Clinical evaluation and biochemical analyses of thiamine deficiency in Pacific harbor seals (Phoca vitulina) maintained at a zoological facility

Croft, Lara; Napoli, Eleonora; Hung, Connie; Leger, Judy St.; Gearhart, Scott; Heym, Kathy; Wong, Shirley; Sakaguchi, Danielle; Lin, Alex Tong‐Long; Puschner, Birgit; Giulivi, Cecilia R

doi:10.2460/javma.243.8.1179

Cited by 15 publications

(23 citation statements)

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“…A study in seals found that pregnant and lactating seals were 2.5 times more likely to develop thiamine deficiency than other female seals [18]. Lactating and maybe pregnant female dolphins should be supplemented with more thiamine than non-breeding dolphins.…”

Section: Discussionmentioning

confidence: 99%

Vitamin blood concentration and vitamin supplementation in bottlenose dolphins (Tursiops truncatus) in European facilities

2016

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BackgroundAs fish eaters bottlenose dolphins (Tursiops truncatus) in human care need to receive daily vitamin supplementation, because whole thawed fish lacks certain vitamins. However, the exact concentration of supplementation has not been established and is a matter of discussion. To ensure adequate vitamin supplementation in pets, vitamin blood concentrations are measured. This is not a common practice in dolphins. The objective of the present study was to collect information about vitamin supplementation in bottlenose dolphins and on vitamin blood concentrations of healthy animals in European facilities. In addition, these results were compared with blood levels of wild animals. Conclusions on how to provide bottlenose dolphins in human care with an effective vitamin supplementation will then be drawn.Initially, fish-handling techniques and vitamin supplementation were evaluated by questionnaire, which was sent to 25 European facilities that house bottlenose dolphins. Secondly, blood samples from 57 dolphins living in 10 facilities were taken and sent by mail to a reference laboratory. They were analysed for retinol, thiamine pyrophosphate, cobalamin, calcidiol and tocopherol. The blood concentrations were then correlated with vitamin supplementation, fish handling techniques and pre-existing blood concentrations of free-ranging dolphins. Finally, the data was subjected to a standard analysis of variance techniques (ANOVA) and a linear model analysis.ResultsFish was mainly thawed in a refrigerator. Further, the 95 % confidence interval for retinol blood concentrations was 0.048 to 0.059 mg/l and for tocopherol 17.95 to 20.76 mg/l. These concentrations were 27 and 53 %, respectively, higher than those found in free-ranging animals. In contrast, calcidiol concentrations (143.9–174.7 ng/ml) of the dolphins in human care were lower than in blood found for free-ranging animals. Regarding thiamine pyrophosphate and cobalamin, concentrations ranged between 0.42 and 0.55 mg/l and 175.55 and 275.22 pg/ml respectively. No reference concentrations for free-ranging Tursiops truncatus were found.ConclusionsThese findings suggest an over-supplementation of retinol (vitamin A) and tocopherol (vitamin E) in bottlenose dolphins (Tursiops truncatus) housed in human care. Therefore, vitamin A supplementation should not exceed 50,000 IU per animal per day and vitamin E supplementation should be around 100 IU per kg fed fish per day.Electronic supplementary materialThe online version of this article (doi:10.1186/s12917-016-0818-1) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Vitamin blood concentration and vitamin supplementation in bottlenose dolphins (Tursiops truncatus) in European facilities

2016

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“…Several studies have indicated a number of symptoms during sub‐lethal thiamine deficiency, including appetite loss or anorexia , memory and learning deficits , lethargy , immune suppression and damage to the blood–brain barrier . However, these early signs are not pathognomonic of thiamine deficiency and they may be overlooked when a well‐balanced diet is provided without considering genetic susceptibilities to this deficiency .…”

Section: Discussionmentioning

confidence: 99%

“…likely that the progression of the neurological disease that culminated in death was caused by a localized thiamine deficiency originated by the presence a loss-of-function mutation in SLC19A3.1, gene encoding for a thiamine transporter. Several studies have indicated a number of symptoms during sub-lethal thiamine deficiency, including appetite loss or anorexia (25), memory and learning deficits (62,63,92), lethargy (34), immune suppression (34) and damage to the blood-brain barrier (20,46). However, these early signs are not pathognomonic of thiamine deficiency and they may be overlooked when a wellbalanced diet is provided (25) without considering genetic susceptibilities to this deficiency (40,78).…”

Section: Discussionmentioning

confidence: 99%

“…Thiamine deficiency can result from multiple factors including: (i) the presence of anti-thiamine activity in the diet [eg, fish or fish-derived products containing thiaminase (25,50,106)]; (ii) thiamine inactivation by heat and/or sulfur dioxide; (iii) changes in thiamine demand [lactation or pregnancy or increased physical activity not matched by the consumption (25,64,94)]; and (iv) genetic defects at the level of any of the thiamine transporters (SLC25A19, SLC19A2, SLC19A3) and/or within the thiamine pathway (TPK1, THTPA, ENTPD5). Primary (genetic defect) or secondary have devastating effects across species (15,22,39,75,76,88,97,103,108,116).…”

Section: Introductionmentioning

confidence: 99%

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Thiamine Deficiency‐Mediated Brain Mitochondrial Pathology in Alaskan Huskies with Mutation in SLC19A3.1

et al. 2014

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Alaskan Husky encephalopathy (AHE1) is a fatal brain disease associated with a mutation in SLC19A3.1 (c.624insTTGC, c.625C>A). This gene encodes for a thiamine transporter 2 with a predominantely central nervous system (CNS) distribution. Considering that brain is particularly vulnerable to thiamine deficiency due to its reliance on TPP-dependent metabolic pathways involved in energy metabolism and neurotransmitter synthesis, we characterized the impact of this mutation on thiamine status, brain bioenergetics, and the contribution of oxidative stress to this phenotype. In silico modeling of the mutated transporter indicated a significant loss of alpha-helices resulting in a more open protein structure suggesting an impaired thiamine transport ability. The cerebral cortex and thalamus of affected dogs were severely deficient in TPP-dependent enzymes accompanied by decreases in mitochondrial mass and OXPHOS capacity, and increases in oxidative stress. These results along with the behavioral and pathological findings indicate that the phenotype associated with AHE is consistent with a brain-specific thiamine deficiency, leading to brain mitochondrial dysfunction and increased oxidative stress. While some of the biochemical deficits, neurobehavior and affected brain areas in AHE were shared by Wernicke's and Korsakoff's syndromes, several differences were noted likely arising from a tissue-specific vs. that from a whole-body thiamine deficiency.

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“…Some factors interfere significantly with thiamin absorption, such as the type of food processing, alcohol intake, protein and folate nutrition level, and the presence of antithiaminic factors in the diet . Intake of raw foods with high thiaminase content (such as crustaceans, sprouts, microorganisms, and some fish) can contribute or even be the direct cause of thiamin deficiency . Thiaminase is also thermolabile, and the act of cooking these foods considerably reduces the risk of thiamin deficiency .…”

Section: Thiamin: Function and Sourcesmentioning

confidence: 99%

Role of Thiamin in Health and Disease

et al. 2019

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Thiamin is a hydrosoluble vitamin that plays a role in several biological processes, mainly in glucose metabolism. There are several risk factors for developing thiamin deficiency, such as malnutrition, refeeding syndrome, gastrointestinal surgery, and alcoholism. Recently, the role of thiamin in critically ill patients has gained prominence, and the prevalence of thiamin deficiency was found to be increased in patients with severe burns, major surgery, septic shock, end-stage renal disease, and heart failure. In adults, thiamin deficiency presents as encephalopathy, dry beriberi (with neurological signs and symptoms), or wet beriberi (with cardiovascular signs and symptoms). Thiamin deficiency can be diagnosed clinically, and all clinicians should be aware of this disease, especially in patients with risk factors for thiamin deficiency. Thiamin supplementation should be started as early as possible in patients suspected to have thiamin deficiency. Treatment is safe, inexpensive, simple, and life-saving. Diagnosis is confirmed on a positive response to treatment. (Nutr Clin Pract. 2019;34:558-564)

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Clinical evaluation and biochemical analyses of thiamine deficiency in Pacific harbor seals (Phoca vitulina) maintained at a zoological facility

Abstract: Results of analyses in this study confirmed a diagnosis of thiamine deficiency for affected seals resulting from high thiaminase activity in dietary fish, inadequate vitamin administration, and increased thiamine demand caused by pregnancy and lactation.

Cited by 15 publications

References 138 publications

Vitamin blood concentration and vitamin supplementation in bottlenose dolphins (Tursiops truncatus) in European facilities

Vitamin blood concentration and vitamin supplementation in bottlenose dolphins (Tursiops truncatus) in European facilities

Thiamine Deficiency‐Mediated Brain Mitochondrial Pathology in Alaskan Huskies with Mutation in SLC19A3.1

Role of Thiamin in Health and Disease

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