A review of thiamine deficiency and its diagnosis, especially in ruminants

Rammell, C. G.; Hill, Justina H.

doi:10.1080/00480169.1986.35350

Cited by 25 publications

(16 citation statements)

References 31 publications

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“…Entretanto, aumentos de piruvato, lactato, oxiglutarato e da atividade do pirofosfato de tiamina (TPP) e diminuição da atividade da trancetolase eritrocitária são descritas na PEM associada e deficiência de tiamina (Rammell & Hill 1986, Radostits et al 2007. A atividade de TPP que, em bovinos e ovinos saudáveis, varia de 30 a 50%, nos casos de PEM pode atingir de 70 a 80% (Radostits et al 2007).…”

Section: Diagnósticounclassified

Polioencefalomalacia em ruminantes

Sant’Ana¹,

Lemos

Nogueira

et al. 2009

Pesq. Vet. Bras.

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Polioencefalomalacia (PEM) de ruminantes é uma doença complexa. O termo indica um diagnóstico morfológico em que necrose neuronal grave resulta em amolecimento da substância cinzenta do cérebro. Interpretada no início como uma doença única, causada por deficiência de tiamina, acredita-se hoje que várias causas e diferentes mecanismos patogênicos, ou um único mecanismo patogênico disparado por diferentes agentes, sejam responsáveis pelo aparecimento da doença. Neste artigo, as possíveis causas e a patogênese de PEM em ruminantes são criticamente revisadas e discutidas. Também são revisadas a epidemiologia, os sinais clínicos, os achados macro e microscópicos e os métodos de diagnóstico, tratamento e controle.

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Section: Diagnósticounclassified

Polioencefalomalacia em ruminantes

Sant’Ana¹,

Lemos

Nogueira

et al. 2009

Pesq. Vet. Bras.

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“…The term polioencephalomalacia also might be used in reference to any neurologic disease syndrome associated with an altered thiamine status . Ruminal lactic acidosis results in decreased ruminal thiamine synthesis, increased thiaminase‐producing bacteria ( Clostridium sporogenes and Bacillus spp), and decreased activity of the thiamine diphosphate‐dependent enzyme transketolase . Transketolase is the rate‐limiting enzyme in the pentose phosphate pathway, which is required for energy metabolism in nervous tissue .…”

Section: Discussionmentioning

confidence: 99%

Seizure Disorders in Goats and Sheep

Chigerwe

Aleman

2016

Veterinary Internal Medicne

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BackgroundGoats and sheep are more likely to be presented for examination for seizures than are cattle, possibly as a consequence of their relatively smaller body size. Currently, no reports describing seizure disorders in goats and sheep are available.ObjectivesTo describe clinical features and treatment outcomes of sheep and goats presented for seizures.AnimalsA total of 59 goats and 21 sheep presented for seizures.MethodsRetrospective study. Medical records from 1994 to 2014 at the Veterinary Medical Teaching Hospital, University of California, Davis, were reviewed. Descriptive statistics were used to summarize data. Logistic regression was performed to determine whether variables were associated with mortality.ResultsThe majority of seizures in goats and sheep had structural or metabolic causes. Polioencephalomalacia (PEM) secondary to ruminal lactic acidosis or PEM of undetermined cause was the most frequently diagnosed cause of seizures in goats and sheep. The proportions of mortality in goats and sheep were 49.2 and 42.9%, respectively. Age increased the odds mortality (odds ratio [OR], 1.51; 95% confidence interval [CI], 1.07, 2.14) in goats. Goats with structural or metabolic causes of seizures had higher odds for mortality (OR, 37.48; 95% CI, 1.12, 99.10) than those with unknown causes. Age and etiological diagnosis were not significant (P > .05) predictors of mortality in affected sheep.Conclusions and Clinical RelevanceSeizure disorders in goats and sheep are associated with high mortality, despite treatment. Current treatment in goats and sheep with seizures warrants further investigation to determine whether treatments are beneficial or detrimental to survival.

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“…Thiamine deficiency induced PEM has been reported in cattle, sheep, horses, dogs [6], goats [14], camels [15], and cats [16]. Thiamine deficiency in ruminants has be associated with several factors such as an impairment of microbial thiamine synthesis, thiamine destroying activity of bacterial thiaminase, along with other dietary factors involved in thiamine destroying activity in the rumen [17].…”

Section: Review Thiamine Deficiency Induced Pemmentioning

confidence: 99%

“…All these factors produce similar brain lesions [3,5]. Regardless of the suspected cause of PEM, affected animals frequently respond to thiamine administration [6][7][8]. For this reason, it is commonly believed that thiamine deficiency is a major metabolic factor involved in the pathogenesis of PEM.…”

Section: Introductionmentioning

confidence: 99%

A review of polioencephalomalacia in ruminants: is the development of malacic lesions associated with excess sulfur intake independent of thiamine deficiency?

Amat

Olkowski²,

Atila³

et al. 2013

Vet Med Anim Sci

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Polioencephalomalacia (PEM), also known as cerebrocortical necrosis, is an important neurologic disease that affects ruminants. Thiamine deficiency and sulfur (S) toxicity have been well recognized as major etiological factors. The mechanism of thiamine deficiency associated PEM has been well elucidated. However, the role of S in PEM pathogenesis remains unclear, although the relationship between S toxicity and PEM has been established for 3 decades. The development of S-induced malacic lesions is believed to be independent of thiamine deficiency, since blood thiamine levels in affected individuals remain in the range of normal animals. However, cattle affected by S-induced PEM frequently respond to thiamine treatment in early disease stages. Thiamine supplementation is reported to reduce the incidence and severity of S-induced PEM. This suggests a possible metabolic relationship between excess S intake and thiamine in the development of malacic lesions. Such an association is further supported by recent studies reporting that high dietary S may increase the metabolic demand for thiamine pyrophosphate (TPP), a critical cofactor in several metabolic pathways. Systemic failure to synthesize metabolically requisite levels of TPP in the brain may be an important precursor in the pathogenesis of S-induced PEM. There is increasing evidence of the importance of thiamine in the pathogenesis of S-induced PEM. Thus, understanding the potential role of S-thiamine interaction in the development of malacic lesions is important step to determine the mechanism of S-induced PEM. The objective of this article is to provide an overview of thiamine deficiency and S toxicity associated PEM, and to discuss the potential role of S-thiamine interaction in the pathogenesis of S-induced PEM in ruminants.

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A review of thiamine deficiency and its diagnosis, especially in ruminants

Cited by 25 publications

References 31 publications

Polioencefalomalacia em ruminantes

Polioencefalomalacia em ruminantes

Seizure Disorders in Goats and Sheep

A review of polioencephalomalacia in ruminants: is the development of malacic lesions associated with excess sulfur intake independent of thiamine deficiency?

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