Toxic Pastures Research Articles

165 Does supplementation of beef cattle impact the agronomy performance of tall fescue and bermudagrass pastures?

Abstract In forage-based beef cattle systems, bermudagrass [Cynodon dactylon (L.) Pers.] and tall fescue (Festuca arundinacea Schreb.) stand as widely used forage species. The strategic supplementation of animals may reduce forage intake, thereby potentially affecting the agronomic performance of these grasses. Our objective was to evaluate the impact of beef cattle supplemental feeding on forage accumulation, forage mass, and nutritive value in tall fescue and bermudagrass pastures. Two studies were conducted where pregnant beef cows were supplemental fed 1% of BW on DM basis of corn silage daily (SUP) or received no supplemental feeding (free-choice mineral; NON). Trial 1: conducted on bermudagrass pastures (BERM) grazed from late May to early October. Experimental design for BERM was completely randomized design with 4 pastures per treatment (n = 3 cows/pasture; average 5 years of age; 550 ± 72 kg initial BW). Trial 2: conducted on fescue pastures (FES) with an experimental design of a 2 x 2 factorial arrangement. The two factors evaluated were fescue type [TOXIC (507 ppm ± 0.82 SEM ergot alkaloids; 92.5% endophyte infection)] or non-toxin-producing (NT; 5 ppm ± 2.50 SEM ergot alkaloids; 38.6% endophyte infection) and two levels of supplemental feeding (NON or SUP). There were 3 or 4 replications per fescue x supplemental feeding treatment (n = 15 pastures), stocked with 3 cows/pasture (average age 4.75 years; 558 ± 73 kg initial BW) and grazed from early May through November. Forage accumulation (FA) was estimated every 28 d using the paired-cage method (4 exclosure cages/pasture). On each exclusion period, the forage mass (FM) was estimated both inside and outside the cages through destructive sampling method and samples analyzed for forage quality. Pasture was experimental unit and repeated measures were included in analysis. Bermudagrass FM tended to be increased by 31% with SUP (P = 0.09; 774 kg/ha greater). Forage accumulation tended (P = 0.07) to be affected by feeding method x month. There was greater FA in June for SUP; however, there was greater FA for NON in July. SUP pastures had greater ADF (1% more; P = 0.01) and reduced TDN (1.5%; P < 0.01) than NON. Forage mass tended to be 10% greater for TOXIC pastures (P = 0.09; 409 kg/ha more forage mass). Supplemental feeding on fescue did not impact FM (P = 0.74). Forage accumulation was not impacted by fescue type, feeding method, nor the interaction (P > 0.30). Cows generally do not consume as much toxic fescue, thus more forage is available in pastures and supplemental feeding did not alter forage parameters. However, on a warm-season grass that is growing while supplemental feeding, forage availability was increased and maybe useful as method to increase stocking rates or as mitigation tool during drought.

Extraction and determination of the Pimelea toxin simplexin in complex plant-polymer biocomposites using ultrahigh-performance liquid chromatography coupled with quadrupole Orbitrap mass spectrometry.

In the present paper, we describe how a robust and fundamental methodology was developed for extraction and determination of a principal natural toxin compound, simplexin, from a series of bulk biocomposites. These complex matrices were fabricated by direct encapsulating either ground plant particles or an ethanolic crude extract of the Australian toxic pasture plant Pimelea trichostachya in the biodegradable polymer poly(3-hydroxybutyrate-co-3-hydroxyvalerate). Proton nuclear magnetic resonance spectroscopy was initially employed to examine the chemical compositions of these complicated systems. Then, a more sensitive strategy was developed and validated by combining solid-phase extraction and ultrahigh-performance liquid chromatography hyphenated with a quadrupole Orbitrap mass spectrometer for the quantification of simplexin embedded in different biocomposites. Satisfactory linearity (R2 > 0.99) and recovery ranges (86.8-116%) with precision (relative standard deviations) of between 0.2 and 13% (n = 3) were achieved from seven biocomposites. The established protocol was further shown to be accurate and reliable in confirming the homogeneous distribution of the simplexin in different biocomposite formulations. A limited mass transfer of simplexin (< 3.5%) from one of the biocomposites into a simulated but sterilized in vitro rumen environment after a 10-day incubation was also revealed by utilizing the method. This quantitative analysis of targeted natural product within plant material-integrated polymeric platforms has potential application when controlled release is required in the bovine rumen and other biological systems. Graphical abstract.

Changes in field concentrations of five phalaris alkaloids and their association with toxicity in pastures of Victoria, Australia

Phalaris aquatica is known to cause toxicity in livestock in the form of acute or chronic staggers or sudden death neurological (SDN) syndrome. Breeding of cultivars that produce lower concentrations of suspected alkaloid toxins has been conducted, but these cultivars continue to cause staggers and SDN toxicity. Field samples of grazed phalaris pasture were collected during one growth season (February–June 2016), and from pastures where cases of staggers and/or SDN had occurred in previous years, and immediately after two cases of toxicity. Pasture collected from a paddock where a case of SDN occurred 4 days prior had elevated levels of 5-methoxy-N,N-dimethyltryptamine (5-MeO DMT) and slightly elevated levels of dimethyltryptamine (DMT) compared with other collections from the region. Pasture collected from a paddock at the time of a case of phalaris staggers did not have elevated levels of the quantified alkaloids. Across the measurement period, potentially toxic alkaloids gramine, hordenine, DMT and 5-MeO DMT were observed to decrease in concentration, whereas β-carboline (norharmane) was not detected in any sample. Excessive drying out of dormant plants was hypothesised to be a risk factor for phalaris toxicity. Continued management of potentially toxic phalaris pasture could include measures to manipulate the physiological processes that result in increased toxic alkaloids, including methods to reduce drying out of dormant phalaris plants, and managing stocking rates and grazing species to mitigate potential toxicity.

The aetiology, prevalence and morbidity of outbreaks of photosensitisation in livestock: A review.

BackgroundPhotosensitisation is a clinical condition occurring in both humans and animals that causes significant injury to affected individuals. In livestock, outbreaks of photosensitisation caused by ingestion of toxic plants are relatively common and can be associated with significant economic loss.ObjectivesThe agents that are most commonly implicated in outbreaks of photosensitisation have not been formally investigated on a global scale. To address this question, a systematic review of the literature was undertaken to determine the most common causative agents implicated in outbreaks of photosensitisation in livestock in Australia and globally, as well as the prevalence and morbidity of such outbreaks.MethodsA systematic database search was conducted to identify peer-reviewed case reports of photosensitisation in livestock published worldwide between 1900 and April 2018. Only case reports with a full abstract in English were included. Non peer-reviewed reports from Australia were also investigated. Case reports were then sorted by plant and animal species, type of photosensitisation by diagnosis, location, morbidity and mortality rate and tabulated for further analysis.ResultsOne hundred and sixty-six reports qualified for inclusion in this study. Outbreaks were reported in 20 countries. Australia (20), Brazil (20) and the United States (11) showed the highest number of peer-reviewed photosensitisation case reports from this analysis. Hepatogenous (Type III) photosensitisation was the most frequently reported diagnosis (68.5%) and resulted in higher morbidity. Panicum spp., Brachiaria spp. and Tribulus terrestris were identified as the most common causes of hepatogenous photosensitisation globally.ConclusionsHepatogenous photosensitisation in livestock represents a significant risk to livestock production, particularly in Australia, Brazil, and the United States. Management of toxic pastures and common pasture weeds may reduce the economic impact of photosensitisation both at a national and global level.

Vasoactivity and Vasoconstriction Changes in Cattle Related to Time off Toxic Endophyte-Infected Tall Fescue.

Previous research has indicated that serotonergic and α-adrenergic receptors in peripheral vasculature are affected by exposure of cattle grazing toxic endophyte-infected (E+; Epichlöe coenophialia) tall fescue (Lolium arundinaceum). The objective of this experiment was to determine the period of time necessary for the vascular effects of ergot alkaloids to subside. Two experiments were conducted to investigate changes in vascular contractile response and vasoconstriction over time relative to removal from an ergot alkaloid-containing E+ tall fescue pasture. In Experiment 1, lateral saphenous vein biopsies were conducted on 21 predominantly Angus steers (357 ± 3 kg body weight) at 0 (n = 6), 7 (n = 6), 14 (n = 5), or 28 days (n = 4) after removal from grazing pasture (3.0 ha; endpoint ergovaline + ergovalinine = 1.35 mg/kg DM) for 126 days. In Experiment 2, lateral saphenous veins were biopsied from 24 Angus-cross steers (361 ± 4 kg body weight) at 0, 21, 42, and 63 days (n = 6 per time point) following removal from grazing tall fescue pastures (3.0 ha; first 88 days endpoint ergovaline + ergovalinine = 0.15 mg/kg DM; last 18 days endpoint ergovaline + ergovalinine = 0.57 mg/kg DM) for 106 total days. Six steers (370 ± 18 kg body weight) off of bermudagrass pasture for the same time interval were also biopsied on Day 0 and Day 63 (n = 3 per time point). Additionally, in Experiment 2, cross-sectional ultrasound scans of caudal artery at the fourth coccygeal vertebra were taken on Days 0, 8, 15, 21, 29, 36, 42, and 45 to determine mean artery luminal area to evaluate vasoconstriction. In both experiments, steers were removed from pasture and housed in a dry lot and fed a corn silage diet for the duration of biopsies and ultrasound scans. Biopsied vessels used to evaluate vasoactivity were cleaned, incubated in a multimyograph, and exposed to increasing concentrations of 4-Bromo-3,6-dimethoxybenzocyclobuten-1-yl) methylamine hydrobromide (TCB2; 5HT2A agonist), guanfacine (GF; α2A-adrenergic agonist), and (R)-(+)-m-nitrobiphenyline oxalate (NBP; α2C-adrenergic agonist) in both experiments and ergovaline (ERV) and ergotamine (ERT) in Experiments 1 and 2, respectively. In Experiment 1, days off pasture × agonist concentration was not significant (p > 0.1) for all four compounds tested. In Experiment 2, GF, NBP, TCB2 and ERT were significant for days off pasture × agonist concentration interaction (p < 0.02) and vasoactivity increased over time. Vasoactivity to agonists was reduced (p < 0.05) when steers were initially removed from E+ tall fescue pasture compared to bermudagrass, but did not differ by Day 63 for any variable. Luminal areas of caudal arteries in steers grazed on E+ tall fescue relaxed and were similar to steers that had grazed bermudagrass for 36 days on non-toxic diet (p = 0.15). These data demonstrate changes in peripheral vasoactivity and recovery from vasoconstriction occur beyond five weeks off toxic pasture and 5HT2A receptors appear to be more dramatically affected in the lateral saphenous vein by grazing E+ tall fescue pasture than adrenergic receptors.

A history of facial eczema (pithomycotoxicosis) research

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 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.

Colic Caused by Panicum Maximum Toxicosis in Equidae in Northern Brazil

In the Amazon region of northern Brazil, Panicum maximum cultivars Mombaça, Tanzânia, and Massai cause severe colic and death in horses and mules. The disease occurs in the rainy season, when sprouting pastures are grazed by equidae. In the 8 separate disease outbreaks studied, a total of 52 out of 153 equidae were affected, including 19 that died (10 mules and 9 horses). Clinical signs were colic and abdominal dilatation, with a clinical manifestation period of 12 hr to 4 days. Serum activities of gamma-glutamyl transferase and aspartate aminotransferase were within reference intervals; however, serum urea nitrogen and creatinine concentrations were occasionally elevated. The primary gross and histologic lesions were observed in the digestive system. The stomach, small intestine, and large intestine had severe hemorrhages and occasional mucosal erosions and ulcerations. Ulceration and hemorrhage of the urinary bladder were rarely observed. Histologic examination revealed diffuse lymphoplasmacytic gastritis and enteritis with severe congestion, hemorrhage, and occasional epithelial necrosis and ulceration. Lymphocellular necrosis was occasionally observed within gut-associated lymphoid tissue. Tubular nephrosis occurred in some animals. Degeneration and occasional necrosis of bile duct epithelial cells and degeneration of hepatocytes were observed in the liver. Toxic pastures were negative for diosgenin- and yamogenin-based saponins, and oxalate concentrations were within reference intervals for the species. The toxin or toxins causing disease and the reason for the toxicity of the plant in the northern region are unknown.

Steroidal saponin concentrations in Brachiaria decumbens and B. brizantha at different developmental stages

Brachiaria species contain steroidal saponins and are involved in outbreaks of hepatogenous photosensitization. This research presents the levels of a steroidal saponin, protodioscin, in the seeds and aerial parts of B. brizantha and B. decumbens during different developmental stages (growth, bloom, fructification and seed fall). The butanolic fraction of the ethanolic extract of each stage was submitted to thin layer chromatography (TLC) and spectrophotometric analysis through the Ehrlich reagent in 515nm. The chromatograms in TLC of the butanolic fraction of B. brizantha and B. decumbens showed similar spots as the protodioscin standard. The estimated level of protodioscin isomers in B. brizantha and B. decumbens ranged from 0.5% to 2.1%, having the highest level at the end of their developmental stages during seed falling comparison with the previous one. Protodioscin was not detected in the seeds. Outbreaks of Brachiaria spp. poisoning in central Western Brazil are frequently observed in pastures that had been more than 30 days without animals grazing, and also during the growing or blooming stage of the pastures. Other saponin determinations in toxic and non toxic pastures are necessary to determine the saponin concentrations that cause intoxication.

Sapogenin Levels in Narthecium ossifragum Plants and Ovis aries Lamb Faeces during Two Alveld Outbreaks in Møre og Romsdal, Norway, 2001

The proposal that saponins produced by the lily bog asphodel (Narthecium ossifragum) may be the direct cause of the hepatogenous photosensitization disease alveld seen in Norwegian lambs was investigated by comparing sapogenin levels in two control and two toxic pastures, and in faeces from lambs grazing the four pastures in the Halsa and Surnadal municipalities, Møre og Romsdal county, Norway. Generally similar levels of sapogenins, determined after hydrolysis of parent plant saponins, were found in Narthecium leaves collected in June/July 2001 from the two alveld outbreak areas and two nearby control areas. Differences in the median sapogenin levels determined for leaf samples in outbreak and control areas were not statistically significant. The total level of free and conjugated sapogenins in faeces recovered from the rectums of lambs grazing the outbreak and control pastures areas varied greatly. The results obtained do not support the hypothesis that a dose-response relationship exists between Narthecium saponin levels and the occurrence of alveld outbreaks.

Genetics of susceptibility to facial eczema in Friesian and Jersey cattle

A total of 528 calves from 3 calf crops, sired by 34 Friesian and 28 Jersey bulls, were challenged with sporidesmin, the toxin causing facial eczema (FE), in order to determine the genetic variation in susceptibility to FE. The challenge was either by grazing toxic pasture or by oral dosing, and the response was monitored by blood sampling to measure the elevations of serum gamma‐glutamyltransferase (GGT), glutamate dehydro‐genase (GDH), and other possible indicators (enzymes or metabolites: bilirubin, aspartate transaminase, ferroxidase, bile acids, and 5'nucleo‐tidase). The last calf crop was sired, in part, by bulls phenotypically selected from the second calf crop using GGT records. Data were analysed using the repeated records option of a restricted maximum likelihood programme. A sire model was used, with sires and maternal grandsires included to determine pedigree. The uni‐variate heritability estimates for logeGGT were 0.29 ± 0.15 in Friesians and 0.77 ± 0.13 in Jerseys, and for logeGDH they were 0.20 ± 0.12 and 0.64 ± 0.13, respectively. Corresponding repeatabilities were 0.86 ± 0.01 and 0.84 ± 0.02 for logeGGT, and 0.66 ± 0.03 and 0.69 ± 0.03 for logeGDH. The genetic correlations between the two enzymes were 0.99 for Friesians and 0.95 for Jerseys. Genetic correlations between the five other enzymes or metabolites and logeGGT were generally high (0.79 to 0.99), with the exception of ferroxidase which was not correlated with logeGGT. The next best indicators of FE susceptibility after GGT and GDH were aspartate transaminase and 5'nucleotidase, which were phenotypically correlated with GGT, were heritable (in Jerseys) and repeatable, and showed elevation in response to challenge. The “High” and “Low” GGT‐selected sire groups in the last calf crop had significantly different progeny mean GGT levels in both breeds. It was concluded that selection against high GGT concentrations following FE challenge should reduce the susceptibility to FE in subsequent generations.

Sublethal exposure to corynetoxins affects production of grazing sheep

This paper reports the production losses resulting from treating sheep with sublethal doses of corynetoxins, the causal agent of annual ryegrass toxicity. Merino ewes were given 3 levels of corynetoxins twice weekly for 11 weeks from 26 days before the start of joining to day 51 of pregnancy, giving a cumulative dose of 0 , 0.4 or 0.8 mg/kg liveweight. The effect on ovulation, pregnancy, lamb birth weight, lamb survival and weaning weight were measured along with the liveweight and wool growth of the ewes. Corynetoxin treatment depressed (P&lt;0.005) the activity of uridine diphospho-N-acetylglucosamine: dolichol-phosphate N-acetylglucosamine-1-phosphate transferase and liver damage was detected in ewes on the high toxin treatment (P&lt;0.05). Ewe liveweight was unaffected by treatment but wool growth and wool fibre diameter were reduced by 10 and 7%, respectively (P&lt;0.05). Corynetoxin treatment appeared to increase ovulation (P&lt;0.05) and, as there was no effect on conception and embryo survival, this resulted in a 30-35% increase in the number of lambs weaned. Lamb birth weight and survival were not affected by treatment but weaning weight of the low toxin group was depressed (P&lt;0.05). While reproduction was not adversely affected, the sheep in this trial were exposed to extremely low levels of corynetoxins which did not accumulate to levels capable of causing detectable liver damage until 23 days after joining. Even at these levels of intake, well below those required to show clinical signs (3-5 mg/kg liveweight), wool growth was reduced, suggesting that sheep grazed on mildly toxic pasture experience wool production losses in the absence of signs of the clinical disease.

A note on the genetics of resistance or susceptibility to ryegrass staggers in sheep

Abstract A flock of mainly Romney × Coopworth ewes was established to test sires for genetic differences in resistance to ryegrass staggers (RGS). This disease is a neurotoxic condition caused by ingestion of endophyte‐infected perennial ryegrass containing the mycotoxin, lolitrem B. Lambs, 18‐month males and females, and ewes of all ages were scored from January to March each year for RGS (0 or 1; 0 = no staggers), while grazing toxic pastures during natural outbreaks of RGS. Over 6 years (the autumns of 1988–93) and over all stock classes scored, age‐group means for RGS ranged from 0 to 0.16. A breeding value for RGS was calculated for each animal, incorporating data from all years and all age groups, provided that the mean year x age group score was at least 0.04. RGS data were also recorded on another Romney flock managed at the same site over the same time period. The heritability of RGS score over both flocks was 0.07 ± 0.02 and the repeatability over years was 0.24 ± 0.04. In March 1993, 170 ewes w...

Mechanisms underlying Phalaris aquatica “sudden death” syndrome in sheep

Twenty outbreaks of Phalaris aquatica "sudden death" syndrome in sheep were investigated between 1981 and 1991. Four were confirmed and one was suspected, to be a cardiac disorder; 5 were confirmed and 3 were suspected, to be a polioencephalomalacic disorder; the aetiology of the remaining 7 outbreaks could not be determined. Potentially toxic levels of hydrocyanic acid (20 to 36 mg/100 g) were measured in the 3 toxic phalaris pastures tested. The measurement of potentially toxic levels of nitrate nitrogen (2920 micrograms/g) in toxic phalaris pastures by others, was noted. It is suggested that phalaris "sudden death" syndrome could have as many as 4 different underlying mechanisms, and that these might reflect the presence in the plant of a cardio-respiratory toxin, a thiaminase and amine co-substate, cyanogenic compounds, and nitrate compounds.

FACIAL ECZEMA - PROBLEMS AND SUCCESSES IN CONTROL

Facial eczema is the most important mycotoxin affecting New Zealand lIvestock. It is a partrcular problem in the lower lying warmer and morster areas of the northern North Island where conditions are favourable to rapid fungal growth and sporulation during autumn. In severe years animal deaths and depressed production can lead to losses exceeding $60 mlllion, average losses are estimated to exceed $20 million anually. Production losses. especially despressions in ewe fertility, can occur in the absence of clinical symptoms so most farmers grossly underestimate the financial losses Inflicted by this disease. Research has led to a number of control methods includmg the identification and awldance of toxic pastures, fungicides, zinc dosing and selection for more resistant stock. However these are not widely accepted by the farming industry because of costs, high labour requirements and a disinclination to disturb normal management practices. Keywords: facial eczema, control, productlon losses, resistance, zinc, fungicides.

On the oestrogenic mycotoxin zearalenone, and the pasture fungusFusarium culmorum

Abstract Extract Sir:–During investigations in Palmerston North over the period 1975-1980, into the possible involvement of fungal toxins in rye grass staggers, laboratory cultures of a number of pasture fungi were chemically screened for their ability to produce indole neurotoxins(10)(11)(12) (Gallagher, Latch and Keogh - unpublished). Although it was shown that numerous isolates of a number of Penicillium spp. were able to produce indole neurotoxins in laboratory culture, this ability was not expressed by any of a number of Fusarium spp. The Fusarium spp. examined included several species previously found to be present in high numbers in toxic ryegrass pastures. (16)(17) In view of the high frequency of occurrence of some of these Fusarium species in the pastures, the opportunity was taken to check the isolates for their ability to produce the potent oestrogenic mycotoxin zearaleone. (20) In fact, the most frequently encountered fungal species on several rye grass pastures, F. culmorum (W. G. Smith) Sac...

RYEGRASS STAGGERS: CLINICAL, PATHOLOGICAL AND AETIOLOGICAL ASPECTS

This paper briefly introduces animal disease aspects of ryegrass staggers IFiGS) and describes the occurence and the clinical signs of the disease. Recent suggestions for the production of a reversible biochemical lesion in the central nervous system are mentioned in relation to the apparent lack of specific morphological lesions found in sheep. The recent isolation of novel potent neurotoxins, the lolitrems, from toxic pasture material is reviewed. There is now strong circumstantial evidence that the lolitrems produce the neurotoxic disease of RGS and also that the lolitrems are elaborated in the close association of perennial ryegrass with its parasitic fungus, Lolium endophyte, in pastures. Under what conditions the lolitrems are produced, or their precise locus within the association, are not yet known.

Distribution in South Australia of Anguina funesta, the nematode associated with annual ryegrass toxicity

Rapid techniques, based on grinding ryegrass seedheads and extracting nematodes with a Baermann funnel, were developed to isolate Anguina funesta the nematode involved in annual ryegrass toxicity. From data on more than 500 samples, the distribution was found to be more widespread than the distribution of toxic pastures.

Decreased plasma testosterone concentrations in rams affected by ryegrass staggers

Feeding ryegrass, cut from pasture that had caused an outbreak of ryegrass staggers, to 10 mature rams caused a significant decrease in plasma testosterone concentrations in six animals. Six rams also developed staggers, but these did not all have decreased testosterone levels. This discrepancy suggests that toxic pasture could cause these two effects independently.

The role of fungal tremorgens in ryegrass staggers

Abstract Administration of the fungal tremorgens penitrem A, verruculogen, fumitremorgin B, and paxilline to sheep produced effects similar to signs of ryegrass staggers (RGS); fungi capable of producing tremorgens were present in the environment where RGS was occurring or had occurred; and spores of these fungi were ingested by sheep grazing the pastures. Of 23 species of Penicillium isolated from toxic pastures, 2 common species produced tremorgens: P. crustosum produced penitrem A and P. piscarium produced either verruculogen or verruculogen and fumitremorgin B. Each of these species was isolated from ryegrass, from soil, and from dung of affected animals. When cultured and fed to sheep they produced effects similar to signs of RGS. No direct evidence of tremorgen production in the natural habitat was obtained, nor were tremorgens detected chemically in ryegrass from toxic pastures. The observations are consistent with, but not conclusive proof of, a causative role for fungal tremorgens in RGS. The pos...

Fungi and ryegrass staggers

Abstract Many pastures with a history of ryegrass staggers were examined for fungi before, during and after outbreaks of the disease. No fungi were unique to pastures on which animals were staggering, but some fungi occurred in greater quantities in toxic pastures. Outbreaks of staggers were associated with the presence of litter in pastures. The incidence of staggers increased among animals grazing on plots sprayed with fungicides. In these sprayed plots the numbers of most fungus species were greatly reduced but some were increased. It is possible that fungi resistant to benomyl are responsible for ryegrass staggers.