Ergot of pasture grasses

Note Number: AG0721
Rod Clarke, Knoxfield
Updated: November, 1999

Importance

Ergot, a fungal disease in pasture grasses, is caused by a number of species of Claviceps depending on the grass type, eg. Claviceps purpurea (ryegrasses), Claviceps paspali (paspalum) and Claviceps phalaridis (phalaris).

Severe infection by these fungi can render pasture grasses unsuitable for consumption by stock because of their toxic effects on the animals. Ergot on ryegrass can act as alternate hosts for the same disease on cereals, and in Australia, there is a nil tolerance to grain contaminated with ergot sclerotia (resting bodies). Contaminated seed lots can be rejected altogether or heavily discounted in price. The reason for the nil tolerance is that the sclerotia can be toxic to humans, and animals. Seed yield losses due to ergot are usually negligible, except in phalaris seed crops. Dairy cows grazing ergot infected paspalum, which is highly susceptible this disease, cease milk production and lose condition.

Symptoms

The characteristic symptom of this disease is the dark purplish sclerotia (resting body), that develop in place of healthy seed and protrude from the glume. These ergot sclerotia can be up to four times higher than the normal seed.

The appearance of the sclerotia is preceded by the honey dew stage which appears two to three weeks after flowering. The infected florets exude a yellow, sugary sticky fluid. Insects are attracted to feed on this exudate. Affected heads may appear dirty because of the accumulation of dust and pollen on the sticky honey dew.

The ergot of phalaris is not typical, as all florets of infected plants show symptoms. The fungus is systemic within the plant and, in a perennial grass such as phalaris, will persist in its host from season to season.

Biology

Survival: Claviceps spp. carry-over on alternate hosts and as sclerotia on the soil or mixed with seed.

Environmental conditions: Cool, wet weather in spring that delays pollination, and thus prolongs flowering, also favours germination of the sclerotia. Stands that tiller and flower unevenly or have a high degree of sterility can be severely affected by ergot.

Dispersal: The germinating sclerotia produce spores which are wind-blown and/or rain splashed onto open florets, where they infect the ovary. Within five days a honey dew is produced containing spores which serve as secondary inoculum. These spores are spread to other florets by contact, rain splash and insects.

Host Range: Clavicep. spp. occur on ryegrass, paspalum, water coach, phalaris, canary grass, cocksfoot, fescue, meadow grass, yorkshire grass as well as cereals.

Control

Use seed that is free of ergot sclerotia. Cultivation of infected soil should be greater than 40 mm, so that the germinating sclerotia cannot reach the soil surface to release spores. Paddock rotations using non host crops will help reduce sclerotia levels in the soil. Control of grasses within cereal crops will help prevent cross infection. This is best achieved by preventing seed set in the season before cropping, by clear fallowing, hard grazing or hay cutting, together with the use of selective herbicides. Headlands and roadsides should be mown before grasses mature to eliminate potential ergot reservoirs.

The advice provided in this publication is intended as a source of information only. Always read the label before using any of the products mentioned. The State of Victoria and its employees do not guarantee that the publication is without flaw of any kind or is wholly appropriate for your particular purposes and therefore disclaims all liability for any error, loss or other consequence which may arise from you relying on any information in this publication.