The role of comparative pathology in the study of copper and cobalt deficiencies in ruminants

Suttle, N. F.

doi:10.1016/0021-9975(88)90048-5

Cited by 31 publications

(10 citation statements)

References 73 publications

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“…The effect of excessive Mo intake and Cu deficiency and an imbalance of these 2 metals and sulphur (S) in the feed is a complex nutritional problem in ruminants dependent on a number of variables, including species and age of the animal [ 22 , 31 ]. Biochemical interactions between Cu, Mo and S that can lead to Cu deficiency and/or molybdenosis occur predominantly in the gastrointestinal tract [ 53 , 43 ]. This may explain the differences in Mo toxicity seen between ruminants and non-ruminants that have been fed the same amount of dietary Mo.…”

Section: Introductionmentioning

confidence: 99%

Experimental Copper Deficiency, Chromium Deficiency and Additional Molybdenum Supplementation in Goats – Pathological Findings

2001

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Secondary copper (Cu) deficiency, chromium (Cr) deficiency and molybdenosis (Mo) has been suggested to cause the "mysterious" moose disease in the southwest of Sweden. The present experiment was performed on goats to investigate the clinical, chemical, and pathological alterations after 20 months feeding of a semi-synthetic diet deficient in Cu and Cr. Four groups were included in the study: control group (n = 4), Cu-deficient group (group 1, n = 4), Cr-deficient group (group 2, n = 2) and Cu+Cr-deficient group (group 3, n = 3). Group 3 was additionally supplemented with tetrathiomolybdate during the last 2 months of the experiment. Main histopathological findings in groups 1 and 3 were the lesions in the liver, characterised by a severe active fibrosis, bile duct proliferation, haemosiderosis and mild necroses. Additionally, degenerative alterations of the exocrine pancreas were prominent in groups 1 and 3. Lesions in group 3 were more pronounced than in group 1. In group 3, the skin showed an atrophic dermatosis, while in group 2 a crusty dermatitis caused by Candida spp. was observed. This study shows that liver, pancreas and skin are mainly affected by a long term deficiency of copper and the findings are complicated by molybdenum application while chromium deficiency produced no histomorphological effects in our study.

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Section: Introductionmentioning

confidence: 99%

Experimental Copper Deficiency, Chromium Deficiency and Additional Molybdenum Supplementation in Goats – Pathological Findings

2001

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“…However, since other characteristic gross and histopathological findings, such as squamous metaplasia, defects in cranial bone remodelling, retinal dysplasia or thickening of the carpal joints, were not observed, vitamin A deficiency was considered unlikely (van der Lugt and Prozesky, 1989;Hill et al, 2009). Another possible cause could be copper deficiency, a well-known cause of swayback in young sheep and goats, the clinical signs of which are predominantly those of spinal cord dysfunction caused by myelin degeneration (Suttle, 1988). Nevertheless, this deficiency was ruled out in our cases, as myelodysplasia has not been described in relation to copper deficiency and biochemical analysis of serum and liver samples taken from four of the calves revealed levels of copper within the normal range.…”

Section: Discussionmentioning

confidence: 97%

“…Myelodysplasia has been related to genetic factors in Charolais and Hereford calves, although the mode of inheritance is unknown (Leipold et al, 1969). The origin of the disease in most cases is unknown and several causal agents have been proposed, including: vitamin A (van der Lugt and Prozesky, 1989;Hill et al, 2009) and copper deficiencies (Suttle, 1988), viral infection (Done et al, 1980;Kono et al, 2008) or toxic causes such as consumption of neuroteratogenic plants (Leipold et al, 1969(Leipold et al, , 1977Keeler, 1978;Washburn and Streeter, 2004).…”

Section: Introductionmentioning

confidence: 97%

Recurrent Outbreaks of Myelodysplasia in Newborn Calves

Polledo

Marı́n

Martínez-Fernández

et al. 2012

Journal of Comparative Pathology

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The present study records recurrent outbreaks of myelodysplasia of unknown origin occurring in a specific geographical location in the north of Spain, and involving up to 30% of the calves born in affected herds. The affected calves were of different breeds and displayed non-progressive signs of spinal cord dysfunction. The disease has occurred annually in February-March over a period of at least 15 years. Only calves born to cattle grazed on mountainside pastures and under high grazing pressure were affected. Seven calves were subjected to necropsy examination. Myelodysplasia was not associated with vertebral defects or arthrogryposis and involved the entire length of the spinal cord. Microscopically, there was abnormal distribution of the grey matter, aberrations of the central canal and failure of formation of the ventral median fissure. Infectious, nutritional and physical disorders were ruled out as possible aetiologies. A critical period of embryonic susceptibility to the causal agent was identified. This was during the time of secondary neurulation when cows in the early stages of gestation were grazed on mountainside pastures. Consequently, the presence of neuroteratogenic plants in these pastures is proposed as a likely cause. Two plants, Carex brevicollis and Erythronium dens-canis, which contain alkaloids, were identified on the mountainsides where affected cattle were grazed and not in other pastures, and are proposed as the possible aetiology of the disease.

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“…À medida que a concentração de Mo aumenta nas forragens, há decréscimo na concentração de Cu no organismo (Homse 1981, Suttle 1988, Underwood & Suttle 1999. As exigências nutricionais de Mo para bovinos ainda não foram perfeitamente estabelecidas, ocorrendo uma grande variação de limites, que depende dos teores de Cu e S presentes na dieta (Suttle 1975).…”

Section: Discussionunclassified

“…Outro mineral considerado um potente antagonista do metabolismo do cobre é o ferro (Humphries et al 1983, Suttle 1988, Schonewille et al 1995. Os requerimentos de Fe, na dieta do gado de corte são de aproximadamente 50 ppm (NRC 1996) e concentrações de 250 a 500 ppm de Fe na alimentação causam depleção dos níveis de Cu em bovinos (Bremner et al 1987, Phillippo et al 1987a .…”

Section: Discussionunclassified

Mortes súbitas em bovinos associadas à carência de cobre

Marques¹,

Riet-Correa

Soares³

et al. 2003

Pesq. Vet. Bras.

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Foi estudado um surto de morte súbita em bovinos no sul do Rio Grande do Sul. Nos animais necropsiados não foram observadas lesões macroscópicas ou microscópicas significativas. Para testar se as mortes súbitas teriam sido causadas por plantas tóxicas, 13 espécies de plantas foram coletadas e administradas a coelhos num total de 440 a 600 g/ kg de peso vivo num período de 7 dias. Os resultados foram negativos. Os teores de cobre no fígado dos bovinos foram muito baixos (3,6±1,6 ppm-base seca) sugerindo que as mortes foram causadas por deficiência de cobre. Cinco amostras de pasto, coletadas no local do surto, apresentaram teores normais de Cu (8,4±0,8 ppm-bs) e S (0,2%±0,03%-bs), mas altos teores de Fe (522±122 ppm-bs). Um grupo de 10 novilhas foi suplementado com Cu subcutâneo. Este grupo e um grupo controle foram mantidos em área similar à da ocorrência do surto. Teores séricos de Cu, S, Fe, Mo e ceruloplasmina foram determinados bimensalmente durante um ano de experimento. Os teores médios de Cu (1,76±1,06 a 10,34±3,1 µmol/l no grupo controle e 3,86±1,53 a 10,61±1,34 µmol/l para o grupo suplementado) e ceruloplamina (6,59±3,93 a 18,61±4,14 mg/l para o grupo controle e 10,35±5,48 a 32,49±6,05 mg/l para o grupo suplementado) foram significativamente maiores no grupo suplementado (P=0,0046 para o Cu e P=0,0001 para a ceruloplasmina), mas a maioria das amostras tiveram teores abaixo do normal em ambos os grupos. Houve uma correlação entre os teores de Cu e os de ceruloplasmina (r=0,67, P=0,05). Em ambos os grupos os teores séricos de Fe (40,09±5,22 a 78,48±28,23 µmol/l) estiveram acima dos teores normais. Amostras de forragens foram coletadas bimensalmente em sete pontos do campo onde ocorreu o surto para determinação de Cu, Mo, S, Fe e proteína. Os teores de Cu (1,36±0,56 a 4,76±1,15 ppm-bs) estiveram abaixo dos requerimentos. Os teores de Mo (0,17±0,06 a 0,96±0,47 ppm-bs) estiveram dentro da normalidade. Valores de S (0,21±0,04% a 0,5±0,17%) e Fe (172,92±62,64 a 437,24±205,44 ppm-bs) alcançaram, ocasionalmente, níveis tóxicos. Teores de proteína variaram de 7,77±2,6% a 13,16±3,02%. Seis amostras de água e 6 amostras de pasto submerso foram coletadas no fim do experimento quando o campo estava inundado. Altos teores de Fe (169, 23±83,49 ppm) e S (0,06±0,03%) foram encontrados na água. Os teores de Fe e S no pasto submerso foram de 469,5±218,28 ppm e 0,19±0,05%, respectivamente. Os resultados obtidos sugerem que as mortes súbitas foram causadas por deficiência de Cu. Três fatores parecem ser responsáveis pela deficiência de Cu: 1) altos teores de Fe na pastagem e na água; 2) ocasionalmente baixos teores de Cu na pastagem; e 3) ingestão de S acima dos requerimentos, devido aos teores ocasionalmente altos na pastagem e na água. O surto descrito é similar a outros surtos de morte súbita em bovinos descritos no sul do Rio Grande do Sul durante o inverno, que foram, também, associados a baixos teores de cobre no fígado. As regiões onde ocorre a enfermidade são caracterizadas por solos arenosos e ácidos com inundações freqüentes durante o inverno. Em solos ácidos periodicamente inundáveis o ferro é solubilizado e absorvido pelas plantas, diminuindo o conteúdo de Cu na forragem e aumentando os teores de Fe. Esta parece ser a maior razão para a deficiência de cobre na região.

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The role of comparative pathology in the study of copper and cobalt deficiencies in ruminants

Cited by 31 publications

References 73 publications

Experimental Copper Deficiency, Chromium Deficiency and Additional Molybdenum Supplementation in Goats – Pathological Findings

Experimental Copper Deficiency, Chromium Deficiency and Additional Molybdenum Supplementation in Goats – Pathological Findings

Recurrent Outbreaks of Myelodysplasia in Newborn Calves

Mortes súbitas em bovinos associadas à carência de cobre

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