14.10 Necrotrophic and biotrophic pathogens of plants

Plant pathogens are often divided into biotrophs and necrotrophs, (and, more recently, hemibiotrophs) according to their lifestyles. The definitions of these terms are:

  • biotrophs derive energy from living cells, they are found on or in living plants, can have very complex nutrient requirements and do not kill host plants rapidly;
  • necrotrophs derive energy from killed cells; they invade and kill plant tissue rapidly and then live saprotrophically on the dead remains;
  • hemibiotrophs have an initial period of biotrophy followed by necrotrophy.

This classification suggests a range of generalisations (Table 3) that together indicate clearly that the biotroph/necrotroph division is biologically meaningful. In particular, the genetic analysis of disease resistance with plants for which the full genomes are available, such as Arabidopsis thaliana, demonstrates that the division is based on how defence against fungal pathogens is controlled.

Table 3. Comparison of generalised characteristics of biotrophic and necrotrophic plant pathogens
Opportunistic, unspecialised (‘non-obligate’) pathogens Specialised (‘obligate’) pathogens
Host cells killed rapidly Cause little damage to the host plant; host cells not killed rapidly, but can induce hypersensitive cell death in incompatible interactions
Entry unspecialised via wounds or natural openings Entry specialised e.g. direct (mechanical) entry (powdery mildews) or through natural openings (rusts)
Secrete copious cell-wall-degrading (lytic) enzymes and toxins Few if any lytic enzymes or toxins are produced
Appressoria/haustoria not normally produced Possess appressoria or haustoria
Seldom systemic Often systemic
Usually attack weak, young or damaged plants Plants of all ages and vigour attacked
Wide host range Narrow host range
Easy to culture axenically Not easily cultured axenically
Survive as competitive saprotrophs Frequently survive on host or as dormant propagules
Controlled by quantitative resistance genes (example is Septoria nodorum blotch caused by Stagonospora nodorum) Controlled by specific (gene-for-gene) resistance genes (for example, tomato leaf mould, the rusts, powdery and downy mildews)
Growth within host is intercellular and intracellular through dead cells Growth within host is intercellular
Controlled by jasmonate- and ethylene-dependent host-defence pathways Controlled by salicylate-dependent host-defence pathways

Defence against biotrophic pathogens is largely due to programmed cell death in the host, and to associated activation of defence responses regulated by the salicylic acid-dependent pathway. Necrotrophic pathogens benefit from death of host cells, so they are not limited by this defence, but by responses activated by jasmonate acid and ethylene signalling pathways (see below). Such a ‘mode-of-defence’ division successfully distinguishes necrotrophs and biotrophs but it does limit the biotroph category to fungi that produce haustoria (Oliver & Ipcho, 2004; Glazebrook, 2005).

Table 4 gives some examples of necrotrophic and biotrophic pathogens, and includes some hemibiotrophic pathogens, like Phytophthora infestans, that exhibit characteristics of both biotrophs and necrotrophs.

Table 4. Some common plant pathogens
Botrytis cinerea
Grey mould
Blumeria (Erysiphe) graminis
Powdery mildew
Cochliobolus heterostrophus
Corn leaf blight
Uromyces fabae
Pythium ultimum
Damping off in seedlings
Ustilago maydis
Maize smut
Ophiostoma novo- ulmi
Dutch elm disease
Cladosporium fulvum
Tomato leaf mould
Fusarium oxysporum
Vascular wilt
Puccinia graminis
Black stem rust of cereals
Sclerotinia sclerotiorum
Soft rot
Phytophthora infestans
Potato late blight
Cladosporium fulvum, causing tomato leaf mould (also called a biotroph).
Colletotrichum lindemuthianum, causing anthracnose.
Magnaporthe grisea, causing rice blast (also called a necrotroph).
Phytophthora infestans, causing potato late blight (also called a biotroph by some, necrotroph by others).
Mycosphaerella graminicola, causing Septoria leaf blight.

Updated December 17, 2016