Thiamine deficiency in a dog associated with exclusive consumption of boiled sweet potato (Ipomoea batatas): Serial changes in clinical findings, magnetic resonance imaging findings and blood lactate and thiamine concentrations.

Thiamine (vitamin B1 ) is an essential nutrient that significantly influences ATP production in the body. It needs to be supplemented consistently through an exogenous source to prevent deficiency; however, it is easily affected by a variety of mitigating factors. Additionally, thiamine requirements can be influenced by an individual's dietary composition. The nervous system is particularly vulnerable to thiamine deficiency due to its high metabolic demand. Thiamine deficiency is typically diagnosed based on clinical signs, dietary history and response to thiamine administration. A 5-year-old neutered male Maltese Terrier dog presented with an acute onset of seizures and generalized ataxia. The dog was exclusively fed boiled sweet potato (Ipomoea batatas) as a primary diet source for 4 weeks. MR findings and hyperlactatemic conditions were consistent with thiamine deficiency, and the diagnosis was confirmed by measuring thiamine concentrations in blood using high-performance liquid chromatography (HPLC). Appropriate thiamine supplementation and diet changes resulted in a rapid improvement in neurological signs. Repeated MR imaging 2 weeks after starting the treatment completely resolved the previously identified abnormalities, and repeated measurements of blood lactate and thiamine levels revealed complete recovery of the thiamine-deficient status.

Thiamine status, metabolism and application in dairy cows: a review.

As the co-enzyme of pyruvate dehydrogenase and α-ketoglutarate dehydrogenase, thiamine plays a critical role in carbohydrate metabolism in dairy cows. Apart from feedstuff, microbial thiamine synthesis in the rumen is the main source for dairy cows. However, the amount of ruminal thiamine synthesis, which is influenced by dietary N levels and forage to concentrate ratio, varies greatly. Notably, when dairy cows are overfed high-grain diets, subacute ruminal acidosis (SARA) occurs and results in thiamine deficiency. Thiamine deficiency is characterised by decreased ruminal and blood thiamine concentrations and an increased blood thiamine pyrophosphate effect to >45 %. Thiamine deficiency caused by SARA is mainly related to the increased thiamine requirement during high grain feeding, decreased bacterial thiamine synthesis in the rumen, increased thiamine degradation by thiaminase, and decreased thiamine absorption by transporters. Interestingly, thiamine deficiency can be reversed by exogenous thiamine supplementation in the diet. Besides, thiamine supplementation has beneficial effects in dairy cows, such as increased milk and component production and attenuated SARA by improving rumen fermentation, balancing bacterial community and alleviating inflammatory response in the ruminal epithelium. However, there is no conclusive dietary thiamine recommendation for dairy cows, and the impacts of thiamine supplementation on protozoa, solid-attached bacteria, rumen wall-adherent bacteria and nutrient metabolism in dairy cows are still unclear. This knowledge is critical to understand thiamine status and function in dairy cows. Overall, the present review described the current state of knowledge on thiamine nutrition in dairy cows and the major problems that must be addressed in future research.

Expression of Thiaminase in Zebrafish (Danio rerio) is Lethal and Has Implications for Use as a Biocontainment Strategy in Aquaculture and Invasive Species.

As the world increasingly relies on aquaculture operations to meet rising seafood demands, reliable biocontainment measures for farmed fish stocks are desired to minimize ecological impacts arising from interactions of cultured fish with wild populations. One possible biocontainment strategy is to induce a dietary dependence on a vitamin, such as thiamine (vitamin B1), required for survival. Fish expressing thiaminase (an enzyme that degrades thiamine) within a confined aquaculture facility could receive supplemental thiamine to allow survival and normal growth, whereas escapees lacking this dietary rescue would die from thiamine deficiency. To test the concept and efficacy of such a dietary dependency system (for potential future use in larger aquaculture species), we expressed thiaminase in zebrafish as a test model. We drove the expression of thiaminase under the strong ubiquitous and constitutive control of the CMV promoter which resulted in non-viable fish, indicating that the thiaminase sequence kills fish. However, the CMV promoter is too strong to allow conditional survival since the lethality could not be rescued by exogenous thiamine provided as a supplement to typical food. In addition, microinjection of 0.5 pg of thiaminase mRNA in zebrafish embryos at the one-cell stage resulted in 50% larval mortality at 5 days post-fertilization (dpf), which was partially rescued by thiamine supplementation. Evaluating the efficacy of biocontainment strategies helps assess which methods can reliably prevent ecological impacts arising from breaches in physical containment systems that release engineered organisms to nature, and consequently provides critical information for use in regulatory risk assessment processes.

Outbreak of thiamine deficiency in cats associated with the feeding of defective dry food.

Objectives The objective of this study was to determine disease progression, association between neurological signs and magnetic resonance imaging (MRI) findings, and long-term outcome in feline thiamine deficiency associated with defective dry food. Methods The clinical records of 17 cats diagnosed with thiamine deficiency related to a defective dry food were examined and data collected. The thiamine level in the food was analysed by liquid chromatography-tandem mass spectrometry. Results The thiamine level in the food was below the recommendation of the National Research Council. Fifteen cats were fed the food exclusively. Prior to the acute development of neurological signs, most cats displayed non-specific signs such as anorexia, lethargy or vomiting. Vestibular signs of varying severity were observed in 94% of the cats, and all but one of these presented with bilateral dysfunction. Other main neurological signs included altered mentation (76%), blindness (59%) and seizures (59%). Moreover, 80% of the cats with seizures presented with cluster seizures or status epilepticus. MRI abnormalities consistent with findings reported in the previous literature were detected in five cases. MRI was unremarkable in one cat with ongoing severe neurological signs even though thiamine had been administered. Most surviving cats recovered rapidly within 2 weeks of treatment and had either returned to normal or had minimal neurological signs at the 2 month follow-up. One cat recovered slowly over 6 months. Most cats with seizures in the initial stage of the disease remained seizure free at the 24 month follow-up. Conclusions and relevance This study documented the association between feline thiamine deficiency and defective dry food. MRI examination provided valuable information in the diagnosis. However, normal MRI findings do not exclude the diagnosis of feline thiamine deficiency, especially once thiamine has been supplemented. MRI findings also may not always reflect the neurological status or severity. If treated promptly, most cats will recover rapidly with a good outcome. Occasionally, recovery may be slow and take several months.

Polioencephalomalacia and Heart Failure Secondary to Presumptive Thiamine Deficiency, Hepatic Lipidosis, and Starvation in 2 Abandoned Siamese Cats.

Two 4-year-old spayed female Siamese cats were seized by the British Columbia Society for the Prevention of Cruelty to Animals after confinement to an abandoned housing unit without food for 9 weeks. One cat was found dead, and the second was euthanized within 24 hours due to neurologic deterioration despite therapy. Polioencephalomalacia of the caudal colliculus, hepatic lipidosis, cachexia, and congestive heart failure with cardiomyocyte atrophy were identified in both cats through postmortem examination and attributed to a prolonged period of starvation. Brain lesions were likely the result of thiamine deficiency (Chastek paralysis), which can be associated with both malnutrition and liver disease. This case highlights the importance of thiamine supplementation during realimentation of cats with hepatic lipidosis. Heart failure resulting from cachexia may have contributed to the death of the first cat and the morbidity of the second cat.

Clinical signs, MRI features, and outcomes of two cats with thiamine deficiency secondary to diet change.

Two cats were presented with vestibular signs and seizures. Both cats were diagnosed with thiamine deficiency. The transverse and dorsal T2-weighted magnetic resonance (MR) images revealed the presence of bilateral hyperintense lesions at specific nuclei of the midbrain, cerebellum, and brainstem. After thiamine supplementation, the clinical signs gradually improved. Repeated MR images taken 3 weeks after thiamine supplementation had started showed that the lesions were nearly resolved. This case report describes the clinical and MR findings associated with thiamine deficiency in two cats.

Thiamine deficiency in a cat: resolution of MRI abnormalities following thiamine supplementation.

Thiamine (vitamin B(1)) is an essential component of a number of metabolic pathways and thiamine deficiency results in a progressive encephalopathy in both humans and animals. Confirming thiamine deficiency is problematic and relies on demonstrating reduced red blood cells transketolase activity, or indirect methods including urinary organic acid analysis and dietary analysis. The characteristic and selective vulnerability of different brain regions in carnivores has been demonstrated by magnetic resonance (MR) imaging in the dog and cat as an aid to diagnosis. A 2-year-old, female, domestic shorthair cat was presented with an acute onset of seizures and ataxia. MR imaging was consistent with thiamine deficiency and supplementation resulted in a progressive clinical improvement. Repeated MR imaging 4 days after starting thiamine supplementation revealed near complete resolution of the MR abnormalities. Repeated MR imaging following appropriate therapy may be useful to further confirm thiamine deficiency.

Thiamine deficiency in dogs due to the feeding of sulphite preserved meat.

A 6-year-old dog, a 4-year-old dog and three 7-week-old puppies were diagnosed with thiamine deficiency caused by feeding sulphite treated meat. The 6-year-old dog presented with a history of inappetence, weight loss and vomiting that rapidly progressed to signs of multifocal intracranial disease including mental dullness, paresis, seizures, spontaneous nystagmus and strabismus. Thiamine pyrophosphate effect was elevated at 58% and magnetic resonance imaging revealed bilaterally symmetrical hyperintensity of the caudate nucleus and rostral colliculi. The dog recovered with thiamine supplementation. The 4-year-old dog and three 7-week-old puppies also presented with rapidly progressive multifocal central nervous system signs including ataxia, paresis, increased muscle tone, seizures, nystagmus and exophthalmos. The 4-year-old dog made a rapid recovery with thiamine supplementation. Euthanasia and necropsy of a puppy revealed malacia of multiple brainstem nuclei and oedema of the cerebral cortex. These findings were consistent with thiamine deficiency.

Thiamine deficiency in a cat associated with the preservation of 'pet meat' with sulphur dioxide.

A cat with allergic dermatitis was fed a diet of fresh meat and a multi-vitamin supplement for 38 days to exclude food allergy as a cause of its dermatopathy. The cat died as a result of acute thiamine deficiency, which was caused by inactivation of thiamine by the preservative, sulphur dioxide. The continuing undeclared usage of sulphites in the Australian pet food industry is discussed.

Hypokalaemic episodic polymyopathy in cats fed a vegetarian diet.

A previously undocumented hypokalaemic condition with a cyclical nature, comprising acute bouts of polymyopathy followed by spontaneous recoveries, is described in the cat. Cats being fed a high protein vegetarian diet developed recurrent episodes of polymyopathy, characterised by ventroflexion of the head and neck, stiff forelimb gait, lateral head-resting and generalised muscle weakness. Plasma potassium concentrations (mean +/- standard deviation) were reduced from 3.28 +/- 0.33 mmol/l at the beginning of the experiment to 2.45 +/- 0.24 mmol/l during bouts of myopathy. This hypokalaemia was associated with increased creatine kinase activities indicative of muscle damage, and decreased urinary potassium concentrations, and was caused by insufficient dietary potassium. Cats that received the same diet supplemented with potassium did not develop hypokalaemic polymyopathy. Spontaneous recoveries of affected cats were not associated consistently with increases in plasma potassium concentrations. Plasma taurine concentrations decreased and glutamic acid increased markedly in all cats fed the experimental diet. There was no evidence of thiamin deficiency associated with the high glutamic acid intake. Veterinarians should be aware that hypokalaemic cats, and in particular those on potassium-deficient diets, may show cyclical disease with episodes of polymyopathy recurring after periods of spontaneous clinical recovery. This condition in cats may be a useful animal model for familial hypokalaemic periodic paralysis in humans.

Vitamin deficiencies in cattle.

Deficiencies of vitamins A, D, K, E and thiamin can cause severe limitations in beef production. In particular, vitamin A and E can be common causes of lost profit, secondary to limitations of reproductive and growth potential. Prolonged dry periods will reduce available A and E in pasture forage, as can ensiling and prolonged storage of harvested feedstuffs. Polioencephalomalacia is a thiamin responsive disorder, associated with high concentrate feeding and lush pastures. Antimetabolites, such as amprolium, will cause thiamine deficiency when fed in excess. Recent information has shown improved performance with supplemental beta carotene and niacin. The positive responses in reproductive performance, noted with cattle fed supplemental beta carotene, was independent of vitamin A. Supplementation of vitamins above National Research Council recommendations can be justified. However, proper evaluation of feed and animal status, and documentation of a response to supplementation is necessary before diagnosing deficiencies of specific nutrients.

Thiamin deficiency in cats and dogs associated with feeding meat preserved with sulphur dioxide.

Thiamin deficiency was diagnosed in cats and dogs being fed fresh minced meat, which contained sulphur dioxide as a preservative and less than 0.5 mg/kg thiamin. Thiamin in the meat and in added dietary ingredients, including a supplementary vitamin mixture, was destroyed by the sulphur dioxide.

Comparison of three methods of thiamine supplementation by measurement of urinary thiamine excretion in sheep.

The relative efficacy of thiamine supplementation to sheep by injection, subcutaneous implant and orally administered protected thiamine bolus was compared in two experiments using a grass and hay ration and a ration containing bracken rhizomes to induce thiamine deficiency. In both experiments, urinary excretion of thiamine was significantly higher in supplemented sheep than in the controls, and in sheep supplemented by injection than in sheep supplemented by implant or protected boluses. Thiamine excretion was lower in sheep fed the ration containing bracken rhizomes than in sheep fed the grass ration.

Comparison of transketolase activity and thiamin pyrophosphate levels in erythrocytes and liver of rainbow trout (Salmo gairdneri) as indicators of thiamin status.

Yearling rainbow trout (Salmo gairdneri) were fed a purified diet with and without thiamin supplementation for 30 wk, at which time overt signs of thiamin deficiency appeared in the deficient group. Overt signs of thiamin deficiency were anorexia, darkening and ataxia. Death rapidly followed the development of overt thiamin deficiency. Transketolase activity and thiamin pyrophosphate levels were measured monthly in erythrocyte and liver samples. Significant differences in erythrocyte transketolase activity between fish fed the thiamin-deficient and control diets were measured after 24 wk of feeding. No significant difference in liver transketolase activity was found between trout fed diets with or without thiamin supplementation. Thiamin pyrophosphate levels were significantly lower in erythrocytes and liver of fish fed the thiamin-deficient diet after 16 wk of feeding. Thiamin pyrophosphate levels in erythrocytes and liver were found to be a more sensitive indicator of thiamin status of rainbow trout than erythrocyte or liver transketolase activity.

Influence of thiamin supplements on furazolidone-induced cardiomyopathy in turkey poults.

Furazolidone (700 ppm) was fed to turkey poults from 2 to 5 weeks of age. The drug produced a cardiomyopathy and reduced the feed intake and growth of the birds. Thiamin was concurrently injected into the furazolidone-fed poults to determine whether the vitamin would prevent or reduce the severity of the cardiotoxic effect of the drug. Supplemental injections of thiamin had no significant effect on feed consumption or growth of the birds nor did they protect the heart against the cardiotoxicity. The conclusion is that furazolidone-induced cardiomyopathy is not caused by a thiamin deficiency.

Natural establishment of thiaminase activity in the alimentary tract of newborn lambs and effects on thiamine status and growth rates.

Thiaminase activity was detected in the faeces of lambs at 2 to 5 days of age. Levels of activity increased for 10 days and then declined over the next 3 to 4 weeks. Decreased erythrocyte transketolase activity indicated thiamine insufficiency in lambs with high thiaminase activity. Mean growth rates were 17% less in lambs with high thiaminase activity than in lambs with zero or low thiaminase activity. Bacillus thiaminolyticus was the only organism isolated which produced thiaminase. Treatment of newborn lambs with intramuscular injections of sulphadoxine did not prevent them from excreting thiaminase in their faeces. It is proposed that oral thiamine supplementation of lambs at 2 to 3 weeks of age may be the most appropriate prevention and treatment for subclinical thiamine deficiency of the cause described.

The effect of thiaminase-induced subclinical thiamine deficiency on growth of weaner sheep.

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.

Involvement of water-soluble vitamins in diseases of swine.

The various roles of the water-soluble vitamins (including choline and vitamin C) in diseases of swine are outlined. The most important role is in the prevention of deficiency disease; another important role is in relation to the immune response. Deficiency signs relating to each vitamin are described and the metabolism of each vitamin is outlined. Recent estimates of requirements are set out, together with suggestions on supplementation of practical diets for swine.

Thiamin and niacin in the rumen.

Thiamin analogs, produced in the rumen by thiaminase I, in the presence of a cosubstrate appear to be responsible for the central nervous system disorder, polioencephalomalacia (PEM). For PEM to occur, an analog must be produced that inhibits an essential thiamin-requiring reaction, and results from a cosubstrate present in the rumen. In high concentrate diets, thiaminase I is produced by rumen microbes. However, PEM can also be caused by thiaminase I of plant origin. Based on physical characteristics and cosubstrate specificity, the thiaminase I enzymes produced by Bacillus thiaminolyticus and Clostridium sporogenes appear to be different from the enzyme produced by the rumen. Because niacin and certain antihelmentics are thiaminase I cosubstrates, they should be used cautiously. Supplementary niacin increased microbial protein synthesis in vitro and in vivo, and was more effective with urea than soybean meal. Supplementary niacin (5 to 6 g X cow-1 X d-1) increased milk production in postpartum cows but not in those in mid-lactation, and in cows fed soybean meal but not in those fed urea. We believe the heating of soybean meal during commercial processing decreased the availability of niacin for rumen protozoa. Supplementary niacin for postpartum cows increased blood glucose, decreased blood ketones and reduced the incidence of ketosis. Niacin flow to the small intestine and its absorption from the small intestine increased with niacin supplementation. Supplemental niacin prevented the postpartum decrease in red blood cell niacin observed in control cows.