Moulds on leaves of perennial ryegrass and white clover

Spore trapping llnd a herbage washing technique were used to follow seasonal changes of fungal spore numbers in ryegrass-white clover pasture from November (spring) 1968 to July (mid-winter) 1970. Spores of five parasitic fungi and of eight saprophytes were regularly counted. Numbers were highest in late summer and autumn, and were generally. similar in mown and grazed plots.Numbers of crown rust (Puccinia coronata Corda) spores were greatest when pasture growth rate had fallen to its lowest summer level, and their peak preceded the peak numbers of spores of saprophytic fungi by about 2 weeks. It is concluded that ryegrass killed by crown rust is an important component of the pasture debris on which the saprophytes grew. The importance of clover pathogens in providing substrate for the saprophytes is less obvious.In addition, the effects of benomyl on spore numbers were studied. The fungicide was sprayed on pasture according to recommendations for prevention of facial eczema disease of sheep. In benomyl plots spore populations of the fungi studied decreased, increased, or were unchanged as follows: Decreased: Cercospora zebrina Pass. It is suggested that a fungicide that would control P. coronata and Pithomyces chartarum as effectively as benomyl controls P. chartarum would further reduce the risk of facial eczema disease of sheep.

Section: Discussionsupporting

confidence: 76%

“…di Menna and Parle (1970) cultured the washings from leaves to estimate fungi on live and dead ryegrass and clover leaves. They examined pasture samples at weekly intervals through two years.…”

Section: Introductionmentioning

confidence: 99%

Seasonal changes in fungal spore numbers in ryegrass white clover pasture, and the effects of benomyl on pasture fungi

McKenzie¹

1971

“…However, proportions of non-sporidesmin-producers have been relatively low in New Zealand pastures (Collin et al 1996(Collin et al ,1998a, and Ulocladium spp. seem to be absent from or rare in the New Zealand pasture microflora, as are those of Pithomyces other than P. chartarum (di Menna & Parle 1970;McKenzie 1971;Latch et al 1976). …”

Section: Spore Counts In Pasturementioning

confidence: 99%

A history of facial eczema (pithomycotoxicosis) research

Menna

Smith²,

Miles

2009

Facial eczema (pithomycotoxicosis), a photosensitisation of ruminants grazing pasture, has been known in New Zealand for over 100 years, but its cause, a toxin produced by a largely saprophytic fungus, Pithomyces chartarum, growing on litter at the base of pasture and sporing profusely under warm moist conditions in late summer and autumn, was found only 50 years ago. As the fungus spores it produces the toxin sporidesmin which, when eaten by sheep, cattle, goats or deer, causes liver injury with inflammation and blockage of bile ducts. Phylloerythrin, a photodynamic breakdown product of chlorophyll, is no longer excreted but circulates in the blood, causing lesions of unpigmented skin when the affected animal is exposed to sunlight. Lesions do not appear until at least a week after sporidesmin has been ingested, and this lag period delayed discovery of the causative agent, first thought to have been an abnormal metabolite of rapidly growing ryegrass. However, before the role of P. chartarum was discovered, the pathology of the disease had been described, toxic extracts had been made from herbage mown from pastures A08061; Online publication date 21 October 2009 Received 8 October 2008 accepted 4 September 2009 associated with facial eczema outbreaks, and the weather conditions preceding outbreaks had been defined. When the causative agent was identified, cultures of P. chartarum on artificial media produced sporidesmin for chemical characterisation and animal dosing trials. Control of facial eczema in the field was first by avoiding toxic pasture, detected by P. chartarum spore counts on herbage, later by reducing P. chartarum pasture populations by spray application of substituted thiabendazole fungicides, and later still by protecting animals with oral doses of zinc at close to toxic levels. Sheep vary widely in their sensitivity to sporidesmin, either under field conditions in facial eczema outbreaks or when dosed orally with sporidesmin, and breeding resistant animals by selection after sporidesmin challenge is the best long-term control method at present. Whilst facial eczema outbreaks have been most severe in New Zealand, the disease has been reported from an increasing number of countries with warm temperate climates in which ruminants are intensively grazed on pasture. The great majority of New Zealand isolates of P. chartarum produce sporidesmin, but varying proportions of those in other countries do not.

“…Five replicates were used at each concentration, and the plates were incubated at 27°c for 10 days before final examination. Four of the P. chartarum strains were heavily sporing isolates recovered during a survey of fungi on leaves of pasture plants (di Menna and Parle 1970), and the fifth was strain C, a heavily sporing laboratory isolate used for sporidesmin production.…”

Section: Methodsmentioning

confidence: 99%

Fungicides and the control ofPithomyces chartarum

Parle

Menna

1972

Self Cite

Thiabendazole and 32 other fungicides were tested for in vitro activity against Pithomyces chartarum. Twelve materials, including copper, Captan, and the carbamates, were active only at 100 ppm or more, 14 were active at 10 ppm, and 7 at 1 ppm. Thirteen of those active at 10 ppm or less inhibited growth by prevention of germination, and 8 by prevention of germ tube elongation after germination. It was possible to assay levels of thiabendazole and benornyl between 0.05 and 0.2 ppm by the degree to which germ tube elongation was inhibited. Strain variation in sensitivity of P. chartarum was detected in only four fungicides. Prolonged cultivation on sublethal levels of thiabendazole did not confer resistance on P. chartarum.