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

McKenzie, E. H. C.

doi:10.1080/00288233.1971.10427102

Cited by 30 publications

(12 citation statements)

References 8 publications

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“…The harmful effect of especially wide-spectrum fungicides on the buffering capacity of saprophytic fungi has been discussed, since it was found that fungicides affected the saprophytic colonization (Hislop and Cox, 1969;McKenzie, 1971;Dickinson, 1973;Jenkyn and Prew, 1973;Gross and Kenneth, 1973;Warren, 1974). Frahm (1973) reviewed several reports concerning increased infection after benomyl treatment by 9 pathogens tolerant to this fungicide.…”

Section: Discussionmentioning

confidence: 98%

The buffering capacity of the natural mycoflora of rye leaves to infection by Cochliobolus sativus, and its susceptibility to benomyl

Fokkema¹,

Laar²,

Nelis-Blomberg³

et al. 1975

Netherlands Journal of Plant Pathology

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Different densities of saprophytic colonization of rye leaves were obtained in field experiments by spraying with benomyl or water. In 1972 and in 1973, inoculation with Coehliobolus sativus, just after flowering, resulted in 60 % less necrosis on water-sprayed leaves than on benomyl-sprayed leaves. At that time, the natural mycoflora of the water-sprayed leaves amounted to 10 000 and 3000 propagules per cm 2 leaf surface in 1972 and 1973, respectively. The benomyl treatment reduced the colonization to 1200 and to 400 propagules per cm 2 in 1972 and 1973, respectively, which implied an apparent reduction of the antagonistic capacity of the mycoflora. In 1974, the saprophytic colonization of the water-sprayed leaves reached only 500 propagules per cm 2 just after flowering, a population density not high enough to be antagonistic. Benomyl had a differential effect on the phyllosphere fungi: Cryptoeoceus spp. were not affected, Sporobolomyces roseus and Cladosporium spp. were reduced to less than 6~ of the control populations, and Aureobasidium pullulans was eliminated. When later in the seasons of 1972 and 1974 the 'white yeasts' on the benomyl-sprayed leaves reached population densities of 6500 propagules per cm 2 and more, inoculation of these leaves resulted in a necrosis similar to that of the water-sprayed leaves with higher population densities. Above a population density of 6500 propagules per cm z no correlation existed between the density of the antagonists and their action on C. sativus.

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Section: Discussionmentioning

confidence: 98%

The buffering capacity of the natural mycoflora of rye leaves to infection by Cochliobolus sativus, and its susceptibility to benomyl

Fokkema¹,

Laar²,

Nelis-Blomberg³

et al. 1975

Netherlands Journal of Plant Pathology

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“…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

New Zealand Journal of Agricultural Research

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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.

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“…The seasonal pattern of highest teliospore numbers in spring and autumn, with low numbers in summer and winter, is in contrast with 13 other pasture fungi studied, which had highest spore numbers in a single period from late summer to early autumn (McKenzie 1971). Cole, Massie, and Duich (1970) reported a similar phenomenon in Pennsylvania, where stripe smut damage to 'Merion' Kentucky bluegrass (Poa pratensis L.) is most severe in spring, but less severe during a secondary period of symptom development in autumn.…”

Section: Resultsmentioning

confidence: 48%

“…The maximum count of approximately 8 million teliospores/g dry weight of herbage can be compared with a maximum of 12 million crown rust (Puccinia coronata Corda) spores recorded in the same pasture in March 1969 (McKenzie 1971). During this study many other pastures in the Manawatu were sampled.…”

Section: Resultsmentioning

confidence: 99%

Seasonal incidence of stripe smut (Ustilago striiformis(West.) Niessl) on ryegrass

McKenzie¹

1972

New Zealand Journal of Agricultural Research

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Seasonal changes in the numbers of stripe smut (Ustilago striijormis (West.) Niessl) teliospores on a ryegrass-white clover pasture were followed from spring 1968 to winter 1970. The maximum numbers of teliospores/g dry weight of herbage were approximately 2 million in autumn 1969, when the pasture was 1 year old, 6 million in the following spring, and 8 million in autumn 1970.At other sites teliospores were found on pasture only 3 months old, and increasing numbers were found on pastures up to, at least, 4 years old.

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

Cited by 30 publications

References 8 publications

The buffering capacity of the natural mycoflora of rye leaves to infection by Cochliobolus sativus, and its susceptibility to benomyl

The buffering capacity of the natural mycoflora of rye leaves to infection by Cochliobolus sativus, and its susceptibility to benomyl

A history of facial eczema (pithomycotoxicosis) research

Seasonal incidence of stripe smut (Ustilago striiformis(West.) Niessl) on ryegrass

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