Vol. 19, No.
2 February 1997
Continuing Education Article
FOCAL POINT
★Many transfusion reactions can
be prevented by careful donor
selection and proper collection,
storage, and administration of
blood products.
KEY FACTS
■ Donors can now be quickly
screened for the highly antigenic
blood type DEA 1.1.
■ A universal canine blood donor
is negative for all DEA groups
except DEA 4.
■ Complement activation to the
terminal C5 to C9 steps results in
intravascular hemolysis.
■ Even low levels of IgM antibodies
can cause complete complement
fixation.
■ Dog erythrocyte antigen (DEA)
1.1 antibodies transferred via
colostrum to neonates with DEA
1.1 cause hemolytic anemia.
Canine Transfusion
Reactions. Part I.
Causes and
Consequences
North Carolina State University University of Minnesota
Karyn Harrell, DVM Janice Parrow, CVT, LATg
Novo Nordisk
Gentofte, Denmark
Annemarie Kristensen, DVM, PhD
E xperiments in transfusion began in the early 1600s. The first therapeutic
transfusions (attempted around 1665) were heterologous: sheep or calf
blood given to mental patients to treat certain behavioral disorders.1,2
Not surprisingly, the first evidence of a transfusion reaction (tachycardia, pro-
fuse sweating, nausea, and voiding of black urine) soon followed.1,2 Such reac-
tions halted further investigation of transfusion for nearly two centuries. Re-
search conducted during the past century has produced tremendous advances
in all aspects of transfusion medicine—including blood typing, donor screen-
ing, and optimal techniques for collection, storage, and administration.1–3
Transfusion therapy has evolved into an essential component of veterinary
medicine. This potentially life-saving therapy need not be reserved for referral
institutions. The veterinary literature provides information on the correct and
practical use of blood products. The establishment of veterinary blood banks
has improved access to reliable blood products that have been typed and
screened for infectious disease. Canine donors can now be quickly screened for
the highly antigenic blood type dog erythrocyte antigen (DEA) 1.1.3,4 Various
laboratories in the United States and Canada readily perform complete blood
typing. An understanding of the basic concepts of transfusion medicine cou-
pled with the accessibility of high-quality blood products will help veterinari-
ans perform transfusion safely and effectively.
This article, which is part I of a two-part presentation, discusses the causes
and consequences of transfusion reactions in dogs. It presents an overview of
the immunology and physiology of transfusion medicine. Part II discusses how
the veterinarian can minimize the risk of these reactions in canine patients. It
Small Animal
also discusses the results of an 8-year retrospective study
on the incidence and significance of transfusion reac-
tions in dogs.
TRANSFUSION REACTIONS
A transfusion reaction is any undesirable side effect
resulting from infusion of blood products. These reac-
tions are generally classified
according to whether they
Classification of are immune-mediated (see
5–9
Transfusion Reactions the box). They can be fur-
ther categorized by their tim-
Immunologic ing. An acute reaction occurs
Acute within minutes of the start
■ Hemolysis of a transfusion and up to 48
hours after the transfusion
■ Acute hypersensitivity
ends. Later reactions are clas-
■ Platelet sensitivity sified as delayed.10 Under-
■ Leukocyte sensitivity standing of the underlying
mechanism helps the veteri-
Delayed
narian prevent and treat
■ Hemolysis transfusion reactions.
■ Posttransfusion
purpura CANINE BLOOD TYPES
A basic knowledge of ca-
■ Neonatal
nine blood groups helps the
isoerythrolysis
veterinarian understand the
■ Immunosuppression
basis for an immune-mediat-
Nonimmunologic ed hemolytic transfusion re-
action. Canine blood types
Acute
are named according to the
■ Pretransfusion surface antigens on the red
hemolysis of donor blood cells (DEA).3,11 An im-
cells mune-mediated hemolytic
transfusion reaction occurs
■ Circulatory overload
when a patient has acquired
■ Bacterial
antibodies (or, less common-
contamination
ly, natural antibodies) to the
■ Citrate toxicity donor erythrocyte anti-
■ Coagulopathy gens.3,5,11,12
■ Hyperammonemia Although over 13 different
■ Hypothermia erythrocyte antigens have
■ Air embolism been defined, only 8 of these
are accepted as standards. 3
■ Pulmonary
Table I summarizes canine
microembolism blood groups and their
■ Acidosis prevalence in the general ca-
nine population. Laboratory
Delayed
blood typing is currently
■ Transmission of available for six of these anti-
infectious disease gens.3,8,13–15
■ Hemosiderosis DEA 1.1 and 1.2 are al-
lelic (see the glossary) and
DOG ERYTHROCYTE ANTIGENS ■ NATURAL ANTIBODIES ■ UNIVERSAL DONOR
The Compendium February 1997
therefore do not exist in the same animal; they are also
the most highly antigenic of all the blood types.3,6,8,13,14
Approximately 60% of dogs carry one of these anti-
gens. At present, no naturally occurring antibodies to
these groups have been identified.3 DEA 7 incompati-
bility generally results in delayed (3 to 5 days) destruc-
tion of the transfused red cells.3,14 Although the pres-
ence of natural antibodies to DEA 7 is somewhat
controversial,16 certain reports suggest that these anti-
bodies do occur in 20% to 50% of DEA 7–negative
dogs.3,14,17 Because of these problems, it is recommend-
ed that all donor dogs should be negative for DEA 1.1,
1.2, and 7.3,7,14,18
DEA groups 3 and 5 are uncommon in the general
canine population. A study of greyhounds, however,
found that 23% were DEA 3 positive and 30% were
DEA 5 positive.3 Natural antibodies have also been
found in dogs lacking these antigens.3 As with DEA 7,
incompatible transfusions result in the delayed destruc-
tion of the trans-
fused red cells. Ca- GLOSSARY
nine blood donors
should therefore be Allele—a variant of the same gene
negative for DEA 3
and 5. Alloantibody—an antibody directed
More than 98% of against an antigen from a member of
the same species
the canine popula-
tion is positive for Anaphylaxis—a severe, systemic
DEA 4. 3,16 There is hypersensitivity reaction that may re-
no evidence for the sult in vomiting, dyspnea, hypoten-
existence of natural sion, seizures, collapse, and shock
antibodies to this
antigen, and ac- Natural antibodies—antibodies
quired DEA 4 anti- found in the serum in the absence of
bodies are generally any previous, known antigenic stim-
considered to be be- ulation
3
nign. Urticaria—erythematous and ede-
A universal donor matous pruritic skin lesions; hives
is a dog that is nega-
tive for all of the
DEA groups except DEA 4.3 Because the purpose of an
erythrocyte transfusion is to maximize the number of
viable erythrocytes available to a patient while minimiz-
ing the risk of unwanted side effects, all attempts to de-
crease the unnecessary destruction of the donor’s trans-
fused red cells should be made. Thus, universal red cells
should be given whenever possible.
IMMUNE-MEDIATED REACTIONS
Hemolytic Transfusion Reactions
Pathophysiology
Antigen-antibody–mediated hemolytic transfusion
reactions are classified as type II hypersensitivities and
The Compendium February 1997 Small Animal

TABLE I C3a and C5a, serotonin,

Canine Blood Groups histamine, and brady-
kinin).5,24 The resultant ar-
Population Occurrence of Typing teriolar dilatation and cap-
Antigen Incidence (%) Natural Antibodies Available? Antigenicity illary permeability lead to
1.1 40–42 None Yes High—aute hemolysis systemic hypotension.5 In
response, catecholamines
1.2 20 None Yes High—acute hemolysis are released and lead to
3 5–6 ~20% Yes Moderate—delayed vasoconstriction of pul-
destruction monary, renal, intestinal,
and cutaneous blood ves-
4 98 None Yes None
sels. 24 Cytokines, such as
5 20–25 ~10% Yes Moderate—delayed tumor necrosis factor
destruction (TNF), are also released.25
6 98 None No ? If these interactions pro-
ceed unchecked, shock,
7 45–50 20–50% Yes Moderate—delayed acute renal failure, and or-
destruction gan damage may occur.5,24
8 40 None No ? IgG antibodies may also
activate complement only
to the level of C3b.5 The re-
may be acute or delayed.11 Acute reactions can lead to sult of the interaction of IgG and C3b with erythrocyte
disseminated intravascular coagulation (DIC), shock, surface antigens is extravascular hemolysis.5 This reaction
acute renal failure, and death.5,17,19,20 Severe acute reac- may be acute or delayed. However, the clinical signs even
tions are attributed to DEA 1.1 and 1.2 incompatibili- of the acute reactions are generally mild. Delayed ex-
ties.16,19,21,22 Radiolabeled compatible transfused canine travascular hemolysis is also seen when circulating IgG
erythrocytes have a half-life of approximately 21 days, antibodies cannot activate complement at any level.
whereas labeled incompatible DEA 1.1 and 1.2 red These antibodies coat the erythrocyte surface, thus re-
blood cells have a half-life of 30 minutes.22,23 Because sulting in erythrocyte opsonization and enhanced cell de-
no natural antibodies to these antigens occur, severe struction by phagocytosis.5,11,25
acute reactions are the result of acquired antibodies
(through previous transfusion or pregnancy).16,19,21,22 Clinical Signs
The severity and timing of an acute immune-mediat- Clinical signs of a severe acute immune-mediated
ed hemolytic transfusion reaction depends on the anti- hemolytic transfusion reaction include tachycardia, dys-
body class involved (IgG and/or IgM), the temperature pnea, hypotension, collapse, salivation, tremors, con-
at which these antibodies bind to cell-surface antigen, vulsions, weakness, vomiting, and pyrexia.9,11,19,22,24 Any
and the degree of complement fixation.5,11 Even low lev- of these signs can result from the primary disease pro-
els of IgM class antibodies are capable of complete com- cess and can be seen with other types of transfusion re-
plement fixation.5 In contrast, high levels of IgG anti- actions; none are pathognomonic for an immune-
bodies are required for complete activation of the mediated hemolytic reaction. Acute intravascular
complement cascade.5 Complement activation to the hemolysis results in hemoglobinemia and hemoglobin-
terminal C5 to C9 steps results in intravascular hemoly- uria, which may occur within minutes of the start of
sis due to penetration and lysis of erythrocyte mem- the transfusion.9,26 Less severe acute and delayed reac-
brane.5,9 Anaphylatoxins C3a and C5a are also released.5 tions (occurring 2 to 21 days after transfusion) with
Intravascular hemolysis leads to the activation of the extravascular hemolysis result in hyperbilirubinemia
hemostatic system.5,20 The end result of these interac- and bilirubinuria.5,11,24 In general, clinical signs occur-
tions is fibrin generation and the systemic circulation of ring in these reactions are much less severe.5,24,25 Fever
microthrombi, consumption of platelets and coagula- is commonly documented in human patients with de-
tion factors, fibrinolysis, and ultimately DIC.24 Rapid layed reactions.24 Anorexia and jaundice may also be
injection of incompatible blood results in a more severe seen.9
form of DIC.5,20
Another result of the injection of incompatible blood Acute Hypersensitivity Reactions
is the release of various vasoactive substances (including The majority of acute hypersensitivity transfusion

DIC ■ COMPLEMENT ACTIVATION ■ SYSTEMIC HYPOTENSION

Small Animal
reactions are allergic or anaphylactic and are classified
as type I hypersensitivities.9,25,27 These reactions are
mediated by IgE antibodies, which can stimulate mast
cells to produce or release potent vasoactive sub-
stances. 9,25,27,28 Leukotrienes, prostaglandins, and
platelet activating factor are formed from the phospho-
lipid membrane of these mast cells.7,25,28 Release of pre-
formed compounds (including proteases, serotonin,
histamine, and kallikrein) results in activation of the
complement system and formation of the anaphylatox-
ins C3a and C5a.27–29 The interaction of these media-
tors can cause not only urticaria and pruritus but also
more severe problems (e.g., increased vascular perme-
ability, bronchoconstriction, and hypotension).
Administration of plasma products is often consid-
ered risk free and overlooked as a cause of transfusion
reactions.29 Plasma products contain alloantigens (albu-
min and other proteins), possible allergens (antibiotics
or component preparation chemicals), and donor IgE
antibodies. As a result, transfusion of plasma products
has been associated with acute hypersensitivity reac-
tions; these plasma reactions appear to be more com-
mon than previously recognized.6,12,27,29
Transfusion of plasma containing IgA antibodies to
patients who are IgA deficient and have anti-IgA anti-
bodies has resulted in acute hypersensitivity reactions in
humans.25,27 Although these reactions have not been
documented to occur in dogs, it is reasonable to con-
sider the possibility of their occurrence in breeds that
are predisposed to IgA deficiency. Patients that are
atopic or have received multiple transfusions are also at
a higher risk of an acute hypersensitivity reaction.29,30
Signs of a reaction generally occur within seconds to
45 minutes from the start of the transfusion.25,27,29 The
severity of these signs depends on the extent of mast
cell degranulation and subsequent release of vasoactive
mediators.19,25,26,29 Pruritus, erythema, and urticaria are
common allergic reactions in dogs.12,19,22,26 Anaphylactic
shock with vomiting, dyspnea, pulmonary edema,
seizures, and cardiopulmonary arrest may also occur.5,30
Leukocyte and Platelet Sensitivity Reactions
Binding of recipient antibodies to leukocyte and
platelet antigens in donor blood components has been
documented to cause febrile nonhemolytic transfusion
reactions in humans.9,22,25,31,32 A febrile nonhemolytic
transfusion reaction is defined clinically as an increase in
body temperature of at least 1°C when no other cause
for the fever is found.31,33 These are the most common
transfusion reactions seen in humans and may be the
source of many febrile reactions in dogs.22,34 Pyrexia is
attributed to the release of endogenous pyrogens (e.g.,
interleukin-1) in addition to the activation of the com-
PLASMA ■ TRANSFUSION ■ LEUKOCYTE AND PLATELET ANTIGENS ■ COLOSTRUM
The Compendium February 1997
plement system by leukocyte antigen–antibody interac-
tions.22,25,31,33 The combination of these mediators may
also lead to the accumulation of neutrophils in the
lungs, thus possibly resulting in severe respiratory signs
and shock.25
A mild fever that begins during the first 30 minutes
of the transfusion is the most commonly observed
side effect of leukocyte or platelet sensitivity reac-
tions.12,19,22,31,33,34 The fever may increase for up to 8
hours and persist for a total of 20 hours.31 Tremors and
emesis have also been documented.33 Pulmonary in-
flammatory reactions are infrequent but can be severe
enough to result in adult respiratory distress syn-
drome.25
Delayed Reactions
Neonatal Isoerythrolysis
Transfusion of DEA 1.1–positive red blood cells to a
DEA 1.1–negative breeding bitch will result in the for-
mation of potent antibodies against DEA 1.1.35 If this
female is bred to a DEA 1.1–positive male, it is likely
that some of the pups in the litter will also have DEA
1.1–positive blood.9,35 DEA 1.1 antibodies are trans-
ferred to these puppies via colostrum. As a result,
hemolytic anemia occurs in these neonates after ap-
proximately 3 to 10 days of nursing.35 Clinical signs ob-
servable by the owner include weakness, failure to
thrive, and hemoglobinuria.
Posttransfusion Purpura
Thrombocytopenia is an infrequent delayed transfu-
sion reaction that has been documented to occur in
humans.36 This complication occurs approximately 1
week after the transfusion and is attributed to platelet
destruction by platelet-specific antibodies. 36 The
thrombocytopenia may persist for 2 months. This dis-
order is typically self-limiting, and clinical signs are
generally not noted. In rare cases, severe thrombocy-
topenia has resulted in evidence of bleeding (such as
petechiae, hematuria, and scleral hemorrhage). The in-
cidence of posttransfusion purpura in dogs is un-
known.
Immunosuppression
Several published studies have documented post-
transfusion immunosuppression. For example, transfu-
sion therapy increases renal allograft survival in dogs
and humans.19,22 Postoperative infections have been
more frequent in some cancer patients after transfusion;
the infections were attributed to immunosuppression
and did not correlate to the severity of the primary dis-
ease.22 The immunosuppression might result from im-
munoregulatory substances in plasma.19
The Compendium February 1997
NON–IMMUNE-MEDIATED REACTIONS
Acute Reactions
Hemolysis
Lysis of donor erythrocytes before transfusion can
cause laboratory and clinical signs of hemolysis. Use of
outdated products, inappropriate storage and adminis-
tration techniques, and bacterial contamination can all
cause pretransfusion hemolysis.5,12,19,24 Thermal damage
caused by freezing (<–3°C) or overheating (>37°C) can
also result in significant hemolysis.5,19,24 Mechanical
trauma due to twisted lines, plugged filters, small-bore
needles, and excessively rapid transfusion is another
possible cause.12,19,24 Certain peristaltic pumps cause
varying degrees of hemolysis.22 Outdated erythrocyte
products may have undergone hemolysis during storage
and are more prone to destruction during administra-
tion than are fresh cells.5,24 Osmotic hemolysis occurs
when red blood cells are diluted with inappropriate hy-
potonic solutions.5,19,24
Pretransfusion hemolysis may also indicate bacterial
contamination.24 Transfusion of potentially contami-
nated cells may have serious consequences and should
be avoided at all costs. Contaminated blood is dis-
cussed more fully below.
Except for the transfusion of contaminated blood,
non–immune-mediated hemolysis is generally fairly in-
nocuous and requires no special treatment.5 However,
hemolyzed blood will be less effective clinically. Because
of the risk of contamination and the possibility of di-
minished efficacy, hemolyzed blood should never be
given intentionally.5
Circulatory Overload
Excessively aggressive and rapid transfusion of blood
products can lead to hypervolemia,6,33 especially in nor-
movolemic patients (e.g., dogs that are not bleeding).19
As with any form of fluid therapy, extreme care must be
used in transfusing patients with cardiac diseases (a rate
of 1 ml/kg/hr has been suggested).6,19,26,33 Patients that
are oliguric or anuric or those with chronic anemia are
also at risk.19 Rapid infusion or large amounts of blood
given to these patients may cause an already compro-
mised cardiovascular status to decompensate.19 Clinical
signs of circulatory overload are primarily cardiovascu-
lar and include tachypnea, dyspnea, coughing, and
tachycardia.19,22,26 If this reaction is not addressed quick-
ly, pulmonary edema and congestive heart failure may
develop.9,33 Urticaria and vomiting may also occur.6 Cir-
culatory overload is probably a common transfusion re-
action in dogs.6,19
Bacterial Contamination
Bacterial contamination may result from inappropri-
OLIGURIA ■ SEPTIC SHOCK ■ LIVER DISEASE ■ NEUROLOGIC SIGNS
Small Animal
ate collection technique, contamination of the donor’s
skin, subclinical bacteremia in the donor, or the en-
trance of contaminated air into the collection bag.17,25,37
Blood is an excellent medium for bacteria, and growth
is easily supported. Several gram-negative organisms
(e.g., Pseudomonas, Citrobacter, Yersinia) and various
coliforms can use citrate as a carbon source and can
grow at low temperatures. 5,9,24,25,37
Transfusion of blood products contaminated by
gram-negative bacteria may cause endotoxin-mediated
septic shock.24,38,39 This syndrome results from activa-
tion of the complement, kinin, and coagulation systems
in addition to defects of oxygen transport, myocardial
function, metabolism, and peripheral perfusion.24,38–40
Clinical signs are severe and arise rapidly.5,19 Severe hy-
potension, fever, hemolysis, vomiting, diarrhea, and
bleeding are typically seen and result from DIC.9,12,24,25
Even with appropriate treatment, the mortality rate is
high.25 Bacterial contamination of blood products has
become much rarer as transfusion techniques have be-
come more sophisticated.24,37,41
Citrate Toxicity
Hypocalcemia is a rare transfusion reaction that re-
sults from the ability of the citrate in blood products to
chelate circulating calcium.7,9,12,26,33 Because citrate is
rapidly metabolized to bicarbonate in the liver, the risk
of hypocalcemia is increased in patients with liver dis-
ease.9,12,19,26,33 Fresh-frozen plasma, whole blood, and
platelet-rich plasma have high amounts of citrate.19 Oc-
casionally, rapid infusion of large quantities of these
products overwhelms the liver’s ability to metabolize
citrate.9,22,26 Citrate chelation may also cause hypomag-
nesemia, but the significance of this side effect is un-
known.33
Muscle tremors, hypotension, and cardiac abnormali-
ties are classic signs of hypocalcemia.9,19,24,33 If hypocal-
cemia is suspected, an electrocardiogram should be run.
Prolongation of the Q-T interval, depression of the P
and T waves, and ventricular arrhythmias may be
seen.9,12,19,33 Vomiting can occur, and tetany has been
seen in severe cases.12,33
Other Acute Reactions
Hyperammonemia may result from the use of out-
dated blood products because ammonia levels in stored
blood products rise proportionally with time.19,33 Pa-
tients with significant liver disease and who therefore
cannot metabolize and excrete this ammonia are at
higher risk for this complication.19,33 Clinical signs of
ammonia toxicity include ataxia, head pressing, cir-
cling, dementia, seizures, and other central nervous sys-
tem abnormalities. It is advisable to use fresh, newly
Small Animal
stored, or washed blood products for patients with he-
patic disease.9
Dilutional coagulopathy may be seen when large
amounts of stored blood products that are deficient in
coagulation factors and platelets are rapidly infused.24
Coagulation of the transfused red cells may occur sec-
ondary to recalcification of the anticoagulant if red
blood cell products are diluted with calcium-containing
solutions (e.g., lactated Ringer’s solution).9 Packed red
blood cells should be diluted only with isotonic saline.9
Transfusion of cold blood products may result in hy-
pothermia in young or small animals.24 Significant hy-
pothermia in compromised animals can cause arrhyth-
mia and sudden death.33 Mild warming of the infused
product is suggested to avoid this complication.33
Pulmonary microembolism may occur because plate-
lets, fibrin, and white blood cells form microaggregates
in blood that has been stored longer than 7 days.19,24,33
These particles are too small to be removed with stan-
dard transfusion filters.33 There is much debate about
whether these microaggregates could lead to pulmonary
microembolism.19,33 Although it is worthwhile to be
aware of the possibility of this complication, the actual
occurrence is believed to be low and the routine use of
special filters is unwarranted.19,33
Air embolism can occur when a large amount of air
(not a few bubbles) is infused. Because closed systems
are now frequently used, this problem is rare; but it
may occur when glass bottles are vented.9 The clinical
signs are acute cough and dyspnea.
Glucose metabolism in stored blood leads to an in-
crease in lactic and pyruvic acid and a subsequent de-
crease in pH.42 Theoretically, large transfusions could
produce clinical acidosis. As with citrate, however, pa-
tients with normally functioning livers can convert
these products to bicarbonate within hours of the trans-
fusion.19 Again, it is wise to be aware of this complica-
tion if the patient has liver dysfunction.
Delayed Reactions
Disease Transmission
Transmission of infectious disease is the most com-
mon cause of transfusion-related death in human
medicine.19 Transmission of HIV has accounted for
much of this mortality. Although no retrovirus has yet
been found to cause disease in dogs, several other
pathogenic agents are blood-borne. Ehrlichia and
Babesia organisms can be transmitted to recipient dogs
through blood transfusion and can cause significant
disease.19,21,22,43 A high incidence of seropositivity to
Babesia canis is seen in retired racing greyhounds.43–45
Borrelia spirochetes can survive at 4°C in packed red
blood cells and at –18°C in fresh-frozen plasma.46,47
COAGULOPATHY ■ HYPOTHERMIA ■ AIR EMBOLISM ■ ACIDOSIS ■ IRON OVERLOAD
The Compendium February 1997
Thus, blood transfusion could transmit Borrelia, result-
ing in Lyme disease.47 The actual incidence of such
transmission is unknown.
Heartworm microfilariae may also be transmitted by
transfusion. These microfilariae may confound heart-
worm testing in the recipient dog but will not cause
clinical disease. Although the prevalence of some dis-
eases varies geographically, it is generally recommended
to screen canine blood donors for heartworm disease,
Rocky Mountain spotted fever, ehrlichiosis, brucellosis,
babesiosis, and possibly Lyme disease.19,21,22,48
Hemosiderosis
Hemosiderosis is a form of iron overload that may
occur when multiple red blood cell transfusions are giv-
en to a patient that is not bleeding. Hepatic damage
may occur because as transferrin becomes saturated, the
excess iron is stored in the liver.19 Hemosiderosis is un-
common and can be prevented by appropriate use of
component therapy and by avoiding unnecessary iron
supplementation.19
CONCLUSION
Transfusion reactions can result from immunologic
and nonimmunologic mechanisms and can range from
mild and self-limiting to life-threatening. Some of these
reactions can result from transfusion of incompatible
blood. Others can result from use of outdated or con-
taminated blood products or inappropriate administra-
tion techniques. Part II will discuss how to prevent
transfusion reactions in dogs.
About the Authors
Dr. Harrell is affiliated with the Department of Companion
Animals and Special Species Medicine, College of Veteri-
nary Medicine, North Carolina State University, Raleigh,
North Carolina. Dr. Kristensen is affiliated with Novo
Nordisk in Gentofte, Denmark, and is a Diplomate of the
American College of Veterinary Internal Medicine. Ms.
Parrow is affiliated with the Department of Small Animal
Medicine and Surgery, College of Veterinary Medicine,
University of Minnesota, St. Paul, Minnesota.
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