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At least 73 records · Page 4Linked to original sources
PubMed2006

Copper deficiency in yaks on pasture in western China.

The clinical signs of a disorder in yaks (Bos grunniens), known locally as "swayback ailment," in the Qing Hai-Tibetan Plateau are described. The purpose of this study is to investigate the possibility that swayback ailment is iron (Fe)-induced copper (Cu) deficiency. The mean concentrations of Cu in soil and forage from affected areas and unaffected areas are similar and within the normal ranges. The mean concentrations of Cu in blood and hair from the affected yaks was significantly lower (P < 0.01) than that in unaffected yaks. The mean concentrations of Fe in soil and forage were significantly higher (P < 0.01) in affected than in unaffected areas. Affected yaks showed a hypochromic microcytic anemia and a low level of ceruloplasmin. Oral administration of copper sulphate prevented and cured the disease. We conclude that "swayback disorder" of yaks is caused by secondary Cu deficiency, mainly due to the high Fe content in forage.

Animal Feed↗
PubMed2005

The effect of gastrointestinal parasitism on blood copper and hemoglobin levels in sheep.

Endoparasitism is a problem in Trinidad, as it is in most tropical countries. Parasite infection has been suspected to contribute to the pathogenesis of swayback disease (which is also prevalent in Trinidad), but the mode of action has not been clearly defined, although it has been suggested that parasites interfere with the absorption of copper from the gastrointestinal tract. The objectives of the study were to assess the effect of endoparasitism on blood copper levels and hemoglobin (Hb) concentration in sheep in Trinidad. Copper was administered intramuscularly to parasite infected and noninfected animals. The results showed that parasitism has a depressing effect on blood copper and Hb levels, even when administered parenterally. It is concluded that parasitism can aggravate existing hypocupremia and possibly influence the expression of swayback disease.

Animals↗
PubMed2003

Myelopathy due to copper deficiency following gastrointestinal surgery.

BACKGROUND: Ataxic myelopathy due to copper deficiency has been described in ruminant animals and is called swayback. Neurological manifestations due to inherited copper deficiency secondary to the failure of intestinal copper absorption is well recognized as Menkes disease. The neurological consequences of acquired copper deficiency in humans are not well described. OBJECTIVE: To report 2 cases where patients developed a myelopathy with copper deficiency after gastrointestinal surgery.Patients Two patients developed a myelopathy many years after gastrointestinal surgery. Both had severe copper deficiency, which was the likely cause of the myelopathy. CONCLUSIONS: Acquired copper deficiency may present as a myelopathy. Gastrointestinal surgery and resulting decreased copper absorption may be causative.

Absorption↗
PubMed1990

Copper deficiency and posterior paralysis (Shalal) in small ruminants in the Sultanate of Oman.

A posterior ataxia or paralysis in goats and sheep is a syndrome known as Shalal within the Sultanate of Oman. An investigation was carried out into the etiology of the syndrome. Samples of blood and tissues were obtained from normal and Shalal-affected goats and sheep. Samples of feed were collected from the affected areas of the Sultanate. Chemical analyses of samples showed that affected animals suffered from severe copper deficiency in spite of sufficient copper contents in feed. However, concentrations of sulphur and iron in the feed were high. It was concluded that the Shalal syndrome in Oman is the condition generally known as swayback or enzootic ataxia caused by conditioned copper deficiency. The deficiency is probably due to copper-sulphur and copper-iron interactions in the rumen, enhanced by feeding of fresh roughage containing rumen degradable proteins.

Animal Feed↗
PubMed2004

Myeloneuropathy and anemia due to copper malabsorption.

Dietary deficiency of copper results in a progressive ataxic myelopathy in ruminants called swayback. Menkes disease is a human disease due to an inherited defect in copper absorption; survival into adulthood is typically not known to occur. We report a 63-year-old woman who was evaluated by us for a myeloneuropathy that occurred in the setting of copper malabsorption. Her neurological deterioration stopped with copper supplementation. The limited literature on neurological manifestations of acquired copper deficiency suggests that the clinical presentation resembles the myeloneuropathy seen with vitamin B12 deficiency.

Anemia↗
PubMed1989

Animal models of amyotrophic lateral sclerosis and the spinal muscular atrophies.

The causes of human amyotrophic lateral sclerosis (ALS) and the spinal muscular atrophies (SMA) are, almost without exception, unknown. This ignorance has stimulated the search for animal models to obtain insight into the etiology, pathogenesis and biochemical mechanisms underlying the human disorders. None of the 38 animal models, described in this review, provides an exact animal copy of a specific human motor neuron disease. Most of the models reproduce certain structural or physiological aspects of their human counterparts. The various experimental models can be classified according to the pathogenetic mechanism involved and according to the structural changes observed. Models based on experimentally induced disease, include heavy metals and trace elements (lead intoxication in guinea pigs, rabbits, rats, cats and primates; mercury intoxication in rats; aluminium intoxication in rabbits; swayback in goat kids; calcium and magnesium deficient rabbits and primates and calcium deficient cynomolgus monkeys), toxins (IDPN, vincristine, vinblastine, podophyllotoxin, colchicine, maytansine, maytanprine, L-BMAA, lectins, adriamycin), nutritional factors (ascorbic acid deficient guinea pigs), virus infection (spongiform polioencephalomyelitis, attenuated poliovirus, lactate dehydrogenase-elevating virus), and immunological factors (immunization with motor neurons). Hereditary models comprise hereditary canine spinal muscular atrophy, hereditary neurogenic amyotrophy in the pointer dog, Stockard paralysis, Swedish Lapland dog paralysis, "wobbler" mouse, "shaker" calf, and hereditary spinal muscular atrophy in zebra foals, crossbred rabbits,

Amyotrophic Lateral Sclerosis↗
PubMed1992

Deficiency of copper can cause neuronal degeneration.

The aim of this article is to emphasize the important role that copper plays in the function of nerve cells. We are reporting preliminary data which suggest that the swelling of axons which we produce in rats by iminodipropionitrile, IDPN, is due to its chelating action on copper, and how conversely supplementation with copper abolishes both symptoms and lesions. The copper values we obtained by atomic absorption spectrophotometry of the spinal cord and brain from the animals fully support this contention. In comparing these results with the diseases that are known to be due to copper deficiency, namely Menkes disease in man, swayback in lambs and several neurological mutant mice, we find not only similar axonal swellings, but also amelioration of symptoms and lesions by early administration of copper. Considering the main forms in which copper is present, we discuss the cuproproteins, i.e. ceruloplasmin and metallothionein, and their role in transport and delivery of copper to various organs. Further, the many cuproenzymes i.e. superoxide dismutase, tryptophan-2,3-dioxygenase, lysine oxidase, cytochrome oxidase, monoamine oxidases, tyrosinase, dopamine-beta-hydroxylase and d-amino levulinate dehydratase are noted for their roles in the nervous system. Finally, we suggest that neuronal copper deficiency should be more fully investigated as a possible etiological factor in the more common neurodegenerative diseases, such as Alzheimer's disease and amyotrophic lateral sclerosis, ALS.

Animals↗
PubMed2004

Iron, copper and fetal development.

Pregnancy is a period of rapid growth and cell differentiation for both the mother and fetus. Consequently, it is a period when both are vulnerable to changes in dietary supply, especially of those nutrients that are marginal under normal circumstances. In developed countries this vulnerability applies mainly to micronutrients. Even now, Fe deficiency is a common disorder, especially in pregnancy. Similarly, Cu intake in the UK population is rarely above adequate levels, which is a matter of some concern, both in terms of public health and possible clinical consequences. In early studies it was shown that lambs born to mothers on Cu-deficient pastures develop 'swayback,' with neurological and muscular symptoms that cannot be reversed by postnatal supplementation. More recently, rat studies have shown that responses such as the 'startle' response are lost in offspring of Cu-deficient mothers. Data have shown that prenatal Fe deficiency results in increased postnatal blood pressure, even though the offspring have normal dietary Fe levels from birth. These observations emphasise the importance of Fe and Cu in growth and development. In the present review the importance of these metals and the consequences, both short term and long term, of deficiency will be discussed and some possible mechanisms whereby these effects may be generated will be considered.

Copper↗
PubMedDate not supplied

Prevalence of trunk abnormalities in eleven-year-old schoolchildren in Rotterdam, The Netherlands.

The prevalence of trunk abnormalities was studied in 4,915 children aged 11 years (2,528 boys, 2,387 girls); 33% of the children were of non-Dutch origin. The following measurements were recorded: height, weight, signs of puberty, and menarche. Trunk abnormality was assessed in the erect child (asymmetry of shoulders, waistline, imbalance of the trunk, scoliosis, lordosis, kyphosis, swayback, and flexibility) and by the forward bending test (rib hump or lumbar prominence, persistence of scoliosis, kyphosis, deviant lateral aspect); 85.9% of boys and 81.3% of girls were symmetric, and abnormal forward bending test was noted in 7.1% of boys and 10.6% of girls. In non-Dutch girls, trunk abnormalities were more prevalent.

Anthropometry↗
PubMed1988

Copper heptonate for the treatment of hypocupraemia in sheep.

Trials were carried out to compare the efficacy of copper heptonate with other available therapeutic products. On nine farms with a copper deficiency problem, over 2000 ewes were treated in mid-pregnancy. All the treatments increased whole blood copper levels and plasma caeruloplasmin (ferroxidase) activity in ewes, and protected their lambs from swayback. The lambs from ewes treated with copper heptonate and copper oxide needles had significantly higher blood copper levels than lambs from untreated control ewes. Treatment with copper heptonate was shown to have a therapeutic index of at least 5 in Swaledale ewes of normal copper status. In two groups of Welsh mountain sheep from different backgrounds, both with normal blood copper levels before treatment, the therapeutic indices were 3 to 5.

Animals↗
PubMedDate not supplied

Severe ataxia, myelopathy, and peripheral neuropathy due to acquired copper deficiency in a patient with history of gastrectomy.

BACKGROUND: In animal studies, copper absorption has been demonstrated to occur in the proximal gut via duodenal enterocytes. Acquired copper deficiency is known as "swayback" in ruminant animals and Menkes' disease in humans. Copper is an essential micronutrient necessary for the hematologic and neurologic systems. Acquired copper deficiency in humans has been described, causing a syndrome similar to the subacute combined degeneration of vitamin B(12) deficiency. METHODS: This is a single case report. Our patient developed a neurologic constellation of ataxia, myelopathy, and peripheral neuropathy similar to vitamin B(12) deficiency many years after gastrectomy for severe peptic ulcer disease. The patient was maintained for decades with enteral feedings via jejunostomy that provided the recommended dietary allowance (RDA) for copper. RESULTS: Copper deficiency was suspected, identified, and treated. Over 3 months of follow-up, serum copper levels increased from 4 microg/dL to 20 microg/dL (70-150 microg/dL), and ceruloplasmin increased from 6 mg/dL to 8 mg/dL (14-58 mg/dL). During this short time of follow-up, the patient has had no further progression of his neurologic symptoms. CONCLUSIONS: Ataxia and myelopathy secondary to acquired copper deficiency are rare complications of major gastric resection. This is quite similar to the syndrome of vitamin B(12) deficiency. Vitamin B(12) repletion does not improve symptoms. Bariatric procedures such as gastric bypass surgery result in a similar functional anatomy of the proximal gut and may place more patients at increased risk. Early recognition and therapy with oral or parenteral copper may lead to a decrease in both neurologic and hematologic consequences.

Aged↗
PubMed2005

Deformity in the "Boxing Boys".

The late Bronze Age wall painting the Boxing Boys (c. 17th-16th century BCE) was excavated in the ancient town of Akrotiri on the Greek island of Thera. This article considers a medical interpretation for the spinal-pelvic anomaly in the anatomy of one of the boys. The artist has depicted a combination of structural anatomical adjustments diagnostic of spondylolisthesis, a forward slippage of one of the lumbar vertebrae. The accurate portrayal of the surface appearance of this condition suggests that the artist painted directly from a live subject. Thus, the Boxing Boys mural may be the earliest visual record of a sports-induced injury. Although the meaning of the wall paintings is unclear, the wild goats (agrimia) on the adjoining walls simulate swayback as a reflection of the boy's torso deformity and share other features with the boxers, adding to the unifying characteristics of the room. The abnormal morphology appears to be the earliest achievement of transforming disease into aesthetic charm on a monumental scale.

Archaeology↗
PubMed1991

Footwear and posture. Compensatory strategies for heel height.

The belief that wearing high-heeled shoes increases lumbar lordosis is firmly ingrained in clinical folklore. Proponents of negative heel footwear argue that because high positive heels increase the lumbar lordosis, negative heels will decrease the lumbar lordosis. Quantitative documentation of the assumption regarding high heels is not to be found in the literature, although sporadic attempts to prove this assumption have been made throughout the 20th Century. Although other effects, such as decreased gait speed and step length, and increased knee flexion at heel strike have been found in more than one study, no increase in lumbar lordosis has been found. Where an actual decrease in lordosis has been found, authors tend to explain it away as inconsistent with what every clinician feels that he or she has observed. We felt it appropriate, then, to conduct both a static and a dynamic study to assess the effects of heel height on lumbar spine and lower limb joint kinematics in the sagittal plane, as well as other strategies to compensate for heel height. The results indicate that the greatest compensation is at the ankle and knee. Where a significant effect occurred in the lumbar spine (males, dynamic study), high heels decreased the lumbar lordosis, i.e., resulted in less swayback rather than more.

Adolescent↗
PubMed1993

Cabbage poisoning in ruminants.

A complaint of poor productivity was investigated in a herd of Jersey cattle and a small flock of Dorper sheep that had been fed cabbage for 5 to 6 months per year, over a number of years. During that time a number of lambs were lost as a result of swayback, some cows aborted, milk production was down, and although the farmer was an experienced inseminator, the conception rate in the Jerseys was low. After rectal examination and consulting the records, 26% of the cows were found to have been open for more than 150 d and 28% had been inseminated more than 3 times. The body condition of the cows ranged from poor to moderate, the hair coats were dull and some cows were anaemia. The young lambs had visibly enlarged thyroids. Haematological investigations revealed a typical Heinz body type haemolytic anaemic. In the cattle the anaemia appeared to be macrocytic, hypochromic and associated with thrombocytosis, while in the sheep it seemed to be normochromic and slightly microcytic. Plasma copper concentrations were severely depressed in all cases. Most thyroxine concentrations were within the normal range, although some were on the low side. Analysis of cabbage revealed a high sulphur content and marginally low copper and zinc levels. The main factor in cabbage which is responsible for poor animal performance, is the high sulphur content. High levels of this mineral exert detrimental effects, in order of priority, by elevating s-methyl cystine sulphoxide, diminishing the availability of copper and raising the glucosinolate content of the plant.

Animals↗
PubMed1994

Studies on the relationship between sway disease of bactrian camels and copper status in Gansu province.

The clinical signs of camel sway disease in the Hexi Corridor of Gansu province were defined. The contents of eight minerals in soils, in forage and in the blood and hair of bactrian camels from this region were determined. The related blood indices were also measured. The concentration of molybdenum in soils and forage was 4.8 +/- 0.02 and 4.8 +/- 0.25 micrograms/g (dry matter), respectively, the copper to molybdenum ratio in the forage being only 1.3. The concentration of copper in blood and hair from the camels was 0.28 +/- 0.17 micrograms/ml and 3.50 +/- 1.00 micrograms/g, respectively. There was a hypochromic microcytic anaemia and a low level of ceruloplasmin in the blood. It is therefore suggested that sway disease of bactrian camels in this region is caused by secondary copper deficiency, mainly due to the high molybdenum content in soils and forage. The copper deficiency in the camels was aggravated during reproduction. Oral administration of copper sulphate can prevent and cure the disease.

Animal Feed↗
PubMed1985

Susceptibility of North Ronaldsay sheep to copper from cupric oxide needles.

Three housed North Ronaldsay sheep were treated with copper in the form of cupric oxide "needles", two at the manufacturer's recommended dosage rate and the third at twice this level. Sheep of this breed are especially sensitive to high dietary intake of copper. Pre- and post-dosing blood samples were monitored for changes in packed cell volume and changes in content of plasma copper, bilirubin, AST and SDH. Weight changes were also recorded. The animal dosed at twice the recommended level died on day 19 post-dosing of acute copper poisoning. The two dosed at the standard rate remained healthy and put on weight steadily throughout the six months following treatment. Two Welsh Mountain sheep dosed at the standard rate and maintained and examined in the same way likewise showed no signs of copper toxicity.

Animal Feed↗