Interactions among co‐infecting pathogens are common across host taxa and can affect infectious disease dynamics. Host nutrition can mediate these among‐pathogen interactions, altering the establishment and growth of pathogens within hosts. It is unclear, however, how nutrition‐mediated among‐pathogen interactions affect transmission and the spread of disease through populations. We manipulated the nitrogen (N) and phosphorus (P) supplies to oat plants in growth chambers and evaluated interactions between two aphid‐vectored Barley and Cereal Yellow Dwarf Viruses: PAV and RPV. We quantified the effect of each virus on the other’s establishment, within‐plant density, and transmission. Co‐inoculation significantly increased PAV density when N and P supplies were low and tended to increase RPV density when N supply was high. Co‐infection increased PAV transmission when N and P supplies were low and tended to increase RPV transmission when N supply was high. Despite the parallels between the effects of among‐pathogen interactions on density and transmission, changes in virus density only partially explained changes in transmission, suggesting that virus density‐independent processes contribute to transmission. A mathematical model describing the spread of two viruses through a plant population, parameterized with empirically derived transmission values, demonstrated that nutrition‐mediated among‐pathogen interactions could affect disease spread. Interactions that altered transmission through virus density‐independent processes determined overall disease dynamics. Our work suggests that host nutrition alters disease spread through among‐pathogen interactions that modify transmission.

Application of plant growth promoting bacteria may induce plant salt stress tolerance, however the underpinning microbial and plant mechanisms remain poorly understood. In the present study, the specific role of phenazine production by rhizosphere-colonizing Pseudomonas in mediating the inhibitory effects of salinity on wheat seed germination and seedling growth in four different varieties was investigated using Pseudomonas chlororaphis 30-84 (wild type) and isogenic derivatives deficient or enhanced in phenazine production. The results showed that varieties differed in how they responded to the salt stress treatment and the benefits derived from colonization by P. chlororaphis 30-84. In all varieties, the salt stress treatment significantly reduced seed germination, and in seedlings, reduced relative water content, increased reactive oxygen species (ROS) levels in leaves, and in three of four varieties, reduced shoot and root production compared to the no salt stress treatment. Inoculation of seeds with Pseudomonas chlororaphis 30-84 wild type or derivatives promoted salt-stress tolerance in seedlings of the four commercial winter wheat varieties tested, but the salt-stress tolerance phenotype was not entirely due to phenazine production. For example, all P. chlororaphis derivatives (including the phenazine-producing mutant) significantly improved relative water content in two varieties, Iba and CV 1, for which the salt stress treatment had a large impact. Importantly, all P. chlororaphis derivatives enabled the salt inhibited wheat varieties studied to maintain above ground productivity in saline conditions. However, only phenazine-producing derivatives enhanced the shoot or root growth of seedlings of all varieties under nonsaline conditions. Notably, ROS accumulation was reduced, and antioxidant enzyme (catalase) activity enhanced in the leaves of seedlings grown in saline conditions that were seed-treated with phenazine-producing P. chlororaphis derivatives as compared to noninoculated seedlings. The results demonstrate the capacity of P. chlororaphis to improve salt tolerance in wheat seedlings by promoting plant growth and reducing osmotic stress and a role for bacterial phenazine production in reducing redox stress.

Rhizosphere colonizing plant growth promoting bacteria (PGPB) increase their competitiveness by producing diffusible toxic secondary metabolites, which inhibit competitors and deter predators. Many PGPB also have one or more Type VI Secretion System (T6SS), for the delivery of weapons directly into prokaryotic and eukaryotic cells. Studied predominantly in human and plant pathogens as a virulence mechanism for the delivery of effector proteins, the function of T6SS for PGPB in the rhizosphere niche is poorly understood. We utilized a collection of Pseudomonas chlororaphis 30–84 mutants deficient in one or both of its two T6SS and/or secondary metabolite production to examine the relative importance of each T6SS in rhizosphere competence, bacterial competition, and protection from bacterivores. A mutant deficient in both T6SS was less persistent than wild type in the rhizosphere. Both T6SS contributed to competitiveness against other PGPB or plant pathogenic strains not affected by secondary metabolite production, but only T6SS-2 was effective against strains lacking their own T6SS. Having at least one T6SS was also essential for protection from predation by several eukaryotic bacterivores. In contrast to diffusible weapons that may not be produced at low cell density, T6SS afford rhizobacteria an additional, more immediate line of defense against competitors and predators.

13Ecological theory that predicts the effects of resource availability on species interactions has 14 been explored across a range of systems. Yet, application of this theory to communities of host-15 associated pathogens has been limited. Host resources and diet can impact disease severity and 16 prevalence, and these resource effects on disease may be mediated by pathogen-pathogen 17 interactions within hosts infected with multiple pathogens. As with free-living organisms, 18 pathogen species can alter each other's population growth rates, population densities, and 19 transmission to new hosts through facilitative or antagonistic processes. We used a model grass-20 virus system (Barley and Cereal Yellow Dwarf Viruses) to test the hypothesis that host nutrition 21 can constrain virus-virus interactions by simultaneously determining both within-host density 22 and transmission to new hosts. Hosts (oats) were grown in growth chambers with different 23 concentrations of soil nitrogen (N) and phosphorus (P) and infected with one or both viruses (i.e., 24 coinfection). We quantified the impacts of nutrient addition on virus-virus interactions through 25 within-host density (i.e., the concentration of viruses in a plant) and transmission to new hosts. 26Nutrients promoted facilitation of one virus (CYDV-RPV) through increased density (elevated 27 N) and increased transmission (elevated N and P) with coinfection relative to single infection. 28The other virus (BYDV-PAV) experienced facilitation through increased density when nutrients 29 were limited, but nutrient addition led to antagonistic effects of coinfection on density (elevated 30 N and P) and transmission (elevated N). Our results highlight opportunities for novel insights 31 from testing predictions of community ecology in disease systems, including nutrient-dependent 32 facilitation and nutrient-mediated interactions during transmission that were not predicted by 33 within-host dynamics. This study contributes to the growing literature on ecological interactions 34 among coinfecting pathogens by demonstrating that resource availability can mediate pathogen-35 pathogen interactions both within hosts and during transmission. 36 37