TAMIL NADU VETERINARY AND ANIMAL

SCIENCES UNIVERSITY

CREDIT SEMINAR
ON
FELINE NEONATAL
ISO-ERYTHROLYSIS (FNI)

SUBMITTED BY:
Dr Paunas Kamlesh Joshi
MVM18020
Dept. of Veterinary Clinical Medicine

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 Table of Contents

Sr. No TITLE Pg. No.

1. BACKGROUND AND FELINE BLOOD GROUPS 3

2. BREED PREDISPOSITIONS OF FELINE BLOOD GROUPS 4

3. INTRODUCTION TO FNI 5

PATHOPHYSIOLOGY OF FELINE NEONATAL ISO-

4. 7
ERYTHROLYSIS (FNI)

5. CLINICAL SIGNS 9

6. DIAGNOSIS 11

7. TREATMENT 13

8. PREVENTION 15

9. CONCLUSION 16

10. REFERENCES 17

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 1. Background and Feline Blood Groups
Cat blood grouping works according to the AB Blood Group system. Cats are either
type A, type B, or type AB. Additional antigens outside the AB blood group have been
suspected based on type specific incompatible crossmatches. Recently, the presence of a new
alloantibody produced against a common red cell antigen was described and termed as Mik..
The investigators also report a naturally occurring alloantibody, anti-Mik, in Mik antigen
negative cats. Note that there is no universal blood type in cats, and all cats must be tested
before receiving any type of transfusion. (Beth Davidow, 2013) (Auer and Bell, 1981)
Blood type is determined by 3 alleles, with A being dominant over the rare ab, which
is dominant over b. (Allele A > Allele ab > Allele B). Cats with a genotype A/A, A/ab, or A/b
are type A, whereas only cats with b/b are type B. Rare AB cats are genotypically ab/ab or
ab/b. (Beth Davidow, 2013)

Phenotype Genotype
Feline Blood A A/A, A/ab, A/b
Groups B b/b
AB ab/ab, ab/b
TABLE 1. Genotypes and associated phenotypes in Feline Blood Groups

An important characteristic of the feline AB blood group system is the presence of

naturally occurring alloantibodies against the blood type they lack. Natural means that there is
no need for previous exposition to blood or blood products. Type A cats may have weak anti-
B alloantibodies that can cause shortened RBC survival if a B donor is used. However, type B
cats have strong anti-A antibodies and can have a fatal reaction from as little as 1 mL of
transfused type A blood. All type B cats aged more than three months possess high-titre
naturally occurring anti A alloantibodies with haemolysing and hemagglutinating activity, but
not all of type A cats present measurable titres of naturally occurring anti-B alloantibodies
Type AB cats have no alloantibodies against either type A or B blood in their sera; they should
receive either AB or A blood products if they need a transfusion because of the strong anti-A
antibodies present in B serum. The clinical relevance of anti-Mik alloantibodies was described
as an acute haemolytic transfusion reaction after inadvertent transfusion of Mik-positive blood
to the Mik negative renal transplant recipient. Most cats have MiK antigen but, in cats that do
not, naturally occurring antibodies can lead to a haemolytic transfusion reaction with a first-
time transfusion.
A universal feline blood donor does not exist. Blood typing should be performed in all
donors and patients, and a crossmatch in addition to blood typing is recommended. (Lynel J.
T., 2010)

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 2. Breed Predispositions of Feline Blood Groups

There is a noted breed predisposition amongst the blood groups in pure bred feline populations
across the globe.
Blood Allele frequency Proportion of
Frequency (A +B = 1) mating at risk for
(%) NI (%)
Type A Type B A allele B allele
Abyssinian 86 14 0.63 0.37 12
Birman 84 16 0.60 0.40 13
British 60 40 0.37 0.63 24
Shorthair
Burmese 100 0 1.0 0.00 0
Cornish Rex 66 34 0.42 0.58 23
Devon Rex 59 41 0.36 0.64 24
Domestic 99 1 0.90 0.10 1
Shorthair
Himalayan 93 7 0.74 0.26 6
Japanese 84 16 0.60 0.40 13
bobtail
Maine Coon 98 2 0.86 0.14 2
Norwegian 93 7 0.74 0.26 6
Forest
Persian 86 14 0.63 0.37 12
Scottish Fold 82 18 0.58 0.42 15
Siamese 100 0 1.0 0.00 0
Sphinx 82 18 0.56 0.44 16
Somali 83 17 0.59 0.41 14
Tonkinese 100 0 1.0 0.00 0
Table 2: Breed Predispositions and Allele frequencies in different cat breeds

In a study conducted by Giger et al (1991), No type B cats were found in the Siamese and
related modern breeds such as the Burmese, Oriental Shorthair, and Tonkinese, or in the
American Shorthair and Norwegian Forest breeds. The number of individuals tested in these
breeds were small, and the B allele cannot be assumed to be entirely absent but appears to be
at a very low frequency. In contrast to the above breeds and the DSH/ DLH cats, a number of
other breeds had a variably higher proportion of type B cats. These breeds include the
Abyssinian, Birman, and Persian; related modern breeds such as British Shorthair, Himalayan,
and Somali; and breeds with a characteristic mutation such as Scottish Fold and Devon Rex,
which both commonly use British Shorthairs in their breeding programs. The proportion of
type B cats in these breeds was between 15% and 24%, except for the British Shorthair (59%)
and Devon Rex (43%), which had a higher proportion of type B cats than the other purebreds
studied.

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 3. Introduction to FNI

Definitions:
Feline neonatal iso-erythrolysis (FNI) is a haemolytic disease characterized by
immune-mediated destruction of red blood cells. It occurs when kittens with blood group A
are born from a mother with blood group B (Clara Mariné Canals, 2017)
Neonatal iso-erythrolysis, or NI, is a rare immune-mediated disease that is caused when
newborn kittens with type A blood drink colostrum from a mother with type B blood.
(Lundgren 2004)
NI occurs when a B type queen is bred to an A or AB type tom and the A and AB type
kittens absorb antibodies from the colostrum when they nurse. The haemolytic disease that
ensues can be lethal. (UC DAVIS EDU SERVICES)
According to Hubler et al, 1987, Haemolytic disease of the new born, called
erythroblastosis foetalis in man and neonatal iso erythrolysis (NI) in domestic animals is a well-
known disease. Term NI implies lysis or destruction of erythrocytes by the action of maternal
isoantibodies which gain access to the circulation of the foetus or new born. The antigenic
determinants involved in NI are the same as those that characterize blood groups.
Neonatal iso-erythrolysis occurs when kittens ingest alloantibodies, acquired from the
queen, in colostrum that act against their own blood type during the first day of life. For the
first 72 hours of life the alloantibodies can be absorbed from the digestive tract into the
bloodstream (Casal et al., 1996)
According to Giger et al (1997), Neonatal iso-erythrolysis is a condition which may
occur when kittens of blood type A or AB receive colostral anti – A alloantibodies from a type
B queen.

Introduction
Hubler et al, 2006, suggested that the first report of FNI was by Ditchfield (1968) who
suspected the cause to be a panleukopenia vaccine of homologous origin. Since then other cases
of suspected FNI have been reported. They also stated that, haemolytic disease of the newborn,
called erythroblastosis fetalis in man and neonatal iso-erythrolysis (NI) in domestic animals, is
a well-known disease. There have been reports in horses, mules, cattle, pigs, dogs and cats.
Apart from naturally occurring cases the disease can develop after blood transfusion and after
the use of homologous blood or tissue vaccines. The term NI implies lysis or destruction of
erythrocytes by the action of maternal isoantibodies which gain access to the circulation of the
foetus or new born.
As previously stated, 12% of kittens that die between the ages of 0 and 14 days die an
immune-mediated disease, specifically neonatal isoerythrolysis. This is the most common non-
infectious cause of mortality in kittens 14 days and younger.

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 According to Giger et al (1997), There is apparently no transfer of immunoglobins
across the placenta from the serum of the queen to the foetus because cats have an
endotheliochorial placenta. The transfer of maternal antibodies via colostrum is, therefore, very
important for protecting the neonatal kitten against the infectious agents until its own immune
system if fully developed. Kittens that do not receive colostrum are thought to be more
susceptible to may viral diseases. The Transmission of Igs from the queen to the neonatal kitten
does not only provide protection from infection, but maternal antibodies may also attack the
red blood cells of the new born, thereby being responsible for fatal incompatibility reactions
known as haemolysis of the new born or neonatal iso-erythrolysis (NI). Thus, colostrum may
protect from or contribute to the fading kitten syndrome or kitten mortality complex and
therefore can be considered a friend or foe. Information on the transfer of maternal Ig from the
queen to the kittens and on NI is limited.

The naturally occurring anti-A alloantibodies present in type B cats are responsible for
FNI as well as severe red cell destruction in mismatched blood transfusions in a manner that
inclusively primiparous queens may present FNI litters. (Silvestre and Josep, 2010)

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 4. Pathophysiology of Feline Neonatal Iso-erythrolysis (FNI)
Silvestre and Josep (2010), said that Feline placenta is of endotheliochorial type. Chorionic
endothelium is closely linked to maternal capillary endothelium. It only allows a small and
insignificant passage of maternal antibodies, 5 to 10%.

A Type Tomcat
and B Type Queen

A Type Kitten B Type Kitten AB Type (RARE)

(At risk of NI) (Normal) (At Risk of NI)

Type B Tomcat
and Type A Queen

Type A Kitten Type B Kitten Type AB (RARE)

(Normal) (Normal) (Normal)

Plate 1 & 2: Flow depiction of Blood Group inheritance and susceptibility of kittens born to parents of Different Blood Groups

Kittens get maternal antibodies, IgG in most cases, by suckling colostrum during the first
days of life. The development of the immune system is a critical period for the kitten. In this
period, maternal immunity is an important factor, but in some cases, it can also cause disease.

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Kittens start to produce their own alloantibodies soon after birth, reaching their maximum level
in the first months of life while the level of maternal antibodies is low at 6 to 8 weeks.
According to Giger et al (1997), colostral anti A alloantibodies are responsible for NI,
i.e Type A, or AB blood type kittens, born from a B blood type queens are at risk of developing
NI during the first week of life. No case of NI has been documented in a type B kitten born to
a type A queen.
According to Hubler et al (1997), In man, immunoglobulins are transferred via the
placenta, whereas in domestic animals they are acquired primarily from colostrum in the first
24 to 72 hours). The isoantibodies responsible for erythrolysis react with antigen determinants
of paternal origin present on the erythrocytes of the new born. The subsequent destruction of
erythrocytes takes place in the spleen and liver, but some can occur directly in the blood stream.
If the erythrocytes are destroyed faster than they are replaced then acute anaemia, with varying
degrees of jaundice and haemoglobinuria will develop.
Neonatal iso-erythrolysis occurs when kittens ingest alloantibodies, acquired from the
queen, in colostrum that act against their own blood type during the first day of life. For the
first 72 hours of life the alloantibodies can be absorbed from the digestive tract into the
bloodstream (Casal et al, 1996).

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 5. Clinical Signs

Affected kittens are born healthy and start to nurse vigorously. Once they drink the
colostrum, they start to show clinical signs within hours to days, stop nursing, and fail to thrive.
They develop haemolytic anaemia within one to two days after birth and some or all of the
litter will die. Early clinical signs of the disease are pigmenturia (dark red-brown urine).
Affected kittens will be anaemic, jaundiced, and depressed. Immune mediated haemolysis,
disseminated intravascular coagulation, acute renal failure, and anaemia are the probable
causes of death. (Meade 2015) (Lundgren 2004)
According to Giger and Casal (1997), Kittens with type A or AB blood born to type B
queens may develop signs of NI immediately following colostrum intake. The hallmark sign
of NI is severe pigmenturia due to haemoglobinuria. Other clinical signs include sudden death
failure to thrive (stop nursing), anaemia, icterus, and tail tip necrosis.
FNI clinical features depend on haemolysis grade and severity. Suckling colostrum allows
the passage of naturally occurring alloantibodies from mother to the neonate. Antibodies
recognize the antigenic determinants in the kitten red cell surface, causing intra or extravascular
haemolysis. Extravascular haemolysis can occur in the spleen or liver. Haemolysis leads to
anaemia, nephropathy, or disseminated intravascular coagulation. Determinants to the degree
of haemolysis or severity are still unknown, but the large variation in clinical signs within a
litter suggests differences in colostral antibody uptake as a determinant factor. Generally,
kittens are born healthy and nurse energetically, but after colostrum ingestion, clinical signs
appear in a few hours or days. Some may die in a few hours without presenting any kind of
clinical signs. Others stop suckling in the first days of life and fade.
The key signs to diagnose FNI are dark red-brown urine, indicating severe intravascular
haemolysis and haemoglobinuria, but they may also present jaundice, anaemia, and weakness
with death occurring in the first week of life. Secondary clinical signs are pale mucous
membranes and those related to decreased oxygenation: lethargy, tachycardia, tachypnoea,
collapse, and death. Hypoglycaemia and metabolic acidosis may be present associated to
stopped or decreased suckling. Those who survive may develop tail tip necrosis. (Bucheler,
1999)
In a study conducted by Hubler et al, (1987) in one litter with 3 kittens, one kitten was
found dead within 15 hours after birth while two others were depressed, weak and unwilling to
suckle. On presentation thee queen and one kitten were healthy but the other two kittens were
weak, depressed and unwilling to suckle. On urine analysis of the two affected kittens, free
haemoglobin was detected. The two affected kittens died within one hour of presentation
despite nursing.

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 In another case, amongst a litter of four kittens given by a Persian queen, one kitten was
found dead about 12 hours post suckling while two others were depressed, jaundiced and
voided red-brown urine. Out of the three kittens one kitten died within few hours of
presentation in spite of being artificially fed and temperature maintenance. The other two
affected kittens looked brighter the next day and started to void macroscopically normal urine.

Table 3: Various Clinical Signs in Kittens affected with FIN

However, once the kitten shows clinical signs, the condition is very difficult to treat.
Clinical signs vary and range from sudden death, to anaemia with haemoglobinuria, to necrosis
of the tip of the tail and ears, while some kittens are asymptomatic. Once a type a kitten sucks,
it will absorb the colostrum containing the anti-a antibodies and these will usually result in
hemagglutination and haemolytic anaemia.
According to Omoto (2019), signs of neonatal iso-erythrolysis include: cessation of
nursing, sudden death, haemoglobinuria (i.e. presence of haemoglobin from destroyed red
blood cells in the urine), icterus (i.e. yellow colouring of the mucous membranes), anaemia,
weakness, lethargy, tachycardia, tachypnoea, collapse, hypo-glycemia, and metabolic acidosis.
Death may occur rapidly or after a few days.

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 6. Diagnosis
Diagnosis is performed on the basis of clinical signs and confirmed by blood typing the
queen and the kitten. If blood typing is not possible, a blood crossmatching can be performed.
Kittens with FNI present a positive Coomb's test which confirms the immune-mediated nature
of this process. If FNI is suspected all kittens should be blood typed. At birth, cord blood from
the placenta may be used to type kittens.
The crossmatching checks for serologic compatibility or incompatibility and it may be
possible to detect any incompatibility, even outside the AB system. This is an important
advantage compared to blood typing that only recognizes blood type antigens. When an
incompatible major crossmatching between the queen and the kitten is found, FNI may be
suspected. (Spada and Proverbio, 2019) (Goy-Thollot, 2019)
Most recently researchers from UC Davis have found the gene associated with the B blood
group and its mutation. They developed a diagnostic DNA test so that animals can be tested at
an early age from a buccal swab. The genetic test for the cat blood group identifies the recessive
b allele which is associated with the B serotype. This test has not been fully validated in the
Ragdoll and Turkish Angora breeds, because, in some animals, results from DNA and
serological tests are not concordant, but cat breeders can greatly benefit from this test for
selection of mating pairs.

Table 4: Procedure for Crossmatching feline Blood

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 Necropsy is an important step in FNI and perinatal death diagnosis. As death may occur in
different stages of the disease, pathological findings depend on the moment of death. The
bladder may be filled with dark red-brown urine and precipitated haemoglobin. The body may
appear icteric and the spleen enlarged. The spleen and liver may present marked
erythrophagocytosis and extramedullary haematopoiesis. In the kidneys large red-orange
tubular casts compatible with haemoglobin or acute tubular necrosis may be seen. Systemic
effects of immune-mediated haemolysis, disseminated intravascular coagulation, anaemia, and
acute renal failure, are the apparent cause of death in kittens suffering from FNI.

Plate 3: Pictographic representation of Crossmatching

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 7. Treatment
FNI treatment should be aggressive and immediate. FNI treatment steps comprise
replacement of passive immune protection, a blood transfusion if clinical conditions
deteriorate, and life support treatment. When the first clinical signs appear, type A or AB
kittens should be immediately removed from their mothers, as long as they continue to
suckle more anti-A immunoglobulins they receive. Type B kitten can continue to suckle.
Kittens should receive immunoglobulin-rich colostrum during the first 12 hours of life to
obtain optimal serum antibody titres and acquire adequate passive immune protection
throughout the neonate period. The interval of transfer of maternal antibodies seems to
be of only 16 hours. The IgG are absorbed by the neonate during this period. After this,
intestinal mucosa loses its permeability, and even when administered, immunoglobulins
are not absorbed. Therefore, kittens only need to be removed from their mothers for the
first 16 to 24 hours of life. Kittens may be fed with a commercial milk replacer, previously
frozen milk from a type A blood mother, or be placed with a foster type A blood queen.
Prevention of passive immunity failure will be addressed later on. (Silvestre and Josep,
2010)

If anaemia is severe and becomes worse, a blood transfusion should be considered.

Kittens severely anaemic with hypoxia signs should receive 2 to 3 mL of previously
washed blood cells during the first 3 days of life. Blood donor selection is the key to a
successful transfusion.

In an A or AB blood kitten with FNI, the queen’s circulating colostral antibodies are
anti-A. Transfusion of type A cells simply adds more vulnerable cells to the kitten’s
circulation. The best blood donor would be the queen as she cannot obviously react to
her own antibodies.

Blood can be
transfused via a spinal
needle into the
trochanteric fossa. In
this way, about 90% of
red blood cells are in the
blood stream in 10
minutes. Due to the
shortened life span of
transfused red cells and
a continued destruction
of the kitten’s own cells,
anaemia may worsen
and a new blood
transfusion may be
essential. The kitten
starts form its own anti-
B alloantibodies soon after birth, and maternal antibodies from colostrum start to
decline. Therefore, if another blood transfusion is required after 3 days postpartum, a

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washed type A blood administration should be considered. After anaemia is corrected,
the kitten should receive life support treatment associated with electrolytic changes and
tissular hypoxia. Even when kittens are removed from their mothers, as soon as the first
clinical signs become present, the mortality rate associated with FNI is high, making
prevention the most important step. (Silvestre and Josep, 2010)

Plate 4: Flow representation of recommended treatment for FIN in affected kittens

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 8. Prevention
The best method to prevent FNI is to avoid incompatible mating between type B blood
queens and type A blood toms. Knowledge of the parent’s blood type is essential for FNI
prevention. To assure blood compatibility, blood typing might be done with an in-house blood
typing card, gel, or tube test, that appear to be reliable clinical laboratory methods for feline
blood typing, or with crossmatching. If there is a need to mate a type B queen with a type A
tom, the best way to prevent FNI is to remove the kitten from the mother for 24 hours
preventing them from nursing colostrum. Failure in passive immunity might be solved by using
previously frozen colostrum, from another queen’s milk.
In most mammalian species, the immunoglobulin concentration in colostrum is generally
much higher than that in milk. Although previous studies show that milk immunoglobulin
concentration in queens
is similar to that present
in colostrum, nowadays
we know that cats have
both colostral and milk
phases of lactation
distinguished by the
concentration of IgG and
IgA.
In cats, IgG and IgA
colostrum concentration
is greater than that in
serum, but reduced
concentrations of IgG
and IgA have been
demonstrated in milk
relative to colostrum.
IgM concentrations are
lower in colostrum and
milk than in the queens’
serum. Although
transplacentary
immunoglobulin transfer
is more efficient for IgG,
fostering on queens in
mid-lactation does not
provide protective
concentrations of
immunoglobulins in colostrum deprived kittens. A previous study also shows that parenteral
administration of 150mL/Kg of adult feline serum results in a normal concentration of IgG in
colostrum deprived kittens. Serum donors must be blood typed. (Silvestre and Josep, 2010)
Another study revealed that in vitro neutrophilic and plasmatic activity hosts a defence
against bacterial and other microorganisms, which is similar in kittens suckling colostrum and

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in those that do not suckle. Because maternal IgG levels have a short life span— approximately
4.4 days (IgG life span is shorter in kittens than in puppies) and the onset of IgG and IgA
production is late (IgG production starts by the 5th to 6th week of age and IgA shortly after,
while, in contrast, IgM steadily increases to a plateau on the 60th day of life), kittens are
vulnerable between the third and fourth week of life. For kittens that have been deprived of
colostrum, early vaccination is recommended whenever there is a risk of viral infection.
Prevention is the preferred "treatment" for NI. Affected kittens need supportive care, blood
transfusions, etc.; however, the prognosis is guarded in spite of any treatment, so prevention
should be the main key of defense.

9. Conclusion

Giger et al (1997), concluded that Kittens should receive colostrum during the first 12 h of
life to obtain optimal serum antibody titres and acquire adequate passive immunity. Milk at
anytime of lactation of a queen may be used as an adequate antibody source for kittens deprived
of colostrum from their own queen. Kittens with type A or AB blood from type B queen are at
risk of NI and must be removed from their queens only for the first day of life to avoid
incompatibility reactions. Neonatal kittens at risk of NI may safely receive milk from a foster
queen with blood type A to provide passive immunity. The rapid decline of maternally derived
serum IgGs and the late onset of IgG and IgA production makes kittens particularly vulnerable
between the third and fourth week of life. Early vaccination may, therefore, be indicated in
catteries at high risk for viral infections. These recommendations may lead to a reduction of
losses owing to fading kitten syndrome and kitten mortality complex.
According to Silvestre and Josep (2010), FNI is rare but the mortality rate is high. It results
from random mating between type B blood queens and type A or AB blood toms. The best way
to prevent FNI is to blood type progenitors, mostly those belonging to breeds with high
incidence of animals with type B blood.

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 10. References

Ana C. Silvestre-Ferreira and Josep Pastor, 2010, Feline Neonatal Isoerythrolysis and the
Importance of Feline Blood Types, Veterinary Medicine International, Volume 2010,
8 pages doi:10.4061/2010/753726

Auer, 1. and K. Bell, 1981, The AB blood group system of cats, Animal Blood Groups and
Biochemical Genetics, 12, 187-297.

Bücheler, J., 1999, Fading kitten syndrome and neonatal isoerythrolysis, Vet Clin North Am
Small Anim Practice, Jul;29(4):853-70, v.

Davidow, B., 2013, Transfusion Medicine in Small Animals, Vet Clin Small Anim 43, 735–756
http://dx.doi.org/10.1016/j.cvsm.2013.03.007.

Giger U. and M. L. Casal., 1997, Feline colostrum – friend or foe: maternal antibodies in queens
and kittens, Journal of Reproduction and Fertility Supplement, 51, 313 – 316.

Giger, U., J. Bucheler, and D. F. Patterson, 1991, Frequency and Inheritance of A and B Blood
Types in Feline Breeds of the United States, Journal of Heredity;82:15-20; 0022-
1503/91

Goy-Thollot, I., A. Nectoux, and M. Guidetti., 2019, Detection of naturally occurring

alloantibody by an in-clinic antiglobulin-enhanced and standard crossmatch gel column
test in non-transfused domestic shorthair cats. J Vet Intern Med.;33(2):588-595.

https://vgl.ucdavis.edu/services/abblood.php
Huble, M., S. Kaelin, A. Hagen *, A. Fairburn, P. Canfield, And P. Ruesch,1987, Feline
neonatal isoerythrolysis in two litters, J. small Anim. Pract, 28, 833-838.

Lamm, C.G., and B. L. Njaa, 2012, Clinical Approach to abortion, Stillbirth and Neonatal
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Little, S., 2010, Feline blood types: What you need to know and why (Proceedings), Fetch
DVM360 CE.

Lundgren, B., 2004, Feline Neonatal Iso-erythrolysis,

http://www.veterinarypartner.com/Content.plx?P=A&C=189&A=1639&S=0&EVet

Lynel J. T., 2010, Transfusion Medicine in Small Animal Practice, Vet Clin Small Anim, 40,
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Meade, C., 2015, Fading Syndrome in Kittens, In Practice, Volume 36, 266-276
Omoto, H., 2015, Gross Causes of Neonatal Mortality in Devon Rex and Persian Kittens,
Thesis submitted to Oregon State University Honors College.

Spada, E., and D. Proverbio, 2019, Blood Compatibility in Cats, Clinician’s Brief.

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