A 1984 study found plants that died following treatment with glyphosate were infected with pathogenic fungi, compared to control plants not treated with glyphosate but planted in the same media that did not yield pathogenic fungi.<ref>Gurmukh S. Johal and James E. Rahe, "[http://www.nationalorganiccoalition.org/resources/Biblio/glyphosatepathogenkillRahe.pdf Effect of soilborne plant-pathogenic fungi on the herbicidal action of glyphosate on bean seedlings]," ''Phytopathology'' (1984), 74:950-955.</ref> The study concluded that more research was needed but postulated that glyphosate inhibits the plant's defense mechanisms and/or increases nutrient leakage from treated plants.
When more research was completed, "Rahe and coworkers documented that severe root infection associated with glyphosate-treated plants was due to disruption of synthesis of plant defense compounds, or phytoalexins, through the shikimate pathway there by predisposing plants to attack by soilborne fungal pathogens (Johal and Rahe, 1988; Lévesqueet Lévesque et al., 1987).<ref>Johal, G.S., Rahe, J.E., 1988. Glyphosate, hypersensitivity and phytoalexins accumulation in the incompatible bean anthracnose host-parasite interaction. Physiol. Mol. Plant Pathol. 32, 267-281</ref><ref>Lévesque, C.A., Rahe, J.E., Eaves, D.M., 1987. Effects of glyphosate on ''Fusarium'' spp.: its influence on root colonization of weeds, propagule density in the soil, and crop emergence. Can. J. Microbiol. 33, 354-360.</ref> Thus, infection by soilborne pathogens caused by the inability of plants to synthesize phytoalexins contributed to the overall herbicidal efficacy of glyphosate and was considered a “secondary mode of action” of glyphosate. These findings were significant because the release of glyphosate into the environment was found to have considerably more and far-reaching effects than the original notion that was limited to only the localized disruption of a specific metabolic pathway within a target plant."<ref></ref>
== Impact on Non-Target Plants ==