Plant pathology

Plant pathology differs greatly from animal pathology. First and foremost, animals have an adaptive immune system that allows them to generate defences as new infections arise, but plants lack this capacity. Plants have a fixed immune system that either confers them resistance to a pathogen or doesn’t. Plant pathogens come in three general classes, necrotrophs, biotrophs, and hemibiotrophs. Necrotrophs are organisms that simply kill plant tissue upon infection using cellulase and hemicellulase, they tend to be generalists that can infect many plants. For biotrophs to go through their reproductive cycle they require live plant tissue and thus tend to infect specific hosts. Biotrophs will cause slowed senescence and will hijack plant cell machinery to generate metabolites for themselves rather than the plant. Lastly, hemibiotrophs are a mix between necrotrophs and biotrophs. In the first stage of their life cycle hemibiotrophs will act like biotrophs, hijacking plant tissue for their own purposes. In the second stage of their life cycle they will act as necrotrophs and kill the plant. Pathogens utilize three main ways of egress into a plant. They can either directly penetrate the plant through the use of a pilus or penetration cap, enter through pre-existing openings such as stomata, or enter through wounds. Plants have a series of defencive strategies to resist and counter infection. The first line of defence is physical, plants have a waxy cuticle and cell walls that aim to prevent direct access to plant cells. The second line of defence is specific, and is known as resistance (R) gene immunity that follows a gene for gene model. Pathogens produce effectors that aim to mask their presence, and plants produce proteins that are able to detect effectors. If a plant can produce a detector that recognizes even a single effector in a pathogen then it can defend against it, otherwise the plant will be infected. The methods of defence include production of toxins that kill the pathogen, synthesis of papillae to reinforce the cell wall, and a hypersensitive response that involves rapid cell death around the area of infection.