CASE NOTES
Endophytes of Fescue and Perennial Ryegrass
Chris Bourke, Principal Research Scientist (Poisonous Plants)
Orange Agricultural Institute, Forest Rd Orange NSW
Posted Flock & Herd February 2011
Endophytes are fungi that live inside plants, frequently grasses. They are transmitted in the seeds of the infected plant. There is no sign of their presence when the plant is examined with the naked eye, but they can be seen microscopically using special stains. Endophytes offer the plant protection from diseases and pests and are consequently very beneficial to the plant's survival. Endophytes come as either wild types or as specifically cultivated types. Wild endophyte toxins in Tall fescue (Festuca arundinacea), or Perennial ryegrass (Lolium perenne), or Hybrid ’annual’ ryegrasses (Perennial x Italiani.e. L perenne x L multiflorum), can cause livestock problems but most of the time they do not.
Fescue is predominantly a summer growing plant and the ryegrasses predominantly spring and autumn growing plants. Seed retaining ’autumn saved’ pastures are typically fescue pastures not ryegrass pastures, since the latter will have dropped its seed by this stage. The seed of endophyte plants can be very high in endophyte toxins and consequently it poses the highest livestock risk. However when these plants are grazed very hard the butt of the plant may be ingested and this can be just as high in endophyte toxins as the seed head. Both of these situations can be managed around once they are understood.
Wild endophytes that occur in Australian Tall fescue and Perennial ryegrass can produce an ergot alkaloid called ergovaline. In addition endophytes in PRG can also produce a toxin called lolitrem B. Toxin producing endophyte activity is very seasonal within a year and very variable from year to year. Toxin production tends to kick off in Nov-Dec, peak in Feb-March, and turn off in May-June. A wet spring followed by a dry summer and autumn will favour higher toxin production levels. The highest risk period for potentially toxic egovaline levels is generally around Jan-Feb and for lolitrem B around March-April.
Toxic levels of ergovaline can cause a group of clinical signs collectively referred to as 'summer Ilthrift’ and toxic levels of lolitrem B can cause the syndrome known as Ryegrass Staggers (covered elsewhere under 'staggers syndromes’). The signs of 'summer Ilthrift’ occur together as a single syndrome but some commentators give this a more negative spin by presenting each clinical sign in isolation as though it were a separate disorder.
If either Tall fescue or Perennial ryegrass, in the seeding growth stage, is fed to livestock during cold winter weather, in the form of autumn saved pasture paddocks or as silage or as hay, then it is possible for the ergovaline toxin that it contains to cause a form of peripheral gangrene called ’Fescue foot’. This problem is very rarely seen in Australian livestock, and so far it has only ever occurred with Tall fescue plant material not with Perennial ryegrass.
Endophyte toxin effects in livestock will usually only occur when animals are either grazing very, short pastures, for example in cell grazing or crash grazing systems, or very tall mature pastures that have set seed, for example autumn saved pastures.
Silage and hay that has been made from seeding growth stage endophyte infected grass pastures can also be toxic. The ensiling process will only reduce ergovaline levels by up to 20% but sun curing cut pasture prior to hay baling can reduce levels by up to 70%. Nitrogen fertilisation of at risk pastures should be delayed till late autumn because late summer applications can cause up to a 100% increase in ergovaline levels in subsequent weeks.
Ergovaline induced 'summer Ilthrift’ is a transient syndrome the severity of which is directly related to the amount of ergovaline ingested in the total mixed daily diet. As ergovaline levels rise livestock reduce their voluntary ingestion of those plants and eat more of alternative species. Therefore the measured amount of ergovaline in an endophyte carrying grass sample from a mixed pasture can give a false indication of the overall pasture toxicity risk. Whereas in New Zealand the fescue or ryegrass component of a pasture may be 80 to 100% this is generally not the case in Australia. In fact in northern New South Wales the perennial ryegrass component of pastures is usually less than 20%. If 80 to 100% of a pasture consists of endophyte infected plants then it becomes much more difficult for the livestock grazing it to switch to grazing alternative species, hence the risk of toxicity will be higher.
The anti wild endophyte grass pastures people frequently speak about so called subclinical or hidden livestock health and production effects. This is really a bit of nonsense since all of the potential effects of endophyte toxins can be either seen or measured. The determining factor for toxic effects is the total amount of toxin present in each kg of the total dry matter ingested off a pasture, by each animal, each day.
For ergovaline and sheep, the ingestion of < 0.8 mg ergovaline per kg of dry matter causes no effects. Ingestion of somewhere between 0.8 and 1.2 mg by sheep may cause inappetence, hence a consequent transient decrease in weight gain and milk production. When the ingestion level reaches 2.0 mg or greater, mild diarrhoea may occur, hyperthermia (hence increased salivation and respiration) may occur, and a degree of true agalactia (a direct reduction in milk production) may be experienced. Compensatory weight gain will follow as soon as the ergovaline intake declines. The corresponding ergovaline values for cattle are < 0.4, between 0.4 and 0.8, and 1.2 mg or greater respectively. The values for horses are < 0.4, between 0.4 and 0.6, and 1.0 mg or greater respectively. It remains a possibility that ruminants suffering from a significant ergovaline induced hyperthermia may be at risk of death should they be denied access to shade for more than 3 consecutive hours on a bright sunny day. No cases have so far been reported for endophyte affected animals but they have been reported for animals affected by ergot of rye hyperthermia.
For all animal species lolitrem B ingestion levels of between 1.8 and 2.0 mg of lolitrem per kg of dry matter per day can result in signs of ryegrass staggers. In most years the total amount of toxin present in each kg of total dry matter ingested off a typical New South Wales fescue or perennial ryegrass containing mixed pasture will be less than 1.2 mg for ergovaline and 1.8 mg for lolitrem B, consequently 'summer Ilthrift’ and ’Ryegrass Staggers’ are only very occasionally encountered, and ’Winter Lameness’ is a very, very, rare event.
From the animal health and production information provided above it would not be hard, if it suited your purposes, to present a very negative spin on wild endophyte carrying PRG pastures. However there is very little evidence from Australian pastures that the potential livestock problems associated with PRG are anything more than an occasional nuisance that can be managed around. That said, the New Zealand based commercial pasture seed industry, its Agresearch New Zealand pasture research co-operators, and individuals within the Victorian Dept of Primary Industries have chosen to put a doom and gloom spin, on the speculated potential livestock problems that may or may not occur, on Australian wild endophyte carrying PRG pastures. I can only assume that they are well intentioned in their current enthusiasm for replacing wild endophyte PRG with expensive, tailor made, trademarked, endophyte selected, PRG varieties. In NSW at least this enthusiasm would seem to be misplaced.
In my experience it is better to manage around an existing but predictable low risk pasture plant livestock problem then it is to replace the plant with new varieties that may or may not remove some current livestock problems only to replace them with a different set of new ones. All of the major selected pasture plant species grown in southern Australia come with some degree of livestock risk. The best approach is to understand the risk and manage around it. For example 30 years of phalaris plant breeding has still not produced a livestock safe phalaris variety, despite the hopes, promises, enthusiasm and best intentions of all of those involved in this process. The good news is that 30 years on research directed at the phalaris livestock problems themselves has established a much greater understanding of the problems and as a consequence much better pasture management strategies to avoid them.