An evolutionary trade‐off between parasite virulence and dispersal at experimental invasion fronts

Abstract

Exploitative parasites are predicted to evolve in highly connected populations or in expanding epidemics. However, many parasites rely on host dispersal to reach new populations, potentially causing conflict between local transmission and global spread. We performed experimental range expansions in interconnected microcosms of the protozoan Paramecium caudatum, allowing natural dispersal of hosts infected with the bacterial parasite Holospora undulata. Parasites from range front treatments facilitated host dispersal and were less virulent, but also invested less in horizontal transmission than parasites from range cores. These differences were consistent with parameter estimates derived from an epidemiological model fitted on population‐level time‐series data. Our results illustrate how dispersal selection can have profound consequences for the evolution of parasite life history and virulence. Decrypting the eco‐evolutionary processes that shape parasite 'dispersal syndromes' may be important for the management of spreading epidemics in changing environments, biological invasions or in other spatial non‐equilibrium settings.

Travelling with a parasite: the evolution of resistance and dispersal syndromes during experimental range expansion

“…As we have shown here, parasite-mediated selection may affect some dispersal syndrome components, but not others, or even modify the correlation between these components. Moreover, a full picture would require measurements of growth, dispersal, and movement in the presence of infection, thereby integrating aspects or virulence / tolerance or context-dependent dispersal [53,54]. In a next step towards a more comprehensive understanding of eco-evo feedbacks, future experiments can use multi-microcosm landscapes to actually measure range expansion speeds for the different types of evolved hosts, with and without parasite.…”

“…Each new growth cycle was started by placing on average 200 paramecia from front and core treatments in 20 mL of fresh bacterised medium, and equilibrium density was then reached within the following 3-4 days. The experiment was conducted with a single host line [53]. This line (63D) had undergone three years of parasite-free core selection prior to the present experiment; initially started from a mix of strains, it has become fixed for a single cytochrome oxydase I haplotype [57].…”

Virulence constrains transmission even in the absence of a genetic trade-off

“…S2) and other systems (Dutta et al, 2021;Little et al, 2008;Louhi et al, 2013;Mackinnon and Read, 1999a). This may enhance the ability to cope with variability in host populations (Dutta et al, 2021;Nørgaard et al, 2021), which is particularly relevant for generalist parasites, such as T. urticae. In the absence of a genetic link with virulence, transmission may instead vary with other factors such as host availability and variability (King and Lively, 2012;Parsche and Lattorff, 2018).…”

The three Ts of virulence evolution during zoonotic emergence

“…Mycoplasma gallisepticum [28] (virulence-transmission rate) high susceptible density at the start of an epidemic selects for higher virulence Escherichia coli/bacteriophage lambda [29] structured host populations select for less transmissible, prudent strategies Escherichia coli/T4 coliphage [30]; Plodia interpunctella/granulosis virus [31]; Escherichia coli/ bacteriophage lambda [32] high virulence can trade-off with decreased host movement Danaus plexippus/Ophryocystis elektroscirrha [33]; Haemorhous mexicanu/Mycoplasma gallisepticum [34]; Paramecium caudatum/Holospora undulata [35] virulence evolves in natural epidemics of emerging disease…”