Facial Eczema

Hore, D. E.

doi:10.1111/j.1751-0813.1960.tb15310.x

Cited by 21 publications

(7 citation statements)

References 2 publications

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“…Soon after the cause of facial eczema had been reported from New Zealand, there were reports of cases of the disease in sheep from Victoria, australia (Hore 1960) and from Western Australia (Gardiner & Nairn 1962). Cases in sheep grazing "artificial pasture" in Cape Province, South africa were described by Marasas et al (1972), and in cattle in Uruguay by Riet & diaz (1974).…”

Section: Global Incidence Of Facial Eczemamentioning

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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Section: Global Incidence Of Facial Eczemamentioning

confidence: 99%

A history of facial eczema (pithomycotoxicosis) research

Menna

Smith²,

Miles

2009

New Zealand Journal of Agricultural Research

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“…chartarum, ecological conditions are probably not conducive to its proliferation. This would be supported by the limited geographical distribution of facial eczyma in Australia (Hore 1960;Connole and Johnston 1967;Edwards el a1 1981).…”

Section: Discussionmentioning

confidence: 97%

A syndrome of hepatogenous photosensitisation, resembling geeldikkop, in sheep grazing Tribulus terrestris

et al. 1984

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Two outbreaks of photosensitivity disease occurred in weaner sheep in south western New South Wales during early autumn 1982. In each instance there was a history of access to the annual herb, Tribulus terrestris and both the clinical and pathological findings were consistent with geeldikkop, a major disease in the Republic of South Africa. The prevalence rates of clinical cases were 21 and 37%, while the case fatality rates approached 70%. Clinical signs were dominated by jaundice and photosensitisation. Ochre and khaki discolouration were present in the liver and kidneys, respectively. Histopathologically, the most characteristic lesion was the presence of acicular, cholesterol-like clefts in the lumens of bile ducts and in the cytoplasm of hepatocytes and Kupffer cells. Similar structures were also evident in the lumens of nephrons in association with segmental hyperplasia of the neighbouring tubular epithelium. The possible pathogenesis of the hepatogenous photosensitisation and its resemblance to geeldikkop are discussed.

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“…Hence under these conditions the unaffected portion of the liver was apparently able to partially compensate for the damage. Therefore, it seems unlikely that most sheep with this degree of damage would be readily detected soon after (ie within 2-3 months) an outbreak of facial eczema, even though it has been found in the past that during periods of stress, for example, pregnancy or semi-starvation, such sheep fare much worse than normal sheep (Hore 1960).…”

Section: Discussionmentioning

confidence: 99%