TOWARDS MANAGING THE FUNGUS CAUSING SPORIDESMIN TOXICITY

Background: Sporidesmin toxicity or Facial eczema is a liver disease of cattle caused by a fungus that lives in pasture moribund material of mainly ryegrass. Animals take in the fungal spores as they graze, the toxin damages the liver, condition and milk production decline, and sometimes animals are lost. The fungus responsible is Pseudopithomyces toxicarius. The research on five dairy farms in the Humansdorp district is aimed at understanding this fungus to predict when pastures become risky, and to give farmers practical ways other than counting spores to manage the risk.

How the fungus spreads and reproduces: Twelve new genetic markers were built and used to fingerprint 289 fungal strains collected across all four seasons. Among those strains, 53 distinct genetic types were found, which imply that the population is varied and well established rather than recently arrived. Almost all of the variation, about 98%, occurred within individual farms rather than between them, whereas the same dominant genetic types turned up on all five farms, and no type was confined to one property. This means the fungus moves freely across the district and the five farms share a single population.

The fingerprints also show how the fungus is multiplying. It is spreading mainly by making copies of itself rather than by sexual reproduction. However, the capacity for sexual reproduction has not been lost, and therefore occasional sexual reproduction in the field cannot yet be ruled out.

What this means for farmers:

● Sporidesmin toxicity needs to be managed across the district rather than farm by farm. Neighbouring farms carry the same fungal population, so a single farm acting alone gains only limited benefit from its own efforts.

● Because the fungus is multiplying mainly by copying itself, it appears to change slowly. Control measures developed now are therefore expected to remain effective rather than being outrun by the fungus.

● However, since both mating types are present, the capacity for sexual reproduction remains. This is being monitored, because a shift to sexual reproduction would allow the fungus to change faster.

Only one species makes the toxin: Not every fungus in this group is dangerous. Strains covering eleven species and species groups of Pseudopithomyces were screened; only Pseudopithomyces toxicarius produced sporidesmin, and every one of the twelve strains of P. toxicarius tested positive. Its closest relative, P. palmicola, does not make the toxin at all. Correct identification therefore matters a great deal, because two fungi that look and behave similarly in a pasture differ completely in the risk they carry.

Measuring the toxin, and why a standard is needed: Predicting risk from a pasture sample means measuring how much toxin is present, not simply whether it is there. At present, presence or absence can only be established, because no purified sporidesmin standard exists to measure against. Everything downstream, from comparing strains to estimating pasture risk, waits on that standard. This is currently a priority in development.

The genes behind the toxin: From sequencing the genomes of the fungus, the block of genes it uses to make sporidesmin were located. That block is almost identical to the published sporidesmin gene cluster, so the South African fungus makes the toxin by the same route as the fungus studied overseas. It also belongs to a well characterised family of

fungal toxin pathways. Within the block, two genes of particular interest have been identified: one that appears to build the toxin, and one that appears to act as the switch turning the pathway on. Proving which does what means disabling them one at a time and testing whether the fungus can still make the toxin. If the toxin-building gene and its switch can both be confirmed, two practical outcomes follow: a rapid test that identifies toxin-producing strains directly from their genes, and a target for interrupting toxin production.

What comes next:

● Direct tests for sexual reproduction in the Eastern Cape population, and repeat laboratory crosses at a lower temperature.

● Breaking the fingerprinted strains down by season and by collection trip, to establish whether the same population persists year-round or turns over through the year.

● Completing the purified sporidesmin standard, so that toxin levels can be measured rather than only detected.

● Generating stable mutants to confirm which gene builds the toxin and which controls it.