The Hazard Form Toxic Fungi in Australia

Culvenor, C. C. J.

doi:10.1111/j.1751-0813.1974.tb05254.x

Cited by 13 publications

(12 citation statements)

References 55 publications

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“…The toxicity of ergots is attributable to alkaloids that are amides and polypeptides derived from lysergic acid and isolysergic acid (Culvenor 1974). Some alkaloids have a direct stimulating effect on smooth muscle, causing vasoconstriction, ischemia of the extremities, necrosis and gangrene (Van Rensburg and Altenkirk 1974).…”

Section: Discussionmentioning

confidence: 99%

Induction of heat stress in beef cattle by feeding the ergots of Claviceps purpurea

Ad¹,

Bakau

et al. 1989

Aust Veterinary J

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Two groups of 4 Hereford steers were housed in a controlled environment room and exposed to simulated high summer temperatures. Both groups were fed a barley grain and hay diet ad libitum. The barley in one diet contained 0.5% w/w ergots of Claviceps purpurea. Within one week of feeding the ergot diet mean rectal temperature was significantly elevated (P less than 0.05) each afternoon (up to 41 degrees C) but returned to normal overnight. Elevated rectal temperature was accompanied by other signs of heat stress, reduced feed intake, body weight loss and depression or serum prolactin concentration. Symptoms disappeared within 1 week of ceasing to feed the ergot diet.

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Section: Discussionmentioning

confidence: 99%

Induction of heat stress in beef cattle by feeding the ergots of Claviceps purpurea

Ad¹,

Bakau

et al. 1989

Aust Veterinary J

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“…It is clear that fescue toxicosis results in major impacts on the cardiovascular system. These impacts include vasoconstriction, a thickened medial layer of blood vessels, endothelial cell damage, vascular stasis and thrombosis, ischemia, and finally gangrene (Thompson et al, 1950;Burfening, 1973;Culvenor, 1974;Garner and Cornell, 1978;Seawright, 1982;Coppock et al, 1989;Dyer, 1993;Oliver and Schultze, 1997;Shappell, 2003;Oliver, 1997Oliver, , 2005Klotz et al, 2007). The thickened medial layer of blood vessels in animals with fescue toxicosis has been linked to hyperplasia of the smooth muscle layer induced by ergot alkaloids, as reported by Strickland et al (1996) using isolated vascular smooth muscle cells in vitro.…”

Section: Vascular Functionmentioning

confidence: 99%

Physiological Basis of Fescue Toxicosis

Strickland

Aiken

Spiers

et al. 2015

Agronomy Monographs

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Tall fescue toxicosis continues to be a major syndrome in temperate climates of the world in terms of economic loss to animal producers. Studies with forage-fed animals over the past three decades have provided insight concerning the pathophysiological effects of the alkaloids present in tall fescue [Lolium arundinaceum (Schreb.) DarbyshJ infected with the fungal endophyte Neotyphodium coenophialum (Morgan-Jones and Gams) Glenn, Bacon, and Hanlin. To provide the reader a general understanding of the overall problem, we present a detailed discussion of the clinical signs of fescue toxicosis, the proposed toxicants, and projected solutions to this costly disease condition of ungulates. We also explore the physiological mechanisms proposed to be involved in the expression of the syndrome. Finally, we offer our suggestions for future research efforts in this arena and the potential impact of these approaches. T all fescue is an economically important cool-season perennial forage grass covering about 15 million ha in the United States alone (Buckner et al., 1979) and many more in continents outside North America (see Chapter 3, Hannaway et alv 2009, this publication). The vast majority of the tall fescue in the United States is grown within the transition zone of the eastern and central part of the country. With the development of novel nontoxic endophytes, tall fescue is again becoming increasingly popular for pastures in New Zealand and Australia. The wide distribution of tall fescue has been attributed to its symbiotic relationship (see Chapter 14, Christensen and Voisey, 2009, this publication) with the endophytic fungus Neotyphodium coenophialum (Glenn et al., 1996). Although beneficial to

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“…Chronic hepatotoxicity is the primary presentation for a number of hepatotoxins including pyrrolizidine alkaloids [31], phomopsins [32], sporidesmin [33] and aflatoxin B1 [8,34]. Chronic hepatic or cholestatic injury frequently results in ill-thrift, reduced feed intake and reduced weight gain and thus should be considered a differential diagnosis in cases of unexplained poor production.…”

Section: Clinical Findingsmentioning

confidence: 99%

“…The hepatotoxic agent may be a component of the plant or be produced by fungal organisms that colonize feed. Fungal growth or contamination of feed is highly dependent on environmental factors [7][8][9][10]. As such, disease caused by mycotoxins can be seen in many areas of Australia provided that environmental conditions support growth.…”

Section: Introductionmentioning

confidence: 99%

Plant and Fungal Hepatotoxicities of Cattle in Australia, with a Focus on Minimally Understood Toxins

Manthorpe

Jerrett

Rawlin

et al. 2020

Toxins

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Plant- and fungus-derived hepatotoxins are a major cause of disease and production losses in ruminants in Australia and around the world. Many are well studied and described in the literature; however, this is not the case for a number of hepatotoxicities with economic and animal welfare impacts, such as acute bovine liver disease (ABLD), brassica-associated liver disease (BALD) and Trema tomentosa, Argentipallium blandowskianum and Lythrum hyssopifolia toxicity. Additionally, significant overlap in the clinical presentation and pathology of these conditions can present a diagnostic challenge for veterinarians. This review summarizes the current and most recently published knowledge of common plant- and fungus-associated hepatotoxins affecting cattle in Australia, with a focus on the mechanisms of toxicity and distinguishing diagnostic features. Consolidation of the current understanding of hepatotoxic mechanisms in cattle provides insight into the potential mechanisms of lesser-known toxins, including cellular and subcellular targets and potential metabolic pathways. In the absence of specific etiological investigations, the study of epidemiological, clinical and pathological features of hepatotoxicity provides valuable insights into potential toxic mechanisms and is integral for the successful diagnosis and management of these conditions.

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The Hazard Form Toxic Fungi in Australia

Cited by 13 publications

References 55 publications

Induction of heat stress in beef cattle by feeding the ergots of Claviceps purpurea

Induction of heat stress in beef cattle by feeding the ergots of Claviceps purpurea

Physiological Basis of Fescue Toxicosis

Plant and Fungal Hepatotoxicities of Cattle in Australia, with a Focus on Minimally Understood Toxins

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