A Case of Concurrent Molybdenosis, Secondary Copper, Cobalt and Selenium Deficiency in a Small Sheep Herd in Northern Germany

To the author’s knowledge this paper describes the first proven report of a combined primary molybdenosis, secondary copper (Cu) deficiency, Ovine White Liver Disease—Cobalt (Co) deficiency, and selenium (Se) deficiency in a small pedigree herd of White Horned Heath sheep in Germany (8 ewes, 2 rams, 3 yearling ewes, 17 lambs) for decades. Clinical signs associated with these mineral deficiencies in a group of pastured ram lambs included emaciation, conjunctivitis, anaemia, growth retardation, discolouration of the wool and photodermatitis. Morbidities and mortalities arose in 4–6-month-old lambs despite intensive veterinary treatment in the summer of 2014 and 2015 (n = 13, 23% died). Se (3/5), Cu (4/7), and Co (3/3) deficiencies in combination with elevated values for Molybdenum (Mo, 2/2) were found. Hamburg is a large industrial city and an input of heavy metals from surrounding industries and coal-fired power stations in combination with a sandy, non-fertilised soil and monoculture grass species might offer a potential explanation for the severity of mineral deficiencies observed in this herd.

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Inhibition of hepatic deiodination of thyroxine is caused by selenium deficiency in rats

Biochemical Journal ◽

10.1042/bj2480443 ◽

1987 ◽

Vol 248 (2) ◽

pp. 443-447 ◽

Cited By ~ 99

Author(s):

G J Beckett ◽

S E Beddows ◽

P C Morrice ◽

F Nicol ◽

J R Arthur

Keyword(s):

Thyroid Hormones ◽

Production Rate ◽

Selenium Deficiency ◽

Enzyme Complex ◽

Measurable Effect ◽

Direct Role ◽

Mechanism Of Inhibition ◽

Se Deficiency

Selenium (Se) deficiency produced up to a 14-fold decrease in hepatic tri-iodothyronine (T3) production from thyroxine (T4) in vitro. The T3 production rate could not be restored by the addition of a variety of cofactors, nor by the addition of control homogenate. The impairment in hepatic T3 production observed in Se deficiency was reflected in the concentrations of thyroid hormones circulating in plasma, T4 being increased approx. 40% and T3 being decreased by 30%. However, the fall in plasma T3 concentrations was smaller than might be expected in view of the marked decreased in T3 production. Se deficiency had no measurable effect on plasma reverse-tri-iodothyronine concentrations. The data suggest that Se deficiency produces an inhibition of both 5- and 5′-deiodination, consistent with the widely held view that these reactions are catalysed by the same enzyme complex. The mechanism of inhibition appears not be mediated by changes in thiol levels, but a direct role of Se in the activity of the deiodinase complex cannot be excluded.

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Degenerative axonopathy associated with copper deficiency in pigs

Pesquisa Veterinária Brasileira ◽

10.1590/s0100-736x2017000900002 ◽

2017 ◽

Vol 37 (9) ◽

pp. 911-915 ◽

Cited By ~ 1

Author(s):

Roberio G. Olinda ◽

Lisanka A. Maia ◽

Maria T.S. Frade ◽

Mauro P. Soares ◽

Severo S. Barros ◽

...

Keyword(s):

White Matter ◽

Purkinje Cells ◽

Copper Deficiency ◽

Clinical Signs ◽

Atomic Absorption Spectrophotometry ◽

Semiarid Region ◽

Spastic Paralysis ◽

Myelin Sheaths ◽

Cu Deficiency ◽

Spinal Segments

ABSTRACT: The epidemiological, clinic and morphological (pathological and ultrastructural) aspects of four outbreaks of copper deficiency affecting 21- to 90-day-old pigs in the Northeast region of Brazil are reported. Clinical signs began with paraparesis and ataxia and progressed to flaccid or spastic paralysis of the pelvic and thoracic limbs, followed by sternal and/or lateral recumbence. In addition, some animals showed dog-sitting position and intention tremors. The clinical manifestation period was 5-20 days. Significant gross lesions were not observed; however, microscopically, symmetrical degeneration of the white matter with ballooned myelin sheaths containing occasional macrophages was observed, mainly in the spinal cord. Two pigs presented with necrosis ad loss of Purkinje cells and ectopic Purkinje cells in the granular layer and cerebellar white matter. A ultrastructural analysis showed different degrees of damage of myelinated axons in the spinal segments, including an absence of the axoplasm structures with only axonal residues remaining. The myelin sheaths were degenerated and often collapsed into the space previously occupied by the axon. These results suggest that myelin degeneration is secondary to the axonal lesion. Finally, the concentration of copper in the liver was determined using atomic absorption spectrophotometry and was found to be low (ranging from 2.2 to 10.8 ppm). In conclusion, in the Brazilian semiarid region, Cu deficiency occurs in 21 to 90-day-old pigs that ingested different types of waste in their food.

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Molybdenosis Leading to Type 2 Diabetes Mellitus in Swedish Moose

Geology and Health ◽

10.1093/oso/9780195162042.003.0019 ◽

2003 ◽

Author(s):

Adrian Frank

Keyword(s):

Trace Element ◽

Experimental Studies ◽

Clinical Signs ◽

Corneal Opacity ◽

Chemical Parameters ◽

Trace Element Pattern ◽

Cu Deficiency ◽

Mucosal Oedema ◽

Loss Of Appetite ◽

Physical And Chemical

The “mysterious moose disease” also called “wasting disease” is affecting moose in a strongly acidified region of southwestern Sweden. Chemical investigations of animals from the affected region have been performed since 1988 and several articles are already published (Frank et al. 1994, Frank 1998, Frank et al. 1999, 2000a, b, c, d). The numerous clinical signs and necropsy findings have included diarrhea, loss of appetite, emaciation, discoloration and loss of hair, apathy, osteoporosis, and neurological signs such as behavioral and locomotor disturbances (Rehbinder et al. 1991, Stéen et al. 1993). Further findings were mucosal oedema, hyperemia, hemorrhages and lesions of the mucosa in the gastrointestinal tract, hemosiderosis of the spleen and liver, dilated flabby heart, alveolar emphysema, and uni- or bilateral corneal opacity. Not all the symptoms appear simultaneously in one and the same animal. About 150—180 affected animals have been reported annually since the late 1980s. An increase in molybdenum (Mo) and a decrease in copper and cadmium (Cu, Cd) content in organ tissues (e.g., liver) are signs of a disturbed trace element balance found in affected animals (Frank 1998). To confirm the findings and to elucidate the mechanisms leading to molybdenosis and Cu deficiency, experimental studies were performed in goats. The feeding studies were performed in a controlled laboratory environment and a semi-synthetic diet was supplied (Frank et al. 2000c). Despite considerable differences in species and living conditions between goat and moose, similar changes in trace element pattern and clinical chemical parameters were observed in both species. The study shows that the etiology of the moose disease is basically molybdenosis followed by Cu deficiency, inter alia (Frank et al. 2000a,b,d). Mo is an essential trace element that controls the metabolism of Cu in ruminants. Increased Mo concentrations relative to Cu in feed results in Cu deficiency, whereas the converse leads to an accumulation of Cu, even to Cu poisoning (e.g., in sheep). In an acidified environment, the molybdate anion is adsorbed in the soil, contrary to positively charged metals. The presence of Mo and Cu in the environment is basically dependent mainly on geochemistry, influenced by numerous physical and chemical parameters (Selinus et al. 1996, Selinus and Frank 2000).

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Selenium Deficiency Aggravates Aflatoxin B1–Induced Immunotoxicity in Chick Spleen by Regulating 6 Selenoprotein Genes and Redox/Inflammation/Apoptotic Signaling

Journal of Nutrition ◽

10.1093/jn/nxz019 ◽

2019 ◽

Vol 149 (6) ◽

pp. 894-901 ◽

Cited By ~ 13

Author(s):

Ling Zhao ◽

Yue Feng ◽

Jiang Deng ◽

Ni-Ya Zhang ◽

Wan-Po Zhang ◽

...

Keyword(s):

Aflatoxin B1 ◽

Body Weight Gain ◽

Selenium Deficiency ◽

B Cell Lymphoma ◽

Underlying Mechanism ◽

Protective Role ◽

White Pulp ◽

Feed Conversion ◽

Apoptotic Signaling ◽

Se Deficiency

ABSTRACTBackgroundSelenium (Se) plays a protective role in aflatoxin B1 (AFB1)–induced splenic immunotoxicity in chicks.ObjectiveThis study was designed to reveal the underlying mechanism of Se-mediated protection against AFB1-induced splenic injury in broilers.MethodsFour groups of 1-d-old Cobb male broilers (n = 5 cages/diet, 6 chicks/cage) were arranged in a 3-wk 2 × 2 factorial design trial whereby they were fed an Se-deficient, corn- and soy-based diet [base diet (BD), 36 μg Se/kg], BD plus 1.0 mg AFB1/kg, BD plus 0.3 mg Se/kg, or BD plus 1.0 mg AFB1/kg and 0.3 mg Se/kg (as 2-hydroxy-4-methylselenobutanoic acid). Serum and spleen were collected at week 3 to assay for cytokines, histology, redox status, selected inflammation- and apoptosis-related genes and proteins, and the selenogenome.ResultsDietary AFB1 induced growth retardation and spleen injury, decreasing (P < 0.05) body weight gain, feed intake, feed conversion efficiency, and serum interleukin-1β by 17.8–98.1% and increasing (P < 0.05) the spleen index and serum interleukin-6 by 37.6–113%. It also reduced the splenic lymphocyte number, the white pulp region, and histiocyte proliferation in Se-adequate groups. However, Se deficiency aggravated (P < 0.05) these AFB1-induced alterations by 16.2–103%. Moreover, Se deficiency decreased (P < 0.05) splenic glutathione peroxidase (GPX) activity and glutathione-S transferase and glutathione concentrations by 35.6–89.4% in AFB1-exposed groups. Furthermore, Se deficiency upregulated (P < 0.05) the apoptotic (Caspase 3 and Caspase 9) and antimicrobial (β defensin 1 and 2) genes, but downregulated (P < 0.05) antiapoptotic (B-cell lymphoma 2) and inflammatory (E3 ubiquitin-protein ligase CBL-B) genes at the mRNA and/or protein level in AFB1 supplementation groups. Additionally, Se deficiency downregulated (P < 0.05) GPX3, thioredoxin reductase 1 (TXNRD 1), GPX4, and selenoprotein (SELENO) S, and upregulated (P < 0.05) SELENOT and SELENOU in spleen in AFB1 administered groups.ConclusionsDietary Se deficiency exacerbated AFB1-induced spleen injury in chicks, partially through the regulation of oxidative stress, inflammatory and apoptotic signaling, and 6 selenoproteins.

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Selenium Deficiency Is Widespread and Spatially Dependent in Ethiopia

Nutrients ◽

10.3390/nu12061565 ◽

2020 ◽

Vol 12 (6) ◽

pp. 1565

Author(s):

Adamu Belay ◽

Edward J. M. Joy ◽

Christopher Chagumaira ◽

Dilnesaw Zerfu ◽

E. Louise Ander ◽

...

Keyword(s):

Essential Element ◽

Selenium Deficiency ◽

Sub Saharan Africa ◽

Eastern Ethiopia ◽

North West ◽

Targeted Interventions ◽

North East ◽

Se Deficiency ◽

Western Ethiopia ◽

Se Status

Selenium (Se) is an essential element for human health and livestock productivity. Globally, human Se status is highly variable, mainly due to the influence of soil types on the Se content of crops, suggesting the need to identify areas of deficiency to design targeted interventions. In sub-Saharan Africa, including Ethiopia, data on population Se status are largely unavailable, although previous studies indicated the potential for widespread Se deficiency. Serum Se concentration of a nationally representative sample of the Ethiopian population was determined, and these observed values were combined with a spatial statistical model to predict and map the Se status of populations across the country. The study used archived serum samples (n = 3269) from the 2015 Ethiopian National Micronutrient Survey (ENMS). The ENMS was a cross-sectional survey of young and school-age children, women and men. Serum Se concentration was measured using inductively coupled plasma mass spectrometry (ICPMS). The national median (Q1, Q3) serum Se concentration was 87.7 (56.7, 123.0) μg L−1. Serum Se concentration differed between regions, ranging from a median (Q1, Q3) of 54.6 (43.1, 66.3) µg L−1 in the Benishangul-Gumuz Region to 122.0 (105, 141) µg L−1 in the Southern Nations, Nationalities, and Peoples’ Region and the Afar Region. Overall, 35.5% of the population were Se deficient, defined as serum Se < 70 µg L−1. A geostatistical analysis showed that there was marked spatial dependence in Se status, with serum concentrations greatest among those living in North-East and Eastern Ethiopia and along the Rift Valley, while serum Se concentrations were lower among those living in North-West and Western Ethiopia. Selenium deficiency in Ethiopia is widespread, but the risk of Se deficiency is highly spatially dependent. Policies to enhance Se nutrition should target populations in North-West and Western Ethiopia.

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MiR-196-5p involvement in selenium deficiency-induced immune damage via targeting of NFκBIA in the chicken trachea

Metallomics ◽

10.1039/d0mt00164c ◽

2020 ◽

Vol 12 (11) ◽

pp. 1679-1692 ◽

Cited By ~ 2

Author(s):

Linqian Qin ◽

Yiming Zhang ◽

Chunyan Wan ◽

Zhu Wang ◽

Yimei Cong ◽

...

Keyword(s):

Selenium Deficiency ◽

Dietary Selenium ◽

Immune Injury ◽

Se Deficiency

Dietary selenium (Se) deficiency can induce multifarious immune injury in tissues, accompanied by inflammation and a decreased expression of selenoproteins.

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Ovine Myeloencephalitis-Leukomyelomalacia Associated with a Sarcocystis-Like Protozoan

Journal of Veterinary Diagnostic Investigation ◽

10.1177/104063879300500213 ◽

1993 ◽

Vol 5 (2) ◽

pp. 212-225 ◽

Cited By ~ 9

Author(s):

Donal O'Toole ◽

Martin Jeffrey ◽

Derek Challoner ◽

Roz Maybey ◽

Valerie Welch

Keyword(s):

Spinal Cord ◽

White Matter ◽

Clinical Signs ◽

Recent Exposure ◽

The North ◽

Sarcocystis Spp ◽

The Usa ◽

Pelvic Limb ◽

Ram Lambs ◽

Glial Nodules

Bilateral pelvic limb paresis developed in 7 of 15 10-month-old Blueface Leicester ram lambs on a mixed enterprise farm in the North of England. Clinical signs were principally mild to severe paresis of the pelvic limbs. Two mildly affected lambs recovered. Multifocal spinal cord white matter edema and necrosis, glial nodules, and mild to moderate nonsuppurative encephalomyelitis were the principal findings in 3 severely paretic lambs examined histologically. Protozoan bodies (12.7–23.0 μm) that stained immunocytochemically for Sarcocystis epitopes were in spinal cord glial cells of 2 of 3 lambs. Protozoa did not react immunocytochemically with anti-Toxoplasma gondii or Neospora canium antisera. Serology indicated there was recent exposure to Sarcocystis spp. in some surviving lambs. These cases resembled those in previous reports of paresis due to an unidentified Sarcocystis-like protozoan in sheep (ovine protozoan myeloencephalitis) in the British Isles, the USA, France, Australia, and New Zealand.

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6.16 Some Advances in Clinical Biochemistry Relating to Trace Metals

BSAP Occasional Publication ◽

10.1017/s0263967x00030305 ◽

1983 ◽

Vol 7 ◽

pp. 149-150

Author(s):

C. H. McMurray ◽

W. J. Blanchflower ◽

P. J. McParland ◽

D. G. O'Neill ◽

D. A. Rice

Keyword(s):

Trace Metals ◽

Blood Plasma ◽

Whole Blood ◽

Laboratory Tests ◽

Blood Clotting ◽

Clinical Biochemistry ◽

Clinical Signs ◽

Cu Deficiency ◽

Phenylene Diamine

The clinical signs of copper (Cu) deficiency are largely non-specific and a number of laboratory tests have been used extensively to assist in diagnosis. Among these are whole blood, plasma and serum Cu and caeruloplasmin (McMurray, 1980). However, for any marker to be useful diagnostically, it is necessary to identify any factors which can affect it. Plasma and serum Cu are not equivalent but are related by the equation:Serum Cu (mg/l) = 11.7 + 0.66 plasma Cu (mg/l). The regression was obtained from the means of 24 groups of suckler cows and calves (> 10 animals/group). The equivalent relationship between serum and plasma caeruloplasmin is:Serum caeruloplasmin = 0.0018+ 0.59 plasma caeruloplasmin.Units of caeruloplasmin are absorbance units in the phenylene diamine assay.Thus, the range of normality will depend on the sample being used for the assay. The reduction in serum values is due to the loss of caeruloplasmin during blood clotting.

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Studies of zinc nutrition in sheep. I. The relation of zinc to growth, testicular development, and spermatogenesis in young rams

Australian Journal of Agricultural Research ◽

10.1071/ar9690889 ◽

1969 ◽

Vol 20 (5) ◽

pp. 889 ◽

Cited By ~ 67

Author(s):

EJ Underwood ◽

M Somers

Keyword(s):

Zinc Deficiency ◽

Size Structure ◽

Clinical Signs ◽

Feed Consumption ◽

Testicular Development ◽

Sperm Production ◽

Poor Growth ◽

Testicular Growth ◽

Ram Lambs ◽

And Function

Ram lambs fed on a diet containing 2.4 p.p.m. zinc made poor growth, developed clinical signs of severe zinc deficiency, showed impaired testicular growth, and showed a complete cessation of spermatogenesis within a period of 20–24 weeks. Lambs fed on the same diet supplemented with zinc sulphate to provide total zinc levels of 17.4 and 32.4 p.p.m. had a higher feed intake, made significantly greater liveweight gains, and showed no signs of zinc deficiency. Testicular growth and sperm production were markedly improved by both the zinc supplements. No differences in liveweight gains or feed consumption between the two supplemented groups were observed but testicular growth and sperm production were highly significantly greater in the lambs receiving the larger zinc supplement. It was concluded that a dietary zinc intake of 17.4 p.p.m. is adequate for growth of ram lambs but is inadequate for normal testicular development and function. Lambs in which consumption of the diet containing 32.4 p.p.m. zinc was restricted to that of the zinc-deficient group showed no significant improvement in liveweight gains, but testicular development and sperm production were significantly greater than in the zinc-deficient lambs. Complete remission of all signs of zinc deficiency and full recovery of testicular size, structure, and function were achieved in a zinc repletion period lasting 20 weeks.

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Clinical study of experimentally induced vitamin E and selenium deficiency in Awassi ewes and their newborn lambs

The Iraqi Journal of Veterinary Medicine ◽

10.30539/iraqijvm.v36i2.458 ◽

2012 ◽

Vol 36 (2) ◽

pp. 158-162

Author(s):

H. K. Abood

Keyword(s):

Body Weight ◽

Clinical Study ◽

Vitamin E ◽

Clinical Signs ◽

Selenium Deficiency ◽

Serum Selenium ◽

Deficient Diet ◽

Sheep Industry ◽

Experimental Induction ◽

Deficient Group

Experimental induction of vitamin E and selenium deficiency by deficient diet was carried out on Awassi ewes and their newborn lambs. The clinical signs were characterized by sudden death in 4 lambs out of 14 lambs in deficient group and other lambs showed a variable signs included inability to suckle, arched back, weakness, dullness, emaciation and recumbency. Serum selenium and vitamin E levels of these lambs were 0.01 ppm and 0.34 mg/L respectively. The clinical signs in ewes included loss of body weight and loss of wool, Weakness, dullness and recumbency. Serum selenium and vitamin E levels of these ewes were 0.02 ppm and 0.61mg/L respectively. It was concluded that vitamin E and selenium are essential antioxidants and their deficiency exposes the sheep industry to many serious losses.

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