inevitable consequence of populations evolving in allopatry” (Turelli et al. 2001). On a verbal level this theory of allopatric speciation appears both simple and convincing. This apparent theoretical simplicity has contributed to the view that the allopatric mode of speciation is the prevalent one – a perspective that has found its most prominent advocate in Ernst Mayr (Chapter 2).

Unfortunately, not only is the simplicity of the usual accounts of allopatric speciation based on the poorly understood concept of genetic incompatibility, but simplicity in itself is no guarantee for ubiquitous validity. Other plausible, but theoretically more intricate, mechanisms for the evolution of reproductive isolation in the absence of geographic isolation have been proposed. Recent approaches have focused attention on adaptive processes that lead to ecological and reproductive divergence as an underlying mechanism for speciation processes – a change in emphasis that occurred concomitantly with a shift in biogeographic focus from allopatric scenarios to parapatric speciation between adjacent populations or fully sympatric speciation. This was foreshadowed by the idea of reinforcement (the evolution of prezygotic isolation through selection against hybrids) and has culminated in theories of sympatric speciation, in which the emergence and divergence of new lineages result from frequency-dependent ecological interactions.

The authors of this book have been encouraged by the editors to stick their necks out and dream up strategies for virulence management, phrased as concretely as possible. As editors, we believe that good science proceeds by making definite predictions so that they can be rigorously put to the test. Phrasing predictions in the form of recommendations forces a healthy definitiveness; no one is allowed to hide under a slightly woolly phrasing. It must nevertheless be understood that not all the recommendations outlined here can as yet be taken at face value; many of the issues raised require additional theoretical and experimental research.

The stress on management aspects is the defining feature of this last part of the book. Whereas earlier parts review particular mechanisms of virulence evolution with a perspective on potentially ensuing options for virulence management, for this part of the book the authors were invited to focus on the following questions:

• For which specific empirical settings can the various possible options of virulence management strategies be expected to apply?

• For each given context, which options appear to be particularly promising?

• What are the open research questions that have to be addressed before measures of virulence management can be recommended for implementation?

After an introductory chapter that is meant to summarize what has been achieved so far, each chapter in this part covers one of the main potential arenas for virulence management: human, wildlife, and livestock diseases, crop protection, and pest control.

Part B explores the impact of host population structure on the evolution of infectious diseases. While simple models of disease ecology and evolution conveniently ignore this complication, the following three chapters underline its importance. It is shown that host population structure can qualitatively alter expectations for the course and outcome of virulence evolution.

By linking individual-based mechanisms of transmission to the demographic consequences of epidemics in host populations, simple mathematical models offer an essential prerequisite for understanding and influencing the virulence evolution of a disease. Elaborations on such models, accounting for three different types of host heterogeneity, are discussed in this part. First, even in the absence of any spatial structure, a host population may be physiologically structured with respect to certain features of individual hosts. Relevant features could be age and size or could directly relate to epidemiological processes like disease-induced mortality, recovery from an infection, or disease transmission (investigated in Chapter 6). Second, host populations can be viscous in the sense that individual hosts are connected, by spatial proximity or social relations, not to the host population as a whole but to a relatively small number of neighbors. Implications of such connectivity structures are analyzed in Chapter 7. Third, connections between hosts may be organized in a hierarchical way such that infections spread more easily within host groups than between groups.