Subclinical thiamine deficiency results in failed reproduction in Arctic foxes.

Thiamine deficiency can result in life-threatening physiological and neurological complications. While a thiamine-deficient diet may result in the onset of such symptoms, the presence of thiaminase - an enzyme that breaks down thiamine - is very often the cause. In such instances, thiaminase counteracts the bioavailability and uptake of thiamine, even when food-thiamine levels are adequate. Here, we report on a case of failed reproduction in seven Arctic fox (Vulpes lagopus) breeding pairs kept at a captive breeding facility, including the presentation of severe thiamine deficiency symptoms in two male foxes. Symptoms included ataxia, obtundation, truncal sway, star-gazing and visual impairment. Blood tests were inconclusive, yet symptoms resolved following treatment with a series of thiamine hydrochloride injections, thereby verifying the diagnosis. A fish-dominated feed, which for the first time had been frozen for a prolonged period, was identified as the likely source of thiaminase and subsequent deterioration in the animals' health. Symptoms in the two males arose during the annual mating period. All seven breeding pairs at the captive breeding station failed to reproduce - a phenomenon never recorded during the captive breeding facility's preceding 17-year operation. Relating our findings to peer-reviewed literature, the second part of this case report assesses how thiamine deficiency (due to thiaminase activity) likely resulted in subclinical effects that impaired the production of reproduction hormones, and thereby led to a complete breeding failure. While previous work has highlighted the potentially lethal effects of thiamine deficiency in farmed foxes, this is, to our knowledge the first study showing how subclinical effects in both males and females may inhibit reproduction in foxes in general, but specifically Arctic foxes. The findings from our case report are not only relevant for captive breeding facilities, but for the welfare and management of captive carnivorous animals in general.

Establishment of a reference interval for thiamine concentrations in healthy dogs and evaluation of the prevalence of absolute thiamine deficiency in critically ill dogs with and without sepsis using high-performance liquid chromatography.

OBJECTIVE: To determine the normal reference interval (RI) for thiamine concentrations in healthy dogs and investigate the prevalence of thiamine deficiency in critically ill dogs with and without sepsis. DESIGN: Prospective, observational, multicenter study, conducted between 2019 and 2021. SETTING: Two veterinary university teaching hospitals. ANIMALS: A total of 109 dogs were enrolled into 3 groups: 40 healthy dogs, 33 dogs with suspected or confirmed sepsis and evidence of tissue hypoperfusion (Doppler blood pressure ≤90 mm Hg or plasma lactate ≥3 mmol/L), and 36 dogs with other critical illnesses and evidence of tissue hypoperfusion. INTERVENTIONS: For each dog, CBC, serum biochemistry, plasma lactate concentration, whole-blood thiamine concentration, blood pressure, vital parameters, Acute Patient Physiologic and Laboratory Evaluation (APPLE)fast score, and clinical outcomes were recorded, alongside basic patient parameters and dietary history. Whole-blood thiamine pyrophosphate (TPP) concentrations were measured using high-performance liquid chromatography. MEASUREMENTS AND MAIN RESULTS: The RI for whole-blood TPP in healthy dogs was 70.9-135.3 µg/L. Median TPP concentrations were significantly lower in septic dogs compared to healthy controls (P = 0.036). No significant difference in median TPP concentrations was found between septic dogs and nonseptic critically ill dogs, or between healthy dogs and nonseptic critically ill dogs. TPP concentrations were below the normal RI in 27.3% of septic dogs, compared to 19.4% of nonseptic critically ill dogs (P = 0.57). No correlations were found between TPP concentrations and lactate concentrations, age, body condition scores, time since last meal, RBC count, serum alanine aminotransferase, APPLEfast scores, or patient outcomes. CONCLUSIONS: TPP concentrations were significantly lower in septic dogs compared to healthy controls, with an absolute thiamine deficiency found in 27.3% of septic dogs. The established TPP RI allows for further investigation of thiamine deficiency in critically ill dogs.

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.

Clinical reasoning in feline vestibular syndrome: which presenting features are the most important?

OBJECTIVES: The aim of this study was to evaluate whether clinical variables from the history, clinical presentation, and physical and neurological examinations of cats with vestibular syndrome were statistically predictive of the underlying diagnosis. METHODS: In total, 174 cats presenting with vestibular syndrome between January 2010 and May 2019 were investigated. Univariate statistical analysis of clinical variables was performed and those statistically associated with a diagnosis were retained for multivariable binary logistic regression modelling. RESULTS: The seven most prevalent diagnoses represented 95% of vestibular presentations, which included: otitis media/interna (n = 48), idiopathic vestibular syndrome (n = 39), intracranial neoplasia (n = 24), middle ear polyp (n = 17), feline infectious peritonitis (n = 13), thiamine deficiency (n = 13) and intracranial empyema (n = 11). Idiopathic vestibular syndrome was commonly associated with non-purebred cats and had 17.8 times the odds of an improving clinical progression (95% confidence interval [CI] 1.3-250.0; P = 0.03). Intracranial neoplasia was associated with older age and chronic onset of clinical signs, and was significantly more likely to have a central vestibular neuroanatomical localisation (95% CI 8.5-344,349,142.0; P = 0.015) with postural deficits on neurological examination. Thiamine deficiency was more common in female cats, with 52.6 times the odds of a waxing and waning clinical progression (95% CI 1.2-1000; P = 0.038) and 6.8 times the odds of presenting with bilateral vestibular signs (95% CI 1.0-45.7; P = 0.047) and wide excursions of the head (95% CI 1.0-45.7; P = 0.047). Middle ear polyps were associated with 8.8 times the odds of presenting with Horner syndrome (95% CI 1.5-50.0; P = 0.015). CONCLUSIONS AND RELEVANCE: Although it may be difficult to identify the underlying diagnosis in cats with vestibular syndrome from the presenting features alone, there are instances in which discrete clinical features may help to guide clinical reasoning when evaluating cats with vestibular presentations.

Severe thiamine deficiency in eastern Baltic cod (Gadus morhua).

The eastern Baltic cod (Gadus morhua) population has been decreasing in the Baltic Sea for at least 30 years. Condition indices of the Baltic cod have decreased, and previous studies have suggested that this might be due to overfishing, predation, lower dissolved oxygen or changes in salinity. However, numerous studies from the Baltic Sea have demonstrated an ongoing thiamine deficiency in several animal classes, both invertebrates and vertebrates. The thiamine status of the eastern Baltic cod was investigated to determine if thiamine deficiency might be a factor in ongoing population declines. Thiamine concentrations were determined by chemical analyses of thiamine, thiamine monophosphate and thiamine diphosphate (combined SumT) in the liver using high performance liquid chromatography. Biochemical analyses measured the activity of the thiamine diphosphate-dependent enzyme transketolase to determine the proportion of apoenzymes in both liver and brain tissue. These biochemical analyses showed that 77% of the cod were thiamine deficient in the liver, of which 13% had a severe thiamine deficiency (i.e. 25% transketolase enzymes lacked thiamine diphosphate). The brain tissue of 77% of the cod showed thiamine deficiency, of which 64% showed severe thiamine deficiency. The thiamine deficiency biomarkers were investigated to find correlations to different biological parameters, such as length, weight, otolith weight, age (annuli counting) and different organ weights. The results suggested that thiamine deficiency increased with age. The SumT concentration ranged between 2.4-24 nmol/g in the liver, where the specimens with heavier otoliths had lower values of SumT (P = 0.0031). Of the cod sampled, only 2% of the specimens had a Fulton's condition factor indicating a healthy specimen, and 49% had a condition factor below 0.8, indicating poor health status. These results, showing a severe thiamine deficiency in eastern Baltic cod from the only known area where spawning presently occurs for this species, are of grave concern.

Deficiency syndromes in top predators associated with large-scale changes in the Baltic Sea ecosystem.

Vitamin B1 (thiamin) deficiency is an issue periodically affecting a wide range of taxa worldwide. In aquatic pelagic systems, thiamin is mainly produced by bacteria and phytoplankton and is transferred to fish and birds via zooplankton, but there is no general consensus on when or why this transfer is disrupted. We focus on the occurrence in salmon (Salmo salar) of a thiamin deficiency syndrome (M74), the incidence of which is highly correlated among populations derived from different spawning rivers. Here, we show that M74 in salmon is associated with certain large-scale abiotic changes in the main common feeding area of salmon in the southern Baltic Sea. Years with high M74 incidence were characterized by stagnant periods with relatively low salinity and phosphate and silicate concentrations but high total nitrogen. Consequently, there were major changes in phytoplankton and zooplankton, with, e.g., increased abundances of Cryptophyceae, Dinophyceae, Diatomophyceae and Euglenophyceae and Acartia spp. during high M74 incidence years. The prey fish communities also had increased stocks of both herring and sprat in these years. Overall, this suggests important changes in the entire food web structure and nutritional pathways in the common feeding period during high M74 incidence years. Previous research has emphasized the importance of the abundance of planktivorous fish for the occurrence of M74. By using this 27-year time series, we expand this analysis to the entire ecosystem and discuss potential mechanisms inducing thiamin deficiency in salmon.

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.

Thiamine Levels in Muscle and Eggs of Adult Pacific Salmon from the Fraser River, British Columbia.

Multiple species and stocks of Pacific salmon Oncorhynchus spp. have experienced large declines in the number of returning adults over a wide region of the Pacific Northwest due to poor marine survival (low smolt-to-adult survival rates). One possible explanation for reduced survival is thiamine deficiency. Thiamine (vitamin B1 ) is an essential vitamin with an integral role in many metabolic processes, and thiamine deficiency is an important cause of salmonid mortality in the Baltic Sea and in the Laurentian Great Lakes. To assess this possibility, we (1) compared muscle thiamine content over time in a holding experiment using Fraser River (British Columbia) Sockeye Salmon O. nerka to establish whether adults that died during the holding period had lower thiamine levels than survivors, (2) measured infectious loads of multiple pathogens in held fish, and (3) measured egg thiamine content from four species of Pacific salmon collected on Fraser River spawning grounds. Chinook Salmon O. tshawytscha had the lowest egg thiamine, followed by Sockeye Salmon; however, egg thiamine concentrations were above levels known to cause overt fry mortality. Thiamine vitamers in the muscle of Fraser River adult Sockeye Salmon shifted over a 13-d holding period, with a precipitous decline in thiamine pyrophosphate (the active form of thiamine used in enzyme reactions) in surviving fish. Survivors also carried lower loads of Flavobacterium psychrophilum than fish that died during in the holding period. Although there is no evidence of thiamine deficiency in the adults studied, questions remain about possible thiamine metabolism-fish pathogen relationships that influence survival.

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.

Physiological changes and reproductive performance of Sterlet sturgeon Acipenser ruthenus injected with thiamine.

To evaluate the effects of thiamine on physiological changes and spawning performance of Sterlet sturgeon Acipenser ruthenus, 45 farmed female fish (698.6±8.9g) were randomly distributed in 9 tanks (1000L) and fed a diet with 1g/kg of an anti-thiamine drug. This was provided for 5 months prior to spawning. Thiamine hydrochloride was intraperitoneally injected to fish at three different doses: 0 (T0, as control), 5 (T5) and 50 (T50) mg/kg body weight at days 30, 90 and 150 after the experiment started. After five months, the results showed no significant differences in weight gain and hemoglobin level, but hematocrit significantly increased in T5 group. There was no significant difference in glucose-6-phosphate dehydrogenase and estradiol-17ß, but testosterone was significantly increased in the T50 group. Total thiamine concentration in the eggs was significantly higher in T50 than that detected in the control group. Fecundity and larval mortality at 6day post hatch (dph) showed no significant differences among treatments, while the number of eggs per gram was significantly lower in T0 than that observed in T50. Larval weights at 1 (11.6mg) and 6 (23.1mg) dph and larval lengths at 6 (15.6mm) dph were significantly affected by the treatment with the highest level of thiamine injection (T50). Diseases symptoms such as yolk sac deformation, erratic pattern of swimming, and loss of equilibrium were observed at 4 dph in T0 and T5 groups. The overall results revealed that thiamine injection has positive effects on reproductive performance in the sturgeon and the negative impacts of anti-thiamine in the offspring can be reduced by the injection of this vitamin to the broodstock.

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.

Thiamin deficiency induces impaired fish gill immune responses, tight junction protein expression and antioxidant capacity: Roles of the NF-κB, TOR, p38 MAPK and Nrf2 signaling molecules.

In this study, we investigate the effects of dietary thiamin deficiency on immune responses, tight junctions, antioxidant capacity and related signaling molecules in the gills of young grass carp (Ctenopharyngodon idella). Fish were fed diets that contained 0.12-2.04 mg thiamin kg(-1) for 8 weeks. We found that dietary thiamin deficiency resulted in reduced complement 3 content, lysozyme and acid phosphatase activities, mRNA levels of hepcidin, liver-expressed antimicrobial peptides 2, transforming growth factor (TGF)-ß1, interleukin (IL)-10, inhibitor protein-κBα (IκBα), ribosomal S6 protein kinase 1 and target of rapamycin (TOR) and increased expression of interferon-γ2, tumor necrosis factor-α, TGF-ß2, IL-1ß, IL-8, IκB kinases (IKKß and IKKγ) and nuclear factor-κB p65 (NF-κB p65). Our findings showed that thiamin deficiency reduced the immune status of fish gills. Furthermore, thiamin deficiency resulted in reduced mRNA transcript levels of claudin b, claudin 3, claudin 12, zonula occludens 1 (ZO-1) and occludin and increased mRNA transcript levels of claudin 15a, myosin light-chain kinase (MLCK) and p38 mitogen-activated protein kinase (p38 MAPK) in fish gill tissues. These data suggested that thiamin deficiency disrupted tight junction-mediated fish gill barrier function. Additionally, reactive oxygen species, malondialdehyde and protein carbonyl levels and both the activities and expression levels of Cu/Zn superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferases and glutathione reductase, as well as NF-E2-related factor 2 gene expression in fish gills, were lower in fish fed a thiamin-deficient diet. By contrast, thiamin deficiency increased levels of Kelch-like-ECH-associated protein 1a (Keap1a) and Keap1b mRNA transcript expression in fish gills. Taken together, our findings indicated that thiamin deficiency impaired fish gill health by effects on the expression of genes encoding cytokines, tight junction proteins, antioxidant enzymes, NF-κB p65, MLCK and Nrf2.

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.

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

Alaskan Husky encephalopathy (AHE(1) ) 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 predominately (CNS) central nervous system distribution. Considering that brain is particularly vulnerable to thiamine deficiency because of its reliance on thiamine pyrophosphate (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 oxidative phosphorylation (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.

In vitro immune functions in thiamine-replete and -depleted lake trout (Salvelinus namaycush).

In this study we examined the impacts of in vivo thiamine deficiency on lake trout leukocyte function measured in vitro. When compared outside the context of individual-specific thiamine concentrations no significant differences were observed in leukocyte bactericidal activity or in concanavalin A (Con A), and phytohemagglutinin-P (PHA-P) stimulated leukocyte proliferation. Placing immune functions into context with the ratio of in vivo liver thiamine monophosphate (TMP--biologically inactive form) to thiamine pyrophosphate (TPP--biologically active form) proved to be the best indicator of thiamine depletion impacts as determined using regression modeling. These observed relationships indicated differential effects on the immune measures with bactericidal activity exhibiting an inverse relationship with TMP to TPP ratios, Con A stimulated mitogenesis exhibiting a positive relationship with TMP to TPP ratios and PHA-P stimulated mitogenesis exhibiting no significant relationships. In addition, these relationships showed considerable complexity which included the consistent observation of a thiamine-replete subgroup with characteristics similar to those seen in the leukocytes from thiamine-depleted fish. When considered together, our observations indicate that lake trout leukocytes experience cell-type specific impacts as well as an altered physiologic environment when confronted with a thiamine-limited state.

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

OBJECTIVE: To determine thiamine-dependent enzyme activities in various tissue samples of Pacific harbor seals (Phoca vitulina) and thiaminase activities in dietary fish. DESIGN: Cross-sectional study. ANIMALS: 11 Pacific harbor seals with thiamine deficiency and 5 control seals. PROCEDURES: Seals underwent evaluation to rule out various diseases and exposure to toxins. For seals that died, measurement of thiamine-dependent enzymes in liver and brain samples and determination of mitochondrial DNA (mtDNA) copy number in liver, brain, and muscle samples were performed. Thiaminase activity in dietary fish was determined. RESULTS: 8 seals with thiamine deficiency died. Affected seals typically had acute neurologic signs with few nonspecific findings detected by means of clinicopathologic tests and histologic examination of tissue samples. Thiamine-dependent enzyme activities in liver samples of affected seals were significantly lower than those in control liver samples. The primary activation ratios and latencies for enzymes indicated that brain tissue was more affected by thiamine deficiency than liver tissue. Activities of pyruvate dehydrogenase were more affected by thiamine deficiency than those of transketolase and ketoglutarate dehydrogenase. For control seals, the mtDNA copy number in muscle samples was significantly lower than that for affected seals; conversely, the copy number in control liver samples was significantly greater than that of affected seals. Thiaminase activity was substantially higher in smelt than it was in other types of dietary fish. CONCLUSIONS AND CLINICAL RELEVANCE: 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.

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.

Impact of thiamine deficiency on T-cell dependent and T-cell independent antibody production in lake trout.

Lake trout Salvelinus namaycush on thiamine-replete and thiamine-depleted diets were evaluated for the effects of thiamine status on in vivo responses to the T-dependent antigen trinitophenol (TNP)-keyhole limpet hemocyanin (TNP-KLH), the T-independent antigen trinitrophenol-lipolysaccaharide (TNP-LPS), or Dulbecco's phosphate-buffered saline (DPBS; negative control fish). Plasma antibody concentrations were evaluated for possible differences in total anti-TNP activity as well as differences in response kinetics. Associations between anti-TNP activity and muscle and liver thiamine concentrations as well as ratios of muscle-to-liver thiamine to anti-TNP activity were also examined. Thiamine-depleted lake trout that were injected with TNP-LPS exhibited significantly more anti-TNP activity than thiamine-replete fish. The depleted fish injected with TNP-LPS also exhibited significantly different response kinetics relative to thiamine-replete lake trout. No differences in activity or kinetics were observed between the thiamine-replete and -depleted fish injected with TNP-KLH or in the DPBS negative controls. Anti-TNP activity in thiamine-depleted lake trout injected with TNP-KLH was positively associated with muscle thiamine pyrophosphate (thiamine diphosphate; TPP) concentration. A negative association was observed between the ratio of muscle-to-liver TPP and T-independent responses. No significant associations between anti-TNP activity and tissue thiamine concentration were observed in the thiamine-replete fish. We demonstrated that thiamine deficiency leads to alterations in both T-dependent and T-independent immune responses in lake trout.