Anemia Infecciosas felinas

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Vol 19 No 2 / / 2009 / / Veterinary Focus / / 31
Introduction
Anemia is a commonly recognized problem in
cats, and although infectious diseases often
underlie anemia in cats, there are an abundance
of other underlying causes. The primary purpose
of this article is to review the most common
infectious causes of anemia in cats. Theoretically,
all pathogens have the ability to cause anemia
through induction of an inflammatory response,
and development of anemia of inflammatory
disease, although this tends to be mild to moderate
and is usually not the primary reason for present-
ation. Pathogenic microorganisms that may cause
cats to present to veterinarians with anemia as the
primary clinical abnormality are the focus of this
article (Table 1). 
Diagnostic approach to anemia
A diagnosis of anemia may be suspected when
a cat presents with lethargy, decreased appetite
and pale or white mucous membranes. Consumpt-
ion of litter or dirt may also be part of the
history. Findings on physical examination may
include tachycardia, tachypnea, or a systolic
cardiac murmur as a result of decreased blood
viscosity. Definitive diagnosis of anemia depends
on the demonstration of a decreased hematocrit,
hemoglobin, or total erthrocyte count. In order
not to overlook the many causes of anemia,
causes of anemia can be grouped broadly into
those resulting in decreased red blood cell
(RBC) production, those causing blood loss, and
those resulting in increased RBC destruction
(Table 2). Anemia resulting from decreased red
blood cell production is always non-regenerative.
Blood loss and increased RBC destruction are
generally followed by a regenerative response 3-5
days after the initial insult, although chronic
gastrointestinal blood loss may become non-
regenerative due to iron deficiency. The presence
Jane Sykes, BVSc (Hons), PhD,
Dipl. DACVIM
University of California, Davis, USA
Dr. Sykes is currently an associate professor of Small
Animal Internal Medicine at the University of
California, Davis, with a special interest in small
animal infectious diseases and hematology. She
completed her veterinary degree at the University of
Melbourne, Australia, in 1993. She has a PhD in the
field of feline upper respiratory tract diseases and
molecular diagnostics for infectious diseases. She
completed a residency in Small Animal Internal
Medicine at the University of Minnesota in 2001 and is
a Diplomate of the American College of Veterinary
Internal Medicine. 
Infectious causes 
of anemia in cats
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of a regenerative response is suggested by the
presence of polychromasia, basophilic stippling,
normoblastosis (the presence of nucleated red
blood cells), anisocytosis, increased numbers
of Howell-Jolly bodies following microscopic
evaluation of blood smears (Figure 1). Reticulo-
cytosis is evident following new methylene
blue staining of blood smears, or automated
counting using flow cytometric methods. Using
visual methods, two types of reticulocytes can
be identified following the regenerative response
to anemia in cats: aggregate and punctate
reticulocytes. Aggregate reticulocytes are the
most immature form of reticulocytes. The pres-
ence of > 1% of these in the peripheral blood
indicates active regeneration. Laboratories that
report a single reticulocyte count for cats
generally are reporting the aggregate reticulocyte
count. Punctate reticulocytes are more mature
and increased numbers (> 10%) suggest a previ-
ous regenerative response, generally within the
last 1-2 weeks. Feline aggregate reticulocytosis
may not always be very pronounced, even though
regeneration is occurring (Table 3). 
Decreased red blood cell production generally
reflects impaired bone marrow function. Causes
in cats include:
a) Renal failure: This results in a normocytic,
normochromic anemia due to decreased
secretion of erythropoietin. 
b) Myelophthisis: Myelophthisic anemia results
from replacement of the marrow by neo-
plastic cells or fibrosis. Usually deficiencies
in other cell lines are present concurrently. 
c) Iron deficiency: Iron deficiency anemia is
classically microcytic and hypochromic,
but occasionally a normocytic, normo-
chromic anemia develops. The combination
of low serum iron concentration, low
ferritin concentration, and increased total
iron binding capacity can be used to dia-
gnose iron deficiency. However, because
serum ferritin is an acute phase reactant
protein, serum ferritin can increase with
inflammatory disease, sometimes impairing
the diagnosis of concurrent iron deficiency
anemia. In dogs and humans, a lack of
bone marrow stainable iron can be used in
such situations to aid diagnosis of iron
Table 1. 
Infectious diseases that may present as
anemia in cats
Organism
Feline leukemia virus
Feline immunodeficiency virus
Feline infectious peritonitis virus
Hemotropic mycoplasmas, primarily
Mycoplasma haemofelis
Cytauxzoon felis
Babesia felis
Ctenocephalides felis 
Ancylostoma spp.
Geographic 
distribution
Worldwide
Worldwide
Worldwide
Worldwide
Southcentral, 
southeastern, and mid-
Atlantic United States
Coastal South Africa
Worldwide
Worldwide
Mechanism
Decreased RBC
Production
RBC Loss
Increased RBC
Destruction
Underlying cause
• Renal failure
• Myelophthisis
• Iron deficiency
• Anemia of inflammatory disease
• Infectious disease (primarily FeLV
infection)
• Immune-mediated disease at the level
of RBC precursors
• Toxins and drugs
• Inherited coagulopathies and platelet
disorders
• Acquired coagulopathies and platelet
disorders
• Neoplasia
• Eosinophilic gastroenteritis
• Trauma
• Feline idiopathic lower urinary tract
disease
• Flea infestations
• Hookworm infestations
• Primary immune-mediated hemolytic
anemia
• Immune-mediated hemolytic anemia
secondary to drugs, neoplasia, or
infectious disease
• Inherited RBC defects (increased
osmotic fragility, pyruvate kinase
deficiency)
• Hypophosphatemia
• Oxidative toxins (e.g. onions, garlic,
local anesthetics, propofol,
acetaminophen, zinc)
• Microangiopathy
Table 2. 
Differential diagnosis of pathologic anemia in cats
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Vol 19 No 2 / / 2009 / / Veterinary Focus / / 33
INFECTIOUS CAUSES OF ANEMIA IN CATS
deficiency anemia. Unfortunately, normal
cats lack stainable marrow iron. As a result,
iron deficiency anemia may be difficult to
confirm in some cats. One of the most
common causes of iron deficiency anemia
in cats is chronic gastrointestinal blood
loss. 
d) Anemia of inflammatory disease: This is
usually a mild to moderate, normocytic,
normochromic anemia. The hematocrit is
seldom lower than 14-15% (1). Anemia of
inflammatory disease is suggested by the
presence of a decreased to normal serum
iron concentration, increased total iron
binding capacity, and normal to elevated
ferritin concentration. 
e) Infectious: The most common infectious
cause of decreased red cell production in
cats is FeLV infection (see below).
f) Immune-mediated disease at the level of
red blood cell precursors.
g) Toxins: As with myelophthisic disease, toxic
causes of anemia operating at the level of the
marrow usually cause deficiencies in other
cell lines. Examples include chloramphenicol
and chemotherapeutic drugs.
Red blood cell loss may be the result of bleeding
from the GI tract, urinary tract, or internal
hemorrhage, such as that due to splenic rupture,
or hemothorax. Chronic gastrointestinal bleeding
may be associated with thrombocytosis and an
elevated BUN to creatinine ratio.
Causes of bleeding include:
a) Inheritedcoagulopathies and platelet dis-
orders
b) Acquired coagulopathies and platelet disord-
ers, including anticoagulant rodenticide
toxicity, immune-mediated thrombocyto-
penia, and hepatopathies
c) Neoplasia, including hemangiosarcoma,
intestinal lymphosarcoma, and intestinal
adenocarcinoma
d) Severe ulcerative gastroenteritis, such as
eosinophilic gastroenteritis 
e) Trauma
f) Feline idiopathic lower urinary tract disease
g) Parasitic infections, in particular heavy
flea and hookworm infestations
• Sick cats, even if tested negative in the past
• All cats and kittens when first acquired, followed by a
second test at least 60 days later
• Following exposure to a retrovirus positive cat, or following a
cat bite, followed by a second test at least 60 days later
(at least 30 days if the exposure was to FeLV)
• Annually for cats living with retrovirus positive cats, or cats
that go outdoors
• Before the first vaccination for FeLV or FIV
• Blood donors should test negative using ELISA and,
if available, real-time PCR for FeLV and FIV
• Intermittent retesting of negative cats is only recommended
if they have an opportunity for exposure to infected cats or if
they become ill
Table 3. 
Current guidelines for testing cats for FeLV
and FIV (7)
Figure 1. 
Blood smear from a cat showing a strongly regenerative
response, with a nucleated red blood cell (medium sized arrow),
polychromasia and anisocytosis (thin arrows), and a Howell-
Jolly body (thick arrow).
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Clinical signs of blood loss include petechiae,
ecchymoses, epistaxis, hematemesis, melena,
hematomas and hemarthrosis. Internal hemor-
rhage may be manifest by abdominal distention
or tachypnea.
Increased RBC destruction may result from:
a) Primary immune-mediated disease: This
is less common in cats than in dogs.
b) Immune-mediated disease that is secondary
to infection, neoplasia, or drugs: The most
common secondary causes of immune-
mediated hemolytic anemia in cats are
infectious (see below).
c) Inherited RBC defects: Osmotic fragility
defects and pyruvate kinase deficiency have
been particularly recognized in Somali and
Abyssinian cats, which may occasionally
be misdiagnosed with immune-mediated
hemolytic anemia (2,3).
d) Hypophosphatemia: Acute hemolysis follow-
ing hypophosphatemia may occur following
refeeding after prolonged anorexia, or with
insulin therapy of diabetic ketoacidosis.
e) Toxic causes that result in oxidative damage
to red blood cells including Heinz body
formation (Figure 2). Feline erythrocytes
are more sensitive to such oxidative insults
than canine erythrocytes, because of the
increased numbers of sulfhydryl groups on
feline hemoglobin when compared with
canine hemoglobin. Examples of oxidative
toxins include acetaminophen, zinc, onions,
garlic, and local anesthetics. 
f) Microangiopathic damage to erythrocytes:
Damage to the endothelium of small vessels
results in fibrin deposition and platelet
aggregation. As red blood cells travel through
the damaged vessels, they are fragmented,
resulting in intravascular hemolysis, some-
times evidenced by the presence of schisto-
cytes on blood smears. 
Clinical signs suggestive of hemolysis include
splenomegaly, icterus, hemoglobinemia, and hemo-
globinuria. Compared with canine RBCs, feline
RBCs are smaller and lack central pallor, so
spherocytes are not normally identified in the cat. 
There are several pathogenic microorganisms
that may cause anemia in cats, the most wide-
spread being feline leukemia virus and feline
immunodeficiency virus infections, feline hemo-
tropic mycoplasma infections, and feline infec-
tious peritonitis virus infection. The approach to
diagnosis of these infections, and the mechanisms
by which they cause anemia are outlined below.
Other infectious causes of feline anemia that
have a more restricted geographic distribution
include the vector-borne protozoan parasites
Cytauxzoon felis and Babesia felis. Cytauxzoon
felis occurs in south-central and southeastern
regions of the United States, and was recently
detected in a cat in France (4). Babesia felis
infects cats in coastal regions of South Africa
(5,6). Other Babesia species have been identified
in cats in Europe, India, other parts of Africa,
and Israel.
Feline leukemia virus and
feline immunodeficiency virus
Feline leukemia virus (FeLV) and feline immuno-
deficiency virus (FIV) are retroviruses that
continue to be an important cause of immuno-
deficiency syndromes, anemia, neurologic signs
and neoplasia in cats worldwide. Initial diagnosis
of FeLV infection relies on detection of viral antigen
in peripheral blood. In contrast, diagnosis of FIV
Figure 2. 
Blood smear from a cat showing large numbers of Heinz
bodies (arrows).
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INFECTIOUS CAUSES OF ANEMIA IN CATS
infection is usually made following detection of
circulating anti-FIV antibodies. Except in kittens
with maternal antibody and cats vaccinated for
FIV, a positive antibody titer correlates with
active infection, because FIV infection persists for
the life of the cat. Assays available commercially for
screening purposes use enzyme-linked immuno-
sorbent assay (ELISA) technology, and include
lateral-flow devices (such as the SNAP FIV
Antibody/FeLV Antigen Combo Test, IDEXX
Laboratories), that have been marketed as a
point of care test, and microwell plate assays.
For both viral infections, false negatives may
occur early in the course of infection, so cats
testing negative should be retested > 30 days
after possible exposure for FeLV, and > 60 days
for FIV (7). The majority of assays for FeLV
infection are highly sensitive and specific (8,9),
and false negatives appear to be rare in cats with
FeLV-related disease. Cats may undergo regressive
infection with FeLV, whereby viral DNA integrates
into the host genome but is contained by the
immune system and does not go on to cause
disease. As a result, confirmation of progressive
infection (infection that is progressing to FeLV-
related disease) is required using immuno-
fluorescent antibody testing of the blood or bone
marrow or repeated ELISA testing at 3-4 month
intervals. Cats testing positive using these latter
methods are likely to develop FeLV-related disease.
Currently, the use of another ELISA assay or
Western immunoblotting is recommended to
confirm infection with FIV. Western immuno-
blotting detects antibodies to a range of FIV
antigens that have been separated and transferred
to a nitrocellulose membrane, but may be less
sensitive than ELISA. False negatives may also
occur with FIV infection of cats with advanced
disease that are unable to synthesize sufficient
antibody for detection using ELISA or Western
immunoblot methodology. Such cats may test
positive with assays designed to detect retrovirus
nucleic acid (polymerase chain reaction assays).
Unfortunately quality assurance may be problem-
atic in some laboratories offering polymerase
chain reaction assays for veterinary pathogens,
and such assays are not readily available in some
countries. Extensive guidelines for retrovirus
testing, prevention, treatment and management
have recently been published (7). The guidelines
for testing are summarized in Table 3.
A recent study including over 18,000 North
American cats estimated the overall prevalence
of FeLV and FIV infections as around 2.3% and
2.5%, respectively (2). Transmission of FIV occurs
primarily through biting, and as such, male cats
that spend time outdoors are at increased risk for
infection. Accordingly, a prevalence of infection
of 18.2% was documentedin sick, feral cats,
whereas the prevalence in healthy indoor cats was
only 0.7%. The predominant means of trans-
mission of FeLV is following prolonged close
contact with salivary secretions from infected
cats. Biting may be a lesser mode of trans-
mission. Recently, fecal shedding and urinary
shedding of FeLV were documented and may
play a role in transmission (10,11).
Progressive infection with FeLV is associated
with a variety of clinical outcomes, including
neoplasia, especially lymphoma and leukemia,
neurologic disorders, anemia and immuno-
deficiency with opportunistic infections (Table 4).
Anemia may result from multiple different mechan-
isms, including decreased RBC production and
increased RBC destruction. Approximately 90%
of FeLV-associated anemias are non-regenerative,
usually as a consequence of decreased red blood
cell production (Table 5). Decreased red blood
cell production can result from a variety of bone
marrow disorders. Infection with FeLV subtype
C infection results in pure red cell aplasia, a
severe non-regenerative anemia associated with
severe depletion of erythroid precursors in the
bone marrow. This was recently shown to result
from binding and interference with a heme
exporter protein and subsequent heme toxicosis
to the developing erythrocyte (12). Cats infected
with FeLV may develop erythrocyte macrocytosis
and non-regenerative anemia. FeLV has been
associated with development of aplastic anemia
in some cats, which is a deficiency in all cell
lineages (platelets, myeloid, and erythroid) within
the bone marrow, with the bone marrow space
being replaced by adipose tissue. Bone marrow
dysfunction may also result from myelophthisis
secondary to leukemia, myeloid and erythroid
dysplasia (disordered maturation of marrow
precursors), and myelofibrosis (Figure 3). Anemia
in cats with FeLV infection may also result from
anemia of inflammatory disease, which may be
secondary to FeLV infection itself, opportunistic
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infections or neoplastic disease. Increased
destruction of red blood cells may occur in
some FeLV-infected cats as a result of secondary
immune-mediated hemolytic anemia, or co-
infection with other hemolytic pathogens,
especially hemoplasmas. Finally, anemia may
reflect hemorrhage as a result of thrombo-
cytopenia. 
Although severe anemias are less common in
FIV-infected cats when compared with FeLV-
infected cats, mild to moderate non-regenerative
anemia can result from anemia of inflammatory
disease and bone marrow hypofunction second-
ary to the viral infection itself, although the
mechanism by which this occurs is unclear (13).
Many cats with FIV infection are geriatric, and
the presence of concurrent chronic renal failure
may also contribute to anemia. Concurrent
hemoplasma infections may also cause anemia
in FIV-positive cats.
As with any ill cat, all anemic cats should be
tested for FIV and FeLV infections. Once a retro-
virus infection is established, an attempt to
identify the underlying cause of the anemia
should be made. This involves careful evaluation
of the CBC, with attention to erythrocyte indices
and morphology, and a careful blood smear
evaluation. Testing for coinfection with hemo-
tropic mycoplasmas using the polymerase chain
reaction, if possible, should also be performed
(see below). A bone marrow evaluation, including
aspirate and core biopsy, is indicated in the
presence of pancytopenia or unexplained non-
regenerative anemia. Treatment of severe anemia
in retrovirus positive cats requires blood trans-
fusion after cross-matching and blood typing,
and treatment of any underlying cause, if evident.
Use of recombinant erythropoietin, together
with iron supplementation, may be beneficial in
some cats with severe non-regenerative anemia.
A response to immunosuppressive doses of
prednisolone (1-2 mg/kg, PO, q 12h) may occur
in some cats. Because glucocorticoids impair
the immune response and may compound the
risk of infection, prednisolone should only be
used if an underlying immune-mediated patho-
genesis is strongly suspected, and after coinfection
with other pathogens has been ruled out with a
thorough work-up, ideally including a thorough
Table 4. 
Possible outcomes of infection with feline
leukemia and feline immunodeficiency virus
Feline 
leukemia virus
• Immunosuppression leading to
opportunistic or severe
infections, such as stomatitis
• Lymphoma, especially
mediastinal, multicentric, renal,
and epidural lymphoma
• Leukemia
• Reproductive failure and fading
kitten syndrome
• Fibrosarcomas (with feline
sarcoma virus)
• Olfactory neuroblastomas
• Multiple osteochondromas
• Cutaneous horns
• Pure red cell aplasia
• Myelodysplasia
• Myelofibrosis
• Aplastic anemia
• Neurologic disease, including
mydriasis and urinary
incontinence
• Immune-mediated disease
• Enteritis
Feline 
immunodeficiency virus
• Immunosuppression
leading to opportunistic or
severe infections, such as
stomatitis
• Neoplasia, especially
lymphoma and squamous
cell carcinoma, but also
myeloproliferative disease
• Chronic wasting
• Neurologic signs
• Enteritis
Category
Decreased RBC Production
RBC Loss
Increased RBC Destruction
Table 5. 
Mechanisms of anemia in cats infected
with FeLV
Underlying mechanism
Pure red cell aplasia (FeLV-C)
Aplastic anemia
Leukemia
Myelofibrosis
Anemia of inflammatory
disease
Thrombocytopenia secondary
to immune-mediated or bone
marrow disease
FeLV-associated IMHA
Co-infection with
hemoplasmas
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physical examination, bloodwork, urinalysis and
urine culture, chest radiographs and abdominal
ultrasound.
Hemotropic mycoplasmas
The hemotropic mycoplasmas, also known as
hemoplasmas, that are currently known to infect
cats are Mycoplasma haemofelis (Mhf), ‘Candidatus
Mycoplasma haemominutum’ (Mhm), and
Mycoplasma turicensis (Mtc). Previously known
as Haemobartonella felis, these organisms are
small, gram negative bacteria that adhere to the
surface of erythrocytes, and have been identified
worldwide. Recently, Mycoplasma suis, a porcine
hemoplasma, was shown to invade erythrocytes,
and the same is probably true for the feline
hemoplasmas, although further studies are
required to confirm this (14). The mode of trans-
mission of these organisms remains enigmatic.
Arthropods, especially fleas, have been suggested
as possible vectors, and recently, Mhm and Mtc
have been detected in saliva, suggesting possible
transmission through biting (15,16). Male cats
with outdoor exposure have increased likelihood
of testing positive for hemoplasmas, also support-
ing a possible role of bite wounds in transmission.
Transmission studies using infected saliva are
required to determine whether such transmission
might occur. 
The pathogenicity of each of the three hemo-
plasma species appears to vary. Mhf is the most
pathogenic species, causing severe hemolytic
anemia, marked reticulocytosis, normoblastosis,
and sometimes leucopenia and thrombocytopenia,
sometimes accompanied by fever and icterus,
even in immunocompetent cats. Young cats may
be more likely to develop severe disease. Healthy,
nonanemic cats are rarely found to be infected
with Mhf. In contrast, Mhm is generally consid-
ered non-pathogenic or only mildly pathogenic
in immunocompetent cats. Mhm infects approxim-
ately 15-25% of all cats, and because Mhm is found
commonly in both non-anemic and anemic cats,
other causes of anemia should be sought in anemic
cats testing positive for Mhm, because its presence
may be coincidental.More severe anemia may be
observed in immuno-suppressed cats that are
infected with Mhm, such as those concurrently
infected with FeLV. The true pathogenicity of Mtc
has not been well established, although it also
appears to be considerably less pathogenic than Mhf
in naturally infected cats (17). It is less prevalent
than Mhm, and in most studies, of similar preval-
ence to that of Mhf (Table 6). Coinfections with
multiple hemoplasma species may occur in some
cats (17-21).
Diagnosis of hemoplasmosis is based on cyto-
logic examination of blood smears, PCR, or both.
Using light microscopy, Mhm is very small
(0.3 µm), and difficult to identify. Mhf appears
as small (0.3-0.6 µm) basophilic coccoid bodies
on the surface of erythrocytes, sometimes
forming short chains of organisms, although it is
not always possible to differentiate Mhm and
Mhf based on light microscopic evaluation
of blood smears (Figure 4). Mtc was recently
discovered in Switzerland, and studies suggest
it has a worldwide distribution. Levels of bacter-
emia with Mtc are much lower than with Mhm
and Mhf, and Mtc has never been identified on
blood smears, even in studies involving exper-
imental infections. The sensitivity of cytologic
blood smear evaluation for diagnosis of hemo-
plasmosis is as low as 30%, because stainable
organisms may be absent from blood smears,
Figure 3. 
Cytology from a bone marrow aspirate showing leukemia,
erythroid aplasia, granulocytic dysplasia and increased
eosinophilopoiesis in an anemic cat suspected to be infected
with FeLV (courtesy Dr. Amir Kol).
INFECTIOUS CAUSES OF ANEMIA IN CATS
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even in severely anemic cats. Stain precipitate
and drying artifacts may be misinterpreted as
hemoplasmas, resulting in low specificity. 
PCR tests for detection of hemoplasma DNA in
blood samples vary in their ability to detect and
identify different species, and so it is best to
consult with your diagnostic laboratory to
determine the species identified. Detection of
Mhf has much greater significance in an anemic
cat than detection of Mhm. Real-time PCR assays
have been developed by a number of workers
that specifically detect Mhm, Mtc or Mhf, and are
offered by certain diagnostic laboratories in
Europe and the United States. These assays are
also capable of approximate quantitation of the
organism load in a particular cat, which has
contributed to an increased understanding of
the pathogenesis of these infections in cats. 
Treatment of hemoplasmosis involves use of
doxycycline (10 mg/kg PO q 24h) for at least
2 weeks. Cats that do not tolerate doxycycline
may be treated with enrofloxacin as an altern-
ative. Blood transfusions may also be necessary.
Concurrent prednisone therapy to treat secondary
immune-mediated hemolytic anemia is controv-
ersial and should be avoided if possible, as
glucocorticoids have the potential to reactivate
latent hemoplasma infections. Although anemia
resolves in treated cats, most cats remain
Table 6. 
Prevalence of hemoplasma species infecting cats worldwide as determined using real-time PCR
methodology (17-21)
Geographic location
United Kingdom
United Kingdom
South Africa
Australia
Switzerland
Northern Italy
United States
United States
Population sampled
1585 sick cats
426 sick and healthy cats
69 cats suspected to have
hemoplasmosis
147 mostly sick cats
713 sick and healthy cats
307 anemic and non-
anemic cats
263 sick cats
310 cats with possible
hemoplasmosis
Mycoplasma
haemofelis
2.8
1.6
14.5
4.8
1.5
5.9
0.5
4.8
Mycoplasma 
turicensis
1.7
2.3
26.1
10.2
1.3
1.3
0.5
6.1
‘Candidatus
Mycoplasma
haemominutum’
11.2
17.1
37.7
23.8
10.0
17.3
16.0
23.5
Prevalence (%)
Figure 4. 
Blood smear from an anemic cat showing Mycoplasma
haemofelis organisms (arrows).
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INFECTIOUS CAUSES OF ANEMIA IN CATS
latently infected, and disease may reappear
following immunosuppression or concurrent
illness. Antimicrobials appear to be less effective
in reducing organism burden in cats infected
with Mhm (22). 
Recently, Mhf was identified in Brazil using PCR
in an HIV-positive human patient with anemia,
who was also coinfected with Bartonella (23).
Thus, these organisms appear to have the
potential to infect humans. The extent and
significance of human infection with hemo-
plasmas remains to be determined. 
Feline infectious peritonitis
virus infection
Feline infectious peritonitis virus is the cause
of a progressive, systemic pyogranulomatous
vasculitis, which most commonly infects young,
purebred cats (Figure 5). The relatively avirulent
feline enteric coronavirus is thought to acquire
mutations that allow it to infect and replicate
within the macrophage, which in genetically
susceptible cats leads to overproduction of pro-
inflammatory cytokines and development of
feline infectious peritonitis. Mild to severe anemia
may develop in cats with FIP. Most commonly
cats have a mild nonregenerative anemia, probably
relating to inflammatory disease. More severe
anemia may result from hemorrhage secondary
to coagulopathies resulting from hepatic failure
and/or thrombocytopenia. Secondary immune-
mediated hemolytic anemia may occur as a
result of virus-induced immune dysregulation,
or increased erythrocyte destruction may be the
result of microangiopathic damage to erythrocytes
as a result of widespread vasculitis. Diagnosis
of FIP remains challenging because no single
mutation differentiates the avirulent feline enteric
coronavirus and virulent feline infectious periton-
itis virus. The serologic response to infection
with each organism is similar. PCR can be used
to detect feline coronavirus in tissues, but feline
enteric coronavirus may be found in the non-
enteric tissues and blood of healthy cats, so
positive PCR results do not necessarily correlate
with FIP. Although a novel PCR assay for detection
of feline coronavirus mRNA in peripheral blood
was initially suggested to be sensitive and specific
for diagnosis of FIP (24), a recent publication from
Turkey using a similar assay reported positive
test results in the blood of 14 of 25 healthy cats,
suggesting that such assays may not be specific for
diagnosis of FIP (25). Currently, diagnosis depends
Figure 5. 
Pyogranulomatous lesions within the kidney from a cat with FIP (courtesy Dr. Megan Jones).
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REFERENCES
on a combination of supportive clinical abnormal-
ities, the ruling out other possible causes and
ideally demonstration of characteristic histopatho-
logical lesions in tissues, following biopsy or
necropsy. At the time of writing this article,
the mainstay of treatment involves the use of
supportive care and glucocorticoid therapy. Work
is ongoing to identify other antivirals and/or
immunomodulators that might have efficacy for
the treatment of this progressively fatal disease. 
INFECTIOUS CAUSES OF ANEMIA IN CATS
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