Coinfection by multiple pathogen strains can alter disease dynamics at the within-host and population level. Yet, in wild plant populations, little is known about how sequential challenge by multiple pathogen strains affects epidemiology. For Plantago lanceolata and its fungal pathogen Podosphaera plantaginis, prior infection has been found to reduce subsequent infection severity in laboratory experiments. However, a field experiment showed no disease reduction in primed plants after weeks of exposure to natural epidemics. Here, we tested the genetic specificity and durability of immune priming in the Plantago-Podosphaera interaction. In Experiment 1, replicates of four host genotypes were divided into control and primed treatments. Priming involved inoculating a single leaf with one of four pathogen strains, then sealing the inoculated (or uninfected control) leaf in a spore-proof pouch. At 4 and 8 days later, plants were challenged with all four pathogen strains. In Experiment 2, the same host genotypes were exposed to epidemics in three natural populations for 10 days. These plants were either healthy controls, or were infected with a pathogen strain from that population 4 or 8 days prior. After both experiments, leaves were screened for infection, and lesions were genotyped to determine which pathogen strains succeeded in infecting.
Results/Conclusions
Previous infection did not protect plants from subsequent pathogen attack in either experiment. Instead, prior infection of a single leaf – sealed off to prevent transmission to other leaves on that plant – increased the probability that other leaves on the plant became infected following later inoculation or exposure to ambient pathogen strains. These results are consistent with previous work showing that coinfection by multiple pathogen strains promotes disease levels at the within-host and population levels. However, forthcoming results from a SNP genotyping panel will reveal the degree of genotype specificity in priming. That is, the multilocus genotype data will allow us to determine the frequency with which primed plants became infected with the priming strain, versus the other three strains they were exposed to in Experiment 1, or versus all other strains sequenced from natural populations in Experiment 2. Because our experiment employed multiple host genotypes, we will also be able to test whether specificity in priming varies with host genetic background. Understanding mechanisms by which repeated infections promote or mitigate disease is essential for assessing their potential as control strategies for agricultural plant species. Our results contribute valuable information about the epidemiological consequences of sequential infections.