Locomotor effects in sheep of alkaloids identified in Australian Tribulus terrestris

Fresh, mature, ungrazed Tribulus terrestris plant material was subjected to a standard alkaloid extraction procedure. The extract was fractionated by thin layer chromatography (TLC) and high performance liquid chromatography (HPLC). Two major alkaloid fractions were demonstrated. These fractions were identified by means of TLC, ultraviolet spectrofluorimetry (UVS) and HPLC, as the beta-carboline indoleamines harmane and norharmane. The extractable alkaloid content was determined to be 44 mg/kg dry matter. Synthetic harmane and norharmane were administered subcutaneously to sheep at a dose rate of 54 mg/kg. Both compounds caused similar nervous effects. The main effect observed was limb paresis, which in some sheep was body side blased. The clinical signs observed in the experimental sheep were consistent with those described for naturally occurring cases of Tribulus terrestris staggers. It was proposed that harmane and norharmane accumulate in tryptamine-associated neurones of the central nervous system, during months of tribulus ingestion, and gradually interact irreversibly with a specific neuronal gene DNA sequence.     

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

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.     

Motor neurone disease in molybdenum-deficient sheep fed the endogenous purine xanthosine: possible mechanism for Tribulus staggers

Background The occurrence of Tribulus terrestris motor neurone disease (MND) in sheep is linked with grazing Tribulus growing on cultivation paddocks. A previous survey found that the molybdenum (Mo) content of Tribulus growing on uncultivated soils in the Coonabarabran district of New South Wales was 3.03 ppm, but on cultivated soils it was <0.04 ppm. Tribulus contains the purine, xanthosine, which functions as a neuromodulator, and the catabolism of xanthosine is Mo‐dependent. Design To investigate the relationship between xanthosine ingestion and low Mo concentration, eight sheep were fed Mo‐deficient lucerne chaff (<0.10 ppm), the Mo antagonist, sodium tungstate, and xanthosine (25 mg/kg/day) over 18 weeks and then returned to pasture. Results Signs of MND developed in two sheep 30 months later and astrocyte degeneration occurred in all sheep. Conclusion The findings were similar to those observed in sheep with T. terrestris MND, suggesting that the combination of xanthosine ingestion and Mo deficiency may be the cause of this disorder.     

The occurrence of phalaris staggers in sheep

Extract

Typical cases of the “staggers” syndrome associated with Phalaris tuberosa poisoning occurred at Invermay Research Station in October, 1954. It is being recorded because detailed records of pasture management and climatic conditions are available for the period when symptoms were seen, also the pasture composition of the Phalaris plot.     

Photosensitivity in South Africa. VI. The experimental induction of geeldikkop in sheep with crude steroidal saponins from Tribulus terrestris

Geeldikkop was induced in sheep by the oral administration of crude steroidal saponins from Tribulus terrestris. Two of the sheep developed typical lesions of geeldikkop, including birefringent crystalloid material in bile ducts and concentric periductal lamellar fibrosis. The clinical pathological changes in these sheep were also consistent with those of geeldikkop: aspartate transaminase and gamma-glutamyl transferase activities in the sera of both were elevated, and one had bilirubinaemia. A third sheep became photosensitive without typical lesions of geeldikkop in the liver or changes in the activities of liver enzymes before euthanasia. The findings of these trials are consistent with reports from abroad that ovine hepatogenous photosensitization, caused by Agave lechuguilla and Narthecium ossifragum, can be induced with crude saponins from the respective plants.     

Decreased plasma testosterone concentrations and weight gain in young bulls affected by ryegrass staggers

Ryegrass staggers caused a significant depression of plasma testosterone concentrations in prepubertal bulls, and the most severely affected animals had a marked reduction in liveweight gain.     

Decreased plasma testosterone concentrations and weight gain in young bulls affected by ryegrass staggers

Ryegrass staggers caused a significant depression of plasma testosterone concentrations in prepubertal bulls, and the most severely affected animals had a marked reduction in liveweight gain.     

蒺藜皂苷对体外瘤胃发酵的影响

试验旨在利用人工瘤胃双外流连续培养系统,初步研究日粮中添加不同浓度(0、0.15、0.30、0.60 g/L)蒺藜皂苷(GSTT)对反刍动物瘤胃发酵参数的影响。结果表明,日粮添加不同水平GSTT对瘤胃pH、总挥发性脂肪酸(TVFA)浓度无显著影响(P>0.05);随着GSTT添加水平的提高,人工瘤胃液内NH₃-N浓度、乙酸摩尔比例和乙酸/丙酸比例显著降低(P<0.05),丙酸摩尔比例显著升高(P<0.05)。提示,GSTT可望作为一种潜在的反刍动物瘤胃发酵调控剂来改变瘤胃发酵模式,改善对饲料能量和蛋白质的利用效率。综合考虑,0.30 g/L GSTT为较适宜添加量。     

Staggers in sheep associated with the ingestion of Tributes terrestris

The history of an unusual locomotory disturbance of sheep is traced from its first recognition in 1937 through to the most recent outbreak in 1981-83. The condition occurred only at certain times and in restricted areas of the central and northern slopes districts of New South Wales. Outbreaks were repeatedly associated with drought periods during which sheep grazed large areas of Tribulus terrestris for many months at a time. Many thousands of sheep were affected, but the prevalence varied greatly between flocks. The course of the disease was characterised by a slowly developing, irreversible, asymmetrical, weakness of the hindlimbs. The clinical signs suggested that a lesion of the thoraco-lumbar spinal cord region was present. The macroscopic and microscopic examination of the nervous and musculoskeletal systems failed to demonstrate abnormalities which would account for the clinical signs. Haematological, biochemical and toxicological test results supported the concept of a neuromuscular disease process being present, but failed to indicate its aetiology.     

Amino acid neurotransmitter release from cerebrocortical synaptosomes of sheep with severe ryegrass staggers in New Zealand

Enhanced unstimulated release of the excitatory amino acid neurotransmitters aspartic acid and glutamic acid was measured in cerebrocortical synaptosomes prepared from sheep showing severe symptoms of ryegrass staggers. A similar pattern of deviation from neurologically normal animals was seen whether the sheep had contracted the disorder naturally or whether they had been deliberately caused to develop the disorder by grazing specific pastures rich in endophyte infected ryegrass. Deranged neurotransmitter release may reasonably be involved in the chemical pathology of ryegrass staggers and the findings are in accord with the putative synonymy of lolitrem toxicosis and ryegrass staggers.     

Abnormal turning behaviour, GABAergic inhibition and the degeneration of astrocytes in ovine Tribulus terrestris motor neuron disease

OBJECTIVE: To observe the clinical signs of sheep affected by Tribulus terrestris motor neuron disease, to ascertain their response to striatal dopamine reducing drugs, and to examine their brains and spinal cords for microscopic changes. PROCEDURES: Twenty-eight sheep displaying well developed clinical signs of the disorder were observed. Twenty-two of these and 22 normal sheep were then randomly allocated to three groups and treated with diazepam, chlorpromazine, or xylazine. The time that it took an animal to return to a standing position following drug administration was recorded. The brain and complete spinal cord were removed from each of the other six affected sheep and fixed in formalin. Brains were sectioned throughout at 5 mm intervals and spinal cords at 10 mm intervals. All tissues were paraffin embedded and examined by light microscopy. A few samples were examined by electron microscopy. RESULTS: Clinical signs included postural asymmetry with a right:left body-side dominance within the group of 50:50, unequal flaccid paresis in the pelvic limbs, extensor muscle atrophy and adduction of the weaker pelvic limb, and concurrent abduction of the stronger. Forward motion followed either a fixed left or right hand curved trajectory, the sheep no longer being able to choose which. Twelve animals intermittently displayed rotational behaviour that involved loss of postural balance without locomotor activation. The administration of diazepam, chlorpromazine, or xylazine caused limb paresis and sedation, with affected sheep being slower than normal sheep by factors of 8, 3 and 2 respectively, to return to a standing position. There were scattered areas of mild Wallerian degeneration throughout the spinal cord, and in both the brain and the cord there were small numbers of degenerate astrocytes containing novel cytoplasmic pigment granules. CONCLUSIONS: Affected sheep had a dysfunction in the control of directional change and this provides a new insight into the normal mechanism for 'turning' in quadrupeds. Directional change requires a functional asymmetry or lateralisation within the upper motor neuron to accommodate a difference in the rate of forward progression of each body side and, simultaneously, a lateral shift of the centre of gravity. The sensitivity of affected sheep to diazepam is consistent with a pre-existing elevation in GABAergic neuronal inhibition, probably as a result of a reduction in glutamatergic neuronal excitation. The cytoplasmic pigment found in degenerate astrocytes was novel and its presence in the brain nuclei known to contribute to turning behaviour could have aetiological significance. The motor output of the basal ganglia in Tribulus neurotoxicity appeared to be excessively inhibitory to the pelvic limb extensor muscles and was asymmetric, causing fixation of the turning posture but not locomotor activation. An intoxication of specific purine sensitive, glutamate releasing astrocytes, located in nuclei controlling turning, was suspected.     

A neurological locomotor disorder in sheep grazing Stachys arvensis

OBJECTIVE: To describe the clinical signs and pathology of a neurological locomotor disorder in sheep associated with ingestion of Stachys arvensis. DESIGN: Field observations and laboratory examinations. PROCEDURE: Clinical and pathological examinations were performed on sheep with suspected S arvensis intoxication. FIELD OBSERVATIONS: Merino sheep in a flock on the southwestern slopes of New South Wales developed a neurological disorder after grazing S arvensis. Affected animals had pelvic limb paresis and a proprioceptive deficit. When forced to exercise they stumbled and collapsed. Recovery following removal from the plant was slow. Many deaths were associated with the outbreak. RESULTS: Affected sheep developed a mild degenerative myelopathy and peripheral neuropathy. Deficiencies of vitamins A and E were also observed in the affected flock. CONCLUSION: Grazing S arvensis is sometimes associated with a neurological locomotor disorder in sheep.