CHAPTER 19

Feline Panleukopenia Virus Infection

and Other Viral Enteritides
Jane E. Sykes

have been reported in households of fully vaccinated kittens,

Overview of Feline Parvoviral Enteritis possibly because of exposure to large amounts of virus in the
First Described: 1928, Verge and Christoforoni, France1 environment.4 Outbreaks of panleukopenia in cats correlate
seasonally with increases in susceptible newborn kitten num-
Cause: Feline panleukopenia virus (FPV); also canine parvo-
bers. Panleukopenia occurs most commonly in multicat house-
virus (CPV)-2a, CPV-2b, and CPV-2c (Family Parvoviridae,
holds, and especially in enclosed, shelter environments. It can
subfamily Parvovirinae, genus Parvovirus)
also occur in cats with outdoor exposure, such as barn, feral,
Affected Hosts: Domestic and wild cats; foxes, mink, and and stray cats. In one study, the prevalence of protective anti-
raccoons body titers to FPV in feral cats in Florida was only 33%, which
Geographic Distribution: Worldwide suggested a low rate of exposure to the virus.5 In some North
American shelters, devastating outbreaks of panleukopenia have
Mode of Transmission: Direct contact with virus in feces and
led to euthanasia of large numbers of cats. Contact with other
vomitus and contaminated fomites.
cats may not be present in the history, because fomite transmis-
Major Clinical Signs: Fever, lethargy, inappetence, vomiting, sion is so effective.3 FPV replicates to a limited extent in dogs,
diarrhea, dehydration, sudden death. Neurologic signs without disease or virus shedding. Some feline panleukopenia
(primarily cerebellar signs) may also occur. results from infection of cats by the related mink enteritis virus,
Differential Diagnoses: Other feline viral enteritides, toxins, CPV-2a, CPV-2b, or CPV-2c.6-8 Mixed infections with FPV and
gastrointestinal foreign body, enteric parasitic infections CPV-2 variants have been detected in cats, and there is evidence
such as giardiasis and nematode infections, enteric bac- for recombination between FPV and CPV-2 variants.7,9 Infec-
terial infections such as salmonellosis, pancreatitis, or tion of cats with CPV-2 variants is uncommon in Europe but
inflammatory bowel disease. Congenital central nervous predominated among cats with panleukopenia in Asia.10
system defects should be considered in cats with neuro- Other viral pathogens that have been associated with gas-
logic signs. troenteritis in cats include feline enteric coronavirus (see
Chapter 20), FeLV, rotaviruses, caliciviruses, reoviruses, and
Human Health Significance: FPV is not known to infect astroviruses. A torovirus-like agent has been associated with
humans, but was isolated from a monkey. a ­syndrome of diarrhea and protrusion of the nictating mem-
branes in cats.11 Togavirus-like and picornavirus-like particles
have been identified in the feces of Australian cats, but their
Etiology and Epidemiology significance is uncertain.12

Feline panleukopenia virus (FPV) is a parvovirus that causes Clinical Features

enteritis and panleukopenia in domestic and wild cat species
worldwide.2 It has also been associated with disease in rac- Signs and Their Pathogenesis
coons, mink, foxes, and a monkey, and can replicate in ferrets The pathogenesis of FPV infection is similar to that of CPV
without causing disease. Feline panleukopenia is sometimes infection (see Chapter 14). Transmission is by the fecal-oral
confusingly referred to as “cat plague” and “feline distemper.” route, and indirect transmission through contaminated fomites
FPV is a small, single-stranded non-enveloped DNA virus that represents the most important means of infection. Like CPV,
is closely related to CPV-2, but in contrast to CPV-2, which FPV enters cells using transferrin receptors13 and replicates in
emerged in the late 1970s, the existence of FPV has been known cells that are in the S-phase of the mitotic cycle. Initially, the
since the 1920s.1 FPV has the same ability as CPV-2 to survive virus replicates in oropharyngeal lymphoid tissue, after which
long periods in the environment and resist disinfection, and has it disseminates in blood to all tissues. Infection of lymphoid tis-
the same preference for replication in rapidly dividing cells (see sues leads to lymphoid tissue necrosis. Infection of the marrow
Chapter 14). is associated with leukopenia, which is compounded by neutro-
Feline panleukopenia is most likely to occur in cats younger phil sequestration in damaged gastrointestinal tissue. The virus
than 1 year of age, but it can occur in unvaccinated or improp- replicates in the intestinal crypt epithelial cells, with shortening
erly vaccinated cats of all ages. The median age of affected cats of villi, increased intestinal permeability, and malabsorption.
in one study was 4 months, and when disease occurred in vac- Subclinical infection is probably widespread, especially in
cinated cats, it occurred only in cats that had not received a young adult or adult, immune-competent cats. Disease severity
booster vaccine after 12 weeks of age.3 However, kitten deaths depends on factors such as age, immune status, and concurrent

187
188 SECTION 1  Viral Diseases

infections with other bacterial or viral pathogens, which increase Kittens with cerebellar signs are generally bright and alert
the turnover rate of intestinal epithelial cells and enhance viral but exhibit intention tremors, incoordination, ataxia, hyper-
replication and cellular destruction. Co-infections can occur with metria, a broad-based stance, decreased postural reactions, a
feline enteric coronavirus, Clostridium piliforme, Salmonella truncal sway, and absence of a menace response. Cats with fore-
spp., FeLV, or astroviruses.14-17 Disease generally occurs after an brain disease may show abnormal behavior, such as aggression
incubation period of 2 to 10 days. The peracute form of disease or decreased mentation. Examination of the ocular fundus may
involves death without apparent premonitory signs. Infection of reveal folding of the retina, evidence of retinal degeneration
kittens or adult cats results in clinical signs of fever, lethargy, with discrete gray spots, and optic nerve hypoplasia. Retinal
vocalization, weakness, and inappetence, which may progress lesions may be an incidental finding in older, recovered cats,
to profound dehydration, vomiting, sometimes watery to hem- which includes surviving cats with cerebellar hypoplasia.
orrhagic diarrhea, and rapid loss of weight. Some cats develop
only anorexia and lethargy, in the absence of vomiting, diar- Diagnosis
rhea, or leukopenia.3 Secondary bacterial infections appear to be
essential for signs of disease to occur. Death ­usually results from Laboratory Abnormalities
complications relating to dehydration, electrolyte imbalances, Complete Blood Count
hypoglycemia, hemorrhage, or bacteremia and endotoxemia. The most common abnormality on the CBC in feline panleu-
In the developing fetus or neonate, FPV replicates in a vari- kopenia is leukopenia, which is due to a neutropenia and lym-
ety of tissues. Abortion, congenital abnormalities, or infertil- phopenia (Box 19-1).3 Total leukocyte counts may be as low
ity can result from infection early in pregnancy, although the as 50 cells/µL, and toxic band neutrophils may be present. In
queen is generally otherwise unaffected. Later in pregnancy or one study, only 65% of 187 cats with panleukopenia were leu-
in neonates up to approximately 1 week of age, viral destruc- kopenic, so an absence of leukopenia does not rule out FPV
tion of Purkinje cells and granule precursor cells located in the infection. Recovery may be associated with lymphocytosis and
cerebellar external granular layer leads to cerebellar hypoplasia
(Figure 19-1). The severity of infection can vary between kittens
in a litter. Sometimes a portion of the litter fails to survive and
the remainder develop neurologic signs.18 Signs of cerebellar
ataxia are nonprogressive and are most apparent when kittens
begin to walk at about 2 to 3 weeks of age, although menta-
tion and appetite are otherwise normal, and these kittens can
sometimes make acceptable pets. Other developmental central
nervous system (CNS) abnormalities have been reported less
commonly, and include hydrocephalus, porencephaly (cystic
lesions within the cerebral hemispheres), or hydranencephaly
(complete replacement of the cerebral hemispheres with cystic
lesions). These abnormalities may be accompanied by signs of
forebrain damage, such as seizures and behavioral changes.
Unlike canine parvoviruses, FPV appears to be able to infect
neurons other than the cerebellar Purkinje cells, which are ter-
minally differentiated cells.19 Ocular lesions can also develop
and include retinal folding, dysplasia and degeneration, and A
optic nerve hypoplasia.
The DNA of FPV has been detected in the myocardium of
cats with hypertrophic, dilated, and restrictive cardiomyopathy,
but was not detected in a subset of healthy control cats.20 Addi-
tional studies to assess the role of FPV in feline myocarditis and
cardiomyopathy are needed.
Fecal shedding of virus usually lasts for several days, and in
some cats, it may persist for up to 6 weeks. Kittens infected in
utero have been reported to develop immune tolerance to the
virus, with viral persistence in the kidneys and lungs for up to
1 year in the absence of shedding.

Physical Examination Findings

The most common physical examination findings are weakness,
lethargy, and dehydration. Fever (103°F to 107°F or 39.5°C to
42.5°C) may be present early in the course of illness. Pain may
be noted on palpation of the abdomen, or a hunched posture B
may be present. The perianal region may be contaminated with FIGURE 19-1  A, Severe cerebellar hypoplasia in a 1-year-old male neutered domes-
feces. Oral ulceration and mucosal pallor may be present in tic shorthair that was euthanized for cerebellar signs and seizures. The neurologic signs
severely affected cats, and rarely, bacteremia may be accompa- had been present since the cat was found at approximately 4 months of age. There is a
nied by icterus. Terminally, affected cats may be hypothermic, paucity of neurons and glial cells in all layers. B, Normal feline cerebellum. Note the dra-
bradycardic, and comatose. matically increased width of the molecular layer when compared to (A).
 CHAPTER 19  Feline Panleukopenia Virus Infection and Other Viral Enteritides 189

leukocytosis. Thrombocytopenia and mild anemia are also com- Serum Biochemical Tests
mon. Thrombocytopenia may result from damage to the mar- Serum biochemistry analysis may show hypoalbuminemia,
row or, possibly, disseminated intravascular coagulation (DIC). hypoglobulinemia, and/or hypocholesterolemia; electrolyte
abnormalities such as hyponatremia or hypernatremia, hypo-
chloremia, hyperkalemia, or, less commonly hypokalemia; and
BOX 19-1 acid-base abnormalities (see Box 19-1). In severely affected cats,
azotemia, increased serum activities of AST or ALT, or hyper-
Prevalence of Laboratory Abnormalities in Cats with bilirubinemia may be present. Hyperglycemia or hypoglycemia
Panleukopenia may also be identified.

Diagnostic Imaging
Leukopenia: 122/187 (65%) Plain Radiography
Thrombocytopenia: 83/153 (54%) As in dogs with parvoviral enteritis, abdominal radiography
Anemia: 91/187 (48%) in cats with panleukopenia may show evidence of poor serosal
Neutropenia: 64/137 (47%) detail and a fluid- and gas-filled gastrointestinal tract.
Lymphopenia: 53/137 (39%)
Hypoalbuminemia: 45/101 (45%) MRI Findings
Hypochloremia: 40/112 (36%) MRI of cats with neurologic signs due to FPV may reveal evi-
Hyponatremia: 41/127 (32%) dence of cerebellar agenesis or hypoplasia. Rarely, hydrocepha-
Hypoproteinemia: 46/153 (30%) lus, porencephaly, or hydranencephaly can be detected.18
Hyperglycemia: 48/168 (29%)
Increased AST activity: 26/98 (27%) Microbiologic Tests
Hyperkalemia: 30/132 (23%) Diagnostic assays available for feline panleukopenia are listed
Increased BUN: 36/168 (21%) in Table 19-1.
Hyperbilirubinemia: 19/134 (14%)
Increased ALT activity: 18/135 (13%) Serologic Diagnosis
Increased creatinine: 12/155 (8%) Use of serology for diagnosis of feline panleukopenia is com-
Hypokalemia: 9/132 (7%) plicated by widespread exposure or immunization, so serologic
Hypernatremia: 8/127 (6%) assays that detect antibody against FPV are generally used to
Hypoglycemia: 10/168 (6%) assess the need for vaccination rather than for diagnosis. They
can also be used in outbreak situations in order to determine
Modified from Kruse BD, Unterer S, Horlacher K, et al. Prognos- which cats are at risk for development of disease and virus shed-
tic factors in cats with feline panleukopenia. J Vet Intern Med ding, and which cats are protected and therefore at low risk.
2010;24:1271-1276. The gold standard method for FPV serology is hemagglutination

TABLE 19-1
Diagnostic Assays Available for Feline Panleukopenia
Assay Specimen Type Target Performance
Canine parvovirus Feces Parvoviral antigen Sensitivity varies with the assay used and the timing
fecal antigen of specimen collection. False negatives are common,
ELISA but a positive result generally indicates infection.
Histopathology Usually necropsy Crypt necrosis with intra- Can be used for necropsy diagnosis.
specimens, especially nuclear inclusions; FPV
gastrointestinal tissues antigen with IHC or IFA
Polymerase chain Feces, tissue samples FPV DNA Sensitivity and specificity varies depending on assay
reaction (PCR) design. The extent to which attenuated live vaccine
virus can be detected after vaccination is not well
understood. Because of the high sensitivity of some
assays, the significance of a positive result may be dif-
ficult to interpret. False-negative results may occur as
a result of inhibition of PCR by components of feces.
Fecal electron Feces Virus particles Not widely available, turnaround time can be slow,
microscopy and may be expensive. Requires the presence of
large amounts of virus.
Virus isolation Feces, tissues FPV Difficult, not widely available. Used primarily as a
research tool.

FPV, feline panleukopenia virus; IFA, immunofluorescent antibody; IHC, immunohistochemistry.

190 SECTION 1  Viral Diseases

inhibition, which measures the ability of serum to prevent agglu- Molecular Diagnosis Using the Polymerase Chain Reaction
tination of erythrocytes by the virus (see Chapter 2). Serum neu- Specific real-time PCR assays have been developed for detection
tralization assays may also be used. Point-of-care assays designed of FPV and differentiation of FPV from CPV-2 variants and are
to detect antibody titers to CPV have a low sensitivity (28%) offered by veterinary diagnostic laboratories. Clinicians should
for detection of antibodies to FPV in cats.21 A point-of-care contact their laboratory to determine the specificity of the assay
assay designed to detect feline antibodies (ImmunoComb Feline offered.25 These assays can be used on whole blood or feces.
VacciCheck Test Kit, Biogal, Galed Labs, Israel) also had a low The extent to which these assays detect attenuated live vaccine
sensitivity (49%), although specificity was high.21 The use of virus after vaccination requires further study. Assays have also
this test for risk analysis in shelter situations may lead to inap- been developed that differentiate between field and vaccine
propriate removal or isolation of cats with false-negative results strains of FPV.26
for protective antibody titers, which might waste time, space,
and financial resources.21 However, positive results should Pathologic Findings
­reliably indicate protection. The test can be performed quickly Gross Pathologic Findings
(30 minutes) and requires as little as 5 µL of serum or plasma, Gross pathologic findings in feline panleukopenia include thymic
so provided it is understood that a negative result means either involution; thickening, distention, and discoloration of the intes-
a protected or susceptible status, and a positive result equates tinal wall with serosal hemorrhage (Figure 19-2); and enlarged,
to protection, the test still has the potential to provide useful edematous mesenteric lymph nodes. The intestine may contain
information. bloody liquid contents, and mucosal hemorrhage may be identi-
fied. Hemorrhages may be visible on the surface of other organs
Antigen Detection Enzyme Linked Immunosorbent Assay as well. In some cats, mild pleural or peritoneal effusion is pres-
FPV can be detected in feces or rectal swabs using antigen ent. Cats infected prenatally may have cerebellar aplasia, or more
assays designed to detect CPV.22,23 The sensitivity and speci- commonly a small cerebellum (often half to three-quarters normal
ficity of these assays varies from one assay to another and with size).27 Rarely other developmental CNS abnormalities such as
the stage of infection, because virus shedding may be tran- hydrocephalus, hydranencephaly, or porencephaly are observed.18
sient. In general, false-negative results are common with these
assays, but false positives are uncommon, so a positive test Histopathologic Findings
result in a cat with consistent clinical signs suggests a diag- Histopathologic findings in the intestinal tract are similar to those
nosis of feline panleukopenia. The specificity of one point-of- described for CPV-2 infection, with crypt dilation and necrosis
care device (SNAP Parvo, IDEXX Laboratories, Westbrook, of crypt epithelial cells, accumulation of cellular debris, neutro-
ME) was high; 54 of 55 positive assay results were confirmed phil infiltration, loss of villi, and submucosal edema throughout
with a PCR assay. Another study of 52 cats with diarrhea the small and large intestines; the jejunum and ileum are usually
and 148 healthy cats showed variability in the sensitivity most severely affected (Figure 19-3, A). Acutely affected cats
and specificity of five different test kits when compared with show widespread lymphoid depletion and there may be hyper-
fecal electron microscopy.23 Sensitivity ranged from 50% to plasia of mononuclear phagocytes. Intranuclear inclusions are
80%, and specificity ranged from 94% to 100%. This study found in some cats (Figure 19-3, B). Examination of the bone
included only 10 cats with FPV as determined with electron marrow may reveal bone marrow hypoplasia. Examination of
microscopy. Additional studies are warranted that evaluate the cerebellum shows cellular depletion; reactive astrocytosis
the sensitivity and specificity of these assays in larger numbers may be present. Immunohistochemistry or immunofluorescent
of cats with FPV infection when both real-time PCR and elec-
tron microscopy are used as the gold standard. False-positive
fecal antigen assay results after vaccination with attenuated
live viral vaccines appear to be uncommon, but again vary
with the test used.24 Of the SNAP Parvo (IDEXX Laborato-
ries), AGEN CPV (AGEN Biomedical Ltd., Brisbane, Austra-
lia), and the Witness CPV (Synbiotics Corp, San Diego, CA),
the SNAP Parvo was least likely to yield positive results after
vaccination.

Fecal Electron Microscopy

Fecal electron microscopy is still offered by some institutions
for diagnosis of viral enteritis. It may also facilitate diagnosis
of other infections such as rotavirus, astrovirus, torovirus, and
coronavirus infections. Turnaround time may be slow. Gener-
ally speaking, large amounts of virus must be present for results
to be positive, and technical expertise is required to accurately
identify virus in the stool.

Virus Isolation
FPV can be isolated in feline cells, but as with CPV, isolation
can difficult, and the virus shows minimal cytopathic effects. FIGURE 19-2  Intestinal tract of a 2-year-old intact female domestic longhair cat
As a result, isolation of FPV is a specialized procedure that is with severe feline panleukopenia. The intestinal loops are dilated and flaccid and discol-
uncommonly used for diagnosis. ored red to purple. Ruler = 1 cm.
 CHAPTER 19  Feline Panleukopenia Virus Infection and Other Viral Enteritides 191

antibody may be used to document the presence of the virus vaccines. An intranasal FPV, FHV-1 and feline calicivirus vac-
within tissues (see Figure 19-3, C). cine is available; its use has been controversial, because panleu-
kopenia is a systemic disease. An outbreak of salmonellosis and
Treatment and Prognosis panleukopenia occurred in one cattery that used an intranasal
FPV vaccine.4 No difference was noted in seroconversion rates
Antimicrobial Treatment and Supportive Care between five cats vaccinated with the intranasal vaccine and five
Treatment of cats with feline panleukopenia is with supportive cats vaccinated with a parenteral attenuated live vaccine, but
care, especially intravenous crystalloids and parenteral antimi- the number of cats in this study was small, and a larger number
crobial drug treatment as for CPV-2 infections (see Chapter 14). of cats that were vaccinated with the parenteral vaccine had
Dextrose supplementation of the fluids may be required, and protective antibody titers on day 7.30
blood glucose concentration should be monitored. Oral intake Both inactivated and attenuated live vaccine types induce
of food and water should be withheld until vomiting has ceased. protective antibody titers after vaccination in a high propor-
Experience with early enteral nutrition has not been reported tion of cats,5 although the attenuated live vaccine may be
in cats, and extreme care is warranted to prevent aspiration more likely to induce protective titers than the inactivated vac-
pneumonia. Antiemetics such as metoclopramide or ondanse- cine.24 Provided maternally-derived antibody (MDA) is absent,
tron may be effective. In contrast to canine parvoviral enteritis, immunity occurs within 1 week after a single vaccination with
treatment with rfIFN-ω has not been beneficial for treatment of an attenuated live viral vaccine31 and lasts for at least 3 years,
feline panleukopenia, although increased antibody production and possibly for life.32 Nevertheless, two doses, 3 to 4 weeks
and a reduced acute inflammatory response was observed.28 apart, have been recommended for initial vaccination with
attenuated live vaccines in the absence of MDA. Two injec-
Prognosis tions are always required for inactivated vaccines, and maxi-
Cats with panleukopenia that survive the first 5 days of treat- mal immunity does not occur until 1 week after the second
ment usually recover, although recovery is often more pro- dose. However, even with an inactivated vaccine, challenge
longed than it is for dogs with parvoviral enteritis. In 244 cats 7.5 years after vaccination was associated with protection.33 The
with feline panleukopenia from Europe, the survival rate was use of inactivated vaccines should be reserved for immunosup-
51.1%.3 Nonsurvivors had lower leukocyte and platelet counts pressed cats or colostrum-deprived neonates that are less than
than survivors, and cats with white cell counts below 1000/µL 4 weeks of age, or when there is a need to vaccinate pregnant cats.
were almost twice as likely to die than those with white cell In shelter situations, the use of attenuated live vaccines is always
counts above 2500/µL. Only total leukopenia, and not lym- recommended because of the slow onset of immunity with inac-
phopenia, was correlated with mortality. Hypoalbuminemia tivated vaccines.34 FPV vaccines protect cats against challenge
and hypokalemia were also associated with an increased risk of with CPV-2b strains.35,36 However, cross-reactivity of antibod-
mortality. In contrast to dogs with parvoviral enteritis, mortal- ies induced by FPV vaccination to CPV-2 strains was lower than
ity in cats does not appear to be correlated with age. that to FPV as determined using hemagglutination inhibition.37
Cerebellar signs in kittens with cerebellar hypoplasia typi- The extent to which FPV vaccines protect against infection with
cally do not progress and may improve slightly as a result of other CPV-2 variants requires further investigation.38
compensatory responses from other senses such as vision.29 The most common reason for vaccine failure is interference
by MDA. Maternal antibody persists until at least 12 weeks,
Immunity and Vaccination and possibly longer in some cats. Virus neutralization titers
above 1:10 are likely to interfere with vaccination, and kittens
Recovery from feline panleukopenia is thought to confer life- with titers below 1:40 are generally considered to be suscep-
long immunity. Effective vaccines are widely available, and tible to infection by FPV. Kittens should be vaccinated every
include both parenteral inactivated and attenuated live viral 3 to 4 weeks from 6 to 8 weeks of age, and it is recommended

A B C
FIGURE 19-3  A, Histopathology of the jejunum from a kitten with panleukopenia. Villi are rounded and blunted with nearly complete epithelial loss and crypt dilation. H&E stain.
B, Histopathology of the jejunum from a young barn cat that died after several days of profound weakness and neurologic signs. Six other cats in the barn died with the same signs. Mucosal
crypts are dilated and contain debris, and intranuclear inclusions are present (small arrows). Another cell (large arrow) is foamy and degenerate and has a hyperchromatic nucleus. H&E
stain. C, Same cat as in B. The presence of FPV in the intestinal tract is confirmed with immunohistochemistry (brown stain). (Courtesy Dr. Patricia Pesavento, University of California, Davis
Veterinary Anatomic Pathology Service.)
192 SECTION 1  Viral Diseases

that the last vaccine in the kitten series be given no earlier 2 mL of type-matched serum from cats with a high antibody
than 14 to 16 weeks of age. When there is a history of an out- titer.39,40 However, this is only effective when administered
break situation, the final booster could be given no earlier than before the onset of clinical signs, and it can interfere with subse-
18 to 20 weeks of age.39 In all situations, a booster should be quent vaccination. For these kittens, it has been recommended
administered at 1 year, and every 3 years thereafter. that vaccination be withheld for 3 weeks after the serum has
Vaccination of pregnant queens with attenuated live viral been administered.39 Passive immunization may be useful when
vaccines can cause cerebellar hypoplasia or fetal losses. The fre- cats are introduced into a shelter situation where a known prob-
quency with which this occurs is unknown. As a result, it has lem exists. Repeated treatment with serum should be avoided
been suggested that pregnant queens only be vaccinated with because hypersensitivity reactions may occur. Prevention of
attenuated live FPV vaccines if they are being introduced into feline panleukopenia should also include proper disinfection
a shelter and quarantine while immunization with inactivated with disinfectants that are effective against parvoviruses, such
vaccines is performed is not possible. Alternatively, assessment as bleach, accelerated hydrogen peroxide, or potassium peroxy-
for protective antibody titers with an in-house test kit (where monosulfate (see Chapter 11) and, in shelter situations, isola-
available) could be performed. tion or removal of cats that develop gastrointestinal illness, and
separate housing for healthy kittens.
Prevention
Public Health Aspects
New kittens should not be introduced into households that
previously contained cats infected with FPV unless they are Although FPV is not known to infect humans, a unique strain of
fully vaccinated. In the face of an outbreak, exposed and sus- FPV was recently isolated from a diarrheic monkey in China.41
ceptible kittens may be effectively protected for 2 to 4 weeks This strain was shown to cause panleukopenia in inoculated
through subcutaneous or intraperitoneal administration of cats.

CASE EXAMPLE Laboratory Findings:

CBC:
HCT 46% (30-50%)
Signalment: “Callie”, a 2 year-old, female intact domestic MCV 49.8 fL (42-53 fL)
longhair from Woodland, CA MCHC 30.4 g/dL (30-33.5 g/dL)
History: Callie was brought to an emergency clinic for acute WBC 150 cells/µL (4500-14,000 cells/µL)
onset of collapse and severe illness. The current owner had Neutrophils 0 cells/µL (2000-9000 cells/µL)
fostered the cat for 1 week after she was found as a stray. The Lymphocytes 141 cells/µL (1000-7000 cells/µL)
cat had been nursing a litter of kittens. The kittens were 4 Highly reactive lymphocytes 6 cells/µL
weeks old, being weaned and apparently healthy. Since be- Monocytes 3 cells/µL (50-600 cells/µL)
ing fostered, the cat had exhibited a progressive decrease Platelets 32,000 platelets/µL (180,000-500,000 platelets/µL).
in appetite and thirst, and her feces had become soft and Serum Chemistry Profile:
pasty. The night before she was brought to the emergency Sodium 141 mmol/L (151-158 mmol/L)
clinic, she had been bathed, and afterwards she vomited Potassium 4.0 mmol/L (3.6-4.9 mmol/L)
bile-stained fluid twice and was placed on a heating pad. Chloride 111 mmol/L (117-126 mmol/L)
The following morning she was found laterally recumbent Bicarbonate 23 mmol/L (15-21 mmol/L)
and minimally responsive. Phosphorus 6.0 mg/dL (3.2-6.3 mg/dL)
Physical Examination: Calcium 7.4 mg/dL (9.0-10.9 mg/dl)
Body Weight: 2.3 kg BUN 24 mg/dL (18-33 mg/dL)
General: Stuporous mentation, estimated to be 8% to 10% Creatinine 0.5 mg/dL (1.1-2.2 mg/dL)
dehydrated, T < 92°F (<33°C), HR = 132 beats/min, RR = 32 Glucose 68 mg/dL (63-118 mg/dL)
breaths/min, mucous membranes pale and tacky, unable Total protein 3.2 g/dL (6.6-8.4 g/dL)
to assess CRT. Fecal and urinary stains were present Albumin 1.6 g/dL (2.2-4.6 g/dL)
around the perineum and on the caudal aspect of the Globulin 1.6 g/dL (2.8-5.4 g/dL)
pelvic limbs. ALT 125 U/L (27-101 U/L)
Musculoskeletal: Body condition score 2/9. Diffuse muscle AST 143 U/L (17-58 U/L)
wasting was present. The cat was laterally recumbent and ALP 4 U/L (14-71 U/L)
nonambulatory. Creatine kinase 2409 U/L (73-260 U/L)
Cardiovascular: Weak femoral pulses. No murmurs or Gamma GT <3 U/L (0-4 U/L)
arrhythmias were detected. Cholesterol 68 mg/dL (89-258 mg/dL)
Gastrointestinal and Urogenital: The abdomen was soft Total bilirubin 0.2 mg/dL (0-0.2 mg/dL)
and nonpainful on palpation. Fluid-filled intestinal loops Magnesium 2.5 mg/dL (1.5-2.5 mg/dL).
were palpated, and the urinary bladder was small (<5 cm) and Imaging: An abdominal ultrasound showed marked fluid dis-
soft. tention of the small intestines.
All Other Systems: No abnormalities were detected. Microbiologic Testing: In-clinic ELISA serology for FeLV anti-
gen and FIV antibody: negative.
 CHAPTER 19  Feline Panleukopenia Virus Infection and Other Viral Enteritides 193

Treatment and Outcome: Callie was treated with active to purple and contained a small amount of dark red mucoid
warming, and a central venous access line was placed. Intra- material. The mesenteric lymph nodes were prominent, and
venous crystalloids (four warmed 60-mL boluses of lactated their cut surface was discolored red to dark pink. The liver
Ringer’s solution [LRS], each given over 20 minutes) were ad- was pale yellow and extended beyond the costal arches. Nu-
ministered, after which an venous acid-base panel showed merous petechial hemorrhages were present on the serosal
a pH of 7.267 (7.31-7.46), bicarbonate of 17.5 mmol/L (14- surface of the urinary bladder.
22 mmol/L), base excess of −8.1 mmol/L (−4 to +2 mmol/L), Histopathologic Findings: Within the duodenum, jejunum,
pCO2 of 39.7 mm Hg (25-37 mmHg), lactate of 4.5 mEq/L and ileum there was severe, subacute, diffuse necrotizing
(<2 mEq/L), glucose of 52 mg/dL, potassium of 3.1 mEq/L, and fibrinohemorrhagic enteritis. The villi were necrotic,
sodium of 141 mEq/L, and ionized calcium of 1.17 (1.1-1.4 fused, and markedly blunted with a minimal inflammatory
mmol/L). A dextrose bolus and ticarcillin-clavulanic acid response. Necrosis extended into the crypts, and there was
(22 mg/kg, q6h, IV) were administered. The cat repeatedly some evidence of a regenerative response that included en-
vomited blood-tinged fluid, and so treatment with meto- terocyte hypertrophy, karyomegaly, and rare mitotic figures.
clopramide (0.02 mg/kg/hr) and famotidine (0.5 mg/kg IV Mixed bacteria, which included small gram-negative rods
q12h) was initiated. Aggressive crystalloid fluid therapy was and large numbers of gram-positive cocci, lined and effaced
continued (LRS supplemented with 30 mEq/L KCl and 2.5% the denuded villi. There was diffuse lymphoid depletion in
dextrose), and treatment with hetastarch was also initiated. lymph nodes, as well as the mucosa-associated lymphoid
Systolic blood pressure (Doppler) was 60 to 90 mm Hg, heart tissue in the cecum and colon. Marked depletion of ery-
rate increased to 170 beats/min, and rectal temperature in- throid and myeloid precursors was present in the bone mar-
creased to 100°F. When the CBC results were available, the row. There were multifocal areas of hemorrhage in the skel-
cat was placed in the isolation ward. etal and cardiac muscle, intestinal tract, and lungs, as well
Pasty diarrhea that contained sloughed mucosa occurred as fibrin thrombi in the lungs. FPV antigen was identified in
every 1 to 2 hours, which transitioned to liquid red feces intestinal epithelial cells using immunohistochemistry. Cul-
over 24 hours. A CBC again showed absolute neutropenia ture of the jejunum for Salmonella spp. was negative.
and 15,000 platelets/µL. After another 24 hours, the cat’s Diagnosis: Feline panleukopenia
condition deteriorated despite aggressive treatment and Comments: The cat in this report was a stray with an un-
monitoring. Partial parenteral nutrition was initiated. That known vaccination history, which demonstrates that severe
evening, pyrexia developed (104.6°F) as well as tachypnea disease can occur even in adult cats. Antemortem diagnos-
and increased respiratory effort. The owner elected eutha- tic testing for FPV with a fecal antigen ELISA assay or PCR
nasia. The cat regurgitated approximately 200 mL of dark assay was discussed with the owner, but was declined be-
brown fluid at the time of euthanasia. cause of the high degree of suspicion for the disease and
Gross Necropsy Findings: Ten mL of semiopaque red fluid the lack of impact that a positive or negative result would
was present in the peritoneal cavity. Streaks of hemorrhage have had on the treatment plan. Secondary bacterial sepsis
were noted throughout the skeletal muscle. Between the was suspected. Additional co-infections with other viruses,
pylorus and the ileocecocolic junction, the serosa of the such as feline coronavirus, or enteropathogenic bacteria
small intestinal tract was dark red to purple to black (see could not be ruled out. During the cat’s treatment, one of
Figure 19-2). The entire small and large intestinal tract was the kittens in the litter died suddenly and the other devel-
dilated and flaccid. The small intestinal mucosa was dark red oped signs of illness.

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