Vol. 19, No.
3 March 1997
Continuing Education Article
Refereed Peer Review
FOCAL POINT
★Aggressive treatment can
dramatically increase survival of
patients with canine parvovirus
enteritis.
KEY FACTS
■ In-house ELISAs allow for rapid
diagnosis, but false-positives
can result when dogs have
been recently vaccinated with
attenuated virus vaccine, and
false-negatives can result when
antibodies from blood in the
feces bind to antigen.
■ If serum albumin drops below 1.5
g/dl or total protein decreases
below 3.5 g/dl, an intravenous
colloid should be given.
■ Intravenous bactericidal
antibiotics are indicated for
puppies with neutropenia and
hemorrhagic diarrhea.
■ Antiendotoxin should be given
before antibiotics because
endotoxins are released as
bacteria are killed.
Small Animal Gastroenterology
Canine Parvovirus.
Part II.Clinical
Signs, Diagnosis,
and Treatment*
Auburn University
Douglass K. Macintire, DVM, MS
Saralyn Smith-Carr, DVM, PhD
T wo clinical syndromes occur in dogs infected with canine parvovirus
(CPV): enteritis and myocardial failure. Myocardial failure can occur in
neonatal puppies infected in utero or shortly after birth as a result of
failure of passive transfer of colostral antibodies. In these puppies, CPV infects
rapidly dividing cells of the myocardium, thus resulting in delayed signs of car-
diac failure, syncope, arrhythmia, or sudden death. Sometimes, the only evi-
dence of myocardial disease is found at necropsy.
The myocardial form of CPV infection was seen primarily in the early 1980s.
It is rare today because of the effectiveness of current vaccination protocols in
promoting maternal antibody protection in young puppies. This article focuses
on the enteric form of CPV infection.
DIAGNOSIS
Clinical Findings
The initial clinical signs of enteric CPV infection are nonspecific and include
anorexia, depression, lethargy, and fever. Within 24 to 48 hours, most affected
puppies begin vomiting. Intestinal disease is more severe in puppies with enter-
ic parasites, environmental stresses, low maternal antibody titers, and delayed
or impaired humoral immune response.1,2 With severe dehydration, protein
loss, concomitant infection, and inability to produce a rapid immune response,
this syndrome can rapidly progress to systemic shock and death.
*Part I of this two-part presentation appeared in the February 1997 (Vol. 19, No. 2)
issue of Compendium.
Small Animal The Compendium March 1997

Necrosis of mucosal and Pathologic Findings

lymphoid tissue of the small
intestine disrupts the gastro-
intestinal mucosal barrier,
thus permitting bacterial
translocation. Gram-negative
and anaerobic bacteria can
enter the general circulation,
producing septic shock and
the systemic inflammatory
response syndrome (SIRS).
The outer cell wall of gram-
negative bacteria contains
endotoxins (lipopolysaccha- Figure 1—Photomicrograph of the duodenal mucosa from a orrhagic contents. The mesen-
rides [LPS]) that are also po- dog with parvovirus enteritis. There is severe villus collapse teric lymph nodes are usually
tent mediators of systemic and dilatation of the crypt glands secondary to viral-induced enlarged and swollen, with
inflammation.3 necrosis of crypt epithelium. (Courtesy of Dr. J. Newton, petechial hemorrhages in the
In humans, bacterial Department of Pathobiology, Auburn University, Auburn, AL) cortex. Cortical necrosis and
translocation and gut-origin
sepsis are believed to be pre-
disposing factors for adult respiratory distress syndrome
(ARDS) and multiple-organ failure.4 In one study of 88
dogs that died of severe CPV infection, E. coli was isolat-
ed from the lung and/or liver of 90% of the dogs, and
pulmonary lesions similar to those found in humans with
ARDS were detected in 69% of the dogs.5 Secondary bac-
terial infection with clostridia, Campylobacter species, and
salmonellae has also been reported to occur with par-
vovirus infection.6,7 Septicemia and/or endotoxemia may
occur as a direct result of these bacterial pathogens.
Transient lymphopenia is the most consistent hema-
tologic finding associated with parvovirus infection.2,8
Panleukopenia, particularly neutropenia, occurs with
severe disease. Blood-loss anemia, often associated with
concurrent internal parasite infection, may be manifest-
ed as anemia with panhypoproteinemia. Serum chem-
istry analyses are nonspecific. Severe potassium loss sec-
ondary to anorexia, vomiting, and diarrhea may
contribute to the depression and weakness. Elevated
blood urea nitrogen (BUN) and creatinine may occur
as a result of dehydration. Elevation in serum alkaline
phosphatase and alanine transaminase activities may
also occur as a result of hepatic hypoxia caused by seri-
ous hypovolemia. Other electrolyte abnormalities may
occur secondary to vomiting and severe diarrhea and
should be monitored.
No specific radiographic findings are associated with
parvovirus infection. Radiographic signs of gastroen-
teritis are fluid- and gas-filled bowel loops. Radiogra-
phy or abdominal ultrasonography may be used to in-
vestigate the possibility that a foreign body is causing
the clinical signs or to identify intussusception as a
complication of severe parvovirus disease.
The gross intestinal lesions
of parvovirus are nonspecific
and variable.1,8 The lesions, if
present, are usually segmen-
tally distributed, with the
ileum and jejunum most of-
ten affected. These affected
sections may be flaccid and
may exhibit serosal hemor-
rhage or congestion. The
bowel lumen is usually empty
but may contain watery hem-
atrophy of the thymus can be
observed in puppies.
The microscopic lesions of CPV are seen in the prolif-
erating population of cells in the intestinal tract, bone
marrow, and lymphoid tissue. In the intestinal tract, the
early lesions are necrosis of the crypt epithelium, result-
ing in dilated crypts that are filled with necrotic debris
and/or intranuclear inclusions within crypt epithelial
cells. With the progression of disease, the villi become
blunted and malabsorption/maldigestion results (Figure
1). Complete collapse and destruction of the villi occurs
in severe cases. These lesions may be focal or may occur
segmentally throughout the small intestine (and infre-
quently in the large intestine). There is usually evidence
of intestinal regeneration, even in severe cases.
The germinal centers of mesenteric and gut-associated
lymph nodes and the cortical area of the thymus are de-
pleted of lymphoid cells. Myeloid and erythroid hy-
poplasia occur in the bone marrow during acute dis-
ease. During recovery, there is hyperplasia of lymphoid,
erythroid, and myeloid cells.
Diagnostic Testing
Many tests are available to practicing veterinarians
for detecting CPV in the feces of infected animals. Solid-
phase enzyme-linked immunosorbent assays (ELISAs)
have enabled in-house testing, which allows for rapid
identification, isolation, and treatment of animals with
CPV infection while clinical signs are still vague. False-
negative results may occur because of binding of test
antigen with serum-neutralizing antibodies in bloody
diarrhea. False-positive results may occur shortly after
vaccination with attenuated virus vaccines because of
fecal shedding of vaccine virus. Samples may also be
submitted to commercial laboratories for diagnosis, al-

CLINICAL FINDINGS ■ DESCRIPTION OF LESIONS ■ IN-HOUSE ELISAs

The Compendium March 1997
though submission may de-
lay definitive diagnosis by 1
or 2 days.
Other tests that are avail-
able through university and
state diagnostic laboratories
include electron microscopy,
hemagglutination (HA),
virus isolation, latex aggluti-
nation, and ELISA. These
tests are performed on feces
from animals in the acute
phase of the disease. Com-
mercial laboratories can also Figure 2—Canine parvovirus enteritis can be a debilitating ing recommendations should
diagnose parvovirus infec- disease, but most puppies can survive with intensive, aggres- be considered in the treat-
tion in fresh-frozen and for- sive supportive care.
malin-fixed tissue samples
by immunocytochemistry,
immunofluorescence assay (IFA), radioimmunoassay
(RIA), or immunoperoxidase staining procedures. Spe-
cialized ELISAs (e.g., indirect ELISA, competitive
ELISA, and double-antibody sandwich ELISA [DAS-
ELISA]) that are currently being developed for detect-
ing CPV-specific antibodies in serum are reportedly
more sensitive than hemagglutination inhibition (HI).
Various assays that use a polymerase chain reaction
(PCR) for the detection of parvovirus in feces have
been developed. The PCR test can detect fewer parti-
cles of CPV than can conventional methods.9–11 This
sensitivity may reduce the number of false-negative re-
sults that occur with fecal ELISAs. The PCR assays are
also highly specific and can differentiate wild-type virus test, animals with a compatible history should receive ap-
from vaccine virus, thus eliminating false-positive re-
sults due to recent vaccination.12
Serum IgM and IgG titers were used to detect par-
vovirus infection when the disease first emerged. A high
IgM titer with a low-to-negative IgG titer was used to
determine acute CPV infection in dogs with hemor-
rhagic diarrhea. Serologic testing was established before
antigen tests were developed and could not be used to
differentiate between previous subclinical infection, ac-
tive infection, or vaccination.
Currently, serum antibody testing for parvovirus is
used to determine whether a dog has been immunized
by vaccination or whether susceptible dogs have been
exposed to parvovirus. Diagnostic laboratories use HI,
radial hemolysis, virus or serum neutralization (VN or
SN), IFA, and RIA to detect CPV antibodies. The stan-
dard for demonstration of protective antibody titer has
long been the HI test, which measures both IgM and
IgG antibodies in serum. More recently, many laborato-
ries have used the IFA and SN titers to determine the
level of protective immunity.
OUTSIDE TESTING ■ FECAL ANTIGEN TEST ■ RAPID SCREENING TESTS
Small Animal
TREATMENT
Canine parvovirus infec-
tion can produce severe dehy-
dration, endotoxic or septic
shock, and multiple-organ
failure. Without treatment, it
is often fatal. However, ag-
gressive therapy and support-
ive care (Figure 2) have
achieved an 85% to 95% sur-
vival rate at our hospital (see
Treatment of Canine Par-
vovirus Enteritis). The follow-
ment of all dogs infected with
CPV.
Initial Assessment
When an animal is presented to the hospital with a
history suggestive of CPV enteritis, a fecal antigen test
should be performed to confirm the diagnosis if possi-
ble. If the test is positive, the animal should be isolated
from other hospitalized patients, and all contaminated
surfaces should be cleaned with a 1:30 dilution of house-
hold bleach. Strict cleanliness should be observed to
avoid spread of the disease to other animals. If the test is
negative, other causes of gastroenteritis (e.g., foreign
body, pancreatitis, intestinal parasitism, toxicity, or di-
etary indiscretion) should be ruled out. Because of the
possibility of false-negative results with the fecal antigen
propriate supportive care and be retested 48 hours later.
Disease severity should be assessed through evalua-
tion of physical examination findings and blood drawn
for an initial minimum data base. Rapid screening tests
that aid in patient assessment and fluid choice include
hematocrit, total solids, serum electrolytes, blood gases,
and reagent sticks for blood glucose and BUN. A com-
plete blood count or blood smear also aids in patient
assessment because leukopenia is generally associated
with more severe disease and a more guarded prognosis.
Dehydration should be estimated through physical ex-
amination findings. Animals with mild dehydration
(5% to 7%) have dry, tacky mucous membranes; ani-
mals with moderate dehydration (7% to 10%) have
slow capillary refill time (>1.5 seconds), skin tenting,
and sunken eyeballs; and animals with severe dehydra-
tion (10% to 12%) are usually moribund and in a state
of circulatory collapse.
Initial Fluid Therapy
Fluid replacement for losses incurred through vomit-
Small Animal
Treatment of Canine Parvovirus Enteritis
Intravenous Fluids
■ Begin with balanced electrolyte solution
■ Replace deficit (dehydration [%] × body weight [kg])
■ Immediately if the patient is in shock (90 ml/kg/hr)
■ Over 2 to 6 hours if the patient is only dehydrated
■ Add to replacement volume
■ Maintenance needs (44–66 ml/kg/day)
■ Continuing losses (estimate amount lost through
vomiting and diarrhea)
Antibiotics (parenteral, bactericidal)
■ For severe cases (leukopenia, hemorrhagic diarrhea),
choose one of the following:
■ Enrofloxacin (5 mg/kg every 12 hours intravenously)
and ampicillin (22 mg/kg every 8 hours
intravenously)
■ Gentamicina (2.2 mg/kg every 8 hours or 6.6 mg/kg
every 24 hours intravenously) or amikacina (10 mg/kg
every 12 hours or 20 mg/kg every 24 hours
intravenously) and amoxicillin (15 mg/kg every 12
hours intravenously)
■ Cefoxitin (25 mg/kg every 6 hours intravenously)
■ For milder cases, choose one of the following:
■ Ampicillin (22 mg/kg every 8 hours intravenously)
■ Cefazolin (20 mg/kg every 8 hours intravenously)
■ Trimethoprim-sulfadiazine (30 mg/kg every 12 hours
subcutaneously)
Electrolyte Replacement
■ Monitor serum sodium and potassium
■ Expect hypokalemia after initial fluid replacement
■ Supplement fluids with potassium (14–20 mEq/L)
Increase Oncotic Pressure
■ Give plasma if total solids <3.5 g/dl (10–20 ml/kg)
■ Give whole blood if patient is anemic
■ Give synthetic colloids (hetastarch) if patient is septic
and edematous (10–20 ml/kg over 24 hours)
a Should not be used in dehydrated animals.
ing and diarrhea is the cornerstone of treatment for
dogs with CPV enteritis and should be continued until
oral intake is resumed. The initial fluid of choice is a
balanced electrolyte solution (e.g., lactated Ringer’s so-
lution). These solutions mimic plasma electrolyte con-
centrations, are isotonic, and can be given rapidly, if
necessary, to replace acute fluid losses.
The route and rate of initial fluid therapy varies with
the patient. If CPV infection has resulted in hypovolemic
shock, a rapid intravenous fluid bolus of up to 90
FLUID REPLACEMENT ■ SHOCK ■ CIRCULATORY COLLAPSE
The Compendium March 1997
Glucose Replacement
■ If patient is hypoglycemic, give 0.5 g/kg 10% dextrose
slowly intravenously
■ After rehydration, add 50–100 ml of 50% dextrose/L of
replacement fluids to make 2.5% to 5% solution
■ Consider partial parenteral nutrition for puppies that
have been anorectic for more than 3 days
Consider Anthelmintic
■ Check stool for Giardia organisms, coccidia, or
nematodes
■ Consider injectable ivermectin (250 µg/kg) for
nonvomiting dogs—except for collies and related breeds
Control Vomiting
■ No oral intake until 24 hours after vomiting has ceased
■ Choose one or more antiemetics:
■ Metoclopramide (1–2 mg/kg over 24 hours in fluids)
■ Chlorpromazine (0.1 mg/kg every 4 to 6 hours
intravenously)
■ Ondansetron (0.1–0.15 mg/kg every 6 to 12 hours
intravenously )
Immunotherapy
■ Antiendotoxin (4.4 mg/kg diluted 1:1 with fluids,
administered over 30 to 60 minutes)
■ Hyperimmune serum (1.1–2.2 ml/kg intravenously or
subcutaneously)
■ Recombinant granulocyte colony-stimulating factor
(5–10 µg/kg/day subcutaneously)
Nutrition
■ Partial parenteral nutrition (3% amino acids, 5%
dextrose in balanced electrolyte solution)
■ Early enteral diet
■ Liquid diet (small amounts frequently)
■ Glutamine (0.5 g/kg/day in two divided doses in
drinking water)
■ Easily digestible recovery diet
ml/kg/hr may be necessary to restore perfusion. Animals
in shock will have pale or muddy mucous membranes
and a slow capillary refill time. Fluid therapy should be
administered at a fairly rapid rate until mucous mem-
brane color becomes pinker and capillary refill time is re-
stored to 1 to 1.5 seconds. If circulatory collapse prevents
venous access, fluids can be administered initially via a
20-gauge, 3.8-cm (1.5-inch) spinal needle placed into the
intraosseous space in the shaft of the femur. Once circula-
tion has improved with intraosseous fluids, an intra-
The Compendium March 1997 Small Animal

venous catheter can be placed aise. 13 Serum potassium

for continued fluid therapy. should be monitored daily
Animals that are severely de- in these patients. If it is low,
hydrated or in a state of cir- potassium chloride should
culatory collapse cannot ab- be added to the fluids
sorb subcutaneous fluid (Table I). If potassium is in
because of peripheral vaso- the normal range, potassi-
constriction. Also, hypertonic um chloride (14 to 20
solutions should be avoided mEq/L) should be added to
in dehydrated patients. prevent the levels from
Animals that are dehy- dropping.
drated but not in shock Puppies with CPV enteri-
should be rehydrated over 4 tis often experience severe
hours. The amount of fluid Figure 3— Toy-breed puppies, such as this 9-week-old protein-losing enteropathy
given is estimated by the fol- pomeranian, are prone to hypoglycemia secondary to gas- because of destruction of
lowing formula: trointestinal disease and often require intravenous glucose the intestinal villi. If the al-
supplementation. bumin decreases below 1.5
Dehydration (%) × Body g/dl, the total protein de-
weight (kg) = Deficit (L) creases below 3.5 g/dl, or
the animal develops evidence of pitting edema, admin-
Maintenance requirements (2 to 3 ml/kg/hr) as well as istration of a colloidal fluid is indicated to maintain in-
continuing losses from vomiting and diarrhea must also travascular oncotic pressure.14
be taken into consideration during initial fluid therapy. If the puppy is anemic because of parasitism or gas-
trointestinal blood loss, a transfusion of whole blood
Maintenance Fluid Therapy (preferably from a recovered animal with a high CPV
Once perfusion has been restored, the fluid rate can antibody titer) is indicated. A dose of 10 to 20 ml/kg
be decreased to 4 to 6 ml/kg/hr for most patients. Hy- can safely be administered to most puppies over a 4-
dration should be monitored by evaluating mucous hour period. If the puppy is not anemic but is hy-
membrane color, capillary refill time, pulse quality, poproteinemic, a plasma transfusion (10 to 20 ml/kg
packed cell volume and total solids, urine output intravenously) should be administered through an in-
(which should be approximately 1 to 2 ml/kg/hr), and line filter over 2 to 4 hours. In addition to providing
urine specific gravity (which should range from 1.015 oncotic components, whole blood and plasma contain
to 1.020). Fluid therapy must be adjusted to replace antibodies and serum protease inhibitors that may help
continuing losses through vomiting and diarrhea. As neutralize circulating virus and control the systemic in-
fluid losses subside, the fluid rate is gradually tapered. flammatory response associated with the disease. Plas-
Many puppies, particular- ma and blood products are
ly toy breeds or those with TABLE I available though commer-
sepsis, are prone to hypo- Potassium Replacement cial blood banks.
glycemia as a result of CPV If natural colloids are un-
Potassium available, puppies with de-
enteritis (Figure 3). After re-
Chloride
hydration, 2.5% to 5% dex- Serum Added
creased total protein and
trose can be added to the Potassium to Fluid Maximum Infusion Rate a edema should receive a syn-
balanced electrolyte solution (mEq/L) (mEq/L) ml/lb/hr ml/kg/hr thetic colloid, such as heta-
(100 ml of 50% dextrose starch or dextran 70. To
added to 1 L will make a avoid potential volume
5% solution). 3.6–5.0 20 11 25 overload, the dosage of 20
Puppies with anorexia, 3.1–3.5 30 8 17 ml/kg/day should not be ex-
vomiting, and diarrhea are 2.6–3.0 40 5.5 12 ceeded; however, colloid in-
also prone to hypokalemia, 2.1–2.5 60 4 8 fusions can be repeated after
which can result in muscle <2.0 80 3 6 24 hours if needed.15 Col-
weakness, gastrointestinal loids can be given rapidly to
ileus, polyuria, cardiac ar- aSo as not to exceed 0.5 mEq/kg/hr. patients in shock or as a
rhythmia, and general mal- continuous infusion over 24

HYDRATION MAINTENANCE ■ COLLOIDS ■ TRANSFUSIONS

The Compendium March 1997
hours to more stable patients. General guidelines are to
supply one third of fluid needs as a colloid and two
thirds as a crystalloid solution.
Systemic Antibiotics
Hemorrhagic diarrhea and mucosal sloughing are
commonly seen in dogs with CPV enteritis and indi-
cate breakdown of the gastrointestinal mucosal barrier,
which can lead to bacterial translocation, endotoxemia,
and sepsis.5,16 Severe neutropenia often coincides with
the severe enteritis and contributes to the risk of sys-
temic sepsis. For these reasons, intravenous broad-spec-
trum, bactericidal antibiotics are indicated for severely
affected puppies.1 A combination of an aminoglycoside
(gentamicin [2.2 mg/kg] or amikacin [10 mg/kg] every
8 hours) with a β-lactam antibiotic (ampicillin [2
mg/kg] or cefazolin [22 mg/kg] every 8 hours) provides
excellent coverage against gram-negative and anaerobic
bacteria that may originate from the gut.17
Aminoglycosides can cause acute renal failure and
should only be administered after rehydration has been
accomplished.18 Once-a-day dosing of aminoglycosides
may minimize renal damage while maximizing bacterial
kill because of high peak and low trough antibiotic con-
centrations.19 The high dose, however, should never be
given to dehydrated patients. Urine sediment should be
monitored for proteinuria or renal tubule casts, which
would warrant discontinuation of aminoglycoside thera-
py.
Enrofloxacin (5 mg/kg every 12 hours) is an alterna-
tive to the aminoglycosides. It has an excellent gram-
negative spectrum but is not approved for intravenous
use and may cause cartilage abnormalities in young,
growing animals.20 We have not encountered any prob-
lems with enrofloxacin when it is diluted 1:1 with
saline and administered slowly (intravenously) for a rel-
atively short term (usually 3 to 5 days) in puppies with
CPV enteritis. Rapid administration may cause vomit-
ing.
Mildly affected dogs with adequate white blood cell
counts generally do not require combination antibiotic
therapy. Appropriate antibiotic choices include ampi-
cillin, first-generation cephalosporins, or trimetho-
prim–sulfonamide in these patients.
Antiemetics
Vomiting often decreases when oral intake of food
and fluid is discontinued; but in some patients, the
problem persists and must be treated to reduce fluid
losses and increase patient comfort.
The two antiemetics most commonly used in dogs
with CPV enteritis are metoclopramide and chlorpro-
mazine. Metoclopramide is a gastric promotility drug
BACTERICIDAL ANTIBIOTICS ■ ANTIEMETICS ■ ONDANSETRON
Small Animal
that can reduce vomiting by stimulating gastric empty-
ing and inhibiting the chemoreceptor trigger zone.21
The promotility effect may prevent gastric atony and
ileus from occurring in dogs with CPV infection.
Metoclopramide can be added to the intravenous fluids
or administered as a constant-rate infusion of 1.0 to 2.0
mg/kg over 24 hours.
If metoclopramide is ineffective in controlling vomit-
ing, a more effective antiemetic is chlorpromazine.22
This drug is a phenothiazine derivative and acts on the
emetic center, the chemoreceptor trigger zone, and pe-
ripheral receptors to reduce the vomiting reflex. The
recommended dosage is 0.1 mg/kg intravenously every
4 to 6 hours or 0.2 to 0.5 mg/kg intramuscularly every
6 to 8 hours, as needed. Phenothiazine derivatives can
cause hypotension and systemic vasodilatation through
their α-adrenergic blocking effect and should only be
given after the patient is well hydrated.22
In dogs with intractable vomiting, metoclopramide
and chlorpromazine may be used together, but only
with caution because the potential for side effects may
increase. Dogs should be monitored for restlessness, hy-
peractivity, bizarre behavior, or extreme drowsiness. If
any of these signs occur, antiemetic therapy should be
discontinued.
Intractable vomiting may respond to treatment with
the new serotonin antagonist ondansetron HCl
(Zofran®, Glaxo Wellcome Inc) at dose of 0.1 to 0.15
mg/kg intravenously every 6 to 12 hours.23 Although
the drug is highly effective and safe, it is also very ex-
pensive.
Anticholinergic drugs should not be given to dogs
with CPV enteritis because these drugs increase the po-
tential for gastric atony, ileus, and intussusception of an
irritated bowel segment.22 Dogs with intractable vomit-
ing should always be evaluated for foreign body ob-
struction or intussusception. Other causes of continued
vomiting include reflux esophagitis and acute pancre-
atitis. Reflux esophagitis may be manifested by signs of
drooling, nausea, and exaggerated swallowing motions.
Treatment involves administration of a systemic antacid
(famotidine [0.5 mg/kg] or ranitidine [5 mg/kg] intra-
venously every 12 hours) and an oral suspension of su-
cralfate (1 g dissolved in 10 ml warm water, every 8
hours). Ideally, the antacid should be administered 1 to
2 hours after the sucralfate.
Immunotherapy
Bacterial endotoxemia is believed to be an impor-
tant factor in the terminal acute shock that occurs in
dogs with severe CPV enteritis. A polyvalent equine-
origin antiserum against LPS endotoxin is available
for use in small animals (SEPTI-serum®—IMMVAC
Small Animal
Inc). In one study, the mortality rate for dogs with
CPV enteritis treated conventionally was 48% (10 of
21 dogs) compared with 17% (5 of 30 dogs) for dogs
that received antiendotoxin plus conventional treat-
ment.24 It is recommended that the product be ad-
ministered over 30 to 60 minutes at the dosage of 4.4
ml/kg and diluted 1:1 with intravenous crystalloid
fluids.25
Antiendotoxin should be most effective if it is ad-
ministered before antibiotic therapy because circulat-
ing plasma LPS concentrations can increase dramati-
cally after an antibiotic kills off gram-negative
bacteria.26 Patients receiving equine-origin antiserum
must be observed closely during administration for
signs of anaphylaxis. If a second administration of an-
tiserum is deemed necessary, it should be given within
5 to 7 days after the initial treatment. After that time,
a severe immunologic reaction is more likely to oc-
cur.27
Anecdotal reports describe the use of convalescent
serum (1.1 to 2.2 ml/kg intravenously or subcuta-
neously) collected from dogs that have recovered
from CPV infection in an effort to provide passive
immunity to exposed or infected dogs.2,28 Research is
needed to determine the efficacy and safety of this
practice.
Aggressive Adjunctive Treatments
Steroids and Flunixin Meglumine
Corticosteroids and flunixin meglumine have shown
beneficial effects in animal models of septic and endo-
toxic shock if administered early in the shock state.29
Potential beneficial effects of corticosteroids include
improved tissue perfusion, decreased leukocyte mar-
gination, enhanced membrane stabilization, and re-
duced absorption of endotoxins. Flunixin meglumine is
a potent nonsteroidal antiinflammatory analgesic that
has antidiarrheal and antipyretic effects and that may
reduce the severity of the intestinal inflammation asso-
ciated with CPV infection.
Corticosteroids and flunixin meglumine can cause se-
vere gastrointestinal ulceration.30 Because of this possi-
bility, we reserve use of these agents for animals exhibit-
ing early signs of sepsis or endotoxemia: fever,
tachycardia, injected or muddy mucous membranes,
and evidence of breakdown of the gastrointestinal mu-
cosal barrier. These agents should not be administered
until after the initial fluid bolus has been given. In se-
lect cases, we use either dexamethasone sodium phos-
phate (2 to 4 mg/kg intravenously) or flunixin meglu-
mine (1 mg/kg intravenously). Repeated doses are not
recommended because they increase the likelihood of
side effects.
ANTIENDOTOXIN ■ STEROIDS ■ FLUNIXIN MEGLUMINE ■ PPN
The Compendium March 1997
Recombinant Granulocyte
Colony-Stimulating Factor
Recently, the use of recombinant granulocyte colony-
stimulating factor (rG-CSF) in dogs with leukopenia
secondary to CPV enteritis has been described.31 The
recommended dose is 5 to 10 µg/kg per day subcuta-
neously. Animals that respond generally show an in-
crease in white blood cell count within 24 hours. Un-
fortunately, preliminary findings do not show an
increased survivability associated with use of this prod-
uct,32 and it is very expensive (approximately $130 to
$150 to treat a puppy).
Eradication of Intestinal Parasites
Intestinal parasites can exacerbate CPV enteritis by
enhancing intestinal cell turnover and subsequent viral
replication.2 Fecal samples should be evaluated to iden-
tify coccidia, Giardia species, hookworms, round-
worms, or whipworms. Appropriate oral therapy can be
initiated as soon as vomiting ceases, or ivermectin (250
µg/kg subcutaneously) can be given–except to collies
and related breeds.
Nutrition
Dogs with severe CPV enteritis may have a pro-
longed course of hospitalization and may require nutri-
tional support to prevent catabolism and immune dys-
function associated with negative nitrogen balance.
Partial parenteral nutrition (PPN) does not supply all
of the patient’s nutrient needs but can provide short-
term support for animals that are expected to recover
soon. PPN solutions can be delivered through a periph-
eral vein rather than through a large central vein.33
These solutions are usually given at a maintenance dose
(60 ml/kg/day); additional fluid needs are met with
crystalloid solutions. A commercial product that con-
tains 3% amino acids, 3% glycerol, and electrolytes can
be used. A PPN solution can be made by adding 300
ml of 8.5% amino acid solution to 700 ml of lactated
Ringer’s solution with 5% dextrose. The addition of
lipid emulsions is controversial. Although lipids are rich
in calories, they have been associated with immunosup-
pression through impairment of reticuloendothelial
function and white blood cell phagocytosis.34
Partial parenteral nutrition solutions are hypertonic
and therefore often cause phlebitis near the catheter
site. Catheters must be placed aseptically and the site
monitored carefully for redness, swelling, or pain.35
Dextrose solutions should be tapered off gradually to
prevent rebound hypoglycemia.
Most practitioners offer water after vomiting has
ceased for 12 to 24 hours. Early enteral nutrition is im-
portant to promote intestinal regeneration. A liquid
Small Animal
diet can be offered initially, or a gruel can be made with
an easily digestible, high-carbohydrate, low-fat diet.
The addition of glutamine powder (0.5 g/kg/day in
two divided doses) to drinking water has been recom-
mended to promote gastrointestinal healing in dogs re-
covering from CPV enteritis.36
Various commercial diets are formulated for animals
that are recovering from gastrointestinal illness. Intesti-
nal malabsorption and protein-losing enteropathy may
persist until the intestinal villi are repaired. Initial
feeding should consist of small amounts of an easily
digestible diet fed frequently. The normal diet is grad-
ually reintroduced after appetite and stool have re-
turned to normal. After recovery, immunity to par-
vovirus infection lasts at least 2 years and may even be
lifelong.
About the Authors
Drs. Macintire and Smith-Carr are affiliated with the
Department of Small Animal Surgery and Medicine, Col-
lege of Veterinary Medicine, Auburn University, Alabama.
Dr. Macintire is a Diplomate of the American College of
Veterinary Internal Medicine and the American College of
Veterinary Emergency and Critical Care.
REFERENCES
1. Pollack RVH, Coyne MJ: Canine parvovirus. Vet Clin North
Am Small Anim Pract 23:555–568, 1993.
2. Brunner CJ, Swango LJ: Canine parvovirus infection: Effects
on the immune system and factors that predispose to severe
disease. Compend Contin Educ Pract Vet 7(12):979–989,
1985.
3. Wessels BC, Gaffin SL: Anti-endotoxin immunotherapy for
canine parvovirus endotoxaemia. J Small Anim Pract 27:
609–615, 1986.
4. Fein AM, Lippmann M, Holtzman H, et al. The risk fac-
tors, incidence, and prognosis of ARDS following sep-
ticemia. Chest 83:40–42, 1983.
5. Turk J, Miller M, Brown T, et al: Coliform septicemia and
pulmonary disease associated with canine parvoviral enteri-
tis: 88 cases (1987–1988). JAVMA 196:771–773, 1990.
6. Turk J, Fales W, Miller M, et al: Enteric Clostridium perfrin-
gens infection associated with parvoviral enteritis in dogs: 74
cases (1987–1990). JAVMA 200:991–994, 1992.
7. Sandstedt K, Wienup M: Concomitant occurrence of
Campylobacter and parvoviruses in dogs with gastroenteritis.
Vet Res Comm 4:271–273, 1981.
8. Macartney L, McCandlish IAP, Thompson H, Cornwell
HJC: Canine parvovirus enteritis 1: Clinical, hematological
and pathological features of experimental infection. Vet Rec
115:201–210, 1984.
9. Mochizuki M, San Gabriel MC, Nakatani H, et al: Compar-
ison of polymerase chain reaction with virus isolation and
hemagglutination assays for the detection of canine par-
voviruses in faecal specimens. Res Vet Sci 55:60–63, 1993.
10. Hirasawa T, Kaneshige T, Mikazuki K: Sensitive detection
The Compendium March 1997
of canine parvovirus DNA by the nested polymerase chain
reaction. Vet Microbiol 41:135–145, 1994.
11. Schunk B, Kraft W, Truyen U: A simple touch-down poly-
merase chain reaction for the detection of canine parvovirus
and feline panleukopenia in feces. J Virol Methods 55:427–
433, 1995.
12. Senda M, Parrish CR, Harasawa R, Gamoh K: Detection by
PCR of wild type canine parvovirus which contaminates dog
vaccines. J Clin Microbiol 33:110–113, 1995.
13. DiBartola SP, Autran de Morais HS: Disorders of potassi-
um: Hypokalemia and hyperkalemia, in DiBartola SP (ed):
Fluid Therapy in Small Animal Practice. Philadelphia, WB
Saunders Co, 1992, pp 89–115.
14. Navar PD, Navar LG: Relationship between colloid osmotic
pressure and protein concentration in the dog. Am J Physiol
233: H295–H298, 1977.
15. Kirby R: Synthetic colloids. Proc 5th Int Vet Emerg Crit Care
Symp:159–163, 1996.
16. Kreeger TJ, Jeraj KP, Manning PJ: Bacteremia concomitant
with canine parvovirus infection in a pup. JAVMA 184:195–
197, 1984.
17. Weeran FR, Muir WW: Clinical aspects of septic shock and
comprehensive approaches to treatment in dogs and cats.
JAVMA 200:1859–1866, 1992.
18. Brown SA, Barsanti SA: Gentamicin nephrotoxicosis in the
dog, in Kirk RW (ed): Current Veterinary Therapy. IX.
Philadelphia, WB Saunders Co, 1986, pp 1146–1149.
19. Munckhof WJ, Grayson ML, Turnidge JD: A meta-analysis
on the safety and efficacy of aminoglycosides given either
once daily or as divided doses. J Antimicrob Chemother
37:645–663, 1996.
20. Boothe DM: Antibiotics in critical care. Proc 5th Int Vet
Emerg Crit Care Symp:330–337, 1996.
21. Alibibi R, McCallum RW: Metoclopramide: Pharmacology
and clinical application. Ann Intern Med 98:86–95, 1982.
22. DeNovo RC Jr: Therapeutics of gastrointestinal diseases, in
Kirk RW (ed): Current Veterinary Therapy. IX. Philadelphia,
WB Saunders Co, 1986, pp 862–872.
23. Cubeddu LX, Hoffman IS, Fuenmayor NT, Finn AL: Effi-
cacy of ondansetron and the role of serotonin in cisplatin-in-
duced nausea and vomiting. N Engl J Med 322:810-816,
1990.
24. Dimmitt R: Clinical experience with cross-protective antien-
dotoxin antiserum in dogs with parvoviral enteritis. Canine
Pract 16:23–26, 1991.
25. Abood S, Dunn T, Hoskins J, et al: Clinical management of
canine parvovirus, part 2. Canine Pract 20:11–16, 1995.
26. Sheneb JL, Morgan KA: Kinetics of endotoxin release during
antibiotic therapy for experimental gram negative sepsis. J
Infect Dis 150:380–387, 1984.
27. SEPTI-serum Fact Sheet, IMMVAC, Inc., Columbia,
MO, 1996.
28. Pollock RVH, Carmichael LE: Maternally derived immunity
to canine parvovirus infection: Transfer, decline, and inter-
ference with vaccination. JAVMA 180: 37–42, 1982.
29. Hardie EM: Sepsis versus septic shock, in Murtaugh RJ, Ka-
plan PM (eds): Veterinary Emergency and Critical Care
Medicine. St Louis, Mosby Year Book, 1992, pp 176–193.
30. Dow SW, Rosychuk RAW, McChesney AE: Effects of flu-
nixin plus prednisone on the gastrointestinal tract of dogs.
Am J Vet Res 51:1131–1138, 1990.
31. Fox LM, Bruederle JB: (Nearly) Foolproof parvovirus treat-
ment. Vet Forum:36–38, 1996.
32. Rewerts JM, Harrington DP, et al: Effect of rhG-CSF ad-
Small Animal
ministration on the clinical outcome of neutropenic, par-
vovirus-infected puppies. Proc 14th Annu ACVIM Vet
Forum:760, 1996.
33. Lippert AC: The metabolic response to injury: Enteral and
parenteral nutritional support, in Murtaugh RJ, Kaplan PM
(eds): Veterinary Emergency and Critical Care Medicine. St
Louis, Mosby Year Book, 1992, pp 593–617.
34. Moore FA, Feliciano DV, Andrassy RJ, et al: Early enteral
The Compendium March 1997
feeding, compared with parenteral, reduces postoperative
septic complications: The results of a meta-analysis. Ann
Surg 216:172–183, 1992.
35. Lippert AC, Armstrong PJ: Parenteral nutritional support, in
Kirk RW (ed): Current Veterinary Therapy. X. Philadelphia,
WB Saunders Co, 1989, pp 26–30.
36. Abood S, Dunn T, Hoskins J: Clinical management of ca-
nine parvovirus, Part 3. Canine Pract 21:20–26, 1996.