Diagnostic aspects of cerebrocortical necrosis

Edwin, E. E.; Markson, L.M.; Shreeve, J.; Jackman, R.; Carroll, PJ

doi:10.1136/vr.104.1.4

Cited by 39 publications

(15 citation statements)

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“…Already 14 days after the administration of Amprolium the TK activity decreased while the TPP effect was found to increase in calves with the experimentally induced CCN. The increase of the TPP effect observed by us was always substantially lower than the values reported by Edwin et al (1979). When studying the dynamics of plasma levels of vitamin A, E and C, of minerals Na, K, Ca, Mg, inorganic P, Zn, and Cu, of urea, glucose, aspartate aminotransferase and gamma glutamyl transferase activity, blood acid-base balance and of some other parameters in rumen fluid no significant differences were found between the ex-perimental and control group.…”

Section: Discussioncontrasting

confidence: 49%

Syndrome of Cerebrocortical Necrosis Experimentally Induced in Calves by Administration of Amprolium

Bouda¹,

Jagos²,

Dvořák³

et al. 1982

Acta Vet. Brno

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Bouda J., P. Jagoi, V. DvoUk, L. Pivnik: Syndrome of Cerebrocortical Necrosis Experimentally Induced in Calves by Administration of Amprolium. Acta vet. Bmo, SO,1981: 109-116 In the experiment into which three experimental and four control calves were included the syndrome of cerebrocortical necrosis (CCN) was induced by the administration of Amprolium. Pathogenesis and symptomlltology of the condition were followed. After the intraruminal administration of Amprolium (O.5g/calf/day) the clinical signs appeared in two calves after six weeks while in the third calf after 56 days. The main clinical features were: inappetence, blindness, increased excitability, symptoms of static and kinetic ataxia. Calves rose with difficulties, had difficulty avoiding objects, muscular tremor and opisthotonus appeared, when falling tonic--clonic convulsions and paddling movements were observed. The observed clinical signs were identical with those of spontaneous cases of CCN in calves.Statistically significant decrease of thiamine content was determined in cerebral cortex, cardiac and skeletal muscle of experimental calves. In liver tissue there was no significant decrease of thiamine level. Fourteen days after the administration of Amprolium the erythrocyte transketolase activity was found to decrease while the thiamine pyrophosphate effect in blood increased. Pathologico-anatomical examination of brain revealed cerebral oedema and yellow coloured foci on some gyri. Histopathological changes in these parts were characterized by necrosis of the grey matter and enormous infiltration of macrophages. However, when compiuing the plasma levels of vitamin A, E and C, minerals, Na, K, Ca, Mg, inorganic P, Zn, Cu, or urea, glucose, asparateaminotransferase and gamma glutamyl transferase activity, acid-base balance in the blood and of some parameters in the rumen fluid, no significant differences were found between experimental and control groups.

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Section: Discussioncontrasting

confidence: 49%

Syndrome of Cerebrocortical Necrosis Experimentally Induced in Calves by Administration of Amprolium

Bouda¹,

Jagos²,

Dvořák³

et al. 1982

Acta Vet. Brno

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“…No entanto, em 1956, no Colorado, EUA, o termo PEM foi empregado para designar não somente urna lesão, mas uma doença especí-fica de ruminantes, presumivelmente causada por deficiência de tiamina e caracterizada por necrose do córtex telencefálico (Jensen et al 1956), e tem sido usado desde então como sinônimo dessa condição em ruminantes. A denominação necrose cerebrocortical é usada para designar a mesma condição na Europa (Markson et al 1972, Edwin et al 1979, Jeffrey et al 1994.…”

Section: Introductionunclassified

Polioencefalomalacia em bovinos: epidemiologia, sinais clínicos e distribuição das lesões no encéfalo

et al. 2009

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Thirty one cases of polioencephalomalacia (PEM) diagnosed from 1999-2008 in cattle from the Southern (13 cases) and Midwestern (18 cases) Brazil were studied. Morbidity (0.04%-6.66 %), mortality (0.04%-6.66 %), and lethality (50%-100%) rates were similar in both regions studied. There was no clear association between PEM cases and age, sex or seasonality. Cases occurred mainly in cattle raised at pasture; in the Southern the disease affected mainly young cattle (one-year old or less) while mainly older cattle (three-year-old or older) were affected in the Midwest. Clinical signs more frequently observed included blindness, incoordination, circling, opisthotonus, recumbence and peddling movements. Clinical course varied from 12 hours to 8 days (average three days and a half). In 11 cases no gross changes were observed in the brain. Main gross findings in the brain of remaining cases included congestion with swelling and flattening of gyri, softening and yellow discoloration of cerebral cortex, hemorrhagic foci in the brain stem, cerebellum and telencephalon, and cerebellar herniation. The main histopathological changes were in the cortex of occipital, parietal and frontal telencephalic lobes; however less prominent and less frequently found lesions occurred in the hippocampus, basal nuclei, thalamus, midbrain, and cerebellum. The type of microscopic cortical lesions was consistent in all cases and included segmentar laminar neuronal necrosis (red neurons), spongiosis, swollen of vascular endothelial nuclei, Alzheimer type II astrocytes and infiltration of gitter cells. In 20% of the cases there was mild lymphohistiocytic cellular infiltrate and in 13% of the cases there was mild infiltrate by neutrophils and eosinophils. Additionally, mild to moderate necrohemorrhagic lesions were observed in 49% of the cases in the basal nuclei, in 39% of the cases in brain stem and in 26% of the cases in the thalamus. Brain lesions were consistently found in the cortical laminae of the occipital, parietal and frontal telencephalic lobes. In such locations, most frequently affected cortical layers both by neuronal necrosis and edema were external and internal granular layers. Both gyri and sulci were equally affected.INDEX TERMS: Diseases of cattle, neuropathology, distribution of lesions, polioencephalomalacia.

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“…Gejala klinis yang muncul akibat keracunan molasses tersebut meliputi penurunan suhu tubuh, kelelahan, air liur berlebihan, peningkatan respirasi dan hewan terlihat seperti mabuk (Pate, 1983;Rowe et al, 1977). Gejala keracunan molasses yang lain adalah gangguan syaraf dan kebutaan akibat dari nekrosis pada otak (Edwin et al, 1979). Nekrosis pada otak tersebut kemungkinan disebabkan oleh pasokan energi ke otak yang terganggu akibat defisiensi enzim transketolase pirofosfat yang berfungsi untuk metabolisme glukosa lebih lanjut (Losada and Preston 1973;Rowe et al, 1977).…”

Section: Toksisitas Molassesunclassified

Molasses : dampak negatif pada ruminansia

Yanuartono¹,

Nururrozi²,

Indarjulianto

et al. 2017

JIIP

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ABSTRACT:Molasses is a by-product or end product of sugar cane (Saccharum officcinarum L.) or sugar-beet (Beta vulgaris L. var. Conditiva) resulting from the manufacture of raw or refined sugar and consisting of structural sugars, hemicelluloses and minerals. It is mainly used to improve appetite of animals or add extra energy when prices of molasses are lower than that of other energy sources. Molasses can be a key ingredient for cost effective management of feeds and pastures. Supplementing poor quality feeds with molasses will increase feed intake and improve palatability. However, molasses can be toxic if fed at ad libitum or free for choice, therefore, it is recommended that molasses should be supplemented in a restrictive form. These molasses poisoning papers and the negative impacts arose from long-standing studies because the poisoning is now rare. However, although this time is rare but did not close the possibility will appear again, Especially if given in an uncontrolled amount. Thus, this paper aims to remind users of molasses in the livestock industry to be wiser in their use.

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Diagnostic aspects of cerebrocortical necrosis

Cited by 39 publications

References 0 publications

Syndrome of Cerebrocortical Necrosis Experimentally Induced in Calves by Administration of Amprolium

Syndrome of Cerebrocortical Necrosis Experimentally Induced in Calves by Administration of Amprolium

Polioencefalomalacia em bovinos: epidemiologia, sinais clínicos e distribuição das lesões no encéfalo

Molasses : dampak negatif pada ruminansia

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