Abstract
How do pathogens, whether they parasitize plants or animals, acquire virulence to new hosts and resistance to the arms we deploy to control disease? The significance of these questions for microbiology and for society at large can be illustrated by the recent worldwide efforts to track and limit the emergence of human transmissible strains of swine and avian influenza virus and of multidrug-resistant lines of human pathogenic bacteria, and to restrain the spread of Ug99, a strain of stem rust of wheat. Recent research in medical epidemiology has elucidated the impact of pathogen ecology in environmental reservoirs on the evolution of novel or enhanced pathogen virulence. In contrast, the evolution of virulence in plant pathogens has been investigated from a predominantly agro-centric perspective, and has focused overwhelmingly on evolutionary forces related to interactions with the primary plant host. Here, we argue that current concepts from the field of medical epidemiology regarding mechanisms that lead to acquisition of novel virulence, biocide resistance, and enhanced pathogenic fitness can serve as an important foundation for novel hypotheses about the evolution of plant pathogens. We present numerous examples of virulence traits in plant pathogenic microorganisms that also have a function in their survival and growth in nonagricultural and nonplant habitats. Based on this evidence, we make an appeal to expand concepts of the life history of plant pathogens and the drivers of pathogen evolution beyond the current agro-centric perspective.
Highlights
How do pathogens, whether they parasitize plants or animals, acquire virulence to new hosts and resistance to the arms we deploy to control disease? The significance of these questions for microbiology and for society at large can be illustrated by the recent worldwide efforts to track and limit the emergence of human transmissible strains of swine and avian influenza virus and of multidrug-resistant lines of human pathogenic bacteria, and to restrain the spread of Ug99, a strain of stem rust of wheat
A nonexhaustive list of its dual-use traits includes capsule formation and production of melanin, laccase, phospholipase, proteases, and ureases [8]. In the environment these traits contribute to survival and in human hosts they contribute to the capacity of C. neoformans to avoid host resistance mechanisms and to attack host tissue
A striking characteristic of many of the virulence factors of these plant pathogens is that they are linked to—or are in themselves—traits critical to adaptation to the nonplant environment, as will be illustrated below. This provides a compelling reason to adopt a holistic view of the life history and evolution of plant pathogens, to move beyond the traditional borders of agriculture and the presumed ‘‘primary’’ plant host
Summary
Whether they parasitize plants or animals, acquire virulence to new hosts and resistance to the arms we deploy to control disease? The significance of these questions for microbiology and for society at large can be illustrated by the recent worldwide efforts to track and limit the emergence of human transmissible strains of swine and avian influenza virus and of multidrug-resistant lines of human pathogenic bacteria, and to restrain the spread of Ug99, a strain of stem rust of wheat. Sapronoses are diseases transmitted to humans from environmental reservoirs where the pathogen thrives saprophytically These habitats include soil, water, and decaying plant and animal matter. Numerous environmental pathogens, including Cryptococcus neoformans, Legionella spp., Chlamydophila pneumoniae, Mycobacterium avium, Listeria monocytogenes, Pseudomonas aeruginosa, and Francisella tularensis, might have acquired virulence traits via their resistance to predation by amoebae This resistance, associated with the ability to grow inside the amoebae—which are essentially alternate hosts—has likely led to the selection of traits conferring survival in macrophages [7]. A nonexhaustive list of its dual-use traits includes capsule formation and production of melanin, laccase, phospholipase, proteases, and ureases [8] In the environment these traits contribute to survival and in human hosts they contribute to the capacity of C. neoformans to avoid host resistance mechanisms and to attack host tissue.
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