scholarly journals Degenerative axonopathy associated with copper deficiency in pigs

2017 ◽  
Vol 37 (9) ◽  
pp. 911-915 ◽  
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.

The copper nutrition of grazing deer

2003 ◽  
Vol 9 ◽  
pp. 113-119
Author(s):  
N.D. Grace ◽  
P.R. Wilson ◽  
A.M. Nicol
Keyword(s):  
Trace Elements ◽  
Distribution Function ◽  
Trace Element ◽  
Cervus Elaphus ◽  
Red Deer ◽  
Copper Deficiency ◽  
Clinical Signs ◽  
Cu Deficiency ◽  
Dietary Requirements ◽  
Important Trace Element

The first deer farms were established in New Zealand about 30 years ago and much of the early deer research was focussed on general nutrition, infectious diseases, management and husbandry practices, while little attention was given to trace elements. Limited trace element studies have identified copper (Cu) as the most important trace element for deer in terms of observed clinical signs of deficiency, namely enzootic ataxia and osteochrondrosis, and their possible impact on animal performance (Wilson et al. 1979; Thompson et al. 1994). To ensure that the Cu status of deer is adequate, and to determine if a Cu supplementation strategy is necessary, it is important to understand the distribution, function and metabolism of Cu, as well as dietary Cu requirements and criteria to diagnosis Cu deficiency. Keywords: Cervus elaphus, copper, deficiency, dietary requirements, fertiliser, forage, red deer, supplementation strategies

scholarly journals Biochemical and pathological changes in tissues of Friesian cattle during the experimental induction of copper deficiency

1976 ◽  
Vol 35 (3) ◽  
pp. 309-331 ◽  
Author(s):  
C. F. Mills ◽  
A. C. Dalgarno ◽  
G. Wenham
Keyword(s):  
Monoamine Oxidase ◽  
Cytochrome Oxidase ◽  
Copper Deficiency ◽  
Early Recognition ◽  
Clinical Signs ◽  
Clinical Appearance ◽  
Cu Content ◽  
Metabolic Defects ◽  
Cu Deficiency ◽  
Friesian Cattle

1. Copper deficiency was induced in five Friesian cattle offered a semi-synthetic diet containing < 1 mg Cu/kg. Changes in blood and liver Cu contents and in the Cu-containing enzymes, ferroxidase I (caeruloplasmin;EC1.16.3.1) and monoamine oxidase (EC1.4.3.4) of plasma and cytochrome oxidase (EC1.9.3.1) of liver and skeletal muscle were monitored during Cu depletion.2. Rapid decreases in blood and liver Cu and plasma ferroxidase I activity were found at least 80 d before the first appearance of overt clinical signs of deficiency. Plasma monoamine oxidase and liver cytochrome oxidase activities decreased less rapidly and thus may provide useful indices of chronic Cu depletion.3. Although results of these assays indicated that Cu depletion was occurring and metabolic defects supervening, none facilitated the early recognition of individuals that subsequently showed marked overt clinical signs of Cu deficiency compared with those less severely affected.4. Irrespective of their clinical appearance at slaughter, Cu-depleted cattle showed gross or microscopic lesions of the skeleton and cardiovascular system and, in some instances, lesions of the ligamentum nuchae and small intestine. The aetiology of these lesions is considered with particular respect to changes in the activities of the Cu-dependent enzymes studied and to the interpretation of field surveys based solely upon determination of blood or liver Cu content.5. A second group of five cattle was offered the same diet supplemented with Cu to provide 8 mg Cu/kg and, later, 15 mg Cu/kg. Although no pathological lesions attributable to Cu deficiency were detected at slaughter a marked reduction in liver Cu content, a decrease in plasma ferroxidase I activity and, in four animals, the development of a diarrhoea controlled by oral administration of Cu, suggested that 8 mg Cu/kg diet did not meet their requirement for Cu.

scholarly journals Treatment of copper deficiency in Texel-crossbred sheep by the feeding of a concentrate formulated for dairy cows

2020 ◽  
Vol 89 (6) ◽  
pp. 325-328
Author(s):  
L. Noorman ◽  
A. F. G. Antonis ◽  
R. Jorritsma ◽  
J. T. Schonewille
Keyword(s):  
Veterinary Medicine ◽  
Dairy Cows ◽  
Copper Deficiency ◽  
Clinical Signs ◽  
Practical Method ◽  
Serum Ceruloplasmin ◽  
Cu Content ◽  
Cu Deficiency ◽  
History Of ◽  
Mild Diarrhea

Six Texel-crossbred sheep, from a flock with a history of a dull appearance and mild diarrhea, were presented to the faculty of veterinary medicine (University of Utrecht) . The clinical signs were found to be related to Copper (Cu) deficiency as indicated by low hepatic Cu values. It was decided to treat the animals by feeding them concentrates specifically formulated for dairy cows because such concentrates have a rather high Cu content compared to concentrates designed for sheep. Sheep Cu status was monitored by measuring liver Cu concentrations. Current results indicate the potential of feeding cow concentrate as a practical method to treat Cu deficiency in Texel-crossbred sheep. In contrast to hepatic Cu concentrations, serum Ceruloplasmin concentration (Cp) values did not respond to the treatment thereby indicating that serum Cp is inferior to evaluate Cu status in sheep compared to liver Cu measurements.

scholarly journals Glutamine synthetase expression in the brain during experimental acute liver failure (immunohistochemical study)

2021 ◽  
Vol 11 (10) ◽  
pp. 342-356
Author(s):  
T. Shulyatnikova ◽  
V. Tumanskiy
Keyword(s):  
White Matter ◽  
Glutamine Synthetase ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Caudate Nucleus ◽  
Immunohistochemical Study ◽  
Clinical Signs ◽  
Brain Regions ◽  
Progressive Increase ◽  
The Brain

The aim of the study was to determine the immunohistochemical level of glutamine synthetase (GS) expression in different brain regions in the conditions of experimental acute liver failure in rats. Materials and methods. The study was conducted in Wistar rats: 5 sham (control) animals and 10 rats with acetaminophen induced liver failure model (AILF). The immunohistochemical study of GS expression in the sensorimotor cortex, white matter, hippocampus, thalamus, caudate nucleus/putamen was carried out in the period of 12-24 h after acetaminophen treatment. Results. Beginning from the 6th hour after acetaminophen treatment all AILF-animals showed the progressive increase in clinical signs of acute brain disfunction finished in 6 rats by comatose state up to 24 h - they constituted subgroup AILF-B, “non-survived”. 4 animals survived until the 24 h - subgroup AILF-A, “survived”. In the AILF-B group, starting from 16 to 24 hours after treatment, a significant (relative to control) regionally-specific dynamic increase in the level of GS expression was observed in the brain: in the cortex – by 307.33 %, in the thalamus – by 249.47%, in the hippocampus – by 245.53%, in the subcortical white matter – by 126.08%, from 12th hour – in the caudate nucleus/putamen, by 191.66 %; with the most substantive elevation of GS expression in the cortex: by 4.07 times. Conclusion. Starting from the 16th hours after the acetaminophen treatment (from the 12th h in the caudate nucleus/putamen region) and up to 24 h, it is observed reliable compared to control dynamic increase in GS protein expression in the cortex, white matter, hippocampus, thalamus, caudate nucleus/putamen of the rat brain with the most significant elevation in the cortex among other regions. The heterogeneity in the degree of GS expression rising in different brain regions potentially may indicate regions more permeable for ammonia and/or other systemic toxic factors as well as heterogeneous sensitivity of brain regions to deleterious agents in conditions of AILF. Subsequently, revealed diversity in the GS expression reflects the specificity of reactive response of local astroglia in the condition of AILF-encephalopathy during specific time-period. The dynamic increase in the GS expression associated with impairment of animal state, indicates involvement of increased GS levels in the mechanisms of experimental acute hepatic encephalopathy.

Molybdenosis Leading to Type 2 Diabetes Mellitus in Swedish Moose

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).

scholarly journals Outbreak of Clostridium perfringens type D enterotoxemia in sheep

2019 ◽  
Vol 40 (6) ◽  
pp. 2593
Author(s):  
Felipe Masiero Salvarani ◽  
Mayane Faccin ◽  
Nayra Fernanda de Queiroz Ramos Freitas ◽  
Mônica Regina de Matos ◽  
Edismair Carvalho Garcia ◽  
...  
Keyword(s):  
Clostridium Perfringens ◽  
Clinical Signs ◽  
Necrotic Enteritis ◽  
Spastic Paralysis ◽  
Type D ◽  
Laboratory Confirmation ◽  
Intestinal Contents ◽  
Epsilon Toxin ◽  
History Of ◽  
Diagnostic Modalities

This work describes the first Brazilian laboratory-confirmed outbreak of enterotoxemia caused by Clostridium perfringens type D in sheep, which occurred in the state of Paraná. We address the epidemiological aspects involved, the diagnostic modalities employed, and the clinical signs and pathological findings observed. Eight healthy pregnant female sheep with no history of vaccination for clostridiosis presented with a history of abrupt feeding changes and neurological manifestations that quickly evolved to illness, coma and death. Four other females with clinical neurological signs were referred to the Veterinary Hospital of the Universidade Federal do Paraná, Palotina Sector. These animals presented with lethargy, motor incoordination, opisthotonus, pedal movements, muscle tremors, spastic paralysis, bruxism, mandibular trismus, sialorrhea, hyperexcitability and the inability to stand. They were examined and euthanized due to the seriousness of the clinical picture with an unfavorable prognosis. We performed gross anatomical and microscopic analyses of the organs and intestinal contents. We also performed bacterial isolation with molecular typing. From the intestinal contents, we detected toxins by means of the seroneutralization technique in mice. At necropsy, we noted pulmonary edema (2/4), necrotizing enteritis (4/4) and hyperemia of the leptomeninges (1/4). Microscopically, we observed lymphohistiocytic interstitial pneumonia, necrotic enteritis associated with the presence of rods, and nephrosis with interstitial lymphohistiocytic nephritis. No significant brain lesions were observed. Using serum neutralization, we identified epsilon toxin in the intestinal contents of all four animals. C. perfringens type D was identified. Based on the history, clinical signs, postmortem findings, and laboratory confirmation of the presence of epsilon toxin, we concluded that C. perfringens type D enterotoxemia caused this outbreak of sheep deaths.

scholarly journals Review of idiopathic eosinophilic meningitis in dogs and cats, with a detailed description of two recent cases in dogs : review and clinical communication

2008 ◽  
Vol 79 (4) ◽  
Author(s):  
J.H. Williams ◽  
L.S. Koster ◽  
V. Naidoo ◽  
L. Odendaal ◽  
A. Van Veenhuysen ◽  
...  
Keyword(s):  
White Matter ◽  
Immunohistochemical Staining ◽  
Nervous Tissue ◽  
Mononuclear Cells ◽  
Age Of Onset ◽  
Neospora Caninum ◽  
Clinical Signs ◽  
Post Mortem ◽  
Central Nervous Tissue ◽  
Eosinophilic Meningoencephalitis

Eosinophilic meningoencephalitis (EME) has been described in various species of animals and in humans. In dogs it has been associated with protozoal infections, cuterebral myiasis and various other aetiologies. Ten cases of idiopathic eosinophilic meningoencephalitis have been reported in dogs and one in a cat where the origin was uncertain or unknown. The dogs were all males, of various breeds but with a predominance of Golden Retrievers and Rottweilers; they generally had a young age of onset. Two cases with no apparent underlying aetiology were diagnosed on post mortem examination. The 18-month-old, male Boerboel presented with sudden onset of cerebellar ataxia, as well as various asymmetrical cranial nerve deficits of 2 weeks' duration and without progression. Haematology revealed a peripheral eosinophilia. Necropsy showed extreme generalised congestion especially of the meninges and blood smear and histological sections of various tissues showed intravascular erythrocyte fragmentation with the formation of microcytes. Histopathology revealed severe diffuse cerebrocortical subarachnoidal meningitis and submeningeal encephalitis, the exudate containing variable numbers of eosinophils together with neutrophils and mononuclear cells. There was also deeper white matter and hippocampal multifocal perivascular mononuclear encephalitis and multifocal periventricular malacia, gliosis and phagocytosis of white matter. The cerebellum, brain stem and spinal cord showed only mild multifocal oedema or scattered occasional axon and myelin degeneration respectively, with no inflammation. Immunohistochemical staining of central nervous tissue for Toxoplasma gondii failed to show any antigen in the central nervous tissue. Ultrastructure of a single submeningeal suspected parasitic cyst showed it to be chromatin clumping within a neuron nucleus indicating karyorrhexis. Gram stain provided no evidence of an aetiological agent. The 3-year-old Beagle bitch had a Caesarian section after developing a non-responsive inertia 8 days prior to presentation. This animal's clinical signs included status epilepticus seizures unrelated to hypocalcaemia and warranted induction of a barbiturate coma. She died 4 hours later. Post mortem and histopathological findings in the brain were almost identical to those of the Boerboel and she also showed histological evidence of recent active intravascular haemolysis with microcyte formation. Rabies, distemper and Neospora caninum immunohistochemical stains were negative in the brains of both dogs. Immunohistochemical staining of the cerebral and meningeal exudates of the Beagle for T- and B-lymphocyte (CD3 and CD79a) markers showed a predominance of T-lymphocytes with fewer scattered B lymphocytes. A possible allergic response to amoxicillin / clavulanate is considered, as this appeared to be the only feature common to the recent history of both animals. An overview of EME in humans, dogs and cats is given and the previously published cases of idiopathic EME in dogs and the single published cat case are briefly reviewed.

scholarly journals Ovine Myeloencephalitis-Leukomyelomalacia Associated with a Sarcocystis-Like Protozoan

1993 ◽  
Vol 5 (2) ◽  
pp. 212-225 ◽  
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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