In cooperation with
Timely Topics in Nutrition
Thiamine deficiency in dogs and cats
Jessica E. Markovich, DVM, DACVIM; Cailin R. Heinze, VMD, MS, DACVN; Lisa M. Freeman, DVM, PhD, DACVN
I n past years, nutritional deficiencies were considered
to be an important problem in dogs and cats. Cur-
rently, most pet owners in many countries, such as the
United States and Canada, feed nutritionally balanced
commercial pet foods. As a result, nutritional deficien-
cies have become uncommon because reputable pet
food manufacturers regularly test their products to en-
sure that they contain adequate amounts of all nutri-
ents. Anecdotally, most reported deficiencies currently
arise from animals eating incomplete or unbalanced
homemade, vegetarian, or raw meat diets. Therefore,
veterinarians may not consider deficiencies as differen-
tial diagnoses in animals eating traditional commercial
diets. However, thiamine (vitamin B1) deficiency is of
clinical concern even today. Since 2009, there have been
5 major voluntary pet food recalls involving thiamine-
deficient pet foods in the United States that ultimately
involved 9 brands of cat foods and at least 23 clinically
affected cats.1 Most of these recalls were instituted in
response to a report from a consumer or veterinarian af-
ter treating a cat that had clinical signs consistent with
thiamine deficiency.
In addition to the possibility of a deficiency in
commercial pet foods, there are a variety of situations in
which a deficiency may arise in dogs or cats with medi-
cal conditions. Clinical manifestations of a deficiency
of thiamine are variable, and the disease is likely under-
reported because of the wide array of clinical signs in
combination with a lack of specific clinicopathologic
changes detected via laboratory analysis.
Thiamine has received much attention as a vitamin
deficiency that is common in ruminants, primarily as
a result of rumen bacterial inactivation of the vitamin,
which results in characteristic cerebrocortical necrosis
and neurologic signs.2 Dogs and cats can also be affected
by deficiency of this vitamin because of an inability to
endogenously synthesize large quantities of thiamine.
Therefore, both cats and dogs need to have a consis-
tent dietary supply of thiamine. As with all B vitamins,
thiamine is water soluble, stored in the body in small
amounts, and subject to urinary losses.3 Thiamine is also
particularly labile and easily destroyed by typical food-
processing techniques.4 In fact, many early experiments
From the Department of Clinical Sciences, Cummings School of
Veterinary Medicine, Tufts University, North Grafton, MA 01536.
Support for Dr. Markovich was provided by VCA Antech Inc.
Address correspondence to Dr. Freeman (Lisa.Freeman@tufts.edu).
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13-01-0012_TTN.indd 649
AAFCO
ABBREVIATIONS
Association of American Feed Control
Officials
GFR Glomerular filtration rate
HPLC High-performance liquid chromatography
NRC National Research Council
TCA Tricarboxylic acid cycle
TPP Thiamine pyrophosphate
on thiamine deficiency were performed by autoclaving a
pet food and then feeding it.5 Most pet food manufactur-
ers add additional sources of thiamine to compensate for
thiamine lost through processing.4 However, despite best
efforts, thiamine-deficient commercial pet foods some-
times are still produced. The information provided here
is intended to describe the clinical syndrome of thiamine
deficiency in companion animals as well as to highlight
several causes of thiamine deficiency that have been de-
scribed in the literature.
Physiologic Functions of Thiamine
The B vitamins are numbered in order of their
isolation. In 1911, thiamine, as the name vitamin B1
implies, was the first B vitamin isolated.6 Thiamine
is found naturally in many plants, particularly whole
grains and grain products (eg, rice and wheat germ) as
well as yeast and legumes. Thiamine is also found in
meat products, often concentrated in the liver, heart,
and kidneys.7 After ingestion, thiamine is absorbed in
the small intestine, primarily the jejunum and ileum.7
Studies6,8 in rats, humans, and dogs have revealed that
the amount of thiamine in the diet dictates the amount
and process of absorption because there are both active
and passive carrier transport processes. When there are
excessive amounts of thiamine in the diet, thiamine is
absorbed from the intestinal lumen via a passive dif-
fusive process, whereas when there is a paucity of thia-
mine in the diet, thiamine is actively absorbed from the
intestinal tract.8 In contrast to cobalamin, a genetic de-
fect of the intestinal thiamine transporter has not been
identified in dogs or cats.3
Once absorbed, most of the thiamine is carried
within RBCs, whereas the remaining thiamine is bound
to plasma proteins or is free in plasma.9,10 Thiamine par-
ticipates in several vital biochemical pathways within
Vet Med Today: Timely Topics in Nutrition 649
8/16/2013 1:31:33 PM
 the body, namely the TCA cycle in the process of carbo-
hydrate metabolism and the pentose phosphate pathway
(Figure 1). It is these important roles in carbohydrate
metabolism that dictate the pathological findings and
clinical signs seen in animals with thiamine deficiency.
There are 4 naturally occurring forms or deriva-
tives of thiamine in the body. Most of the thiamine
in an animal is found in a phosphorylated form, TPP,
whereas the nonphosphorylated forms are more com-
mon in plants.7 Thiamine pyrophosphate, also known
as thiamine diphosphate, is the most biologically ac-
tive form within the body because TPP is the form of
thiamine that is a cofactor in both the TCA cycle and
the pentose phosphate pathway (Figure 1). Within the
TCA cycle, TPP is an integral cofactor in the conver-
sion of pyruvate to acetyl-CoA. Without TPP, an excess
amount of pyruvate and lactate is produced, which can
lead to type B lactic acidosis.11
Cats are more susceptible to thiamine deficiency
than dogs because cats have approximately a 3-fold
higher requirement for the vitamin than their canine
counterparts.7 For example, the NRC-recommended
allowance for adult cats is 1.4 mg of thiamine/1,000
kcal of metabolizable energy, whereas the NRC-recom-
mended allowance for adult dogs is 0.56 mg of thia-
mine/1,000 kcal of metabolizable energy.7 Although
AAFCO does not adjust minimum amounts of thia-
mine on the basis of life stage, the NRC-recommended
allowance for thiamine is higher for reproduction,
compared with the allowance for adult maintenance,
for cats.7,12 Interestingly, although AAFCO and NRC
have no specific guidelines for vitamin or other nu-
trient requirements for geriatric animals, older people
appear to be more susceptible to thiamine deficiency
than are younger individuals, irrespective of health
status.13

Figure 1—Schematic diagram of the role of TPP as an integral cofactor in both the TCA cycle and the pentose phosphate (PP) pathway
for glucose metabolism. The important roles of TPP in these pathways dictate the clinicopathologic findings and clinical importance of
thiamine deficiency. Large black arrows indicate that multiple steps were condensed. NADPH = Reduced form of nicotinamide adenine
dinucleotide phosphate.

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 Mechanisms of Thiamine Deficiency
Systemic disease states can affect absorption, reten-
tion, and metabolism of thiamine in the body. In terms
of absorption, intestinal malabsorptive or other chronic
enteropathy conditions can affect the uptake of thia-
mine from the diet,6 whereas medications (eg, diuretics)
that increase urinary losses can potentiate the excretion
of vitamin B1.14 Furthermore, the number and efficiency
of thiamine transporters in the small intestines, heart,
liver, and brain correlate with the overall absorption
and usage of thiamine within the body. Investigators
of a recent study15 found that rats with chronic kidney
disease (5/6 nephrectomy scale) developed downregu-
lation of thiamine and folate transporters in the small
intestines, heart, liver, and brain. Thiamine primarily
undergoes renal excretion in a nonlinear manner that
is largely dependent on a combination of GFR, tubular
secretion, and tubular reabsorption.14 As the GFR is re-
duced as a result of kidney disease, plasma concentra-
tions of thiamine may actually increase.16 In contrast,
in the physiologic normal state, medications such as di-
uretics or other diseases that cause an increase in GFR
may also cause total body depletion of thiamine.14,17
Clinical Signs of Thiamine Deficiency
Clinical signs associated with thiamine deficiency
are variable and nonspecific, and may involve several
body systems2,5,9,18–22 (Table 1). Gastrointestinal signs
are typically the first manifestation, but neurologic
signs are often the ones most commonly associated with
thiamine deficiency.2,18 In cats, spastic cervical ventro-
flexion may be detected that initially resembles marked
hypokalemia; however, in cats with thiamine deficiency,
the ventroflexion worsens and the cats will continue to
look at the ground when held upside down (eg, wheel-
barrow position).2,18 Ocular examination often reveals
anisocoria or mydriasis with decreased to absent pu-
pillary light reflexes and lack of menace responses but
no abnormalities evident during fundic examination.2
Nystagmus or blindness may also be evident. It is im-
portant to remember that in the early stages of thiamine
deficiency, clinical signs are often nonspecific and can
therefore lead to a misdiagnosis until overt neurologic
signs are evident.
Thiamine deficiency can result in several electro-
cardiographic abnormalities, which may be evident as
Table 1—Common clinical signs of thiamine deficiency in dogs
and cats.2,5,9,18–22
Neurologic Ocular
• Acute blindness
• Altered mentation
• Acute blindness • Mydriasis or aniscoria
• Proprioceptive deficits • Nystagmus
• Ataxia
• Polyneuropathy Gastrointestinal tract
• Spastic ventroflexion • Anorexia or hyporexia
of the head and neck • Weight loss
• Extensor rigidity • Vomiting
• Vestibular signs • Constipation
• Paresis
• Hyperesthesia Cardiac
• Tremors • Tachycardia
• Seizures • Brachycardia
• Coma
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bradycardia or tachycardia.23 In 1 study,23 investigators
found an excitement syndrome that consisted of a brief
period of tachycardia, followed by severe bradycardia
and rhythm irregularity in nearly all of the cats during
the end stages of thiamine deficiency. Electrocardio-
graphic changes can include flattening or inversion of
the T wave, QRS prolongation, or prolongation of the
ST segment.23
Three progressive stages associated with thiamine
deficiency have been described: induction, critical, and
terminal.2,5 As described in a controlled study5 and a
retrospective report,2 the induction stage generally de-
velops within 1 week after animals begin eating a diet
severely deficient in thiamine and is characterized by
hyporexia, vomiting, or both. Typically, an animal must
be thiamine deficient for slightly more than 1 month
before the terminal stage is reached.5 However, once the
terminal stage has started, an animal will die within a
few days if the deficiency is not corrected immediately.5
Despite this, nearly all reported cases of thiamine de-
ficiency in dogs and cats have been diagnosed in the
third or terminal stage. Although these time periods
were described in a study5 performed in 1944, and cats
with experimentally induced thiamine deficiency were
included in that study, there is much more variation
in clinical signs, which makes it more challenging to
arrive at the diagnosis. Typically, it can take weeks to
months for the development of clinical signs, which are
attributable to subchronic deficiency because most di-
ets are not entirely devoid of thiamine. Mitigating fac-
tors include the amount of thiamine in the food, nutri-
ent composition of the diet, whether the animal eats
a consistent diet, and species and health status of the
animal.
Risk Factors for Developing
Thiamine Deficiency
Diets that have low concentrations of thiamine are
a clear risk factor for the development of deficiency.
However, a variety of other diet factors can increase or
decrease an animal’s risk for developing a deficiency of
thiamine. In particular, animals that are fed unconven-
tional diets (eg, raw food diets, nutritionally incomplete
or unbalanced commercial pet foods, or home-prepared
diets) have a number of unique risks.
The composition of the diet can affect an animal’s
dietary thiamine requirements. Diets that are high in
protein and fat can have a thiamine-sparing effect,
whereas those that are high in carbohydrates can actu-
ally increase thiamine requirements and worsen the ef-
fects of thiamine deficiency.19,24 The reason for this dis-
crepancy is that high-carbohydrate diets require greater
use of the TCA cycle, which requires thiamine to com-
plete the conversion of glucose into energy (Figure 1).
Thus, when there are more carbohydrates in the diet,
thiamine is depleted more rapidly.
In addition, the rate of metabolism and the require-
ment of the TCA cycle for energy differ among tissue
types within the body. Tissues with a higher require-
ment for glucose as the primary source of energy (eg,
neural tissues in the brain) are more affected by thia-
mine deficiency than are other tissues in the body that
have the ability to use lactate or pyruvate for energy.
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 Furthermore, some areas of the brain are more affected
than other areas, depending on the metabolic require-
ment for glucose. Those areas that are most affected de-
fine the primary neurologic signs associated with thia-
mine deficiency.
Although dry foods can be deficient in thiamine,
it is more common in canned foods for a number of
reasons. Canned food production is a multistep process
that involves grinding and mixing of the food, filling
and sealing of the cans, and sterilizing the food within
the cans.25 The sterilization (retort) step is important
for destroying common pathogenic bacteria. However,
thiamine is a heat-labile vitamin, and losses of > 50%
of the thiamine content have been considered to be a
result of processing.25 In addition, some canned diets
include alkalinizing gelling agents that can alter the pH
and therefore the availability of thiamine.7 Manufac-
turers should consider all of these factors, use analytic
methods to estimate the amount of thiamine lost to
processing or inactivated because of pH, and supple-
ment the diet with additional sources of thiamine prior
to the sterilization process to compensate for impend-
ing losses.25 In addition, reputable manufacturers will
analyze the final diet to determine the content of thia-
mine and other nutrients to ensure that they meet mini-
mum values.
The duration and environmental conditions associ-
ated with storage of a commercial cat or dog food after
manufacturing can further affect the amount of vitamin
loss over time. Although B vitamins are not as suscep-
tible to loss during storage as are fat-soluble vitamins,
thiamine is one of the B vitamins most susceptible to
loss during storage.7 For dry pet foods, overall vitamin
B loss has been estimated to be as high as 2% to 4%/mo
under ideal environmental conditions.7 It has been sug-
gested25 that thiamine losses can be as great as 57% in
dry dog food and 34% in dry cat food after 18 months
of storage; however, the loss of thiamine appears to be
minimal in canned food. Heat, humidity, and exposure to
air can affect the amount of nutrient losses in a diet, and
owners should be questioned and educated as to their
techniques for storage of pet foods at home. In a recent
study,a investigators found that 30% of owners do not
store pet food in an air-conditioned environment, despite
the fact that they live in a warm climate. Improper stor-
age or feeding techniques could include food that is fed
after the manufacturer’s expiration date, bags that have
been opened and not resealed between meals, or food
that has been allowed during the summer to remain in
the trunk of a car or in a garage prior to feeding.
In addition to nutrient losses from processing and
storage, specific diet ingredients can also affect thiamine
availability. Fish and shellfish, in particular, are known
sources of thiaminases. Thiaminases are enzymes that
degrade and inactivate thiamine in fish or other ingre-
dients with which the fish are combined. Species of fish
and shellfish differ in the amounts of thiaminase activ-
ity, as do parts within the same fish.26 The viscera of thi-
aminase-containing fish species tend to contain more
thiaminase than that found in the muscles or skeleton
of fish.20 Therefore, potentially inadequate amounts of
thiamine would be of particular concern for owners
feeding raw fish– or shellfish-based diets or any time
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13-01-0012_TTN.indd 652
substantial amounts of raw fish are included in the diet.
Raw fish are not the only sources of thiaminase, which
can also be found in some species of plants, bacteria,
and fungi.27 These could potentially be an issue for pet
food when added as ingredients or indirectly through
contamination. Although thiaminases are heat labile
and are destroyed by cooking and standard food-pro-
cessing techniques, the amount of time that thiaminase
is in contact with thiamine-containing foods within a
diet prior to cooking plays a role in the amount of thia-
mine that is ultimately destroyed.7 Therefore, contact
between thiamine-containing foods and thiaminase-
containing foods can lead to inactivation of thiamine.
This issue may be important in fish-based commer-
cial pet foods produced by manufacturers that do not
routinely test their ingredients and end-products for
thiamine. Processed fish meal is heat treated; thus, it
would pose no risk because the thiaminase has been
denatured.
The use of certain food preservatives can also im-
pact the availability of thiamine, as indicated by several
outbreaks of thiamine deficiency in Australia second-
ary to the use of sulfur-based preservatives.21,28 Sulfur
dioxide can cause concentration-dependent inactiva-
tion of thiamine.21,24,28,29 Sulfur derivatives are used for
preserving meat through inhibition of bacterial growth,
extending the storage life, and maintaining the red color
of the meat.24,28 Many countries have banned the use of
sulfur preservatives in the production of meat products
intended for human consumption; however, in some
countries, the same bans do not apply to meat intended
for pet foods or to all types of meats available for human
consumption. In the United States, sulfur dioxide is spe-
cifically prohibited for use as a preservative in meats or
in products that serve as sources of vitamin B1.12
Not surprisingly, incomplete or unbalanced com-
mercial diets are also a cause of vitamin deficiencies.
Diets intended for supplementary or intermittent feed-
ing (ie, supplementary diets) are not nutritionally com-
plete and balanced. This is not always readily apparent
to consumers from the label and can result in a number
of nutritional deficiencies, including thiamine deficien-
cy, when a supplementary diet is fed as a sole or pri-
mary diet. Although some veterinary therapeutic diets
may be labeled for intermittent or supplemental feed-
ing to specifically address certain disease conditions,
over-the-counter commercial foods should always be
complete and balanced because these products are not
dispensed under the guidance of a veterinarian. Thia-
mine deficiency was identified in a published report2 of
a colony of cats fed 2 supplementary diets over a course
of 6 months, which resulted in the death of 5 cats and
clinical signs in 23 others. When in doubt, pet owners
should bring the food label for their pet’s food to their
veterinarian so that it can be evaluated to help identify
this potential cause of thiamine deficiency. It is also im-
portant for veterinarians to proactively educate owners
that an over-the-counter food label that states “for in-
termittent or supplemental use” indicates the diet is not
complete and balanced and should be fed in only small
amounts as a treat, rather than as a sole or primary diet.
Nutritional imbalances are of major concern for
owners who prefer to feed a home-prepared diet.30–33
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 Anecdotally, home-prepared diets fed by most owners
include a protein and carbohydrate source with or with-
out other ingredients, but all-meat diets are not uncom-
mon. Although it might be expected that a diet consist-
ing primarily of meat would be sufficient in thiamine,
the amount of thiamine differs among cuts of meat and
the species from which the meat is obtained; thus, these
diets are not consistent and may not provide adequate
thiamine intake.34 More importantly, as mentioned pre-
viously, cooking will destroy between 73% and 100% of
the thiamine content in most meat.35 Additionally, the
thiamine in the meat and other ingredients is likely to
be destroyed (regardless of any effects from cooking) in
home-prepared diets that are high in thiaminase-con-
taining fish or sulfite-preserved meat.
Certain medications have also been associated
with the induction of thiamine deficiency. Amprolium
is a coccidiostat medication that has been associated
with thiamine deficiency in ruminants and dogs.36
Amprolium works within parasites by mimicking the
action of thiamine; however, prolonged administra-
tion or excessive doses can lead to thiamine deficiency
in the host. Conversely, diets high in thiamine or di-
etary supplementation with thiamine can render amp-
rolium less effective, and this factor should be consid-
ered for animals to which amprolium is prescribed.37
A similar medication is pyrimethamine, which is an
inhibitor of folic acid synthesis. Pyrimethamine is
often prescribed to treat protozoal infections such as
toxoplasmosis, neosporosis, or hepatozoonosis. Py-
rimethamine can induce thiamine deficiency in dogs
and cats and has been used to experimentally induce
thiamine deficiency in cats and rats.38
The aforementioned risk factors, many of which are
dietary factors, highlight the importance of collecting a
good diet history as the key to determining the various
components of an animal’s diet, the duration of feeding
of that diet, and clinical signs. The American Animal
Hospital Association and World Small Animal Veteri-
nary Association have developed nutritional assessment
guidelines that include collection of a thorough diet
history on every animal at every visit. A diet history
should include the type and amount of diet fed, dura-
tion of feeding of that diet, frequency of feeding, treats,
supplement-type products, foods used for medication
administration, and appetite of the animal. This infor-
mation will be instrumental in identifying risk factors
for thiamine deficiency as well as other deficiencies, ex-
cesses, or other forms of suboptimal nutritional status.
Diagnosis of Thiamine Deficiency
The diagnosis of thiamine deficiency is initiated
by recognition of relevant clinical signs and evalua-
tion of the medical and diet history. Results of serum
biochemical analyses, CBCs, and urinalyses are often
within reference limits in dogs and cats with thiamine
deficiency and may not aid in the diagnosis.3,20 Simi-
larly, evaluation of CSF is unhelpful in obtaining a diag-
nosis, but it may aid in ruling out other infectious and
inflammatory causes. Magnetic resonance imaging can
provide characteristic findings suggestive of thiamine
deficiency, namely bilateral hyperintense areas that cor-
relate with several brainstem nuclei (Figure 2).39,40 A
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definitive diagnosis is obtained by determining a reduc-
tion in blood or tissue thiamine concentrations.
Several forms of thiamine exist within the body;
however, there currently is no single test that mea-
sures all forms of thiamine. The 2 most commonly
used methods for assessing thiamine status in vivo are
the erythrocyte transketolase activity assay and HPLC.
The erythrocyte transketolase activity assay is a func-
tional assay that measures the activity of TPP in eryth-
rocytes.10 Because this method measures transketolase
activity rather than measuring thiamine directly, it can
be affected by other systemic processes (eg, diabetes
mellitus or liver disease10) in an animal. By contrast, the
HPLC method directly measures the TPP form of thia-
mine within RBCs. The HPLC method is more sensi-
tive, specific, and stable than the erythrocyte transketo-
lase activity assay for the measurement of thiamine.10 In
humans, HPLC (which typically is performed on whole
blood) has the additional benefit of better representing
total body status.10 However, neither method can mea-
sure the small percentage of thiamine in the plasma;
they only measure the thiamine in the erythrocytes or
tissue.9 Furthermore, these assays are not available at
all diagnostic laboratories, and specific procedures for
collection and transport of samples may apply.
Other less commonly used methods that can lead
to a diagnosis include the measurement of urinary thia-
mine or urinary organic acid concentrations or analysis
of dietary thiamine content.3 Because of the difficulties
in obtaining a definitive diagnosis, some clinicians may
elect an empirical treatment trial in an animal with a
relevant medical history and clinical signs while wait-
ing for test results or in lieu of testing.3,9
Unfortunately, some cases of thiamine deficiency
are not diagnosed until after an animal dies or is eu-
thanatized. Gross postmortem examination of animals
with thiamine deficiency may reveal bilateral symmet-
ric focal hemorrhages clearly visible in the paraventric-
ular gray matter.22,27 Brainstem nuclei typically involved
in companion animals with thiamine deficiency include
the lateral geniculate nuclei, caudal colliculi nuclei, dor-
Figure 2—Transverse T2-weighted fluid-attenuated inversion re-
covery image at the level of the thalamus in an adult cat with thia-
mine deficiency. Notice the bilateral hyperintense lesions (white
arrow) in the region of the lateral geniculate nuclei. R = Right.
Vet Med Today: Timely Topics in Nutrition 653
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 sal cochlear nuclei, oculomotor nuclei, mamillary nu-
clei, medial vestibular nuclei, and red nuclei, although
not all nuclei are involved in every animal.22,38,41 The
cerebellar vermis, cerebral cortex, basal ganglia, and
hippocampus may also be variably affected.22,41 Com-
parison of postmortem histopathologic results with
results from T2-weighted MRI reveals areas of hemor-
rhage and necrosis that typically correspond to regions
of hyperintensity visible on MRI images. Although both
T1- and T2-weighted images can be used for diagnosis,
changes are typically more prominent on T2-weighted
images.9,39,40 Changes evident on MRI images may be
inconsistently enhanced with IV administration of con-
trast medium.9,39,40 Microscopically, changes in affected
regions include cerebral edema, endothelial prolifera-
tion, neuronal necrosis, and myelin degeneration.27,41
Peripherally, myelin degeneration and axonal disinte-
gration may also be evident. Postmortem changes are
not limited to the peripheral nerves and CNS; there also
can be a wide range of changes in the heart, including
myocardial degeneration, multifocal myocardial necro-
sis, dilation, fibrosis, or mineralization.22,36,42
Treatment
Treatment of thiamine deficiency involves paren-
teral administration of thiamine for 3 to 5 days, fol-
lowed by oral administration for an additional 2 to 4
weeks. In 1 veterinary formulary,37 dosages for paren-
teral administration to dogs or cats ranged from 1 to
250 mg every 12 to 24 hours. The ideal dose of thia-
mine is unknown; however, doses described for clinical
cases range from 25 to 150 mg in cats2,9,39,40 and 100 to
600 mg in dogs.20,21 The authors typically use a dose of
50 to 100 mg every 12 hours for cats, but further re-
search is needed to determine the optimal dose needed
to correct thiamine deficiency.
Route of administration and duration of treatment
differ widely. In addition, some clinicians initiate treat-
ment with a loading dose, whereas others prefer a con-
sistent dose throughout treatment. Irrespective of the
dose, response to treatment is often noticeable within
hours.5 Parenteral administration of thiamine is partic-
ularly important in an animal with concurrent vomit-
ing or gastrointestinal tract disease because intestinal
absorption of the vitamin may be impaired. Pure thia-
mine hydrochloride, which commonly is provided at a
concentration of 100, 200, or 500 mg/mL, is preferred
over solutions of vitamin B complex because the com-
position of vitamin B complex products differs widely.
For example, the thiamine content of 8 commercial so-
lutions of vitamin B complex ranged from 10 to 150
mg/mL (up to one-fiftieth the content of a solution of
pure thiamine). To achieve a dose of 100 mg for a cat,
between 0.66 and 10 mL of vitamin B complex would
be required every 12 hours, depending on the brand of
the vitamin B complex.
Intravenous administration of thiamine should
be avoided because dose-dependent hemodynamic ef-
fects (eg, acute hypotension, cardiac arrhythmias, neu-
romuscular or ganglionic blockade, apnea, or death)
could result.7,43,44 In 1 study,44 investigators found that
IV administration of thiamine at doses ≥ 20 mg/kg (9.1
mg/lb) to cats and 80 mg/kg (36 mg/lb) to dogs led
654 Vet Med Today: Timely Topics in Nutrition
13-01-0012_TTN.indd 654
to neuromuscular paralysis and ganglionic blockade.
Therefore, parenteral administration should be provid-
ed via SC or IM injection. In the event that an overdose
of thiamine is administered IV, norepinephrine may re-
duce the adverse hemodynamic effects of the vitamin.43
It is important to mention that oral intake of an excess
of thiamine via supplementation of a commercial diet
or as a supplement-type product has not been found to
induce adverse clinical effects.7,19
Improvement in thiamine status can be monitored
via clinical signs, repeated MRI, and measurement of
thiamine status via HPLC or erythrocyte transketo-
lase activity.39 There may be residual neurologic defi-
cits such as mild ataxia after treatment is completed.40
In addition, an animal’s diet should be evaluated and
changed to a good-quality, complete, and balanced diet
if a home-prepared, raw, or supplementary diet is be-
ing fed. For a cat or dog that is consuming a complete
and balanced commercial diet and that has no medi-
cal reason for developing thiamine deficiency, diagnosis
or suspicion of thiamine deficiency should be reported
to the food manufacturer and the FDA. Concerns can
be reported to the FDA by calling the FDA Consumer
Complaint Coordinators for each state that are listed on
the FDA website or by reporting concerns to the FDA
Safety Reporting Portal online.45 Ideally, the lot and ex-
piration date should be obtained from each bag or can
of pet food, and multiple cans from the same lot or sam-
ples of dry food from the same bag should be retained
for testing as needed.
Other Issues of Clinical
Importance Related to Thiamine
Dietary thiamine supplementation should be con-
sidered when starting parenteral provision of nutrients
(ie, parenteral nutrition) in dogs and cats because there
have been several reported cases of the development of
thiamine deficiency in humans receiving parenteral nu-
trition without vitamin supplementation.46 The authors
recommend that most parenteral nutrition mixtures in-
clude B vitamins because animals in need of parenteral
nutrition frequently have increased metabolic require-
ments for these vitamins and may have an extended
history of inadequate caloric and nutrient intake as a
result of illness. The provision of thiamine should pre-
cede IV administration of dextrose because thiamine is
required for the conversion of glucose to energy via the
TCA cycle. Therefore, dextrose administration could
potentiate an underlying deficiency.46
The addition of vitamin B complex products to
crystalloid solutions is a popular technique to provide
additional B vitamins to hospitalized dogs and cats or to
animals receiving fluids administered at home (eg, pets
with chronic kidney disease). Most commercial solu-
tions of vitamin B complex contain thiamine, ribofla-
vin, niacinamide, pyridoxine hydrochloride, D-panthe-
nol, and cyanocobalamin; however, the concentration
of each B vitamin (including thiamine) differs widely
among commercial solutions. Similar to thiamine, the
optimal dose of vitamin B complex is unknown. A com-
mon standard dose in use by many veterinarians is 1 to
2 mL/L of fluids administered IV, irrespective of the rate
of fluid administration or the brand of vitamin B com-
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8/16/2013 1:31:35 PM
 plex.47 However, the actual dose of B vitamins adminis-
tered via this method differs widely depending on the
brand of vitamin B complex selected as well as the rate
of fluid administration. As mentioned previously, there
may be a 15-fold difference in thiamine concentration,
and the other B vitamins have similar wide variations
for the various formulations. In addition, possible con-
cerns with the use of B vitamins in IV fluid therapy in-
clude potential interactions with concurrent additives
(eg, potassium chloride) and the degradation of B vita-
mins via light exposure. Key points to consider for the
administration of vitamin B complex is the route and
rate of administration and knowledge of the content of
the specific vitamin B complex used so that clinicians
are able to calculate an appropriate dose for each ani-
mal requiring thiamine.
A common dietary supplement, brewer’s yeast, re-
portedly is a rich source of B vitamins and is sometimes
used as part of home-prepared diets to provide addi-
tional B vitamins to animals with diseases (eg, chronic
kidney disease) or for its reported insect-repellant ef-
fects.48,49 There are differences in formulations of brew-
er’s yeast, but 30 mg (2 tablespoons) of brewer’s yeast
provides approximately 1 mg of thiamine. This means
that the typical cat would need 3,000 mg (200 table-
spoons) of brewer’s yeast/d to provide the amount of
thiamine used to correct thiamine deficiency. In addi-
tion, 2 prospective case-controlled clinical studies49,50
revealed that there was no flea-repellant benefit for
dogs administered brewer’s yeast.
Clinical Summary
Thiamine deficiency is unlikely to be diagnosed on
initial evaluation until overt neurologic signs develop;
therefore, thiamine deficiency may be underreported in
companion animals. A thorough and complete dietary
history is integral to the initial identification of at-risk
or affected animals. Identification and diagnosis of this
disease remain the biggest challenges for clinicians, and
treatment should not be delayed because of a lack of
a definitive diagnosis. Treatment results in complete
resolution of clinical signs in most animals, providing
extensive neurologic damage has not already occurred.
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