Pathogen evolution poses the critical challenge for infectious disease management in the twenty-first century. As is already painfully obvious in many parts of the world, the spread of drug-resistant and vaccine-escape (epitope) mutants can impair and even debilitate public and animal health programs. But there may also be another way in which pathogen evolution can erode the effectiveness of medical and veterinary interventions. Virulence- and transmission-related traits are intimately linked to pathogen fitness and are almost always genetically variable in pathogen populations. They can therefore evolve. Moreover, virulence and infectiousness are the target of medical and veterinary interventions. Here, we focus on vaccination and ask whether large-scale immunization programs might impose selection that results in the evolution of more-virulent pathogens.
The word virulence is used in a variety of ways in different disciplines. We take a parasite-centric view as follows. We use “disease severity” (morbidity and/or mortality) to mean the harm to the host following infection. Disease severity is thus a phenotype measured at the whole-organism (host) level that is determined by host genes, parasite genes, environmental effects, and the interaction between those factors. One component of this is virulence, a phenotypic trait of the pathogen whose expression depends on the host. Thus, virulence is the component of disease severity that is due to pathogen genes, and it can be measured only on a given host. We assume no specificity in the interaction between host and pathogen (more-virulent strains are always more virulent, whatever host they infect).
We review methods for studying the adaptive basis of sex allocation in the phylum Apicomplexa, a group of parasitic protozoa that includes the aetiological agents of malaria. It is our contention that analysis of apicomplexan sex ratios is not only interesting in its own right, but may actually provide insights into matters of clinical and epidemiological importance. We begin by justifying that position, and then summarize the natural history of these parasites and the sex ratio expectations that flow from that. Broadly speaking, these expectations are supported, but the evidence is scanty relative to that for many multicelled taxa. In the second half of the chapter, we give an overview of the theoretical and empirical methods available to take this work further. Much remains to be done: many key assumptions are currently little more than acts of faith.
Almost all work on the evolution of sex allocation is motivated by and tested on multicelled organisms. Yet the causative agents of some of the most serious diseases of humans and livestock have anisogamous sexual stages (Figure 15.1). These are all members of the protozoan phylum Apicomplexa, and include the malaria parasites (Plasmodium spp.). Species in other protozoan phyla can also have anisogamous sexual stages (e.g. some dinoflagellates, volvocidians and perhaps some foraminiferans; Lee et al. 1985) but we are unaware of any analysis of sex allocation in micro-organisms other than the Apicomplexa.
Malaria, a disease caused by protozoan parasites of the genus Plasmodium, can substantially reduce host fitness in wild animals (Atkinson and Van Riper 1991; Schall 1996). In humans, the major disease syndromes – severe anemia, coma, and organ failure, as well as general pathology such as respiratory distress, aches, and nausea – cause considerable mortality and morbidity (Marsh and Snow 1997).
Biomedical research attributes malaria to red cell destruction, infected cell sequestration in vital organs, and the parasite-induced release of cytokines (Marsh and Snow 1997). But mechanistic explanations are just one type of explanation for any biological phenomenon, and, in recent years, evolutionary biologists have become interested in offering evolutionary explanations of infectious disease virulence. This is entirely appropriate (Read 1994). In the context of malaria, for example, the clinical outcome of infection has an important impact on parasite and host fitness and is – at least in part – determined by heritable variation in host and parasite factors (Greenwood et al. 1991). Yet in the recent rush to provide evolutionary explanations of disease, there has been, in our view, too little interaction between the models built by evolutionary biologists and reality. There is unlikely to be a simple, general model of virulence: the causes of disease and the fitness consequences for host and parasite are too variable. Instead, different models, and even different frameworks, will be relevant in different contexts.
Email your librarian or administrator to recommend adding this to your organisation's collection.