Abstract
The coincidental virulence evolution hypothesis suggests that outside-host selection, such as predation, parasitism and resource competition can indirectly affect the virulence of environmentally-growing bacterial pathogens. While there are some examples of coincidental environmental selection for virulence, it is also possible that the resource acquisition and enemy defence is selecting against it. To test these ideas we conducted an evolutionary experiment by exposing the opportunistic pathogen bacterium Serratia marcescens to the particle-feeding ciliate Tetrahymena thermophila, the surface-feeding amoeba Acanthamoeba castellanii, and the lytic bacteriophage Semad11, in all possible combinations in a simulated pond water environment. After 8 weeks the virulence of the 384 evolved clones were quantified with fruit fly Drosophila melanogaster oral infection model, and several other life-history traits were measured. We found that in comparison to ancestor bacteria, evolutionary treatments reduced the virulence in most of the treatments, but this reduction was not clearly related to any changes in other life-history traits. This suggests that virulence traits do not evolve in close relation with these life-history traits, or that different traits might link to virulence in different selective environments, for example via resource allocation trade-offs.
Highlights
Compared to the vast knowledge on the prevention and treatment of bacterial infectious disease, relatively little is known about how the virulence of bacteria has evolved
This is a plausible expectation when considering opportunistic, environmentally growing bacterial pathogens because they typically live in a complex web of interactions with biotic and abiotic selection pressures that might not be directly connected to their potential hosts [7]
The population dynamics of bacterial prey and amoeba predators during the experiment The presence of predators generally reduced the bacterial biomass in free water phase (OD of the medium: F7, 52 = 674.620, p,0.001; Figure 2A)
Summary
Compared to the vast knowledge on the prevention and treatment of bacterial infectious disease, relatively little is known about how the virulence of bacteria has evolved. Virulence evolution is often exemplified as a tug of war between the multicellular host and the pathogen, where the virulence (the degree of host damage or mortality caused by the pathogen) [1] evolves solely through host-pathogen interaction [2,3,4] Contrary to this idea, the ‘‘coincidental evolution of virulence hypothesis’’ suggests that virulence evolves indirectly due to selection forces that are not related to the host-pathogen interaction per se, but because of selection that occurs outside host environments [2,3,5,6]. The biofilm-forming ability of many bacteria can be directly linked to the virulence of bacteria as it can prevent macrophage phagocytosis inside the multicellular host [11,14,15,16]
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