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Thiaminase type I-producing bacilli and ovine Polioencephalomalacia

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Thiaminase type 1 producing bacilli were isolated from sheep, several of which had died from polioencephalomalacia. The thiaminase type 1 was apparently identical to the thiaminase which has been implicated in the etiology of this disease. It is postulated that the thiaminases present in the rumen contents and feces of sheep may be of bacterial origin.

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... Diets high in soluble carbohydrates and low in fiber and sudden feeding changes, especially in the transfer of poor pastures to good pastures (JENSEN et al., 1956;MORO et al., 1994) may favor the occurrence of PEM. However, diets rich in soluble carbohydrates are easily fermentable, reducing rumen pH leading to rumen lactic acidosis, which inhibits the development of thiamine producing microorganisms and favors the multiplication of some thiamine degrading bacteria by thiaminase enzymes such as Clostridium sporogenes and Bacillus thiaminollyticus (MORGAN & LAWSON, 1974;SHREEVE & EDWIN, 1974;HAVEN et al., 1983). ...
... Thiaminase enzymes can also occur in plants, such as Amaranthus blitoides, Malva parviflora, Pteridium aquilinum, Marsilea drummondii, Cheilanthes sieberi and Equisetum arvense (MEYER, 1989;RAMOS et al., 2005), but they are rare and isolated. Other conditions that may lead to thiamine deficiency are the administration of vitamin B1 antimetabolic substances, such as piritiamine, oxytiamine and amprolium (LOEW & DUNLOP, 1972;MARKSON et al., 1972;MORGAN, 1974;SANT'ANA et al., 2009b) and also the use of some anthelmintics, such as levaisol and thiabendazole (LINKLATER et al., 1977). ...
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Polioencephalomalacia (PEM) is a nervous disease with neuronal necrosis. He previously believed that this condition was related to thiamine deficiency, but studies suggest that it can be determined by different nutritional and dietary factors. In this context, objectified to perform a literature review on the main causes of polioencephalomalacia caused by nutritional and dietary factors as well as the appropriate treatment and prevention in ruminants. Therefore, PEM disease can be caused by the classic thiamine deficiency, lead poisoning, sulfur and salt associated with drinking water deprivation. To prevent PEM, avoid contaminated material in pastures (avoid lead and sulfur), invasive plants (avoid thiaminases) and nutritional management of dietary thiamine concentrations and sulfur levels in water and diet. For treatment it is recommended to identify the source that causes the disease, deprivation of contaminated material and use of food management techniques, drugs needed to restore the metabolic parameters.
... However, the thiamin status can be altered and lead to cerebrocortical necrosis (CCN), a nervous syndrome well documented throughout the world. Previous studies (Edwin & Jackman, 1973;Morgan & Lawson, 1974;Shreeve & Edwin, 1974;Boyd & Walton, 1977;Boyd, 1985) have related this neurological disease to the development of high thiaminase activity in the rumen which destroys the vitamin and could induce a vitamin deficiency. However, little is known about micro-organisms which produce thiaminases in pathological conditions, and nutritional conditions which lead to the selection of thiaminase-producing strains cannot be reproduced experimentally. ...
... Despite the very low thiaminase activity, the presence of this species in RUSITEC was suspected as it can multiply within the pH range of 5-5-6-5 (Russell & Dombrowski, 1980). However, a high thiaminase activity has been attributed to species like Bacillus thiaminolyticus (Morgan & Lawson, 1974) or Clostridium sporogenes (Shreeve & Edwin, 1974) which are not usual constituents of the rumen microbial population. In this sense, the in vitro model is limited as it does not take into account accidental contamination by such species. ...
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The effects of acidogenic conditions, a high S level and the addition of thiamin on the rumen microbial metabolism of thiamin were investigated in vitro in a semi-continuous fermenter (RUSITEC), using a factorial design. Acidogenic conditions were obtained by simultaneously increasing the starch: cellulose ratio and the amount of solid substrate fed, and by decreasing the buffering capacity of the liquid phase of the fermenter. S in the form of sulfate was supplied at two levels, one corresponding to a control amount of S (2 g/kg dietary DM), the second to an excess (5 g/kg DM) which is sufficient to trigger cerebrocortical necrosis (CCN) when used in vivo. Acidogenic conditions decreased the pH of the fermenters, CH4 production and cellulose digestibility, increased the short-chain fatty acid production, but had no effect on thiamin production. The high S level enhanced the production of sulfide considerably, had no effect ont he microbial metabolism of energy and N, and decreased thiamin production (326 v. 266 nmol/d). The added thiamin was rapidly converted into phosphorylated compounds which largely decreased the apparent synthesis of this vitamin by the rumen microflora. The total thiamin flow was increased by added thiamin. In no case was thiaminase activity in the fermenter liquid phase significantly modified. The high level of S induced only a limited decrease of total thiamin flow. Consequently, it is unlikely that the investigated factors could be considered to be high risk factors for the thiamin-dependent CCN.
... A queda brusca do pH ruminal leva a inibição de componentes da microbiota que produzem tiamina e também favorece o desenvolvimento de outros que produzem tiaminases. (Morgan & Lawson, 1974). ...
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A produção leiteira pode ser influenciada por diversas enfermidades que afetam rebanhos bovinos. Dentre estas, a Síndrome da Vaca Caída (SVC) é um dos principais transtornos que acometem vacas leiteiras, principalmente no periparto. Essa síndrome possui definições variadas que são correlacionadas ao decúbito prolongado e incapacidade do animal de se manter em estação. Devido a variabilidade relacionada a etiologia, patogenia e medidas terapêuticas, as informações relacionadas a SVC se encontram dispersas na literatura científica veterinária. Objetivou-se consolidar uma base de informações técnico-científicas revisadas sistemicamente, proporcionando um material completo, pertinente e acessível para auxiliar a conduta clínica de médicos veterinários. O levantamento foi realizado através das principais bases de dados do meio cientifico e acadêmico. A seleção passou por um processo criterioso de avaliação, filtrando somente trabalhos com assunto pertinente ao tema proposto. Alguns aspectos relacionados a SVC apresentam maior relevância, como a caracterização de etiologia multifacetada. Além disso, pode ocorrer devido a doenças primárias ou secundária a lesões decorrentes do decúbito. O estabelecimento de prognóstico e tratamento adequado é dependente da causa inicial deste acometimento, necessitando de avaliação clínica correta. Contudo, alguns pontos importantes são os cuidados de enfermagem que buscam proporcionar melhores condições aos animais afetados e na maioria das vezes, consistem na utilização de diversos métodos e equipamentos na tentativa de manter o paciente em estação. O conhecimento apropriado em relação as ferramentas terapêuticas disponíveis na clínica médica de bovinos, visa minimizar consequências a saúde e proporcionar bem-estar aos animais.
... 11 The term polioencephalomalacia also might be used in reference to any neurologic disease syndrome associated with an altered thiamine status. 11 Ruminal lactic acidosis results in decreased ruminal thiamine synthesis, increased thiaminase-producing bacteria (Clostridium sporogenes and Bacillus spp), [12][13][14] and decreased activity of the thiamine diphosphate-dependent enzyme transketolase. 15,16 Transketolase is the ratelimiting enzyme in the pentose phosphate pathway, which is required for energy metabolism in nervous tissue. ...
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Background: Goats 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. Objectives: To describe clinical features and treatment outcomes of sheep and goats presented for seizures. Animals: A total of 59 goats and 21 sheep presented for seizures. Methods: Retrospective 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. Results: The 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 relevance: Seizure 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.
... The disease occurs primarily in beef calves aged 6-18 months. Under normal circumstances, thiaminase is not produced in the rumen, but under microbial conditions, as seen in rumen acidosis, a microbial flora is formed, presumably capable of producing thiaminase (Edwin et al., 1968;Morgan 1974). However, recent research show a connection between the occurrence of CCN and the quantity of intra-ruminally produced H 2 S (Cummings et al., 1995a; Cummings et al., 1995b). ...
... Dietas ricas em carboidratos e pobres em fibra e mudanças bruscas na alimentação, principalmente na transferência de pastos pobres para pastagem de boa qualidade (Jensen et al. 1956, Moro et al. 1994) favorecem a ocorrência da PEM. Dietas ricas em carboidratos são facilmente fermentáveis reduzindo o pH ruminal, levando a acidose láctica, o que inibe o desenvolvimento dos microorganismos produtores de tiamina e favorece a multiplicação de algumas bactérias que sintetizam tiaminase, como Clostridium sporogenes e Bacillus thiaminollyticus (Morgan & Lawson 1974, Shreeve & Edwin 1974, Haven et al. 1983. As reservas hepáticas de tiamina são exauridas, desencadeando deficiência sistêmica, inclusive no tecido nervoso, ocasionando as manifestações clínicas características da doença. ...
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Sant'Ana F.J.F., Lemos R. A. A., Nogueira A. P. A., Togni M., Tessele B. & Barros C. S. L. 2009. [Polioencephalomalacia in ruminants.] Polioencefalomalacia em ruminantes. Pesquisa Veterinaria Brasileira 29(9): 681-694. Laboratorio de Patologia Veterinaria, Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900, Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Polioencephalomalacia (PEM) of ruminants is a complex disease. The term indicates a morphological diagnosis where severe neuronal necrosis results in softening of cerebral grey matter. Initially though as a single disease caused by thiamine deficiency, PEM is currently believe to have several causes and different pathogenic mechanisms or a single pathogenic organism triggered by different agents are responsible for the disease. In this paper the possible causes and pathogenesis of PEM in ruminants are critically reviewed and discussed. Also are reviewed the epidemiology, clinical signs, gross and histological findings, methods of diagnosis, treatment and control.
... The disease occurs primarily in beef calves aged 6-18 months. Under normal circumstances, thiaminase is not produced in the rumen, but under microbial conditions, as seen in rumen acidosis, a microbial flora is formed, presumably capable of producing thiaminase (Edwin et al., 1968;Morgan 1974). However, recent research show a connection between the occurrence of CCN and the quantity of intra-ruminally produced H 2 S (Cummings et al., 1995a; Cummings et al., 1995b). ...
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Increased genetic potential for high milk yield and economic increased benefits in feeding rations high in starch, may increase the occurrence of rumen acidosis in Danish dairy herds. Together with enhanced focus on nutritional production diseases in recent years, the demand for professional knowledge and advisory work is substantial. The present paper reviews rumen acidosis, its etiology, pathogenesis, occurrence, significance, diagnostics and prophylaxis with special attention to Subclinical Rumen Acidosis (SRA). Details of the rumenenocentesis procedure for obtaining rumen fluid are presented together with original observations on rumen pH determinations performed on such samples compared to samples obtained by stomach tube. Differences and similarities between the subclinical and the acute form are illustrated. Our understanding of fundamental parts of pathogenesis, significance and diagnostic of set is still insufficient. It appears that the resulting metabolic acidosis is best reflected in urine. Most other suggested diagnostic parameters lack evidence of usefulness under practical conditions. Adjustments of suboptimal feeding and management routines are believed to be essential prophylactic steps.
... The action of these antagonists in enzyme systems in caused by the mechanism of competitive inhibition. The significant role in the incidence of hypovitaminosis Bl in ruminants is ascribed to thiaminases which decompose vitamin Bl (Shreeve, Edwin 1974;Morgan, Lawson 1974). ...
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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 inclu-ded the syndrome of cerebrocortical necrosis (CCN) was induced by the admini-stration 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 excitabili-ty, 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 examina-tion of brain revealed cerebral oedema and yellow coloured foci on some gyri. Histo-pathological 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 dif-ferences were found between experimental and control groups. Calf, plasma, hYPOfJitaminosis BlJ transketolase, TPP effect, vitamins A, E, C, minerals Na, K, Mg, Ca, inorg. P,Zn, and Cu, urea, glucose, acid-base balance, rumenfluid.
... Dietas ricas em carboidratos e pobres em fibra e mudanças bruscas na alimentação, principalmente na transferência de pastos pobres para pastagem de boa qualidade (Jensen et al. 1956, Moro et al. 1994) favorecem a ocorrência da PEM. Dietas ricas em carboidratos são facilmente fermentáveis reduzindo o pH ruminal, levando a acidose láctica, o que inibe o desenvolvimento dos microorganismos produtores de tiamina e favorece a multiplicação de algumas bactérias que sintetizam tiaminase, como Clostridium sporogenes e Bacillus thiaminollyticus (Morgan & Lawson 1974, Shreeve & Edwin 1974, Haven et al. 1983. As reservas hepáticas de tiamina são exauridas, desencadeando deficiência sistêmica, inclusive no tecido nervoso, ocasionando as manifestações clínicas características da doença. ...
Article
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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.Polioencephalomalacia (PEM) of ruminants is a complex disease. The term indicates a morphological diagnosis where severe neuronal necrosis results in softening of cerebral grey matter. Initially though as a single disease caused by thiamine deficiency, PEM is currently believe to have several causes and different pathogenic mechanisms or a single pathogenic organism triggered by different agents are responsible for the disease. In this paper the possible causes and pathogenesis of PEM in ruminants are critically reviewed and discussed. Also are reviewed the epidemiology, clinical signs, gross and histological findings, methods of diagnosis, treatment and control.
... The disease has been associated with the presence, in rumen digesta and faeces, of thiaminase-producing Clostridium spovogenes (Shreeve and Edwin 1974) and Bacillus spp. (Morgan and Lawson 1974). These associations were based, however, on the identification of isolates only, and were not supported by estimates of the numbers of viable organisms present in the digesta. ...
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In an attempt to clarify the reported relationship between cobalt deficiency and the incidence of cerebrocortical necrosis (CCN), sheep were fed on a diet deficient in cobalt. High levels of thiaminase activity were found regularly in rumen and faeces samples from cobalt-deficient animals, and also from controls supplemented with cobalt or vitamin B12. There was a poor correlation between thiaminase activity and viable counts of the thiaminase-producing organisms Clostvidium spovogenes and Bacillus spp. Urinary excretion of thiamine appeared normal. When the sheep were killed, normal concentrations of thiamine were found in the liver. The sheep were deficient in vitamin B12, as judged by the concentrations in serum and liver, by urinary excretion of methylmalonic acid, and by clinical condition. Twitching and weakness were observed, but clinical signs of CCN did not develop.
... Further links between sulfur-induced PEM and ruminal pH change have been explored by Gould (1998), who concluded that in diets with S concentrations exceeding 0.3%, the combination of dietary S concentration, ruminal sulfide production, and increased thiaminase production may increase incidence of PEM. Alves de Oliveria et al. (1996) reported that decreased ruminal pH did not decrease microbial production of thiamine; however, the decrease in rumen pH does favor thiaminase-producing bacteria (Morgan and Lawson, 1974;Boyd and Walton, 1977;Thomas et al., 1987). Lambs in study 2 were fed a similar finishing ration as lambs in study 1 but were adapted from a medium-concentrate diet to a high-concentrate diet concurrently with increases in DDGS concentration (and thus S content). ...
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Limited data are available regarding the influence of thiamine supplementation on the incidence of polioencephalomalacia (PEM) in lambs fed diets containing increased concentrations of S in the diet (>0.7%). Therefore, our objective was to evaluate the influence of thiamine supplementation on feedlot performance, carcass quality, ruminal hydrogen sulfide gas concentrations, and incidence of PEM in lambs fed a finishing diet containing 60% distillers dried grains with solubles (DDGS; DM basis). Two studies were conducted using completely randomized designs to evaluate the influence of concentration of thiamine supplementation. Study 1 used 240 lambs fed in 16 pens, whereas study 2 used 55 individually fed lambs. Lamb finishing diets contained 60% DDGS, which resulted in a dietary S concentration of 0.73% (DM basis). Treatments diets were based on the amount of supplemental thiamine provided: 1) no supplemental thiamine (CON), 2) 50 mg/animal per day (LO), 3) 100 mg/animal per day (MED), or 4) 150 mg/animal per day (HI). Additionally, in study 2, a fifth treatment was included, which contained 0.87% S (DM basis; increased S provided by addition of dilute sulfuric acid) and provided 150 mg of thiamine/animal per day (HI+S). In study 1, ADG decreased quadratically (P = 0.04), with lambs fed the CON, LO, and MED diets gaining BW at a greater rate than lambs fed the HI diet. In study 1, DMI responded quadratically (P < 0.01), whereas G:F tended to differ linearly (P = 0.08) to concentration of thiamine supplementation, with MED lambs having greater DMI and decreased G:F. No differences (P > or = 0.17) in lamb performance were observed in study 2. In both studies, most carcass characteristics were unaffected, with the exception of a tendency for decreased carcass conformation (study 1; P = 0.09) and greater flank streaking (study 2; P = 0.03). No differences in ruminal hydrogen sulfide concentration (P > 0.05) among treatments were apparent until d 10, at which point lambs fed the LO diet had less hydrogen sulfide concentrations than all other treatments. Lambs fed HI had the greatest concentrations of hydrogen sulfide on d 31 (1.07 g of hydrogen sulfide /m(3); P < 0.009). Ruminal pH did not differ (P = 0.13) and averaged 5.6 +/- 0.06. No clinical cases of PEM were observed during the course of either study. The use of thiamine as a dietary additive to aid in the prevention of PEM in finishing lambs does not appear to be necessary under the conditions of this study.
... Increased breakdown of thiamin in the rumen is, however, usually associated with the presence of certain microbial species e.g. Bacteroides thiaminolyticus (Morgan & Lawson, 1974; Thomas, 19866) and other Bacteroides species, Clostridium sporogenes, Megasphaera elsdenii and Streptococcus bovis (Edwin & Jackman, 1982;Wilson et al. 1984). Bact. ...
... The pH optimum for bacterial thiaminase I was 5.0. Morgan and Lawson (1974) isolated from the rumens and feces of PEM sheep, thiaminase I-producing bacilli that were weakly gram-positive and formed rods after 48 hours. Pyrimidinybnicotinic acid was isolated as a reaction end-product, indicating that a base-exchange reaction had occurred. ...
Article
SUMMARY Laminitis often follows lactic acidosis and is accompanied by increased blood and rumen histamine. However, since histamine is poorly absorbed and absorbed histamine is rapidly metabolized, and since high levels of oral histamine have not produced laminitis, it is unlikely that ruminal histamine causes lami- nitis. Lactic acidosis leads to rumenitis, which, in turn, leads to liver abscesses because the causa- tive microorganism can now cross the rumen wall into portal circulation. In cattle, hair ingested during grooming may penetrate the rumen wall and aid in this passage. Immunizing cattle against liver abscesses may be possible. Polioencephalomalacia occurs because an en- zyme, thiaminase, develops in the rumen, cata- lyzing the production of a thiamin antagonist. Lactic acidosis may set up ruminal conditions that encourage this chain of events.
... Worldwide, there is a large body of literature regarding the relationship between altered thiamine metabolism and PEM. Several investigators have measured markedly decreased concentrations of thiamine in body tissues, decreased activity of a thiamine diphosphate dependent enzyme (transketolase) in blood, (Edwin and Jackman, 1973; Roberts and Boyd, 1974; Spicer and Horton, 1981; Jackman, 1985; Rammell and Hill, 1986; Fakhruddin et al., 1987a), and increased levels of thiamine-destroying thiaminases in the gastrointestinal tract of animals with PEM (Edwin et al., 1968; Morgan, 1974). Thiamine analogues with impaired biological activity may be produced in the rumen by thiaminase I (Edwin and Jackman, 1982). ...
Article
Polioencephalomalacia (PEM) is a neuropathologic condition of ruminants that can be induced by a variety of neural metabolic disruptions. These include altered thiamine status, water deprivation-sodium ion toxicosis, lead poisoning, and high sulfur intake. Investigations of sulfur-related PEM have demonstrated that the onset of the clinical signs coincides with excessive ruminal sulfide production. A number of ruminal factors could modulate the production and absorption of ruminal sulfide. The development of a convenient method to estimate ruminal gas cap H2S has made it possible to identify cattle with high levels of ruminal H2S and evaluate their risk of developing PEM.
... The survey identified cerebrocortical necrosis as a widespread neurological disorder affecting lambs in Sardinia. Many toxins are associated with cerebrocortical necrosis, including the excessive production of sulphides in the rumen and the presence of thiaminase produced by rumen bacteria belonging to the genus Bacillus (Morgan andLawson 1974, Gould andothers 1991). Because these aetiological factors are more common after the onset of rumen function, this disease would be expected to be more common after weaning, as was observed. ...
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Histopathological and bacteriological examinations were performed on 178 brains from Sardinian sheep which were showing neurological signs. The sheep represented the total number of sheep with neurological syndromes submitted for diagnostic investigations over a three-year period in Sardinia. Scrapie was detected in 57 cases, cerebrocortical necrosis in 25, intoxication by a typical Mediterranean plant (Cistus species) was suspected in 25, coenurosis was detected in 11 cases, Listeria monocytogenes in eight cases and focal symmetrical encephalomalacia in six cases. Non-suppurative inflammatory changes were observed in three of the brains and suppurative changes were noted in two. Lesions restricted to the spinal cord were found in three cases. In the remaining 38 cases there were no significant neuropathological changes.
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This review aims first to provide specific information on microbial synthesis, the absorption and the metabolism of vitamin Bl in healthy ruminants, and on the influence of low thiamin production on rumen microbial activity. In the second part the authors discuss the etiology and the pathogenesis of cerebrocortical necrosis in the light of the most recent data. The factors involved in the microbial synthesis and catabolism of thiamin under usual feeding conditions are well known; however factors liable to disturb the net production or absorption of thiamin in the digestive tract under low- or overfeeding conditions, or in the case of inbalanced diets, are not well understood. Classical pathogenesis of cerebrocortical necrosis involves the ruminal overproduction of thiaminases I. This theory is not entirely satisfactory, since the normal rumen microflora has a low thiaminase I activity and since factors which allow the establishment of thiaminase producing bacteria are not known. Excess of sulphur in the diet also induces typical signs of cerebrocortical necrosis but its relation to a thiamin deficiency is not clear. It is more likely that we are dealing with two independant etiologies which are expressed by the same clinical syndrome.
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The interaction between ruminal metabolism and toxic or potentially toxic substances of plant and fungal origin is reviewed. Toxic compounds were classified into substances which are detoxified in the rumen, toxic substances produced in the rumen and substances which affect ruminal metabolism. Due to the large number of toxic substances in plants and to the large volume of specialized literature, this report only considers compounds of major importance under field conditions. The pathological characteristics of the diseases produced by the different toxins are described.
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Synopsis The toxicity of bracken fern ( Pteridium aquilinum (L) Kuhn) is complicated because this plant elaborates more than one type of agent potentially harmful to livestock. When simple-stomached animals are fed a diet containing some green fronds or rhizomes for a few weeks, they develop anorexia and inco-ordination symptoms; this polyneuritic syndrome shows all the characteristics of thiamine deficiency. Thiamine therapy is effective in curing the animal provided it is administered at the onset of clinical symptoms. Bracken staggers in the horse and rhizome poisoning of pigs are diseases of this nature,i.e. an avitaminosis B ¹ has been induced. The causative agent in the fern is a steam-labile enzyme, thiaminase I, which destroys thiamine in such a way that it is no longer active in animal nutrition. Acute cattle bracken poisoning occurs after frequent eating of the fern over a period of weeks.Haemorrhages and fever are the characteristic clinical symptoms, and the animal usually dies within a few days. The fundamental lesion is bone marrow aplasia resulting in a severe leucopenia and thrombocytopenia.Thiaminase I is not involved in this disease. Bracken contains an organic chemical(s) which poisons rapidly dividing cells in the bovine animal. Sheep are less sensitive to this toxic agent, although the condition has been described along with 'bright-blindness* in some parts of Britain (e.g. North York Moors). Purification of the active principle causing cattle bracken poisoning from green fronds and rhizomes is far advanced; these methods are described, along with calf toxicity tests on each fraction. Chemical investigations are also under way to determine the nature of the components. Whether the cattle factor, in small doses over an extended period of time (years), is also the agent causing tumours in livestock, is probable but not certain. Some bracken constituents shown to be carcinogenic in small animals, e.g. shikimic acid, quercetin or the tannin fraction, are not capable of producing acute cattle bracken poisoning; neither does safrole or 1-indanone. Some of the sesquiterpene glycosides—the 'pterosides' and/or their aglycones, the 'pterosins', of which over 30 have been identified in bracken—are likely candidates. On the other hand, the active principle(s) may be something quite different; the search continues.
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Bacterial thiaminase I associated with cerebrocortical necrosis of cattle and sheep is shown to utilise Δ1-pyrroline and related compounds as cosubstrates. The product resulting from the reaction of thiamine and Δ1-pyrroline is 1-(4-amino-2-methylpyrimidin-5-ylmethyl)-1-pyrrolinium chloride. This compound has been identified in the brains of calves suffering from cerebrocortical necrosis. The implications of these findings in the aetiology of other thiamine-responsive diseases of the central nervous system are briefly discussed.
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Kinetic studies of thiaminase I in extracts of ruminant faeces showed that the affinity for one substrate varied with the concentration of the other substrate in the manner of a two-step transfer mechanism. When the alternate substrate concentration was optimal, the apparent Michaelis constant ( K m ) for thiamine was 176 μΜ and the apparent K m for aniline was 3·19 mΜ. It is recommended that in routine thiaminase assays, the thiamine and aniline concentrations should be at least 1·5 and 25 mΜ, respectively. When non-saturating concentrations of thiamine are used in thiaminase assays the results should be reported as unimolecular reaction constants since the enzyme activity can be calculated only if suitable K m data have been determined. Improved radioactive and colorimetric thiaminase assays with saturating substrate concentrations gave similar results. The analytical variation of the colorimetric method was rather high but this method may be useful for laboratories which lack radioactive isotope facilities. Thiaminase assays were performed on cultures of 14 species of rumen bacteria. Only Megasphaera elsdenii had thiaminase activity and its cosubstrate specificity was different from the rumen thiaminase associated with cerebrocortical necrosis in ruminants. It was concluded that the source of rumen thiaminase in that disease has yet to be identified.
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Thiaminases from different sources exhibit varied responses to change in pH and to differing activators, cosubstrates and inhibitors. These properties are used in an attempt to characterize the extracellular thiaminases of 17 strains of Bacillus spp. isolated from the rumen contents of animals affected with cerebrocortical necrosis and to compare these with the endogenous thiaminase present in the rumen content of such animals and with other known thiaminase-producing bacteria. Statistical analysis of the results obtained using different activators classified the isolates into two main groups corresponding to the presence of thiaminase I or thiaminase II. The pH characteristics of the rumen content enzyme differed significantly from any of the bacterial isolates examined.
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The possibility of a sub-clinical state of thiamine deficiency in young cattle and sheep is discussed. A trial was carried out on six MAFF experimental husbandry farms in which groups of animals were given 100 mg of thiamine per day orally throughout the rearing period. Measurement of erythrocyte transketolase showed that the dosed group gave a significantly lower percentage thiamine pyrophosphate effect than the control group. There was no difference in weight gain of the two groups during the limited period of the trial.(Received April 14 1976)
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A rapid method for the detection of very small amounts of thiaminase activity produced by bacterial colonies is described. It can be used routinely in screening for thiaminase-producing bacteria and other colony-forming micro-organisms and offers considerable advantages over other methods.
Article
The toxicity of bracken (Pteridium aquilinum (L.) Kuhn) to animals is complicated because this plant elaborates more than one type of agent harmful to livestock. An enzyme, thiaminase I, which destroys thiamine, is responsible for the neurotoxic syndrome. Using a radiochemical assay, the distribution of thiaminase I activity in bracken throughout the growing season has been ascertained: levels are high in the rhizome and young buds, but fall sharply in the fronds as the aerial parts of the plant unfold. The so-called thermostable ‘antithiamine’ factors present in bracken and other plant species are discussed. The biochemical lesions of thiamine deficiency in animals are briefly outlined, and the clinical syndrome caused by the inclusion of bracken fronds or rhizomes in the diet for simple-stomached animals (rat, horse, pig) and a ruminant (sheep) are described. All these neurotoxic syndromes respond to thiamine therapy in a dramatic way, if administered during the early stages of the disease.
Article
Polioencephalomalacia was diagnosed histologically in cattle from two herds on the Darling Downs, Queensland, during July-August 2007. In the first incident, 8 of 20 18-month-old Aberdeen Angus steers died while grazing pastures comprising 60%Sisymbrium irio (London rocket) and 40%Capsella bursapastoris (shepherd's purse). In the second incident, 2 of 150 mixed-breed adult cattle died, and another was successfully treated with thiamine, while grazing a pasture comprising almost 100%Raphanus raphanistrum (wild radish). Affected cattle were either found dead or comatose or were seen apparently blind and head-pressing in some cases. For both incidents, plant and water assays were used to calculate the total dietary sulfur content in dry matter as 0.62% and 1.01% respectively, both exceeding the recommended 0.5% for cattle eating more than 40% forage. Blood and tissue assays for lead were negative in both cases. No access to thiaminase, concentrated sodium ion or extrinsic hydrogen sulfide sources were identified in either incident. Below-median late summer and autumn rainfall followed by above-median unseasonal winter rainfall promoted weed growth at the expense of wholesome pasture species before these incidents.
Article
The growth of strains of Bacillus thiaminolyticus was found to be inhibited by many other bacteria in glucose-containing media. The properties of the substances responsible for the inhibition were such as to suggest that they could be carboxylic acids. Carboxylic acids were found to produce a similar inhibition of B. thiaminolyticus and another thiaminase type I-producing organism, Clostridium sporogenes.
Article
We have calculated that the high thiaminase activity in the rumen of CCN-affected animals could degrade all the thiamine usually ingested and synthesized.We have confirmed that thiaminase-producing B. thiaminolyticus and Cl. sporogenes can be isolated from heat-treated rumen contents of CCN-affected sheep and cattle. The thiaminase from cultures of these bacteria is more active with the co-substrates pyridine, 3-picoline and pyridoxine than with aniline, whereas with the thiaminase from rumen fluid and faecal extracts the converse is true. The thiaminase of faecal extracts can use certain pyrrole and imidazole derivatives as co-substrates whereas the bacterial thiaminases cannot. There are also marked differences in membrane filtration, gel filtration, electrophoretic mobility and pH dependence. We conclude that neither B. thiaminolyticus nor Cl. sporogenes is the real source of rumen thiaminase.
Article
In recent years considerable progress has been made in the chemical identification of the so called thermostable 'antithiamine' factors of plants and the ways in which they may react with thiamine. The role of thiaminases in the etiology of some naturally occurring diseases of livestock has also been clarified, but the physiological significance of thiaminases within the living organisms in which they are found is still unclear. The author gives a survey of the physiology and clinical effects in animals.
Article
Polioencephalomalacia was confirmed histologically in Western Australia in sheep from 100 farms and cattle from 14 farms during the period 1965 to 1974. The condition affected sheep and cattle in good physical condition of all ages, throughout the year. Mortality rates in sheep flocks ranged from less than 1% to in excess of 10% and occurred under a number of management systems.
Article
Polioencephalomalacia (PEM) was induced in calves by feeding a semipurified, low-roughage diet of variable copper and molybdenum composition. Two formulations resulting in Cu-insufficient and Cu-sufficient forms of the diet were fed (n = 10 and 4 calves, respectively); both diets induced PEM. Clinical signs of disease developed as early as 15 days after transition to the experimental diets and included impaired vision, decreased response to external stimuli, and abnormal gait. Grossly evident cerebrocortical lesions consisted of laminar areas of cavitation and/or autofluorescence seen under UV illumination. Hepatic Cu concentration was decreased in calves fed the Cu-insufficient diet, but not below normal range. During the course of feeding either diet, rumen pH decreased, rumen volatile fatty acid concentrations increased, rumen and blood lactic acid concentrations increased, and rumen and plasma thiamine concentrations increased. The thiamine pyrophosphate effect on erythrocyte transketolase activity was unaltered in calves of either diet group. This nutritionally induced form of PEM does not appear to be related to Cu deficiency or reduction in plasma or rumen thiamine concentration.
Article
Three experiments were performed to examine for causes of poor growth of young Merino sheep. Weekly testing of animals 42 weeks of age for 10 weeks revealed that 90% of clinically poor animals were excreting high levels of thiaminase in their faeces; low levels of activity were present in 20% of clinically normal animals. There were significant differences in the mean erythrocyte transketolase activity of the thiaminase excreting poor animals and the thiaminase free normal animals. Other known causes of poor growth could not be demonstrated. Weekly monitoring of thiaminase activity in the faeces from 80 lambs 6 weeks of age showed 23% to be excreting significant levels of enzyme (greater than 3mUg-1 DM) throughout a 10 week test period. Mean growth rates of these lambs were significantly below those of lambs not excreting thiaminase or excreting low levels intermittently. Supplementation of thiaminase excreting lambs with intra-muscular injections of thiamine HCl was associated with a statistically significant improved growth rate (P less than 0.01) compared to unsupplemented sheep excreting thiaminase. Mean growth rates of lambs not excreting thiaminase on a continuous basis (sampled weekly) were the same with or without thiamine HCl supplementation. High thiaminase levels were found in the ruminal fluids of trial animals excreting the enzyme in their faeces, confirming this previously established association. Bacillus thiaminolyticus was isolated from faeces and ruminal fluids from clinically poor animals and is the most likely source of the thiaminase. Subclinical thiamine deficiency was indicated by low erythrocyte transketolase activities and elevated TPP effects and is proposed as the cause of the poor growth by the young sheep.
Article
Thiaminases play an important role in the aetiology of CCN being responsible for the state of thiamine-deficiency which is an essential feature of the disease, evidence for which is presented here. These studies have led to a greater appreciation of the role of thiamine and thiaminases in ruminant nutrition especially as ruminal thiaminase activity is not confined to clinically affected animals but is of wider distribution. The importance of thiaminases in intensive beef production and the possibility of the need for thiamine supplementation in the form of a thiaminase resistant derivative is discussed.
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