Claviceps Purpurea - Life Cycle

Life Cycle

An ergot kernel called Sclerotium clavus develops when a floret of flowering grass or cereal is infected by a spore of C. purpurea. The infection process mimics a pollen grain growing into an ovary during fertilization. Because infection requires access of the fungal spore to the stigma, plants infected by C. purpurea are mainly outcrossing species with open flowers, such as rye (Secale cereale) and Alopecurus.

The proliferating fungal mycelium then destroys the plant ovary and connects with the vascular bundle originally intended for feeding the developing seed. The first stage of ergot infection manifests itself as a white soft tissue (known as Sphacelia segetum) producing sugary honeydew, which often drops out of the infected grass florets. This honeydew contains millions of asexual spores (conidia) which are dispersed to other florets by insects or rain. Later, the Sphacelia segetum convert into a hard dry Sclerotium clavus inside the husk of the floret. At this stage, alkaloids and lipids (e.g. ricinoleic acid) accumulate in the Sclerotium.

When a mature Sclerotium drops to the ground, the fungus remains dormant until proper conditions trigger its fruiting phase (onset of spring, rain period, need of fresh temperatures during winter, etc.). It germinates, forming one or several fruiting bodies with head and stipe, variously colored (resembling a tiny mushroom). In the head, threadlike sexual spores are formed, which are ejected simultaneously, when suitable grass hosts are flowering. Ergot infection causes a reduction in the yield and quality of grain and hay produced, and if infected grain or hay is fed to livestock it may cause a disease called ergotism.

Insects, including flies and moths, have been shown to carry conidia of Claviceps species, but if insects play a role in spreading the fungus from infected to healthy plants is unknown.